FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Hambright, D
Park, KY
Brooks, M
McKay, R
Swaroop, A
Nasonkin, IO
AF Hambright, Dustin
Park, Kye-Yoon
Brooks, Matthew
McKay, Ron
Swaroop, Anand
Nasonkin, Igor O.
TI Long-term survival and differentiation of retinal neurons derived from
human embryonic stem cell lines in un-immunosuppressed mouse retina
SO MOLECULAR VISION
LA English
DT Article
ID HUMAN NEURAL PROGENITORS; NEUROTROPHIC FACTOR; PHOTORECEPTOR
DEGENERATION; SUBRETINAL SPACE; PARKINSONS-DISEASE; CHONDROITINASE ABC;
PRECURSOR CELLS; GROWTH-FACTORS; HOST RETINA; RAT MODEL
AB Purpose: To examine the potential of NIH-maintained human embryonic stem cell (hESC) lines TE03 and UC06 to differentiate into retinal progenitor cells (hESC-RPCs) using the noggin/Dkk-1/IGF-1/FGF9 protocol. An additional goal is to examine the in vivo dynamics of maturation and retinal integration of subretinal and epiretinal (vitreous space) hESC-RPC grafts without immunosuppression.
Methods: hESCs were neuralized in vitro with noggin for 2 weeks and expanded to derive neuroepithelial cells (hESC-neural precursors, NPs). Wnt (Integration 1 and wingless) blocking morphogens Dickkopf-1 (Dkk-1) and Insulin-like growth factor 1 (IGF-1) were used to direct NPs to a rostral neural fate, and fibroblast growth factor 9 (FGF9)/fibroblast growth factor-basic (bFGF) were added to bias the differentiation of developing anterior neuroectoderm cells to neural retina (NR) rather than retinal pigment epithelium (RPE). Cells were dissociated and grafted into the subretinal and epiretinal space of young adult (4-6-week-old) mice (C57BL/6J x129/Sv mixed background). Remaining cells were replated for (i) immunocytochemical analysis and (ii) used for quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis. Mice were sacrificed 3 weeks or 3 months after grafting, and the grafts were examined by histology and immunohistochemistry for survival of hESC-RPCs, presence of mature neuronal and retinal markers, and the dynamics of in vivo maturation and integration into the host retina.
Results: At the time of grafting, hESC-RPCs exhibited immature neural/neuronal immunophenotypes represented by nestin and neuronal class III beta-tubulin, with about half of the cells positive for cell proliferation marker Kiel University raised antibody number 67 (Ki67), and no recoverin-positive (recoverin [+]) cells. The grafted cells expressed eye field markers paired box 6 (PAX6), retina and anterior neural fold homeobox (RAX), sine oculis homeobox homolog 6 (SIX6), LIM homeobox 2 (LHX2), early NR markers (Ceh-10 homeodomain containing homolog [CHX10], achaete-scute complex homolog 1 [MASH1], mouse atonal homolog 5 [MATH5], neurogenic differentiation 1 [NEUROD1]), and some retinal cell fate markers (brain-specific homeobox/POU domain transcription factor 3B [BRN3B], prospero homeobox 1 [PROX1], and recoverin). The cells in the subretinal grafts matured to predominantly recoverin [+] phenotype by 3 months and survived in a xenogenic environment without immunosuppression as long as the blood-retinal barrier was not breached by the transplantation procedure. The epiretinal grafts survived but did not express markers of mature retinal cells. Retinal integration into the retinal ganglion cell (RGC) layer and the inner nuclear layer (INL) was efficient from the epiretinal but not subretinal grafts. The subretinal grafts showed limited ability to structurally integrate into the host retina and only in cases when NR was damaged during grafting. Only limited synaptogenesis and no tumorigenicity was observed in grafts.
Conclusions: Our studies show that (i) immunosuppression is not mandatory to xenogenic graft survival in the retina, (ii) the subretinal but not the epiretinal niche can promote maturation of hESC-RPCs to photoreceptors, and (iii) the hESC-RPCs from epiretinal but not subretinal grafts can efficiently integrate into the RGC layer and INL. The latter could be of value for long-lasting neuroprotection of retina in some degenerative conditions and glaucoma. Overall, our results provide new insights into the technical aspects associated with cell-based therapy in the retina.
C1 [Hambright, Dustin; Brooks, Matthew; Swaroop, Anand; Nasonkin, Igor O.] NEI, N NRL, NIH, Bethesda, MD 20892 USA.
[Park, Kye-Yoon; McKay, Ron] Natl Inst Neurol Disorders & Stroke, Mol Biol Lab, NIH, Bethesda, MD USA.
[Park, Kye-Yoon; McKay, Ron] Natl Inst Neurol Disorders & Stroke, NIH Stem Cell Unit, NIH, Bethesda, MD USA.
RP Nasonkin, IO (reprint author), NEI, N NRL, NIH, 6 Ctr Dr,MSC0610,Bldg 6,Room 341, Bethesda, MD 20892 USA.
EM nasonkini@mail.nih.gov
OI Swaroop, Anand/0000-0002-1975-1141
FU National Eye Institute (NEI); National Institute of Neurologic Disorders
and Stroke (NINDS)
FX This research was supported by intramural programs of the National Eye
Institute (NEI) and National Institute of Neurologic Disorders and
Stroke (NINDS). We are grateful to Dr. Ginger Tansey (NEI) for help with
experimental animals, Dr. Robert Fariss for help with confocal
microscopy and Dr. Jacob Nellissery for help with selecting the
antibodies. We thank the members of N-NRL laboratory for discussion of
our results, and especially Dr. James Friedman for carefully reading the
manuscript.
NR 78
TC 37
Z9 39
U1 0
U2 9
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD APR 12
PY 2012
VL 18
IS 96-97
BP 920
EP 936
PG 17
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 947NJ
UT WOS:000304436400001
PM 22539871
ER
PT J
AU Lickwar, CR
Mueller, F
Hanlon, SE
McNally, JG
Lieb, JD
AF Lickwar, Colin R.
Mueller, Florian
Hanlon, Sean E.
McNally, James G.
Lieb, Jason D.
TI Genome-wide protein-DNA binding dynamics suggest a molecular clutch for
transcription factor function
SO NATURE
LA English
DT Article
ID GLUCOCORTICOID-RECEPTOR; EUKARYOTIC GENOME; BUDDING YEAST; LIVING CELLS;
CHROMATIN; PROMOTER; EQUILIBRIUM; MECHANISM; EXCHANGE; SITES
AB Dynamic access to genetic information is central to organismal development and environmental response. Consequently, genomic processes must be regulated by mechanisms that alter genome function relatively rapidly(1-4). Conventional chromatin immunoprecipitation (ChIP) experiments measure transcription factor occupancy(5), but give no indication of kinetics and are poor predictors of transcription factor function at a given locus. To measure transcription-factor-binding dynamics across the genome, we performed competition ChIP (refs 6, 7) with a sequence-specific Saccharomyces cerevisiae transcription factor, Rap1 (ref. 8). Rap1-binding dynamics and Rap1 occupancy were only weakly correlated (R-2 = 0.14), but binding dynamics were more strongly linked to function than occupancy. Long Rap1 residence was coupled to transcriptional activation, whereas fast binding turnover, which we refer to as 'treadmilling', was linked to low transcriptional output. Thus, DNA-binding events that seem identical by conventional ChIP may have different underlying modes of interaction that lead to opposing functional outcomes. We propose that transcription factor binding turnover is a major point of regulation in determining the functional consequences of transcription factor binding, and is mediated mainly by control of competition between transcription factors and nucleosomes. Our model predicts a clutch-like mechanism that rapidly engages a treadmilling transcription factor into a stable binding state, or vice versa, to modulate transcription factor function.
C1 [Lickwar, Colin R.; Hanlon, Sean E.; Lieb, Jason D.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Curriculum Genet & Mol Biol, Dept Biol,Carolina Ctr Genome Sci, Chapel Hill, NC 27599 USA.
[Mueller, Florian; McNally, James G.] NCI, LRBGE, NIH, Bethesda, MD 20892 USA.
[Mueller, Florian] Ctr Natl Rech Sci, Inst Pasteur, Grp Imagerie & Modelisat, Unite Rech Associee 2582, F-75015 Paris, France.
RP Lieb, JD (reprint author), Univ N Carolina, Lineberger Comprehens Canc Ctr, Curriculum Genet & Mol Biol, Dept Biol,Carolina Ctr Genome Sci, CB 3280,408 Fordham Hall, Chapel Hill, NC 27599 USA.
EM jlieb@bio.unc.edu
RI Mueller, Florian/C-9075-2012
OI Mueller, Florian/0000-0002-9622-4396
FU US National Institutes of Health (NIH) [R01-GM072518]; NIH, National
Cancer Institute, Center for Cancer Research; Region Ile-de-France in
the framework of C'Nano IdF, the nanoscience competence center of Paris
Region
FX We thank T. Kaplan and O. Rando for help with their turnover model, T.
Palpant and S. Adar for help with time course experiments, and A.
Leonardo Iniguez and H. Rosenbaum of Roche Nimblegen for pre-release
custom HD4 12-plex microarrays. This work was supported by the US
National Institutes of Health (NIH) Grant R01-GM072518 (to J.D.L.), and
the intramural program of the NIH, National Cancer Institute, Center for
Cancer Research (to J.G.M. and F.M.). F.M. was also supported in part by
the Region Ile-de-France in the framework of C'Nano IdF, the nanoscience
competence center of Paris Region.
NR 38
TC 105
Z9 107
U1 1
U2 34
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD APR 12
PY 2012
VL 484
IS 7393
BP 251
EP U141
DI 10.1038/nature10985
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 930OV
UT WOS:000303149900037
PM 22498630
ER
PT J
AU Ishaq, M
Lin, BR
Bosche, M
Zheng, X
Yang, J
Huang, DW
Lempicki, RA
Aguilera-Gutierrez, A
Natarajan, V
AF Ishaq, Mohammad
Lin, Bor-Ruei
Bosche, Marjorie
Zheng, Xin
Yang, Jun
Huang, Dawei
Lempicki, Richard A.
Aguilera-Gutierrez, Angelica
Natarajan, Ven
TI LIM kinase 1 - dependent cofilin 1 pathway and actin dynamics mediate
nuclear retinoid receptor function in T lymphocytes (vol 12, 41, 2011)
SO BMC MOLECULAR BIOLOGY
LA English
DT Correction
C1 [Ishaq, Mohammad; Lin, Bor-Ruei; Aguilera-Gutierrez, Angelica; Natarajan, Ven] NCI, Mol Cell Biol Lab, SAIC Frederick, Frederick, MD 21702 USA.
[Bosche, Marjorie; Zheng, Xin; Yang, Jun; Huang, Dawei; Lempicki, Richard A.] NCI, Lab Immunopathogenesis & Bioinformat, SAIC Frederick, Frederick, MD 21702 USA.
RP Ishaq, M (reprint author), NCI, Mol Cell Biol Lab, SAIC Frederick, Frederick, MD 21702 USA.
EM mishaq@mail.nih.gov
RI Lempicki, Richard/E-1844-2012
OI Lempicki, Richard/0000-0002-7059-409X
NR 1
TC 0
Z9 0
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2199
J9 BMC MOL BIOL
JI BMC Mol. Biol.
PD APR 12
PY 2012
VL 13
AR 14
DI 10.1186/1471-2199-13-14
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 939NK
UT WOS:000303818100001
ER
PT J
AU Abdollahpour, H
Appaswamy, G
Kotlarz, D
Diestelhorst, J
Beier, R
Schaffer, AA
Gertz, EM
Schambach, A
Kreipe, HH
Pfeifer, D
Engelhardt, KR
Rezaei, N
Grimbacher, B
Lohrmann, S
Sherkat, R
Klein, C
AF Abdollahpour, Hengameh
Appaswamy, Giridharan
Kotlarz, Daniel
Diestelhorst, Jana
Beier, Rita
Schaeffer, Alejandro A.
Gertz, E. Michael
Schambach, Axel
Kreipe, Hans H.
Pfeifer, Dietmar
Engelhardt, Karin R.
Rezaei, Nima
Grimbacher, Bodo
Lohrmann, Sabine
Sherkat, Roya
Klein, Christoph
TI The phenotype of human STK4 deficiency
SO BLOOD
LA English
DT Article
ID ORGAN SIZE CONTROL; CONGENITAL NEUTROPENIA; OXIDATIVE-STRESS; CASPASE
CLEAVAGE; KINASE MST1; APOPTOSIS; PHOSPHORYLATION; ACTIVATION;
MUTATIONS; PATHWAY
AB We describe a novel clinical phenotype associating T- and B-cell lymphopenia, intermittent neutropenia, and atrial septal defects in 3 members of a consanguineous kindred. Their clinical histories included recurrent bacterial infections, viral infections, mucocutaneous candidiasis, cutaneous warts, and skin abscesses. Homozygosity mapping and candidate gene sequencing revealed a homozygous premature termination mutation in the gene STK4 (serine threonine kinase 4, formerly having the symbol MST1). STK4 is the human ortholog of Drosophila Hippo, the central constituent of a highly conserved pathway controlling cell growth and apoptosis. STK4-deficient lymphocytes and neutrophils exhibit enhanced loss of mitochondrial membrane potential and increased susceptibility to apoptosis. STK4 deficiency is a novel human primary immunodeficiency syndrome. (Blood. 2012; 119(15):3450-3457)
C1 [Kotlarz, Daniel; Diestelhorst, Jana; Klein, Christoph] Dr von Haunersches Kinderspital, Univ Childrens Hosp Munich, D-80337 Munich, Germany.
[Abdollahpour, Hengameh; Appaswamy, Giridharan; Kotlarz, Daniel; Diestelhorst, Jana; Beier, Rita; Klein, Christoph] Hannover Med Sch, Dept Pediat Hematol Oncol, D-3000 Hannover, Germany.
[Schaeffer, Alejandro A.; Gertz, E. Michael] NIH, Natl Ctr Biotechnol Informat, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Schambach, Axel] Hannover Med Sch, Dept Expt Hematol, D-3000 Hannover, Germany.
[Kreipe, Hans H.] Hannover Med Sch, Inst Pathol, D-3000 Hannover, Germany.
[Pfeifer, Dietmar] Univ Freiburg, Med Ctr, Dept Hematol Oncol, Core Facil Genom 2, Freiburg, Germany.
[Engelhardt, Karin R.; Grimbacher, Bodo] Royal Free Hosp, Dept Immunol & Mol Pathol, London NW3 2QG, England.
[Engelhardt, Karin R.; Grimbacher, Bodo] UCL, London, England.
[Rezaei, Nima] Univ Tehran Med Sci, Childrens Med Ctr, Pediat Ctr Excellence, Res Ctr Immunodeficiencies, Tehran, Iran.
[Lohrmann, Sabine] Hannover Med Sch, Dept Pediat Cardiol, D-3000 Hannover, Germany.
[Sherkat, Roya] Isfahan Univ Med Sci, Dept Infect Dis, Infect Dis Res Ctr, Esfahan, Iran.
RP Klein, C (reprint author), Dr von Haunersches Kinderspital, Univ Childrens Hosp Munich, Lindwurmstr 4, D-80337 Munich, Germany.
EM christoph.klein@med.uni-muenchen.de
RI Schaffer, Alejandro/F-2902-2012; Rezaei, Nima/B-4245-2008;
OI Rezaei, Nima/0000-0002-3836-1827; Gertz, E. Michael/0000-0001-8390-4387
FU Deutsche Forschungsgemeinschaft [SFB900, KFO250]; Care-for-Rare
Foundation; Deutsche Jose Carreras Leukamie-Stiftung; European Union
commission [MEXT-CT-2006-042316, FP7/2007-2013]; EURO-PADnet
[HEALTH-F2-2008-201549]; National Institutes of Health, National Library
of Medicine
FX This work was supported by the Deutsche Forschungsgemeinschaft (SFB900,
KFO250, and Gottfried-Wilhelm-Leibniz program), the Care-for-Rare
Foundation, the Deutsche Jose Carreras Leukamie-Stiftung, the European
Union commission Marie-Curie (grants MEXT-CT-2006-042316 and
FP7/2007-2013), EURO-PADnet (grant HEALTH-F2-2008-201549), and in part
by the Intramural Research Program of the National Institutes of Health,
National Library of Medicine. H. A. is a graduated member of the
international MD-PhD program at Hannover Medical School.
NR 39
TC 95
Z9 98
U1 1
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 APR 12
PY 2012
VL 119
IS 15
BP 3450
EP 3457
DI 10.1182/blood-2011-09-378158
PG 8
WC Hematology
SC Hematology
GA 927OK
UT WOS:000302917200017
PM 22294732
ER
PT J
AU Walz, C
Ahmed, W
Lazarides, K
Betancur, M
Patel, N
Hennighausen, L
Zaleskas, VM
Van Etten, RA
AF Walz, Christoph
Ahmed, Wesam
Lazarides, Katherine
Betancur, Monica
Patel, Nihal
Hennighausen, Lothar
Zaleskas, Virginia M.
Van Etten, Richard A.
TI Essential role for Stat5a/b in myeloproliferative neoplasms induced by
BCR-ABL1 and JAK2(V617F) in mice
SO BLOOD
LA English
DT Article
ID CHRONIC MYELOID-LEUKEMIA; DNA-BINDING ACTIVITY; BONE-MARROW; BCR-ABL;
LYMPHOBLASTIC-LEUKEMIA; INDUCED TRANSFORMATION; LYMPHOID DEVELOPMENT;
EFFICIENT INDUCTION; GENE-EXPRESSION; STEM-CELLS
AB STAT5 proteins are constitutively activated in malignant cells from many patients with leukemia, including the myeloproliferative neoplasms (MPNs) chronic myeloid leukemia (CML) and polycythemia vera (PV), but whether STAT5 is essential for the pathogenesis of these diseases is not known. In the present study, we used mice with a conditional null mutation in the Stat5a/b gene locus to determine the requirement for STAT5 in MPNs induced by BCR-ABL1 and JAK2(V617F) in retroviral transplantation models of CML and PV. Loss of one Stat5a/b allele resulted in a decrease in BCR-ABL1-induced CML-like MPN and the appearance of B-cell acute lymphoblastic leukemia, whereas complete deletion of Stat5a/b prevented the development of leukemia in primary recipients. However, BCR-ABL1 was expressed and active in Stat5-null leukemic stem cells, and Stat5 deletion did not prevent progression to lymphoid blast crisis or abolish established B-cell acute lymphoblastic leukemia. JAK2(V617F) failed to induce polycythemia in recipients after deletion of Stat5a/b, although the loss of STAT5 did not prevent the development of myelofibrosis. These results demonstrate that STAT5a/b is essential for the induction of CML-like leukemia by BCR-ABL1 and of polycythemia by JAK2(V617F), and validate STAT5a/b and the genes they regulate as targets for therapy in these MPNs. (Blood. 2012;119(15):3550-3560)
C1 [Walz, Christoph; Ahmed, Wesam; Lazarides, Katherine; Betancur, Monica; Patel, Nihal; Zaleskas, Virginia M.; Van Etten, Richard A.] Tufts Med Ctr, Mol Oncol Res Inst, Boston, MA 02111 USA.
[Ahmed, Wesam; Zaleskas, Virginia M.; Van Etten, Richard A.] Tufts Med Ctr, Div Hematol Oncol, Boston, MA 02111 USA.
[Hennighausen, Lothar] NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD USA.
RP Van Etten, RA (reprint author), Tufts Med Ctr, Mol Oncol Res Inst, 800 Washington St,Box 5609, Boston, MA 02111 USA.
EM rvanetten@tuftsmedicalcenter.org
FU National Institutes of Health [CA090576, HL089747, T32 CA09429]; German
Research Foundation Deutsche Forschungsgemeinschaft
FX This work was supported by the National Institutes of Health (grants
CA090576 and HL089747 to R. A. V. and grant T32 CA09429 to W.A.) and the
German Research Foundation Deutsche Forschungsgemeinschaft (to C.W.).
NR 47
TC 62
Z9 65
U1 0
U2 0
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 APR 12
PY 2012
VL 119
IS 15
BP 3550
EP 3560
DI 10.1182/blood-2011-12-397554
PG 11
WC Hematology
SC Hematology
GA 927OK
UT WOS:000302917200027
PM 22234689
ER
PT J
AU Sheng, JS
Wu, LG
AF Sheng, Jiansong
Wu, Ling-Gang
TI Cysteine String Protein alpha: A New Role in Vesicle Recycling
SO NEURON
LA English
DT Editorial Material
ID CSP-ALPHA; ENDOCYTOSIS; MECHANISMS; SNAP-25; SYNAPSE
AB Zhang et al. (2012) and Rozas et al. (2012) in this issue of Neuron find that cysteine string protein a, a protein involved in neurodegeneration, regulates vesicle endocytosis via interaction with dynamin 1, which may participate in regulating synaptic transmission and possibly in maintaining synapses.
C1 [Sheng, Jiansong; Wu, Ling-Gang] Natl Inst Neurol Disorders & Stroke, Synapt Transmiss Sect, Bethesda, MD 20892 USA.
RP Wu, LG (reprint author), Natl Inst Neurol Disorders & Stroke, Synapt Transmiss Sect, 35 Convent Dr,Bldg 35,Rm 2B-1012, Bethesda, MD 20892 USA.
EM wul@ninds.nih.gov
RI SHENG, JIANSONG/K-1914-2013
FU Intramural NIH HHS [ZIA NS003009-08]
NR 15
TC 2
Z9 2
U1 1
U2 4
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 APR 12
PY 2012
VL 74
IS 1
BP 6
EP 8
DI 10.1016/j.neuron.2012.03.013
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA 927FZ
UT WOS:000302893800003
PM 22500624
ER
PT J
AU Dong, ZQ
Yang, N
Yeo, SY
Chitnis, A
Guo, S
AF Dong, Zhiqiang
Yang, Nan
Yeo, Sang-Yeob
Chitnis, Ajay
Guo, Su
TI Intralineage Directional Notch Signaling Regulates Self-Renewal and
Differentiation of Asymmetrically Dividing Radial Glia
SO NEURON
LA English
DT Article
ID NEURAL STEM-CELLS; C-ELEGANS EMBRYOS; NERVOUS-SYSTEM; NEUROEPITHELIAL
CELLS; MIND BOMB; INTERMEDIATE PROGENITORS; RETINAL DEVELOPMENT; NUCLEAR
MIGRATION; CORTICAL-NEURONS; IN-VIVO
AB Asymmetric division of progenitor/stem cells generates both self-renewing and differentiating progeny and is fundamental to development and regeneration. How this process is regulated in the vertebrate brain remains incompletely understood. Here, we use time-lapse imaging to track radial glia progenitor behavior in the developing zebrafish brain. We find that asymmetric division invariably generates a basal self-renewing daughter and an apical differentiating sibling. Gene expression and genetic mosaic analysis further show that the apical daughter is the source of Notch ligand that is essential to maintain higher Notch activity in the basal daughter. Notably, establishment of this intralineage and directional Notch signaling requires the intrinsic polarity regulator Partitioning defective protein-3 (Par-3), which segregates the fate determinant Mind bomb unequally to the apical daughter, thereby restricting the self-renewal potential to the basal daughter. These findings reveal with single-cell resolution how self-renewal and differentiation become precisely segregated within asymmetrically dividing neural progenitor/stem lineages.
C1 [Dong, Zhiqiang; Yang, Nan; Guo, Su] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, Program Human Genet, San Francisco, CA 94143 USA.
[Dong, Zhiqiang; Yang, Nan; Guo, Su] Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, Program Biol Sci, San Francisco, CA 94143 USA.
[Yeo, Sang-Yeob; Chitnis, Ajay] NICHHD, Sect Neural Dev Dynam, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
RP Guo, S (reprint author), Univ Calif San Francisco, Dept Bioengn & Therapeut Sci, Program Human Genet, San Francisco, CA 94143 USA.
EM su.guo@ucsf.edu
RI Yang, Nan/H-3174-2012
FU NIH [NS042626]
FX We thank Dr. J. Lewis for zebrafish Dla and Did antibodies, Drs. P. Soba
and Y.N. Jan for the UAS-TdTomato plasmids, Drs. A. Kriegstein, J.
Rubenstein, and S. Wilson and the S.G. lab members for discussions; Dr.
B. Lu and S.G. lab members for critically reading the manuscript; Dr. K.
Thorn and the UCSF Nikon imaging center for assistance with confocal
microscopy; and M. Munchua for fish husbandry. This work was supported
by the NIH Grant NS042626. S.G. was a Searle Scholar and a Science and
Engineering Fellow of the David and Lucile Packard foundation.
NR 74
TC 48
Z9 50
U1 1
U2 16
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD APR 12
PY 2012
VL 74
IS 1
BP 65
EP 78
DI 10.1016/j.neuron.2012.01.031
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA 927FZ
UT WOS:000302893800010
PM 22500631
ER
PT J
AU Rai, G
Vyjayanti, VN
Dorjsuren, D
Simeonov, A
Jadhav, A
Wilson, DM
Maloney, DJ
AF Rai, Ganesha
Vyjayanti, Vaddadi N.
Dorjsuren, Dorjbal
Simeonov, Anton
Jadhav, Ajit
Wilson, David M., III
Maloney, David J.
TI Synthesis, Biological Evaluation, and Structure-Activity Relationships
of a Novel Class of Apurinic/Apyrimidinic Endonuclease 1 Inhibitors
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID BASE EXCISION-REPAIR; HUMAN APURINIC ENDONUCLEASE; SMALL-MOLECULE
INHIBITOR; DNA-REPAIR; CANCER CELLS; BREAST-CANCER; MAJOR HUMAN; APE1;
PROTEIN; TEMOZOLOMIDE
AB APE1 is an essential protein that operates in the base excision repair (BER) pathway and is responsible for >= 95% of the total apurinic/apyrimidinic (AP) endonuclease activity in human cells. BER is a major pathway that copes with DNA damage induced by several anticancer agents, including ionizing radiation and temozolomide. Overexpression of APEI and enhanced AP endonuclease activity have been linked to increased resistance of tumor cells to treatment with monofunctional alkylators, implicating inhibition of APEI as a valid strategy for cancer therapy. We report herein the results of a focused medicinal chemistry effort around a novel APEI inhibitor, N-(3-(benzo[d]thiazol-2-yl)-6-isopropyl-4,5,6,7-tetrahydrothieno[2,3-c]pyridin-2-yl)acetamide (3). Compound 3 and related analogues exhibit single-digit micromolar activity against the purified APE1 enzyme and comparable activity in HeLa whole cell extract assays and potentiate the cytotoxicity of the alkylating agents methylmethane sulfonate and temozolomide. Moreover, this class of compounds possesses a generally favorable in vitro ADME profile, along with good exposure levels in plasma and brain following intraperitoneal dosing (30 mg/kg body weight) in mice.
C1 [Rai, Ganesha; Dorjsuren, Dorjbal; Simeonov, Anton; Jadhav, Ajit; Maloney, David J.] Natl Ctr Adv Translat Sci, NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
[Vyjayanti, Vaddadi N.; Wilson, David M., III] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Maloney, DJ (reprint author), Natl Ctr Adv Translat Sci, NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
EM wilsonda@mail.nih.gov; maloneyd@mail.nih.gov
FU NIH, National Institute on Aging; NIH [R03 MH086444-01]; Molecular
Libraries Initiative of the National Institutes of Health Roadmap for
Medical Research
FX The authors thank William Leister, Paul Shinn, Danielle Van Leer, James
Bougie, and Tom Daniel for assistance with compound management and
purification. We also thank Christina Greco for critical reading of the
manuscript and technical assistance. This research was supported by the
Intramural Research Program of the NIH, National Institute on Aging, as
well as by the NIH Grant R03 MH086444-01 (D.M.W.), and the Molecular
Libraries Initiative of the National Institutes of Health Roadmap for
Medical Research.
NR 34
TC 19
Z9 21
U1 0
U2 7
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD APR 12
PY 2012
VL 55
IS 7
BP 3101
EP 3112
DI 10.1021/jm201537d
PG 12
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 923AT
UT WOS:000302591100020
PM 22455312
ER
PT J
AU Rodrigues, J
Oliveira, GA
Kotsyfakis, M
Dixit, R
Molina-Cruz, A
Jochim, R
Barillas-Mury, C
AF Rodrigues, Janneth
Oliveira, Giselle A.
Kotsyfakis, Michalis
Dixit, Rajnikant
Molina-Cruz, Alvaro
Jochim, Ryan
Barillas-Mury, Carolina
TI An Epithelial Serine Protease, AgESP, Is Required for Plasmodium
Invasion in the Mosquito Anopheles gambiae
SO PLOS ONE
LA English
DT Article
ID TIME BOMB MODEL; OOKINETE INVASION; MIDGUT CELLS; MALARIA PARASITES;
SALIVARY-GLANDS; REAL-TIME; FALCIPARUM; STEPHENSI; VECTOR; SPOROZOITES
AB Background: Plasmodium parasites need to cross the midgut and salivary gland epithelia to complete their life cycle in the mosquito. However, our understanding of the molecular mechanism and the mosquito genes that participate in this process is still very limited.
Methodology/Principal Findings: We identified an Anopheles gambiae epithelial serine protease (AgESP) that is constitutively expressed in the submicrovillar region of mosquito midgut epithelial cells and in the basal side of the salivary glands that is critical for Plasmodium parasites to cross these two epithelial barriers. AgESP silencing greatly reduces Plasmodium berghei and Plasmodium falciparum midgut invasion and prevents the transcriptional activation of gelsolin, a key regulator of actin remodeling and a reported Plasmodium agonist. AgESP expression is highly induced in midgut cells invaded by Plasmodium, suggesting that this protease also participates in the apoptotic response to invasion. In salivary gland epithelial cells, AgESP is localized on the basal side-the surface with which sporozoites interact. AgESP expression in the salivary gland is also induced in response to P. berghei and P. falciparum sporozoite invasion, and AgESP silencing significantly reduces the number of sporozoites that invade this organ.
Conclusion: Our findings indicate that AgESP is required for Plasmodium parasites to effectively traverse the midgut and salivary gland epithelial barriers. Plasmodium parasites need to modify the actin cytoskeleton of mosquito epithelial cells to successfully complete their life cycle in the mosquito and AgESP appears to be a major player in the regulation of this process.
C1 [Rodrigues, Janneth; Oliveira, Giselle A.; Kotsyfakis, Michalis; Dixit, Rajnikant; Molina-Cruz, Alvaro; Jochim, Ryan; Barillas-Mury, Carolina] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
RP Rodrigues, J (reprint author), Univ Washington, Dept Chem, Seattle, WA 98195 USA.
EM cbarillas@niaid.nih.gov
RI Jochim, Ryan/C-6756-2013; Kotsyfakis, Michail/G-9525-2014;
OI Kotsyfakis, Michail/0000-0002-7526-1876; Oliveira,
Giselle/0000-0002-5898-7843; DIXIT, RAJNIKANT/0000-0002-3536-8329
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health. The funders had no
role in study design, data collection and analysis, decision to publish,
or preparation of the manuscript.
NR 29
TC 10
Z9 10
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 11
PY 2012
VL 7
IS 4
AR e35210
DI 10.1371/journal.pone.0035210
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 959TP
UT WOS:000305336600093
PM 22509400
ER
PT J
AU Xiong, W
Wu, XW
Lovinger, DM
Zhang, L
AF Xiong, Wei
Wu, Xiongwu
Lovinger, David M.
Zhang, Li
TI A Common Molecular Basis for Exogenous and Endogenous Cannabinoid
Potentiation of Glycine Receptors
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID SUBUNIT-SPECIFIC MODULATION; SWISS-MODEL; ALLOSTERIC MODULATION;
MEDIATED RESPONSES; 5-HT3A RECEPTORS; XENOPUS OOCYTES; KNOCKOUT MICE; SR
141716A; ANANDAMIDE; LIGANDS
AB Both exogenous and endogenous cannabinoids can allosterically modulate glycine receptors (GlyRs). However, little is known about the molecular basis of cannabinoid-GlyR interactions. Here we report that sustained incubation with the endocannabinoid anandamide (AEA) substantially increased the amplitude of glycine-activated current in both rat cultured spinal neurons and in HEK-293 cells expressing human alpha 1, rat alpha 2 and alpha 3 GlyRs. While the alpha 1 and alpha 3 subunits were highly sensitive to AEA-induced potentiation, the alpha 2 subunit was relatively insensitive to AEA. Switching a serine at 296 and 307 in the TM3 (transmembrane domain 3) of the alpha 1 and alpha 3 subunits with an alanine (A) at the equivalent position in the alpha 2 subunit converted the alpha 1/alpha 3 AEA-sensitive receptors to sensitivity resembling that of alpha 2. The S296 residue is also critical for exogenous cannabinoid-induced potentiation of I-Gly. The magnitude of AEA potentiation decreased with removal of either the hydroxyl or oxygen groups on AEA. While desoxy-AEA was significantly less efficacious in potentiating I-Gly, desoxy-AEA inhibited potentiation produced by both Delta(9)-tetrahydrocannabinol (THC), a major psychoactive component of marijuana, and AEA. Similarly, didesoxy-THC, a modified THC with removal of both hydroxyl/oxygen groups, did not affect I-Gly when applied alone but inhibited the potentiation of I-Gly induced by AEA and THC. These findings suggest that exogenous and endogenous cannabinoids potentiate GlyRs via a hydrogen bonding-like interaction. Such a specific interaction likely stems from a common molecular basis involving the S296 residue in the TM3 of the alpha 1 and alpha 3 subunits.
C1 [Xiong, Wei; Lovinger, David M.; Zhang, Li] NIAAA, Lab Integrat Neurosci, NIH, Bethesda, MD 20892 USA.
[Wu, Xiongwu] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Zhang, L (reprint author), NIAAA, Lab Integrat Neurosci, NIH, 5625 Fishers Lane, Bethesda, MD 20892 USA.
EM lzhang@mail.nih.gov
FU National Institute on Alcohol Abuse and Alcoholism
FX This work was supported by funds from the intramural program of the
National Institute on Alcohol Abuse and Alcoholism. We thank Drs. Kejun
Cheng and Fuying Li for providing modified cannabinoids (didesoxy-THC,
desoxy-AEA, and dehydroxyl-AEA). We also thank Dr. Zhifeng Zhou for
technical assistance with DNA sequencing.
NR 50
TC 14
Z9 15
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 APR 11
PY 2012
VL 32
IS 15
BP 5200
EP 5208
DI 10.1523/JNEUROSCI.6347-11.2012
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 925WT
UT WOS:000302793500018
PM 22496565
ER
PT J
AU Tao, R
Li, C
Newburn, EN
Ye, TZ
Lipska, BK
Herman, MM
Weinberger, DR
Kleinman, JE
Hyde, TM
AF Tao, Ran
Li, Chao
Newburn, Erin N.
Ye, Tianzhang
Lipska, Barbara K.
Herman, Mary M.
Weinberger, Daniel R.
Kleinman, Joel E.
Hyde, Thomas M.
TI Transcript-Specific Associations of SLC12A5 (KCC2) in Human Prefrontal
Cortex with Development, Schizophrenia, and Affective Disorders
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID GLUTAMIC-ACID DECARBOXYLASE; CATION-CHLORIDE COTRANSPORTERS; BIPOLAR
DISORDER; GENE-EXPRESSION; GABA; NEURONS; GAD1; PATHOPHYSIOLOGY;
GAD(67); REELIN
AB The neuron-specific K+-Cl- cotransporter SLC12A5, also known as KCC2, helps mediate the electrophysiological effects of GABA. The pattern of KCC2 expression during early brain development suggests that its upregulation drives the postsynaptic switch of GABA from excitation to inhibition. We previously found decreased expression of full-length KCC2 in the postmortem hippocampus of patients with schizophrenia, but not in the dorsolateral prefrontal cortex (DLPFC). Using PCR and rapid amplification of cDNA ends, we discovered several previously unrecognized alternative KCC2 transcripts in both human adult and fetal brain in addition to the previously identified full-length (NM_020708.3) and truncated (AK098371) transcripts. We measured the expression levels of four relatively abundant truncated splice variants, including three novel transcripts (Delta EXON6, EXON2B, and EXON6B) and one previously described transcript (AK098371), in a large human cohort of nonpsychiatric controls across the lifespan, and in patients with schizophrenia and affective disorders. In SH-SY5Y cell lines, these transcripts were translated into proteins and expressed at their predicted sizes. Expression of the EXON6B transcript is increased in the DLPFC of patients with schizophrenia (p = 0.03) but decreased in patients with major depression (p = 0.04). The expression of AK098371 is associated with a GAD1 single nucleotide polymorphism (rs3749034) that previously has been associated with GAD67 expression and risk for schizophrenia. Our data confirm the developmental regulation of KCC2 expression, and provide evidence that KCC2 transcripts are differentially expressed in schizophrenia and affective disorders. Alternate transcripts from KCC2 may participate in the abnormal GABA signaling in the DLPFC associated with schizophrenia.
C1 [Tao, Ran; Li, Chao; Newburn, Erin N.; Ye, Tianzhang; Lipska, Barbara K.; Herman, Mary M.; Weinberger, Daniel R.; Kleinman, Joel E.; Hyde, Thomas M.] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
[Ye, Tianzhang; Weinberger, Daniel R.; Hyde, Thomas M.] Johns Hopkins Univ, Med Ctr, Lieber Inst Brain Dev, Baltimore, MD 21205 USA.
RP Hyde, TM (reprint author), NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Intramural Res Program,NIH, 10 Ctr Dr,Room 4N312, Bethesda, MD 20892 USA.
EM hydet@mail.nih.gov
RI Tao, Ran/C-2662-2013; Tao, Ran/L-3460-2014
FU National Institute of Mental Health (NIMH), National Institutes of
Health
FX This research was supported by the Intramural Research Program of the
National Institute of Mental Health (NIMH), National Institutes of
Health. We thank Amy Deep-Soboslay, M.Ed., and Llewellyn B. Bigelow, M
D., of the Clinical Brain Disorders Branch, Genes, Cognition and
Psychosis Program, Intramural Research Program, and NIMH for their
efforts in clinical diagnosis and demographic characterization, and
Vesna Imamovic, Yeva Snitkovsky, Jewell King, Jonathan Sirovatka, and
Liqin Wang, M.D., for their excellent technical assistance. Special
gratitude also is extended to H. Ronald Zielke, Ph.D., Robert D.
Vigorito, M.S., P.A., and Robert M. Johnson, B.S., of the National
Institute of Child Health and Human Development Brain and Tissue Bank
for Developmental Disorders at the University of Maryland for their
provision of fetal, child, and adolescent brain specimens for this
study.
NR 40
TC 28
Z9 29
U1 1
U2 6
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 11
PY 2012
VL 32
IS 15
BP 5216
EP 5222
DI 10.1523/JNEUROSCI.4626-11.2012
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 925WT
UT WOS:000302793500020
PM 22496567
ER
PT J
AU Colegate, SM
Gardner, DR
Joy, RJ
Betz, JM
Panter, KE
AF Colegate, Steven M.
Gardner, Dale R.
Joy, Robert J.
Betz, Joseph M.
Panter, Kip E.
TI Dehydropyrrolizidine Alkaloids, Including Monoesters with an Unusual
Esterifying Acid, from Cultivated Crotalaria juncea (Sunn Hemp
cv.'Tropic Sun')
SO JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
LA English
DT Article
DE Crotalaria juncea; 'Tropic Sun'; pyrrolizidine alkaloids; N-oxides;
HPLC-ESI/MS; junceine; trichodesmine; isohemijunceine; hemijunceine
ID TOXIC RANGE PLANTS; PYRROLIZIDINE ALKALOIDS; N-OXIDES; SENECIO; MS;
SPECTROSCOPY; CHEMISTRY
AB Cultivation of Crotalaria juncea L. (Sunn Hemp cv. 'Tropic Sun') is recommended as a green manure crop in a rotation cycle to improve soil condition, help control erosion, suppress weeds, and reduce soil nematodes. Because C. juncea belongs to a genus that is known for the production of toxic dehydropyrrolizidine alkaloids, extracts of the roots, stems, leaves, and seeds of 'Tropic Sun' were analyzed for their presence using HPLC-ESI/MS. Qualitative analysis identified previously unknown alkaloids as major components along with the expected macrocyclic dehydropyrrolizidine alkaloid diesters, junceine and trichodesmine. The dehydropyrrolizidine alkaloids occurred mainly as the N-oxides in the roots, stems, and, to a lesser extent, leaves, but mainly as the free bases in the seeds. Comprehensive spectrometric and spectroscopic analysis enabled elucidation of the unknown alkaloids as diastereoisomers of isohemijunceine, a monoester of retronecine with an unusual necic acid. The dehydropyrrolizidine alkaloid contents of the roots, stems, and leaves of immature plants were estimated to be 0.05, 0.12, and 0.01% w/w, respectively, whereas seeds were estimated to contain 0.15% w/w.
C1 [Colegate, Steven M.; Gardner, Dale R.; Panter, Kip E.] ARS, Poisonous Plant Res Lab, USDA, Logan, UT 84341 USA.
[Joy, Robert J.] USDA, Nat Resources Conservat Serv, Plant Mat Ctr, Hoolehua, HI 96729 USA.
[Betz, Joseph M.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
RP Colegate, SM (reprint author), ARS, Poisonous Plant Res Lab, USDA, 1150 E 1400 N, Logan, UT 84341 USA.
EM steven.colegate@ars.usda.gov
FU Agricultural Research Service of the U.S. Department of Agriculture;
Office of Dietary Supplements of the National Institutes of Health
FX This research is supported by the Agricultural Research Service of the
U.S. Department of Agriculture and an Interagency Agreement with the
Office of Dietary Supplements of the National Institutes of Health.
NR 30
TC 18
Z9 18
U1 0
U2 21
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0021-8561
J9 J AGR FOOD CHEM
JI J. Agric. Food Chem.
PD APR 11
PY 2012
VL 60
IS 14
BP 3541
EP 3550
DI 10.1021/jf205296s
PG 10
WC Agriculture, Multidisciplinary; Chemistry, Applied; Food Science &
Technology
SC Agriculture; Chemistry; Food Science & Technology
GA 922CS
UT WOS:000302525000001
PM 22429238
ER
PT J
AU Sinthuvanich, C
Veiga, AS
Gupta, K
Gaspar, D
Blumenthal, R
Schneider, JP
AF Sinthuvanich, Chomdao
Veiga, Ana Salome
Gupta, Kshitij
Gaspar, Diana
Blumenthal, Robert
Schneider, Joel P.
TI Anticancer beta-Hairpin Peptides: Membrane-Induced Folding Triggers
Activity
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID TUMOR BLOOD-VESSELS; ANTIMICROBIAL PEPTIDE; PLASMA-MEMBRANE;
AMINOPHOSPHOLIPID TRANSLOCASE; ANIONIC PHOSPHOLIPIDS; CANCER-TREATMENT;
LYTIC PEPTIDES; CELLS; PHOSPHATIDYLSERINE; CONFORMATION
AB Several cationic antimicrobial peptides (AMPs) have recently been shown to display anticancer activity via a mechanism that usually entails the disruption of cancer cell membranes. In this work, we designed an 18-residue anticancer peptide, SVS-1, whose mechanism of action is designed to take advantage of the aberrant lipid composition presented on the outer leaflet of cancer cell membranes, which makes the surface of these cells electronegative relative to the surface of noncancerous cells. SVS-1 is designed to remain unfolded and inactive in aqueous solution but to preferentially fold at the surface of cancer cells, adopting an amphiphilic beta-hairpin structure capable of membrane disruption. Membrane-induced folding is driven by electrostatic interaction between the peptide and the negatively charged membrane surface of cancer cells. SVS-1 is active against a variety of cancer cell lines such as A549 (lung carcinoma), KB (epidermal carcinoma), MCF-7 (breast carcinoma), and MDA-MB-436 (breast carcinoma). However, the cytotoxicity toward noncancerous cells having typical membrane compositions, such as HUVEC and erythrocytes, is low. CD spectroscopy, appropriately designed peptide controls, cell-based studies, liposome leakage assays, and electron microscopy support the intended mechanism of action, which leads to preferential killing of cancerous cells.
C1 [Sinthuvanich, Chomdao; Veiga, Ana Salome; Schneider, Joel P.] NCI, Biol Chem Lab, Frederick, MD 21702 USA.
[Sinthuvanich, Chomdao] Univ Delaware, Dept Chem & Biochem, Newark, DE 19716 USA.
[Veiga, Ana Salome; Gaspar, Diana] Univ Lisbon, Inst Mol Med, Fac Med, P-1649028 Lisbon, Portugal.
[Gupta, Kshitij; Blumenthal, Robert] NCI, Membrane Struct & Funct Sect, Nanobiol Program, Frederick, MD 21702 USA.
RP Schneider, JP (reprint author), NCI, Biol Chem Lab, Frederick, MD 21702 USA.
EM Joel.Schneider@nih.gov
RI Schneider, Joel/N-2610-2014; Gaspar, Diana/M-9562-2015
OI Gaspar, Diana/0000-0002-9602-567X
FU Strategic Scholarship for Frontier Research Network (SFR) from the
Office of the Higher Education Commission, Ministry of Education,
Thailand; European Community [PIOE-GA-2009-235154]; Fundacao para a
Ciencia e a Tecnologia (Ministerio da Educacao e Ciencia, Portugal)
[SFRH/BPD/73500/2010]; National Cancer Institute, National Institutes of
Health
FX We thank Adam Harned, Christina Burks, and Ulrich Baxa from the Electron
Microscopy Laboratory (SAIC-Frederick) for electron microscopy images
and Marco Domingues for assistance with preliminary leakage experiments.
This work was partially supported by a graduate fellowship awarded to
C.S. through the Strategic Scholarship for Frontier Research Network
(SFR) from the Office of the Higher Education Commission, Ministry of
Education, Thailand. A Marie Curie International Outgoing Fellowship
within the 7th European Community Framework Programme partilly supported
A.S.V. (PIOE-GA-2009-235154). D.G. acknowledges Fundacao para a Ciencia
e a Tecnologia (Ministerio da Educacao e Ciencia, Portugal) for
Fellowship SFRH/BPD/73500/2010. Research funding was provided by the
Intramural Research Program of the National Cancer Institute, National
Institutes of Health.
NR 38
TC 55
Z9 56
U1 6
U2 49
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD APR 11
PY 2012
VL 134
IS 14
BP 6210
EP 6217
DI 10.1021/ja210569f
PG 8
WC Chemistry, Multidisciplinary
SC Chemistry
GA 922CQ
UT WOS:000302524800030
PM 22413859
ER
PT J
AU Zhang, YL
Muthana, SM
Farnsworth, D
Ludek, O
Adams, K
Barchi, JJ
Gildersleeve, JC
AF Zhang, Yalong
Muthana, Saddam M.
Farnsworth, David
Ludek, Olaf
Adams, Kristie
Barchi, Joseph J., Jr.
Gildersleeve, Jeffrey C.
TI Enhanced Epimerization of Glycosylated Amino Acids During Solid-Phase
Peptide Synthesis
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID TOTAL CHEMICAL-SYNTHESIS; ANTIPROLIFERATIVE FACTOR; GLYCOPEPTIDE
SYNTHESIS; POSTTRANSLATIONAL MODIFICATION; GLYCAN MICROARRAYS;
CLINICAL-TRIALS; O-GLYCOPEPTIDE; TN-ANTIGEN; CANCER; ANTIBODIES
AB Glycopeptides are extremely useful for basic research and clinical applications, but access to structurally defined glycopeptides is limited by the difficulties in synthesizing this class of compounds. In this study, we demonstrate that many common peptide coupling conditions used to prepare O-linked glycopeptides result in substantial amounts of epimerization at the a position. In fact, epimerization resulted in up to 80% of the non-natural epimer, indicating that it can be the major product in some reactions. Through a series of mechanistic studies, we demonstrate that the enhanced epimerization relative to nonglycosylated amino acids is due to a combination of factors, including a faster rate of epimerization, an energetic preference for the unnatural epimer over the natural epimer, and a slower overall rate of peptide coupling. In addition, we demonstrate that use of 2,4,6-trimethylpyridine (TMP) as the base in peptide couplings produces glycopeptides with high efficiency and low epimerization. The information and improved reaction conditions will facilitate the preparation of glycopeptides as therapeutic compounds and vaccine antigens.
C1 [Zhang, Yalong; Muthana, Saddam M.; Farnsworth, David; Ludek, Olaf; Adams, Kristie; Barchi, Joseph J., Jr.; Gildersleeve, Jeffrey C.] NCI, Biol Chem Lab, Frederick, MD 21702 USA.
RP Gildersleeve, JC (reprint author), NCI, Biol Chem Lab, 376 Boyles St,Bldg 376, Frederick, MD 21702 USA.
EM gildersj@mail.nih.gov
RI Gildersleeve, Jeffrey/N-3392-2014; Barchi Jr., Joseph/N-3784-2014
FU NIH, NCI
FX This research was supported by the Intramural Research Program of the
NIH, NCI. We gratefully acknowledge James A. Kelley (NIH/NCI) for
obtaining mass spectrometry data for all the compounds.
NR 66
TC 25
Z9 25
U1 3
U2 28
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD APR 11
PY 2012
VL 134
IS 14
BP 6316
EP 6325
DI 10.1021/ja212188r
PG 10
WC Chemistry, Multidisciplinary
SC Chemistry
GA 922CQ
UT WOS:000302524800041
PM 22390544
ER
PT J
AU Eddy, MT
Ong, TC
Clark, L
Teijido, O
van der Wel, PCA
Garces, R
Wagner, G
Rostovtseva, TK
Griffin, RG
AF Eddy, Matthew T.
Ong, Ta-Chung
Clark, Lindsay
Teijido, Oscar
van der Wel, Patrick C. A.
Garces, Robert
Wagner, Gerhard
Rostovtseva, Tatiana K.
Griffin, Robert G.
TI Lipid Dynamics and Protein-Lipid Interactions in 2D Crystals Formed with
the beta-Barrel Integral Membrane Protein VDAC1
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID NUCLEAR-MAGNETIC-RESONANCE; SOLID-STATE NMR; OUTER
MITOCHONDRIAL-MEMBRANE; ANION-SELECTIVE CHANNEL; ANGLE-SPINNING NMR;
2-DIMENSIONAL CRYSTALS; NEUROSPORA-CRASSA; CELL-MEMBRANES; SCHIFF-BASE;
H-2 NMR
AB We employ a combination of C-13/N-15 magic angle spinning (MAS) NMR and H-2 NMR to study the structural and functional consequences of different membrane environments on VDAC1 and, conversely, the effect of VDAC1 on the structure of the lipid bilayer. MAS spectra reveal a well-structured VDAC1 in 2D crystals of dimyristoylphosphatidylcholine (DMPC) and diphytanoylphosphatidylcholine (DPhPC,), and their temperature dependence suggests that the VDAC structure does not change conformation above and below the lipid phase transition temperature. The same data show that the N-terminus remains structured at both low and high temperatures. Importantly, functional studies based on electrophysiological measurements on these same samples show fully functional channels, even without the presence of Triton X-100 that has been found necessary for in vitro-refolded channels. H-2 solid-state NMR and differential scanning calorimetry were used to investigate the dynamics and phase behavior of the lipids within the VDAC1 2D crystals. H-2 NMR spectra indicate that the presence of protein in DMPC results in a broad lipid phase transition that is shifted from 19 to similar to 27 degrees C and show the existence of different lipid populations, consistent with the presence of both annular and bulk lipids in the functionally and structurally homogeneous samples.
C1 [Eddy, Matthew T.; Ong, Ta-Chung; Clark, Lindsay; van der Wel, Patrick C. A.; Griffin, Robert G.] MIT, Dept Chem, Cambridge, MA 02139 USA.
[Eddy, Matthew T.; Ong, Ta-Chung; Clark, Lindsay; van der Wel, Patrick C. A.; Griffin, Robert G.] MIT, Francis Bitter Magnet Lab, Cambridge, MA 02139 USA.
[Teijido, Oscar; Rostovtseva, Tatiana K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Garces, Robert; Wagner, Gerhard] Harvard Univ, Sch Med, Dept Biol & Mol Pharmacol, Boston, MA 02115 USA.
RP Griffin, RG (reprint author), MIT, Dept Chem, Cambridge, MA 02139 USA.
EM rgg@mit.edu
RI van der Wel, Patrick/B-1428-2009
OI van der Wel, Patrick/0000-0002-5390-3321
FU NIH [EB001960, EB002026, GM075879]; Eunice Kennedy Shriver National
Institute of Child Health and Human Development, NIH
FX We wish to thank Nicki Watson from the Whitehead Institute and Maria
Ericsson from Harvard Medical School for acquiring EM images and Dr.
David Ruben for help with de-Pake-ing. The Biophysical Instrumentation
Facility for the Study of Complex Macromolecular Systems (NSF-0070319
and NIH GM68762) is gratefully acknowledged for help acquiring the DSC
data. This research was supported by NIH grants EB001960, EB002026, and
GM075879. O.T. and T.K.R. wish to thank Sergey Bezrukov for fruitful
discussions and Kely Sheldon for help with experiments and acknowledge
support by the Intramural Research Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, NIH.
NR 109
TC 30
Z9 30
U1 3
U2 29
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD APR 11
PY 2012
VL 134
IS 14
BP 6375
EP 6387
DI 10.1021/ja300347v
PG 13
WC Chemistry, Multidisciplinary
SC Chemistry
GA 922CQ
UT WOS:000302524800047
PM 22435461
ER
PT J
AU Milman, G
Schwope, DM
Gorelick, DA
Huestis, MA
AF Milman, Garry
Schwope, David M.
Gorelick, David A.
Huestis, Marilyn A.
TI Cannabinoids and metabolites in expectorated oral fluid following
controlled smoked cannabis
SO CLINICA CHIMICA ACTA
LA English
DT Article
DE Oral fluid; Expectoration; Cannabinoids; Delta 9-Tetrahydrocannabinol;
Detection window; Cannabis
ID MARIJUANA SMOKING; DELTA(9)-TETRAHYDROCANNABINOL; DRUGS;
DELTA-9-TETRAHYDROCANNABINOL; DISPOSITION; COLLECTION; SPECIMENS;
SALIVA; ABUSE; HAIR
AB Background: Delta(9)-Tetrahydrocannabinol (THC) in oral fluid (OF) implies cannabis intake, but eliminating passive exposure and improving interpretation of test results requires additional research.
Methods: Ten adult cannabis users smoked ad libitum one 6.8% THC cigarette. Expectorated OF was collected for up to 22 h, and analyzed within 24 h of collection. THC, 11-nor-9-carboxy-THC (THCCOOH), cannabidiol, and cannabinol were quantified by 2-dimensional-GCMS.
Results: Eighty specimens were analyzed: 6 could not be collected due to dry mouth. THC was quantifiable in 95.2%, cannabidiol in 69.3%, cannabinol in 62.3%, and THCCOOH in 94.7% of specimens. Highest THC, cannabidiol, and cannabinol concentrations were 22370, 1000, and 1964 mu g/l, respectively, 0.25 h after the start of smoking; THCCOOH peaked within 2 h (up to 560 ng/l). Concentrations 6 h after smoking were THC (0.9-90.4 mu g/l) and THCCOOH (17.0-151 ng/l) (8 of 9 positive for both); only 4 were positive for cannabidiol (0.5-2.4 mu g/l) and cannabinol (1.0-3.0 mu g/l). By 22 h, there were 4 THC (0.4-10.3 mu g/l), 5 THCCOOH (6.0-24.0 ng/l), 1 cannabidiol (0.3 mu g/l), and no cannabinol positive specimens.
Conclusions: THCCOOH in OF suggests no passive contamination, and CBD and CBN suggest recent cannabis smoking. Seventeen alternative cutoffs were evaluated to meet the needs of different drug testing programs. Published by Elsevier B.V.
C1 [Huestis, Marilyn A.] Natl Inst Drug Abuse, IRP, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), Natl Inst Drug Abuse, IRP, NIH, Biomed Res Ctr, 251 Bayview Blvd,Room 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
FU National Institute on Drug Abuse, National Institutes of Health
FX We acknowledge the contributions of the clinical staff of the National
Institute on Drug Abuse, Intramural Research Program and the Behavioral
Research Pharmacology Unit. Funding was provided by the Intramural
Research Program, National Institute on Drug Abuse, National Institutes
of Health.
NR 28
TC 27
Z9 28
U1 4
U2 17
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 APR 11
PY 2012
VL 413
IS 7-8
BP 765
EP 770
DI 10.1016/j.cca.2012.01.011
PG 6
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 913WL
UT WOS:000301908000021
PM 22285315
ER
PT J
AU Farkas, S
Nagy, K
Jia, ZS
Harkany, T
Palkovits, M
Donohou, SR
Pike, VW
Halldin, C
Mathe, D
Csiba, L
Gulyas, B
AF Farkas, Szabolcs
Nagy, Katalin
Jia, Zhisheng
Harkany, Tibor
Palkovits, Miklos
Donohou, Sean R.
Pike, Victor W.
Halldin, Christer
Mathe, Domokos
Csiba, Laszlo
Gulyas, Balazs
TI The decrease of dopamine D-2/D-3 receptor densities in the putamen and
nucleus caudatus goes parallel with maintained levels of CB1 cannabinoid
receptors in Parkinson's disease: A preliminary autoradiographic study
with the selective dopamine D-2/D-3 antagonist [H-3]raclopride and the
novel CB1 inverse agonist [I-125]SD7015
SO BRAIN RESEARCH BULLETIN
LA English
DT Article
DE Parkinson's disease; Endocannabinoid CB1 receptor; Dopamine D-2/D-3
receptor; Molecular imaging biomarker; Human brain autoradiography;
Striatum
ID MESSENGER-RNA EXPRESSION; RAT BASAL GANGLIA; ENDOCANNABINOID SYSTEM;
HUMAN BRAIN; IN-VIVO; HUNTINGTONS-DISEASE; D2 RECEPTORS; ENDOGENOUS
CANNABINOIDS; DENERVATED STRIATUM; SUBSTANTIA-NIGRA
AB Cannabinoid type-1 receptors (CB1 Rs) modulate synaptic neurotransmission by participating in retrograde signaling in the adult brain. Increasing evidence suggests that cannabinoids through CB1 Rs play an important role in the regulation of motor activities in the striatum. In the present study, we used human brain samples to examine the relationship between CB1 R and dopamine receptor density in case of Parkinson's disease (PD).
Post mortem putamen, nucleus caudatus and medial frontal gyrus samples obtained from PD patients were used for CB1 R and dopamine D-2/D-3 receptor autoradiography. [I-125]SD7015, a novel selective CB1 R inverse agonist, developed by a number of the present co-authors, and [H-3]raclopride, a dopamine D-2/D-3 antagonist, were used as radioligands. Our results demonstrate unchanged CB1 R density in the putamen and nucleus caudatus of deceased PD patients, treated with levodopa (L-DOPA). At the same time dopamine D-2/D-3 receptors displayed significantly decreased density levels in case of PD putamen (control: 47.97 +/- 10.00 fmol/g, PD: 3.73 +/- 0.07 fmol/g (mean +/- SEM), p < 0.05) and nucleus caudatus (control: 30.26 +/- 2.48 fmol/g, PD: 12.84 +/- 5.49 fmol/g, p < 0.0005) samples. In contrast to the putamen and the nucleus caudatus, in the medial frontal gyrus neither receptor densities were affected.
Our data suggest the presence of an unaltered CB1 R population even in late stages of levodopa treated PD. This further supports the presence of an intact CB1 R population which, in line with the conclusion of earlier publications, may be utilized as a pharmacological target in the treatment of PD. Furthermore we found discrepancy between a maintained CB1 R population and a decreased dopamine D-2/D-3 receptor population in PD striatum. The precise explanation of this conundrum requires further studies with simultaneous examination of the central cannabinoid and dopaminergic systems in PD using higher sample size. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Jia, Zhisheng; Halldin, Christer; Gulyas, Balazs] Karolinska Inst, Dept Clin Neurosci, Psychiat Sect, S-17176 Stockholm, Sweden.
[Farkas, Szabolcs; Nagy, Katalin] Univ Debrecen, Dept Neurol, H-4012 Debrecen, Hungary.
[Harkany, Tibor] Karolinska Inst, Dept Med Biochem & Biophys, Div Mol Neurobiol, S-17177 Stockholm, Sweden.
[Palkovits, Miklos] Semmelweis Univ, Dept Anat, H-1094 Budapest, Hungary.
[Donohou, Sean R.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Mathe, Domokos] Semmelweis Univ, Dept Biophys & Radiat Biol, H-1094 Budapest, Hungary.
[Mathe, Domokos] CROmed Translat Res Ctr, H-1047 Budapest, Hungary.
RP Gulyas, B (reprint author), Karolinska Inst, Dept Clin Neurosci, Psychiat Sect, S-17176 Stockholm, Sweden.
EM balazs.gulyas@ki.se
RI Palkovits, Miklos/F-2707-2013; Gulyas, Balazs/F-9508-2015
FU Hungarian National Science Found (OTKA) [K 68864]
FX The study was supported by the Hungarian National Science Found (OTKA)
(K 68864) and was performed partly within a collaborative master
research agreement between Karolinska Institutet, Mediso Medical Imaging
Systems and CROmed Translational.
NR 106
TC 6
Z9 6
U1 0
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0361-9230
J9 BRAIN RES BULL
JI Brain Res. Bull.
PD APR 10
PY 2012
VL 87
IS 6
BP 504
EP 510
DI 10.1016/j.brainresbull.2012.02.012
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 934ZT
UT WOS:000303487300002
PM 22421165
ER
PT J
AU Zhang, XX
Eden, HS
Chen, XY
AF Zhang, Xiao-Xiang
Eden, Henry S.
Chen, Xiaoyuan
TI Peptides in cancer nanomedicine: Drug carriers, targeting ligands and
protease substrates
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Review
DE Peptides; Cancer; Nanomedicine; Drug delivery; Tumor targeting;
Protease-responsive
ID CELL-PENETRATING PEPTIDES; MATRIX METALLOPROTEINASES MMPS;
BIOLOGICALLY-ACTIVE PROTEINS; NUCLEIC-ACID DELIVERY; SMALL INTERFERING
RNA; TAT-FUSION PROTEINS; VIRUS TYPE-1 VP22; IN-VIVO; MAMMALIAN-CELLS;
GENE DELIVERY
AB Peptides are attracting increasing attention as therapeutic agents, as the technologies for peptide development and manufacture continue to mature. Concurrently, with booming research in nanotechnology for biomedical applications, peptides have been studied as an important class of components in nanomedicine, and they have been used either alone or in combination with nanomaterials of every reported composition. Peptides possess many advantages, such as smallness, ease of synthesis and modification, and good biocompatibility. Their functions in cancer nanomedicine, discussed in this review, include serving as drug carriers, as targeting ligands, and as protease-responsive substrates for drug delivery. Published by Elsevier B.V.
C1 [Chen, Xiaoyuan] NIBIB, LOMIN, NIH, Intramural Res Program, Bethesda, MD 20892 USA.
RP Chen, XY (reprint author), NIBIB, LOMIN, NIH, Intramural Res Program, Bldg 31,Room 1C22, Bethesda, MD 20892 USA.
EM shawn.chen@nih.gov
FU National Institute of Biomedical Imaging and Bioengineering (NIBIB),
National Institutes of Health (NIH)
FX This work was supported by the intramural research program of the
National Institute of Biomedical Imaging and Bioengineering (NIBIB),
National Institutes of Health (NIH). This work was performed while X-X
Zhang held a National Research Council Research Associateship Award at
NIH/NIBIB.
NR 190
TC 71
Z9 76
U1 6
U2 106
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-3659
J9 J CONTROL RELEASE
JI J. Control. Release
PD APR 10
PY 2012
VL 159
IS 1
BP 2
EP 13
DI 10.1016/j.jconrel.2011.10.023
PG 12
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA 938LG
UT WOS:000303734400002
PM 22056916
ER
PT J
AU Emens, LA
Silverstein, SC
Khleif, S
Marincola, FM
Galon, J
AF Emens, Leisha A.
Silverstein, Samuel C.
Khleif, Samir
Marincola, Francesco M.
Galon, Jerome
TI Toward integrative cancer immunotherapy: targeting the tumor
microenvironment
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
ID ENDOTHELIAL GROWTH-FACTOR; ENHANCES ANTITUMOR IMMUNITY; CELL
LUNG-CANCER; T-CELLS; COLORECTAL-CANCER; CLINICAL ACTIVITY; MODULATION;
EXPRESSION; CARCINOMA; CHEMOTHERAPY
AB The development of cancer has historically been attributed to genomic alterations of normal host cells. Accordingly, the aim of most traditional cancer therapies has been to destroy the transformed cells themselves. There is now widespread appreciation that the progressive growth and metastatic spread of cancer cells requires the cooperation of normal host cells (endothelial cells, fibroblasts, other mesenchymal cells, and immune cells), both local to, and at sites distant from, the site at which malignant transformation occurs. It is the balance of these cellular interactions that both determines the natural history of the cancer, and influences its response to therapy. This active tumor-host dynamic has stimulated interest in the tumor microenvironment as a key target for both cancer diagnosis and therapy. Recent data has demonstrated both that the presence of CD8(+) T cells within a tumor is associated with a good prognosis, and that the eradication of all malignantly transformed cells within a tumor requires that the intra-tumoral concentration of cytolytically active CD8(+) effector T cells remain above a critical concentration until every tumor cell has been killed. These findings have stimulated two initiatives in the field of cancer immunotherapy that focus on the tumor microenvironment. The first is the development of the immune score as part of the routine diagnostic and prognostic evaluation of human cancers, and the second is the development of combinatorial immune-based therapies that reduce tumor-associated immune suppression to unleash pre-existing or therapeutically-induced tumor immunity. In support of these efforts, the Society for the Immunotherapy of Cancer (SITC) is sponsoring a workshop entitled "Focus on the Target: The Tumor Microenvironment" to be held October 24-25, 2012 in Bethesda, Maryland. This meeting should support development of the immune score, and result in a position paper highlighting opportunities for the development of integrative cancer immunotherapies that sculpt the tumor microenvironment to promote definitive tumor rejection.
C1 [Emens, Leisha A.] Johns Hopkins Univ, Sch Med, Tumor Immunol Program, Baltimore, MD 21231 USA.
[Emens, Leisha A.] Johns Hopkins Univ, Sch Med, Breast Canc Res Program, Baltimore, MD 21231 USA.
[Emens, Leisha A.] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21231 USA.
[Silverstein, Samuel C.] Columbia Univ Coll Phys & Surg, Dept Physiol & Cellular Biophys, New York, NY 10032 USA.
[Silverstein, Samuel C.] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA.
[Khleif, Samir] Georgia Hlth Sci Univ, Ctr Canc, Atlanta, GA USA.
[Marincola, Francesco M.] NIH, IDIS, Bethesda, MD 20891 USA.
[Marincola, Francesco M.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20891 USA.
[Marincola, Francesco M.] NIH, TransNIH Ctr Human Immunol CHI, Bethesda, MD 20891 USA.
[Galon, Jerome] INSERM, UMRS872, Cordeliers Res Ctr, Lab Integrat Canc Immunol, F-75006 Paris, France.
[Galon, Jerome] Georges Pompidou European Hosp, AP HP, Paris, France.
[Galon, Jerome] Univ Paris 06, Paris, France.
[Galon, Jerome] Univ Paris 05, Paris, France.
[Emens, Leisha A.] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Baltimore, MD 21231 USA.
RP Emens, LA (reprint author), Johns Hopkins Univ, Sch Med, Tumor Immunol Program, Baltimore, MD 21231 USA.
EM emensle@jhmi.edu
NR 47
TC 21
Z9 22
U1 0
U2 7
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 APR 10
PY 2012
VL 10
AR 70
DI 10.1186/1479-5876-10-70
PG 5
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 934CE
UT WOS:000303417600001
PM 22490302
ER
PT J
AU Aldworth, ZN
Stopfer, M
AF Aldworth, Zane N.
Stopfer, Mark
TI Olfactory Coding: Tagging and Tuning Odor-Activated Synapses for Memory
SO CURRENT BIOLOGY
LA English
DT Editorial Material
ID EVOKED NEURAL OSCILLATIONS; MUSHROOM BODY; INFORMATION; DROSOPHILA;
ASSEMBLIES; HONEYBEES; LOCUST; BRAIN
C1 [Aldworth, Zane N.; Stopfer, Mark] NIH NICHD, Bethesda, MD 20892 USA.
RP Aldworth, ZN (reprint author), NIH NICHD, Bldg 35,35 Lincoln Dr,Room 3A-102,Msc 3715, Bethesda, MD 20892 USA.
EM stopferm@mail.nih.gov
FU Intramural NIH HHS [Z99 HD999999]; NIDCD NIH HHS [F32 DC000234]
NR 20
TC 2
Z9 4
U1 0
U2 9
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 APR 10
PY 2012
VL 22
IS 7
BP R227
EP R229
DI 10.1016/j.cub.2012.02.047
PG 3
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 926QC
UT WOS:000302844900009
PM 22497937
ER
PT J
AU Stein, U
Fleuter, C
Siegel, F
Smith, J
Kopacek, A
Scudiero, DA
Hite, KM
Schlag, PM
Shoemaker, RH
Walther, W
AF Stein, U.
Fleuter, C.
Siegel, F.
Smith, J.
Kopacek, A.
Scudiero, D. A.
Hite, K. M.
Schlag, P. M.
Shoemaker, R. H.
Walther, W.
TI Impact of mutant beta-catenin on ABCB1 expression and therapy response
in colon cancer cells
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE colon cancer; beta-catenin; multidrug resistance; ABCB1; therapy
response
ID PRODUCT P-GLYCOPROTEIN; MULTIDRUG-RESISTANCE; COLORECTAL-CANCER;
MULTIDRUG-RESISTANCE-1 GENE; MDR1 GENE; LINES; METASTASIS; MUTATIONS;
CARCINOMA; CARCINOGENESIS
AB BACKGROUND: Colorectal cancers are often chemoresistant toward antitumour drugs that are substrates for ABCB1-mediated multidrug resistance (MDR). Activation of the Wnt/beta-catenin pathway is frequently observed in colorectal cancers. This study investigates the impact of activated, gain-of-function beta-catenin on the chemoresistant phenotype.
METHODS: The effect of mutant (mut) beta-catenin on ABCB1 expression and promoter activity was examined using HCT116 human colon cancer cells and isogenic sublines harbouring gain-of-function or wild-type beta-catenin, and patients' tumours. Chemosensitivity towards 24 anticancer drugs was determined by high throughput screening.
RESULTS: Cell lines with mut beta-catenin showed high ABCB1 promoter activity and expression. Transfection and siRNA studies demonstrated a dominant role for the mutant allele in activating ABCB1 expression. Patients' primary colon cancer tumours shown to express the same mut beta-catenin allele also expressed high ABCB1 levels. However, cell line chemosensitivities towards 24 MDR-related and non-related antitumour drugs did not differ despite different beta-catenin genotypes.
CONCLUSION: Although ABCB1 is dominantly regulated by mut beta-catenin, this did not lead to drug resistance in the isogenic cell line model studied. In patient samples, the same beta-catenin mutation was detected. The functional significance of the mutation for predicting patients' therapy response or for individualisation of chemotherapy regimens remains to be established. British Journal of Cancer (2012) 106, 1395-1405. doi: 10.1038/bjc.2012.81 www.bjcancer.com Published online 29 March 2012 (C) 2012 Cancer Research UK
C1 [Stein, U.; Fleuter, C.; Siegel, F.; Smith, J.; Kopacek, A.; Walther, W.] Expt & Clin Res Ctr, D-13125 Berlin, Germany.
[Scudiero, D. A.; Hite, K. M.] NCI, SAIC Frederick, Frederick, MD 21702 USA.
[Schlag, P. M.] Charite, Charite Comprehens Canc Ctr, D-10117 Berlin, Germany.
[Shoemaker, R. H.] NCI, Screening Technol Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Frederick, MD 21702 USA.
RP Stein, U (reprint author), Expt & Clin Res Ctr, D-13125 Berlin, Germany.
EM ustein@mdc-berlin.de
NR 52
TC 11
Z9 11
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD APR 10
PY 2012
VL 106
IS 8
BP 1395
EP 1405
DI 10.1038/bjc.2012.81
PG 11
WC Oncology
SC Oncology
GA 925SX
UT WOS:000302782800006
PM 22460269
ER
PT J
AU Cook, NR
Paynter, NP
Eaton, CB
Manson, JE
Martin, LW
Robinson, JG
Rossouw, JE
Wassertheil-Smoller, S
Ridker, PM
AF Cook, Nancy R.
Paynter, Nina P.
Eaton, Charles B.
Manson, JoAnn E.
Martin, Lisa W.
Robinson, Jennifer G.
Rossouw, Jacques E.
Wassertheil-Smoller, Sylvia
Ridker, Paul M.
TI Comparison of the Framingham and Reynolds Risk Scores for Global
Cardiovascular Risk Prediction in the Multiethnic Women's Health
Initiative
SO CIRCULATION
LA English
DT Article
DE cardiovascular diseases; forecasting; prevention; models statistical;
risk factors; statins; risk assessment
ID C-REACTIVE PROTEIN; CORONARY-HEART-DISEASE; EVALUATING ROSUVASTATIN
JUPITER; CASE-COHORT DESIGNS; PRIMARY PREVENTION; VALIDATION; MODELS;
TRIAL; RECLASSIFICATION; JUSTIFICATION
AB Background-Framingham-based and Reynolds Risk scores for cardiovascular disease (CVD) prediction have not been directly compared in an independent validation cohort.
Methods and Results-We selected a case-cohort sample of the multiethnic Women's Health Initiative Observational Cohort, comprising 1722 cases of major CVD (752 myocardial infarctions, 754 ischemic strokes, and 216 other CVD deaths) and a random subcohort of 1994 women without prior CVD. We estimated risk using the Adult Treatment Panel III (ATP-III) score, the Reynolds Risk Score, and the Framingham CVD model, reweighting to reflect cohort frequencies. Predicted 10-year risk varied widely between models, with >= 10% risk in 6%, 10%, and 41% of women with the ATP-III, Reynolds, and Framingham CVD models, respectively. Calibration was adequate for the Reynolds model, but the ATP-III and Framingham CVD models overestimated risk for coronary heart disease and major CVD, respectively. After recalibration, the Reynolds model demonstrated improved discrimination over the ATP-III model through a higher c statistic (0.765 versus 0.757; P=0.03), positive net reclassification improvement (NRI; 4.9%; P=0.02), and positive integrated discrimination improvement (4.1%; P<0.0001) overall, excluding diabetics (NRI=4.2%; P=0.01), and in white (NRI=4.3%; P=0.04) and black (NRI=11.4%; P=0.13) women. The Reynolds (NRI=12.9%; P<0.0001) and ATP-III (NRI=5.9%; P=0.0001) models demonstrated better discrimination than the Framingham CVD model.
Conclusions-The Reynolds Risk Score was better calibrated than the Framingham-based models in this large external validation cohort. The Reynolds score also showed improved discrimination overall and in black and white women. Large differences in risk estimates exist between models, with clinical implications for statin therapy. (Circulation. 2012; 125:1748-1756.)
C1 [Cook, Nancy R.] Harvard Univ, Brigham & Womens Hosp, Div Prevent Med, Sch Med, Boston, MA 02215 USA.
[Eaton, Charles B.] Brown Univ, Sch Med, Providence, RI 02912 USA.
[Martin, Lisa W.] George Washington Univ, Sch Med, Washington, DC USA.
[Robinson, Jennifer G.] Univ Iowa, Iowa City, IA USA.
[Rossouw, Jacques E.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Wassertheil-Smoller, Sylvia] Albert Einstein Coll Med, Bronx, NY 10467 USA.
RP Cook, NR (reprint author), Harvard Univ, Brigham & Womens Hosp, Div Prevent Med, Sch Med, 900 Commonwealth Ave E, Boston, MA 02215 USA.
EM ncook@rics.bwh.harvard.edu
OI Martin, Lisa Warsinger/0000-0003-4352-0914
FU National Heart, Lung, and Blood Institute's Broad Agency Announcement
[HHSN268200960011C]; National Heart, Lung, and Blood Institute; National
Institutes of Health; US Department of Health and Human Services
[N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-9,
32122, 42107-26, 42129-32, 44221]
FX This project was supported by National Heart, Lung, and Blood
Institute's Broad Agency Announcement contract HHSN268200960011C. The
Women's Health Initiative program is funded by the National Heart, Lung,
and Blood Institute, National Institutes of Health, and the US
Department of Health and Human Services through contracts N01WH22110,
24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-9, 32122,
42107-26, 42129-32, and 44221.
NR 39
TC 85
Z9 87
U1 1
U2 15
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD APR 10
PY 2012
VL 125
IS 14
BP 1748
EP U112
DI 10.1161/CIRCULATIONAHA.111.075929
PG 20
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 925WR
UT WOS:000302793300016
PM 22399535
ER
PT J
AU Kovacic, JC
Mercader, N
Torres, M
Boehm, M
Fuster, V
AF Kovacic, Jason C.
Mercader, Nadia
Torres, Miguel
Boehm, Manfred
Fuster, Valentin
TI Epithelial-to-Mesenchymal and Endothelial-to-Mesenchymal Transition From
Cardiovascular Development to Disease
SO CIRCULATION
LA English
DT Article
DE endothelium; epithelium; development; endocardium; vasculature;
cardiovascular diseases
ID GROWTH-FACTOR-BETA; PLASMINOGEN-ACTIVATOR INHIBITOR-1; CORONARY-ARTERY
FORMATION; CHRONIC PULMONARY-HYPERTENSION; TRANSCRIPTION FACTOR SNAIL;
EPICARDIUM-DERIVED CELLS; CARDIAC-VALVE FORMATION; VASCULAR
SMOOTH-MUSCLE; CHICK-EMBRYO; IN-VIVO
C1 [Kovacic, Jason C.; Fuster, Valentin] Mt Sinai Sch Med, Zena & Michael A Wiener Cardiovasc Inst, New York, NY 10029 USA.
[Mercader, Nadia; Torres, Miguel; Fuster, Valentin] CNIC, Madrid, Spain.
[Boehm, Manfred] NHLBI, Ctr Mol Med, Bethesda, MD 20892 USA.
[Fuster, Valentin] Mt Sinai Sch Med, Marie Josee & Henry R Kravis Cardiovasc Hlth Ctr, New York, NY USA.
RP Kovacic, JC (reprint author), Mt Sinai Sch Med, Zena & Michael A Wiener Cardiovasc Inst, 1 Gustave L Levy Pl,Box 1030, New York, NY 10029 USA.
EM jason.kovacic@mountsinai.org
RI Mercader, Nadia/L-2728-2014; Torres, Miguel/A-7388-2013; Fuster,
Valentin/H-4319-2015
OI Mercader, Nadia/0000-0002-0905-6399; Torres, Miguel/0000-0003-0906-4767;
Fuster, Valentin/0000-0002-9043-9986
FU National Institutes of Health [1K08HL111330-01, 5U01HL071988-07];
Fundacion Centro Nacional de Investigaciones Cardiovasculares Carlos
III; Spanish Ministry of Economy and Competitiveness [BFU200800212/BMC,
BFU2011-25297, RYC-2006-001694]; Comunidad de Madrid [S2011/BMD-2321];
Spanish 'Ministerio de Economia y Competitividad'; Instituto de Salud
Carlos III; proCNIC foundation; National Heart, Lung and Blood Institute
FX Dr Kovacic is supported by National Institutes of Health grant
1K08HL111330-01. Dr Mercader is supported by the Fundacion Centro
Nacional de Investigaciones Cardiovasculares Carlos III, the Spanish
Ministry of Economy and Competitiveness (BFU200800212/BMC,
BFU2011-25297, and RYC-2006-001694) as well as the Comunidad de Madrid
(S2011/BMD-2321). Dr Torres is funded by grants from the Spanish
'Ministerio de Economia y Competitividad'. CNIC is funded by the
Instituto de Salud Carlos III and the proCNIC foundation. Dr Boehm is
supported by the intramural research program of the National Heart, Lung
and Blood Institute. Dr Fuster is in receipt of National Institutes of
Health grant 5U01HL071988-07.
NR 160
TC 88
Z9 90
U1 2
U2 30
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD APR 10
PY 2012
VL 125
IS 14
BP 1795
EP 1808
DI 10.1161/CIRCULATIONAHA.111.040352
PG 14
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 925WR
UT WOS:000302793300021
PM 22492947
ER
PT J
AU Glancy, B
Balaban, RS
AF Glancy, Brian
Balaban, Robert S.
TI Role of Mitochondrial Ca2+ in the Regulation of Cellular Energetics
SO BIOCHEMISTRY
LA English
DT Article
ID PYRUVATE-DEHYDROGENASE PHOSPHATASE; RAT-LIVER MITOCHONDRIA;
CYTOCHROME-C-OXIDASE; NICOTINAMIDE ADENINE-DINUCLEOTIDE;
NUCLEAR-MAGNETIC-RESONANCE; KIDNEY ALPHA-KETOGLUTARATE; POSITIVE
INOTROPIC AGENTS; CALCIUM-BINDING PROTEIN; BROWN ADIPOSE-TISSUE;
OXIDATIVE-PHOSPHORYLATION
AB Calcium is an important signaling molecule involved in the regulation of many cellular functions. The large free energy in the Ca2+ ion membrane gradients makes Ca2+ signaling inherently sensitive to the available cellular free energy, primarily in the form of ATP. In addition, Ca2+ regulates many cellular ATP-consuming reactions such as muscle contraction, exocytosis, biosynthesis, and neuronal signaling. Thus, Ca2+ becomes a logical candidate as a signaling molecule for modulating ATP hydrolysis and synthesis during changes in numerous forms of cellular work Mitochondria are the primary source of aerobic energy production in mammalian cells and also maintain a large Ca2+ gradient across their inner membrane, providing a signaling potential for this molecule. The demonstrated link between cytosolic and mitochondrial Ca2+ concentrations, identification of transport mechanisms, and the proximity of mitochondria to Ca2+ release sites further supports the notion that Ca2+ can be an important signaling molecule in the energy metabolism interplay of the cytosol with the mitochondria. Here we review sites within the mitochondria where Ca2+ plays a role in the regulation of ATP generation and potentially contributes to the orchestration of cellular metabolic homeostasis. Early work on isolated enzyme's pointed to several matrix dehydrogenases that are stimulated by Ca2+, which were confirmed in the intact mitochondrion as well as cellular and in vivo systems. However, studies in these intact systems suggested a more expansive influence of Ca2+ on mitochondrial energy conversion. Numerous noninvasive approaches monitoring NADH, mitochondrial membrane potential, oxygen consumption, and workloads suggest significant effects of Ca2+ on other elements of NADH generation as well as downstream elements of oxidative phosphorylation, including the F1Fo-ATPase and the cytochrome chain. These other potential elements of Ca2+ modification of mitochondrial energy conversion will be the focus of this review. Though most specific molecular mechanisms have yet to be elucidated, it is clear that Ca2+ provides a balanced activation of mitochondrial energy metabolism that exceeds the alteration of dehydrogenases alone.
C1 [Glancy, Brian; Balaban, Robert S.] NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20817 USA.
RP Balaban, RS (reprint author), NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20817 USA.
EM rsb@nih.gov
RI Glancy, Brian/P-3163-2016
OI Glancy, Brian/0000-0002-8571-244X
FU Intramural NIH HHS [ZIA HL004601-23, ZIA HL004610-03]
NR 173
TC 151
Z9 153
U1 1
U2 30
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 10
PY 2012
VL 51
IS 14
BP 2959
EP 2973
DI 10.1021/bi2018909
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 921NL
UT WOS:000302484200001
PM 22443365
ER
PT J
AU Connelly, L
Jang, H
Arce, FT
Ramachandran, S
Kagan, BL
Nussinov, R
Lal, R
AF Connelly, Laura
Jang, Hyunbum
Arce, Fernando Teran
Ramachandran, Srinivasan
Kagan, Bruce L.
Nussinov, Ruth
Lal, Ratnesh
TI Effects of Point Substitutions on the Structure of Toxic Alzheimer's
beta-Amyloid Channels: Atomic Force Microscopy and Molecular Dynamics
Simulations
SO BIOCHEMISTRY
LA English
DT Article
ID FORMS ION CHANNELS; ALL-D-ENANTIOMER; IN-VITRO; PROTEIN; DISEASE;
PEPTIDE; FIBRILS; MUTAGENESIS; PORES; A-BETA-42
AB Alzheimer's disease (AD) is a misfolded protein disease characterized by the accumulation of beta-amyloid (A beta) peptide as senile plaques, progressive neurodegeneration, and memory loss. Recent evidence suggests that AD pathology is linked to the destabilization of cellular ionic homeostasis mediated by toxic pores made of A beta peptides. Understanding the exact nature by which these pores conduct electrical and molecular signals could aid in identifying potential therapeutic targets for the prevention and treatment of AD. Here using atomic force microscopy (AFM) and molecular dynamics (MD) simulations, we compared the imaged pore structures with models to predict channel conformations as a function of amino acid sequence. Site-specific amino acid (AA) substitutions in the wild-type A beta(1-42) peptide yield information regarding the location and significance of individual AA residues to its characteristic structure activity relationship. We selected two AAs that our MD simulation predicted to inhibit or permit pore conductance. The substitution of Phe19 with Pro has previously been shown to eliminate conductance in the planar lipid bilayer system. Our MD simulations predict a channel-like shape with a collapsed pore, which is supported by the AFM channel images. We suggest that proline, a known beta-sheet breaker, creates a kink in the center of the pore and prevents conductance via blockage. This residue may be a viable target for drug development studies aiming to inhibit A beta from inducing ionic destabilization toxicity. The substitution of Phe20 with Cys exhibits pore structures indistinguishable from the wild type in AFM images. MD simulations predict site 20 to face the solvated pore. Overall, the mutations support the previously predicted beta-sheet-based channel structure.
C1 [Jang, Hyunbum; Nussinov, Ruth] SAIC Frederick Inc, Basic Sci Program, Ctr Canc Res Nanobiol Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Connelly, Laura; Arce, Fernando Teran; Ramachandran, Srinivasan; Lal, Ratnesh] Univ Calif San Diego, Mat Sci Program, La Jolla, CA 92093 USA.
[Connelly, Laura; Arce, Fernando Teran; Ramachandran, Srinivasan; Lal, Ratnesh] Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA.
[Connelly, Laura; Arce, Fernando Teran; Ramachandran, Srinivasan; Lal, Ratnesh] Univ Calif San Diego, Dept Mech & Aerosp Engn, La Jolla, CA 92093 USA.
[Kagan, Bruce L.] Univ Calif Los Angeles, Dept Psychiat, David Geffen Sch Med, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90024 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Dept Human Mol Genet & Biochem, IL-69978 Tel Aviv, Israel.
RP Nussinov, R (reprint author), SAIC Frederick Inc, Basic Sci Program, Ctr Canc Res Nanobiol Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
EM ruthnu@helix.nih.gov; rlal@ucsd.edu
RI Ramachandran, Srinivasan/G-5300-2010
OI Ramachandran, Srinivasan/0000-0002-4912-0279
FU National Institutes of Health (National Institute on Aging) [AG028709];
Frederick National Laboratory for Cancer Research; National Institutes
of Health [HHSN261200800001E]; National Institutes of Health, Frederick
National Lab, Center for Cancer Research
FX This research was supported by the National Institutes of Health
(National Institute on Aging Grant AG028709 to R.L.). This project has
been funded in whole or in part with Federal funds from the Frederick
National Laboratory for Cancer Research, National Institutes of Health,
under Contract HHSN261200800001E. This research was supported (in part)
by the Intramural Research Program of the National Institutes of Health,
Frederick National Lab, Center for Cancer Research.
NR 43
TC 28
Z9 29
U1 4
U2 41
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 10
PY 2012
VL 51
IS 14
BP 3031
EP 3038
DI 10.1021/bi300257e
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 921NL
UT WOS:000302484200007
PM 22413858
ER
PT J
AU Do Kwon, Y
Finzi, A
Wu, XL
Dogo-Isonagie, C
Lee, LK
Moore, LR
Schmidt, SD
Stuckey, J
Yang, YP
Zhou, TQ
Zhu, J
Vicic, DA
Debnath, AK
Shapiro, L
Bewley, CA
Mascola, JR
Sodroski, JG
Kwong, PD
AF Do Kwon, Young
Finzi, Andres
Wu, Xueling
Dogo-Isonagie, Cajetan
Lee, Lawrence K.
Moore, Lucas R.
Schmidt, Stephen D.
Stuckey, Jonathan
Yang, Yongping
Zhou, Tongqing
Zhu, Jiang
Vicic, David A.
Debnath, Asim K.
Shapiro, Lawrence
Bewley, Carole A.
Mascola, John R.
Sodroski, Joseph G.
Kwong, Peter D.
TI Unliganded HIV-1 gp120 core structures assume the CD4-bound conformation
with regulation by quaternary interactions and variable loops
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE conformational equilibrium; viral evasion; X-ray crystallography
ID VIRAL MEMBRANE-FUSION; ENVELOPE GLYCOPROTEIN; NEUTRALIZATION
SENSITIVITY; MONOCLONAL-ANTIBODIES; VIRUS; CD4; BINDING; REVEALS; ENTRY;
ARCHITECTURE
AB The HIV-1 envelope (Env) spike (gp120(3)/gp41(3)) undergoes considerable structural rearrangements to mediate virus entry into cells and to evade the host immune response. Engagement of CD4, the primary human receptor, fixes a particular conformation and primes Env for entry. The CD4-bound state, however, is prone to spontaneous inactivation and susceptible to antibody neutralization. How does unliganded HIV-1 maintain CD4-binding capacity and regulate transitions to the CD4-bound state? To define this mechanistically, we determined crystal structures of unliganded core gp120 from HIV-1 clades B, C, and E. Notably, all of these unliganded HIV-1 structures resembled the CD4-bound state. Conformational fixation with ligand selection and thermodynamic analysis of full-length and core gp120 interactions revealed that the tendency of HIV-1 gp120 to adopt the CD4-bound conformation was restrained by the V1/V2- and V3-variable loops. In parallel, we determined the structure of core gp120 in complex with the small molecule, NBD-556, which specifically recognizes the CD4-bound conformation of gp120. Neutralization by NBD-556 indicated that Env spikes on primary isolates rarely assume the CD4-bound conformation spontaneously, although they could do so when quaternary restraints were loosened. Together, the results suggest that the CD4-bound conformation represents a "ground state" for the gp120 core, with variable loop and quaternary interactions restraining unliganded gp120 from "snapping" into this conformation. A mechanism of control involving deformations in unliganded structure from a functionally critical state (e. g., the CD4-bound state) provides advantages in terms of HIV-1 Env structural diversity and resistance to antibodies and inhibitors, while maintaining elements essential for entry.
C1 [Finzi, Andres; Sodroski, Joseph G.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Dept Pathol,Div AIDS, Boston, MA 02115 USA.
[Do Kwon, Young; Wu, Xueling; Schmidt, Stephen D.; Stuckey, Jonathan; Yang, Yongping; Zhou, Tongqing; Zhu, Jiang; Shapiro, Lawrence; Mascola, John R.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Sodroski, Joseph G.] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA.
[Dogo-Isonagie, Cajetan; Bewley, Carole A.] NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Lee, Lawrence K.] Victor Chang Cardiac Res Inst, Struct & Computat Biol Div, Darlinghurst, NSW 2010, Australia.
[Moore, Lucas R.; Vicic, David A.] Univ Arkansas, Dept Chem & Biochem, Fayetteville, AR 72701 USA.
[Vicic, David A.] Univ Hawaii, Dept Chem, Honolulu, HI 96822 USA.
[Debnath, Asim K.] New York Blood Ctr, Lindsley F Kimball Res Inst, Lab Mol Modeling & Drug Design, New York, NY 10065 USA.
[Shapiro, Lawrence] Columbia Univ, Dept Biochem & Mol Biophys, New York, NY 10032 USA.
RP Sodroski, JG (reprint author), Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS,Dept Pathol,Div AIDS, 44 Binney St, Boston, MA 02115 USA.
EM joseph_sodroski@dfci.harvard.edu; pdkwong@nih.gov
RI Kwon, Young Do/A-6957-2010; Zhou, Tongqing/A-6880-2010; Cheng,
Yushao/E-6256-2011; Schmidt, Stephen/B-5398-2012
OI Zhou, Tongqing/0000-0002-3935-4637;
FU National Institutes of Health (NIH); International AIDS Vaccine
Initiative's Neutralizing Antibody Consortium; US Department of Energy,
Basic Energy Sciences, Office of Science [W-31-109-Eng-38]
FX We thank J. Hoxie, R. Sandier, I. A. Wilson, and members of the
Structural Biology Section and Structural Bioinformatics Core, Vaccine
Research Center, for discussions and comments on the manuscript. Support
for this work was provided by the Intramural Research Program of the
National Institutes of Health (NIH) and by grants from the NIH and from
the International AIDS Vaccine Initiative's Neutralizing Antibody
Consortium. 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 Contract
W-31-109-Eng-38.
NR 46
TC 117
Z9 117
U1 3
U2 31
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 10
PY 2012
VL 109
IS 15
BP 5663
EP 5668
DI 10.1073/pnas.1112391109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 922FX
UT WOS:000302533500028
ER
PT J
AU Baron, BW
Anastasi, J
Hyjek, EM
Bies, J
Reddy, PL
Dong, JF
Joseph, L
Thirman, MJ
Wroblewski, K
Wolff, L
Baron, JM
AF Baron, Beverly W.
Anastasi, John
Hyjek, Elizabeth M.
Bies, Juraj
Reddy, Poluru L.
Dong, Jingfang
Joseph, Loren
Thirman, Michael J.
Wroblewski, Kristen
Wolff, Linda
Baron, Joseph M.
TI PIM1 gene cooperates with human BCL6 gene to promote the development of
lymphomas
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID B-CELL LYMPHOMA; GERMINAL-CENTER FORMATION; BURKITTS-LYMPHOMA; C-MYC;
EXPRESSION; DIFFERENTIATION; PROTOONCOGENE; KINASE; LEUKEMIA; ACTIVATION
AB Diffuse large B-cell lymphomas in humans are associated with chromosomal rearrangements (similar to 40%) and/or mutations disrupting autoregulation (similar to 16%) involving the BCL6 gene. Studies of lymphoma development in humans and mouse models have indicated that lymphomagenesis evolves through the accumulation of multiple genetic alterations. Based on our prior studies, which indicated that carcinogen-induced DNA mutations enhance the incidence of lymphomas in our mouse model expressing a human BCL6 transgene, we hypothesized that mutated genes are likely to play an important cooperative role in BCL6-associated lymphoma development. We used retroviral insertional mutagenesis in an effort to identify which genes cooperate with BCL6 in lymphomagenesis in our BCL6 transgenic mice. We identified PIM1 as the most frequently recurring cooperating gene in our murine BCL6-associated lymphomas (T- and B-cell types), and we observed elevated levels of PIM1 mRNA and protein expression in these neoplasms. Further, immunohistochemical staining, which was performed in 20 randomly selected BCL6-positive human B-and T-cell lymphomas, revealed concurrent expression of BCL6 and PIM1 in these neoplasms. As PIM1 encodes a serine/threonine kinase, PIM1 kinase inhibition may be a promising therapy for BCL6/PIM1-positive human lymphomas.
C1 [Baron, Beverly W.; Anastasi, John; Hyjek, Elizabeth M.; Reddy, Poluru L.; Joseph, Loren] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA.
[Bies, Juraj; Wolff, Linda] NCI, Leukemogenesis Sect, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
[Dong, Jingfang; Thirman, Michael J.; Baron, Joseph M.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Wroblewski, Kristen] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
RP Baron, BW (reprint author), Univ Chicago, Dept Pathol, 5841 S Maryland Ave, Chicago, IL 60637 USA.
EM beverly.baron@uchospitals.edu
FU Department of Pathology at the University of Chicago; University of
Chicago Cancer Center [P30 CA014599]; University of Chicago
FX We thank Dr. B. Gladstone for technical assistance, Dr. I. Aifantis for
antibodies for flow cytometry, D. Kane for expertise in
immunohistochemistry, R. Duggan for assistance with FACS, and G. Musa
for assistance with illustrations. This work was supported by the
Department of Pathology at the University of Chicago (B. W. B.),
University of Chicago Cancer Center Support Grant P30 CA014599 (to B. W.
B.), and Hematology Research Funds at the University of Chicago donated
by S. Samsky and E. Lanzl (to J.M.B.).
NR 45
TC 9
Z9 9
U1 0
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 APR 10
PY 2012
VL 109
IS 15
BP 5735
EP 5739
DI 10.1073/pnas.1201168109
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 922FX
UT WOS:000302533500040
PM 22451912
ER
PT J
AU Chang, YF
Lee-Chang, JS
Imam, JS
Buddavarapu, KC
Subaran, SS
Sinha-Hikim, AP
Gorospe, M
Rao, MK
AF Chang, Yao-Fu
Lee-Chang, Jennifer S.
Imam, J. Saadi
Buddavarapu, Kalyan Chakravarthy
Subaran, Sarah S.
Sinha-Hikim, Amiya P.
Gorospe, Myriam
Rao, Manjeet K.
TI Interaction between microRNAs and actin-associated protein Arpc5
regulates translational suppression during male germ cell
differentiation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE spermiogenesis; messenger ribonucleoprotein; Arp2/3; processing body
ID RNA-BINDING-PROTEIN; SPERMATOGENIC CELLS; TRANSITION PROTEINS; ARP2/3
COMPLEX; MESSENGER-RNA; MOUSE; MICE; PHOSPHORYLATION; SPERMATIDS;
SERTOLI
AB Decoupling of transcription and translation during postmeiotic germ cell differentiation is critical for successful spermatogenesis. Here we establish that the interaction between microRNAs and actin-associated protein Arpc5 sets the stage for an elaborate translational control mechanism by facilitating the sequestration of germ cell mRNAs into translationally inert ribonucleoprotein particles until they are later translated. Our studies reveal that loss of microRNA-dependent regulation of Arpc5, which controls the distribution of germ cell mRNAs between translationally active and inactive pools, results in abnormal round spermatid differentiation and impaired fertility. Interestingly, Arpc5 functions as a broadly acting translational suppressor, as it inhibits translation initiation by blocking 80S formation and facilitates the transport of mRNAs to chromatoid/P bodies. These findings identify a unique role for actin-associated proteins in translational regulation, and suggest that mRNA-specific and general translational control mechanisms work in tandem to regulate critical germ cell differentiation events and diverse somatic cell functions.
C1 [Chang, Yao-Fu; Lee-Chang, Jennifer S.; Imam, J. Saadi; Buddavarapu, Kalyan Chakravarthy; Rao, Manjeet K.] Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, San Antonio, TX 78229 USA.
[Chang, Yao-Fu; Rao, Manjeet K.] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
[Subaran, Sarah S.; Gorospe, Myriam] NIA, Lab Mol Biol & Immunol, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Sinha-Hikim, Amiya P.] Charles R Drew Univ Med & Sci, Div Endocrinol Metab & Mol Med, Los Angeles, CA 90059 USA.
RP Rao, MK (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Greehey Childrens Canc Res Inst, San Antonio, TX 78229 USA.
EM raom@uthscsa.edu
OI Imam, J Saadi/0000-0003-3463-838X
FU National Institute of Child Health and Human Development [HD057118];
National Institutes of Health (NIH); National Institute on Aging, NIH
FX We thank Yidong Chen, Krystle Harris, Jennifer Rebeles, and Jennifer
Martindale for assistance with experiments and evaluation of data. We
also thank Daniel Schoenberg, Rod Balhorn, Marvin Fritzler, and Peter
Sarnow for generously providing us with reagents. Thanks to Alexander
Pertsemlidis for critical reading of the manuscript. M. K. R. was
supported by National Institute of Child Health and Human Development
Grant HD057118, National Institutes of Health (NIH); and S. S. S. and M.
G. were supported by the Intramural Research Program, National Institute
on Aging, NIH.
NR 29
TC 14
Z9 15
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 10
PY 2012
VL 109
IS 15
BP 5750
EP 5755
DI 10.1073/pnas.1117837109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 922FX
UT WOS:000302533500043
PM 22447776
ER
PT J
AU Vertes, PE
Alexander-Bloch, AF
Gogtay, N
Giedd, JN
Rapoport, JL
Bullmore, ET
AF Vertes, Petra E.
Alexander-Bloch, Aaron F.
Gogtay, Nitin
Giedd, Jay N.
Rapoport, Judith L.
Bullmore, Edward T.
TI Simple models of human brain functional networks
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE neuroimaging; graph theory; systems; trade-off
ID SMALL-WORLD NETWORKS; GRAPH-THEORETICAL ANALYSIS; COMMON STEREOTACTIC
SPACE; GLOBAL OPTIMIZATION; SCHIZOPHRENIA; CONNECTIVITY; SYSTEMS;
IMAGES; ROBUST; REGISTRATION
AB Human brain functional networks are embedded in anatomical space and have topological properties-small-worldness, modularity, fat-tailed degree distributions-that are comparable to many other complex networks. Although a sophisticated set of measures is available to describe the topology of brain networks, the selection pressures that drive their formation remain largely unknown. Here we consider generative models for the probability of a functional connection (an edge) between two cortical regions (nodes) separated by some Euclidean distance in anatomical space. In particular, we propose a model in which the embedded topology of brain networks emerges from two competing factors: a distance penalty based on the cost of maintaining long-range connections; and a topological term that favors links between regions sharing similar input. We show that, together, these two biologically plausible factors are sufficient to capture an impressive range of topological properties of functional brain networks. Model parameters estimated in one set of functional MRI (fMRI) data on normal volunteers provided a good fit to networks estimated in a second independent sample of fMRI data. Furthermore, slightly detuned model parameters also generated a reasonable simulation of the abnormal properties of brain functional networks in people with schizophrenia. We therefore anticipate that many aspects of brain network organization, in health and disease, may be parsimoniously explained by an economical clustering rule for the probability of functional connectivity between different brain areas.
C1 [Vertes, Petra E.; Alexander-Bloch, Aaron F.; Bullmore, Edward T.] Univ Cambridge, Behav & Clin Neurosci Inst, Dept Psychiat, Cambridge CB2 0SZ, England.
[Alexander-Bloch, Aaron F.; Gogtay, Nitin; Giedd, Jay N.; Rapoport, Judith L.] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
[Alexander-Bloch, Aaron F.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Bullmore, Edward T.] Cambridgeshire & Peterborough Natl Hlth Serv Fdn, Cambridge CB21 5EF, England.
[Bullmore, Edward T.] Addenbrookes Hosp, GlaxoSmithKline Clin Unit Cambridge, Cambridge CB2 0QQ, England.
RP Bullmore, ET (reprint author), Univ Cambridge, Behav & Clin Neurosci Inst, Dept Psychiat, Cambridge CB2 0SZ, England.
EM etb23@cam.ac.uk
RI Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015; Bullmore,
Edward/C-1706-2012;
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978;
Bullmore, Edward/0000-0002-8955-8283; Alexander-Bloch,
Aaron/0000-0001-6554-1893; Vertes, Petra E./0000-0002-0992-3210
FU Wellcome Trust; Medical Research Council; Engineering and Physical
Sciences Research Council; NIH
FX The Behavioural and Clinical Neuroscience Institute is supported by the
Wellcome Trust and the Medical Research Council. P. E. V. was supported
by a grant from the Engineering and Physical Sciences Research Council.
Data collection was supported by the intramural research program of the
National Institute of Mental Health, NIH. A.F.A.-B. is supported by the
NIH Cambridge Graduate Partnership Program.
NR 52
TC 87
Z9 89
U1 3
U2 18
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 10
PY 2012
VL 109
IS 15
BP 5868
EP 5873
DI 10.1073/pnas.1111738109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 922FX
UT WOS:000302533500063
PM 22467830
ER
PT J
AU Gaiser, MR
Lammermann, T
Feng, X
Igyarto, BZ
Kaplan, DH
Tessarollo, L
Germain, RN
Udey, MC
AF Gaiser, Maria R.
Laemmermann, Tim
Feng, Xu
Igyarto, Botond Z.
Kaplan, Daniel H.
Tessarollo, Lino
Germain, Ronald N.
Udey, Mark C.
TI Cancer-associated epithelial cell adhesion molecule (EpCAM; CD326)
enables epidermal Langerhans cell motility and migration in vivo
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID DERMAL DENDRITIC CELLS; CONTACT HYPERSENSITIVITY; E-CADHERIN; EP-CAM;
DEFICIENT MICE; STEM-CELLS; NULL MICE; RESPONSES; MATURATION; DISTINCT
AB After activation, Langerhans cells (LC), a distinct subpopulation of epidermis-resident dendritic cells, migrate from skin to lymph nodes where they regulate the magnitude and quality of immune responses initiated by epicutaneously applied antigens. Modulation of LC-keratinocyte adhesion is likely to be central to regulation of LC migration. LC express high levels of epithelial cell adhesion molecule (EpCAM; CD326), a cell-surface protein that is characteristic of some epithelia and many carcinomas and that has been implicated in intercellular adhesion and metastasis. To gain insight into EpCAM function in a physiologic context in vivo, we generated conditional knockout mice with EpCAM-deficient LC and characterized them. Epidermis from these mice contained increased numbers of LC with normal levels of MHC and costimulatory molecules and T-cell-stimulatory activity in vitro. Migration of EpCAM-deficient LC from skin explants was inhibited, but chemotaxis of dissociated LC was not. Correspondingly, the ability of contact allergen-stimulated, EpCAM-deficient LC to exit epidermis in vivo was delayed, and strikingly fewer hapten-bearing LC subsequently accumulated in lymph nodes. Attenuated migration of EpCAM-deficient LC resulted in enhanced contact hypersensitivity responses as previously described in LC-deficient mice. Intravital microscopy revealed reduced translocation and dendrite motility in EpCAM-deficient LC in vivo in contact allergen-treated mice. These results conclusively link EpCAM expression to LC motility/migration and LC migration to immune regulation. EpCAM appears to promote LC migration from epidermis by decreasing LC-keratinocyte adhesion and may modulate intercellular adhesion and cell movement within in epithelia during development and carcinogenesis in an analogous fashion.
C1 [Gaiser, Maria R.; Feng, Xu; Udey, Mark C.] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Laemmermann, Tim; Germain, Ronald N.] NIAID, Lymphocyte Biol Sect, Lab Syst Biol, NIH, Bethesda, MD 20892 USA.
[Igyarto, Botond Z.; Kaplan, Daniel H.] Univ Minnesota, Dept Dermatol, Ctr Immunol, Minneapolis, MN 55455 USA.
[Tessarollo, Lino] NCI, Mouse Canc Genet Program, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Udey, MC (reprint author), NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM udey@helix.nih.gov
RI Kaplan, Daniel/N-2779-2013
OI Kaplan, Daniel/0000-0002-7851-7320
FU Center for Cancer Research, National Cancer Institute; National
Institues of Allergy and Infectious Diseases, National Institutes of
Health; National Institutes of Health [R01-AR056632]; International
Human Frontier Science Program fellowship
FX We thank Drs. William Telford and Michael Kruhlak for their advice and
assistance with flow cytometry and conventional microscopy; Joshua
Drago, Mallorie Heneghan, and Olga Milgrom for mouse husbandry and
genotyping; Jay Linton, Michael Lu, Dr. Chuanjin Wu, and Dr. Sei-ichiro
Motegi for advice and assistance with experimental procedures; and Dr.
Stephen I. Katz for helpful discussions. This work was supported by the
Intramural Research Program, Center for Cancer Research, National Cancer
Institute, and the National Institues of Allergy and Infectious
Diseases, National Institutes of Health, by National Institutes of
Health Grant R01-AR056632 (to D.H.K.), and an International Human
Frontier Science Program fellowship grant (to T.L.).
NR 57
TC 29
Z9 30
U1 0
U2 8
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 10
PY 2012
VL 109
IS 15
BP E889
EP E897
DI 10.1073/pnas.1117674109
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 922FX
UT WOS:000302533500005
PM 22411813
ER
PT J
AU Safaeian, M
Hildesheim, A
Gonzalez, P
Yu, K
Porras, C
Li, QZ
Rodriguez, AC
Sherman, ME
Schiffman, M
Wacholder, S
Burk, R
Herrero, R
Burdette, L
Chanock, SJ
Wang, SS
AF Safaeian, Mahboobeh
Hildesheim, Allan
Gonzalez, Paula
Yu, Kai
Porras, Carolina
Li, Qizhai
Cecilia Rodriguez, Ana
Sherman, Mark E.
Schiffman, Mark
Wacholder, Sholom
Burk, Robert
Herrero, Rolando
Burdette, Laurie
Chanock, Stephen J.
Wang, Sophia S.
TI Single Nucleotide Polymorphisms in the PRDX3 and RPS19 and Risk of HPV
Persistence and Cervical Precancer/Cancer
SO PLOS ONE
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS INFECTION; FAMILY-CANCER DATABASE; COSTA-RICA;
NEOPLASIA; PROGRESSION; VARIANTS; GENES
AB Background: Host genetic factors might affect the risk of progression from infection with carcinogenic human papillomavirus (HPV), the etiologic agent for cervical cancer, to persistent HPV infection, and hence to cervical precancer and cancer.
Methodology/Principal Findings: We assessed 18,310 tag single nucleotide polymorphisms (SNPs) from 1113 genes in 416 cervical intraepithelial neoplasia 3 (CIN3)/cancer cases, 356 women with persistent carcinogenic HPV infection (median persistence of 25 months) and 425 randomly selected women (non-cases and non-HPV persistent) from the 10,049 women from the Guanacaste, Costa Rica HPV natural history cohort. For gene and SNP associations, we computed age-adjusted odds ratio and p-trend. Three comparisons were made: 1) association with CIN3/cancer (compared CIN3/cancer cases to random controls), 2) association with persistence (compared HPV persistence to random controls), and 3) progression (compared CIN3/cancers with HPV-persistent group). Regions statistically significantly associated with CIN3/cancer included genes for peroxiredoxin 3 PRDX3, and ribosomal protein S19 RPS19. The single most significant SNPs from each gene associated with CIN3/cancer were PRDX3 rs7082598 (P-trend < 0.0001), and RPS19 rs2305809 (P-trend = 0.0007), respectively. Both SNPs were also associated with progression.
Conclusions/Significance: These data suggest involvement of two genes, RSP19 and PRDX3, or other SNPs in linkage disequilibrium, with cervical cancer risk. Further investigation showed that they may be involved in both the persistence and progression transition stages. Our results require replication but, if true, suggest a role for ribosomal dysfunction, mitochondrial processes, and/or oxidative stress, or other unknown function of these genes in cervical carcinogenesis.
C1 [Safaeian, Mahboobeh; Hildesheim, Allan; Yu, Kai; Sherman, Mark E.; Schiffman, Mark; Wacholder, Sholom] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Gonzalez, Paula; Porras, Carolina; Cecilia Rodriguez, Ana; Herrero, Rolando] Fdn INCIENSA, Proyecto Epidemiol Guanacaste, San Jose, Costa Rica.
[Li, Qizhai] Chinese Acad Sci, Acad Math & Syst Sci, Beijing, Peoples R China.
[Burk, Robert] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Burdette, Laurie; Chanock, Stephen J.] NCI Frederick, Core Genotyping Facil, Div Canc Epidemiol & Genet, Adv Technol Program,SAIC Frederick Inc, Frederick, MD USA.
[Wang, Sophia S.] City Hope Natl Med Ctr, Dept Populat Sci, Div Etiol, Duarte, CA USA.
RP Safaeian, M (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM safaeianm@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU NCI; NIH Office of Research On Women's Health; National Young Science
Foundation of China [10901155]; SAIC-Frederick Inc.; Information
Management Services, Inc.
FX The study was funded by intramural NCI and the NIH Office of Research On
Women's Health. The authors are grateful to Sabrina Chen from the
Information Management Services, Inc. (IMS) for data management and
programming support. They are also grateful to Amy Hutchinson and
Belynda Hicks for their management of this genotyping effort at the NCI
Core Genotyping Facility and for their scientific contributions to the
authors' research efforts. Q. Li is partially supported by National
Young Science Foundation of China No. 10901155. The funders had no role
in study design, data collection and analysis, decision to publish, or
preparation of the manuscript.; Laurie Burdette and Stephen J. Chanock
are employed by The Core Genotyping Facility (CGF) which is within the
Division of Cancer Epidemiology and Genetics (DCEG) of the National
Cancer Institute (NCI) and supported by SAIC-Frederick Inc. Information
Management Services, Inc. also supported this study, along with Amy
Hutchinson and Belynda Hicks with their management of this genotyping
effort at the NCI Core Genotyping Facility and for their scientific
contributions to the authors' research efforts. This does not alter the
authors' adherence to all PloS ONE policies on sharing data and
materials.
NR 21
TC 17
Z9 19
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 APR 9
PY 2012
VL 7
IS 4
AR e33619
DI 10.1371/journal.pone.0033619
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 955JO
UT WOS:000305014500013
PM 22496757
ER
PT J
AU Bennett, GG
Warner, ET
Glasgow, RE
Askew, S
Goldman, J
Ritzwoller, DP
Emmons, KM
Rosner, BA
Colditz, GA
AF Bennett, Gary G.
Warner, Erica T.
Glasgow, Russell E.
Askew, Sandy
Goldman, Julie
Ritzwoller, Debra P.
Emmons, Karen M.
Rosner, Bernard A.
Colditz, Graham A.
CA Be Fit
Be Well Study Investigators
TI Obesity Treatment for Socioeconomically Disadvantaged Patients in
Primary Care Practice
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Article
ID BODY-MASS INDEX; NUTRITION EXAMINATION SURVEY; WEIGHT-LOSS MAINTENANCE;
BLOOD-PRESSURE; LIFE-STYLE; AFRICAN-AMERICAN; UNITED-STATES;
CARDIOVASCULAR RISK; ETHNIC DISPARITIES; CANCER PREVENTION
AB Background: Few evidence-based weight loss treatment options exist for medically vulnerable patients in the primary care setting.
Methods: We conducted a 2-arm, 24-month randomized effectiveness trial in 3 Boston community health centers (from February 1, 2008, through May 2, 2011). Participants were 365 obese patients receiving hypertension treatment (71.2% black, 13.1% Hispanic, 68.5% female, and 32.9% with less than a high school educational level). We randomized participants to usual care or a behavioral intervention that promoted weight loss and hypertension self-management using eHealth components. The intervention included tailored behavior change goals, self-monitoring, and skills training, available via a website or interactive voice response; 18 telephone counseling calls; primary care provider endorsement; 12 optional group support sessions; and links with community resources.
Results: At 24 months, weight change in the intervention group compared with that in the usual care group was -1.03 kg (95% CI, -2.03 to -0.03 kg). Twenty-four-month change in body mass index (calculated as weight in kilograms divided by height in meters squared) in the intervention group compared with that in the usual care group was -0.38 (95% CI, -0.75 to -0.004). Intervention participants had larger mean weight losses during the 24 months compared with that in the usual care group (area under the receiver operating characteristic curve, -1.07 kg; 95% CI, -1.94 to -0.22). Mean systolic blood pressure was not significantly lower in the intervention arm compared with the usual care arm.
Conclusion: The intervention produced modest weight losses, improved blood pressure control, and slowed systolic blood pressure increases in this high-risk, socio-economically disadvantaged patient population.
C1 [Bennett, Gary G.; Askew, Sandy] Duke Univ, Duke Obes Prevent Program, Durham, NC 27708 USA.
[Bennett, Gary G.] Duke Univ, Dept Psychol & Neurosci, Durham, NC 27708 USA.
[Bennett, Gary G.; Askew, Sandy] Duke Univ, Duke Global Hlth Inst, Durham, NC 27708 USA.
[Warner, Erica T.; Colditz, Graham A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Bennett, Gary G.; Emmons, Karen M.] Harvard Univ, Sch Publ Hlth, Dept Soc, Boston, MA 02115 USA.
[Bennett, Gary G.; Emmons, Karen M.] Harvard Univ, Sch Publ Hlth, Dept Human Dev, Boston, MA 02115 USA.
[Bennett, Gary G.; Emmons, Karen M.] Harvard Univ, Sch Publ Hlth, Dept Hlth, Boston, MA 02115 USA.
[Rosner, Bernard A.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Rosner, Bernard A.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Bennett, Gary G.; Warner, Erica T.; Askew, Sandy; Goldman, Julie; Emmons, Karen M.] Dana Farber Canc Inst, Ctr Community Based Res, Div Populat Sci, Boston, MA 02115 USA.
[Glasgow, Russell E.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Ritzwoller, Debra P.] Kaiser Permanente, Inst Hlth Res, Denver, CO USA.
[Colditz, Graham A.] Washington Univ, Sch Med, Div Publ Hlth Sci, Alvin J Siteman Canc Ctr,Dept Surg, St Louis, MO USA.
RP Bennett, GG (reprint author), Duke Univ, Duke Obes Prevent Program, POB 90086, Durham, NC 27708 USA.
EM gary.bennett@duke.edu
RI Colditz, Graham/A-3963-2009
OI Colditz, Graham/0000-0002-7307-0291
FU National Heart, Lung, and Blood Institute [U01-HL087071]; National
Cancer Institute [K22CA126992, K05CA124415-04]
FX This work was supported in part by grant U01-HL087071 from the National
Heart, Lung, and Blood Institute and grants K22CA126992 (Dr Bennett) and
K05CA124415-04 (Dr Emmons) from the National Cancer Institute.
NR 58
TC 67
Z9 68
U1 2
U2 28
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 APR 9
PY 2012
VL 172
IS 7
BP 565
EP 574
DI 10.1001/archinternmed.2012.1
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 922NV
UT WOS:000302555300006
PM 22412073
ER
PT J
AU Pilotto, A
Panza, F
Ferrucci, L
AF Pilotto, Alberto
Panza, Francesco
Ferrucci, Luigi
TI A Multidimensional Prognostic Index in Common Conditions Leading to
Death in Older Patients
SO ARCHIVES OF INTERNAL MEDICINE
LA English
DT Letter
ID COMPREHENSIVE GERIATRIC ASSESSMENT; LONG-TERM MORTALITY
C1 [Pilotto, Alberto] S Antonio Hosp, Geriatr Unit, Azienda ULSS Padova 16, I-35127 Padua, Italy.
[Pilotto, Alberto; Panza, Francesco] IRCCS Casa Sollievo Sofferenza, Geriatr Unit, San Giovanni Rotondo, Italy.
[Pilotto, Alberto; Panza, Francesco] IRCCS Casa Sollievo Sofferenza, Gerontol Geriatr Res Lab, San Giovanni Rotondo, Italy.
[Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
RP Pilotto, A (reprint author), S Antonio Hosp, Geriatr Unit, Azienda ULSS Padova 16, Via Facciolati 71, I-35127 Padua, Italy.
EM alberto.pilotto@sanita.padova.it
NR 5
TC 9
Z9 9
U1 1
U2 2
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 APR 9
PY 2012
VL 172
IS 7
BP 594
EP 594
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 922NV
UT WOS:000302555300015
PM 22493470
ER
PT J
AU Okoye, AA
Rohankhedkar, M
Abana, C
Pattenn, A
Reyes, M
Pexton, C
Lum, R
Sylwester, A
Planer, SL
Legasse, A
Park, BS
Piatak, M
Lifson, JD
Axthelm, MK
Picker, LJ
AF Okoye, Afam A.
Rohankhedkar, Mukta
Abana, Chike
Pattenn, Audrie
Reyes, Matthew
Pexton, Christopher
Lum, Richard
Sylwester, Andrew
Planer, Shannon L.
Legasse, Alfred
Park, Byung S.
Piatak, Michael, Jr.
Lifson, Jeffrey D.
Axthelm, Michael K.
Picker, Louis J.
TI Naive T cells are dispensable for memory CD4(+) T cell homeostasis in
progressive simian immunodeficiency virus infection
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID CD8(+) LYMPHOCYTE DEPLETION; RHESUS MACAQUES; SIV INFECTION;
PATHOGENESIS; PROTECTION; EXPANSION; IMMUNITY; DECLINE; MONKEYS; DISEASE
AB The development of AIDS in chronic HIV/simian immunodeficiency virus (SIV) infection has been closely linked to progressive failure of CD4(+) memory T cell (T-M) homeostasis. CD4(+) naive T cells (T-N) also decline in these infections, but their contribution to disease progression is less clear. We assessed the role of CD4(+) T-N in SIV pathogenesis using rhesus macaques (RMs) selectively and permanently depleted of CD4(+) T-N before SIV infection. CD4(+) T-N-depleted and CD4(+) T-N-repleted RMs were created by subjecting juvenile RMs to thymectomy versus sham surgery, respectively, followed by total CD4(+) T cell depletion and recovery from this depletion. Although thymectomized and sham-treated RMs manifested comparable CD4(+) T-M recovery, only sham-treated RMs reconstituted CD4(+) T-N. CD4(+) T-N-depleted RMs responded to SIVmac239 infection with markedly attenuated SIV-specific CD4(+) T cell responses, delayed SIVenv-specific Ab responses, and reduced SIV-specific CD8(+) T cell responses. However, CD4(+) T-N-depleted and -repleted groups showed similar levels of SIV replication. Moreover, CD4(+) T-N deficiency had no significant effect on CD4(+) T-M homeostasis (either on or off anti-retroviral therapy) or disease progression. These data demonstrate that the CD4(+) T-N compartment is dispensable for CD4+ T-M homeostasis in progressive SIV infection, and they confirm that CD4(+) T-M comprise a homeostatically independent compartment that is intrinsically capable of self-renewal.
C1 [Okoye, Afam A.; Rohankhedkar, Mukta; Abana, Chike; Pattenn, Audrie; Reyes, Matthew; Pexton, Christopher; Lum, Richard; Sylwester, Andrew; Planer, Shannon L.; Legasse, Alfred; Axthelm, Michael K.; Picker, Louis J.] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Vaccine & Gene Therapy Inst, Dept Pathol, Beaverton, OR 97006 USA.
[Okoye, Afam A.; Rohankhedkar, Mukta; Abana, Chike; Pattenn, Audrie; Reyes, Matthew; Pexton, Christopher; Lum, Richard; Sylwester, Andrew; Planer, Shannon L.; Legasse, Alfred; Axthelm, Michael K.; Picker, Louis J.] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Vaccine & Gene Therapy Inst, Dept Mol Microbiol & Immunol, Beaverton, OR 97006 USA.
[Park, Byung S.] Oregon Hlth & Sci Univ, Dept Publ Hlth & Prevent Med, Div Biostat, Portland, OR 97239 USA.
[Piatak, Michael, Jr.; Lifson, Jeffrey D.] NCI, AIDS Vaccine Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Picker, LJ (reprint author), Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Vaccine & Gene Therapy Inst, Dept Pathol, Beaverton, OR 97006 USA.
EM pickerl@ohsu.edu
OI /0000-0003-3516-7516
FU National Institutes of Health [R37-AI054292, P51-RR00163]; National
Cancer Institute, National Institutes of Health [HHSN261200800001E]
FX This work was supported by National Institutes of Health grants
R37-AI054292 and P51-RR00163 and federal funds from the National Cancer
Institute, National Institutes of Health, under Contract No.
HHSN261200800001E.
NR 32
TC 15
Z9 15
U1 0
U2 3
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 APR 9
PY 2012
VL 209
IS 4
BP 641
EP 651
DI 10.1084/jem.20112071
PG 11
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 925SS
UT WOS:000302782300001
PM 22451717
ER
PT J
AU Scheibye-Knudsen, M
Ramamoorthy, M
Sykora, P
Maynard, S
Lin, PC
Minor, RK
Wilson, DM
Cooper, M
Spencer, R
de Cabo, R
Croteau, DL
Bohr, VA
AF Scheibye-Knudsen, Morten
Ramamoorthy, Mahesh
Sykora, Peter
Maynard, Scott
Lin, Ping-Chang
Minor, Robin K.
Wilson, David M., III
Cooper, Marcus
Spencer, Richard
de Cabo, Rafael
Croteau, Deborah L.
Bohr, Vilhelm A.
TI Cockayne syndrome group B protein prevents the accumulation of damaged
mitochondria by promoting mitochondrial autophagy
SO JOURNAL OF EXPERIMENTAL MEDICINE
LA English
DT Article
ID LIFE-SPAN EXTENSION; BASE EXCISION-REPAIR; NEURODEGENERATIVE DISEASES;
CALORIE RESTRICTION; C-ELEGANS; DNA; CELLS; TRANSCRIPTION; MICE;
DYSFUNCTION
AB Cockayne syndrome (CS) is a devastating autosomal recessive disease characterized by neurodegeneration, cachexia, and accelerated aging. 80% of the cases are caused by mutations in the CS complementation group B (CSB) gene known to be involved in DNA repair and transcription. Recent evidence indicates that CSB is present in mitochondria, where it associates with mitochondrial DNA (mtDNA). We report an increase in metabolism in the CSBm/m mouse model and CSB-deficient cells. Mitochondrial content is increased in CSB-deficient cells, whereas autophagy is down-regulated, presumably as a result of defects in the recruitment of P62 and mitochondrial ubiquitination. CSB-deficient cells show increased free radical production and an accumulation of damaged mitochondria. Accordingly, treatment with the autophagic stimulators lithium chloride or rapamycin reverses the bioenergetic phenotype of CSB-deficient cells. Our data imply that CSB acts as an mtDNA damage sensor, inducing mitochondrial autophagy in response to stress, and that pharmacological modulators of autophagy are potential treatment options for this accelerated aging phenotype.
C1 [Scheibye-Knudsen, Morten; Ramamoorthy, Mahesh; Sykora, Peter; Wilson, David M., III; Croteau, Deborah L.; Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
[Maynard, Scott; Lin, Ping-Chang; Spencer, Richard] NIA, Magnet Resonance Imaging & Spect Sect, NIH, Baltimore, MD 21224 USA.
[Minor, Robin K.; de Cabo, Rafael] NIA, Lab Expt Gerontol, NIH, Baltimore, MD 21224 USA.
[Bohr, Vilhelm A.] Univ Copenhagen, Ctr Hlth Aging, Inst Cellular & Mol Med, DK-1165 Copenhagen, Denmark.
[Cooper, Marcus] Univ Massachusetts, Sch Med, Div Cardiovasc Med, Worcester, MA 01655 USA.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
EM vbohr@nih.gov
RI de Cabo, Rafael/J-5230-2016;
OI de Cabo, Rafael/0000-0002-3354-2442; Maynard, Scott/0000-0001-5625-936X;
Lin, Ping-Chang/0000-0003-0918-4072; Scheibye-Knudsen,
Morten/0000-0002-6637-1280; Ramamoorthy, Mahesh/0000-0002-2359-5647; ,
rafael/0000-0003-2830-5693
FU NIH, National Institute on Aging
FX This research was supported entirely by the Intramural Research Program
of the NIH, National Institute on Aging.
NR 58
TC 69
Z9 69
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 APR 9
PY 2012
VL 209
IS 4
BP 855
EP 869
DI 10.1084/jem.20111721
PG 15
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 925SS
UT WOS:000302782300016
PM 22473955
ER
PT J
AU Lloyd-Sherlock, P
McKee, M
Ebrahim, S
Gorman, M
Greengross, S
Prince, M
Pruchno, R
Gutman, G
Kirkwood, T
O'Neill, D
Ferrucci, L
Kritchevsky, SB
Vellas, B
AF Lloyd-Sherlock, Peter
McKee, Martin
Ebrahim, Shah
Gorman, Mark
Greengross, Sally
Prince, Martin
Pruchno, Rachel
Gutman, Gloria
Kirkwood, Tom
O'Neill, Desmond
Ferrucci, Luigi
Kritchevsky, Stephen B.
Vellas, Bruno
TI Population ageing and health
SO LANCET
LA English
DT Letter
C1 [Lloyd-Sherlock, Peter] Univ E Anglia, Sch Dev Studies, Norwich NR4 7TJ, Norfolk, England.
[McKee, Martin] London Sch Hyg & Trop Med, European Ctr Hlth Soc Transit, London WC1, England.
[Ebrahim, Shah] Publ Hlth Fdn India, S Asia Network Chron Dis, New Delhi, India.
[Gorman, Mark] HelpAge Int, London, England.
[Greengross, Sally] Int Longev Ctr UK, London, England.
[Prince, Martin] Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
[Pruchno, Rachel] New Jersey Inst Successful Aging, Stratford, NJ USA.
[Gutman, Gloria] Int Network Prevent Elder Abuse, Vancouver, BC, Canada.
[Kirkwood, Tom] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[O'Neill, Desmond] European Union Geriatr Med Soc, Brussels, Belgium.
[Ferrucci, Luigi] NIA, Bethesda, MD 20892 USA.
[Kritchevsky, Stephen B.] Sticht Ctr Aging, Winston Salem, NC USA.
[Vellas, Bruno] Int Assoc Gerontol & Geriatr, Liege, Belgium.
RP Lloyd-Sherlock, P (reprint author), Univ E Anglia, Sch Dev Studies, Norwich NR4 7TJ, Norfolk, England.
EM p.lloyd-sherlock@uea.ac.uk
RI Prince, Martin/A-9170-2010;
OI Prince, Martin/0000-0003-1379-7146; Gutman, Gloria/0000-0001-8810-2287;
Pruchno, Rachel/0000-0001-7440-4495; Kritchevsky,
Stephen/0000-0003-3336-6781; O'Neill, Desmond/0000-0002-5542-9897
FU Wellcome Trust [084674]
NR 3
TC 35
Z9 36
U1 1
U2 13
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 APR 7
PY 2012
VL 379
IS 9823
BP 1295
EP 1296
DI 10.1016/S0140-6736(12)60519-4
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 922FB
UT WOS:000302531100015
PM 22480756
ER
PT J
AU Zhou, XL
Yang, XY
Popescu, NC
AF Zhou, Xiaoling
Yang, Xu-Yu
Popescu, Nicholas C.
TI Preclinical evaluation of combined antineoplastic effect of DLC1 tumor
suppressor protein and suberoylanilide hydroxamic acid on prostate
cancer cells
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE DLC1; Tumor suppressor gene; SAHA; Apoptosis; RhoA activity; Inhibition
prostate tumor growth in vivo
ID HISTONE-DEACETYLASE INHIBITORS; RHO-GTPASES; GENE; THERAPY;
TRANSFORMATION; PERSPECTIVES; METASTASIS; CARCINOMA; MIGRATION; GROWTH
AB Deleted in liver cancer (DLC1), a tumor suppressor gene in multiple cancers, is recurrently down regulated or inactivated by epigenetic mechanisms in primary prostate carcinomas (PCAs). In this study the methylation and acetylation profile of the DLC1 promoter region was examined in three PCA cell lines with low or undetectable DLC1 expression: LNCaP, its derivative C4-2B-2, and 22Rv1. Two histone deacetylase inhibitors (HDAC), suberoylanilide hydroxamic acid (SAHA) and trichostatin A (TSA) induced histone acetylation of the DLC1 promoter in all three lines. DLC1 promoter methylation and deacetylation were detected in LNCaP and C4-2B-2 cells while in 22Rv1 cells DLC1 is silenced by deacetylation. Treatment with SAHA or TSA efficiently increased DLC1 expression in all lines, particularly in 22Rv1 cells, and activated the DLC1 promoter through the same Spl sites. The 22Rv1 cell line was selected to evaluate the efficacy of combined DLC1 transduction and SAHA treatment on tumor growth in athymic mice. Individually. DLC1 transduction and SAHA exposure reduced the tumor size by 75-80% compared to controls and in combination almost completely inhibited tumor growth. The antitumor effect was associated with the induction of apoptosis and inhibition of RhoA activity. SAHA alone significantly reduced RhoA activity, showing that this RhoGTPase is a target for SAHA. These results, obtained with a reliable preclinical in vivo test, predict that combined therapeutic agents targeting the pathways governing DLC1 function and HDAC inhibitors may be beneficial in management of prostate cancer. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Zhou, Xiaoling; Yang, Xu-Yu; Popescu, Nicholas C.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Popescu, NC (reprint author), NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, 37 Convent Dr,MSC 4262, Bethesda, MD 20892 USA.
EM popescun@mail.nih.gov
RI yang, xuyu/D-1414-2012
FU National Cancer Institute, NIH
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, NIH.
NR 26
TC 5
Z9 5
U1 0
U2 1
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 APR 6
PY 2012
VL 420
IS 2
BP 325
EP 330
DI 10.1016/j.bbrc.2012.02.158
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 969FW
UT WOS:000306042100020
PM 22425986
ER
PT J
AU Teijido, O
Ujwal, R
Hillerdal, CO
Kullman, L
Rostovtseva, TK
Abramson, J
AF Teijido, Oscar
Ujwal, Rachna
Hillerdal, Carl-Olof
Kullman, Lisen
Rostovtseva, Tatiana K.
Abramson, Jeff
TI Reply to Thinnes: To Include Plasmalemmal VDAC/Porin Pays
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Letter
ID CHANNEL; VDAC
C1 [Teijido, Oscar; Rostovtseva, Tatiana K.] Eunice Kennedy Shriver NICHD, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Ujwal, Rachna; Abramson, Jeff] Univ Calif Los Angeles, Dept Physiol, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Hillerdal, Carl-Olof; Kullman, Lisen] Uppsala Univ, Dept Med Cell Biol, S-75123 Uppsala, Sweden.
RP Teijido, O (reprint author), Eunice Kennedy Shriver NICHD, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
EM jabramson@mednet.ucla.edu
NR 6
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 6
PY 2012
VL 287
IS 15
BP 12156
EP 12156
DI 10.1074/jbc.N111.314229
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 925SR
UT WOS:000302782200055
ER
PT J
AU Murase, S
McKay, RD
AF Murase, Sachiko
McKay, Ronald D.
TI Matrix Metalloproteinase-9 Regulates Survival of Neurons in Newborn
Hippocampus
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID OCCURRING CELL-DEATH; MATRIX METALLOPROTEINASE-3; ALZHEIMERS-DISEASE;
MOUSE HIPPOCAMPUS; LAMININ; EXPRESSION; RAT; SPECIFICITY; ACTIVATION;
INTEGRINS
AB The number of neurons in the adult rodent brain is strongly influenced by events in early postnatal life that eliminate approximately half of the neurons. Recently, we reported that neurotrophins induced survival of neonatal rat hippocampal neurons by promoting neural activity and activation of the Ser/Thr kinase, Akt. The survival of neurons also depended on integrin signaling, but a role for the extracellular matrix (ECM) in this mechanism was yet to be explored. Here, we show that levels of the matrix metalloproteinase-9 (MMP9) decrease, and the level of the ECM protein laminin increases in rat hippocampus during the period of neuronal death. Hippocampi from MMP9 null mice showed higher levels of laminin expression than wild type at P1 and no further increase at P10. In vitro, the matrix metalloproteinase inhibitor FN-439 promoted survival of neurons in a laminin-integrin beta 1-dependent manner. Blocking laminin signaling attenuated activation of Akt by depolarization. In vivo, injecting FN-439 into the neonatal hippocampus increased the level of laminin and promoted neuronal survival through an integrin-dependent mechanism. These results show signals from the ECM are not simply permissive but rather actively regulated, and they interact with neuronal activity to control the number of hippocampal neurons. This work is the first to report a role for MMP9 in regulating neuronal survival through the developmental process that establishes the functional brain.
C1 [Murase, Sachiko; McKay, Ronald D.] NINDS, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[McKay, Ronald D.] Lieber Inst Brain Dev, Baltimore, MD 21205 USA.
RP Murase, S (reprint author), NINDS, Mol Biol Lab, NIH, 35 Lincoln Dr, Bethesda, MD 20892 USA.
EM sachikom@ninds.nih.gov
FU National Institutes of Health from NINDS
FX This work was supported by a National Institutes of Health grant from
the Intramural Research Program, NINDS.
NR 39
TC 15
Z9 15
U1 0
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 6
PY 2012
VL 287
IS 15
BP 12184
EP 12194
DI 10.1074/jbc.M111.297671
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 925SR
UT WOS:000302782200060
PM 22351756
ER
PT J
AU Duverger, O
Zah, A
Isaac, J
Sun, HW
Bartels, AK
Lian, JB
Berdal, A
Hwang, J
Morasso, MI
AF Duverger, Olivier
Zah, Angela
Isaac, Juliane
Sun, Hong-Wei
Bartels, Anne K.
Lian, Jane B.
Berdal, Ariane
Hwang, Joonsung
Morasso, Maria I.
TI Neural Crest Deletion of Dlx3 Leads to Major Dentin Defects through
Down-regulation of Dspp
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CHIP-SEQ DATA; TRICHODENTOOSSEOUS SYNDROME; SIALOPHOSPHOPROTEIN
EXPRESSION; TOOTH DEVELOPMENT; MURINE DENTITION; GENE-EXPRESSION;
HOMEOBOX GENES; ENAMEL DEFECTS; DIFFERENTIATION; MUTATION
AB During development, Dlx3 is expressed in ectodermal appendages such as hair and teeth. Thus far, the evidence that Dlx3 plays a crucial role in tooth development comes from reports showing that autosomal dominant mutations in DLX3 result in severe enamel and dentin defects leading to abscesses and infections. However, the normal function of DLX3 in odontogenesis remains unknown. Here, we use a mouse model to demonstrate that the absence of Dlx3 in the neural crest results in major impairment of odontoblast differentiation and dentin production. Mutant mice develop brittle teeth with hypoplastic dentin and molars with an enlarged pulp chamber and underdeveloped roots. Using this mouse model, we found that dentin sialophosphoprotein (Dspp), a major component of the dentin matrix, is strongly down-regulated in odontoblasts lacking Dlx3. Using ChIP-seq, we further demonstrate the direct binding of Dlx3 to the Dspp promoter in vivo. Luciferase reporter assays determined that Dlx3 positively regulates Dspp expression. This establishes a regulatory pathway where the transcription factor Dlx3 is essential in dentin formation by directly regulating a crucial matrix protein.
C1 [Duverger, Olivier; Zah, Angela; Isaac, Juliane; Bartels, Anne K.; Hwang, Joonsung; Morasso, Maria I.] NIAMS, Dev Skin Biol Sect, NIH, Bethesda, MD 20892 USA.
[Sun, Hong-Wei] NIAMS, Biodata Min & Discovery Sect, NIH, Bethesda, MD 20892 USA.
[Lian, Jane B.] Univ Massachusetts, Dept Cell Biol, Sch Med, Worcester, MA 01655 USA.
[Lian, Jane B.] Univ Massachusetts, Dept Orthoped Surg, Sch Med, Worcester, MA 01655 USA.
[Berdal, Ariane] Univ Paris 05, INSERM, UMRS 872, Team 5, F-75006 Paris, France.
[Berdal, Ariane] Univ Paris 06, INSERM, UMRS 872, Team 5, F-75006 Paris, France.
RP Morasso, MI (reprint author), NIAMS, Dev Skin Biol Sect, NIH, 50 South Dr,Room 1523, Bethesda, MD 20892 USA.
EM morasso@nih.gov
FU NIAMS, National Institutes of Health; National Institutes of Health [R37
DE012528]
FX This work was supported by the Intramural Research Program of the NIAMS,
National Institutes of Health.; Supported by National Institutes of
Health Grant R37 DE012528.
NR 51
TC 22
Z9 23
U1 0
U2 9
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
EI 1083-351X
J9 J BIOL CHEM
JI J. Biol. Chem.
PD APR 6
PY 2012
VL 287
IS 15
BP 12230
EP 12240
DI 10.1074/jbc.M111.326900
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 925SR
UT WOS:000302782200064
PM 22351765
ER
PT J
AU Lee, MS
Bonner, JR
Bernard, DJ
Sanchez, EL
Sause, ET
Prentice, RR
Burgess, SM
Brody, LC
AF Lee, Marina S.
Bonner, Jenna R.
Bernard, David J.
Sanchez, Erica L.
Sause, Eric T.
Prentice, R. Reid
Burgess, Shawn M.
Brody, Lawrence C.
TI Disruption of the folate pathway in zebrafish causes developmental
defects
SO BMC DEVELOPMENTAL BIOLOGY
LA English
DT Article
ID DEPENDENT METHYLENETETRAHYDROFOLATE DEHYDROGENASE; METHIONINE
ADENOSYLTRANSFERASE; RISK-FACTOR; REDUCTASE; GENE; CANCER; MICE;
IDENTIFICATION; MITOCHONDRIA; METHOTREXATE
AB Background: Folic acid supplementation reduces the risk of neural tube defects and congenital heart defects. The biological mechanisms through which folate prevents birth defects are not well understood. We explore the use of zebrafish as a model system to investigate the role of folate metabolism during development.
Results: We first identified zebrafish orthologs of 12 human folate metabolic genes. RT-PCR and in situ analysis indicated maternal transcripts supply the embryo with mRNA so that the embryo has an intact folate pathway. To perturb folate metabolism we exposed zebrafish embryos to methotrexate (MTX), a potent inhibitor of dihydrofolate reductase (Dhfr) an essential enzyme in the folate metabolic pathway. Embryos exposed to high doses of MTX exhibited developmental arrest prior to early segmentation. Lower doses of MTX resulted in embryos with a shortened anterior-posterior axis and cardiac defects: linear heart tubes or incomplete cardiac looping. Inhibition of dhfr mRNA with antisense morpholino oligonucleotides resulted in embryonic lethality. One function of the folate pathway is to provide essential one-carbon units for dTMP synthesis, a rate-limiting step of DNA synthesis. After 24 hours of exposure to high levels of MTX, mutant embryos continue to incorporate the thymidine analog BrdU. However, additional experiments indicate that these embryos have fewer mitotic cells, as assayed with phospho-histone H3 antibodies, and that treated embryos have perturbed cell cycles.
Conclusions: Our studies demonstrate that human and zebrafish utilize similar one-carbon pathways. Our data indicate that folate metabolism is essential for early zebrafish development. Zebrafish studies of the folate pathway and its deficiencies could provide insight into the underlying etiology of human birth defects and the natural role of folate in development.
C1 [Lee, Marina S.; Bonner, Jenna R.; Bernard, David J.; Sanchez, Erica L.; Sause, Eric T.; Prentice, R. Reid; Burgess, Shawn M.; Brody, Lawrence C.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Brody, LC (reprint author), NHGRI, NIH, Bethesda, MD 20892 USA.
EM lbrody@mail.nih.gov
OI Burgess, Shawn/0000-0003-1147-0596
FU Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health
FX We thank Stacie Anderson for help with FACS analysis, Darryl Leja for
help with figures, Settara Chandrasekharappa for equipment, Amy Singer
of the ZFIN Nomenclature Committee for naming help, and Charles River
Aquatic Staff for fish care. This research was supported by the
Intramural Research Program of the National Human Genome Research
Institute, National Institutes of Health (S.M.B, L.C.B).
NR 40
TC 11
Z9 13
U1 0
U2 22
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-213X
J9 BMC DEV BIOL
JI BMC Dev. Biol.
PD APR 5
PY 2012
VL 12
AR 12
DI 10.1186/1471-213X-12-12
PG 11
WC Developmental Biology
SC Developmental Biology
GA 982TH
UT WOS:000307067800001
PM 22480165
ER
PT J
AU Dakshinamoorthy, G
Samykutty, AK
Munirathinam, G
Shinde, GB
Nutman, T
Reddy, MV
Kalyanasundaram, R
AF Dakshinamoorthy, Gajalakshmi
Samykutty, Abhilash Kumble
Munirathinam, Gnanasekar
Shinde, Gangadhar Bhaurao
Nutman, Thomas
Reddy, Maryada Venkatarami
Kalyanasundaram, Ramaswamy
TI Biochemical Characterization and Evaluation of a Brugia malayi Small
Heat Shock Protein as a Vaccine against Lymphatic Filariasis
SO PLOS ONE
LA English
DT Article
ID ALPHA-CRYSTALLIN DOMAIN; WUCHERERIA-BANCROFTI; PROTECTIVE IMMUNITY; DNA
VACCINATION; ANTIBODY-RESPONSES; INFECTIVE LARVAE; ANTIGEN;
TUBERCULOSIS; IMMUNOGENICITY; MICE
AB Filarial nematodes enjoy one of the longest life spans of any human pathogen due to effective immune evasion strategies developed by the parasite. Among the various immune evasion strategies exhibited by the parasite, Interleukin 10 (IL-10) productions and IL-10 mediated immune suppression has significant negative impact on the host immune system. Recently, we identified a small heat shock protein expressed by Brugia malayi (BmHsp12.6) that can bind to soluble human IL-10 receptor alpha (IL-10R) and activate IL-10 mediated effects in cell lines. In this study we show that the IL-10R binding region of BmHsp12.6 is localized to its N-terminal region. This region has significant sequence similarity to the receptor binding region of human IL-10. In vitro studies confirm that the N-terminal region of BmHsp12.6 (N-BmHsp12.6) has IL-10 like activity and the region containing the alpha crystalline domain and C-terminus of BmHsp12.6 (BmHsp12.6ac) has no IL-10 like activity. However, BmHsp12.6ac contains B cell, T cell and CTL epitopes. Members of the sHSP families are excellent vaccine candidates. Evaluation of sera samples from putatively immune endemic normal (EN) subjects showed IgG1 and IgG3 antibodies against BmHsp12.6ac and these antibodies were involved in the ADCC mediated protection. Subsequent vaccination trials with BmHsp12.6ac in a mouse model using a heterologous prime boost approach showed that 83% protection can be achieved against B. malayi L3 challenge. Results presented in this study thus show that the N-BmHsp12.6 subunit of BmHsp12.6 has immunoregulatory function, whereas, the BmHsp12.6ac subunit of BmHsp12.6 has significant vaccine potential.
C1 [Dakshinamoorthy, Gajalakshmi; Samykutty, Abhilash Kumble; Munirathinam, Gnanasekar; Kalyanasundaram, Ramaswamy] Univ Illinois, Coll Med Rockford, Dept Biomed Sci, Rockford, IL USA.
[Samykutty, Abhilash Kumble; Reddy, Maryada Venkatarami] Mahatma Gandhi Inst Med Sci, Dept Biochem, Sevagram, Maharashtra, India.
[Shinde, Gangadhar Bhaurao] Rashtrasant Tukadoji Maharaj Nagpur Univ, Dept Biochem, Nagpur, Maharashtra, India.
[Nutman, Thomas] NIH, Helminth Immunol Sect, Bethesda, MD 20892 USA.
RP Dakshinamoorthy, G (reprint author), Univ Illinois, Coll Med Rockford, Dept Biomed Sci, Rockford, IL USA.
EM ramswamy@uic.edu
FU NIH [AI064745]; Department of Biotechnology, Ministry of Science and
Technology, New Delhi [BT/INF/22/1/2007]
FX This study was funded by an NIH RO1 grant (AI064745). Additional funding
was received from the Department of Biotechnology, Ministry of Science
and Technology, New Delhi (BT/INF/22/1/2007). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 61
TC 22
Z9 22
U1 2
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 APR 5
PY 2012
VL 7
IS 4
AR e34077
DI 10.1371/journal.pone.0034077
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 955IH
UT WOS:000305010500004
PM 22496777
ER
PT J
AU Dunleavy, K
Wilson, WH
AF Dunleavy, Kieron
Wilson, Wyndham H.
TI How I treat HIV-associated lymphoma
SO BLOOD
LA English
DT Review
ID HUMAN-IMMUNODEFICIENCY-VIRUS; B-CELL LYMPHOMA; NON-HODGKINS-LYMPHOMA;
PRIMARY EFFUSION LYMPHOMA; ACTIVE ANTIRETROVIRAL THERAPY; AIDS-RELATED
LYMPHOMA; NERVOUS-SYSTEM LYMPHOMA; GENE-EXPRESSION PROFILE; NF-KAPPA-B;
BURKITTS-LYMPHOMA
AB Over the past 10 years, significant progress has been made in understanding HIV-associated lymphomas and improving the prognosis of these diseases. With the advent of combination antiretroviral therapy and the development of novel therapeutic strategies, most patients with HIV-associated lymphomas are cured. The outcome for the majority of patients with HIV-associated diffuse large B-cell lymphoma and Burkitt lymphoma in particular, is excellent, with recent studies supporting the role of rituximab in these diseases. Indeed, in the combination antiretroviral therapy era, the curability of many patients with HIV-associated lymphoma is similar to their HIV-negative counterparts. New treatment frontiers need to focus on improving the outcome for patients with advanced immune suppression and for those with adverse tumor biology, such as the activated B-cell type of diffuse large B-cell lymphoma and the virally driven lymphomas. Future clinical trials need to investigate novel targeted agents alone and in combination with chemotherapy. (Blood. 2012; 119(14): 3245-3255)
C1 [Dunleavy, Kieron] NCI, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Dunleavy, K (reprint author), NCI, Metab Branch, Ctr Canc Res, Bldg 10,Rm 4N-115,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM dunleavk@mail.nih.gov
FU National Cancer Institute of the National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Cancer Institute of the National Institutes of Health.
NR 89
TC 51
Z9 55
U1 0
U2 9
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 0006-4971
EI 1528-0020
J9 BLOOD
JI Blood
PD APR 5
PY 2012
VL 119
IS 14
BP 3245
EP 3255
DI 10.1182/blood-2011-08-373738
PG 11
WC Hematology
SC Hematology
GA 925PL
UT WOS:000302773200014
PM 22337719
ER
PT J
AU Xi, LQ
Arons, E
Navarro, W
Calvo, KR
Stetler-Stevenson, M
Raffeld, M
Kreitman, RJ
AF Xi, Liqiang
Arons, Evgeny
Navarro, Winnifred
Calvo, Katherine R.
Stetler-Stevenson, Maryalice
Raffeld, Mark
Kreitman, Robert J.
TI Both variant and IGHV4-34-expressing hairy cell leukemia lack the BRAF
V600E mutation
SO BLOOD
LA English
DT Article
ID DIAGNOSIS; CLADRIBINE; DISEASE; CANCER
AB Recently, the BRAF V600E mutation was reported in all cases of hairy cell leukemia (HCL) but not in other peripheral B-cell neoplasms. We wished to confirm these results and assess BRAF status in well-characterized cases of HCL associated with poor prognosis, including the immunophenotypically defined HCL variant (HCLv) and HCL expressing the IGHV4-34 immunoglobulin rearrangement. Fifty-three classic HCL (HCLc) and 16 HCLv cases were analyzed for BRAF, including 5 HCLc and 8 HCLv expressing IGHV4-34. BRAF was mutated in 42 (79%) HCLc, but wild-type in 11 (21%) HCLc and 16 (100%) HCLv. All 13 IGHV4-34(+) HCLs were wild-type. IGHV gene usage in the 11 HCLc BRAF wild-type cases included 5 IGHV4-34, 5 other, and 1 unknown. Our results suggest that HCLv and IGHV4-34(+) HCLs have a different pathogenesis than HCLc and that a significant minority of other HCLc are also wild-type for BRAF V600. (Blood. 2012; 119(14): 3330-3332)
C1 [Arons, Evgeny; Kreitman, Robert J.] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Xi, Liqiang; Navarro, Winnifred; Stetler-Stevenson, Maryalice; Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Kreitman, RJ (reprint author), NCI, Mol Biol Lab, NIH, 37-5124b,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA.
EM kreitmar@mail.nih.gov
RI Calvo, Katherine/A-8109-2009;
OI Calvo, Katherine/0000-0002-0771-4191
FU National Cancer Institute, National Institutes of Health
FX This work was supported by the intramural program of the National Cancer
Institute, National Institutes of Health.
NR 24
TC 82
Z9 85
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD APR 5
PY 2012
VL 119
IS 14
BP 3330
EP 3332
DI 10.1182/blood-2011-09-379339
PG 3
WC Hematology
SC Hematology
GA 925PL
UT WOS:000302773200024
PM 22210875
ER
PT J
AU Borotikar, BS
Sipprell, WH
Wible, EE
Sheehan, FT
AF Borotikar, Bhushan S.
Sipprell, William H., III
Wible, Emily E.
Sheehan, Frances T.
TI A methodology to accurately quantify patellofemoral cartilage contact
kinematics by combining 3D image shape registration and cine-PC MRI
velocity data
SO JOURNAL OF BIOMECHANICS
LA English
DT Article
DE Knee; MRI; Dynamic; Femur; Patella; Contact kinematics
ID IN-VIVO; TIBIOFEMORAL KINEMATICS; ARTICULAR-CARTILAGE; PATELLAR
TRACKING; WEIGHT-BEARING; PAIN; JOINT; OSTEOARTHRITIS; PROGRESSION
AB Patellofemoral osteoarthritis and its potential precursor patellofemoral pain syndrome (PFPS) are common, costly, and debilitating diseases. PFPS has been shown to be associated with altered patellofemoral joint mechanics; however, an actual variation in joint contact stresses has not been established due to challenges in accurately quantifying in vivo contact kinematics (area and location). This study developed and validated a method for tracking dynamic, in vivo cartilage contact kinematics by combining three magnetic resonance imaging (MRI) techniques, cine-phase contrast (CPC), multi-plane cine (MPC), and 3D high-resolution static imaging. CPC and MPC data were acquired from 12 healthy volunteers while they actively extended/flexed their knee within the MRI scanner. Since no gold standard exists for the quantification of in vivo dynamic cartilage contact kinematics, the accuracy of tracking a single point (patellar origin relative to the femur) represented the accuracy of tracking the kinematics of an entire surface. The accuracy was determined by the average absolute error between the PF kinematics derived through registration of MPC images to a static model and those derived through integration of the CPC velocity data. The accuracy ranged from 0.47 mm to 0.77 mm for the patella and femur and from 0.68 mm to 0.86 mm for the patellofemoral joint. For purely quantifying joint kinematics, CPC remains an analytically simpler and more accurate (accuracy <0.33 mm) technique. However, for application requiring the tracking of an entire surface, such as quantifying cartilage contact kinematics, this combined imaging approach produces accurate results with minimal operator intervention. Published by Elsevier Ltd.
C1 [Borotikar, Bhushan S.; Wible, Emily E.; Sheehan, Frances T.] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Sipprell, William H., III] SUNY Buffalo, Sch Med & Biomed Sci, Buffalo, NY 14260 USA.
RP Sheehan, FT (reprint author), NIH, Dept Rehabil Med, Bldg 10,CRC RM 1-1469,10 Ctr Dr,MSC 1604, Bethesda, MD 20892 USA.
EM fsheehan@cc.nih.gov
RI sheehan, frances/B-6962-2009
FU NIH at the Clinical Center; Diagnostic Radiology Department at the
National Institutes of Health
FX This research was supported in its entirety by the Intramural Research
Program of the NIH at the Clinical Center at the NIH. The authors wish
to thank Sara Sadeghi, Bonnie Damaska, and the Diagnostic Radiology
Department at the National Institutes of Health for their support and
research time.
NR 28
TC 11
Z9 12
U1 0
U2 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0021-9290
J9 J BIOMECH
JI J. Biomech.
PD APR 5
PY 2012
VL 45
IS 6
BP 1117
EP 1122
DI 10.1016/j.jbiomech.2011.12.025
PG 6
WC Biophysics; Engineering, Biomedical
SC Biophysics; Engineering
GA 928KC
UT WOS:000302980600033
PM 22284428
ER
PT J
AU Raghunathan, M
Zubovski, Y
Venable, RM
Pastor, RW
Nagle, JF
Tristram-Nagle, S
AF Raghunathan, Mohit
Zubovski, Yuriy
Venable, Richard M.
Pastor, Richard W.
Nagle, John F.
Tristram-Nagle, Stephanie
TI Structure and Elasticity of Lipid Membranes with Genistein and Daidzein
Bioflavinoids Using X-ray Scattering and MD Simulations
SO JOURNAL OF PHYSICAL CHEMISTRY B
LA English
DT Article
ID ION-CHANNEL FUNCTION; BILAYER ELASTICITY; ESTROGEN-RECEPTOR; PROTEIN
FUNCTION; GRAMICIDIN; BINDING; PHASE; BETA; PHYTOESTROGENS; ISOFLAVONES
AB This work reports the effects of the bioflavinoids genistein and daidzein on lipid bilayers as determined by volume measurements, X-ray scattering, and molecular dynamics simulations. The experimental and simulated total molecular volumes were found to be in outstanding agreement with each other before the addition of genistein and daidzein and also after their addition. Both bioflavinoids inserted into the hydrocarbon region of both DOPC and diphytanoylPC near the carbonyls of the lipids and both decreased the bilayer thicknesses. The long axes of both bioflavinoids were oriented nearly parallel to the plane of the bilayer with their carbonyl groups preferentially pointed toward the proximal surface. A difference is that daidzein had a solubility limit of similar to 0.14 mol fraction in DOPC (similar to 0.12 mol fraction in diphytanoyIPC), whereas genistein was soluble at least to 0.20 mol fraction in both lipid membranes. Measurements of bending modulus K-C and simulation results for area compressibility modulus K-A indicate that both bioflavinoids soften bilayers.
C1 [Raghunathan, Mohit; Zubovski, Yuriy; Nagle, John F.; Tristram-Nagle, Stephanie] Carnegie Mellon Univ, Dept Phys, Biol Phys Grp, Pittsburgh, PA 15213 USA.
[Venable, Richard M.; Pastor, Richard W.] NHLBI, Lab Computat Biol, Rockville, MD 20852 USA.
RP Tristram-Nagle, S (reprint author), Carnegie Mellon Univ, Dept Phys, Biol Phys Grp, 5000 Forbes Ave, Pittsburgh, PA 15213 USA.
EM stn@cmu.edu
RI Tristram-Nagle, Prof. Stephanie/N-7811-2014; Nagle, John/B-1917-2015
OI Tristram-Nagle, Prof. Stephanie/0000-0003-2271-7056; Nagle,
John/0000-0002-9844-5934
FU NIGMS/NIH [GM 44976]; Howard Hughes Medical Institute; Charles E.
Kaufman Foundation; NIH, National Heart, Lung and Blood Institute;
National Science Foundation; National Institutes of Health/National
Institute of General Medical Sciences under National Science Foundation
[DMR-0225180]
FX This research was supported in part by Grant No. GM 44976 from NIGMS/NIH
(S.T.-N., J.N.), the Howard Hughes Medical Institute (M.R., Y.Z.), and
the Charles E. Kaufman Foundation (S.T.-N.). It was supported in part
(R.V., R.P.) by the Intramural Research Program of the NIH, National
Heart, Lung and Blood Institute and utilized the high-performance
computational capabilities at the National Institutes of Health,
Bethesda, MD (NHLBI LoBoS cluster). X-ray scattering data were taken at
the Cornell High Energy Synchrotron Source (CHESS), which is supported
by the National Science Foundation and the National Institutes of
Health/National Institute of General Medical Sciences under National
Science Foundation Award DMR-0225180. We especially thank Dr. Arthur
Woll for obtaining our beam and for general support during our data
collection at the G1 station. We thank Dr. Jianjun Pan for help with
sample preparation and X-ray data collection at CHESS, Prof. Olaf
Andersen for helpful discussions, and especially Dr. Gilman Toombes for
very insightful criticism of a first draft.
NR 44
TC 32
Z9 33
U1 2
U2 15
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1520-6106
J9 J PHYS CHEM B
JI J. Phys. Chem. B
PD APR 5
PY 2012
VL 116
IS 13
BP 3918
EP 3927
DI 10.1021/jp211904j
PG 10
WC Chemistry, Physical
SC Chemistry
GA 919OG
UT WOS:000302337000002
PM 22324769
ER
PT J
AU Hakim, O
Resch, W
Yamane, A
Klein, I
Kieffer-Kwon, KR
Jankovic, M
Oliveira, T
Bothmer, A
Voss, TC
Ansarah-Sobrinho, C
Mathe, E
Liang, GQ
Cobell, J
Nakahashi, H
Robbiani, DF
Nussenzweig, A
Hager, GL
Nussenzweig, MC
Casellas, R
AF Hakim, Ofir
Resch, Wolfgang
Yamane, Arito
Klein, Isaac
Kieffer-Kwon, Kyong-Rim
Jankovic, Mila
Oliveira, Thiago
Bothmer, Anne
Voss, Ty C.
Ansarah-Sobrinho, Camilo
Mathe, Ewy
Liang, Genqing
Cobell, Jesse
Nakahashi, Hirotaka
Robbiani, Davide F.
Nussenzweig, Andre
Hager, Gordon L.
Nussenzweig, Michel C.
Casellas, Rafael
TI DNA damage defines sites of recurrent chromosomal translocations in B
lymphocytes
SO NATURE
LA English
DT Article
ID CLASS-SWITCH RECOMBINATION; SEQUENCING REVEALS; HUMAN GENOME; BREAKS;
CELLS; AID; IDENTIFICATION; REARRANGEMENTS; ORGANIZATION; MECHANISMS
AB Recurrent chromosomal translocations underlie both haematopoietic and solid tumours. Their origin has been ascribed to selection of random rearrangements, targeted DNA damage, or frequent nuclear interactions between translocation partners; however, the relative contribution of each of these elements has not been measured directly or on a large scale. Here we examine the role of nuclear architecture and frequency of DNA damage in the genesis of chromosomal translocations by measuring these parameters simultaneously in cultured mouse B lymphocytes. In the absence of recurrent DNA damage, translocations between Igh or Myc and all other genes are directly related to their contact frequency. Conversely, translocations associated with recurrent site-directed DNA damage are proportional to the rate of DNA break formation, as measured by replication protein A accumulation at the site of damage. Thus, non-targeted rearrangements reflect nuclear organization whereas DNA break formation governs the location and frequency of recurrent translocations, including those driving B-cell malignancies.
C1 [Klein, Isaac; Jankovic, Mila; Oliveira, Thiago; Bothmer, Anne; Robbiani, Davide F.; Nussenzweig, Michel C.] Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
[Hakim, Ofir; Voss, Ty C.; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
[Resch, Wolfgang; Yamane, Arito; Kieffer-Kwon, Kyong-Rim; Ansarah-Sobrinho, Camilo; Liang, Genqing; Cobell, Jesse; Nakahashi, Hirotaka; Casellas, Rafael] NCI, NIAMS, NIH, Bethesda, MD 20892 USA.
[Oliveira, Thiago] Univ Sao Paulo, Med Sch Ribeirao Preto, Dept Genet, Natl Inst Sci & Technol Stem Cells & Cell Therapy, BR-14051140 Ribeirao Preto, SP, Brazil.
[Oliveira, Thiago] Ctr Cell Based Therapy, BR-14051140 Ribeirao Preto, SP, Brazil.
[Nussenzweig, Andre] NCI, Lab Genome Integr, NIH, Bethesda, MD 20892 USA.
[Nussenzweig, Michel C.] Rockefeller Univ, Howard Hughes Med Inst, New York, NY 10065 USA.
[Casellas, Rafael] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Nussenzweig, MC (reprint author), Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
EM nussen@rockefeller.edu; casellar@mail.nih.gov
RI perumal, murugiah/D-1565-2012; Yamane, Arito/A-2959-2013;
OI Oliveira, Thiago/0000-0002-2654-0879
FU Starr Foundation; NIH [AI037526]; NIAMS; NCI, NIH
FX We thank members of the Casellas and Nussenzweig laboratories for
discussions; G. Gutierrez from NIAMS genomics facility for technical
assistance. This work was supported in part by a grant from the Starr
Foundation to M.C.N., by NIH grant number AI037526 to M.C.N. and the
Intramural Research Program of NIAMS and NCI, NIH. M.C.N. is an HHMI
investigator. This study made use of the high-performance computational
capabilities of the Biowulf Linux cluster at the NIH
(http://biowulf.nih.gov), and the resources of NCI's High-Throughput
Imaging Facility.
NR 28
TC 102
Z9 106
U1 1
U2 16
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD APR 5
PY 2012
VL 484
IS 7392
BP 69
EP +
DI 10.1038/nature10909
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919QN
UT WOS:000302343400035
PM 22314321
ER
PT J
AU Alexander, GM
Graef, JD
Hammarback, JA
Nordskog, BK
Burnett, EJ
Daunais, JB
Bennett, AJ
Friedman, DP
Suomi, SJ
Godwin, DW
AF Alexander, G. M.
Graef, J. D.
Hammarback, J. A.
Nordskog, B. K.
Burnett, E. J.
Daunais, J. B.
Bennett, A. J.
Friedman, D. P.
Suomi, S. J.
Godwin, D. W.
TI DISRUPTIONS IN SEROTONERGIC REGULATION OF CORTICAL GLUTAMATE RELEASE IN
PRIMATE INSULAR CORTEX IN RESPONSE TO CHRONIC ETHANOL AND NURSERY
REARING
SO NEUROSCIENCE
LA English
DT Article
DE anterior insula; ethanol; serotonin; stress; 5-HT1A
ID POSITRON-EMISSION-TOMOGRAPHY; MEDIAL PREFRONTAL CORTEX; EARLY-LIFE
STRESS; 5-HYDROXYINDOLEACETIC ACID CONCENTRATIONS; SEROTONIN(1A)
RECEPTOR-BINDING; DIMINISHED SOCIAL COMPETENCE; REDUCES SYNAPTIC
EXCITATION; RAT BASOLATERAL AMYGDALA; HUMAN CHRONIC-ALCOHOLICS;
ANXIETY-PRONE SUBJECTS
AB Early-life stress has been shown to increase susceptibility to anxiety and substance abuse. Disrupted activity within the anterior insular cortex (AIC) has been shown to play a role in both of these disorders. Altered serotonergic processing is implicated in controlling the activity levels of the associated cognitive networks. We therefore investigated changes in both serotonin receptor expression and glutamatergic synaptic activity in the AIC of alcohol-drinking rhesus monkeys. We studied tissues from male rhesus monkeys raised under two conditions: Male rhesus monkeys (1) "mother reared" (MR) by adult females (n=9) or (2) "Nursery reared" (NR), that is, separated from their mothers and reared as a separate group under surrogate/peer-reared conditions (n=9). The NR condition represents a long-standing and well-validated nonhuman primate model of early life stress. All monkeys were trained to self-administer ethanol (4% w/v) or an isocaloric maltose dextrin control solution. Subsets from each rearing condition were then given daily access to ethanol, water, or maltose dextrin for 12 months. Tissues were collected at necropsy and were further analyzed. Using real time RT-PCR we found that ethanol-naive, NR monkeys had lower AIC levels of 5-HT1A and 5-HT2A receptor mRNA compared with ethanol-naive, MR animals. Although NR monkeys consumed more ethanol over the 12-month period compared with MR animals, both MR and NR animals expressed greater 5-HT1A and 5-HT2A receptor mRNA levels following chronic alcohol self-administration. The interaction between nursery-rearing conditions and alcohol consumption resulted in a significant enhancement of both 5-HT1A and 5-HT2A receptor mRNA levels such that lower expression levels observed in nursery-rearing conditions were not found in the alcohol self-administration group. Using voltage clamp recordings in the whole cell configuration we recorded excitatory postsynaptic currents in both ethanol-naive and chronic self-administration groups of NR and MR monkeys. Both groups that self-administered ethanol showed greater glutamatergic activity within the AIC. This AIC hyperactivity in MR alcohol-consuming monkeys was accompanied by an increased sensitivity to regulation by presynaptic 5-HT1A receptors that was not apparent in the ethanol-naive, MR group. Our data indicate that chronic alcohol consumption leads to greater AIC activity and may indicate a compensatory upregulation of presynaptic 5-HT1A receptors. Our results also indicate that AIC activity may be less effectively regulated by 5-HT in ethanol-naive NR animals than in NR monkeys in response to chronic ethanol self-administration. These data suggest possible mechanisms for increased alcohol seeking and possible addiction potential among young adults who had previously experienced early-life stress that include disruptions in both AIC activity and serotonin system dynamics. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
C1 [Hammarback, J. A.; Nordskog, B. K.; Godwin, D. W.] Wake Forest Univ, Bowman Gray Sch Med, Dept Neurobiol & Anat, Winston Salem, NC 27157 USA.
[Alexander, G. M.] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA.
[Graef, J. D.; Burnett, E. J.] Wake Forest Univ, Bowman Gray Sch Med, Neurosci Program, Winston Salem, NC 27157 USA.
[Daunais, J. B.; Bennett, A. J.; Friedman, D. P.] Wake Forest Univ, Bowman Gray Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27157 USA.
[Suomi, S. J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, NIH, Anim Ctr, Poolesville, MD 20837 USA.
RP Godwin, DW (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Dept Neurobiol & Anat, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM dgodwin@wakehealth.edu
RI Reis, Aline/G-9573-2012;
OI Burnett, Elizabeth/0000-0001-5037-7576
FU NIH [AA014106, AA015568, AA016748, AA016852, AA017056, EY018159]; Tab
Williams Family Fund
FX We thank Dr. Satoru Hayasaka for statistical support. These studies were
supported by NIH grants AA014106 and AA015568 (D.P.F.), AA016748
(J.B.D.), AA016852, AA017056, EY018159, and the Tab Williams Family Fund
(D.W.G.).
NR 112
TC 2
Z9 2
U1 1
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD APR 5
PY 2012
VL 207
BP 167
EP 181
DI 10.1016/j.neuroscience.2012.01.027
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 917UB
UT WOS:000302203000014
PM 22305886
ER
PT J
AU Mejias-Aponte, CA
Kiyatkin, EA
AF Mejias-Aponte, C. A.
Kiyatkin, E. A.
TI VENTRAL TEGMENTAL AREA NEURONS ARE EITHER EXCITED OR INHIBITED BY
COCAINE'S ACTIONS IN THE PERIPHERAL NERVOUS SYSTEM
SO NEUROSCIENCE
LA English
DT Article
DE cocaine methiodide; peripheral nervous system; cocaine; ventral
tegmental area; single-unit recordings
ID MIDBRAIN DOPAMINE NEURONS; FREELY MOVING RATS; NUCLEUS-ACCUMBENS
NEURONS; INTRAVENOUS COCAINE; SUBSTANTIA-NIGRA; IMPULSE ACTIVITY;
SODIUM-CHANNELS; EXTRACELLULAR ELECTROPHYSIOLOGY; NONDOPAMINERGIC
NEURONS; SYNAPTIC-TRANSMISSION
AB Cocaine's multiple pharmacological substrates are ubiquitously present in the peripheral and central nervous system. Thus, upon its administration, cocaine acts in the periphery before directly acting in the brain. We determined whether cocaine alters ventral tegmental area (VTA) neuronal activity via its peripheral actions. In urethane-anesthetized rats, we recorded VTA neuron's responses to intravenous injections of two cocaine analogs: cocaine-hydrochloride (HCl, 0.25 mg/kg), which readily cross the blood brain barrier (BBB), and cocaine-methiodide (MI, 0.33 mg/kg), which does not cross the BBB. Both cocaine analogs produced sustained changes in discharge rates that began 5 s after the initiation of a 10-s drug infusion. Within the first 90 s post-injection, the magnitudes of neuronal responsiveness of both cocaine analogs were comparable, but later the effects of cocaine-HCl were stronger and persisted longer than those of cocaine-MI. The proportion of neurons responsive to cocaine-HCl was twice that of cocaine-MI (74% and 35%, respectively). Both analogs also differed in their response onsets. Cocaine-MI rarely evoked responses after 1 min, whereas cocaine-HCl continued to evoke responses within 3 min post-injection. VTA neurons were either excited or inhibited by both cocaine analogs. Most units responsive to cocaine-MI, regardless of whether they were excited or inhibited, had electrophysiological characteristics of putative dopamine (DA) neurons. Units inhibited by cocaine-HCl also had characteristics of DA neurons, whereas excited neurons had widely varying action potential durations and discharge rates. Cocaine-MI and cocaine-HCl each produced changes in VTA neuron activity under full DA receptor blockade. However, the duration of inhibition was shortened and the number of excitations increased, and they occurred with an earlier onset during DA receptor blockade. These findings indicate that cocaine acts peripherally with a short latency and alters the activity of VTA neurons before its well-known direct actions in the brain. Published by Elsevier Ltd on behalf of IBRO.
C1 [Mejias-Aponte, C. A.; Kiyatkin, E. A.] NIDA, Behav Neurosci Branch, Intramural Res Program, NIH,DHHS,Triad Technol Ctr, Baltimore, MD 21224 USA.
RP Mejias-Aponte, CA (reprint author), NIDA, Behav Neurosci Branch, Intramural Res Program, NIH,DHHS,Triad Technol Ctr, Suite 2200,333 Cassell Dr, Baltimore, MD 21224 USA.
EM mejiasca@mail.nih.gov
FU National Institute on Drug Abuse
FX This work was supported by the National Institute on Drug Abuse,
Intramural Research Program. We thank Cameron Good, Carl Lupica, and Roy
Wise for their insight and comments on the manuscript and for their
helpful editorial assistance. We also thank Mary Pfeiffer for her
helpful editorial assistance.
NR 77
TC 3
Z9 3
U1 2
U2 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD APR 5
PY 2012
VL 207
BP 182
EP 197
DI 10.1016/j.neuroscience.2012.01.026
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 917UB
UT WOS:000302203000015
PM 22300980
ER
PT J
AU Wu, J
Lou, H
Alerte, TNM
Stachowski, EK
Chen, J
Singleton, AB
Hamilton, RL
Perez, RG
AF Wu, J.
Lou, H.
Alerte, T. N. M.
Stachowski, E. K.
Chen, J.
Singleton, A. B.
Hamilton, R. L.
Perez, R. G.
TI LEWY-LIKE AGGREGATION OF alpha-SYNUCLEIN REDUCES PROTEIN PHOSPHATASE 2A
ACTIVITY IN VITRO AND IN VIVO
SO NEUROSCIENCE
LA English
DT Article
DE synucleinopathy; hyperphosphorylation; dephosphorylation; phosphatase;
enzymatic regulation
ID TYROSINE-HYDROXYLASE PHOSPHORYLATION; FAMILIAL PARKINSONS-DISEASE;
ALZHEIMER-DISEASE; NACP/ALPHA-SYNUCLEIN; TAU PHOSPHORYLATION; INCLUSION
FORMATION; TRANSGENIC MICE; BODY DISEASE; PP2A; SUBUNIT
AB alpha-synuclein (alpha-Syn) is a chaperone-like protein that is highly implicated in Parkinson's disease (PD) as well as in dementia with Lewy bodies (DLB). Rare forms of PD occur in individuals with mutations of alpha-Syn or triplication of wild type alpha-Syn, and in both PD and DLB the intraneuronal inclusions known as Lewy bodies contain aggregated alpha-Syn that is highly phosphorylated on serine 129. In neuronal cells and in the brains of alpha-Syn overexpressing transgenic mice, soluble alpha-Syn stimulates the activity of protein phosphatase 2A (PP2A), a major serine/threonine phosphatase. Serine 129 phosphorylation of alpha-Syn attenuates its stimulatory effects on PP2A and also accelerates alpha-Syn aggregation; however, it is unknown if aggregation of alpha-Syn into Lewy bodies impairs PP2A activity. To assess for this, we measured the impact of alpha-Syn aggregation on PP2A activity in vitro and in vivo. In cell-free assays, aggregated alpha-Syn had similar to 50% less PP2A stimulatory effects than soluble recombinant alpha-Syn. Similarly in DLB and alpha-Syn triplication brains, which contain robust alpha-Syn aggregation with high levels of serine 129 phosphorylation, PP2A activity was also similar to 50% attenuated. As alpha-Syn normally stimulates PP2A activity, our data suggest that overexpression of alpha-Syn or sequestration of alpha-Syn into Lewy bodies has the potential to alter the phosphorylation state of key PP2A substrates; raising the possibility that all forms of synucleinopathy will benefit from treatments aimed at optimizing PP2A activity. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
C1 [Wu, J.; Lou, H.; Alerte, T. N. M.; Stachowski, E. K.; Chen, J.; Perez, R. G.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA.
[Perez, R. G.] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA.
[Hamilton, R. L.] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA USA.
[Wu, J.; Lou, H.; Alerte, T. N. M.; Stachowski, E. K.; Chen, J.; Perez, R. G.] Univ Pittsburgh, Sch Med, Pittsburgh Inst Neurodegenerat Dis, Pittsburgh, PA 15260 USA.
[Wu, J.] Fudan Univ, Huashan Hosp, Dept Neurol, Shanghai 200433, Peoples R China.
[Lou, H.] Shandong Univ, Dept Pharmacol, Sch Med, Jinan 250012, Shandong, Peoples R China.
[Singleton, A. B.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Perez, RG (reprint author), Texas Tech Univ, Hlth Sci Ctr, Ctr Excellence Neurosci, Paul L Foster Sch Med, Med Sci Bldg 1,Suite 4002,5001 El Paso Dr, El Paso, TX 79905 USA.
EM ruth.g.perez@ttuhsc.edu
RI Singleton, Andrew/C-3010-2009
FU University of Pittsburgh Alzheimer's Disease Research Center - National
Institutes of Health [P50 AG005133]; National Institute of Neurological
Disorders and Stroke [R01 [NS42094]]; China Scholarship Council;
Foundation for Excellent Young and Middle-Aged Scientists of Shandong
Province [BS2010YY036]; National Institute on Aging-National Institutes
of Health [Z01 AG000957-05]
FX We thank W Halfter for the dialysis advice, J Worley for preparing human
cortex slides, S Slusher for technical help, K Farrell and A Fisher for
insightful comments, and E Villanueva for editorial assistance. This
work is dedicated to MJ Fox, R Byer, J Cordy, and to the memory of L
"Rusty" Lanelli and was supported by a seed award from the University of
Pittsburgh Alzheimer's Disease Research Center - National Institutes of
Health [P50 AG005133, to R.G.P.]; National Institute of Neurological
Disorders and Stroke R01 [NS42094, to R.G.P.]; China Scholarship Council
[to LH]; Foundation for Excellent Young and Middle-Aged Scientists of
Shandong Province [BS2010YY036, to LH]; and an Intramural Research
Program of the National Institute on Aging-National Institutes of Health
[Z01 AG000957-05, to AS]. The funding agencies played no role in study
design; collection, analysis and interpretation of data; nor in writing
the report or in decision to submit the paper for publication.
NR 68
TC 20
Z9 20
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD APR 5
PY 2012
VL 207
BP 288
EP 297
DI 10.1016/j.neuroscience.2012.01.028
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 917UB
UT WOS:000302203000024
PM 22326202
ER
PT J
AU Kaplan, RM
Satterfield, JM
Kington, RS
AF Kaplan, Robert M.
Satterfield, Jason M.
Kington, Raynard S.
TI Building a Better Physician - The Case for the New MCAT
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 [Kaplan, Robert M.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Satterfield, Jason M.] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Kington, Raynard S.] Grinnell Coll, Off President, Grinnell, IA 50112 USA.
RP Kaplan, RM (reprint author), NIH, Off Behav & Social Sci Res, Bldg 10, Bethesda, MD 20892 USA.
NR 5
TC 25
Z9 25
U1 0
U2 2
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD APR 5
PY 2012
VL 366
IS 14
BP 1265
EP 1268
PG 4
WC Medicine, General & Internal
SC General & Internal Medicine
GA 919QJ
UT WOS:000302343000002
PM 22475589
ER
PT J
AU Haynes, BF
Gilbert, PB
McElrath, MJ
Zolla-Pazner, S
Tomaras, GD
Alam, SM
Evans, DT
Montefiori, DC
Karnasuta, C
Sutthent, R
Liao, HX
DeVico, AL
Lewis, GK
Williams, C
Pinter, A
Fong, Y
Janes, H
DeCamp, A
Huang, YD
Rao, M
Billings, E
Karasavvas, N
Robb, ML
Ngauy, V
de Souza, MS
Paris, R
Ferrari, G
Bailer, RT
Soderberg, KA
Andrews, C
Berman, PW
Frahm, N
De Rosa, SC
Alpert, MD
Yates, NL
Shen, XY
Koup, RA
Pitisuttithum, P
Kaewkungwal, J
Nitayaphan, S
Rerks-Ngarm, S
Michael, NL
Kim, JH
AF Haynes, Barton F.
Gilbert, Peter B.
McElrath, M. Juliana
Zolla-Pazner, Susan
Tomaras, Georgia D.
Alam, S. Munir
Evans, David T.
Montefiori, David C.
Karnasuta, Chitraporn
Sutthent, Ruengpueng
Liao, Hua-Xin
DeVico, Anthony L.
Lewis, George K.
Williams, Constance
Pinter, Abraham
Fong, Youyi
Janes, Holly
DeCamp, Allan
Huang, Yunda
Rao, Mangala
Billings, Erik
Karasavvas, Nicos
Robb, Merlin L.
Ngauy, Viseth
de Souza, Mark S.
Paris, Robert
Ferrari, Guido
Bailer, Robert T.
Soderberg, Kelly A.
Andrews, Charla
Berman, Phillip W.
Frahm, Nicole
De Rosa, Stephen C.
Alpert, Michael D.
Yates, Nicole L.
Shen, Xiaoying
Koup, Richard A.
Pitisuttithum, Punnee
Kaewkungwal, Jaranit
Nitayaphan, Sorachai
Rerks-Ngarm, Supachai
Michael, Nelson L.
Kim, Jerome H.
TI Immune-Correlates Analysis of an HIV-1 Vaccine Efficacy Trial
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS; V1/V2 DOMAIN; ANTIBODY; PROTECTION; GP120;
INFECTION; RESPONSES; ENVELOPE; MONKEYS; SIV
AB BACKGROUND
In the RV144 trial, the estimated efficacy of a vaccine regimen against human immunodeficiency virus type 1 (HIV-1) was 31.2%. We performed a case-control analysis to identify antibody and cellular immune correlates of infection risk.
METHODS
In pilot studies conducted with RV144 blood samples, 17 antibody or cellular assays met prespecified criteria, of which 6 were chosen for primary analysis to determine the roles of T-cell, IgG antibody, and IgA antibody responses in the modulation of infection risk. Assays were performed on samples from 41 vaccinees who became infected and 205 uninfected vaccinees, obtained 2 weeks after final immunization, to evaluate whether immune-response variables predicted HIV-1 infection through 42 months of follow-up.
RESULTS
Of six primary variables, two correlated significantly with infection risk: the binding of IgG antibodies to variable regions 1 and 2 (V1V2) of HIV-1 envelope proteins (Env) correlated inversely with the rate of HIV-1 infection (estimated odds ratio, 0.57 per 1-SD increase; P = 0.02; q = 0.08), and the binding of plasma IgA antibodies to Env correlated directly with the rate of infection (estimated odds ratio, 1.54 per 1-SD increase; P = 0.03; q = 0.08). Neither low levels of V1V2 antibodies nor high levels of Env-specific IgA antibodies were associated with higher rates of infection than were found in the placebo group. Secondary analyses suggested that Env-specific IgA antibodies may mitigate the effects of potentially protective antibodies.
CONCLUSIONS
This immune-correlates study generated the hypotheses that V1V2 antibodies may have contributed to protection against HIV-1 infection, whereas high levels of Env-specific IgA antibodies may have mitigated the effects of protective antibodies. Vaccines that are designed to induce higher levels of V1V2 antibodies and lower levels of Env-specific IgA antibodies than are induced by the RV144 vaccine may have improved efficacy against HIV-1 infection.
C1 [Haynes, Barton F.; Tomaras, Georgia D.; Alam, S. Munir; Montefiori, David C.; Liao, Hua-Xin; Ferrari, Guido; Soderberg, Kelly A.; Yates, Nicole L.; Shen, Xiaoying] Duke Univ, Human Vaccine Inst, Durham, NC 27710 USA.
[Haynes, Barton F.; Tomaras, Georgia D.; Alam, S. Munir; Montefiori, David C.; Liao, Hua-Xin; Ferrari, Guido; Soderberg, Kelly A.; Yates, Nicole L.; Shen, Xiaoying] Duke Univ, Sch Med, Ctr HIV AIDS Vaccine Immunol, Durham, NC 27710 USA.
[Gilbert, Peter B.; Fong, Youyi; Janes, Holly; DeCamp, Allan; Huang, Yunda] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
[McElrath, M. Juliana; Frahm, Nicole; De Rosa, Stephen C.] Fred Hutchinson Canc Res Ctr, Div Clin Res, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[Zolla-Pazner, Susan; Williams, Constance] Vet Affairs New York Harbor Healthcare Syst, New York, NY USA.
[Zolla-Pazner, Susan; Williams, Constance] NYU, Sch Med, Dept Pathol, New York, NY USA.
[Evans, David T.; Alpert, Michael D.] Harvard Univ, Sch Med, New England Reg Primate Ctr, Dept Microbiol & Immunobiol, Southborough, MA 01772 USA.
[Rao, Mangala; Billings, Erik; Robb, Merlin L.; Paris, Robert; Andrews, Charla; Michael, Nelson L.; Kim, Jerome H.] Walter Reed Army Inst Res, US Mil Res Program, Silver Spring, MD USA.
[Bailer, Robert T.; Koup, Richard A.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Karnasuta, Chitraporn; Karasavvas, Nicos; Ngauy, Viseth; de Souza, Mark S.] Armed Forces Res Inst Med Sci, US Army Component, Bangkok 10400, Thailand.
[Nitayaphan, Sorachai] Armed Forces Res Inst Med Sci, Royal Thai Army, Bangkok 10400, Thailand.
[Sutthent, Ruengpueng] Siriraj Hosp, Dept Microbiol, Natl HIV Repository & Bioinformat Ctr, Bangkok, Thailand.
[Pitisuttithum, Punnee; Kaewkungwal, Jaranit] Mahidol Univ, Fac Trop Med, Bangkok 10700, Thailand.
[Rerks-Ngarm, Supachai] Minist Publ Hlth, Dept Dis Control, Nonthaburi, Thailand.
[Berman, Phillip W.] Univ Calif Santa Cruz, Dept Biomol Engn, Santa Cruz, CA 95064 USA.
[DeVico, Anthony L.; Lewis, George K.] Univ Maryland, Sch Med, Inst Human Virol, Baltimore, MD 21201 USA.
[Pinter, Abraham] Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA.
RP Haynes, BF (reprint author), Duke Univ, Med Ctr, Duke Human Vaccine Inst, 2 Genome Ct,Box 103020, Durham, NC 27710 USA.
EM hayne002@mc.duke.edu
RI Ferrari, Guido/A-6088-2015; Tomaras, Georgia/J-5041-2016
FU Bill and Melinda Gates Foundation Collaboration for AIDS Vaccine
Discovery; U.S. Army Medical Research and Materiel Command; NIAID
[Y1-AI-2642-12, U01-AI-067854]; Henry M. Jackson Foundation for the
Advancement of Military Medicine; Department of Defense
[W81XWH-07-2-0067]; HIV Vaccine Trials Network Laboratory
[UM1-AI-068618]
FX Supported in part by grants from the Bill and Melinda Gates Foundation
Collaboration for AIDS Vaccine Discovery (to Drs. Haynes, Koup, and
Montefiori); an interagency agreement between the U.S. Army Medical
Research and Materiel Command and the NIAID (Y1-AI-2642-12); a
cooperative agreement between the Henry M. Jackson Foundation for the
Advancement of Military Medicine and the Department of Defense
(W81XWH-07-2-0067); and grants from the NIAID to the Center for HIV/AIDS
Vaccine Immunology (U01-AI-067854) and the HIV Vaccine Trials Network
Laboratory Program (UM1-AI-068618).
NR 40
TC 724
Z9 742
U1 10
U2 96
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 APR 5
PY 2012
VL 366
IS 14
BP 1275
EP 1286
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 919QJ
UT WOS:000302343000005
PM 22475592
ER
PT J
AU Somerville, RPT
Devillier, L
Parkhurst, MR
Rosenberg, SA
Dudley, ME
AF Somerville, Robert P. T.
Devillier, Laura
Parkhurst, Maria R.
Rosenberg, Steven A.
Dudley, Mark E.
TI Clinical scale rapid expansion of lymphocytes for adoptive cell transfer
therapy in the WAVE (R) bioreactor
SO JOURNAL OF TRANSLATIONAL MEDICINE
LA English
DT Article
DE Human; T Cells; Tumor Immunity; T Cell Receptors; Adoptive Immunotherapy
ID CD8(+) T-CELLS; RECOMBINANT INTERLEUKIN-2 THERAPY; TUMOR-INFILTRATING
LYMPHOCYTES; METASTATIC MELANOMA; CANCER REGRESSION; ANTIGEN;
IMMUNOTHERAPY; CULTURES; RESPONSES; EFFICACY
AB Background: To simplify clinical scale lymphocyte expansions, we investigated the use of the WAVE (R), a closed system bioreactor that utilizes active perfusion to generate high cell numbers in minimal volumes.
Methods: We have developed an optimized rapid expansion protocol for the WAVE bioreactor that produces clinically relevant numbers of cells for our adoptive cell transfer clinical protocols.
Results: TIL and genetically modified PBL were rapidly expanded to clinically relevant scales in both static bags and the WAVE bioreactor. Both bioreactors produced comparable numbers of cells; however the cultures generated in the WAVE bioreactor had a higher percentage of CD4+ cells and had a less activated phenotype.
Conclusions: The WAVE bioreactor simplifies the process of rapidly expanding tumor reactive lymphocytes under GMP conditions, and provides an alternate approach to cell generation for ACT protocols.
C1 [Somerville, Robert P. T.; Devillier, Laura; Parkhurst, Maria R.; Rosenberg, Steven A.; 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 DudleyM@mail.nih.gov
FU National Cancer Institute; Adelson Medical Research Foundation
FX This research was supported in part by the intramural research program
of the National Cancer Institute. Robert Somerville is supported by the
Adelson Medical Research Foundation. We would like to thank Kate Hogan,
Michelle Langhan, Thomas Shelton, Azam Nahvi, Linda Parker, Colin Gross
and Marcos Garcia for assisting with this research.
NR 34
TC 19
Z9 20
U1 0
U2 13
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 APR 4
PY 2012
VL 10
AR 69
DI 10.1186/1479-5876-10-69
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 975OL
UT WOS:000306520500001
PM 22475724
ER
PT J
AU Cheng, C
Wang, LS
Gall, JGD
Nason, M
Schwartz, RM
McElrath, J
DeRosa, SC
Hural, J
Corey, L
Buchbinder, SP
Nabel, GJ
AF Cheng, Cheng
Wang, LingShu
Gall, Jason G. D.
Nason, Martha
Schwartz, Richard M.
McElrath, Juliana
DeRosa, Steven C.
Hural, John
Corey, Lawrence
Buchbinder, Susan P.
Nabel, Gary J.
TI Decreased Pre-existing Ad5 Capsid and Ad35 Neutralizing Antibodies
Increase HIV-1 Infection Risk in the Step Trial Independent of
Vaccination
SO PLOS ONE
LA English
DT Article
ID ADENOVIRUS SEROTYPE 5; T-CELLS; SOLUBLE ANTIGENS; GENE-THERAPY;
IMMUNITY; VECTORS; IMMUNIZATION; VOLUNTEERS; EXPANSION; HUMANS
AB Background: The Step trial raised the possibility that uncircumcised men with pre-existing Ad5 neutralizing antibodies carried an increased risk of HIV infection after vaccination. Thus, understanding Ad seropositivity in humans is important to the development of an AIDS vaccine. Here, we analyze the impact of different Ad5-specific neutralizing antibodies on immune function and clinical outcome.
Methods and Findings: Ad seropositivity in the Step trial volunteers was analyzed using chimeric rAd5/35 vectors to characterize their specificity for Ad5 fiber and non-fiber external (capsid) proteins. Immune responses and HIV seropositivity were correlated with the specificity of Ad5-neutralizing antibodies. Neutralizing antibodies induced by the vaccine in Ad5 seronegative subjects were directed preferentially to Ad5 capsid proteins, although some fiber-neutralizing antibodies could be detected. Pre-vaccination Ad5 serostatus did not affect the capsid-directed response after three vaccinations. In contrast, anti-fiber antibody titers were significantly higher in volunteers who were Ad5 seropositive prior to vaccination. Those Ad5 seropositive subjects who generated anti-capsid responses showed a marked reduction in vaccine-induced CD8 responses. Unexpectedly, anti-vector immunity differed qualitatively in Ad5 seropositive participants who became HIV-1 infected compared to uninfected case controls; Ad5 seropositive participants who later acquired HIV had lower neutralizing antibodies to capsid. Moreover, Ad35 seropositivity was decreased in HIV-infected subjects compared with uninfected case controls, while seroprevalence for other serotypes including Ad14, Ad28 and Ad41 was similar in both groups.
Conclusions: Together, these findings suggest that the case subjects were less immunologically responsive prior to infection. Subjects infected during the Step trial had qualitative differences in immunity that increased their risk of HIV-1 infection independent of vaccination.
C1 [Cheng, Cheng; Wang, LingShu; Schwartz, Richard M.; Nabel, Gary J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Nason, Martha] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Gall, Jason G. D.] GenVec Inc, Gaithersburg, MD USA.
[McElrath, Juliana; DeRosa, Steven C.; Hural, John; Corey, Lawrence] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[McElrath, Juliana; DeRosa, Steven C.; Hural, John; Corey, Lawrence; Buchbinder, Susan P.] HIV Vaccine Trials Network, Seattle, WA USA.
[Buchbinder, Susan P.] San Francisco Dept Publ Hlth, HIV Res Sect, San Francisco, CA USA.
RP Cheng, C (reprint author), NIAID, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM gnabel@nih.gov
FU National Institutes of Health intramural research
FX The study was funded by National Institutes of Health intramural
research. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 25
TC 11
Z9 11
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD APR 4
PY 2012
VL 7
IS 4
AR e33969
DI 10.1371/journal.pone.0033969
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 953GO
UT WOS:000304855200028
ER
PT J
AU O'Seaghdha, CM
Hwang, SJ
Vasan, RS
Larson, MG
Hoffmann, U
Wang, TJ
Fox, CS
AF O'Seaghdha, Conall M.
Hwang, Shih-Jen
Vasan, Ramachandran S.
Larson, Martin G.
Hoffmann, Udo
Wang, Thomas J.
Fox, Caroline S.
TI Correlation of renin angiotensin and aldosterone system activity with
subcutaneous and visceral adiposity: the framingham heart study
SO BMC ENDOCRINE DISORDERS
LA English
DT Article
ID BODY-MASS INDEX; ESSENTIAL-HYPERTENSION; INSULIN-RESISTANCE;
CARDIOVASCULAR-DISEASE; TISSUE COMPARTMENTS; SERUM ALDOSTERONE;
RISK-FACTORS; OBESITY; ADULTS; DIET
AB Background: Animal studies suggest that local adipocyte-mediated activity of the renin-angiotensin-aldosterone system (RAAS) contributes to circulating levels, and may promote the development of obesity-related hypertension in rodents.
Methods: We examined relations of systemic RAAS activity, as assessed by circulating plasma renin activity (PRA), serum aldosterone level, and aldosterone: renin ratio (ARR), with specific regional adiposity measures in a large, community-based sample. Third Generation Framingham Heart Study participants underwent multidetector computed tomography assessment of SAT and VAT volumes during Exam 1 (2002 and 2005). PRA and serum aldosterone were measured after approximately 10 minutes of supine rest; results were log-transformed for analysis. Correlation coefficients between log-transformed RAAS measures and adiposity measurements were calculated, adjusted for age and sex. Partial correlations between log-transformed RAAS measures and adiposity measurements were also calculated, adjusted for standard CVD risk factors.
Results: Overall, 992 women and 897 men were analyzed (mean age 40 years; 7% hypertension; 3% diabetes). No associations were observed with SAT (renin r = 0.04, p = 0.1; aldosterone r = -0.01, p = 0.6) or VAT (renin r = 0.03, p = 0.2; aldosterone r = -0.03, p = 0.2). Similar results were observed for ARR, in sex-stratified analyses, and for BMI and waist circumference. Non-significant partial correlations were also observed in models adjusted for standard cardiovascular risk factors.
Conclusions: Regional adiposity measures were not associated with circulating measures of RAAS activity in this large population-based study. Further studies are required to determine whether adipocyte-derived RAAS components contribute to systemic RAAS activity in humans.
C1 [O'Seaghdha, Conall M.; Hwang, Shih-Jen; Vasan, Ramachandran S.; Larson, Martin G.; Wang, Thomas J.; Fox, Caroline S.] Nat Heart Lung & Blood Inst, Framingham Heart Study, Framingham, MA USA.
[O'Seaghdha, Conall M.; Hwang, Shih-Jen; Fox, Caroline S.] Ctr Populat Studies, Framingham, MA USA.
[O'Seaghdha, Conall M.] Brigham & Womens Hosp, Div Renal, Boston, MA 02115 USA.
[O'Seaghdha, Conall M.; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Larson, Martin G.] Boston Univ, Dept Math & Stat, Boston, MA 02215 USA.
[Larson, Martin G.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02215 USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Dept Radiol, Boston, MA 02114 USA.
[Wang, Thomas J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Cardiol, Boston, MA USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol, Boston, MA 02115 USA.
RP Fox, CS (reprint author), Nat Heart Lung & Blood Inst, Framingham Heart Study, 73 Mt Wayte Ave Suite 2, Framingham, MA USA.
EM foxca@nhlbi.nih.gov
OI Larson, Martin/0000-0002-9631-1254; Ramachandran,
Vasan/0000-0001-7357-5970
FU National Heart, Lung, and Blood Institute [N01-HC-25195];
[R01-HL-086875]
FX The Framingham Heart Study is supported by the National Heart, Lung, and
Blood Institute (N01-HC-25195). Dr. Wang is supported by R01-HL-086875.
NR 42
TC 12
Z9 12
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6823
J9 BMC ENDOCR DISORD
JI BMC Endocr. Disord.
PD APR 4
PY 2012
VL 12
AR 3
DI 10.1186/1472-6823-12-3
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 943AN
UT WOS:000304092900001
PM 22475205
ER
PT J
AU Sinka, ME
Bangs, MJ
Manguin, S
Rubio-Palis, Y
Chareonviriyaphap, T
Coetzee, M
Mbogo, CM
Hemingway, J
Patil, AP
Temperley, WH
Gething, PW
Kabaria, CW
Burkot, TR
Harbach, RE
Hay, SI
AF Sinka, Marianne E.
Bangs, Michael J.
Manguin, Sylvie
Rubio-Palis, Yasmin
Chareonviriyaphap, Theeraphap
Coetzee, Maureen
Mbogo, Charles M.
Hemingway, Janet
Patil, Anand P.
Temperley, William H.
Gething, Peter W.
Kabaria, Caroline W.
Burkot, Thomas R.
Harbach, Ralph E.
Hay, Simon I.
TI A global map of dominant malaria vectors
SO PARASITES & VECTORS
LA English
DT Article
ID ANOPHELES-FUNESTUS GROUP; BIONOMIC PRECIS; NICHE MODELS; POPULATION;
ABUNDANCE; ASSAY; ASIA
AB Background: Global maps, in particular those based on vector distributions, have long been used to help visualise the global extent of malaria. Few, however, have been created with the support of a comprehensive and extensive evidence-based approach.
Methods: Here we describe the generation of a global map of the dominant vector species (DVS) of malaria that makes use of predicted distribution maps for individual species or species complexes.
Results: Our global map highlights the spatial variability in the complexity of the vector situation. In Africa, An. gambiae, An. arabiensis and An. funestus are co-dominant across much of the continent, whereas in the Asian-Pacific region there is a highly complex situation with multi-species coexistence and variable species dominance.
Conclusions: The competence of the mapping methodology to accurately portray DVS distributions is discussed. The comprehensive and contemporary database of species-specific spatial occurrence (currently available on request) will be made directly available via the Malaria Atlas Project (MAP) website from early 2012.
C1 [Sinka, Marianne E.; Patil, Anand P.; Temperley, William H.; Gething, Peter W.; Hay, Simon I.] Univ Oxford, Spatial Ecol & Epidemiol Grp, Dept Zool, Oxford OX1 3PS, England.
[Bangs, Michael J.] PT Freeport Indonesia, Publ Hlth & Malaria Control Dept, Kuala Kencana, Papua, Indonesia.
[Manguin, Sylvie] Univ Montpellier I, Inst Rech Dev, Lab Immunophysiopathol Mol Comparee, Fac Pharm,UMR MD3, F-34093 Montpellier, France.
[Rubio-Palis, Yasmin] Univ Carabobo, Maracay 2101A, Venezuela.
[Rubio-Palis, Yasmin] Minist Poder Popular Salud, Direcc Control Vectores & Fauna Nociva, Lab Ecol Vectores, Maracay, Venezuela.
[Chareonviriyaphap, Theeraphap] Kasetsart Univ, Dept Entomol, Fac Agr, Bangkok, Thailand.
[Coetzee, Maureen] Univ Witwatersrand, Malaria Entomol Res Unit, Sch Pathol, Fac Hlth Sci, Johannesburg, South Africa.
[Chareonviriyaphap, Theeraphap] Natl Hlth Lab Serv, Natl Inst Communicable Dis, Vector Control Reference Unit, ZA-2131 Johannesburg, South Africa.
[Mbogo, Charles M.] KEMRI Wellcome Trust Programme, Ctr Geog Med Res Coast, Kilifi, Kenya.
[Hemingway, Janet] Univ Liverpool, Liverpool Sch Trop Med, Liverpool L3 5QA, Merseyside, England.
[Kabaria, Caroline W.] Univ Oxford, Malaria Publ Hlth & Epidemiol Grp, Kenyatta Natl Hosp Grounds,Ctr Geog Med, Wellcome Trust Collaborat Programme,KEMRI, Nairobi, Kenya.
[Burkot, Thomas R.] James Cook Univ, Trop Hlth Alliance, Townsville, Qld, Australia.
[Harbach, Ralph E.] Nat Hist Museum, Dept Entomol, London SW7 5BD, England.
[Hay, Simon I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Sinka, ME (reprint author), Univ Oxford, Spatial Ecol & Epidemiol Grp, Dept Zool, Tinbergen Bldg,S Parks Rd, Oxford OX1 3PS, England.
EM marianne.sinka@zoo.ox.ac.uk; simon.hay@zoo.ox.ac.uk
RI Burkot, Thomas/C-6838-2013; Manguin, Sylvie/G-1787-2015; Hay,
Simon/F-8967-2015;
OI Manguin, Sylvie/0000-0002-5925-7164; Hay, Simon/0000-0002-0611-7272;
Hemingway, Janet/0000-0002-3200-7173; Gething, Peter/0000-0001-6759-5449
FU Technical Advisory Group; Wellcome Trust [083534, 079091, 091835]; Bill
and Melinda Gates Foundation via the VFCNet consortium; RAPIDD of the
Science & Technology Directorate, Department of Homeland Security;
Fogarty International Center; National Institutes of Health; Wellcome
Trust, U.K; Global Fund to fight AIDS, Tuberculosis, and Malaria;
University of Oxford-Li Ka Shing Foundation; Oxford Tropical Network
FX We wish to thank Robi Okara, Rosalind Howes, Edward Haynes, Philip
Mbithi, Owen Yang, Carolynn Tago and Elisabeth Thiveyrat for primary
data abstraction and to Katherine Battle and David Pigott for proof
reading the manuscript. We are very grateful for insightful comments and
encouragement from Anthony Kiszewski on the global and regional
composite maps. We also thank unreservedly our Technical Advisory Group
for their extended support over the duration of the project. The initial
vector database and species distribution maps were created while MES was
funded by a project grant from the Wellcome Trust (#083534) to SIH. The
current work was conducted with support and funding from the Bill and
Melinda Gates Foundation via the VFCNet consortium
http://www.vecnet.org/[36], which also provides support for TRB. SIH is
funded by a Senior Research Fellowship from the Wellcome Trust
(#079091), which also supported CWK and supports PWG. APP and WHT are
funded by a Wellcome Trust Biomedical Resources Grant (#091835). SIH and
PWG also acknowledge support from the RAPIDD program of the Science &
Technology Directorate, Department of Homeland Security, and the Fogarty
International Center, National Institutes of Health
http://www.fic.nih.gov. This work forms part of the output of the
Malaria Atlas Project (MAP, http://www.map.ox.ac.uk), principally funded
by the Wellcome Trust, U.K. MAP also acknowledges the support of the
Global Fund to fight AIDS, Tuberculosis, and Malaria
http://www.theglobalfund.org and grants from the University of Oxford-Li
Ka Shing Foundation Global Health Program and the Oxford Tropical
Network. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 31
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U1 8
U2 52
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-3305
J9 PARASITE VECTOR
JI Parasites Vectors
PD APR 4
PY 2012
VL 5
AR 69
DI 10.1186/1756-3305-5-69
PG 11
WC Parasitology
SC Parasitology
GA 940GM
UT WOS:000303878000001
PM 22475528
ER
PT J
AU Smith, MR
Hamson, DK
Poort, JE
Jordan, CL
Breedlove, SM
AF Smith, Milo R.
Hamson, Dwayne K.
Poort, Jessica E.
Jordan, Cynthia L.
Breedlove, S. Marc
TI Ontogeny of androgen receptor expression in spinal nucleus of the
bulbocavernosus motoneurons and their target muscles in male mice
SO NEUROSCIENCE LETTERS
LA English
DT Article
DE Androgen receptor; Bulbocavernosus; Motoneuron; Sexual differentiation
ID LEVATOR ANI MUSCLE; DEVELOPING NEUROMUSCULAR SYSTEM; MALE-RATS;
GENITOFEMORAL NERVE; HORMONAL-CONTROL; KNOCKOUT MICE; CELL-DEATH;
TESTOSTERONE; IMMUNOREACTIVITY; FLUTAMIDE
AB The spinal nucleus of the bulbocavernosus (SNB) in rodents is a neuromuscular system consisting of lumbar motoneurons and the perineal muscles they innervate, the bulbocavernosus and levator ani. This system is present prenatally in both males and females but degenerates postnatally in females because of the lack of perinatal androgens. Whether androgens act on the motoneurons or muscles in the SNB system to promote survival is a longstanding question. Evidence in rats suggests androgens act primarily on the muscles in development, given that the muscles express androgen receptor (AR) before the critical period of androgen-dependent cell rescue, whereas motoneurons develop AR after this period. We now report, based on a novel AR-reporter mouse model, that AR is expressed in the bulbocavernosus muscles of C57/BL6(J) mice as early as embryonic day 15, while, based on AR-immunocytochemistry, SNB motoneurons do not express AR until postnatal day 4. These results indicate that the ontogeny of AR expression in the mouse SNB system resembles that found in rats, suggesting that androgens may also act on perineal muscles in mice to rescue the SNB system. (c) 2012 Elsevier Ireland Ltd. All rights reserved.
C1 [Smith, Milo R.; Hamson, Dwayne K.; Poort, Jessica E.; Jordan, Cynthia L.; Breedlove, S. Marc] Michigan State Univ, Neurosci Program, E Lansing, MI 48824 USA.
RP Smith, MR (reprint author), NIH, BG 10 RM 2D39,10 Ctr Dr, Bethesda, MD 20892 USA.
EM milo.smith@nih.gov
FU National Institutes of Health [R01 NS28241, NS045195]; Michigan State
University
FX We thank Diane Redenius for dedicated research support. This work was
made possible by National Institutes of Health Grants R01 NS28241 (SMB)
and NS045195 (CLJ) and with the support of the Michigan State University
Summer Research Opportunities Program.
NR 22
TC 5
Z9 5
U1 0
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PD APR 4
PY 2012
VL 513
IS 2
BP 119
EP 123
DI 10.1016/j.neulet.2012.01.067
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA 929UD
UT WOS:000303090300003
PM 22330750
ER
PT J
AU Wallace, GL
Shaw, P
Lee, NR
Clasen, LS
Raznahan, A
Lenroot, RK
Martin, A
Giedd, JN
AF Wallace, Gregory L.
Shaw, Philip
Lee, Nancy Raitano
Clasen, Liv S.
Raznahan, Armin
Lenroot, Rhoshel K.
Martin, Alex
Giedd, Jay N.
TI Distinct Cortical Correlates of Autistic versus Antisocial Traits in a
Longitudinal Sample of Typically Developing Youth
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PROCESS SCREENING DEVICE; AUTOMATED 3-D EXTRACTION; PSYCHOPATHIC TRAITS;
SPECTRUM DISORDER; SOCIAL COGNITION; MENTAL-HEALTH; CHILDREN; BRAIN;
RELIABILITY; VALIDITY
AB In humans, behaviors associated with autism and antisociality, disorders characterized by distinct social impairments, can be viewed as quantitative traits that range from frank impairment to normal variation, as found in the general population. Neuroimaging investigations of autism and antisociality demonstrate diagnostically specific aberrant cortical brain structure. However, little is known about structural brain correlates of social behavior in nonclinical populations. Therefore, we sought to determine whether autistic and antisocial traits exhibit dissociable cortical correlates and whether these associations are stable across development among typically developing youth. Three hundred twenty-three typically developing youth (age at first scan: mean = 10.63, SD = 3.71 years) underwent anatomic magnetic resonance imaging (1-6 scans each; total = 742 scans), and provided ratings of autistic and antisocial traits. Higher autistic trait ratings were associated with thinner cortex most prominently in right superior temporal sulcus while higher antisocial trait ratings were associated with thinner cortex in primarily bilateral anterior prefrontal cortices. There was no interaction with age, indicating that these brain-behavior associations were stable across development. Using assessments of both subclinical autistic and subclinical antisocial traits within a large longitudinal sample of typically developing youth, we demonstrate dissociable neuroanatomic correlations that parallel those found in the frank clinical disorders of autism (e. g., superior temporal cortex) and antisociality (e. g., anterior prefrontal cortex). Moreover, these correlations appear to be established in early childhood and remain fixed into early adulthood. These results support the dimensional view of psychopathology and provide neural signatures that can serve as informative endophenotypes for future genetic studies.
C1 [Wallace, Gregory L.; Martin, Alex] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
[Shaw, Philip; Lee, Nancy Raitano; Clasen, Liv S.; Raznahan, Armin; Lenroot, Rhoshel K.; Giedd, Jay N.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
RP Wallace, GL (reprint author), NIMH, Lab Brain & Cognit, NIH, 10 Ctr Dr,Room 4C104,MSC 1366, Bethesda, MD 20892 USA.
EM gregwallace@mail.nih.gov
RI martin, alex/B-6176-2009; Raznahan, Armin/F-4534-2012; Giedd,
Jay/B-7302-2012; Giedd, Jay/J-9644-2015; Lee, Nancy/M-7492-2016;
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978; Lee,
Nancy/0000-0002-6663-0713; Wallace, Gregory/0000-0003-0329-5054
FU NIH, National Institute of Mental Health
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Mental Health. We thank the participants and
their families who volunteered their time to contribute to this
research.
NR 49
TC 27
Z9 28
U1 4
U2 18
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 4
PY 2012
VL 32
IS 14
BP 4856
EP 4860
DI 10.1523/JNEUROSCI.6214-11.2012
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA 925TD
UT WOS:000302783500016
PM 22492041
ER
PT J
AU Iruarrizaga-Lejarreta, M
Varela-Rey, M
Lozano, JJ
Fernandez-Ramos, D
Rodriguez-Ezpeleta, N
Embade, N
Lu, SC
van der Kraan, PM
Davidson, ENB
Gorospe, M
Mirsky, R
Jessen, KR
Aransay, AM
Mato, JM
Martinez-Chantar, ML
Woodhoo, A
AF Iruarrizaga-Lejarreta, Marta
Varela-Rey, Marta
Jose Lozano, Juan
Fernandez-Ramos, David
Rodriguez-Ezpeleta, Naiara
Embade, Nieves
Lu, Shelly C.
van der Kraan, Peter M.
Davidson, Esmeralda N. Blaney
Gorospe, Myriam
Mirsky, Rhona
Jessen, Kristjan R.
Maria Aransay, Ana
Mato, Jose M.
Martinez-Chantar, Maria L.
Woodhoo, Ashwin
TI The RNA-Binding Protein Human Antigen R Controls Global Changes in Gene
Expression during Schwann Cell Development
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PERIPHERAL NERVOUS-SYSTEM; NF-KAPPA-B; GROWTH-FACTOR-BETA;
MESSENGER-RNA; IN-VITRO; EMBRYONIC-DEVELOPMENT; EXTRACELLULAR-MATRIX;
WIDE ANALYSIS; CYCLIN D1; KINASE-C
AB An important prerequisite to myelination in peripheral nerves is the establishment of one-to-one relationships between axons and Schwann cells. This patterning event depends on immature Schwann cell proliferation, apoptosis, and morphogenesis, which are governed by coordinated changes in gene expression. Here, we found that the RNA-binding protein human antigen R (HuR) was highly expressed in immature Schwann cells, where genome-wide identification of its target mRNAs in vivo in mouse sciatic nerves using ribonomics showed an enrichment of functionally related genes regulating these processes. HuR coordinately regulated expression of several genes to promote proliferation, apoptosis, and morphogenesis in rat Schwann cells, in response to NRG1, TGF beta, and laminins, three major signals implicated in this patterning event. Strikingly, HuR also binds to several mRNAs encoding myelination-related proteins but, contrary to its typical function, negatively regulated their expression, likely to prevent ectopic myelination during development. These functions of HuR correlated with its abundance and subcellular localization, which were regulated by different signals in Schwann cells.
C1 [Iruarrizaga-Lejarreta, Marta; Varela-Rey, Marta; Fernandez-Ramos, David; Rodriguez-Ezpeleta, Naiara; Embade, Nieves; Maria Aransay, Ana; Mato, Jose M.; Martinez-Chantar, Maria L.; Woodhoo, Ashwin] Ctr Invest Biomed Red Enfermedades Hepat & Digest, CIC BioGUNE, Derio 48160, Bizkaia, Spain.
[Jose Lozano, Juan] Hosp Clin Ctr Esther Koplovitz, Ctr Invest Biomed Red Enfermedades Hepat & Digest, Barcelona 08036, Spain.
[Lu, Shelly C.] Univ So Calif, Keck Sch Med, Res Ctr Liver Dis, Div Gastrointestinal & Liver Dis, Los Angeles, CA 90033 USA.
[van der Kraan, Peter M.; Davidson, Esmeralda N. Blaney] Radboud Univ Nijmegen, Med Ctr, Dept Rheumatol, Nijmegen Ctr Mol Life Sci,Med Ctr Nijmegen, NL-6525 GA Nijmegen, Netherlands.
[Gorospe, Myriam] NIA, Lab Cellular & Immunol, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Mirsky, Rhona; Jessen, Kristjan R.] UCL, Dept Cell & Dev Biol, London WC1E 6BT, England.
RP Woodhoo, A (reprint author), Ctr Invest Biomed Red Enfermedades Hepat & Digest, CIC BioGUNE, Technol Pk Bizkaia, Derio 48160, Bizkaia, Spain.
EM awoodhoo@cicbiogune.es
RI MATO, JOSE/A-5187-2011; Aransay, Ana/F-8086-2011; Rodriguez-Ezpeleta,
Naiara/B-7138-2014; van der Kraan, Peter/D-9115-2011; embade,
Nieves/K-5190-2014; woodhoo, ashwin/A-4904-2015; Martinez Chantar, Maria
Luz/F-5190-2011; Blaney Davidson, E.N./L-4204-2015; Fernandez-Ramos,
David/S-5231-2016
OI Aransay, Ana/0000-0002-8271-612X; Rodriguez-Ezpeleta,
Naiara/0000-0001-6735-6755; embade, Nieves/0000-0001-9878-3290; woodhoo,
ashwin/0000-0002-8395-2837; Martinez Chantar, Maria
Luz/0000-0002-6446-9911;
FU Instituto de Salud Carlos III (FIS) [PS09/00094]; Fundacion Cientifica
de la Asociacion Espanola Contra el Cancer; Ministry of Science and
Innovation, Spain; Royal Society of Great Britain; National Institutes
of Health [AT-1576]; Spanish Ministry of Science [SAF2011-29851];
Sanidad Gobierno Vasco; Educacion Gobierno Vasco; Instituto de Salud
Carlos III; National Institute on Aging, National Institutes of Health;
[PI11/01588]
FX This work was supported by grants from Instituto de Salud Carlos III
(FIS, PS09/00094; Ministry of Health, Spain), Fundacion Cientifica de la
Asociacion Espanola Contra el Cancer (Cancer Infantil), and the Program
Ramon y Cajal (Ministry of Science and Innovation, Spain) (A. W.), an
International Joint Project grant from the Royal Society of Great
Britain (K.R.J., A. W.), National Institutes of Health Grant AT-1576 (S.
C. L., M. L. M.-C., J.M.M.), Plan Nacional from the Spanish Ministry of
Science SAF2011-29851 (J.M.M.), Sanidad Gobierno Vasco 2012 (M.V.-R.),
ETORTEK-2010 (M. L. M.-C.), Sanidad Gobierno Vasco 2008 (M. L. M.-C.),
Educacion Gobierno Vasco 2011 (M. L. M.-C.), and PI11/01588 (M. L.
M.-C.). Centro de Investigacion Biomedica en Red de Enfermedades
Hepaticas y Digestivas is funded by the Instituto de Salud Carlos III.
M. G. was supported by the National Institute on Aging-Intramural
Research Program, National Institutes of Health.
NR 87
TC 4
Z9 4
U1 0
U2 7
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 4
PY 2012
VL 32
IS 14
BP 4944
EP 4958
DI 10.1523/JNEUROSCI.5868-11.2012
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 925TD
UT WOS:000302783500025
PM 22492050
ER
PT J
AU Bossert, JM
Stern, AL
Theberge, FRM
Marchant, NJ
Wang, HL
Morales, M
Shaham, Y
AF Bossert, Jennifer M.
Stern, Anna L.
Theberge, Florence R. M.
Marchant, Nathan J.
Wang, Hui-Ling
Morales, Marisela
Shaham, Yavin
TI Role of Projections from Ventral Medial Prefrontal Cortex to Nucleus
Accumbens Shell in Context-Induced Reinstatement of Heroin Seeking
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PHASEOLUS-VULGARIS-LEUKOAGGLUTININ; DOPAMINE D-1-FAMILY RECEPTORS;
PRIMING-INDUCED REINSTATEMENT; COCAINE-INDUCED REINSTATEMENT;
CUE-INDUCED REINSTATEMENT; C-FOS IMMUNOREACTIVITY; BASOLATERAL AMYGDALA;
DRUG-SEEKING; INDUCED RELAPSE; PRELIMBIC CORTEX
AB In humans, exposure to contexts previously associated with heroin use can provoke relapse. In rats, exposure to heroin-paired contexts after extinction of drug-reinforced responding in different contexts reinstates heroin seeking. This effect is attenuated by inhibition of glutamate or dopamine transmission in nucleus accumbens shell, or inactivation of ventral medial prefrontal cortex (mPFC). Here, we used an anatomical asymmetrical disconnection procedure to demonstrate that an interaction between glutamatergic projections from ventral mPFC to accumbens shell and local dopamine D-1 postsynaptic receptors contributes to context-induced reinstatement of heroin seeking. We also combined the marker of neuronal activity, Fos, with the retrograde tracer Fluoro-Gold to assess activation in this pathway during context-induced reinstatement. Rats were trained to self-administer heroin for 12 d; drug infusions were paired with a discrete tone-light cue. Lever pressing was subsequently extinguished in a nondrug-associated context in the presence of the discrete cue. Rats were then tested in the heroin- or extinction-associated contexts under extinction conditions. Injections of muscimol + baclofen into ventral mPFC in one hemisphere and D-1-family receptor antagonist SCH 23390 into the contralateral or ipsilateral accumbens shell decreased context-induced reinstatement. Unilateral injections of muscimol + baclofen into ventral mPFC or SCH 23390 into the accumbens shell had no effect. Context-induced reinstatement was associated with increased Fos expression in ventral mPFC neurons, including those projecting to accumbens shell, with higher double-labeling in the ipsilateral projection than in the contralateral projection. Our results demonstrate that activation of glutamatergic projections from ventral mPFC to accumbens shell, previously implicated in inhibition of cocaine relapse, promotes heroin relapse.
C1 [Bossert, Jennifer M.; Stern, Anna L.; Theberge, Florence R. M.; Marchant, Nathan J.; Shaham, Yavin] NIDA, Behav Neurosci Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
[Wang, Hui-Ling; Morales, Marisela] NIDA, Cellular Neurobiol Res Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
RP Bossert, JM (reprint author), NIDA, Behav Neurosci Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM jbossert@intra.nida.nih.gov
RI shaham, yavin/G-1306-2014;
OI Marchant, Nathan/0000-0001-8269-0532
FU National Institute on Drug Abuse (NIH, DHHS)
FX This work was supported by the Intramural Research Program of the
National Institute on Drug Abuse (NIH, DHHS). We thank Brittany Navarre,
Carlo Cifani, and Sanya Fanous for their help in conducting the
experiments. We also thank Susan Sesack, Stan Floresco, Kue Tseng,
Anthony Grace, Patricio O'Donnell, and Bita Moghaddam for helpful advice
on anatomical and circuit issues discussed in this paper.
NR 85
TC 85
Z9 93
U1 0
U2 6
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD APR 4
PY 2012
VL 32
IS 14
BP 4982
EP 4991
DI 10.1523/JNEUROSCI.0005-12.2012
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 925TD
UT WOS:000302783500028
PM 22492053
ER
PT J
AU Kim, T
Lee, KI
Morris, P
Pastor, RW
Andersen, OS
Im, W
AF Kim, Taehoon
Lee, Kyu Il
Morris, Phillip
Pastor, Richard W.
Andersen, Olaf S.
Im, Wonpil
TI Influence of Hydrophobic Mismatch on Structures and Dynamics of
Gramicidin A and Lipid Bilayers
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID MEMBRANE-PROTEIN FUNCTION; MOLECULAR-DYNAMICS; H-2 NMR; ENSEMBLE
DYNAMICS; CHANNEL LIFETIME; CHAIN DYNAMICS; ION PERMEATION;
FORCE-FIELDS; FREE-ENERGY; SIDE-CHAIN
AB Gramicidin A (gA) is a 15-amino-acid antibiotic peptide with an alternating L-D sequence, which forms (dimeric) bilayer-spanning, monovalent cation channels in biological membranes and synthetic bilayers. We performed molecular dynamics simulations of gA dimers and monomers in all-atom, explicit dilauroylphosphatidylcholine (DLPC), dimyristoylphosphatidylcholine (DMPC), dioleoylphosphatidylcholine (DOPC), and 1-palmitoy1-2-oleoyl-phosphatidylcholine (POPC) bilayers. The variation in acyl chain length among these different phospholipids provides a way to alter gA-bilayer interactions by varying the bilayer hydrophobic thickness, and to determine the influence of hydrophobic mismatch on the structure and dynamics of both gA channels (and monomeric subunits) and the host bilayers. The simulations show that the channel structure varied little with changes in hydrophobic mismatch, and that the lipid bilayer adapts to the bilayer-spanning channel to minimize the exposure of hydrophobic residues. The bilayer thickness, however, did not vary monotonically as a function of radial distance from the channel. In all simulations, there was an initial decrease in thickness within 4-5 angstrom from the channel, which was followed by an increase in DOPC and POPC or a further decrease in DLPC and DMPC bilayers. The bilayer thickness varied little in the monomer simulations except one of three independent simulations for DMPC and all three DLPC simulations, where the bilayer thinned to allow a single subunit to form a bilayer-spanning water-permeable pore. The radial dependence of local lipid area and bilayer compressibility is also nonmonotonic in the first shell around gA dimers due to gA-phospholipid interactions and the hydrophobic mismatch. Order parameters, acyl chain dynamics, and diffusion constants also differ between the lipids in the first shell and the bulk. The lipid behaviors in the first shell around gA dimers are more complex than predicted from a simple mismatch model, which has implications for understanding the energetics of membrane protein-lipid interactions.
C1 [Andersen, Olaf S.] Weill Cornell Med Coll, Dept Physiol & Biophys, New York, NY USA.
[Kim, Taehoon; Lee, Kyu Il; Morris, Phillip; Im, Wonpil] Univ Kansas, Dept Mol Biosci, Lawrence, KS 66045 USA.
[Kim, Taehoon; Lee, Kyu Il; Morris, Phillip; Im, Wonpil] Univ Kansas, Ctr Bioinformat, Lawrence, KS 66045 USA.
[Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Andersen, OS (reprint author), Weill Cornell Med Coll, Dept Physiol & Biophys, New York, NY USA.
EM sparre@med.cornell.edu; wonpil@ku.edu
FU National Science Foundation [MCB-0918374]; Purdue University (National
Science Foundation) [OCI-0503992]; National Institutes of Health
[GM021342]; National Institutes of Health, National Heart, Lung and
Blood Institute
FX This work was supported in part by the National Science Foundation
(MCB-0918374 to W.I.); TeraGrid resources were provided by Purdue
University (National Science Foundation, OCI-0503992 to W.I.), the
National Institutes of Health (GM021342 to O.S.A.), and the Intramural
Research Program of the National Institutes of Health, National Heart,
Lung and Blood Institute (to R.W.P.).
NR 57
TC 47
Z9 47
U1 4
U2 37
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 APR 4
PY 2012
VL 102
IS 7
BP 1551
EP 1560
DI 10.1016/j.bpj.2012.03.014
PG 10
WC Biophysics
SC Biophysics
GA 920XR
UT WOS:000302443100010
PM 22500755
ER
PT J
AU Mazumder, A
Bandyopadhyay, S
Dhar, A
Lewis, DEA
Deb, S
Dey, S
Chakrabarti, P
Roy, S
AF Mazumder, Abhishek
Bandyopadhyay, Sumita
Dhar, Amlanjyoti
Lewis, Dale E. A.
Deb, Sunanda
Dey, Sucharita
Chakrabarti, Pinak
Roy, Siddhartha
TI A Genetic Network That Balances Two Outcomes Utilizes Asymmetric
Recognition of Operator Sites
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID LAMBDA-CI-REPRESSOR; BACTERIOPHAGE-LAMBDA; CONFORMATIONAL-CHANGES;
TERMINAL DOMAIN; O-R; DNA; BINDING; TRANSCRIPTION; ENERGETICS; COLI
AB Stability and induction of the lysogenic state of bacteriophage A are balanced by a complex regulatory network. A key feature of this network is the mutually exclusive cooperative binding of a repressor dimer (Cl) to one of two pairs of binding sites, O(R)1-O(R)2 or O(R)2-O(R)3. The structural features that underpin the mutually exclusive binding mode are not well understood. Recent studies have demonstrated that Cl is an asymmetric dimer. The functional importance of the asymmetry is not fully clear. Due to the asymmetric nature of the Cl dimer as well as its binding sites, there are two possible bound orientations. By fluorescence resonance energy transfer measurements we showed that Cl prefers one bound orientation. We also demonstrated that the relative configuration of the binding sites is important for Cl dimer-dimer interactions and consequent cooperative binding. We proposed that the operator configuration dictates the orientations of the bound Cl molecules, which in turn dictates Cl cooperative interaction between the O(R)1-O(R)2 or O(R)2-O(R)3, but not both. Modeling suggests that the relative orientation of the C- and N-terminal domains may play an important role in the mutually exclusive nature of the cooperative binding. This work correlates unique structural features of a transcription regulatory protein with the functional properties of a gene regulatory network.
C1 [Mazumder, Abhishek; Roy, Siddhartha] Indian Inst Chem Biol, Council Sci & Ind Res, Div Struct Biol & Bioinformat, Kolkata 700032, W Bengal, India.
[Dey, Sucharita; Chakrabarti, Pinak] Bose Inst, Dept Biochem, Kolkata 700009, W Bengal, India.
[Bandyopadhyay, Sumita; Deb, Sunanda] Bose Inst, Dept Biophys, Kolkata 700009, W Bengal, India.
[Dhar, Amlanjyoti; Lewis, Dale E. A.] NCI, Mol Biol Lab, Bethesda, MD 20892 USA.
RP Roy, S (reprint author), Indian Inst Chem Biol, Council Sci & Ind Res, Div Struct Biol & Bioinformat, 4 Raja Sc Mullick Rd, Kolkata 700032, W Bengal, India.
EM sidroykolkata@gmail.com
FU Department of Science and Technology, Government of India; Council of
Scientific and Industrial Research; National Institutes of Health;
National Cancer Institute; Center for Cancer Research
FX We acknowledge the Department of Science and Technology, Government of
India, for JC Bose Fellowship to SR., Council of Scientific and
Industrial Research for funding the work and fellowship to A.M. This
work was also supported by the Intramural Research Program of the
National Institutes of Health, the National Cancer Institute, and the
Center for Cancer Research.
NR 29
TC 0
Z9 0
U1 0
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
EI 1542-0086
J9 BIOPHYS J
JI Biophys. J.
PD APR 4
PY 2012
VL 102
IS 7
BP 1580
EP 1589
DI 10.1016/j.bpj.2012.01.052
PG 10
WC Biophysics
SC Biophysics
GA 920XR
UT WOS:000302443100013
PM 22500758
ER
PT J
AU Mueller, F
Morisaki, T
Mazza, D
McNally, JG
AF Mueller, Florian
Morisaki, Tatsuya
Mazza, Davide
McNally, James G.
TI Minimizing the Impact of Photoswitching of Fluorescent Proteins on FRAP
Analysis
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID NUCLEAR PROTEINS; HUMAN-CELLS; CHROMATIN; RECOVERY; DYNAMICS; BINDING;
DIFFUSION; MOLECULES; MOBILITY
AB Fluorescence recovery after photobleaching (FRAP) is a widely used imaging technique for measuring the mobility of fluorescently tagged proteins in living cells. Although FRAP presumes that high-intensity illumination causes only irreversible. photobleaching, reversible photoswitching of many fluorescent molecules, including GFP, can also occur. Here, we show that this photoswitching is likely to contaminate many FRAPs of GFP, and worse, the size of its contribution can be up to 60% under different experimental conditions, making it difficult to compare FRAPs from different studies. We develop a procedure to correct FRAPs for photoswitching and apply it to FRAPs of the GFP-tagged histone H2B, which, depending on the precise photobleaching conditions exhibits apparent fast components ranging from 9-36% before correction and similar to 1% after correction. We demonstrate how this similar to 1% fast component of H28-GFP can be used as a benchmark both to estimate the role of photoswitching in previous FRAP studies of TATA binding proteins (TBP) and also as a tool to minimize the contribution of photoswitching to tolerable levels in future FRAP experiments. In sum, we show how the impact of photoswitching on FRAP can be identified, minimized, and corrected.
C1 [Mueller, Florian; Morisaki, Tatsuya; Mazza, Davide; McNally, James G.] NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
RP McNally, JG (reprint author), NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
EM mcnallyj@exchange.nih.gov
RI Mueller, Florian/C-9075-2012; Mazza, Davide/R-5340-2016
OI Mueller, Florian/0000-0002-9622-4396; Mazza, Davide/0000-0003-2776-4142
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX This research was supported in part by the intramural program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 21
TC 23
Z9 23
U1 1
U2 9
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 APR 4
PY 2012
VL 102
IS 7
BP 1656
EP 1665
DI 10.1016/j.bpj.2012.02.029
PG 10
WC Biophysics
SC Biophysics
GA 920XR
UT WOS:000302443100021
PM 22500766
ER
PT J
AU Ulrich, CM
Grady, C
AF Ulrich, Connie M.
Grady, Christine
TI Perceptions of Appropriateness of Care in the Intensive Care Unit
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
ID ETHICS CONSULTATION
C1 [Ulrich, Connie M.] Univ Penn, Sch Nursing, Dept Med Eth & Hlth Policy, Philadelphia, PA 19104 USA.
[Grady, Christine] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Ulrich, CM (reprint author), Univ Penn, Sch Nursing, Dept Med Eth & Hlth Policy, Philadelphia, PA 19104 USA.
EM culrich@nursing.upenn.edu
FU Intramural NIH HHS [Z99 CL999999]
NR 3
TC 0
Z9 0
U1 1
U2 3
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 APR 4
PY 2012
VL 307
IS 13
BP 1370
EP 1371
DI 10.1001/jama.2012.394
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 919AY
UT WOS:000302294200015
PM 22474196
ER
PT J
AU Alberts, SR
Sargent, DJ
Nair, S
Mahoney, MR
Mooney, M
Thibodeau, SN
Smyrk, TC
Sinicrope, FA
Chan, E
Gill, S
Kahlenberg, MS
Shields, AF
Quesenberry, JT
Webb, TA
Farr, GH
Pockaj, BA
Grothey, A
Goldberg, RM
AF Alberts, Steven R.
Sargent, Daniel J.
Nair, Suresh
Mahoney, Michelle R.
Mooney, Margaret
Thibodeau, Stephen N.
Smyrk, Thomas C.
Sinicrope, Frank A.
Chan, Emily
Gill, Sharlene
Kahlenberg, Morton S.
Shields, Anthony F.
Quesenberry, James T.
Webb, Thomas A.
Farr, Gist H., Jr.
Pockaj, Barbara A.
Grothey, Axel
Goldberg, Richard M.
TI Effect of Oxaliplatin, Fluorouracil, and Leucovorin With or Without
Cetuximab on Survival Among Patients With Resected Stage III Colon
Cancer A Randomized Trial
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; EPITHELIAL-MESENCHYMAL TRANSITION; MRC
COIN TRIAL; 1ST-LINE TREATMENT; ADJUVANT TREATMENT; PHASE-III;
CHEMOTHERAPY; PANITUMUMAB; FLUOROPYRIMIDINE; IRINOTECAN
AB Context Leucovorin, fluorouracil, and oxaliplatin (FOLFOX) is the standard adjuvant therapy for resected stage III colon cancer. Adding cetuximab to FOLFOX benefits patients with metastatic wild-type KRAS but not mutated KRAS colon cancer.
Objective To assess the potential benefit of cetuximab added to the modified sixth version of the FOLFOX regimen (mFOLFOX6) in patients with resected stage III wild-type KRAS colon cancer.
Design, Setting, and Participants A randomized trial of 2686 patients aged 18 years or older at multiple institutions across North America enrolled following resection and informed consent between February 10, 2004, and November 25, 2009. The primary randomized comparison was 12 biweekly cycles of mFOLFOX6 with and without cetuximab. KRAS mutation status was centrally determined. The trial was halted after a planned interim analysis of 48% of predicted events (246/515) occurring in 1863 (of 2070 planned) patients with tumors having wild-type KRAS. A total of 717 patients with mutated KRAS and 106 with indeterminate KRAS were accrued. The 2070 patients with wild-type KRAS provided 90% power to detect a hazard ratio (HR) of 1.33 (2-sided alpha=.05), with planned interim efficacy analyses after 25%, 50%, and 75% of expected relapses.
Main Outcome Measures Disease-free survival in patients with wild-type KRAS mutations. Secondary end points included overall survival and toxicity.
Results Median (range) follow-up was 28 (0-68) months. The trial demonstrated no benefit when adding cetuximab. Three-year disease-free survival for mFOLFOX6 alone was 74.6% vs 71.5% with the addition of cetuximab (HR, 1.21; 95% CI, 0.98-1.49; P=.08) in patients with wild-type KRAS, and 67.1% vs 65.0% (HR, 1.12; 95% CI, 0.86-1.46; P=.38) in patients with mutated KRAS, with no significant benefit in any subgroups assessed. Among all patients, grade 3 or higher adverse events (72.5% vs 52.3%; odds ratio [OR], 2.4; 95% CI, 2.1-2.8; P<.001) and failure to complete 12 cycles (33% vs 23%; OR, 1.6; 95% CI, 1.4-1.9; P<.001) were significantly higher with cetuximab. Increased toxicity and greater detrimental differences in all outcomes were observed in patients aged 70 years or older.
Conclusion Among patients with stage III resected colon cancer, the use of cetuximab with adjuvant mFOLFOX6 compared with mFOLFOX6 alone did not result in improved disease-free survival.
C1 [Alberts, Steven R.; Sinicrope, Frank A.; Grothey, Axel] Mayo Clin, Dept Oncol, Rochester, MN 55905 USA.
[Sargent, Daniel J.; Mooney, Margaret] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Nair, Suresh] Lehigh Valley Hosp, Allentown, PA USA.
[Mooney, Margaret] NCI, Clin Invest Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Chan, Emily] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Gill, Sharlene] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Kahlenberg, Morton S.] Surg Oncol Associates S Texas, San Antonio, TX USA.
[Shields, Anthony F.] Karmanos Canc Inst, Detroit, MI USA.
[Quesenberry, James T.] Siouxland Hematol Oncol Associates, Sioux City, IA USA.
[Webb, Thomas A.] Illinois Oncol Res Assoc, Community Clin Oncol Program, Peoria, IL USA.
[Farr, Gist H., Jr.] Ochsner Community Clin Oncol Program, New Orleans, LA USA.
[Goldberg, Richard M.] Ohio State Univ, Columbus, OH 43210 USA.
RP Alberts, SR (reprint author), Mayo Clin, Dept Oncol, Rochester, MN 55905 USA.
RI Goldberg , Richard/M-1311-2013;
OI Sargent, Daniel/0000-0002-2684-4741
FU National Cancer Institute, Department of Health and Human Services
[CA-25224, CA-37404, CA-35103, CA-35113, CA-35272, CA-114740, CA-32102,
CA-14028, CA49957, CA21115, CA31946, CA12027, CA37377]; Bristol-Myers
Squibb; ImClone; sanofi-aventis; Pfizer; sanofi-aventis by the North
Central Cancer Treatment Group (NCCTG); Merck Serono; Eastern
Cooperative Oncology Group; National Comprehensive Cancer Network;
Genentech; Southwest Oncology Group
FX All authors have completed and submitted the ICMJE Form for Disclosure
of Potential Conflicts of Interest. Dr Alberts reported receiving grants
from Pfizer, Bristol-Myers Squibb, and sanofi-aventis by the North
Central Cancer Treatment Group (NCCTG) for support of the conduct of
this trial. Dr Sargent reported receiving grants from Pfizer,
Bristol-Myers Squibb, and sanofi-aventis for support to NCCTG for
conduct of this trial. Dr Nair reported receiving support for travel to
meetings from National Cancer Institute Cooperative Group. Dr Sinicrope
reported receiving consultancy fees from Merck Serono, receiving grants
from the National Institutes of Health, payment for lectures including
service on service bureaus from the University of Kansas, and travel
meeting expenses from the American Society of Clinical Oncology. Dr Chan
reported receiving a grant from the Eastern Cooperative Oncology Group;
being a board member of Colorectal Cancer Index and Reviews and
HCPLive.com Oncology Advisory Board; being a consultant on advisory
boards of Amgen, ImClone, Bristol-Myers Squibb, Genentech, Pfizer, and
Celgene; receiving grants and travel meeting expenses from National
Comprehensive Cancer Network; receiving travel meeting expenses from
Chemotherapy Foundation; and being an institutional investigator in
numerous clinical trials involving multiple pharmaceutical companies. Dr
Gill reported receiving payment for lectures including service on
speakers bureaus from Bristol-Myers Squibb. Dr Kahlenberg reported
receiving payment for lectures including service on speakers bureaus
from Genentech. Dr Shields reported receiving grant and support for
travel to meetings for the study from Southwest Oncology Group. Dr
Grothey reported receiving grants and consultancy fees from
sanofi-aventis. No other authors provided any financial disclosures.;
This trial was conducted as a collaborative trial of the North Central
Cancer Treatment Group (NCCTG), Mayo Clinic, and was supported in part
by Public Health Service grants CA-25224, CA-37404, CA-35103, CA-35113,
CA-35272, CA-114740, CA-32102, CA-14028, CA49957, CA21115, CA31946,
CA12027, CA37377 from the National Cancer Institute, Department of
Health and Human Services. Bristol-Myers Squibb, ImClone,
sanofi-aventis, and Pfizer provided unrestricted support to NCCTG for
conduct of trial. Bristol-Myers Squibb provided cetuximab to NCCTG.
NR 33
TC 172
Z9 176
U1 1
U2 11
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 APR 4
PY 2012
VL 307
IS 13
BP 1383
EP 1393
DI 10.1001/jama.2012.385
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 919AY
UT WOS:000302294200025
PM 22474202
ER
PT J
AU Millum, J
AF Millum, Joseph
TI Canada's new ethical guidelines for research with humans: a critique and
comparison with the United States
SO CANADIAN MEDICAL ASSOCIATION JOURNAL
LA English
DT Article
ID BOARD; MULTICENTER
C1 [Millum, Joseph] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
[Millum, Joseph] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Millum, J (reprint author), NIH, Dept Bioeth, Bldg 10, Bethesda, MD 20892 USA.
EM millumj@cc.nih.gov
NR 24
TC 1
Z9 1
U1 1
U2 3
PU CMA-CANADIAN MEDICAL ASSOC
PI OTTAWA
PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 5W8, CANADA
SN 0820-3946
J9 CAN MED ASSOC J
JI Can. Med. Assoc. J.
PD APR 3
PY 2012
VL 184
IS 6
BP 657
EP 661
DI 10.1503/cmaj.111217
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 007NJ
UT WOS:000308894700033
PM 22249987
ER
PT J
AU Moon, AF
Xu, YM
Woody, SM
Krahn, JM
Linhardt, RJ
Liu, J
Pedersen, LC
AF Moon, Andrea F.
Xu, Yongmei
Woody, Susan M.
Krahn, Joseph M.
Linhardt, Robert J.
Liu, Jian
Pedersen, Lars C.
TI Dissecting the substrate recognition of 3-O-sulfotransferase for the
biosynthesis of anticoagulant heparin
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE oligosaccharides; substrate specificity; ternary complex; heparan
sulfate
ID SULFATE; ANTITHROMBIN; CONFORMER; RESIDUES; BINDING; ENTRY
AB Heparin is a polysaccharide-based natural product that is used clinically as an anticoagulant drug. Heparan sulfate 3-O-sulfotransferase (3-OST) is an enzyme that transfers a sulfo group to the 3-OH position of a glucosamine unit. 3-OST is present in multiple isoforms, and the polysaccharides modified by these different isoforms perform distinct biological functions. 3-OST isoform 1 (3-OST-1) is the key enzyme for the biosynthesis of anticoagulant heparin. Here, we report the crystal structure of the ternary complex of 3-OST-1, 3'-phosphoadenosine 5'-phosphate, and a heptasaccharide substrate. Comparisons to previously determined structures of 3-OST-3 reveal unique binding modes used by the different isoforms of 3-OST for distinguishing the fine structures of saccharide substrates. Our data demonstrate that the saccharide substrates display distinct conformations when interacting with the different 3-OST isoforms. Site-directed mutagenesis data suggest that several key amino residues, including Lys259, Thr256, and Trp283 in 3-OST-3 and Arg268 in 3-OST-1, play important roles in substrate binding and specificity between isoforms. These results deepen our understanding of the biosynthetic mechanism of heparan sulfate and provide structural information for engineering enzymes for an enhanced biosynthetic approach to heparin production.
C1 [Xu, Yongmei; Woody, Susan M.; Liu, Jian] Univ N Carolina, Div Chem Biol & Med Chem, Eshelman Sch Pharm, Chapel Hill, NC 27599 USA.
[Moon, Andrea F.; Krahn, Joseph M.; Pedersen, Lars C.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Linhardt, Robert J.] Rensselaer Polytech Inst, Ctr Biotechnol & Interdisciplinary Studies, Dept Chem & Chem Biol, Troy, NY 12180 USA.
RP Liu, J (reprint author), Univ N Carolina, Div Chem Biol & Med Chem, Eshelman Sch Pharm, Chapel Hill, NC 27599 USA.
EM jian_liu@unc.edu
FU Division of Intramural Research of the National Institute of
Environmental Health Sciences, National Institutes of Health (NIH) [1
ZIA ES102645-03]; NIH [AI050050, HL094463, HL096972]; US Department of
Energy, Office of Science, Office of Basic Energy Sciences
[W-31-109-Eng-38]
FX We thank G. Mueller and S. Garantziotis for critical reading of the
manuscript, and Prof. Peng George Wang (Georgia State University) for
providing the plasmid expressing NAHK. This research was supported by
the Division of Intramural Research of the National Institute of
Environmental Health Sciences, National Institutes of Health (NIH) Grant
1 ZIA ES102645-03; and NIH Grants AI050050, HL094463, and HL096972. Use
of the Advanced Photon Source was supported by the US Department of
Energy, Office of Science, Office of Basic Energy Sciences Contract
W-31-109-Eng-38.
NR 19
TC 28
Z9 28
U1 1
U2 19
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP 5265
EP 5270
DI 10.1073/pnas.1117923109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700037
PM 22431632
ER
PT J
AU Zhao, J
Jitkaew, S
Cai, ZY
Choksi, S
Li, QN
Luo, J
Liu, ZG
AF Zhao, Jie
Jitkaew, Siriporn
Cai, Zhenyu
Choksi, Swati
Li, Qiuning
Luo, Ji
Liu, Zheng-Gang
TI Mixed lineage kinase domain-like is a key receptor interacting protein 3
downstream component of TNF-induced necrosis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID NONAPOPTOTIC CELL-DEATH; NF-KAPPA-B; PROGRAMMED NECROSIS; ACTIVATION;
APOPTOSIS; PATHWAY; ACCUMULATION; INDUCTION; ALPHA; JNK
AB Tumor necrosis factor (TNF) is an important inflammatory cytokine and induces many cellular responses, including inflammation, cell proliferation, apoptosis, and necrosis. It is known that receptor interacting protein (RIP) kinases, RIP1 and RIP3, are key effectors of TNF-induced necrosis, but little is known about how these two RIP kinases mediate this process, although reactive oxygen species (ROS) generation and JNK activation have been suggested to be two downstream events of RIP kinases. Here we report the identification of mixed lineage kinase domain-like, MLKL, as a key RIP3 downstream component of TNF-induced necrosis. Through screening a kinase/phosphatase shRNA library in human colon adenocarcinoma HT-29 cells, we found that knockdown of MLKL blocked TNF-induced necrosis. Our data suggest that MLKL functions downstream of RIP1 and RIP3 and is recruited to the necrosome through its interaction with RIP3. Finally, we found that MLKL is required for the generation of ROS and the late-phase activation of JNK during TNF-induced necrosis. However, because these two events are not involved in TNF-induced necrosis in HT-29 cells, the target of MLKL during TNF-induced necrosis remains elusive. Taken together, our study suggests that MLKL is a key RIP3 downstream component of TNF-induced necrotic cell death.
C1 [Zhao, Jie; Jitkaew, Siriporn; Cai, Zhenyu; Choksi, Swati; Liu, Zheng-Gang] NCI, Cell & Canc Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Li, Qiuning; Luo, Ji] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Liu, ZG (reprint author), NCI, Cell & Canc Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM zgliu@box-z.nih.gov
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health
FX We thank Drs. Francis Ka Ming Chan and Jiahuai Han for the RIP3
plasmids. This research was supported by the Intramural Research Program
of the Center for Cancer Research, National Cancer Institute, National
Institutes of Health.
NR 28
TC 218
Z9 224
U1 0
U2 18
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP 5322
EP 5327
DI 10.1073/pnas.1200012109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700047
PM 22421439
ER
PT J
AU Fox, JT
Sakamuru, S
Huang, RL
Teneva, N
Simmons, SO
Xia, MH
Tice, RR
Austin, CP
Myung, K
AF Fox, Jennifer T.
Sakamuru, Srilatha
Huang, Ruili
Teneva, Nedelina
Simmons, Steven O.
Xia, Menghang
Tice, Raymond R.
Austin, Christopher P.
Myung, Kyungjae
TI High-throughput genotoxicity assay identifies antioxidants as inducers
of DNA damage response and cell death
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE chemotherapy; high-throughput screening
ID POSTMENOPAUSAL WOMEN; PHYTOESTROGEN GENISTEIN; XERODERMA-PIGMENTOSUM;
CHEMICAL LIBRARIES; POLYMERASE ETA; CANCER CELLS; HUMAN ELG1; NUDE-MICE;
IN-VIVO; RESVERATROL
AB Human ATAD5 is a biomarker for identifying genotoxic compounds because ATAD5 protein levels increase posttranscriptionally in response to DNA damage. We screened over 4,000 compounds with a cell-based quantitative high-throughput ATAD5-luciferase assay detecting genotoxic compounds. We identified 22 antioxidants, including resveratrol, genistein, and baicalein, that are currently used or investigated for the treatment of cardiovascular disease, type 2 diabetes, osteopenia, osteoporosis, and chronic hepatitis, as well as for antiaging. Treatment of dividing cells with these compounds induced DNA damage and resulted in cell death. Despite their genotoxic effects, resveratrol, genistein, and baicalein did not cause mutagenesis, which is a major side effect of conventional anticancer drugs. Furthermore, resveratrol and genistein killed multidrug-resistant cancer cells. We therefore propose that resveratrol, genistein, and baicalein are attractive candidates for improved chemotherapeutic agents.
C1 [Fox, Jennifer T.; Teneva, Nedelina; Myung, Kyungjae] NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
[Sakamuru, Srilatha; Huang, Ruili; Xia, Menghang; Austin, Christopher P.] NIH, Natl Ctr Adv Translat Sci, Bethesda, MD 20892 USA.
[Simmons, Steven O.] US EPA, Integrated Syst Toxicol Div, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA.
[Tice, Raymond R.] NIEHS, Div Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
RP Myung, K (reprint author), NHGRI, Genome Instabil Sect, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
EM kmyung@mail.nih.gov
OI Simmons, Steven/0000-0001-9079-1069
FU National Institute of Environmental Health Sciences [Y2-ES-7020-01];
National Human Genome Research Institute, National Institutes of Health;
[R03 MH092164-01]
FX We thank S. Anderson in the FACS core, A. Dutra in the cytogenetics
core, and D. Bodine, F. Candotti, P. Schwartzberg, and Y. Yang of the
National Human Genome Research Institute for helpful discussions and
comments on the manuscript; M. Gottesman and C. Cardarelli of the
National Cancer Institute for cell lines; and K.M. especially thanks E.
Cho. This research was supported by the Intramural Research Programs
(Interagency Agreement Y2-ES-7020-01) of the National Toxicology
Program, National Institute of Environmental Health Sciences, and the
National Human Genome Research Institute, National Institutes of Health,
and by Grant R03 MH092164-01 (to K.M and M.X.).
NR 36
TC 46
Z9 47
U1 5
U2 26
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP 5423
EP 5428
DI 10.1073/pnas.1114278109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700064
PM 22431602
ER
PT J
AU Waisberg, M
Cerqueira, GC
Yager, SB
Francischetti, IMB
Lu, JH
Gera, N
Srinivasan, P
Miura, K
Rada, B
Lukszo, J
Barbian, KD
Leto, TL
Porcella, SF
Narum, DL
El-Sayed, N
Miller, LH
Pierce, SK
AF Waisberg, Michael
Cerqueira, Gustavo C.
Yager, Stephanie B.
Francischetti, Ivo M. B.
Lu, Jinghua
Gera, Nidhi
Srinivasan, Prakash
Miura, Kazutoyo
Rada, Balazs
Lukszo, Jan
Barbian, Kent D.
Leto, Thomas L.
Porcella, Stephen F.
Narum, David L.
El-Sayed, Najib
Miller, Louis H.
Pierce, Susan K.
TI Plasmodium falciparum merozoite surface protein 1 blocks the
proinflammatory protein S100P
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE placental; yeast two-hybrid; surface plasmon resonance; high-throughput
screen
ID MALARIA PARASITE; CELL INVASION; IMMUNITY; ANTIBODIES; HEMOZOIN;
DISEASE; VACCINE; FAMILY; DNA
AB The malaria parasite, Plasmodium falciparum, and the human immune system have coevolved to ensure that the parasite is not eliminated and reinfection is not resisted. This relationship is likely mediated through a myriad of host-parasite interactions, although surprisingly few such interactions have been identified. Here we show that the 33-kDa fragment of P. falciparum merozoite surface protein 1 (MSP1(33)), an abundant protein that is shed during red blood cell invasion, binds to the proinflammatory protein, S100P. MSP1(33) blocks S100P-induced NF kappa B activation in monocytes and chemotaxis in neutrophils. Remarkably, S100P binds to both dimorphic alleles of MSP1, estimated to have diverged >27 Mya, suggesting an ancient, conserved relationship between these parasite and host proteins that may serve to attenuate potentially damaging inflammatory responses.
C1 [Waisberg, Michael; Yager, Stephanie B.; Lu, Jinghua; Gera, Nidhi; Pierce, Susan K.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Rada, Balazs; Leto, Thomas L.] NIAID, Host Def Lab, NIH, Rockville, MD 20852 USA.
[Francischetti, Ivo M. B.; Srinivasan, Prakash; Miura, Kazutoyo; Miller, Louis H.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
[Lukszo, Jan; Barbian, Kent D.; Porcella, Stephen F.] NIAID, Res Technol Branch, NIH, Rockville, MD 20852 USA.
[Narum, David L.] NIAID, Lab Malaria Immunol & Vaccinol, NIH, Rockville, MD 20852 USA.
[Cerqueira, Gustavo C.; El-Sayed, Najib] Univ Maryland, Maryland Pathogen Res Inst, College Pk, MD 20742 USA.
RP Waisberg, M (reprint author), NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
EM waisbergm@niaid.nih.gov; lmiller@niaid.nih.gov
RI lu, jinghua/G-5872-2012; El-Sayed, Najib/K-7266-2015
OI El-Sayed, Najib/0000-0001-7970-3312
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases
FX The authors thank Dr. George Makhatadze for sharing reagents, Ms. Julie
Kim for logistic support, and Ms. Terri Fantasia for editorial support.
This study was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 31
TC 8
Z9 8
U1 0
U2 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP 5429
EP 5434
DI 10.1073/pnas.1202689109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700065
PM 22431641
ER
PT J
AU Veenstra-VanderWeele, J
Muller, CL
Iwamoto, H
Sauer, JE
Owens, WA
Shah, CR
Cohen, J
Mannangatti, P
Jessen, T
Thompson, BJ
Ye, R
Kerr, TM
Carneiro, AM
Crawley, JN
Sanders-Bush, E
McMahon, DG
Ramamoorthy, S
Daws, LC
Sutcliffe, JS
Blakely, RD
AF Veenstra-VanderWeele, Jeremy
Muller, Christopher L.
Iwamoto, Hideki
Sauer, Jennifer E.
Owens, W. Anthony
Shah, Charisma R.
Cohen, Jordan
Mannangatti, Padmanabhan
Jessen, Tammy
Thompson, Brent J.
Ye, Ran
Kerr, Travis M.
Carneiro, Ana M.
Crawley, Jacqueline N.
Sanders-Bush, Elaine
McMahon, Douglas G.
Ramamoorthy, Sammanda
Daws, Lynette C.
Sutcliffe, James S.
Blakely, Randy D.
TI Autism gene variant causes hyperserotonemia, serotonin receptor
hypersensitivity, social impairment and repetitive behavior
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE development; monoamine; neurotransmitter
ID ACTIVATED PROTEIN-KINASE; WHOLE-BLOOD SEROTONIN; SPECTRUM DISORDERS;
MOUSE MODEL; IN-VIVO; TRANSPORTER; MICE; EXPRESSION; PHOSPHORYLATION;
ABNORMALITIES
AB Fifty years ago, increased whole-blood serotonin levels, or hyperserotonemia, first linked disrupted 5-HT homeostasis to Autism Spectrum Disorders (ASDs). The 5-HT transporter (SERT) gene (SLC6A4) has been associated with whole blood 5-HT levels and ASD susceptibility. Previously, we identified multiple gain-of-function SERT coding variants in children with ASD. Here we establish that transgenic mice expressing the most common of these variants, SERT Ala56, exhibit elevated, p38 MAPK-dependent transporter phosphorylation, enhanced 5-HT clearance rates and hyperserotonemia. These effects are accompanied by altered basal firing of raphe 5-HT neurons, as well as 5HT(1A) and 5HT(2A) receptor hypersensitivity. Strikingly, SERT Ala56 mice display alterations in social function, communication, and repetitive behavior. Our efforts provide strong support for the hypothesis that altered 5-HT homeostasis can impact risk for ASD traits and provide a model with construct and face validity that can support further analysis of ASD mechanisms and potentially novel treatments.
C1 [Veenstra-VanderWeele, Jeremy; Muller, Christopher L.; Sauer, Jennifer E.; Shah, Charisma R.; Cohen, Jordan; Sanders-Bush, Elaine; Sutcliffe, James S.; Blakely, Randy D.] Vanderbilt Univ, Dept Psychiat, Nashville, TN 37232 USA.
[Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pediat, Nashville, TN 37232 USA.
[Veenstra-VanderWeele, Jeremy; Iwamoto, Hideki; Jessen, Tammy; Ye, Ran; Kerr, Travis M.; Carneiro, Ana M.; Sanders-Bush, Elaine; McMahon, Douglas G.; Blakely, Randy D.] Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37232 USA.
[Veenstra-VanderWeele, Jeremy; Carneiro, Ana M.; Sanders-Bush, Elaine; McMahon, Douglas G.; Sutcliffe, James S.; Blakely, Randy D.] Vanderbilt Univ, Inst Brain, Nashville, TN 37232 USA.
[Veenstra-VanderWeele, Jeremy; Carneiro, Ana M.; Sanders-Bush, Elaine; McMahon, Douglas G.; Sutcliffe, James S.; Blakely, Randy D.] Vanderbilt Univ, Kennedy Ctr Res Human Dev, Nashville, TN 37232 USA.
[Owens, W. Anthony; Daws, Lynette C.] Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA.
[Mannangatti, Padmanabhan; Ramamoorthy, Sammanda] Univ Texas Hlth Sci Ctr San Antonio, Dept Neurosci, San Antonio, TX 78229 USA.
[Thompson, Brent J.] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
[Thompson, Brent J.; Daws, Lynette C.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
[Crawley, Jacqueline N.] NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA.
[Sanders-Bush, Elaine; McMahon, Douglas G.; Blakely, Randy D.] Vanderbilt Univ, Silvio O Conte Ctr Neurosci Res, Nashville, TN 37232 USA.
[McMahon, Douglas G.] Vanderbilt Univ, Dept Biol Sci, Nashville, TN 37232 USA.
[Sutcliffe, James S.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
RP Veenstra-VanderWeele, J (reprint author), Vanderbilt Univ, Dept Psychiat, 221 Kirkland Hall, Nashville, TN 37232 USA.
EM j.vvw@vanderbilt.edu; randy.blakely@vanderbilt.edu
RI Sutcliffe, James/C-1348-2012; Thompson, Brent/L-1336-2014;
Veenstra-VanderWeele, Jeremy/K-1935-2015
OI Sutcliffe, James/0000-0001-5200-6007; Thompson,
Brent/0000-0002-2302-0886; Veenstra-VanderWeele,
Jeremy/0000-0002-6349-1076
FU National Institutes of Health (NIH) [MH081066, MH094604, DA07390,
MH078098, HD065278, MH62612, HD15052, RR024975]; Autism Speaks Pilot
Award; American Academy of Child and Adolescent Psychiatry; Seaside
Therapeutics; Roche Pharmaceuticals; Novartis; Forest Pharmaceuticals
FX Michelle Carter, Lauren Huntress, and Clinton Canal provided technical
assistance; Mu Yang and Jill Silverman provided advice on behavioral
data analysis; and Warren Lambert provided statistical assistance. The
authors thank the families who participated in the original genetic
study. This work was supported by National Institutes of Health (NIH)
Grants MH081066 (to J.V.), MH094604 (to J.V.), DA07390 (to R.D.B.),
MH078098 (to R.D.B.), HD065278 (to R.D.B.), and MH62612 (to S.R.); an
Autism Speaks Pilot Award (to J.V.), an American Academy of Child and
Adolescent Psychiatry Pilot Research Award (to J.V.), and NIH Grants
HD15052 (to the Vanderbilt Kennedy Center) and RR024975 (to the
Vanderbilt Institute for Clinical and Translational Research).; The
authors have no direct competing financial interests. J.V. receives
research funding for nonoverlapping work from Seaside Therapeutics,
Roche Pharmaceuticals, and Novartis, and has served as a consultant to
Novartis. R.D.B. receives research funding for nonoverlapping work from
Forest Pharmaceuticals and serves on the Lundbeck Pharmaceuticals
Advisory Board and as a consultant to JubilantInnovation.
NR 62
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PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP 5469
EP 5474
DI 10.1073/pnas.1112345109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700072
PM 22431635
ER
PT J
AU Gonzalez-Castillo, J
Saad, ZS
Handwerker, DA
Inati, SJ
Brenowitz, N
Bandettini, PA
AF Gonzalez-Castillo, Javier
Saad, Ziad S.
Handwerker, Daniel A.
Inati, Souheil J.
Brenowitz, Noah
Bandettini, Peter A.
TI Whole-brain, time-locked activation with simple tasks revealed using
massive averaging and model-free analysis
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE fMRI; activation extent; transient responses; clustering
ID BOLD HEMODYNAMIC-RESPONSES; FUNCTIONAL CONNECTIVITY; NEURONAL-ACTIVITY;
SPATIAL EXTENT; FMRI DATA; TRANSIENT; MRI; IDENTIFICATION; NETWORKS;
SIGNALS
AB The brain is the body's largest energy consumer, even in the absence of demanding tasks. Electrophysiologists report on-going neuronal firing during stimulation or task in regions beyond those of primary relationship to the perturbation. Although the biological origin of consciousness remains elusive, it is argued that it emerges from complex, continuous whole-brain neuronal collaboration. Despite converging evidence suggesting the whole brain is continuously working and adapting to anticipate and actuate in response to the environment, over the last 20 y, task-based functional MRI (fMRI) have emphasized a localizationist view of brain function, with fMRI showing only a handful of activated regions in response to task/stimulation. Here, we challenge that view with evidence that under optimal noise conditions, fMRI activations extend well beyond areas of primary relationship to the task; and blood-oxygen level-dependent signal changes correlated with task-timing appear in over 95% of the brain for a simple visual stimulation plus attention control task. Moreover, we show that response shape varies substantially across regions, and that whole-brain parcellations based on those differences produce distributed clusters that are anatomically and functionally meaningful, symmetrical across hemispheres, and reproducible across subjects. These findings highlight the exquisite detail lying in fMRI signals beyond what is normally examined, and emphasize both the pervasiveness of false negatives, and how the sparseness of fMRI maps is not a result of localized brain function, but a consequence of high noise and overly strict predictive response models.
C1 [Gonzalez-Castillo, Javier; Handwerker, Daniel A.; Brenowitz, Noah; Bandettini, Peter A.] NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
[Inati, Souheil J.; Bandettini, Peter A.] NIMH, Funct MRI Facil, NIH, Bethesda, MD 20892 USA.
RP Gonzalez-Castillo, J (reprint author), NIMH, Sect Funct Imaging Methods, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
EM javier.gonzalez-castillo@nih.gov
OI Gonzalez-Castillo, Javier/0000-0002-6520-5125
NR 39
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PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP 5487
EP 5492
DI 10.1073/pnas.1121049109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700075
PM 22431587
ER
PT J
AU Hartley, CA
McKenna, MC
Salman, R
Holmes, A
Casey, BJ
Phelps, EA
Glatt, CE
AF Hartley, Catherine A.
McKenna, Morgan C.
Salman, Rabia
Holmes, Andrew
Casey, B. J.
Phelps, Elizabeth A.
Glatt, Charles E.
TI Serotonin transporter polyadenylation polymorphism modulates the
retention of fear extinction memory
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID GENETIC-VARIATION; DEPRESSION; ANXIETY; 5-HTTLPR; STRESS; METAANALYSIS;
REGION; BRAIN; MICE; ABNORMALITIES
AB Growing evidence suggests serotonin's role in anxiety and depression is mediated by its effects on learned fear associations. Pharmacological and genetic manipulations of serotonin signaling in mice alter the retention of fear extinction learning, which is inversely associated with anxious temperament in mice and humans. Here, we test whether genetic variation in serotonin signaling in the form of a common human serotonin transporter polyadenylation polymorphism (STPP/rs3813034) is associated with spontaneous fear recovery after extinction. We show that the risk allele of this polymorphism is associated with impaired retention of fear extinction memory and heightened anxiety and depressive symptoms. These STPP associations in humans mirror the phenotypic effects of serotonin transporter knockout in mice, highlighting the STPP as a potential genetic locus underlying interindividual differences in serotonin transporter function in humans. Furthermore, we show that the serotonin transporter polyadenylation profile associated with the STPP risk allele is altered through the chronic administration of fluoxetine, a treatment that also facilitates retention of extinction learning. The propensity to form persistent fear associations due to poor extinction recall may be an intermediate phenotype mediating the effects of genetic variation in serotonergic function on anxiety and depression. The consistency and specificity of these data across species provide robust support for this hypothesis and suggest that the little-studied STPP may be an important risk factor for mood and anxiety disorders in humans.
C1 [Hartley, Catherine A.; Salman, Rabia; Phelps, Elizabeth A.] NYU, Dept Psychol, New York, NY 10003 USA.
[Phelps, Elizabeth A.] NYU, Ctr Neural Sci, New York, NY 10003 USA.
[McKenna, Morgan C.; Glatt, Charles E.] Weill Cornell Med Coll, Dept Psychiat, New York, NY 10065 USA.
[Casey, B. J.] Weill Cornell Med Coll, Sackler Inst Dev Psychobiol, New York, NY 10065 USA.
[Holmes, Andrew] NIAAA, Lab Behav & Genom Neurosci, Rockville, MD 20852 USA.
RP Hartley, CA (reprint author), NYU, Dept Psychol, 6 Washington Pl, New York, NY 10003 USA.
EM cate@nyu.edu; ceg2004@med.cornell.edu
FU National Science Foundation; James S. McDonnell Foundation; National
Institutes of Health (NIH) [MH072279, MH80758, MH079513, MH091401];
National Institute on Alcohol Abuse; Hartwell Foundation; Pritzker
Neuropsychiatric Disorders Research Consortium
FX We thank A. Gorun and A. Richman for assistance with data collection and
analysis. A. Izquierdo and A. Holmes collected the original 5-HTT
knockout mouse data. This research was supported by the National Science
Foundation (C. A. H.); the James S. McDonnell Foundation, and National
Institutes of Health (NIH) Grants MH072279 and MH80758 (to E. A. P.);
The National Institute on Alcohol Abuse and Alcoholism Intramural
Research Program (A. H.); a generous gift by the Mortimer D. Sackler, MD
family (to B.J.C.); NIH Grant MH079513 (to B.J.C. and C. E. G.); and The
Hartwell Foundation, the Pritzker Neuropsychiatric Disorders Research
Consortium, and NIH Grant MH091401 (to C. E. G.).
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PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP 5493
EP 5498
DI 10.1073/pnas.1202044109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700076
PM 22431634
ER
PT J
AU Jabbi, M
Kippenhan, JS
Kohn, P
Marenco, S
Mervis, CB
Morris, CA
Meyer-Lindenberg, A
Berman, KF
AF Jabbi, Mbemba
Kippenhan, J. Shane
Kohn, Philip
Marenco, Stefano
Mervis, Carolyn B.
Morris, Colleen A.
Meyer-Lindenberg, Andreas
Berman, Karen Faith
TI The Williams syndrome chromosome 7q11.23 hemideletion confers
hypersocial, anxious personality coupled with altered insula structure
and function
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE brain; genetics; copy number variant; MRI; PET
ID OLD-WORLD MONKEY; ANTERIOR INSULA; GENETIC CONTRIBUTIONS; SOCIAL
COGNITION; WHITE-MATTER; NEURAL BASIS; GREAT APES; BRAIN; CORTEX;
BEHAVIOR
AB Although it is widely accepted that genes can influence complex behavioral traits such as human temperament, the underlying neurogenetic mechanisms remain unclear. Williams syndrome (WS), a rare disorder caused by a hemizygous deletion on chromosome 7q11.23, including genes important for neuronal migration and maturation (LIMK1 and CLIP2), is typified by a remarkable hypersocial but anxious personality and offers a unique opportunity to investigate this open issue. Based on the documented role of the insula in mediating emotional response tendencies and personality, we used multimodal imaging to characterize this region in WS and found convergent anomalies: an overall decrease in dorsal anterior insula (AI) gray-matter volume along with locally increased volume in the right ventral AI; compromised white-matter integrity of the uncinate fasciculus connecting the insula with the amygdala and orbitofrontal cortex; altered regional cerebral blood flow in a pattern reminiscent of the observed gray-matter alterations (i.e., widespread reductions in dorsal AI accompanied by locally increased regional cerebral blood flow in the right ventral AI); and disturbed neurofunctional interactions between the AI and limbic regions. Moreover, these genetically determined alterations of AI structure and function predicted the degree to which the atypical WS personality profile was expressed in participants with the syndrome. The AI's rich anatomical connectivity, its transmodal properties, and its involvement in the behaviors affected in WS make the observed genetically determined insular circuitry perturbations and their association with WS personality a striking demonstration of the means by which neural systems can serve as the interface between genetic variability and alterations in complex behavioral traits.
C1 [Jabbi, Mbemba; Kippenhan, J. Shane; Kohn, Philip; Meyer-Lindenberg, Andreas; Berman, Karen Faith] NIMH, Sect Integrat Neuroimaging, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Jabbi, Mbemba; Kippenhan, J. Shane; Kohn, Philip; Marenco, Stefano; Meyer-Lindenberg, Andreas; Berman, Karen Faith] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
[Mervis, Carolyn B.] Univ Louisville, Dept Psychol & Brain Sci, Neurodev Sci Lab, Louisville, KY 40208 USA.
[Morris, Colleen A.] Univ Nevada, Sch Med, Dept Pediat, Las Vegas, NV 89128 USA.
RP Jabbi, M (reprint author), NIMH, Sect Integrat Neuroimaging, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
EM jabbim@gmail.com; karen.berman@nih.gov
RI Marenco, Stefano/A-2409-2008; Meyer-Lindenberg, Andreas/H-1076-2011
OI Marenco, Stefano/0000-0002-2488-2365; Meyer-Lindenberg,
Andreas/0000-0001-5619-1123
FU National Institute of Mental Health, National Institutes of Health;
National Institute of Neurological Disorders and Stroke [R01 NS35102]
FX The authors thank Rosanna Olsen, Aaron Bonner-Jackson, and Paul Koch for
their contribution toward data collection and management of the
experiments and Dwight Dickinson for comments. This research was
supported by the Intramural Research Program of the National Institute
of Mental Health, National Institutes of Health and by National
Institute of Neurological Disorders and Stroke Grant R01 NS35102 (to
C.B.M.).
NR 62
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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 APR 3
PY 2012
VL 109
IS 14
BP E860
EP E866
DI 10.1073/pnas.1114774109
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700013
PM 22411788
ER
PT J
AU Mulkidjanian, AY
Bychkov, AY
Dibrova, DV
Galperin, MY
Koonin, EV
AF Mulkidjanian, Armen Y.
Bychkov, Andrew Yu.
Dibrova, Daria V.
Galperin, Michael Y.
Koonin, Eugene V.
TI Origin of first cells at terrestrial, anoxic geothermal fields
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE prebiotic chemistry; abiotic photosynthesis; hydrothermal alteration;
origin of life; Na+/K+ gradient
ID TEMPLATE-DIRECTED SYNTHESIS; HYDROTHERMAL ORE-DEPOSITS; INFORMATIONAL
POLYMERS; PREBIOTIC SYNTHESIS; EARLY EARTH; DIFFERENTIAL STABILITY;
FORMAMIDE SOLUTIONS; MANGANESE SULFIDE; COMMON ANCESTOR; NUCLEIC-ACIDS
AB All cells contain much more potassium, phosphate, and transition metals than modern (or reconstructed primeval) oceans, lakes, or rivers. Cells maintain ion gradients by using sophisticated, energy-dependent membrane enzymes (membrane pumps) that are embedded in elaborate ion-tight membranes. The first cells could possess neither ion-tight membranes nor membrane pumps, so the concentrations of small inorganic molecules and ions within protocells and in their environment would equilibrate. Hence, the ion composition of modern cells might reflect the inorganic ion composition of the habitats of protocells. We attempted to reconstruct the "hatcheries" of the first cells by combining geochemical analysis with phylogenomic scrutiny of the inorganic ion requirements of universal components of modern cells. These ubiquitous, and by inference primordial, proteins and functional systems show affinity to and functional requirement for K+, Zn2+, Mn2+, and phosphate. Thus, protocells must have evolved in habitats with a high K+/Na+ ratio and relatively high concentrations of Zn, Mn, and phosphorous compounds. Geochemical reconstruction shows that the ionic composition conducive to the origin of cells could not have existed in marine settings but is compatible with emissions of vapor-dominated zones of inland geothermal systems. Under the anoxic, CO2-dominated primordial atmosphere, the chemistry of basins at geothermal fields would resemble the internal milieu of modern cells. The precellular stages of evolution might have transpired in shallow ponds of condensed and cooled geothermal vapor that were lined with porous silicate minerals mixed with metal sulfides and enriched in K+, Zn2+, and phosphorous compounds.
C1 [Mulkidjanian, Armen Y.; Dibrova, Daria V.] Univ Osnabruck, Sch Phys, D-49069 Osnabruck, Germany.
[Mulkidjanian, Armen Y.] Moscow MV Lomonosov State Univ, AN Belozersky Inst Physicochem Biol, Moscow 119992, Russia.
[Bychkov, Andrew Yu.] Moscow MV Lomonosov State Univ, Sch Geol, Moscow 119992, Russia.
[Dibrova, Daria V.] Moscow MV Lomonosov State Univ, Sch Bioengn & Bioinformat, Moscow 119992, Russia.
[Galperin, Michael Y.; Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Mulkidjanian, AY (reprint author), Univ Osnabruck, Sch Phys, D-49069 Osnabruck, Germany.
EM amulkid@uos.de; koonin@ncbi.nlm.nih.gov
RI Galperin, Michael/B-5859-2013; Mulkidjanian, Armen/J-8086-2013; Bychkov,
Andrey/R-6693-2016
OI Galperin, Michael/0000-0002-2265-5572; Mulkidjanian,
Armen/0000-0001-5844-3064; Bychkov, Andrey/0000-0003-2560-6423
FU Deutsche Forschungsgemeinschaft (DFG) [DFG-Mu-1285/1-10, DFG-436-RUS
113/963/0-1]; Russian Government [02.740.11.5228]; Volkswagen
Foundation; EU COST [CM0902]; Deutscher Akademischer Austausch Dienst;
Russian Foundation for Basic Research [10-05-00320, 0-04-91331];
National Library of Medicine at the National Institutes of Health
FX Valuable discussions with Drs. D. A. Cherepanov, M. Eigen, R. M. Hazen,
G. F. Joyce, M. J. van Kranendonk, V. N. Kompaninchenko, D.-H. Lankenau,
D. L. Pinti, M. J. Russell, V. P. Skulachev, H.-J. Steinhoff, J.
Szostak, N. E. Voskoboynikova, R. J. P. Williams, Y. I. Wolf and A.
Yonath are greatly appreciated. The authors are thankful to Drs. A. S.
Karyagina and I. Y. Nikolaeva for providing photographs of boiling mud
pots. This study was supported by Deutsche Forschungsgemeinschaft (DFG)
Grants DFG-Mu-1285/1-10 and DFG-436-RUS 113/963/0-1 (to A. Y. M.),
Russian Government Grant 02.740.11.5228 (to A. Y. M.), the Volkswagen
Foundation (A. Y. M.), EU COST CM0902 Action (A. Y. M.), Deutscher
Akademischer Austausch Dienst (D.V.D.), Russian Foundation for Basic
Research Grants 10-05-00320 (to A. Y. B.) and 0-04-91331 (to D. V. D.),
and the Intramural Research Program of the National Library of Medicine
at the National Institutes of Health (M. Y. G. and E.V.K).
NR 145
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U2 91
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD APR 3
PY 2012
VL 109
IS 14
BP E821
EP E830
DI 10.1073/pnas.1117774109
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 919BD
UT WOS:000302294700009
PM 22331915
ER
PT J
AU Pallan, PS
Marquez, VE
Egli, M
AF Pallan, Pradeep S.
Marquez, Victor E.
Egli, Martin
TI The Conformationally Constrained N-Methanocarba-dT Analogue Adopts an
Unexpected C4 '-exo Sugar Pucker in the Structure of a DNA Hairpin
SO BIOCHEMISTRY
LA English
DT Article
ID NUCLEOSIDE ANALOGS; CRYSTAL-STRUCTURE; NUCLEIC-ACIDS; RNA; NUCLEOTIDES;
OLIGONUCLEOTIDES; THERAPEUTICS; NORTH; RING
AB Incorporation of a bicyclo[3.1.0]hexane scaffold into the nucleoside sugar was devised to lock the embedded cyclopentane ring in conformations that mimic the furanose North and South sugar puckers. To analyze the effects of North-methanocarba-2'-deoxythymidine (N-MCdT) on the B-form DNA, we crystallized d(CGCGAA[mcTmcT]CGCG) with two N-MCdTs. Instead of a duplex, the 12mer forms a tetraloop hairpin, whereby loop N-MCdTs adopt the C4'-exo pucker (NE; P = 50 degrees). Thus, the bicyclic framework does not limit the pucker to the anticipated C2'-exo range (NNW; P = 18 degrees).
C1 [Pallan, Pradeep S.; Egli, Martin] Vanderbilt Univ, Dept Biochem, Sch Med, Nashville, TN 37232 USA.
[Marquez, Victor E.] NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21702 USA.
RP Egli, M (reprint author), Vanderbilt Univ, Dept Biochem, Sch Med, Nashville, TN 37232 USA.
EM martin.egli@vanderbilt.edu
FU NIH [GM55237]; U.S. DOE, Office of Science, Office of Basic Energy
Sciences [DE-AC02-06CH11357]
FX Supported by NIH Grant GM55237 (to M.E.). Use of the APS was supported
by the U.S. DOE, Office of Science, Office of Basic Energy Sciences,
Contract DE-AC02-06CH11357.
NR 35
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U1 0
U2 4
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 3
PY 2012
VL 51
IS 13
BP 2639
EP 2641
DI 10.1021/bi300215k
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 926KW
UT WOS:000302830900001
PM 22409313
ER
PT J
AU Agniswamy, J
Shen, CH
Aniana, A
Sayer, JM
Louis, JM
Weber, IT
AF Agniswamy, Johnson
Shen, Chen-Hsiang
Aniana, Annie
Sayer, Jane M.
Louis, John M.
Weber, Irene T.
TI HIV-1 Protease with 20 Mutations Exhibits Extreme Resistance to Clinical
Inhibitors through Coordinated Structural Rearrangements
SO BIOCHEMISTRY
LA English
DT Article
ID VIRUS TYPE-1 PROTEASE; RESOLUTION CRYSTAL-STRUCTURES; DRUG-RESISTANCE;
ACTIVE-SITE; MOLECULAR CHARACTERIZATION; MULTIDRUG-RESISTANCE; MUTANTS;
BINDING; AMPRENAVIR; DARUNAVIR
AB The escape mutant of HIV-1 protease (PR) containing 20 mutations (PR20) undergoes efficient polyprotein processing even in the presence of clinical protease inhibitors (PIs). PR20 shows >3 orders of magnitude decreased affinity for Pis darunavir (DRV) and saquinavir (SQV) relative to PR Crystal structures of PR20 crystallized with yttrium, substrate analogue p2-NC, DRV, and SQV reveal three distinct conformations of the flexible flaps and diminished interactions with inhibitors through the combination of multiple mutations. PR20 with yttrium at the active site exhibits widely separated flaps lacking the usual intersubunit contacts seen in other inhibitor-free dimers. Mutations of residues 35-37 in the hinge loop eliminate interactions and perturb the flap conformation. Crystals of P PR20/p2-NC contain one uninhibited dimer with one very open flap and one closed flap and a second inhibitor-bound dimer in the closed form showing six fewer hydrogen bonds with the substrate analogue relative to wild-type PR PR20 complexes with PIs exhibit expanded S2/S2' pockets and fewer PI interactions arising from coordinated effects of mutations throughout the structure, in agreement with the strikingly reduced affinity. In particular, insertion of the large aromatic side chains of L10F and L33F alters intersubunit interactions and widens the PI binding site through a network of hydrophobic contacts. The two very open conformations of PR20 as well as the expanded binding site of the inhibitor-bound closed form suggest possible approaches for modifying inhibitors to target extreme drug-resistant HIV.
C1 [Agniswamy, Johnson; Shen, Chen-Hsiang; Weber, Irene T.] Georgia State Univ, Dept Biol, Mol Basis Dis Program, Atlanta, GA 30303 USA.
[Aniana, Annie; Sayer, Jane M.; Louis, John M.] NIDDK, Chem Phys Lab, NIH, DHHS, Bethesda, MD 20892 USA.
RP Weber, IT (reprint author), Georgia State Univ, Dept Biol, Mol Basis Dis Program, POB 4010, Atlanta, GA 30303 USA.
EM iweber@gsu.edu
RI shen, chen-hsiang/D-7309-2016
FU NIDDK; National Institutes of Health (NIH) [GM062920]; Office of the
Director, NIH; U.S. Department of Energy, Office of Science, Office of
Basic Energy Sciences [W-31-109-Eng-38]; Georgia State University
FX This research was supported, in whole or in part, by the Intramural
Research Program of the NIDDK, National Institutes of Health (NIH),
Intramural AIDS-Targeted Antiviral Program of the Office of the
Director, NIH, and Grant GM062920 from the NIH. 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
W-31-109-Eng-38.; Chen-Hsiang Shen was supported in part by the Georgia
State University Molecular Basis of Disease Fellowship and the Georgia
State University Research Program Enhancement Award in Bioinformatics.
This research was authored, in whole or in part, by National Institutes
of Health staff. Data were collected at the Southeast Regional
Collaborative Access Team (SER-CAT) beamline 22ID at the Advanced Photon
Source, Argonne National Laboratory. Supporting institutions may be
found at www.ser-cat.org/members.html. DRV and SQV were obtained through
the NIH AIDS Research and Reference Reagent Program, Division of AIDS,
NIAID, NIH.
NR 51
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U1 0
U2 14
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 3
PY 2012
VL 51
IS 13
BP 2819
EP 2828
DI 10.1021/bi2018317
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 926KW
UT WOS:000302830900019
PM 22404139
ER
PT J
AU Mandal, D
Moitra, K
Ghosh, D
Xia, D
Dey, S
AF Mandal, Debjani
Moitra, Karobi
Ghosh, Debabrata
Xia, Di
Dey, Saibal
TI Evidence for Modulatory Sites at the Lipid-Protein Interface of the
Human Multidrug Transporter P-Glycoprotein
SO BIOCHEMISTRY
LA English
DT Article
ID NICOTINIC ACETYLCHOLINE-RECEPTOR; DRUG-BINDING; MEMBRANE-PROTEINS;
ALLOSTERIC MODULATION; PLASMA-MEMBRANE; LIPID/PROTEIN INTERFACE;
CYTOPLASMIC LEAFLET; TRANSITION-STATE; KINETIC-ANALYSIS; ATPASE ACTIVITY
AB The human multidrug transporter P-glycoprotein (Pgp or ABCB1) sets up pharmacological barriers to many clinically important drugs, a therapeutic remedy for which has yet to be formulated. For the rational design of mechanism-based inhibitors (or modulators), it is necessary to map the potential sites for modulator interaction and understand their modes of communication with the other functional domains of Pgp. In this study, combining directed mutagenesis with homology modeling, we provide evidence of two modulator-specific sites at the lipid protein interface of Pgp. Targeting 21 variant positions in the COOH-terminal transmembrane (TM) regions, we find residues M948 (in TM11) and F983, M986, V988, and Q990 (all four in TM12) critically involved in substrate-site modulation by a thioxanthene-based allosteric modulator cis-(Z)-flupentixol. Interestingly, for ATP-site modulation by the same modulator, only two (M948 and Q990) of those four residues appear indispensable, together with two additional residues, T837 and I864 in TM9 and TM10, respectively, suggesting independent modes of communication linking the allosteric site with the substrate binding and ATPase domains. None of the seven residues identified prove to be critical for modulation of the substrate or ATP sites by Pgp modulators that are transported by the pump, such as cyclosporin A or verapamil, indicating their specificity for cis-(Z)-flupentixol. On the other hand, ATP-site modulation by verapamil proves to be highly sensitive to replacement at positions F716 (in TM7) and 1765 (in TM8), and to a more moderate extent at 1764 and L772 (both in TM8). Homology modeling based on the known crystal structures of the bacterial multidrug transporter SAV1866 and the mouse Pgp homologue maps the identified residues primarily at the lipid-protein interface of Pgp, in two spatially distinct modulator-specific clusters. The two modulatory sites demonstrate negative synergism in influencing ATP hydrolysis, consolidating their spatial distinctness. Because Pgp is known to recruit drug molecules directly from the lipid bilayer, identification of modulatory sites at the lipid-protein interface and at the same time outside the conventional central drug binding cavity is mechanistically revealing.
C1 [Mandal, Debjani; Moitra, Karobi; Ghosh, Debabrata; Dey, Saibal] Uniformed Serv Univ Hlth Sci, Sch Med, Dept Biochem, Bethesda, MD 20814 USA.
[Xia, Di] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Dey, S (reprint author), Uniformed Serv Univ Hlth Sci, Sch Med, Dept Biochem & Mol Biol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM sdey@usuhs.mil
OI Ghosh, Debabrata/0000-0002-6571-304X
FU U.S. Public Health Services [GM067926]; Uniformed Services University
FX The work was supported by U.S. Public Health Services Grant GM067926 and
Uniformed Services University Grant C071FU.
NR 72
TC 9
Z9 10
U1 0
U2 10
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 3
PY 2012
VL 51
IS 13
BP 2852
EP 2866
DI 10.1021/bi201479k
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 926KW
UT WOS:000302830900022
PM 22360349
ER
PT J
AU Reuven, EM
Dadon, Y
Viard, M
Manukovsky, N
Blumenthal, R
Shai, Y
AF Reuven, Eliran Moshe
Dadon, Yakir
Viard, Mathias
Manukovsky, Nurit
Blumenthal, Robert
Shai, Yechiel
TI HIV-1 gp41 Transmembrane Domain Interacts with the Fusion Peptide:
Implication in Lipid Mixing and Inhibition of Virus-Cell Fusion
SO BIOCHEMISTRY
LA English
DT Article
ID MEMBRANE-SPANNING DOMAIN; GLYCOPROTEIN-MEDIATED FUSION; COLI ASPARTATE
RECEPTOR; ENVELOPE GLYCOPROTEIN; PHOSPHOLIPID-MEMBRANES;
CONFORMATIONAL-CHANGES; IN-VIVO; INFLUENZA HEMAGGLUTININ; COMMON
PRINCIPLES; PORE FORMATION
AB Fusion of the human immunodeficiency virus (HIV) with target cells is mediated by the gp41 subunit of the envelope protein. Mutation and deletion studies within the transmembrane domain (TMD) of intact gp41 influenced its fusion activity. In addition, current models suggest that the TMD is in proximity with the fusion peptide (FP) at the late fusion stages, but there are no direct experimental data to support this hypothesis. Here, we investigated the TMD focusing on two regions: the N-terminal containing the GxxxG motif and the C-terminal containing the GLRI motif; which is conserved among the TMDs of HIV and the T-cell receptor. Studies utilizing the ToxR expression system combined with synthetic peptides and their fluorescent analogues derived from TMD revealed that the GxxxG motif is important for TMD self-association, whereas the C-terminal region is for its heteroassociation with FP. Functionally, all three TMD peptides induced lipid mixing that was enhanced significantly upon mixing with FP. Furthermore, the TMD peptides inhibited virus-cell fusion apparently through their interaction with their endogenous counterparts. Notably, the R2E mutant (in the GLRI) was significantly less potent than the two others. Overall, our findings provide experimental evidence that HIV-1 TMD contributes to membrane assembly and function of the HIV-1 envelope. Owing to similarities between functional domains within viruses, these findings suggest that the TMDs and FPs may contribute similarly in other viruses as well.
C1 [Reuven, Eliran Moshe; Dadon, Yakir; Manukovsky, Nurit; Shai, Yechiel] Weizmann Inst Sci, Dept Biol Chem, IL-76100 Rehovot, Israel.
[Viard, Mathias; Blumenthal, Robert] SAIC Frederick Inc, Basic Res Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Viard, Mathias] NCI, Nanobiol Program, Ctr Canc Res, Frederick, MD 21701 USA.
RP Shai, Y (reprint author), Weizmann Inst Sci, Dept Biol Chem, IL-76100 Rehovot, Israel.
EM Yechiel.Shai@weizmann.ac.il
FU Israel Science Foundation; Frederick National Laboratory for Cancer
Research, National Institutes of Health [HHSN261200800001E]; NIH,
Frederick National Lab, Center for Cancer Research
FX This study was supported by the Israel Science Foundation (to Y.S.) and
in part with Federal funds from the Frederick National Laboratory for
Cancer Research, National Institutes of Health, under contract
HHSN261200800001E (to R.B.). 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. This research
was supported in part by the Intramural Research Program of NIH,
Frederick National Lab, Center for Cancer Research (to R.B.). Y.S. is
the Harold S. and Harriet B. Brady Professorial Chair in Cancer
Research.
NR 90
TC 30
Z9 30
U1 2
U2 14
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD APR 3
PY 2012
VL 51
IS 13
BP 2867
EP 2878
DI 10.1021/bi201721r
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 926KW
UT WOS:000302830900023
PM 22413880
ER
PT J
AU Shah, MR
Starling, RC
Longacre, LS
Mehra, MR
AF Shah, Monica R.
Starling, Randall C.
Longacre, Lisa Schwartz
Mehra, Mandeep R.
CA Working Grp Participants
TI Heart Transplantation Research in the Next Decade-A Goal to Achieving
Evidence-Based Outcomes
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Review
DE heart transplantation; NHLBI; research; working group
ID CARDIAC ALLOGRAFT VASCULOPATHY; ANTIBODY-MEDIATED REJECTION; CONVERTING
ENZYME-INHIBITORS; VENTRICULAR ASSIST DEVICES; PULMONARY-HYPERTENSION;
INTRAVASCULAR ULTRASOUND; INTERNATIONAL SOCIETY; LUNG TRANSPLANTATION;
DONOR; RECIPIENTS
AB The National Heart, Lung, and Blood Institute (NHLBI) convened a Working Group (WG) on August 5 to 6, 2010 in Bethesda, Maryland to discuss future directions of research in heart transplantation (HT). The WG was composed of researchers with expertise in the basic science, clinical science, and epidemiological aspects of advanced heart failure and HT. These experts were asked to identify the highest priority research gaps in the field and make recommendations for future research strategies. The WG was also asked to include approaches that capitalize on current scientific opportunities and focus on areas that required unique NHLBI leadership. Finally, the WG was charged with developing recommendations that would have short-and long-term impact on the field of HT. The WG participants reviewed key areas in HT and identified the most urgent knowledge gaps. These gaps were then organized into the following 4 specific research directions: 1) enhanced phenotypic characterization of the pre-transplant population; 2) donor-recipient optimization strategies; 3) individualized immunosuppression therapy; and, 4) investigations of immune and non-immune factors affecting late cardiac allograft outcomes. Finally, because the HT population is relatively small compared with other patient groups, the WG strongly urged concerted efforts to enroll every transplant recipient into a clinical study and to increase collaborative networks to optimize research in this field. (J Am Coll Cardiol 2012; 59: 1263-9) (C) 2012 by the American College of Cardiology Foundation
C1 [Shah, Monica R.] NHLBI, Heart Failure & Arrhythmias Branch, Div Cardiovasc Sci, Rockledge Ctr 2, Bethesda, MD 20892 USA.
[Starling, Randall C.] Case Western Reserve Univ, Sch Med, Cleveland Clin, Lerner Coll Med, Cleveland, OH USA.
[Starling, Randall C.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Mehra, Mandeep R.] Harvard Univ, Sch Med, Boston, MA USA.
[Mehra, Mandeep R.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RP Shah, MR (reprint author), NHLBI, Heart Failure & Arrhythmias Branch, Div Cardiovasc Sci, Rockledge Ctr 2, 6701 Rockledge Dr,MSC 7956, Bethesda, MD 20892 USA.
EM shahmr@nhlbi.nih.gov
RI Fung, John/A-2679-2012
FU Division of Cardiovascular Sciences, NHLBI, NIH; NIAID/NIH; Johnson and
Johnson Corp.; NHLBI/NIH
FX Support for the working group was provided by the Division of
Cardiovascular Sciences, NHLBI, NIH. Drs. Starling and Mehra served as
Chairs of the Workshop. Drs. Shah and Schwartz Longacre are employees of
NIH. Dr. Starling has received grant support from NIAID/NIH and Johnson
and Johnson Corp., has served as a consultant to Medtronic, WellPoint,
Novartis, Anthem Ins., and Bio Control Medical Ltd., and owns stock in
Cardiomems that is worth <$1,000. Dr. Mehra has received grant support
from NHLBI/NIH and served as a consultant to Medtronic, St. Judes,
Geron, J and J, and GlaxoSmithKline. A full list of the Working Group
Participants is listed in the Appendix at the end of the paper.
NR 34
TC 17
Z9 17
U1 1
U2 4
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 APR 3
PY 2012
VL 59
IS 14
BP 1263
EP 1269
DI 10.1016/j.jacc.2011.11.050
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 916ZD
UT WOS:000302140800002
PM 22464255
ER
PT J
AU Amyot, F
Zimmermann, T
Riley, J
Kainerstorfer, JM
Chernomordik, V
Mooshagian, E
Najafizadeh, L
Krueger, F
Gandjbakhche, AH
Wassermann, EM
AF Amyot, Franck
Zimmermann, Trelawny
Riley, Jason
Kainerstorfer, Jana M.
Chernomordik, Victor
Mooshagian, Eric
Najafizadeh, Laleh
Krueger, Frank
Gandjbakhche, Amir H.
Wassermann, Eric M.
TI Normative database of judgment of complexity task with functional near
infrared spectroscopy-Application for TBI
SO NEUROIMAGE
LA English
DT Article
DE Near infrared spectroscopy; Frameless stereotaxy; Frontal cortex; Group
study
ID TRAUMATIC BRAIN-INJURY; VIETNAM HEAD-INJURY; ACTIVATION; TECHNOLOGY;
LOCATIONS
AB The ability to assess frontal lobe function in a rapid, objective, and standardized way, without the need for expertise in cognitive test administration might be particularly helpful in mild traumatic brain injury (TBI), where objective measures are needed. Functional near infrared spectroscopy (fNIRS) is a reliable technique to noninvasively measure local hemodynamic changes in brain areas near the head surface. In this paper, we are combining fNIRS and frameless stereotaxy which allowed us to co-register the functional images with previously acquired anatomical MRI volumes. In our experiment, the subjects were asked to perform a task, evaluating the complexity of daily life activities, previously shown with fMRI to activate areas of the anterior frontal cortex. We reconstructed averaged oxyhemoglobin and deoxyhemoglobin data from 20 healthy subjects in a spherical coordinate. The spherical coordinate is a natural representation of surface brain activation projection. Our results show surface activation projected from the medial frontopolar cortex which is consistent with previous fMRI results. With this original technique, we will construct a normative database for a simple cognitive test which can be useful in evaluating cognitive disability such as mild traumatic brain injury. Published by Elsevier Inc.
C1 [Amyot, Franck; Riley, Jason; Kainerstorfer, Jana M.; Chernomordik, Victor; Najafizadeh, Laleh; Gandjbakhche, Amir H.] Eunice Kennedy Shriver NICHD, NIH, Program Pediat Imaging & Tissue Sci, Sect Analyt & Funct Biophoton, Bethesda, MD 20892 USA.
[Amyot, Franck; Mooshagian, Eric; Najafizadeh, Laleh] Henry M Jackson Fdn, Rockville, MD 20852 USA.
[Amyot, Franck; Zimmermann, Trelawny; Mooshagian, Eric; Wassermann, Eric M.] Natl Inst Neurol Disorders & Stroke, Behav Neurol Unit, NIH, Bethesda, MD USA.
[Krueger, Frank] George Mason Univ, Krasnow Inst Adv Study, Fairfax, VA 22030 USA.
RP Gandjbakhche, AH (reprint author), Eunice Kennedy Shriver NICHD, NIH, Program Pediat Imaging & Tissue Sci, Sect Analyt & Funct Biophoton, Bethesda, MD 20892 USA.
EM amir@helix.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institute of Neurological Disorders and Stroke;
Center for Neuroscience and Regenerative Medicine
FX We thank Dr. Jordan Grafman for his valuable suggestions and comments on
this project. We also acknowledge the funding of the intramural program
of the Eunice Kennedy Shriver National Institute of Child Health and
Human Development, the National Institute of Neurological Disorders and
Stroke and Center for Neuroscience and Regenerative Medicine.
NR 29
TC 9
Z9 9
U1 2
U2 8
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 APR 2
PY 2012
VL 60
IS 2
BP 879
EP 883
DI 10.1016/j.neuroimage.2012.01.104
PG 5
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 932ED
UT WOS:000303272300005
PM 22306800
ER
PT J
AU Caria, A
de Falco, S
Venuti, P
Lee, S
Esposito, G
Rigo, P
Birbaumer, N
Bornstein, MH
AF Caria, Andrea
de Falco, Simona
Venuti, Paola
Lee, Sangkyun
Esposito, Gianluca
Rigo, Paola
Birbaumer, Niels
Bornstein, Marc H.
TI Species-specific response to human infant faces in the premotor cortex
SO NEUROIMAGE
LA English
DT Article
DE Infant faces; fMRI; Species-specific; Premotor cortex; Supplementary
motor area
ID MATERNAL RESPONSIVENESS; FMRI DATA; BRAIN; SUPPLEMENTARY; PREPAREDNESS;
POTENTIALS; ATTACHMENT; BEHAVIORS; MOVEMENTS; INFERENCE
AB The human infant face represents an essential source of communicative signals on the basis of which adults modulate their interactions with infants. Behavioral studies demonstrate that infants' faces activate sensitive and attuned responses in adults through their gaze, face expression, voice, and gesture. In this study we aimed to identify brain responses that underlie adults' general propensity to respond to infant faces. We recorded fMRI during adults' (non-parents) processing of unfamiliar infant faces compared to carefully matched adult faces and infrahuman mammal infant and adult faces. Human infant faces activated several brain systems including the lateral premotor cortex, supplementary motor area, cingulate cortex, anterior insula and the thalamus. Activation of these brain circuits suggests adults' preparation for communicative behavior with infants as well as attachment and caregiving. The same brain regions preferentially responded to human infant faces when compared to animal infant faces, indicating species-specific adult brain responses. Moreover, results of support vector machine based classification analysis indicated that these regions allowed above chance-level prediction of brain state during perception of human infant faces. The complex of brain responses to human infant faces appears to include biological mechanisms that underlie responsiveness and a caring inclination toward young children which appear to transcend adult's biological relationship to the baby. (c) 2011 Elsevier Inc. All rights reserved.
C1 [Caria, Andrea; Birbaumer, Niels] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, D-72070 Tubingen, Germany.
[Caria, Andrea; de Falco, Simona; Venuti, Paola; Esposito, Gianluca; Rigo, Paola] Univ Trent, Dipartimento Sci Cogniz & Formaz, Trento, Italy.
[Lee, Sangkyun] Max Planck Inst Biol Cybernet, Tubingen, Germany.
[Esposito, Gianluca] RIKEN Brain Sci Inst, Saitama, Japan.
[Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Caria, A (reprint author), Univ Tubingen, Inst Med Psychol & Behav Neurobiol, Gartenstr 29, D-72070 Tubingen, Germany.
EM andrea.caria@uni-tuebingen.de
RI Esposito, Gianluca/B-1374-2012
OI Esposito, Gianluca/0000-0002-9442-0254
FU Intramural NIH HHS [ZIA HD001119-25]
NR 70
TC 28
Z9 28
U1 1
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD APR 2
PY 2012
VL 60
IS 2
BP 884
EP 893
DI 10.1016/j.neuroimage.2011.12.068
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 932ED
UT WOS:000303272300006
PM 22230948
ER
PT J
AU Ozarslan, E
Shepherd, TM
Koay, CG
Blackband, SJ
Basser, PJ
AF Oezarslan, Evren
Shepherd, Timothy M.
Koay, Cheng Guan
Blackband, Stephen J.
Basser, Peter J.
TI Temporal scaling characteristics of diffusion as a new MRI contrast:
Findings in rat hippocampus
SO NEUROIMAGE
LA English
DT Article
DE Diffusion time; q-Space; Scaling; Power law; Fractal; Anomalous
diffusion; Anisotropy; Rician; Noise floor; SHORE; DWI
ID FRACTIONAL ORDER CALCULUS; TIME-DEPENDENT DIFFUSION; ANOMALOUS
DIFFUSION; HUMAN BRAIN; BIOLOGICAL TISSUES; TENSOR; NMR; WATER; SIGNAL;
MODEL
AB Features of the diffusion-time dependence of the diffusion-weighted magnetic resonance imaging (MRI) signal provide a new contrast that could be altered by numerous biological processes and pathologies in tissue at microscopic length scales. An anomalous diffusion model, based on the theory of Brownian motion in fractal and disordered media, is used to characterize the temporal scaling (TS) characteristics of diffusion-related quantities, such as moments of the displacement and zero-displacement probabilities, in excised rat hippocampus specimens. To reduce the effect of noise in magnitude-valued MRI data, a novel numerical procedure was employed to yield accurate estimation of these quantities even when the signal falls below the noise floor. The power-law dependencies characterize the TS behavior in all regions of the rat hippocampus, providing unique information about its microscopic architecture. The relationship between the TS characteristics and diffusion anisotropy is investigated by examining the anisotropy of TS, and conversely, the TS of anisotropy. The findings suggest the robustness of the technique as well as the reproducibility of estimates. TS characteristics of the diffusion-weighted signals could be used as a new and useful marker of tissue microstructure. (c) 2012 Elsevier Inc. All rights reserved.
C1 [Oezarslan, Evren; Basser, Peter J.] NICHD, Sect Tissue Biophys & Biomimet, PPITS, NIH, Bethesda, MD 20892 USA.
[Oezarslan, Evren] Uniformed Serv Univ Hlth Sci, Ctr Neurosci & Regenerat Med, Bethesda, MD 20814 USA.
[Shepherd, Timothy M.] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
[Koay, Cheng Guan] Univ Wisconsin, Dept Med Phys, Madison, WI 53705 USA.
[Blackband, Stephen J.] Univ Florida, Dept Neurosci, Gainesville, FL 32610 USA.
[Blackband, Stephen J.] Natl High Magnet Field Lab, Tallahassee, FL 32310 USA.
RP Ozarslan, E (reprint author), NICHD, Sect Tissue Biophys & Biomimet, PPITS, NIH, Bethesda, MD 20892 USA.
EM evren@helix.nih.gov
RI Ozarslan, Evren/B-4858-2013; Basser, Peter/H-5477-2011
OI Ozarslan, Evren/0000-0003-0859-1311;
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD), National Institutes of Health (NIH); NIH
[1R01EB012874]; Department of Defense in the Center for Neuroscience and
Regenerative Medicine (CNRM); Henry M. Jackson Foundation (HJF);
National Science Foundation (NSF) via the National High Magnetic Field
Laboratory (NHMFL)
FX Support for this work included funding from: (i) the Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development (NICHD), National Institutes of Health (NIH). (ii)
NIH grant number 1R01EB012874. (iii) Department of Defense in the Center
for Neuroscience and Regenerative Medicine (CNRM) and the Henry M.
Jackson Foundation (HJF). (iv) National Science Foundation (NSF) via the
National High Magnetic Field Laboratory (NHMFL). We thank Liz Salak for
editing the manuscript and Alexandru V. Avram for helpful discussions.
NR 76
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Z9 14
U1 0
U2 14
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 APR 2
PY 2012
VL 60
IS 2
BP 1380
EP 1393
DI 10.1016/j.neuroimage.2012.01.105
PG 14
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 932ED
UT WOS:000303272300051
PM 22306798
ER
PT J
AU Burkart, AD
Xiong, B
Baibakov, B
Jimenez-Movilla, M
Dean, J
AF Burkart, Anna D.
Xiong, Bo
Baibakov, Boris
Jimenez-Movilla, Maria
Dean, Jurrien
TI Ovastacin, a cortical granule protease, cleaves ZP2 in the zona
pellucida to prevent polyspermy
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID GOLDEN-HAMSTER EGGS; MOUSE EGGS; SPERM BINDING; SULFATED GLYCOPROTEIN;
ASTACIN FAMILY; BLOCK; MICE; METALLOENDOPEPTIDASES; FERTILIZATION;
ANTIBODIES
AB The mouse zona pellucida is composed of three glycoproteins (ZP1, ZP2, and ZP3), of which ZP2 is proteolytically cleaved after gamete fusion to prevent polyspermy. This cleavage is associated with exocytosis of cortical granules that are peripherally located subcellular organelles unique to ovulated eggs. Based on the cleavage site of ZP2, ovastacin was selected as a candidate protease. Encoded by the single-copy Astl gene, ovastacin is an oocyte-specific member of the astacin family of metalloendoproteases. Using specific antiserum, ovastacin was detected in cortical granules before, but not after, fertilization. Recombinant ovastacin cleaved ZP2 in native zonae pellucidae, documenting that ZP2 was a direct substrate of this metalloendoprotease. Female mice lacking ovastacin did not cleave ZP2 after fertilization, and mouse sperm bound as well to Astl-null two-cell embryos as they did to normal eggs. Ovastacin is a pioneer component of mouse cortical granules and plays a definitive role in the postfertilization block to sperm binding that ensures monospermic fertilization and successful development.
C1 [Burkart, Anna D.; Xiong, Bo; Baibakov, Boris; Jimenez-Movilla, Maria; Dean, Jurrien] NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
RP Dean, J (reprint author), NIDDK, Lab Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
EM jurrien@helix.nih.gov
RI Jimenez-Movilla, Maria/I-1004-2015
OI Jimenez-Movilla, Maria/0000-0002-1572-8219
FU National Institute of Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health
FX This research was support by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health.
NR 42
TC 57
Z9 61
U1 1
U2 24
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD APR 2
PY 2012
VL 197
IS 1
BP 37
EP 44
DI 10.1083/jcb.201112094
PG 8
WC Cell Biology
SC Cell Biology
GA 921KN
UT WOS:000302476600007
PM 22472438
ER
PT J
AU David, A
Dolan, BP
Hickman, HD
Knowlton, JJ
Clavarino, G
Pierre, P
Bennink, JR
Yewdell, JW
AF David, Alexandre
Dolan, Brian P.
Hickman, Heather D.
Knowlton, Jonathan J.
Clavarino, Giovanna
Pierre, Philippe
Bennink, Jack R.
Yewdell, Jonathan W.
TI Nuclear translation visualized by ribosome-bound nascent chain
puromycylation
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID NONSENSE-MEDIATED DECAY; MESSENGER-RNA TRANSLATION; PROTEIN-SYNTHESIS;
MAMMALIAN-CELLS; ESCHERICHIA-COLI; INITIATION; COMPLEXES; INHIBITORS;
EXPRESSION; NUCLEOLUS
AB Whether protein translation occurs in the nucleus is contentious. To address this question, we developed the ribopuromycylation method (RPM), which visualizes translation in cells via standard immunofluorescence microscopy. The RPM is based on ribosome-catalyzed puromycylation of nascent chains immobilized on ribosomes by antibiotic chain elongation inhibitors followed by detection of puromycylated ribosome-bound nascent chains with a puromycin (PMY)-specific monoclonal antibody in fixed and permeabilized cells. The RPM correlates localized translation with myriad processes in cells and can be applied to any cell whose translation is sensitive to PMY. In this paper, we use the RPM to provide evidence for translation in the nucleoplasm and nucleolus, which is regulated by infectious and chemical stress.
C1 [David, Alexandre; Dolan, Brian P.; Hickman, Heather D.; Knowlton, Jonathan J.; Bennink, Jack R.; Yewdell, Jonathan W.] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Clavarino, Giovanna; Pierre, Philippe] Ctr Immunol Marseille Luminy Aix Marseille Univ, F-13288 Marseille, France.
[Clavarino, Giovanna; Pierre, Philippe] INSERM, U1104, F-13288 Marseille, France.
[Clavarino, Giovanna; Pierre, Philippe] CNRS, Unite Mixte Rech 7280, F-13288 Marseille, France.
RP Yewdell, JW (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM jyewdell@nih.gov
RI David, Alexandre/B-2447-2013; Clavarino, Giovanna/M-7174-2014;
OI David, Alexandre/0000-0003-3365-1339; pierre,
philippe/0000-0003-0863-8255
FU Division of Intramural Research; National Institute of Allergy and
Infectious Diseases; Ligue National Contre le Cancer; Human Frontier
Science Program; European Network of Excellence DC-THERA
FX This work was generously supported by the Division of Intramural
Research and the National Institute of Allergy and Infectious Diseases
and by grants to P. Pierre from Ligue National Contre le Cancer, the
Human Frontier Science Program, and the European Network of Excellence
DC-THERA.
NR 50
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U1 1
U2 27
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD APR 2
PY 2012
VL 197
IS 1
BP 45
EP 57
DI 10.1083/jcb.201112145
PG 13
WC Cell Biology
SC Cell Biology
GA 921KN
UT WOS:000302476600008
PM 22472439
ER
PT J
AU Djousse, L
Biggs, ML
Ix, JH
Kizer, JR
Lemaitre, RN
Sotoodehnia, N
Zieman, SJ
Mozaffarian, D
Tracy, RP
Mukamal, KJ
Siscovick, DS
AF Djousse, Luc
Biggs, Mary L.
Ix, Joachim H.
Kizer, Jorge R.
Lemaitre, Rozenn N.
Sotoodehnia, Nona
Zieman, Susan J.
Mozaffarian, Dariush
Tracy, Russell P.
Mukamal, Kenneth J.
Siscovick, David S.
TI Nonesterified Fatty Acids and Risk of Sudden Cardiac Death in Older
Adults
SO CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
LA English
DT Article
DE epidemiology; sudden death; fatty acids; risk factors
ID CARDIOVASCULAR HEALTH; MYOCARDIAL INFARCTION; INSULIN-RESISTANCE;
ARRHYTHMIAS; NIDDM; EPIDEMIOLOGY; PATHOGENESIS; METABOLISM
AB Background-Although nonesterified fatty acids (NEFA) have been positively associated with coronary heart disease risk factors, limited and inconsistent data are available on the relation between NEFA and sudden cardiac death.
Methods and Results-Using a prospective design, we studied 4657 older men and women (mean age, 75 years) from the Cardiovascular Health Study (1992-2006) to evaluate the association between plasma NEFA and the risk of sudden cardiac death in older adults. Plasma concentrations of NEFA were measured using established enzymatic methods, and sudden death was adjudicated using medical records, death certificates, proxy interview, and autopsy reports. We used Cox proportional hazard models to estimate multivariable-adjusted relative risks. During a median follow-up of 10.0 years, 221 new cases of sudden cardiac death occurred. In a multivariable model adjusting for age, sex, race, clinic site, alcohol intake, smoking, prevalent coronary heart disease and heart failure, and self-reported health status, relative risks (95% confidence interval) for sudden cardiac death were 1.0 (ref), 1.15 (0.81-1.64), 1.06 (0.72-1.55), and 0.91 (0.60-1.38) across consecutive quartiles of NEFA concentration. In secondary analyses restricted to the first 5 years of follow-up, we also did not observe a statistically significant association between plasma NEFA and sudden cardiac death.
Conclusions-Our data do not provide evidence for an association between plasma NEFA measured late in life and the risk of sudden cardiac death in older adults. (Circ Arrhythm Electrophysiol. 2012;5:273-278.)
C1 [Djousse, Luc] Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Aging,Dept Med, Boston, MA 02120 USA.
[Djousse, Luc] Boston Vet Affairs Healthcare Syst, Boston, MA USA.
[Biggs, Mary L.] Univ Washington, Sch Publ Hlth & Community Med, Dept Biostat, Seattle, WA 98195 USA.
[Ix, Joachim H.] Univ Calif San Diego, Dept Med, Div Nephrol, Vet Affairs San Diego Healthcare Syst, San Diego, CA 92103 USA.
[Ix, Joachim H.] Univ Calif San Diego, Div Prevent Med, Vet Affairs San Diego Healthcare Syst, San Diego, CA 92103 USA.
[Kizer, Jorge R.] Weill Cornell Med Coll, Dept Med, New York, NY USA.
[Kizer, Jorge R.] Weill Cornell Med Coll, Dept Publ Hlth, New York, NY USA.
[Lemaitre, Rozenn N.; Sotoodehnia, Nona; Siscovick, David S.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Zieman, Susan J.] NIA, NIH, Bethesda, MD 20892 USA.
[Mozaffarian, Dariush] Brigham & Womens Hosp, Dept Med, Div Cardiovasc Med, Boston, MA 02115 USA.
[Djousse, Luc; Mozaffarian, Dariush] Harvard Univ, Sch Med, Boston, MA 02120 USA.
[Tracy, Russell P.] Univ Vermont, Coll Med, Dept Pathol, Colchester, VT USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Dept Gen Med & Primary Care, Boston, MA 02215 USA.
[Siscovick, David S.] Univ Washington, Dept Epidemiol, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
RP Djousse, L (reprint author), Harvard Univ, Sch Med, Brigham & Womens Hosp, Div Aging,Dept Med, 1620 Tremont St,3rd Floor, Boston, MA 02120 USA.
EM ldjousse@rics.bwh.harvard.edu
RI Djousse, Luc/F-5033-2017
OI Djousse, Luc/0000-0002-9902-3047
FU National Heart, Lung, and Blood Institute [R01HL094555, N01-HC-85239,
N01-HC-85079, N01-HC-85086, N01-HC-35129, N01-HC-15103, N01-HC-55222,
N01-HC-75150, N01-HC-45133, HL080295]; National Institute of
Neurological Disorders and Stroke (NINDS); National Institute on Aging
(NIA) [AG-023629, AG-15928, AG-20098, AG-027058]
FX The research reported in this article was supported by the National
Heart, Lung, and Blood Institute (R01HL094555) to Drs Djousse, Ix,
Mukamal, Zieman, and Kizer. The CHS was supported by contracts
N01-HC-85239, N01-HC-85079 through N01-HC-85086, N01-HC-35129,
N01-HC-15103, N01-HC-55222, N01-HC-75150, N01-HC-45133, and grant
HL080295 from the National Heart, Lung, and Blood Institute, with
additional contribution from the National Institute of Neurological
Disorders and Stroke (NINDS). Additional support was provided through
AG-023629, AG-15928, AG-20098, and AG-027058 from the National Institute
on Aging (NIA). A full list of principal CHS investigators and
institutions can be found at http://www.chs-nhlbi.org/pi.htm.
NR 31
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U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1941-3149
J9 CIRC-ARRHYTHMIA ELEC
JI Circ.-Arrhythmia Electrophysiol.
PD APR
PY 2012
VL 5
IS 2
BP 273
EP 278
DI 10.1161/CIRCEP.111.967661
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 071HO
UT WOS:000313582100016
PM 22281952
ER
PT J
AU Dettmer, M
Alekel, DL
Lasrado, JA
Messina, M
Carriquiry, A
Heiberger, K
Stewart, JW
Franke, W
AF Dettmer, Michelle
Alekel, D. Lee
Lasrado, Joanne A.
Messina, Mark
Carriquiry, Alicia
Heiberger, Kevin
Stewart, Jeanne W.
Franke, Warren
TI The Effect of Soy Protein Beverages on Serum Cell Adhesion Molecule
Concentrations in Prehypertensive/Stage 1 Hypertensive Individuals
SO JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION
LA English
DT Article
DE cardiovascular disease risk; cell adhesion molecules; ICAM-1;
E-selectin; VCAM-1; isoflavones; soy beverages
ID VASCULAR ENDOTHELIAL-CELLS; POSTMENOPAUSAL WOMEN; E-SELECTIN; HUMAN
ATHEROSCLEROSIS; BLOOD-PRESSURE; CARDIOVASCULAR RISK; INFLAMMATION;
ISOFLAVONES; MECHANISMS; VCAM-1
AB Objective: Prehypertensive and hypertensive individuals are at increased risk of atherosclerotic cardiovascular disease (CVD), in part because hypertension contributes to endothelial dysfunction and increased cell adhesion molecule expression. Soy protein and isoflavones may favorably alter CVD risk factors, and hence the aim of this study was to determine whether intake of cow's milk compared with soy beverage prepared from whole soy bean (WSB) or soy protein isolate (SPI) would lower soluble cell adhesion molecule concentrations as a means of decreasing CVD risk.
Methods: We enrolled healthy prehypertensive/stage 1 hypertensive men (n = 60; 18-63 years) and premenopausal women (n = 8; 20-48 years). Participants were randomized to 1 of 3 groups for 8 weeks: cow's milk (600 mL/d), SPI beverage (840 mL/d; 30.1 mg total isoflavones/d), or WSB beverage (840 mL/d; 91.4 mg total isoflavones/d). We measured soluble vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1), and endothelial-leukocyte adhesion molecule-1 (E-selectin) concentrations at baseline and week 8.
Results: Soluble CAM concentrations were not altered by treatment and did not differ between prehypertensive and hypertensive participants. However, analysis of variance indicated a treatment X gender interaction (gender effect) for ICAM-1 (p = 0.0037) but not for E-selectin (p = 0.067) or VCAM-1 (p = 0.16). Men had higher concentrations of ICAM-1 and E-selectin, respectively, at baseline (p = 0.0071, p = 0.049) and week 8 (p = 0.0054, p = 0.038) than women did.
Conclusion: Neither intake of cow's milk nor soy beverage for 8 weeks altered soluble CAM concentrations in prehypertensive/stage 1 hypertensive individuals, suggesting that neither type of beverage diminished atherosclerotic CVD risk in mildly hypertensive individuals by way of improving circulating CAM concentrations.
C1 [Dettmer, Michelle; Alekel, D. Lee] Iowa State Univ, Dept Food Sci & Human Nutr, Ames, IA USA.
[Dettmer, Michelle; Alekel, D. Lee; Lasrado, Joanne A.; Heiberger, Kevin; Stewart, Jeanne W.] Iowa State Univ, Nutr & Wellness Res Ctr, Ames, IA USA.
[Carriquiry, Alicia] Iowa State Univ, Dept Stat, Ames, IA USA.
[Franke, Warren] Iowa State Univ, Dept Kinesiol, Ames, IA USA.
[Messina, Mark] Loma Linda Univ, Sch Publ Hlth, Dept Nutr, Port Townsend, WA USA.
[Heiberger, Kevin] Univ N Texas, Athlet Dept, Denton, TX 76203 USA.
RP Alekel, DL (reprint author), NIH, NCCAM, 6707 Democracy Blvd,Suite 401, Bethesda, MD 20892 USA.
EM Lee.Alekel@nih.gov
FU Soyfoods Council; Iowa Soybean Association; WhiteWave Foods Company
FX The Soyfoods Council and Iowa Soybean Association provided most of the
funding for this intervention; WhiteWave Foods Company also contributed
funds and soy milk product; Fareway Stores, Inc. also provided milk
product. We acknowledge Linda Funk, executive director of The Soyfoods
Council, and the Iowa Soybean Association, for their contribution to
this study. We thank our participants who diligently adhered to the
dietary intervention and reported faithfully to our research unit. We
are grateful to the dietetics students (particularly Abby Pollard,
Heather Meardon Plizga, and Tiffany McCabe) in the Department of Food
Science and Human Nutrition at Iowa State University who helped with lab
processing, data collection, dietary intake analysis, and data entry. We
thank Dennis Lock, a doctoral student in the Department of Statistics at
Iowa State University, for his efforts with data analysis.
NR 31
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U1 1
U2 5
PU AMER COLLEGE NUTRITION
PI CLEARWATER
PA 300 SOUTH DUNCAN AVENUE, STE 225, CLEARWATER, FL 33755 USA
SN 0731-5724
J9 J AM COLL NUTR
JI J. Am. Coll. Nutr.
PD APR
PY 2012
VL 31
IS 2
BP 100
EP 110
PG 11
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 069XL
UT WOS:000313470300005
PM 22855915
ER
PT J
AU Drake, JW
AF Drake, John W.
TI Contrasting Mutation Rates from Specific-Locus and Long-Term
Mutation-Accumulation Procedures
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE specific-locus mutation rates; genomic sequencing for mutation rates;
synonymous codons; neutral mutations
ID CODON USAGE BIAS; DNA-POLYMERASE; FIDELITY
AB Until recently, the two predominant ways to estimate mutation rates were the specific-locus method and the mutation-accumulation (Bateman-Mukai) method. Both involve seeding a number of parallel lines from a small, genetically uniform population, growing as long as is feasible but not so long as to allow selection to perturb mutant frequencies, and sometimes using extreme bottlenecks to facilitate the retention of deleterious mutations. In the specific-locus method, mutations are selected according to their specific phenotypes and are confirmed by sequencing. In older versions of the mutation-accumulation method, the increase in variance of a quantitative fitness trait is measured and converted into a mutation rate. More recently, a variation on the mutation-accumulation method has become possible based on phenotype-blind genomic sequencing, which might (or might not) provide improved sampling breadth, usually at the expense of sample size. In a recent study, genomic sequencing was applied to Escherichia coli lines propagated for 40,000 generations and passaged daily via 5,000,000 cells. To mitigate the impact of selection, the only targets employed for rate calculations were putatively neutral synonymous mutations. The mutation rate estimate was about 6-fold lower than obtained previously with a robust specific-locus method. Here I argue that purifying selection acting to shape the strong codon preferences of E. coli is the probable cause of the lower estimate, rather than, for instance, a lower mutation rate in nature than in the laboratory.
C1 NIEHS, Mol Genet Lab, Res Triangle Pk, NC 27709 USA.
RP Drake, JW (reprint author), NIEHS, Mol Genet Lab, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM drake@niesh.nih.gov
FU Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences [Z01ES065016]
FX I thank Libertad Garcia-Villada for running the G tests and both her and
Shay Covo for comments on the presubmission draft of this paper. This
research was supported by funds allocated to project Z01ES065016 of the
Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences.
NR 15
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U1 0
U2 13
PU GENETICS SOC AM
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD APR 1
PY 2012
VL 2
IS 4
BP 483
EP 485
DI 10.1534/g3.111.001842
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 055YD
UT WOS:000312453000008
PM 22540039
ER
PT J
AU Liu, QY
Spusta, SC
Mi, RF
Lassiter, RNT
Stark, MR
Hoke, A
Rao, MS
Zeng, XM
AF Liu, Qiuyue
Spusta, Steven C.
Mi, Ruifa
Lassiter, Rhonda N. T.
Stark, Michael R.
Hoeke, Ahmet
Rao, Mahendra S.
Zeng, Xianmin
TI Human Neural Crest Stem Cells Derived from Human ESCs and Induced
Pluripotent Stem Cells: Induction, Maintenance, and Differentiation into
Functional Schwann Cells
SO STEM CELLS TRANSLATIONAL MEDICINE
LA English
DT Article
DE Neural crest; Human embryonic stem cells; Differentiation; Schwann
cells; Peripheral neuron
ID DOPAMINERGIC-NEURONS; DEFINED CONDITIONS; NERVOUS-SYSTEM; SKULL VAULT;
FATE; DERIVATION; EXPRESSION; GENERATION; PATIENT; DISEASE
AB The neural crest (NC) is a transient, multipotent, migratory cell population unique to vertebrates that gives rise to diverse cell lineages. Much of our knowledge of NC development comes from studies of organisms such as chicken and zebrafish because human NC is difficult to obtain because of its transient nature and the limited availability of human fetal cells. Here we examined the process of NC induction from human pluripotent stem cells, including human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs). We showed that NC cells could be efficiently induced from hESCs by a combination of growth factors in medium conditioned on stromal cells and that NC stem cells (NCSCs) could be purified by p75 using fluorescence-activated cell sorting (FACS). FACS-isolated NCSCs could be propagated in vitro in five passages and cryopreserved while maintaining NCSC identity characterized by the expression of a panel of NC markers such as p75, Sox9, Sox10, CD44, and HNK1. In vitro-expanded NCSCs were able to differentiate into neurons and glia (Schwann cells) of the peripheral nervous system, as well as mesenchymal derivatives. hESC-derived NCSCs appeared to behave similarly to endogenous embryonic NC cells when injected in chicken embryos. Using a defined medium, we were able to generate and propagate a nearly pure population of Schwann cells that uniformly expressed glial fibrillary acidic protein, 5100, and p75. Schwann cells generated by our protocol myelinated rat dorsal root ganglia neurons in vitro. To our knowledge, this is the first report on myelination by hESC- or iPSC-derived Schwann cells. STEM CELLS TRANSLATIONAL MEDICINE 2012;1:266-278
C1 [Liu, Qiuyue; Spusta, Steven C.; Rao, Mahendra S.; Zeng, Xianmin] Buck Inst Res Aging, Novato, CA 94945 USA.
[Mi, Ruifa; Hoeke, Ahmet] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Mi, Ruifa; Hoeke, Ahmet] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
[Lassiter, Rhonda N. T.; Stark, Michael R.] Brigham Young Univ, Dept Physiol, Provo, UT 84602 USA.
[Lassiter, Rhonda N. T.; Stark, Michael R.] Brigham Young Univ, Dept Dev Biol, Provo, UT 84602 USA.
[Rao, Mahendra S.] NIH, Natl Ctr Regenerat Med, Bethesda, MD 20892 USA.
RP Zeng, XM (reprint author), Buck Inst Res Aging, Novato, CA 94945 USA.
EM xzeng@buckinstitute.org
OI Hoke, Ahmet/0000-0003-1215-3373
FU California Institute for Regenerative Medicine [CL1-00501-1, TG2-01155];
Maryland Stem Cell Research Fund Grant [302385]
FX This work was supported in part by the California Institute for
Regenerative Medicine Grants CL1-00501-1 (to X.Z.) and TG2-01155 (to
X.Z.) and Maryland Stem Cell Research Fund Grant 302385 (to A.H.). We
thank Dr. L. Cheng at the Johns Hopkins University for providing the
iPSC line and Drs. J. Peng and A. Swistowski (a previous member of our
laboratory) for technical assistance. We also acknowledge the
Developmental Studies Hybridoma Bank maintained by the University of
Iowa (Iowa City, IA) for supply of monoclonal antibodies.
NR 54
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U1 0
U2 16
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 2157-6564
J9 STEM CELL TRANSL MED
JI Stem Cells Transl. Med.
PD APR
PY 2012
VL 1
IS 4
BP 266
EP 278
DI 10.5966/sctm.2011-0042
PG 13
WC Cell & Tissue Engineering
SC Cell Biology
GA 057NZ
UT WOS:000312571600007
PM 23197806
ER
PT J
AU Saphire, EO
Feldmann, H
AF Saphire, Erica Ollmann
Feldmann, Heinz
TI Untitled
SO CURRENT OPINION IN VIROLOGY
LA English
DT Editorial Material
C1 [Saphire, Erica Ollmann] Scripps Res Inst, Dept Immunol & Microbial Sci, La Jolla, CA 92037 USA.
[Feldmann, Heinz] NIAID, Virol Lab, DIR, NIH,Rocky Mt Labs, Hamilton, MT 59840 USA.
RP Saphire, EO (reprint author), Scripps Res Inst, Dept Immunol & Microbial Sci, 10550 N Torrey Pines Rd,IMM-21, La Jolla, CA 92037 USA.
EM erica@scripps.edu
NR 0
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U1 0
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD APR
PY 2012
VL 2
IS 2
BP 157
EP 159
DI 10.1016/j.coviro.2012.03.002
PG 3
WC Virology
SC Virology
GA 051FX
UT WOS:000312112700008
PM 22482713
ER
PT J
AU Pierson, TC
Diamond, MS
AF Pierson, Theodore C.
Diamond, Michael S.
TI Degrees of maturity: the complex structure and biology of flaviviruses
SO CURRENT OPINION IN VIROLOGY
LA English
DT Article
ID TICK-BORNE ENCEPHALITIS; WEST-NILE-VIRUS; ENVELOPE PROTEIN-E;
ANTIBODY-MEDIATED NEUTRALIZATION; CROSS-REACTIVE ANTIBODIES; FUSION-LOOP
ANTIBODY; DENGUE VIRUS; MONOCLONAL-ANTIBODIES; ENDOPLASMIC-RETICULUM;
MEMBRANE-FUSION
AB Flaviviruses are small enveloped virions that enter target cells in a pH-dependent fashion. Virus attachment, entry, and membrane fusion are orchestrated by the envelope (E) and pre-membrane (prM) proteins, the two structural proteins displayed on the surface of virions. Flaviviruses assemble as an immature non-infectious form onto which prM and E form trimeric spikes. During egress from infected cells, flaviviruses undergo dramatic structural changes characterized by the formation of a herringbone arrangement of E proteins that lie flat against the surface of the virion and cleavage of the prM protein by the cellular protease furin. The result is a relatively smooth, infectious mature virion. This dynamic process is now understood in structural detail at the atomic level. However, recent studies indicate that many of the virions released from cells share structural features of both immature and mature virus particles. These mosaic partially mature virions are infectious and interact uniquely with target cells and the host immune response. Here, we will discuss recent advances in our understanding of the biology and significance of partially mature flaviviruses.
C1 [Pierson, Theodore C.] NIAID, Viral Pathogenesis Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Mol Microbiol, St Louis, MO 63110 USA.
[Diamond, Michael S.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
RP Pierson, TC (reprint author), NIAID, Viral Pathogenesis Sect, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM piersontc@mail.nih.gov
FU Intramural Research Program of the NIH, National Institutes of Allergy
and Infectious Diseases (NIAID) [R01-AI077955, U01-AI061373]
FX This work was supported by the Intramural Research Program of the NIH,
National Institutes of Allergy and Infectious Diseases (NIAID),
R01-AI077955 and U01-AI061373. The authors thank Mr. Ethan Tyler and
Phong Lee for preparation of the figures. We are grateful to Drs.
Kimberly Dowd and Swati Mukherjee for their thoughtful comments on our
manuscript. We thank members of our laboratory for useful discussions.
NR 68
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U1 2
U2 12
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD APR
PY 2012
VL 2
IS 2
BP 168
EP 175
DI 10.1016/j.coviro.2012.02.011
PG 8
WC Virology
SC Virology
GA 051FX
UT WOS:000312112700010
PM 22445964
ER
PT J
AU Yang, SC
Karne, NK
Goff, SL
Black, MA
Xu, H
Bischof, D
Cornetta, K
Rosenberg, SA
Morgan, RA
Feldman, SA
AF Yang, Shicheng
Karne, Neel K.
Goff, Stephanie L.
Black, Mary A.
Xu, Hui
Bischof, Daniela
Cornetta, Kenneth
Rosenberg, Steven A.
Morgan, Richard A.
Feldman, Steven A.
TI A Simple and Effective Method to Generate Lentiviral Vectors for Ex Vivo
Gene Delivery to Mature Human Peripheral Blood Lymphocytes
SO HUMAN GENE THERAPY METHODS
LA English
DT Article
ID SEVERE COMBINED IMMUNODEFICIENCY; TUMOR-INFILTRATING LYMPHOCYTES;
T-CELLS; TRANSGENE EXPRESSION; RETROVIRAL VECTORS; CANCER REGRESSION;
STEM-CELLS; THERAPY; VIRUS; TRANSFECTION
AB Human ex vivo gene therapy protocols have been used successfully to treat a variety of genetic disorders, infectious diseases, and cancer. Murine oncoretroviruses (specifically, gammaretroviruses) have served as the primary gene delivery vehicles for these trials. However, in some cases, such vectors have been associated with insertional mutagenesis. As a result, alternative vector platforms such as lentiviral vectors (LVVs) are being developed. LVVs may provide advantages compared with gammaretroviral vectors, including the ability to transduce large numbers of nondividing cells, resistance to gene silencing, and a potentially safer integration profile. The aim of this study was to develop a simplified process for the rapid production of clinical-grade LVVs. To that end, we used a self-inactivating bicistronic LVV encoding an MART (melanoma antigen recognized by T cells)-1-reactive T cell receptor containing oPRE, an optimized and truncated version of woodchuck hepatitis virus posttranslational regulatory element (wPRE). Using our simplified clinical production process, 293T cells were transiently transfected in roller bottles. The LVV supernatant was collected, treated with Benzonase, and clarified by modified step filtration. LVV produced in this manner exhibited titers and a biosafety profile similar to those of cGMP (current Good Manufacturing Practices) LVVs previously manufactured at the Indiana University Vector Production Facility in support of a phase I/II clinical trial. We describe a simple, efficient, and low-cost method for the production of clinical-grade LVV for ex vivo gene therapy protocols.
C1 [Yang, Shicheng; Karne, Neel K.; Goff, Stephanie L.; Black, Mary A.; Xu, Hui; Rosenberg, Steven A.; Morgan, Richard A.; Feldman, Steven A.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Karne, Neel K.] SUNY Upstate Med Univ, Dept Surg Gen Surg, Syracuse, NY 13210 USA.
[Goff, Stephanie L.] Columbia Univ, Coll Phys & Surg, Dept Surg, New York, NY 10032 USA.
[Bischof, Daniela; Cornetta, Kenneth] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Cornetta, Kenneth] Indiana Univ Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA.
[Cornetta, Kenneth] Indiana Univ Sch Med, Dept Med, Indianapolis, IN 46202 USA.
RP Feldman, SA (reprint author), NCI, Surg Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM feldmanst@mail.nih.gov
FU NCRR NIH HHS [P40 RR024928]; PHS HHS [HHSN26820074820]
NR 56
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Z9 3
U1 1
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1946-6536
J9 HUM GENE THER METHOD
JI Hum. Gene Ther. Methods
PD APR
PY 2012
VL 23
IS 2
BP 73
EP 83
DI 10.1089/hgtb.2011.199
PG 11
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 022WM
UT WOS:000309994900001
PM 22515320
ER
PT J
AU Carty, CL
Buzkova, P
Fornage, M
Franceschini, N
Cole, S
Heiss, G
Hindorff, LA
Howard, BV
Mann, S
Martin, LW
Zhang, Y
Matise, TC
Prentice, R
Reiner, AP
Kooperberg, C
AF Carty, Cara L.
Buzkova, Petra
Fornage, Myriam
Franceschini, Nora
Cole, Shelley
Heiss, Gerardo
Hindorff, Lucia A.
Howard, Barbara V.
Mann, Sue
Martin, Lisa W.
Zhang, Ying
Matise, Tara C.
Prentice, Ross
Reiner, Alexander P.
Kooperberg, Charles
TI Associations Between Incident Ischemic Stroke Events and Stroke and
Cardiovascular Disease-Related Genome-Wide Association Studies Single
Nucleotide Polymorphisms in the Population Architecture Using Genomics
and Epidemiology Study
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE genetics of stroke; risk factors for stroke; genetics of cardiovascular
disease; cohort studies
ID ATHEROSCLEROSIS RISK; FOLLOW-UP; DESIGN; METAANALYSIS; HEALTH; VARIANTS;
SURVIVAL; TRAITS
AB Background-Genome-wide association studies (GWAS) have identified loci associated with ischemic stroke (IS) and cardiovascular disease (CVD) in European-descent individuals, but their replication in different populations has been largely unexplored.
Methods and Results-Nine single nucleotide polymorphisms (SNPs) selected from GWAS and meta-analyses of stroke, and 86 SNPs previously associated with myocardial infarction and CVD risk factors, including blood lipids (high density lipoprotein [HDL], low density lipoprotein [LDL], and triglycerides), type 2 diabetes, and body mass index (BMI), were investigated for associations with incident IS in European Americans (EA) N=26 276, African-Americans (AA) N=8970, and American Indians (AI) N=3570 from the Population Architecture using Genomics and Epidemiology Study. Ancestry-specific fixed effects meta-analysis with inverse variance weighting was used to combine study-specific log hazard ratios from Cox proportional hazards models. Two of 9 stroke SNPs (rs783396 and rs1804689) were associated with increased IS hazard in AA; none were significant in this large EA cohort. Of 73 CVD risk factor SNPs tested in EA, 2 (HDL and triglycerides SNPs) were associated with IS. In AA, SNPs associated with LDL, HDL, and BMI were significantly associated with IS (3 of 86 SNPs tested). Out of 58 SNPs tested in AI, 1 LDL SNP was significantly associated with IS.
Conclusions-Our analyses showing lack of replication in spite of reasonable power for many stroke SNPs and differing results by ancestry highlight the need to follow up on GWAS findings and conduct genetic association studies in diverse populations. We found modest IS associations with BMI and lipids SNPs, though these findings require confirmation. (Circ Cardiovasc Genet. 2012;5:210-216.)
C1 [Carty, Cara L.; Mann, Sue; Prentice, Ross; Kooperberg, Charles] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Buzkova, Petra] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Inst Mol Med, Houston, TX USA.
[Fornage, Myriam] Univ Texas Hlth Sci Ctr Houston, Sch Publ Hlth, Div Epidemiol, Houston, TX USA.
[Franceschini, Nora; Heiss, Gerardo] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Cole, Shelley] Texas Biomed Res Inst, Dept Genet, San Antonio, TX USA.
[Hindorff, Lucia A.] NHGRI, Off Populat Genom, Bethesda, MD 20892 USA.
[Howard, Barbara V.] Medstar Hlth Res Inst, Washington, DC USA.
[Howard, Barbara V.; Martin, Lisa W.] George Washington Univ, Sch Med, Washington, DC USA.
[Zhang, Ying] Univ Oklahoma, Hlth Sci Ctr, Oklahoma City, OK USA.
[Matise, Tara C.] Rutgers State Univ, Dept Genet, Piscataway, NJ USA.
[Reiner, Alexander P.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
RP Carty, CL (reprint author), Fred Hutchinson Canc Res Ctr, 1100 Fairview Ave N,M3-A410, Seattle, WA 98109 USA.
EM ccarty@fhcrc.org
RI Carty, Cara/B-8683-2013;
OI Martin, Lisa Warsinger/0000-0003-4352-0914
FU National Human Genome Research Institute (NHGRI); CALiCo [U01HG004803];
EAGLE [U01HG004798]; MEC [U01HG004802]; WHI [U01HG004790]; Coordinating
Center [U01HG004801]; NHGRI PAGE program [U01HG004798-01]; Johns Hopkins
University from NHLBI [N01-HV-48195]; Centers for Disease Control and
Prevention; National Cancer Institute [R37CA54281, R01 CA63, P01CA33619,
U01CA136792, U01CA98758]
FX The Population Architecture Using Genomics and Epidemiology (PAGE)
program is funded by the National Human Genome Research Institute
(NHGRI), supported by U01HG004803 (CALiCo), U01HG004798 (EAGLE),
U01HG004802 (MEC), U01HG004790 (WHI), and U01HG004801 (Coordinating
Center), and their respective NHGRI ARRA supplements. The contents of
this paper are solely the responsibility of the authors and do not
necessarily represent the official views of the NIH.; The "Epidemiologic
Architecture for Genes Linked to Environment (EAGLE)" is funded through
the NHGRI PAGE program (U01HG004798-01 and its NHGRI ARRA supplement).
Genotyping services for select NHANES III SNPs presented here were also
provided by the Johns Hopkins University under federal contract number
(N01-HV-48195) from NHLBI. The study participants derive from the
National Health and Nutrition Examination Surveys (NHANES), and these
studies are supported by the Centers for Disease Control and Prevention.
The findings and conclusions in this report are those of the authors and
do not necessarily represent the views of the Centers for Disease
Control and Prevention.; The Multiethnic Cohort study (MEC)
characterization of epidemiological architecture is funded through the
NHGRI PAGE program (U01HG004802 and its NHGRI ARRA supplement). The MEC
study is funded through the National Cancer Institute (R37CA54281, R01
CA63, P01CA33619, U01CA136792, and U01CA98758).
NR 37
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U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-325X
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD APR
PY 2012
VL 5
IS 2
BP 210
EP 216
DI 10.1161/CIRCGENETICS.111.962191
PG 7
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 021KS
UT WOS:000309884300011
PM 22403240
ER
PT J
AU Kristiansson, K
Perola, M
Tikkanen, E
Kettunen, J
Surakka, I
Havulinna, AS
Stancakova, A
Barnes, C
Widen, E
Kajantie, E
Eriksson, JG
Viikari, J
Kahonen, M
Lehtimoki, T
Raitakari, OT
Hartikainen, AL
Ruokonen, A
Pouta, A
Jula, A
Kangas, AJ
Soininen, P
Ala-Korpela, M
Mannisto, S
Jousilahti, P
Bonnycastle, LL
Jarvelin, MR
Kuusisto, J
Collins, FS
Laakso, M
Hurles, ME
Palotie, A
Peltonen, L
Ripatti, S
Salomaa, V
AF Kristiansson, Kati
Perola, Markus
Tikkanen, Emmi
Kettunen, Johannes
Surakka, Ida
Havulinna, Aki S.
Stancakova, Alena
Barnes, Chris
Widen, Elisabeth
Kajantie, Eero
Eriksson, Johan G.
Viikari, Jorma
Kahonen, Mika
Lehtimaki, Terho
Raitakari, Olli T.
Hartikainen, Anna-Liisa
Ruokonen, Aimo
Pouta, Anneli
Jula, Antti
Kangas, Antti J.
Soininen, Pasi
Ala-Korpela, Mika
Mannisto, Satu
Jousilahti, Pekka
Bonnycastle, Lori L.
Jarvelin, Marjo-Riitta
Kuusisto, Johanna
Collins, Francis S.
Laakso, Markku
Hurles, Matthew E.
Palotie, Aarno
Peltonen, Leena
Ripatti, Samuli
Salomaa, Veikko
TI Genome-Wide Screen for Metabolic Syndrome Susceptibility Loci Reveals
Strong Lipid Gene Contribution But No Evidence for Common Genetic Basis
for Clustering of Metabolic Syndrome Traits
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE metabolic syndrome; risk factors; genome-wide association study;
meta-analysis; lipids
ID ASSOCIATION ANALYSIS; RISK; INSULIN; COMPONENTS; OBESITY
AB Background-Genome-wide association (GWA) studies have identified several susceptibility loci for metabolic syndrome (MetS) component traits, but have had variable success in identifying susceptibility loci to the syndrome as an entity. We conducted a GWA study on MetS and its component traits in 4 Finnish cohorts consisting of 2637 MetS cases and 7927 controls, both free of diabetes, and followed the top loci in an independent sample with transcriptome and nuclear magnetic resonance-based metabonomics data. Furthermore, we tested for loci associated with multiple MetS component traits using factor analysis, and built a genetic risk score for MetS.
Methods and Results-A previously known lipid locus, APOA1/C3/A4/A5 gene cluster region (SNP rs964184), was associated with MetS in all 4 study samples (P=7.23x10(-9) in meta-analysis). The association was further supported by serum metabolite analysis, where rs964184 was associated with various very low density lipoprotein, triglyceride, and high-density lipoprotein metabolites (P=0.024-1.88x10(-5)). Twenty-two previously identified susceptibility loci for individual MetS component traits were replicated in our GWA and factor analysis. Most of these were associated with lipid phenotypes, and none with 2 or more uncorrelated MetS components. A genetic risk score, calculated as the number of risk alleles in loci associated with individual MetS traits, was strongly associated with MetS status.
Conclusions-Our findings suggest that genes from lipid metabolism pathways have the key role in the genetic background of MetS. We found little evidence for pleiotropy linking dyslipidemia and obesity to the other MetS component traits, such as hypertension and glucose intolerance. (Circ Cardiovasc Genet. 2012;5:242-249.)
C1 [Kristiansson, Kati; Perola, Markus; Tikkanen, Emmi; Kettunen, Johannes; Surakka, Ida; Ripatti, Samuli] Univ Helsinki, Publ Hlth Genom Unit, Helsinki, Finland.
[Havulinna, Aki S.; Mannisto, Satu; Jousilahti, Pekka; Salomaa, Veikko] Univ Helsinki, Chron Dis Epidemiol & Prevent Unit, Helsinki, Finland.
[Kajantie, Eero; Eriksson, Johan G.] Univ Helsinki, Diabet Prevent Unit, Dept Chron Dis Prevent, Helsinki, Finland.
[Jousilahti, Pekka] Univ Helsinki, Int Affairs Unit, Natl Inst Hlth & Welf, Helsinki, Finland.
[Kristiansson, Kati; Perola, Markus; Tikkanen, Emmi; Kettunen, Johannes; Surakka, Ida; Widen, Elisabeth; Pouta, Anneli; Ripatti, Samuli] Univ Helsinki, Inst Mol Med Finland FIMM, Helsinki, Finland.
[Eriksson, Johan G.] Univ Helsinki, Dept Gen Practice & Primary Hlth Care, Helsinki, Finland.
[Perola, Markus] Univ Tartu, Estonian Genome Ctr, EE-50090 Tartu, Estonia.
[Stancakova, Alena] Univ Eastern Finland, Inst Clin Med, Dept Med, Kuopio, Finland.
[Barnes, Chris] Univ London Imperial Coll Sci Technol & Med, Ctr Bioinformat, Div Mol Biosci, London, England.
[Barnes, Chris] Univ London Imperial Coll Sci Technol & Med, Inst Math Sci, London, England.
[Jarvelin, Marjo-Riitta] Univ London Imperial Coll Sci Technol & Med, Fac Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
[Kajantie, Eero] Univ Helsinki, Helsinki, Finland.
[Kajantie, Eero] Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland.
[Eriksson, Johan G.] Univ Helsinki, Cent Hosp, Unit Gen Practice, Helsinki, Finland.
[Eriksson, Johan G.] Folkhalsan Res Ctr, Helsinki, Finland.
[Eriksson, Johan G.] Vaasa Cent Hosp, Vaasa, Finland.
[Raitakari, Olli T.] Turku Univ Hosp, FIN-20520 Turku, Finland.
[Raitakari, Olli T.] Univ Turku, Res Ctr Appl & Prevent Cardiovasc Med, Turku, Finland.
[Viikari, Jorma] Univ Turku, Dept Med, Turku, Finland.
[Kahonen, Mika] Univ Tampere, Dept Clin Physiol, FIN-33101 Tampere, Finland.
[Lehtimaki, Terho] Univ Tampere, Dept Clin Chem, FIN-33101 Tampere, Finland.
[Lehtimaki, Terho] Tampere Univ Hosp, Tampere, Finland.
[Hartikainen, Anna-Liisa] Univ Oulu, Inst Clin Med Obstet & Gynaecol, Oulu, Finland.
[Ruokonen, Aimo] Univ Oulu, Dept Clin Chem, Oulu, Finland.
[Pouta, Anneli; Jarvelin, Marjo-Riitta] Natl Inst Hlth & Welf, Dept Children Young People & Families, Oulu, Finland.
[Jula, Antti] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Populat Studies Unit, Turku, Finland.
[Kangas, Antti J.; Soininen, Pasi; Ala-Korpela, Mika] Univ Oulu, Computat Med Res Grp, Inst Clin Med, Oulu, Finland.
[Ala-Korpela, Mika] Univ Oulu, Dept Internal Med, Clin Res Ctr, SF-90220 Oulu, Finland.
[Jarvelin, Marjo-Riitta] Univ Oulu, Inst Hlth Sci, Oulu, Finland.
[Jarvelin, Marjo-Riitta] Univ Oulu, Bioctr Oulu, Oulu, Finland.
[Soininen, Pasi; Ala-Korpela, Mika] Univ Eastern Finland, Dept Biosci, Chem Lab, NMR Metabon Lab, Kuopio, Finland.
[Bonnycastle, Lori L.; Collins, Francis S.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Kuusisto, Johanna; Collins, Francis S.] Kuopio Univ Hosp, SF-70210 Kuopio, Finland.
[Kuusisto, Johanna; Collins, Francis S.] Univ Eastern Finland, Inst Clin Med, Dept Med, Kuopio, Finland.
[Hurles, Matthew E.; Palotie, Aarno; Ripatti, Samuli] Wellcome Trust Sanger Inst, Cambridge, England.
[Palotie, Aarno] Broad Inst & Harvard, Program Med & Populat Genet & Genet Anal Platform, Cambridge, MA USA.
[Palotie, Aarno] Univ Cent Hosp, Helsinki, Finland.
[Palotie, Aarno] Univ Helsinki, Dept Med Genet, Helsinki, Finland.
RP Kristiansson, K (reprint author), Univ Helsinki, Natl Inst Hlth & Welf, PL 104, FI-00251 Helsinki, Finland.
EM kati.kristiansson@thl.fi
RI Ripatti, Samuli/H-9446-2014;
OI Ripatti, Samuli/0000-0002-0504-1202; Jarvelin,
Marjo-Riitta/0000-0002-2149-0630; Eriksson, Johan/0000-0002-2516-2060;
Kristiansson, Kati/0000-0003-4688-107X; Mannisto,
Satu/0000-0002-8668-3046; Barnes, Chris/0000-0002-9459-1395
FU European Community's Seventh Framework Programme, BioSHaRE Consortium
[261433]; Academy of Finland; Orion-Farmos Research Foundation; Finnish
Foundation for Cardiovascular Research; Sigrid Juselius Foundation;
Diabetes Research Foundation; Finnish Foundation for Pediatric Research;
Novo Nordisk Foundation; Jenny and Antti Wihuri Foundation;
Biotechnology and Biological Research Council; Wellcome Trust; Finnish
Diabetes Research Society; Samfundet Folkhalsan; Juho Vainio Foundation;
Finska Lakaresallskapet; Paivikki and Sakari Sohlberg Foundation; Signe
and Ane Gyllenberg Foundation; Yrjo Jahnsson Foundation; Social
Insurance Institution of Finland; University Hospital Medical; Emil
Aaltonen Foundation; University Hospital Oulu, Biocenter; University of
Oulu; NHLBI; ENGAGE; Medical Research Council; Biocentrum Helsinki
FX This research was supported through funds from the European Community's
Seventh Framework Programme (FP7/2007-2013), BioSHaRE Consortium, grant
agreement 261433, Academy of Finland, Orion-Farmos Research Foundation,
Finnish Foundation for Cardiovascular Research, Sigrid Juselius
Foundation, Diabetes Research Foundation, Finnish Foundation for
Pediatric Research, Novo Nordisk Foundation, Jenny and Antti Wihuri
Foundation, Biotechnology and Biological Research Council, Wellcome
Trust, Finnish Diabetes Research Society, Samfundet Folkhalsan, Juho
Vainio Foundation, Finska Lakaresallskapet, Paivikki and Sakari Sohlberg
Foundation, Signe and Ane Gyllenberg Foundation, Yrjo Jahnsson
Foundation, Social Insurance Institution of Finland, University Hospital
Medical funds to Tampere and Turku University Hospitals, Emil Aaltonen
Foundation, University Hospital Oulu, Biocenter, University of Oulu,
NHLBI, ENGAGE, Medical Research Council, and Biocentrum Helsinki (see
online-only Data Supplement).
NR 34
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U1 0
U2 23
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1942-325X
J9 CIRC-CARDIOVASC GENE
JI Circ.-Cardiovasc. Genet.
PD APR
PY 2012
VL 5
IS 2
BP 242
EP 249
DI 10.1161/CIRCGENETICS.111.961482
PG 8
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 021KS
UT WOS:000309884300015
PM 22399527
ER
PT J
AU Abdelazim, SA
Bachran, C
David, A
Leppla, SH
AF Abdelazim, Suzanne Aly
Bachran, Christopher
David, Alexandre
Leppla, Stephen H.
TI A non-radioactive high-throughput assay for the detection of cellular
protein synthesis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Abdelazim, Suzanne Aly; Bachran, Christopher; David, Alexandre; Leppla, Stephen H.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
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PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305936
ER
PT J
AU Adelman, KL
AF Adelman, Karen L.
TI Probing the dynamics of promoter proximally paused Pol II
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Adelman, Karen L.] NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
NR 0
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U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300166
ER
PT J
AU Ahuja, JKC
Bhagwat, S
Haytowitz, D
Holden, J
Bailey, R
Dwyer, J
Milner, J
Moshfegh, A
AF Ahuja, Jaspreet K. C.
Bhagwat, Seema
Haytowitz, David
Holden, Joanne
Bailey, Reagan
Dwyer, Johanna
Milner, John
Moshfegh, Alanna
TI Development of a flavonoid database for assessing population exposures
and its application
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Ahuja, Jaspreet K. C.; Bhagwat, Seema; Haytowitz, David; Holden, Joanne; Moshfegh, Alanna] ARS, USDA, Beltsville Human Nutr Res Ctr, Beltsville, MD USA.
[Bailey, Reagan; Dwyer, Johanna] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Milner, John] NCI, NIH, Rockville, MD USA.
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JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304421
ER
PT J
AU Akinfiresoye, L
Lovinger, DM
Tizabi, Y
AF Akinfiresoye, Luli
Lovinger, D. M.
Tizabi, Y.
TI Antidepressant-like effect of AMPA and ketamine combination in male
Wistar -Kyoto rats
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Akinfiresoye, Luli; Tizabi, Y.] Howard Univ, Coll Med, Dept Pharmacol, Washington, DC 20059 USA.
[Lovinger, D. M.] NIAAA, Lab Integrat Neurosci, Div Intramural Clin & Basic Res, NIH, Rockville, MD 20852 USA.
NR 0
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VL 26
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WC Biochemistry & Molecular Biology; Biology; Cell Biology
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Topics; Cell Biology
GA 032IZ
UT WOS:000310711307213
ER
PT J
AU Andrews, KW
Roseland, JM
Holden, JM
Middleton, AM
Solomon, AM
Douglass, L
Dwyer, JT
Bailey, R
Saldanha, LG
Daniel, MG
AF Andrews, K. W.
Roseland, J. M.
Holden, J. M.
Middleton, A. M.
Solomon, A. M.
Douglass, L.
Dwyer, J. T.
Bailey, R.
Saldanha, L. G.
Daniel, M. G.
TI Release 2 of the US Dietary Supplement Ingredient Database (DSID):
research protocols and ingredient estimates for children's and adult
multivitamins
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Andrews, K. W.; Roseland, J. M.; Holden, J. M.; Middleton, A. M.; Solomon, A. M.; Daniel, M. G.] USDA, Nutrient Data Lab, Beltsville, MD 20705 USA.
[Dwyer, J. T.; Bailey, R.; Saldanha, L. G.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
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VL 26
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SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303114
ER
PT J
AU Arab, L
Su, J
Steck, S
Ang, A
Fontham, E
Bensen, J
Mohler, J
AF Arab, Lenore
Su, Joseph
Steck, Susan
Ang, Alfonso
Fontham, Elizabeth
Bensen, Jeannette
Mohler, James
TI Living WCRF Recommendations associated with less Prostate Cancer
Aggressiveness among African and Caucasian Americans
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Arab, Lenore; Ang, Alfonso] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Su, Joseph] NCI, Bethseda, MD USA.
[Steck, Susan] USC, Columbus, SC USA.
[Fontham, Elizabeth] LSU, New Orleans, LA USA.
[Mohler, James] UNC, Sch Med, Chapel Hill, NC USA.
[Mohler, James] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
NR 0
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PD APR
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Topics; Cell Biology
GA 032IZ
UT WOS:000310711306903
ER
PT J
AU Artis, M
Huestis, D
Lehmann, T
AF Artis, Monica
Huestis, Diana
Lehmann, Tovi
TI Variation in cuticular hydrocarbons with age, feeding, and insemination
status of Anopheles gambiae
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Artis, Monica] Univ Maryland Eastern Shore, Princess Anne, MD USA.
[Huestis, Diana; Lehmann, Tovi] NIAID, NIH, Rockville, MD USA.
NR 0
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U1 1
U2 2
PU FEDERATION AMER SOC EXP BIOL
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PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301054
ER
PT J
AU Barry, CE
AF Barry, Clifton Earl
TI Compensatory Evolution and Fixation of Rfampicin Resistance in MDR and
XDR Tuberculosis.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Barry, Clifton Earl] NIAID, TB Res Sect 3, NIH, Bethesda, MD 20892 USA.
RI Barry, III, Clifton/H-3839-2012
NR 0
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PU FEDERATION AMER SOC EXP BIOL
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PD APR
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VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301980
ER
PT J
AU Benischke, AS
Hemion, C
Neutzner, M
Norris, K
Frank, S
Youle, R
Karbowski, M
Neutzner, A
AF Benischke, Anne-Sophie
Hemion, Charles
Neutzner, Melanie
Norris, Kristi
Frank, Stefan
Youle, Richard
Karbowski, Mariusz
Neutzner, Albert
TI A novel mitochondrial ubiquitin ligase involved in the regulation of
mitochondrial fusion
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Benischke, Anne-Sophie; Hemion, Charles; Neutzner, Melanie; Neutzner, Albert] Dept Biomed, Basel, Switzerland.
[Norris, Kristi; Youle, Richard] NIH, Bethesda, MD 20892 USA.
[Frank, Stefan] Univ Basel, Inst Pathol, Basel, Switzerland.
[Karbowski, Mariusz] Univ Maryland, Inst Biotechnol, Baltimore, MD 21201 USA.
NR 0
TC 0
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PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304218
ER
PT J
AU Bortner, CD
Scoltock, AB
Sifre, MI
Cidlowski, JA
AF Bortner, Carl David
Scoltock, Alyson B.
Sifre, Maria I.
Cidlowski, John A.
TI Osmotic Stress Resistance Imparts Acquired Anti-Apoptotic Properties in
Lymphocytes via Regulatory Cell Volume Mechanisms
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Bortner, Carl David; Scoltock, Alyson B.; Sifre, Maria I.; Cidlowski, John A.] NIEHS, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303102
ER
PT J
AU Branum, A
Singer, B
Bailey, R
AF Branum, Amy
Singer, Barbara
Bailey, Regan
TI Dietary supplement use during pregnancy: results from the National
Health and Nutritional Examination Survey (NHANES)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Branum, Amy] CDC NCHS, Hyattsville, MD USA.
[Singer, Barbara] Univ Maryland, College Pk, MD 20742 USA.
[Bailey, Regan] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301614
ER
PT J
AU Brosh, RM
Sommers, J
Muniandy, P
Coulombe, Y
Masson, JY
Seidman, M
Suhasini, A
AF Brosh, Robert Michael
Sommers, Joshua
Muniandy, Parameswary
Coulombe, Yan
Masson, Jean-Yves
Seidman, Michael
Suhasini, Avvaru
TI Physical and Functional Interaction Between Fanconi Anemia Group J
Helicase and MRE11 Nuclease
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Brosh, Robert Michael; Sommers, Joshua; Muniandy, Parameswary; Seidman, Michael; Suhasini, Avvaru] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
[Coulombe, Yan; Masson, Jean-Yves] Univ Laval, Canc Res Ctr, Genome Stabil Lab, Quebec City, PQ, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303009
ER
PT J
AU Buchowski, M
Whitaker, L
Powers, J
Chen, K
Schnelle, J
AF Buchowski, Maciej
Whitaker, Lauren
Powers, James
Chen, Kong
Schnelle, John
TI Fatigability as a function of physical activity energy expenditure:
proof of concept
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Buchowski, Maciej; Whitaker, Lauren; Powers, James; Schnelle, John] Vanderbilt Univ, Nashville, TN USA.
[Chen, Kong] NIDDK, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304338
ER
PT J
AU Byun, JS
Gardner, K
AF Byun, Jung S.
Gardner, Kevin
TI The ELL component of the SEC complex facilitates RNA polymerase II pause
site entry and release
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Byun, Jung S.; Gardner, Kevin] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301709
ER
PT J
AU Byun, JS
Gardner, K
AF Byun, Jung S.
Gardner, Kevin
TI Reprogramming the cancer epigenome by "metabolic transduction"
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Byun, Jung S.; Gardner, Kevin] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301596
ER
PT J
AU Carlson, B
Kim, JY
Xu, XM
Yoo, MH
Zeng, Y
Chen, S
Gladyshev, V
Lee, BJ
Hatfield, D
AF Carlson, Bradley
Kim, Jin Young
Xu, Xue-Ming
Yoo, Min Hyuk
Zeng, Yu
Chen, Shawn
Gladyshev, Vadim
Lee, Byeong Jae
Hatfield, Dolph
TI Inhibition of selenocysteine tRNA[Ser]Sec aminoacylation provides
evidence that aminoacylation is required for regulatory methylation of
this tRNA
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Carlson, Bradley; Xu, Xue-Ming; Yoo, Min Hyuk; Hatfield, Dolph] NCI, NIH, Bethesda, MD 20892 USA.
[Kim, Jin Young; Lee, Byeong Jae] Seoul Natl Univ, Seoul, South Korea.
[Zeng, Yu; Chen, Shawn] Ohio Univ, Athens, OH 45701 USA.
[Gladyshev, Vadim] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Gladyshev, Vadim] Harvard Univ, Sch Med, Boston, MA USA.
RI Gladyshev, Vadim/A-9894-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302548
ER
PT J
AU Chandra, G
Saha, A
Moralle, MR
Zhang, ZJ
Sarkar, C
Peng, SY
Mukherjee, AB
AF Chandra, Goutam
Saha, Arjun
Moralle, Matthew R.
Zhang, Zhongjian
Sarkar, Chinmoy
Peng, Shiyong
Mukherjee, Anil B.
TI Impaired lysosomal maturation of pro-cathepsin D to active cathepsin D
in a childhood neurodegenerative lysosomal storage disease
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Chandra, Goutam; Saha, Arjun; Moralle, Matthew R.; Zhang, Zhongjian; Sarkar, Chinmoy; Peng, Shiyong; Mukherjee, Anil B.] NICHD, Sect Dev Genet, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303433
ER
PT J
AU Charron, CS
Clevidence, BA
Albaugh, GP
Kramer, M
Vinyard, BT
Milner, JA
Novotny, JA
AF Charron, Craig S.
Clevidence, Beverly A.
Albaugh, George P.
Kramer, Matthew
Vinyard, Bryan T.
Milner, John A.
Novotny, Janet A.
TI Influence of consumption of allyl isothiocyanate or cabbage and mustard
on DNA integrity in humans
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Charron, Craig S.; Clevidence, Beverly A.; Albaugh, George P.; Novotny, Janet A.] USDA, Beltsville Human Nutr Res Ctr, Beltsville, MD 20705 USA.
[Kramer, Matthew; Vinyard, Bryan T.] USDA, Biometr Consulting Serv, Beltsville, MD 20705 USA.
[Milner, John A.] NCI, Div Canc Prevent, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305025
ER
PT J
AU Chavis, JT
Neal, J
Switzer, C
Wink, DA
Garcin, E
AF Chavis, John Taylor, III
Neal, Jacob
Switzer, Christopher
Wink, David A., Jr.
Garcin, Elsa
TI Determining the effect of dithiolethione compounds on the activity of
human glyceraldehyde-3-phosphate dehydrogenase
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Chavis, John Taylor, III; Neal, Jacob; Garcin, Elsa] Univ Maryland Baltimore Cty, Baltimore, MD 21228 USA.
[Switzer, Christopher; Wink, David A., Jr.] NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301068
ER
PT J
AU Chen, F
Hofmann, P
Carlson, BA
Tobe, R
Schomburg, L
Gladyshev, VN
Schweizer, U
Hatfield, DL
AF Chen, Fang
Hofmann, Peter
Carlson, Bradley A.
Tobe, Ryuta
Schomburg, Lutz
Gladyshev, Vadim N.
Schweizer, Ulrich
Hatfield, Dolph L.
TI Mammalian selenocysteine tRNA Um34 methylase and its role in
selenoprotein synthesis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Chen, Fang; Carlson, Bradley A.; Tobe, Ryuta; Hatfield, Dolph L.] NCI, NIH, Bethesda, MD 20892 USA.
[Hofmann, Peter; Schomburg, Lutz; Schweizer, Ulrich] Charite, D-13353 Berlin, Germany.
[Gladyshev, Vadim N.] Harvard Univ, Sch Med, Boston, MD USA.
[Gladyshev, Vadim N.] Brigham & Womens Hosp, Boston, MD USA.
RI Gladyshev, Vadim/A-9894-2013; Schomburg, Lutz/D-8096-2013; Schweizer,
Ulrich/E-8105-2013
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303301
ER
PT J
AU Chen, L
Murray-Kolb, LE
Patel, KV
AF Chen, Lenis
Murray-Kolb, Laura E.
Patel, Kushang V.
TI The Characterization of Iron Status in InCHIANTI: The Use of a Higher
Ferritin Cutoff
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Chen, Lenis; Murray-Kolb, Laura E.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Murray-Kolb, Laura E.] Penn State Univ, Dept Nutr Sci, University Pk, PA 16802 USA.
[Patel, Kushang V.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302275
ER
PT J
AU Chou, CL
Han, L
Wang, G
Gucek, M
Pisitkun, T
Knepper, MA
AF Chou, C. L.
Han, L.
Wang, G.
Gucek, M.
Pisitkun, T.
Knepper, M. A.
TI Stoichiometry determination of UT-A1 and UT-A3 within collecting duct
urea transporter complex
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Chou, C. L.; Han, L.; Wang, G.; Gucek, M.; Pisitkun, T.; Knepper, M. A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305151
ER
PT J
AU Coates, PM
Bailey, RL
AF Coates, Paul M.
Bailey, Regan L.
TI Making sense of dietary supplement research and a framework for the
future
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Coates, Paul M.; Bailey, Regan L.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301077
ER
PT J
AU Conroy, J
Free, RB
Doyle, TB
Southall, N
Ferrer, M
Han, Y
Javitch, JA
Sibley, DR
AF Conroy, Jennie
Free, R. Benjamin
Doyle, Trevor B.
Southall, Noel
Ferrer, Marc
Han, Yang
Javitch, Jonathan A.
Sibley, David R.
TI Identification of a novel dopaminergic agonist that selectively
activates the D-2 dopamine receptor
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Conroy, Jennie; Free, R. Benjamin; Doyle, Trevor B.; Sibley, David R.] NINDS, MNS, NIH, Rockville, MD USA.
[Southall, Noel; Ferrer, Marc] NIH, Ctr Translat Therapeut, Bethesda, MD 20892 USA.
[Han, Yang; Javitch, Jonathan A.] Columbia Univ Coll Phys & Surg, Ctr Mol Recognit, New York, NY 10032 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304809
ER
PT J
AU Costello, RB
Lentino, C
Saldanha, L
Srinivas, P
Sempos, C
AF Costello, Rebecca B.
Lentino, Cindy
Saldanha, Leila
Srinivas, Pothur
Sempos, Chris
TI Review of select dietary supplement interventions for endothelial
dysfunction
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Costello, Rebecca B.; Lentino, Cindy; Saldanha, Leila; Sempos, Chris] Off Dietary Supplements, Bethesda, MD USA.
[Srinivas, Pothur] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304759
ER
PT J
AU Cox, B
Post, J
Bull, G
Gouty, S
Woods, A
AF Cox, Brian
Post, Jeremy
Bull, Gregory
Gouty, Shawn
Woods, Amina
TI Mass-spectrometric analysis of changes in brain lipid expression and
distribution after brain injury
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Cox, Brian; Bull, Gregory; Gouty, Shawn] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Cox, Brian; Post, Jeremy; Bull, Gregory; Woods, Amina] NIH, USU, CNRM, Bethesda, MD USA.
[Post, Jeremy; Woods, Amina] NIDA, Struct Biol Unit, IRP, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304866
ER
PT J
AU Dai, LS
Tsai-Morris, CH
Sato, H
Villar, J
Zhang, JB
Dufau, ML
AF Dai, L-S
Tsai-Morris, C. H.
Sato, H.
Villar, J.
Zhang, J-B
Dufau, M. L.
TI Regulation of exclusively testis-expressed microRNA-469 by
Gonadotropin-Regulated Testicular RNA Helicase controls male germ cells
development
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Dai, L-S; Tsai-Morris, C. H.; Sato, H.; Villar, J.; Dufau, M. L.] NICHD, Sect Mol Endocrinol, PDEGEN, NIH, Bethesda, MD USA.
[Dai, L-S; Zhang, J-B] Jilin Univ, Coll Anim Sci & Vet Med, Lab Anim Ctr, Jilin, Jilin, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300444
ER
PT J
AU Dodd, KW
Verkaik-Kloosterman, J
Dekkers, A
vantVeer, P
Ocke, M
AF Dodd, Kevin Wayne
Verkaik-Kloosterman, Janneke
Dekkers, Arnold
vantVeer, Pieter
Ocke, Marga
TI A three-part mixed-effects model to estimate usual total nutrient
distributions from food and dietary supplements
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Dodd, Kevin Wayne] NCI, Biometry Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
[Verkaik-Kloosterman, Janneke; Dekkers, Arnold; Ocke, Marga] Natl Inst Publ Hlth & Environm RIVM, Ctr Nutr & Hlth CVG, Bilthoven, Netherlands.
[vantVeer, Pieter] Wageningen Univ, Div Human Nutr, Wageningen, Netherlands.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305735
ER
PT J
AU Du, LL
Gao, ZG
van Veldhoven, JPD
IJzerman, AP
Jacobson, KA
Auchampach, JA
AF Du, Lili
Gao, Zhan-Guo
van Veldhoven, Jacobus P. D.
IJzerman, Adriaan P.
Jacobson, Kenneth A.
Auchampach, John A.
TI Activity of LUF6000 and LUF6096 as positive allosteric modulators (PAMs)
for the A3 adenosine receptor (AR) is species-dependent
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Du, Lili; Auchampach, John A.] Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA.
[Gao, Zhan-Guo; Jacobson, Kenneth A.] NIDDKD, NIH, Bethesda, MD 20892 USA.
[van Veldhoven, Jacobus P. D.; IJzerman, Adriaan P.] Leiden Univ, LACDR, Div Med Chem, Leiden, Netherlands.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303182
ER
PT J
AU Duchez, B
Milgram, S
Playford, MP
AF Duchez, Brian
Milgram, Sharon
Playford, Martin Peter
TI Characterization of the interaction between Sorting Nexin 27 and
beta-Catenin in kidney epithelial cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Duchez, Brian; Milgram, Sharon; Playford, Martin Peter] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306343
ER
PT J
AU Duncan, T
Samuel, W
Kutty, RK
Redmond, TM
AF Duncan, Todd
Samuel, William
Kutty, R. Krishnan
Redmond, T. Michael
TI Alteration of sphingolipid metabolism during 4-HPR induced cell death in
the ARPE-19 human retinal pigment epithelial cell line
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Duncan, Todd; Samuel, William; Kutty, R. Krishnan; Redmond, T. Michael] NEI, Lab Retinal Cell & Mol Biol, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300958
ER
PT J
AU Dwyer, JT
Bailey, R
Nahin, R
Rogers, G
Sempos, C
Jacques, P
AF Dwyer, Johanna T.
Bailey, Regan
Nahin, Richard
Rogers, Gail
Sempos, Christopher
Jacques, Paul
TI Dietary supplement (DS) use of children < 18 yr in the 2007 National
Health Interview Survey (NHIS)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Dwyer, Johanna T.; Bailey, Regan; Sempos, Christopher] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Nahin, Richard] NCCAM, NIH, Bethesda, MD USA.
[Rogers, Gail; Jacques, Paul] Tufts Univ, USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301271
ER
PT J
AU Dwyer, JT
Bailey, R
Saldanha, L
Holden, J
Andrews, K
Betz, J
Gahche, J
Hardy, C
Milner, J
Roseland, J
AF Dwyer, Johanna T.
Bailey, Regan
Saldanha, Leila
Holden, Joanne
Andrews, Karen
Betz, Joseph
Gahche, Jaime
Hardy, Constance
Milner, John
Roseland, Janet
TI Progress in development of dietary supplement (DS) composition and label
databases for research
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Dwyer, Johanna T.; Bailey, Regan; Saldanha, Leila; Betz, Joseph] Off Dietary Supplements, Bethesda, MD USA.
[Milner, John] NCI, NIH, Bethesda, MD 20892 USA.
[Holden, Joanne; Andrews, Karen; Roseland, Janet] USDA, Nutrient Data Lab, Beltsville, MD 20705 USA.
[Gahche, Jaime] CDC, NCHS, Hysattsville, MD USA.
[Hardy, Constance] US FDA, CFSAN, Silver Spring, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301264
ER
PT J
AU Fantegrossi, WE
Zimmerman, SM
Rice, KC
AF Fantegrossi, William E.
Zimmerman, Sarah M.
Rice, Kenner C.
TI In vivo effects of "bath salt" constituent
3,4-methylenedioxypyrovalerone (MDPV) in mice: contribution of ambient
temperature and monoamines
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Fantegrossi, William E.; Zimmerman, Sarah M.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Rice, Kenner C.] NIDA, Drug Design & Synth Sect, CBRB, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302560
ER
PT J
AU Free, RB
Dalefield, M
Miller, BN
Doyle, TB
Conroy, JL
Vangveravong, S
Duan, LH
Javitch, JA
Mach, RH
Sibley, DR
AF Free, R. Benjamin
Dalefield, Martin
Miller, Brittney N.
Doyle, Trevor B.
Conroy, Jennie L.
Vangveravong, Suwanna
Duan, Lihua
Javitch, Jonathan A.
Mach, Robert H.
Sibley, David R.
TI The antipsychotic aripiprazole is a non-competitive antagonist of
dopamine-stimulated D-2 receptor interactions with beta-arrestin-2
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Free, R. Benjamin; Dalefield, Martin; Miller, Brittney N.; Doyle, Trevor B.; Conroy, Jennie L.; Sibley, David R.] NINDS, MNS, Rockville, MD USA.
[Vangveravong, Suwanna; Mach, Robert H.] Washington Univ, Sch Med, St Louis, MO USA.
[Duan, Lihua; Javitch, Jonathan A.] Columbia Univ Coll Phys & Surg, Ctr Mol Recognit, New York, NY 10032 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304496
ER
PT J
AU Freeman, LB
AF Freeman, Laura Beane
TI Occupational formaldehyde exposure and cancer risk
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Freeman, Laura Beane] NCI, Occupat & Environm Epidemiol Branch, Bethesda, MD 20892 USA.
RI Beane Freeman, Laura/C-4468-2015
OI Beane Freeman, Laura/0000-0003-1294-4124
NR 0
TC 0
Z9 0
U1 0
U2 5
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300260
ER
PT J
AU Gericke, A
Ross, AH
King, KE
Neuman, BM
Jiang, ZP
AF Gericke, Arne
Ross, Alonzo H.
King, Katrice E.
Neuman, Brittany M.
Jiang, Zhiping
TI PTEN binding properties for different model membrane morphologies
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Gericke, Arne; King, Katrice E.; Neuman, Brittany M.] Worcester Polytech Inst, Worcester, MA 01609 USA.
[Ross, Alonzo H.] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Jiang, Zhiping] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306663
ER
PT J
AU Glancy, B
Hsu, LY
Dao, L
Bakalar, M
French, S
Chess, DJ
Taylor, JL
Daniels, MP
Esfahani, S
Balaban, RS
AF Glancy, Brian
Hsu, Li-Yueh
Dao, Lam
Bakalar, Matthew
French, Stephanie
Chess, David J.
Taylor, Joni L.
Daniels, Mathew P.
Esfahani, Shervin
Balaban, Robert S.
TI Capillaries are Embedded in the Sarcolemma of Murine Slow Twitch
Skeletal Muscle Fibers
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Glancy, Brian; Hsu, Li-Yueh; Dao, Lam; Bakalar, Matthew; French, Stephanie; Chess, David J.; Taylor, Joni L.; Daniels, Mathew P.; Esfahani, Shervin; Balaban, Robert S.] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Glancy, Brian/P-3163-2016
OI Glancy, Brian/0000-0002-8571-244X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304871
ER
PT J
AU Goldstein, DS
AF Goldstein, David S.
TI Clinical Methods to Assess Cardiac Sympathetic Innervation and Function
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Goldstein, David S.] NINDS, Clin Neurocardiol Sect, CNP, DIR,NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300122
ER
PT J
AU Green, ML
Manjerovic, MB
Mateus-Pinilla, NE
Kelly, AC
Shelton, P
Novakofski, J
AF Green, Michelle L.
Manjerovic, Mary Beth
Mateus-Pinilla, Nohra E.
Kelly, Amy C.
Shelton, Paul
Novakofski, Jan
TI Determining source populations of newly identified cases of chronic
wasting disease in white-tailed deer
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Green, Michelle L.; Manjerovic, Mary Beth; Kelly, Amy C.; Novakofski, Jan] Univ Illinois, Urbana, IL 61801 USA.
[Green, Michelle L.; Manjerovic, Mary Beth; Mateus-Pinilla, Nohra E.] Univ Illinois, Illinois Nat Hist Survey, Champaign, IL 61820 USA.
[Kelly, Amy C.] NIDDK, NIH, Bethesda, MD USA.
[Shelton, Paul] Illinois Dept Nat Resources, Div Wildlife Resources, Springfield, IL USA.
NR 0
TC 0
Z9 0
U1 0
U2 9
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305775
ER
PT J
AU Groene, HJ
Wang, SJ
Papatriantafyllou, M
Kaya, Z
Burgdorf, S
Young, MF
Schaefer, L
Popovic, ZV
AF Groene, Hermann-Josef
Wang, Shijun
Papatriantafyllou, Maria
Kaya, Ziya
Burgdorf, Sven
Young, Marian F.
Schaefer, Liliana
Popovic, Zoran V.
TI The proteoglycan biglycan enhances antigen-specific T cell activation
potentially via MyD88 and TRIF pathways and triggers autoimmune
perimyocarditis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Groene, Hermann-Josef; Wang, Shijun; Papatriantafyllou, Maria; Popovic, Zoran V.] German Canc Res Ctr, D-6900 Heidelberg, Germany.
[Kaya, Ziya] Univ Heidelberg, Univ Heidelberg Hosp, Heidelberg, Germany.
[Burgdorf, Sven] Univ Hosp Bonn, Inst Mol Med, Bonn, Germany.
[Burgdorf, Sven] Univ Hosp Bonn, Inst Expt Immunol, Bonn, Germany.
[Young, Marian F.] Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, Bethesda, MD USA.
[Schaefer, Liliana] Goethe Univ Clin, Frankfurt, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305878
ER
PT J
AU Guenther, PM
O'Connell, KM
Reedy, J
Kirkpatrick, SI
Hiza, HAB
Kuczynski, KJ
AF Guenther, Patricia M.
O'Connell, Kellie M.
Reedy, Jill
Kirkpatrick, Sharon I.
Hiza, Hazel A. B.
Kuczynski, Kevin J.
TI Development of the Healthy Eating Index-2010
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Guenther, Patricia M.; O'Connell, Kellie M.; Hiza, Hazel A. B.; Kuczynski, Kevin J.] USDA, Ctr Nutr Policy & Promot, Alexandria, VA USA.
[Reedy, Jill; Kirkpatrick, Sharon I.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 7
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301470
ER
PT J
AU Hager, GL
AF Hager, Gordon L.
TI Molecular dynamics of epigenetic transitions
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304569
ER
PT J
AU Hanover, JA
Wang, P
Ghosh, S
Keembiyehetty, C
Comly, M
Bond, M
Krause, M
Love, D
AF Hanover, John A.
Wang, Peng
Ghosh, Salil
Keembiyehetty, Chithra
Comly, Marcy
Bond, Michelle
Krause, Michael
Love, Dona
TI O-GlcNAc cycling and Epigenetics
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Hanover, John A.; Wang, Peng; Ghosh, Salil; Keembiyehetty, Chithra; Comly, Marcy; Bond, Michelle; Love, Dona] NIDDK, LCMB, Bethesda, MD USA.
[Krause, Michael] NIDDK, LMB, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303247
ER
PT J
AU Hiranita, T
Li, LB
Hayashi, S
Cao, JJ
AF Hiranita, Takato
Li, Libin
Hayashi, Shuichiro
Cao, Jianjing
TI Can the Stereotypy-Inducing Effects of Atypical Dopamine Uptake
Inhibitors Account for Their Blockade of Cocaine Self Administration?
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Hiranita, Takato; Li, Libin; Hayashi, Shuichiro; Cao, Jianjing] NIDA IRP NIH DHHS, Mol Targets & Medicat Discovery Branch, Baltimore, MD USA.
RI Hiranita, Takato/G-6567-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304497
ER
PT J
AU Hueschen, CL
Zimmerman, SP
Milgram, SL
Playford, MP
AF Hueschen, Christina Lynn
Zimmerman, Seth Paul
Milgram, Sharon Lynn
Playford, Martin Peter
TI Sorting Nexin 27 mediates PDZ-directed trafficking of Zona-Occludens
(ZO)-2 to the Tight Junction
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Hueschen, Christina Lynn; Zimmerman, Seth Paul; Milgram, Sharon Lynn; Playford, Martin Peter] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306142
ER
PT J
AU Izumi, Y
Burg, MB
Ferraris, JD
AF Izumi, Yuichiro
Burg, Maurice B.
Ferraris, Joan D.
TI Regulated intramembrane proteolysis contributes to control of the
osmoprotective transcription factor, NFAT5.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Izumi, Yuichiro; Burg, Maurice B.; Ferraris, Joan D.] NHLBI, SBC, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301780
ER
PT J
AU Jensen, TB
Pisitkun, T
Hoffert, JD
Fenton, RA
Praetorius, HA
Jensen, UB
Knepper, MA
Praetorius, J
AF Jensen, Thomas Buus
Pisitkun, Trairak
Hoffert, Jason D.
Fenton, Robert A.
Praetorius, Helle A.
Jensen, Uffe Birk
Knepper, Mark A.
Praetorius, Jeppe
TI Identification of proteins regulated by 24-hour aldosterone treatment in
late distal convoluted tubules, connecting tubules and initial cortical
collecting ducts
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Jensen, Thomas Buus; Fenton, Robert A.; Praetorius, Helle A.; Jensen, Uffe Birk; Praetorius, Jeppe] Aarhus Univ, Dept Biomed, Aarhus, Denmark.
[Pisitkun, Trairak; Hoffert, Jason D.; Knepper, Mark A.] NHLBI, Epithelial Syst Biol Lab, NIH, Bethesda, MD 20892 USA.
[Jensen, Uffe Birk] Aarhus Univ Hosp, Dept Clin Med Clin Genet, DK-8000 Aarhus, Denmark.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300729
ER
PT J
AU Johnson, JM
Tominaga, K
Gorospe, M
Abdelmohsen, K
AF Johnson, Jessica Michelle
Tominaga, Kumiko
Gorospe, Myriam
Abdelmohsen, Kotb
TI Regulation of microRNA Expression by AUF1 Through Dicer
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Johnson, Jessica Michelle] Unvers Maryland Eastern Shore, Dept Nat Sci, Princess Anne, MD USA.
[Tominaga, Kumiko; Gorospe, Myriam; Abdelmohsen, Kotb] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301456
ER
PT J
AU Jovic, M
Bojjireddy, N
Kean, M
Gingras, AC
Brill, J
Balla, T
AF Jovic, Marko
Bojjireddy, Naveen
Kean, Michelle
Gingras, Anne-Claude
Brill, Julie
Balla, Tamas
TI Regulation of PI4KII alpha distribution between the Golgi and endosomal
compartments
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Jovic, Marko; Bojjireddy, Naveen; Balla, Tamas] NICHD, NIH, Bethesda, MD USA.
[Kean, Michelle; Gingras, Anne-Claude] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Toronto, ON M5G 1X5, Canada.
[Brill, Julie] Hosp Sick Children, Cell Biol Program, Toronto, ON M5G 1X8, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306265
ER
PT J
AU Kang, GS
Cates, K
Pacheco-Rodriguez, G
Meza-Carmen, V
Daniels, M
Connelly, P
Moss, J
Vaughan, M
AF Kang, Gi Soo
Cates, Krystal
Pacheco-Rodriguez, Gustavo
Meza-Carmen, Victor
Daniels, Mathew
Connelly, Patricia
Moss, Joel
Vaughan, Martha
TI Role of ADP-ribosylation factor domain protein 1 (ARD1/TRIM23) on
lysosome biogenesis and function
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kang, Gi Soo; Cates, Krystal; Pacheco-Rodriguez, Gustavo; Meza-Carmen, Victor; Daniels, Mathew; Connelly, Patricia; Moss, Joel; Vaughan, Martha] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302936
ER
PT J
AU Kant, AK
Graubard, BI
AF Kant, Ashima K.
Graubard, Barry I.
TI Race/ethnicity, family income, and education differentials in
nutritional biomarkers in American children and adolescents: NHANES
2003-2006
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kant, Ashima K.] CUNY, Queens Coll, FNES, Flushing, NY USA.
[Graubard, Barry I.] NCI, Biostat Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306234
ER
PT J
AU Kaur, S
Kuznetsova, SA
Pendrak, ML
Sipes, JM
Roberts, DD
AF Kaur, Sukhbir
Kuznetsova, Svetlana A.
Pendrak, Michael L.
Sipes, John M.
Roberts, David D.
TI Thrombospondin-1 signaling via CD47 regulates T lymphocyte
glycosaminoglycan biosynthesis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kaur, Sukhbir; Kuznetsova, Svetlana A.; Pendrak, Michael L.; Sipes, John M.; Roberts, David D.] NIH, Pathol Lab, Bethesda, MD 20892 USA.
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302638
ER
PT J
AU Kelly, A
Shewmaker, F
Wickner, R
AF Kelly, Amy
Shewmaker, Frank
Wickner, Reed
TI Molecular Analysis of Genetic Variation in Prions of Saccharomyces
cerevisiae
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kelly, Amy; Wickner, Reed] NIDDK, NIH, Bethesda, MD USA.
[Shewmaker, Frank] Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304834
ER
PT J
AU Khan, FA
Szabo-Fresnais, N
Krall, J
Moss, J
Vaughan, M
Movsesian, M
Manganiello, V
AF Khan, Faiyaz Ahmad
Szabo-Fresnais, Nicolas
Krall, Judy
Moss, Joel
Vaughan, Martha
Movsesian, Matthew
Manganiello, Vincent
TI PKA-induced Interaction of Phosphorylated PDE3A (pPDE3A) and BIG1
(Brefeldin A-inhibited guanine nucleotide exchange protein 1) in
Cytosolic Fractions from Human Myocardium may be Important in Regulation
of BIG1 Function
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Khan, Faiyaz Ahmad; Moss, Joel; Vaughan, Martha; Manganiello, Vincent] NHLBI, NIH, CPB, Bethesda, MD 20892 USA.
[Szabo-Fresnais, Nicolas; Krall, Judy; Movsesian, Matthew] Univ Utah, Div Cardiol, Salt Lake City, UT 84112 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305498
ER
PT J
AU Kim, EK
Kim, YS
Yu, LL
Milner, JA
Wang, TTY
AF Kim, Eun-Kyung
Kim, Young S.
Yu, Liangli
Milner, John A.
Wang, Thomas T. Y.
TI Broccoli-derived compounds modulate androgen up-regulation of C-C
chemokine ligand 2 and enhancement of monocyte attraction to prostate
cancer cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kim, Eun-Kyung; Yu, Liangli] Univ Maryland, College Pk, MD 20742 USA.
[Kim, Young S.; Milner, John A.] NCI, Nutr Sci Res Grp, Rockville, MD USA.
[Wang, Thomas T. Y.] ARS, Diet Genom & Immunol Lab, USDA, Beltsville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304484
ER
PT J
AU Kimura, AK
Kim, HY
AF Kimura, Atsuko Kakio
Kim, Hee-Yong
TI Acyl chain dependent product inhibition by phosphatidylserine synthases
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kimura, Atsuko Kakio; Kim, Hee-Yong] NIAAA, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306538
ER
PT J
AU Kobilo, T
van Praag, H
AF Kobilo, Tali
van Praag, Henriette
TI Cognitive and motor effects of endurance related compound AICAR: from
muscle to brain
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kobilo, Tali; van Praag, Henriette] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300384
ER
PT J
AU Kochukov, MY
Balasubramanian, A
Abramowitz, J
Birnbaumer, L
Marrelli, SP
AF Kochukov, Mikhail Y.
Balasubramanian, Adithya
Abramowitz, Joel
Birnbaumer, Lutz
Marrelli, Sean P.
TI Role of TRPC1 and TRPC3 channels in constriction and relaxation of mouse
thoracic aorta
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kochukov, Mikhail Y.; Balasubramanian, Adithya; Marrelli, Sean P.] Baylor Coll Med, Houston, TX 77030 USA.
[Abramowitz, Joel; Birnbaumer, Lutz] NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305093
ER
PT J
AU Kraft, ML
Klitzing, HA
Lou, KY
Zimmerberg, J
Weber, PK
AF Kraft, Mary L.
Klitzing, Haley A.
Lou, Kaiyan
Zimmerberg, Joshua
Weber, Peter K.
TI Time-dependent changes in long range sphingolipid organization revealed
by high-resolution secondary ion mass spectrometry
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kraft, Mary L.; Lou, Kaiyan] Univ Illinois, Dept Chem & Biomol Engn, Urbana, IL 61801 USA.
[Kraft, Mary L.; Klitzing, Haley A.] Univ Illinois, Dept Chem, Urbana, IL 61801 USA.
[Zimmerberg, Joshua] NICHHD, NIH, Bethesda, MD 20892 USA.
[Weber, Peter K.] Lawrence Livermore Natl Lab, Glenn T Seaborg Inst, Livermore, CA USA.
RI Lou, Kaiyan/D-4199-2012
OI Lou, Kaiyan/0000-0003-3443-0343
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711307263
ER
PT J
AU Kraft, ML
Frisz, JF
Klitzing, HA
Lou, KY
Lizunov, V
Zimmerberg, J
Weber, PK
AF Kraft, Mary L.
Frisz, Jessica F.
Klitzing, Haley A.
Lou, Kaiyan
Lizunov, Vladimir
Zimmerberg, Joshua
Weber, Peter K.
TI Chemical Imaging of Cholesterol and Sphingolipid Distribution in the
Plasma Membranes of Fibroblast Cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Kraft, Mary L.; Lou, Kaiyan] Univ Illinois, Dept Chem & Biomol Engn, Urbana, IL 61801 USA.
[Frisz, Jessica F.; Klitzing, Haley A.] Univ Illinois, Dept Chem, Urbana, IL 61801 USA.
[Lizunov, Vladimir; Zimmerberg, Joshua] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Weber, Peter K.] Lawrence Livermore Natl Lab, Glenn T Seaborg Inst, Livermore, CA USA.
RI Lou, Kaiyan/D-4199-2012
OI Lou, Kaiyan/0000-0003-3443-0343
NR 0
TC 0
Z9 0
U1 0
U2 10
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711307173
ER
PT J
AU Labrique, AB
Klein, S
Kmush, B
Ali, H
Engle, R
Schulze, K
Purcell, R
West, KP
Nelson, KE
AF Labrique, Alain Bernard
Klein, Sabra
Kmush, Brittany
Ali, Hasmot
Engle, Ronald
Schulze, Kerry
Purcell, Robert
West, Keith P., Jr.
Nelson, Kenrad E.
TI IMMUNOLOGIC DYSREGULATION AND MICRONUTRIENT DEFICIENCIES ASSOCIATED WITH
RISK OF INTRAPARTUM HEPATITIS E INFECTIONS IN PREGNANT BANGLADESHI WOMEN
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Labrique, Alain Bernard; Klein, Sabra; Kmush, Brittany; Schulze, Kerry; West, Keith P., Jr.; Nelson, Kenrad E.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Ali, Hasmot] Johns Hopkins Univ Bangladesh, JiVitA Maternal & Child Res Project, Gaibandha, Bangladesh.
[Engle, Ronald; Purcell, Robert] NIH, Hepatitis Viruses Sect, Infect Dis Lab, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306802
ER
PT J
AU Lal, A
Thomas, M
Navarro, F
Li, XL
Lieberman, J
AF Lal, Ashish
Thomas, Marshall
Navarro, Francisco
Li, Xiao Ling
Lieberman, Judy
TI A microRNA pulldown approach uncovers regulation of p53 activity and
growth factor signaling by miR-34a
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Lal, Ashish] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Thomas, Marshall; Navarro, Francisco; Lieberman, Judy] Harvard Univ, Sch Med, Boston, MA USA.
RI Lieberman, Judy/A-2717-2015
NR 0
TC 0
Z9 0
U1 0
U2 5
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300364
ER
PT J
AU Le, K
Pacheco-Rodriguez, G
Moss, J
Vaughan, M
AF Le, Kang
Pacheco-Rodriguez, Gustavo
Moss, Joel
Vaughan, Martha
TI Tripartite motif protein 23 (TRIM23) regulates degradation of epidermal
growth factor receptor (EGFR)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Le, Kang; Pacheco-Rodriguez, Gustavo; Moss, Joel; Vaughan, Martha] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302949
ER
PT J
AU Lezin, G
Kosaka, Y
Yost, HJ
Kuehn, MR
Brunelli, L
AF Lezin, George
Kosaka, Yasuhiro
Yost, H. Joseph
Kuehn, Michael R.
Brunelli, Luca
TI Differentiating frequency of recombination from frequency of
recombinants
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Lezin, George; Kosaka, Yasuhiro; Yost, H. Joseph; Brunelli, Luca] Univ Utah, Salt Lake City, UT USA.
[Kuehn, Michael R.] NCI, Canc Res Ctr, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301203
ER
PT J
AU Lezin, G
Kosaka, Y
Yost, HJ
Kuehn, MR
Brunelli, L
AF Lezin, George
Kosaka, Yasuhiro
Yost, H. Joseph
Kuehn, Michael R.
Brunelli, Luca
TI A novel approach to isolate unselected recombinants facilitates
markerless DNA recombineering
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Lezin, George; Kosaka, Yasuhiro; Yost, H. Joseph; Brunelli, Luca] Univ Utah, Salt Lake City, UT USA.
[Kuehn, Michael R.] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301185
ER
PT J
AU Li, CC
Shen, XY
Aponte, A
Shen, RF
Billings, EM
Moss, J
Vaughan, M
AF Li, Chun-Chun
Shen, Xiaoyan
Aponte, Angel
Shen, Rong-Fong
Billings, Eric M.
Moss, Joel
Vaughan, Martha
TI BIG2, an ARF guanine nucleotide-exchange protein, regulates cell
migration via effects integrin beta 1 cycling and actin cytoskeleton
remodeling
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Li, Chun-Chun; Shen, Xiaoyan; Moss, Joel; Vaughan, Martha] NHLBI, Cardiovasc & Pulm Branch, Bethesda, MD 20892 USA.
[Aponte, Angel; Shen, Rong-Fong; Billings, Eric M.] NHLBI, Prote Core Facil, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302765
ER
PT J
AU Li, HY
Tu, HB
Wang, YH
Levine, M
AF Li, Hongyan
Tu, Hongbin
Wang, Yaohui
Levine, Mark
TI Assay of Vitamin C in Red Blood Cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Li, Hongyan; Tu, Hongbin; Wang, Yaohui; Levine, Mark] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303243
ER
PT J
AU Lyon, AM
Tesmer, VM
Boguth, CA
Dhamsania, VD
Thal, DM
Guiterrez, J
Chowdhury, S
Northup, JK
Tesmer, JJG
AF Lyon, Angeline Marie
Tesmer, Valerie M.
Boguth, Cassandra A.
Dhamsania, Vishan D.
Thal, David M.
Guiterrez, Joanne
Chowdhury, Shoaib
Northup, John K.
Tesmer, John J. G.
TI How G alpha(q) Regulates PIP2 Hydrolysis: Molecular Mechanisms and
Prospects for Drug Development
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Lyon, Angeline Marie; Tesmer, Valerie M.; Boguth, Cassandra A.; Dhamsania, Vishan D.; Thal, David M.; Tesmer, John J. G.] Univ Michigan, Life Sci Inst, Ann Arbor, MI 48109 USA.
[Guiterrez, Joanne; Chowdhury, Shoaib; Northup, John K.] NIDCD, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301100
ER
PT J
AU Malicdan, MC
Momma, K
Nishino, I
Noguchi, S
AF Malicdan, May Christine
Momma, Kazunari
Nishino, Ichizo
Noguchi, Satoru
TI Identification of biomarkers for GNE myopathy
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Malicdan, May Christine] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Malicdan, May Christine; Momma, Kazunari; Nishino, Ichizo; Noguchi, Satoru] Natl Inst Neurosci, Dept Neuromuscular Res, Tokyo, Japan.
[Momma, Kazunari] Natl Def Med Coll, Dept Neurol, Saitama, Japan.
RI Malicdan, May Christine/F-2806-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 2
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306981
ER
PT J
AU Manjerovic, MB
Green, ML
Kelly, AC
Mateus-Pinilla, NE
Shelton, P
Novakofski, J
AF Manjerovic, Mary Beth
Green, Michelle L.
Kelly, Amy C.
Mateus-Pinilla, Nohra E.
Shelton, Paul
Novakofski, Jan
TI Spatial variation in susceptibility to chronic wasting disease in
white-tailed deer
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Manjerovic, Mary Beth; Green, Michelle L.; Mateus-Pinilla, Nohra E.] Univ Illinois, Illinois Nat Hist Survey, Champaign, IL 61820 USA.
[Manjerovic, Mary Beth; Green, Michelle L.; Kelly, Amy C.; Novakofski, Jan] Univ Illinois, Urbana, IL 61801 USA.
[Kelly, Amy C.] NIDDK, NIH, Bethesda, MD USA.
[Shelton, Paul] Illinois Dept Nat Resources, Div Wildlife Resources, Springfield, IL USA.
NR 0
TC 0
Z9 0
U1 0
U2 9
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305776
ER
PT J
AU Mashimo, M
Niere, M
Agledal, L
Dolle, C
Kasamatsu, A
Kato, J
Moss, J
Ziegler, M
AF Mashimo, Masato
Niere, Marc
Agledal, Line
Dolle, Christian
Kasamatsu, Atsushi
Kato, Jiro
Moss, Joel
Ziegler, Mathias
TI ARH3 catalyzes degradation of mitochondrial matrix-accumulated Poly
(ADP-ribose)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Mashimo, Masato; Kasamatsu, Atsushi; Kato, Jiro; Moss, Joel] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Niere, Marc; Agledal, Line; Dolle, Christian; Ziegler, Mathias] Univ Bergen, Dept Mol Biol, Bergen, Norway.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303055
ER
PT J
AU McCarthy, P
Saksena, R
Peterson, D
Lee, CH
An, YM
Vionnet, J
Cipollo, J
Vann, W
AF McCarthy, Pumtiwitt
Saksena, Rina
Peterson, Dwight
Lee, Che-Hung
An, Yanming
Vionnet, Justine
Cipollo, John
Vann, Willie
TI Towards a Well Defined Meningitis Vaccine: Chemoenzymatic Synthesis of
Meningococcal Glycoconjugate Vaccine Candidates
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [McCarthy, Pumtiwitt] NIH NIGMS, Bethesda, MD USA.
[McCarthy, Pumtiwitt; Saksena, Rina; Peterson, Dwight; Lee, Che-Hung; An, Yanming; Vionnet, Justine; Cipollo, John; Vann, Willie] CBER FDA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305767
ER
PT J
AU Mereu, M
Chun, LE
Hiranita, T
Cao, JJ
Newman, A
Katz, JL
Tanda, G
AF Mereu, Maddalena
Chun, Lauren E.
Hiranita, Takato
Cao, Jian Jing
Newman, Amy
Katz, Jonathan L.
Tanda, Gianluigi
TI Rimcazole Attenuates the Cocaine-Induced Stimulation of Mesolimbic
Dopamine related to its Abuse and Dependence
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Mereu, Maddalena; Hiranita, Takato; Cao, Jian Jing; Newman, Amy; Katz, Jonathan L.; Tanda, Gianluigi] NIDA, Mol Targets & Medicat Discovery Branch, NIH, Baltimore, MD USA.
[Chun, Lauren E.] Univ Colorado, Spencer Neuroendocrinol Lab, Boulder, CO 80309 USA.
RI Tanda, Gianluigi/B-3318-2009; Hiranita, Takato/G-6567-2011
OI Tanda, Gianluigi/0000-0001-9526-9878;
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305409
ER
PT J
AU Midthune, DN
Carroll, RJ
Subar, AF
Freedman, LS
Thompson, FE
Kipnis, V
AF Midthune, Douglas Neil
Carroll, Raymond J.
Subar, Amy F.
Freedman, Laurence S.
Thompson, Frances E.
Kipnis, Victor
TI Combining self-report dietary assessment instruments to reduce the
effects of measurement error
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Midthune, Douglas Neil; Kipnis, Victor] NCI, Canc Prevent Div, Biometry Res Grp, Bethesda, MD 20892 USA.
[Subar, Amy F.; Thompson, Frances E.] NCI, Div Canc Control & Populat Sci, Risk Factor Monitoring & Methods Branch, Bethesda, MD 20892 USA.
[Carroll, Raymond J.] Texas A&M Univ, Dept Stat, College Stn, TX 77843 USA.
[Freedman, Laurence S.] Gertner Inst Epidemiol & Publ Hlth Policy, Biostat Unit, Tel Hashomer, Israel.
NR 0
TC 0
Z9 0
U1 1
U2 7
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305805
ER
PT J
AU Miller, DS
Schroeter, C
Wang, XQ
Campos, CR
AF Miller, David S.
Schroeter, Christian
Wang, Xueqian
Campos, Christopher R.
TI ABC Transporter Expression, Function and Regulation at the Blood-Spinal
Cord Barrier
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Miller, David S.; Wang, Xueqian; Campos, Christopher R.] NIEHS, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
[Schroeter, Christian] Univ Heidelberg, Heidelberg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302473
ER
PT J
AU Miller, DS
Campos, CR
Hawkins, BT
Cannon, R
AF Miller, David S.
Campos, Christopher R.
Hawkins, Brian T.
Cannon, Ronald
TI Sphingolipids signal rapid loss of P-glycoprotein transport activity at
the blood-brain barrier
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Miller, David S.; Campos, Christopher R.; Cannon, Ronald] NIEHS, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
[Hawkins, Brian T.] Univ Washington, Div Hematol, Sch Med, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300902
ER
PT J
AU Miller, TW
Song, T
Amarnath, S
Fowler, DH
Roberts, DD
AF Miller, Thomas W.
Song, Timothy
Amarnath, Shoba
Fowler, Daniel H.
Roberts, David D.
TI Hydrogen sulfide (H2S) regulates hypoxic signaling in T cells.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Miller, Thomas W.; Song, Timothy; Roberts, David D.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303260
ER
PT J
AU Mizrahi, V
Warner, D
Ndwandwe, D
Abrahams, G
Venclovas, C
AF Mizrahi, Valerie
Warner, Digby
Ndwandwe, Duduzile
Abrahams, Garth
Venclovas, Ceslovas
TI A novel inducible mutagenesis system in Mycobacterium tuberculosis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Mizrahi, Valerie; Warner, Digby; Abrahams, Garth] Univ Cape Town, Inst Infect Dis & Mol Med, ZA-7925 Cape Town, South Africa.
[Ndwandwe, Duduzile] Univ Witwatersrand, Ctr Excellence Biomed TB Res, Johannesburg, South Africa.
[Abrahams, Garth] NIAID, TB Res Sect, Lab CLin Infect Dis, Bethesda, MD 20892 USA.
[Venclovas, Ceslovas] Inst Biotechnol, Lab Bioinformat, Vilnius, Lithuania.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300201
ER
PT J
AU Murray, DR
Valente, AJ
Siebenlist, U
Chandrasekar, B
AF Murray, David R.
Valente, Anthony J.
Siebenlist, Ulrich
Chandrasekar, Bysani
TI CIKS is critical mediator of isoproterenol/beta-AR induced cardiomyocyte
hypertrophy in vitro and in vivo
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Murray, David R.] William S Middleton Mem Vet Adm Med Ctr, Madison, WI USA.
[Valente, Anthony J.] Univ Texas HSC, San Antonio, TX USA.
[Siebenlist, Ulrich] NIAID, Lab Immunoregulat, NIH, Bethesda, MD 20892 USA.
[Chandrasekar, Bysani] SLVHCS, New Orleans, LA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304479
ER
PT J
AU Nader, SH
Blaylock, BL
Wilson, WD
Banala, A
Newman, AH
Nader, MA
AF Nader, Susan H.
Blaylock, B. L.
Wilson, W. D.
Banala, A.
Newman, A. H.
Nader, M. A.
TI Characterization of Dopamine D3 receptor-selective compounds on
unconditioned behaviors and food/drug choice in cocaine and
methamphetamine self-administering rhesus monkeys
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Nader, Susan H.; Blaylock, B. L.; Wilson, W. D.; Nader, M. A.] Wake Forest Sch Med, Winston Salem, NC USA.
[Banala, A.; Newman, A. H.] NIDA IRP, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301467
ER
PT J
AU Namaste, S
Ashour, F
Porter, A
Raghavan, R
Pilch, S
Raiten, D
AF Namaste, Sorrel
Ashour, Fayrouz
Porter, Alexandra
Raghavan, Ramkripa
Pilch, Susan
Raiten, Daniel
TI Effect modifiers for the safety and efficacy of iron intervention in the
context of malaria: A review of data for an individual patient based
meta-analysis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Namaste, Sorrel; Ashour, Fayrouz; Porter, Alexandra; Raghavan, Ramkripa; Raiten, Daniel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Pilch, Susan] Natl Inst Hlth Lib, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304735
ER
PT J
AU Nanda, JS
Munoz, A
Saini, AK
Hinnebusch, AG
AF Nanda, Jagpreet Singh
Munoz, Antonio
Saini, Adesh K.
Hinnebusch, Alan G.
TI Coordinated movement of eukaryotic translation initiation factors 1, 1A,
and 5 within the 43S ribosomal preinitiation complex (PIC) mediates the
response to start codon recognition.
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Nanda, Jagpreet Singh; Munoz, Antonio] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Saini, Adesh K.] Shoolini Univ Biotechnol, Shimla, India.
[Hinnebusch, Alan G.] NICHD, Lab Gene Regulat & Dev, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300595
ER
PT J
AU Nayeem, MA
Zeldin, DC
Pradhan, I
Mustafa, SJ
Falck, JR
Morisseau, C
Marowsky, A
AF Nayeem, Mohammed A.
Zeldin, Darryl C.
Pradhan, Isha
Mustafa, S. Jamal
Falck, John R.
Morisseau, Christophe
Marowsky, Anne
TI Disruption of soluble epoxide hydrolase modulates adenosine-induced
response: role of adenosine A2A receptor and cyp-epoxygenases
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Nayeem, Mohammed A.; Pradhan, Isha; Mustafa, S. Jamal] W Virginia Univ, Ctr Cardiovasc & Resp Sci, Morgantown, WV 26506 USA.
[Zeldin, Darryl C.] NIEHS, Div Intramural Res, NIH, Res Triangle Pk, NC 27709 USA.
[Falck, John R.] UTSWMC, Dallas, TX USA.
[Morisseau, Christophe] Univ Calif Davis, Dept Entomol, Davis, WV USA.
[Marowsky, Anne] Univ Calif Davis, UCD Canc Ctr, Davis, WV USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300295
ER
PT J
AU Nelson, SM
Carlson, B
Urban, J
Lei, XG
Hatfield, D
Prabhu, KS
AF Nelson, Shakira M.
Carlson, Bradley
Urban, Joseph
Lei, Xingen
Hatfield, Dolph
Prabhu, K. Sandeep
TI Selenoprotein induced M1 to M2 murine macrophage phenotype switching is
imperative in helminth parasite clearance
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Nelson, Shakira M.; Prabhu, K. Sandeep] Penn State Univ, University Pk, PA 16802 USA.
[Carlson, Bradley; Hatfield, Dolph] NCI, Bethesda, MD 20892 USA.
[Urban, Joseph] USDA, Beltsville, MD 20705 USA.
[Lei, Xingen] Cornell Univ, Ithaca, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303681
ER
PT J
AU Ness, EC
Lazrak, A
Jackson, JM
Garantziotis, S
Matalon, S
AF Ness, Emily Christine
Lazrak, Ahmed
Jackson, Justin M.
Garantziotis, Stavros
Matalon, Sadis
TI Inhibition of Epithelial Sodium Channel Activity by Inter-alpha-Trypsin
Inhibitor
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Ness, Emily Christine; Lazrak, Ahmed; Jackson, Justin M.; Matalon, Sadis] Univ Alabama Birmingham, Birmingham, AL USA.
[Garantziotis, Stavros] NIEHS, Clin Res Unit, Res Triangle Pk, NC 27709 USA.
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305518
ER
PT J
AU Noguchi, S
Malicdan, MC
Funato, F
Nishino, I
AF Noguchi, Satoru
Malicdan, May Christine
Funato, Fumiko
Nishino, Ichizo
TI Metabolic changes in sialic acid synthesis pathway in GNE-myopathy model
mice with long-term sialic acid treatment
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Noguchi, Satoru; Funato, Fumiko; Nishino, Ichizo] NCNP, Dept Neuromuscular Res, Natl Inst Neurosci, Tokyo, Japan.
[Malicdan, May Christine] NHGRI, MGB, NIH, Bethesda, MD 20892 USA.
RI Malicdan, May Christine/F-2806-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306949
ER
PT J
AU Oubrahim, H
Wong, A
Wilson, B
Chock, PB
AF Oubrahim, Hammou
Wong, Allison
Wilson, Brenda
Chock, P. Boon
TI On the mechanism of Pasteurella multocida toxin (PMT) induced
mitogenesis: mTOR mediated upregulation of survivin and aurora kinase B
in cultured cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Oubrahim, Hammou; Wong, Allison; Chock, P. Boon] NHLBI, Biochem Lab, BBC, NIH, Bethesda, MD 20892 USA.
[Wilson, Brenda] Univ Illinois, Dept Microbiol, Urbana, IL USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305352
ER
PT J
AU Pathan, AR
Bowlin, BM
Machaca, K
Abramowitz, J
Zheng, F
Rusch, NJ
AF Pathan, Asif R.
Bowlin, Brandi M.
Machaca, Khaled
Abramowitz, Joel
Zheng, Fang
Rusch, Nancy J.
TI Phenylephrine-induced current and vasoconstriction are blunted in
mesenteric arteries of TRPC3 knockout mice
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Pathan, Asif R.; Bowlin, Brandi M.; Zheng, Fang; Rusch, Nancy J.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Machaca, Khaled] Weill Cornell Med Coll Qatar, Doha, Qatar.
[Abramowitz, Joel] NIEHS, Lab Neurobiol, Div Intramural Res, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304530
ER
PT J
AU Patial, S
Stumpo, DJ
Lai, WS
Ward, TW
Blackshear, PJ
AF Patial, Sonika
Stumpo, Deborah J.
Lai, Wi S.
Ward, Toni W.
Blackshear, Perry J.
TI Genetic deletion of an instability motif in the Tristetraprolin (TTP)
transcript: Implications for the treatment of systemic inflammation
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Patial, Sonika; Stumpo, Deborah J.; Lai, Wi S.; Ward, Toni W.; Blackshear, Perry J.] NIEHS, LST, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304454
ER
PT J
AU Pradhan, I
Mustafa, SJ
Zeldin, DC
Ledent, C
Falck, JR
Nayeem, MA
AF Pradhan, Isha
Mustafa, S. Jamal
Zeldin, Darryl C.
Ledent, Catherine
Falck, J. R.
Nayeem, Mohammed A.
TI Salt modulates vascular response through cyp-epoxygenases in the
presence of A(2A) AR
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Pradhan, Isha; Mustafa, S. Jamal; Nayeem, Mohammed A.] W Virginia Univ, Morgantown, WV 26506 USA.
[Zeldin, Darryl C.] NIEHS, Div Pulm, NIH, Res Triangle Pk, NC 27709 USA.
[Ledent, Catherine] Univ Libre Brussels, IRIBHN, B-1070 Brussels, Belgium.
[Falck, J. R.] Univ Texas Dallas, Dallas, TX 75230 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304880
ER
PT J
AU Qu, AJ
Li, F
Krausz, K
Shah, YM
Gonzalez, FJ
AF Qu, Aijuan
Li, Fei
Krausz, Kristopher
Shah, Yatrik M.
Gonzalez, Frank J.
TI Metabolomics Reveals the role of hypoxia-inducible factors in
hypoxia-induced liver metabolic shift
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Qu, Aijuan; Li, Fei; Krausz, Kristopher; Gonzalez, Frank J.] NCI, Lab Metab, CCR, NIH, Bethesda, MD 20892 USA.
[Shah, Yatrik M.] Univ Michigan, Sch Med, Dept Mol & Integrat Physiol, Ann Arbor, MI USA.
RI Li, Fei/F-6849-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301726
ER
PT J
AU Raghavan, R
Darnton-Hill, I
Raiten, DJ
AF Raghavan, Ramkripa
Darnton-Hill, Ian
Raiten, Daniel J.
TI Biomarkers of Nutrition for Development (BOND): An Overview
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Raghavan, Ramkripa; Raiten, Daniel J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Endocrinol Nutr & Growth Branch, Bethesda, MD USA.
[Darnton-Hill, Ian] Univ Sydney, Boden Inst Obes Nutr & Exercise, Sydney, NSW 2006, Australia.
[Darnton-Hill, Ian] Tufts Univ, Friedman Sch Nutr Sci & Policy, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305721
ER
PT J
AU Rahman, GM
Sanker, S
Lewin, N
Prasad, BVV
Blumberg, PM
Das, J
AF Rahman, Ghazi M.
Sanker, Sreejesh
Lewin, Nancy
Prasad, B. V. V.
Blumberg, Peter M.
Das, Joydip
TI Identification of the activator binding residues in protein kinase C
theta C1B domain
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Rahman, Ghazi M.; Das, Joydip] Univ Houston, Dept Pharmacol & Pharmaceut Sci, Houston, TX USA.
[Sanker, Sreejesh; Prasad, B. V. V.] Baylor Coll Med, Dept Mol Virol & Microbiol, Houston, TX 77030 USA.
[Lewin, Nancy; Blumberg, Peter M.] NCI, Lab Canc Biol & Genet, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305724
ER
PT J
AU Rajagopal, V
Park, EH
Hinnebusch, AG
Lorsch, JR
AF Rajagopal, Vaishnavi
Park, Eun-Hee
Hinnebusch, Alan G.
Lorsch, Jon R.
TI Specific domains in yeast eukaryotic Initiation Factor (eIF) 4G bias the
RNA unwinding specificity of eIF4F towards duplexes with a 5 '-overhang
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Rajagopal, Vaishnavi; Lorsch, Jon R.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Park, Eun-Hee; Hinnebusch, Alan G.] NICHD, Program Cellular Regulat & Metab, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300777
ER
PT J
AU Reece, KM
Richardson, ED
Pisle, ST
Holly, AJ
Campbell, TJ
Figg, WD
AF Reece, Kelie M.
Richardson, Emily D.
Pisle, Stephen T.
Holly, Alesia J.
Campbell, Tessa J.
Figg, William D.
TI Disruption of the HIF-1 alpha/p300 interaction as a means of inhibiting
angiogenesis
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Reece, Kelie M.; Richardson, Emily D.; Holly, Alesia J.; Campbell, Tessa J.; Figg, William D.] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[Pisle, Stephen T.] NCI, Clin Pharmacol Program, SAIC Frederick, Frederick, MD 21701 USA.
RI Figg Sr, William/M-2411-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303517
ER
PT J
AU Rhee, DK
Hockman, SC
Ahmad, F
Manganiello, VC
AF Rhee, Dong Keun
Hockman, Steven Craig
Ahmad, Faiyaz
Manganiello, Vincent C.
TI Heterologous expression of human phosphodiesterase 3A (hPDE3A) improves
ethanol production in Saccharomyces cerevisiae
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Rhee, Dong Keun; Hockman, Steven Craig; Ahmad, Faiyaz; Manganiello, Vincent C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304721
ER
PT J
AU Rhee, DK
Hockman, SC
Manganiello, VC
AF Rhee, Dong Keun
Hockman, Steven Craig
Manganiello, Vincent C.
TI Heterologous expression of human phosphodiesterase 3A affects
calcineurin-mediated calcium homeostasis in yeast
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Rhee, Dong Keun; Hockman, Steven Craig; Manganiello, Vincent C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304595
ER
PT J
AU Roof, RA
Bergman, J
Furman, CA
Conroy, JL
Mello, NK
Skolnick, P
Sibley, DR
AF Roof, Rebecca A.
Bergman, Jack
Furman, Chersyse A.
Conroy, Jennie L.
Mello, Nancy K.
Skolnick, Phil
Sibley, David R.
TI Buspirone is a potent antagonist at D-3 and D-4 Dopamine Receptors and
attenuates the reinforcing effects of cocaine in a primate model
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Roof, Rebecca A.; Conroy, Jennie L.; Sibley, David R.] NINDS, Mol Neuropharmacol Sect, NIH, Rockville, MD USA.
[Bergman, Jack; Mello, Nancy K.] Harvard Univ, McLean Hosp, Sch Med, Belmont, MA USA.
[Furman, Chersyse A.] NIH, Off Sci Policy Anal, Rockville, MD USA.
[Skolnick, Phil] NIDA, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300539
ER
PT J
AU Saito, K
Moore, R
Negishi, M
AF Saito, Kosuke
Moore, Rick
Negishi, Masahiko
TI p38 MAPK signaling determines CAR-mediated activation of the CYP2B genes
by xenobiotics
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Saito, Kosuke; Moore, Rick; Negishi, Masahiko] NIEHS, LRDT, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302972
ER
PT J
AU Saldanha, LG
Dwyer, JT
Holden, JM
Andrews, KW
Bailey, RL
Betz, JM
Gahche, JJ
Hardy, CJ
Milner, J
Roseland, JM
AF Saldanha, Leila G.
Dwyer, Johanna T.
Holden, Joanne M.
Andrews, Karen W.
Bailey, Regan L.
Betz, Joseph M.
Gahche, Jaime J.
Hardy, Constance J.
Milner, John
Roseland, Janet M.
TI Identifying non-vitamin & mineral bioactive (non-VM) ingredients for
inclusion in Dietary Supplement (DS) Composition Databases
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Milner, John] NCI, NIH, Bethesda, MD 20892 USA.
[Saldanha, Leila G.; Dwyer, Johanna T.; Bailey, Regan L.; Betz, Joseph M.] Off Dietary Supplements, Bethesda, MD USA.
[Holden, Joanne M.; Andrews, Karen W.; Roseland, Janet M.] ARS, USDA, Beltsville, MD USA.
[Gahche, Jaime J.] CDC, NHANES, NCHS, Hyattsville, MD USA.
[Hardy, Constance J.] US FDA, CFSAN, College Pk, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302966
ER
PT J
AU Samuel, W
Kutty, RK
Duncan, T
Redmond, TM
AF Samuel, William
Kutty, R. Krishnan
Duncan, Todd
Redmond, T. Michael
TI Endoplasmic reticulum stress induces the degradation of stearoyl-CoA
desaturase protein in human retinal pigment epithelial cells via
ubiquitin-proteasome pathway
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Samuel, William; Kutty, R. Krishnan; Duncan, Todd; Redmond, T. Michael] NEI, LRCMB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300959
ER
PT J
AU Sankavaram, K
Mattison, J
de Cabo, R
Pearson, K
Allard, J
AF Sankavaram, Kavitha
Mattison, Julie
de Cabo, Rafael
Pearson, Kevin
Allard, Joanne
TI Resveratrol improves cerebrospinal fluid neuroprotective biomarkers in
monkeys fed with a high-fat high-sugar diet
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Sankavaram, Kavitha; Allard, Joanne] Howard Univ, Washington, DC 20059 USA.
[Sankavaram, Kavitha; Mattison, Julie; de Cabo, Rafael] NIA, Lab Expt Biol, Baltimore, MD 21224 USA.
[Pearson, Kevin] Univ Kentucky, Grad Ctr Nutr Sci, Lexington, KY USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304717
ER
PT J
AU Schindler, C
Baumann, MH
Thorndike, EB
Blough, BE
Goldberg, SR
AF Schindler, Charles
Baumann, Michael H.
Thorndike, Eric B.
Blough, Bruce E.
Goldberg, Steven R.
TI Effects of 3,4-methylenedioxymethamphetamine (MDMA) and its metabolites
on cardiovascular function in rats
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Schindler, Charles; Baumann, Michael H.; Thorndike, Eric B.; Goldberg, Steven R.] NIH NIDA Intramural Reseach, Baltimore, MD USA.
[Blough, Bruce E.] RTI Int, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303235
ER
PT J
AU Scoltock, AB
Bortner, C
Cidlowski, J
AF Scoltock, Alyson Bell
Bortner, Carl
Cidlowski, John
TI Signaling Mechanisms of Apoptosis Resistance in Lymphoid Cells Exposed
to Hyperosmotic Stress
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Scoltock, Alyson Bell; Bortner, Carl; Cidlowski, John] NIEHS, Lab Signal Transduct, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302699
ER
PT J
AU Sempos, CT
Vesper, HW
Phinney, K
AF Sempos, Christopher T.
Vesper, Hubert W.
Phinney, Karen
TI Vitamin D Standardization Program (VDSP)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Sempos, Christopher T.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Vesper, Hubert W.] CSC, Div Sci Lab, Atlanta, GA USA.
[Phinney, Karen] NIST, Div Analyt Chem, Gaithersburg, MD 20899 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301597
ER
PT J
AU Serafine, KM
Briscione, MA
Rice, KC
Riley, AL
AF Serafine, Katherine Marie
Briscione, Maria A.
Rice, Kenner C.
Riley, Anthony L.
TI Assessment of dopaminergic involvement in cocaine-induced conditioned
taste aversions
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Serafine, Katherine Marie; Briscione, Maria A.; Riley, Anthony L.] American Univ, Washington, DC 20016 USA.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, Bethesda, MD 20892 USA.
[Rice, Kenner C.] NIAAA, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301132
ER
PT J
AU Shi, Y
Alpatov, R
Wagner, U
Nakamoto-Kinoshita, M
Ye, Z
Luu, Y
Armache, KJ
Simon, MD
Stuetzer, A
Greer, EL
Wang, ZB
Hu, GQ
Wu, FZ
Xu, C
Beavers, WN
Guo, YH
Bian, CB
Morrison, PT
Vakoc, CR
Min, JR
Fischle, W
Kingston, RE
Zhao, KJ
Ren, B
Warren, ST
AF Shi, Yang
Alpatov, Roman
Wagner, Ulrich
Nakamoto-Kinoshita, Mika
Ye, Zhen
Luu, Ying
Armache, Karim J.
Simon, Matthew D.
Stuetzer, Alexandra
Greer, Eric L.
Wang, Zhibin
Hu, Gang-Qing
Wu, Feizhen
Xu, Chao
Beavers, William N.
Guo, Yahong
Bian, Chuanbing
Morrison, Paul T.
Vakoc, Christopher R.
Min, Jinrong
Fischle, Wolfgang
Kingston, Robert E.
Zhao, Keji
Ren, Bing
Warren, Stephen T.
TI The fragile X mental retardation protein FMRP plays a role in the DNA
damage response
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Shi, Yang; Alpatov, Roman; Greer, Eric L.] Childrens Hosp, Boston, MA 02115 USA.
[Shi, Yang; Alpatov, Roman; Greer, Eric L.] Harvard Univ, Sch Med, Boston, MA USA.
[Wagner, Ulrich; Ye, Zhen; Luu, Ying; Ren, Bing] Univ Calif San Diego, Ludwig Inst Canc Res, La Jolla, CA 92093 USA.
[Nakamoto-Kinoshita, Mika; Warren, Stephen T.] Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA USA.
[Nakamoto-Kinoshita, Mika; Warren, Stephen T.] Emory Univ, Sch Med, Dept Biochem, Atlanta, GA 30322 USA.
[Nakamoto-Kinoshita, Mika; Warren, Stephen T.] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA USA.
[Armache, Karim J.; Simon, Matthew D.; Kingston, Robert E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Stuetzer, Alexandra; Fischle, Wolfgang] Max Planck Inst Biol Chem, Gottingen, Germany.
[Wang, Zhibin; Hu, Gang-Qing; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Wu, Feizhen] Fudan Univ, Inst Biomed Sci, Shanghai 200433, Peoples R China.
[Xu, Chao; Guo, Yahong; Bian, Chuanbing; Min, Jinrong] Univ Toronto, Struct Genom Consortium, Toronto, ON, Canada.
[Beavers, William N.; Morrison, Paul T.] Dana Farber Canc Inst, Mol Biol Core Facil, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711307045
ER
PT J
AU Shi, YB
AF Shi, Yun-Bo
TI Liganded thyroid hormone receptor induces nucleosome removal and histone
modifications to activate transcription during adult stem cell
development
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Shi, Yun-Bo] NICHD, LGRD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300497
ER
PT J
AU Slezak, J
Katz, JL
AF Slezak, Jonathan
Katz, Jonathan L.
TI A comparison of methylphenidate enantiomers on delay discounting in rats
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Slezak, Jonathan; Katz, Jonathan L.] NIDA IRP NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303110
ER
PT J
AU Song, WF
Yu, ZH
Ambalavanan, N
Garantziotis, S
Matalon, S
AF Song, Weifeng
Yu, Zhihong
Ambalavanan, Namasivayam
Garantziotis, Stavros
Matalon, Sadis
TI Respiratory Syncytial Virus Infections Augment Airway Reactivity in Mice
Exposed to Chlorine (Cl-2)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Song, Weifeng; Yu, Zhihong; Ambalavanan, Namasivayam; Matalon, Sadis] Univ Alabama Birmingham, Birmingham, AL USA.
[Garantziotis, Stavros] NIEHS, Clin Res Unit, Res Triangle Pk, NC USA.
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305891
ER
PT J
AU Srivastava, S
Kashiwaya, Y
King, MT
Baxa, U
Tam, J
Niu, G
Chen, XY
Clarke, K
Veech, RL
AF Srivastava, Shireesh
Kashiwaya, Yoshihiro
King, M. Todd
Baxa, Ulrich
Tam, Joseph
Niu, Gang
Chen, Xiaoyuan
Clarke, Kieran
Veech, Richard L.
TI Mitochondrial Biogenesis and Increased Uncoupling Protein 1 in Brown
Adipose Tissue of Mice Fed a Ketone Ester Diet
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Srivastava, Shireesh; Kashiwaya, Yoshihiro; King, M. Todd; Veech, Richard L.] NIAAA, Lab Metab Control, Bethesda, MD 21701 USA.
[Tam, Joseph] NIAAA, Lab Physiol Studies, Bethesda, MD USA.
[Niu, Gang; Chen, Xiaoyuan] Natl Inst Biomed Imaging, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD USA.
[Baxa, Ulrich] NCI, Adv Technol Program, Frederick, MD USA.
[Clarke, Kieran] Univ Oxford, Dept Physiol Anat & Genet, Oxford, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304691
ER
PT J
AU Steiner, J
Davis, JM
McClellan, J
Green, J
Murphy, EA
AF Steiner, Jennifer
Davis, J. Mark
McClellan, Jamie
Green, Jeffrey
Murphy, E. Angela
TI Quercetin decreases tumorigenesis in a high fat diet-enhanced mouse
model of breast cancer
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Murphy, E. Angela] Univ S Carolina, Sch Med, Columbia, SC USA.
[Green, Jeffrey] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302041
ER
PT J
AU Streater, C
An, J
Weng, NP
AF Streater, Courtney
An, Jie
Weng, Nan Ping
TI Posttranscriptional regulation of telomerase reverse transcriptase in
Human T cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Streater, Courtney] Univ Maryland Eastern Shore, Princess Anne, MD USA.
[An, Jie; Weng, Nan Ping] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301036
ER
PT J
AU Subar, AF
Kirkpatrick, SI
Mittl, B
Zimmerman, TP
Thompson, FE
Bingley, C
Willis, G
McNutt, S
Potischman, N
AF Subar, Amy F.
Kirkpatrick, Sharon I.
Mittl, Beth
Zimmerman, Thea P.
Thompson, Frances E.
Bingley, Christopher
Willis, Gordon
McNutt, Suzanne
Potischman, Nancy
TI The National Cancer Institute's automated self-administered 24-hour
dietary recall (ASA24)
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Subar, Amy F.; Kirkpatrick, Sharon I.; Thompson, Frances E.; Willis, Gordon; Potischman, Nancy] NCI, Appl Res Program, Bethesda, MD 20892 USA.
[Mittl, Beth; Zimmerman, Thea P.; Bingley, Christopher; McNutt, Suzanne] WESTAT Corp, Rockville, MD 20850 USA.
NR 0
TC 0
Z9 0
U1 1
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302512
ER
PT J
AU Talan, MI
Ahmet, I
Lakatta, EG
AF Talan, Mark I.
Ahmet, Ismayil
Lakatta, Edward G.
TI Acute, NO-mediated, effects of erythropoietin are not associated with
its cardioprotective properties
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Talan, Mark I.; Ahmet, Ismayil; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300553
ER
PT J
AU Tauseef, M
Knezevic, N
Chava, K
Schraufnagel, D
Smith, M
Vogel, S
Dietrich, A
Birnbaumer, L
Malik, A
Mehta, D
AF Tauseef, Mohammad
Knezevic, Nebojsa
Chava, Koteswara
Schraufnagel, Dean
Smith, Monica
Vogel, Stephen
Dietrich, Alexander
Birnbaumer, Lutz
Malik, Asrar
Mehta, Dolly
TI Cation channel TRPC6 activation of TLR4 in endothelial cells mediates
sepsis-induced acute lung injury
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Tauseef, Mohammad; Knezevic, Nebojsa; Chava, Koteswara; Schraufnagel, Dean; Smith, Monica; Vogel, Stephen; Malik, Asrar; Mehta, Dolly] Univ Illinois Chicago UIC, Chicago, IL USA.
[Dietrich, Alexander] Walter Straub Inst Pharmacol & Toxicol, Munich, Germany.
[Birnbaumer, Lutz] NIEHS, Res Triangle Pk, NC 27709 USA.
RI Dietrich, Alexander/G-8619-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304270
ER
PT J
AU Tobe, R
Naranjo-Suarez, S
Turanov, AA
Carlson, BA
Tsuji, PA
Yoo, MH
Everley, RA
Gladyshev, VN
AF Tobe, Ryuta
Naranjo-Suarez, Salvador
Turanov, Anton A.
Carlson, Bradley A.
Tsuji, Petra A.
Yoo, Min-Hyuk
Everley, Robert A.
Gladyshev, Vadim N.
TI Antibiotics induce mistranslation of selenocysteine residue in
selenoproteins
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Tobe, Ryuta; Naranjo-Suarez, Salvador; Carlson, Bradley A.; Yoo, Min-Hyuk] NCI, NIH, Bethesda, MD 20892 USA.
[Turanov, Anton A.; Everley, Robert A.; Gladyshev, Vadim N.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Turanov, Anton A.; Everley, Robert A.; Gladyshev, Vadim N.] Harvard Univ, Sch Med, Boston, MA USA.
[Tsuji, Petra A.] Towson Univ, Towson, MD USA.
RI Gladyshev, Vadim/A-9894-2013
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303157
ER
PT J
AU Tryba, AK
Chong, JA
Del Camino, D
Lacey, V
Abramowitz, J
Birnbaumer, L
Harder, DR
Gerges, N
Kaczorowski, CC
AF Tryba, Andrew Kieran
Chong, Jayhong A.
Del Camino, D.
Lacey, V.
Abramowitz, Joel
Birnbaumer, Lutz
Harder, David R.
Gerges, Nashaat
Kaczorowski, Catherine C.
TI Role of TRPC3 channels in BDNF-induced plasticity, hippocampal neuronal
excitability and memory
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Tryba, Andrew Kieran; Harder, David R.; Gerges, Nashaat; Kaczorowski, Catherine C.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Chong, Jayhong A.; Del Camino, D.; Lacey, V.] Hydra Biosci, Cambridge, MA USA.
[Abramowitz, Joel; Birnbaumer, Lutz] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711307022
ER
PT J
AU Tsuji, PA
Carlson, BA
Yoo, MH
Xu, XM
Naranjo-Suarez, S
Davis, CD
Gladyshev, VN
Hatfield, DL
AF Tsuji, Petra Akiko
Carlson, Bradley A.
Yoo, Min-Hyuk
Xu, Xue-Ming
Naranjo-Suarez, Salvador
Davis, Cindy D.
Gladyshev, Vadim N.
Hatfield, Dolph L.
TI Independent down-regulation of Sep15 and TR1, but not deficiency in both
genes, affects cancer phenotypes of mouse colon carcinoma cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Tsuji, Petra Akiko] Towson Univ, Towson, MD USA.
[Carlson, Bradley A.; Yoo, Min-Hyuk; Xu, Xue-Ming; Naranjo-Suarez, Salvador; Hatfield, Dolph L.] NCI, MBSS, LCP, Bethesda, MD 20892 USA.
[Davis, Cindy D.] NCI, NSRG, DCP, Bethesda, MD 20892 USA.
[Gladyshev, Vadim N.] Brigham & Womens Hosp, Boston, MA 02115 USA.
RI Gladyshev, Vadim/A-9894-2013
NR 0
TC 0
Z9 0
U1 0
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303061
ER
PT J
AU Turanov, AA
Hatfield, DL
Gladyshev, VN
AF Turanov, Anton A.
Hatfield, Dolph L.
Gladyshev, Vadim N.
TI SECIS- and UGA position-dependent incorporation of selenocysteine into
mammalian selenoproteins
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Turanov, Anton A.; Gladyshev, Vadim N.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Div Genet 1, Boston, MA 02115 USA.
[Hatfield, Dolph L.] NCI, Lab Canc Prevent, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RI Gladyshev, Vadim/A-9894-2013
NR 0
TC 0
Z9 0
U1 1
U2 2
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711302178
ER
PT J
AU Turbyville, TJ
Blonder, J
Das, S
Ye, XY
Prieto, DA
Veenstra, TD
Milner, JA
Romagnolo, DF
AF Turbyville, Tommy J.
Blonder, Josip
Das, Sudipto
Ye, Xiaoying
Prieto, Darue A.
Veenstra, Timothy D.
Milner, John A.
Romagnolo, Donato F.
TI Comparative Proteomic Profiling of Human Breast Cell Lines
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Turbyville, Tommy J.] SAIC NCI, Opt Microscopy & Anal Lab, Frederick, MD USA.
[Blonder, Josip; Das, Sudipto; Ye, Xiaoying; Prieto, Darue A.; Veenstra, Timothy D.] SAIC NCI, Lab Prote & Analyt Technol, Adv Technol Program, Frederick, MD USA.
[Milner, John A.] NCI, Canc Prevent Div, NIH, Rockville, MD USA.
[Romagnolo, Donato F.] Univ Arizona, Dept Nutr Sci, Tucson, AZ USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711306383
ER
PT J
AU Ungvari, Z
Bailey-Downs, LC
Gautam, T
Sosnowska, D
Wang, MY
Monticone, RE
Telljohann, R
de Cabo, R
Sonntag, WE
Lakatta, E
Csiszar, A
AF Ungvari, Zoltan
Bailey-Downs, Lora C.
Gautam, Tripti
Sosnowska, Danuta
Wang Mingyi
Monticone, Robert E.
Telljohann, Richard
de Cabo, Rafael
Sonntag, William E.
Lakatta, Edward
Csiszar, Anna
TI Age-associated vascular oxidative stress, Nrf2 dysfunction and NF-kappa
B activation in the non-human primate Macaca mulatta
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Ungvari, Zoltan; Bailey-Downs, Lora C.; Gautam, Tripti; Sosnowska, Danuta; Sonntag, William E.; Csiszar, Anna] Univ Oklahoma, Hlth Sci Ctr, Reynolds Oklahoma Ctr Aging, Oklahoma City, OK USA.
[Wang Mingyi; Monticone, Robert E.; Telljohann, Richard; de Cabo, Rafael; Lakatta, Edward] NIA, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305123
ER
PT J
AU Wang, PM
Martin, WJ
AF Wang, Ping M.
Martin, William J., II
TI Evidence for proliferation of airway-delivered donor type II cells in
lungs of recipient mice following intratracheal bleomycin
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Wang, Ping M.; Martin, William J., II] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301007
ER
PT J
AU Yadav, H
Quijano, C
Kamaraju, AK
Gavrilova, O
Lonning, S
Skarulis, M
Sumner, AE
Finkel, T
Rane, SG
AF Yadav, Hariom
Quijano, Celia
Kamaraju, Anil K.
Gavrilova, Oksana
Lonning, Scott
Skarulis, Monica
Sumner, Anne E.
Finkel, Toren
Rane, Sushil G.
TI TGF-beta/Smad3 signaling inhibition protects from obesity and diabetes
through modulation of adipocyte biology
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Yadav, Hariom; Kamaraju, Anil K.; Skarulis, Monica; Sumner, Anne E.; Rane, Sushil G.] NIDDK, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD USA.
[Quijano, Celia; Finkel, Toren] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Gavrilova, Oksana] NIDDK, Mouse Metab Core Lab, NIH, Bethesda, MD USA.
[Lonning, Scott] Genzyme Corp, Framingham, MA 01701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303518
ER
PT J
AU Yadav, H
Rane, SG
AF Yadav, Hariom
Rane, Sushil G.
TI Feeding of probiotic formulation protects from obesity and diabetes
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Yadav, Hariom; Rane, Sushil G.] NIDDK, Endocrinol & Obes Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303475
ER
PT J
AU Yadav, H
Rane, SG
AF Yadav, Hariom
Rane, Sushil G.
TI Role of unique miRNAs in development of obesity and type 2 diabetes
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Yadav, Hariom; Rane, Sushil G.] NIDDK, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711301131
ER
PT J
AU Yang, J
Eliasson, B
Smith, U
Cushman, SW
Sherman, A
AF Yang, Jian
Eliasson, Bjorn
Smith, Ulf
Cushman, Samuel W.
Sherman, Arthur
TI Amelioration of insulin resistance by rosiglitazone is associated with
increased adipose cell size in obese type 2 diabetics
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Yang, Jian] Univ S Alabama, Coll Med, Mobile, AL USA.
[Yang, Jian; Cushman, Samuel W.] NIDDK, DEOB, NIH, Bethesda, MD USA.
[Eliasson, Bjorn; Smith, Ulf] Univ Gothenburg, Sahlgrenska Univ Hosp, Gothenburg, Sweden.
[Sherman, Arthur] NIDDK, LBM, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303613
ER
PT J
AU Yang, Y
Evans, S
Escano, C
Asico, L
Zhang, YR
Gonzalez, SC
Villar, VA
Wang, XY
Pisegna, JR
Wank, SA
Armando, I
Jose, P
AF Yang, Yu
Evans, Sarah
Escano, Crisanto
Asico, Laureano
Zhang, Yanrong
Gonzalez, Santiago Cuevas
Villar, Van Anthony
Wang, Xiaoyan
Pisegna, Joseph R.
Wank, Stephen A.
Armando, Ines
Jose, Pedro
TI Expression of gastrin in the thin descending limb of Henle's loop in the
mouse kidney: a molecular, localization, and functional study
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Yang, Yu; Evans, Sarah; Escano, Crisanto; Asico, Laureano; Zhang, Yanrong; Gonzalez, Santiago Cuevas; Villar, Van Anthony; Wang, Xiaoyan; Armando, Ines; Jose, Pedro] George Washington Univ, Childrens Natl Med Ctr, Ctr Mol Physiol Res, Washington, DC USA.
[Pisegna, Joseph R.] Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA 90024 USA.
[Wank, Stephen A.] NIDDK, Gastrointestinal Cell Biol Sect, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304811
ER
PT J
AU Yazawa, I
Yoshida, Y
Yoshimi, R
O'Donovan, M
Ozato, K
AF Yazawa, Itaru
Yoshida, Yuko
Yoshimi, Ryusuke
O'Donovan, Michael
Ozato, Keiko
TI Electrophysiological analysis of the spinal network function in the in
situ adult interferon regulatory factor 8 (IRF8) knockout mice
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Yazawa, Itaru] Showa Univ, Dept Anat, Sch Med, Shinagawa, Japan.
[Yazawa, Itaru; O'Donovan, Michael] NINDS, Bethesda, MD 20892 USA.
[Yoshida, Yuko; Yoshimi, Ryusuke; Ozato, Keiko] NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711304531
ER
PT J
AU Yoo, MH
Carlson, BA
Tsuji, PA
Gladyshev, VN
Hatfield, DL
AF Yoo, Min-Hyuk
Carlson, Bradley A.
Tsuji, Petra A.
Gladyshev, Vadim N.
Hatfield, Dolph L.
TI Thioredoxin reductase 1: Role in oxidative stress within cancer cells
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Yoo, Min-Hyuk; Carlson, Bradley A.; Tsuji, Petra A.; Hatfield, Dolph L.] NCI, NIH, Bethesda, MD 20892 USA.
[Gladyshev, Vadim N.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Gladyshev, Vadim N.] Harvard Univ, Sch Med, Boston, MA USA.
RI Gladyshev, Vadim/A-9894-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711303192
ER
PT J
AU Zhou, XM
Burg, MB
Ferraris, JD
AF Zhou, Xiaoming
Burg, Maurice B.
Ferraris, Joan D.
TI PTG (Protein Targeting to Glycogen) regulates the osmoprotective
transcription factor NFAT5 via SHP-1 phosphatase
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Zhou, Xiaoming] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Burg, Maurice B.; Ferraris, Joan D.] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711300292
ER
PT J
AU Zwicker, JD
Zhang, Y
Hutchinson, MR
Rice, KC
Watkins, LR
Funk, GD
AF Zwicker, Jennifer D.
Zhang, Yong
Hutchinson, Mark R.
Rice, Kenner C.
Watkins, Linda R.
Funk, Gregory D.
TI Microglia attenuate the opioid-induced depression of preBotzinger
Complex (preBotC) inspiratory rhythm in vitro via a TLR4-independent
pathway
SO FASEB JOURNAL
LA English
DT Meeting Abstract
CT Experimental Biology Meeting
CY APR 21-25, 2012
CL San Diego, CA
C1 [Zwicker, Jennifer D.; Zhang, Yong; Funk, Gregory D.] Univ Alberta, Dept Physiol, Edmonton, AB, Canada.
[Hutchinson, Mark R.] Univ Adelaide, Dept Pharmacol, Adelaide, SA, Australia.
[Rice, Kenner C.] NIDA, Chem Biol Res Branch, Bethesda, MD 20892 USA.
[Watkins, Linda R.] Univ Colorado, Dept Psychol, Boulder, CO 80309 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD APR
PY 2012
VL 26
PG 1
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 032IZ
UT WOS:000310711305686
ER
PT J
AU Wang, Y
Dinse, GE
Rogan, WJ
AF Wang, Y.
Dinse, G. E.
Rogan, W. J.
TI Birth weight, early weight gain and pubertal maturation: a longitudinal
study
SO PEDIATRIC OBESITY
LA English
DT Article
DE Age at menarche; birth weight; Tanner stage; weight gain
ID POSTNATAL-GROWTH; DICHLORODIPHENYL DICHLOROETHENE;
POLYCHLORINATED-BIPHENYLS; PROSPECTIVE COHORT; SEXUAL-MATURATION;
CHILDHOOD GROWTH; US CHILDREN; BODY-SIZE; MENARCHE; AGE
AB Objective: To investigate the effect of birth weight and early weight gain on the timing of various measures of puberty in both girls and boys.
Methods: A total of 856 newborns enrolled in the North Carolina Infant Feeding Study were followed to age 5 years, with 600 children followed up at adolescence. Birth weight was obtained from medical records and children were weighed at study visits until age 5 years; gains in standardized weights were calculated over four early age intervals: 0-6 months, 6-12 months, 1-2 years and 2-5 years. Age at menarche in girls and age at advanced Tanner stages in both girls and boys were reported by adolescents and their parents. Survival models were used to analyse the effects of birth weight and early weight gain on these outcomes.
esults: Girls with higher birth weight and greater weight gains during the four early age intervals were younger when they reached menarche and advanced Tanner stages; boys with greater early weight gains also were younger when they reached advanced Tanner stages, but few of these effects were statistically significant.
Conclusions: Higher birth weights and greater weight gains during infancy and early childhood can lead to earlier sexual maturation in girls.
C1 [Wang, Y.; Rogan, W. J.] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Dinse, G. E.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
RP Wang, Y (reprint author), NIEHS, Epidemiol Branch, POB 12233,Mail Drop A3-05, Res Triangle Pk, NC 27709 USA.
EM wangy13@niehs.nih.gov
RI Rogan, Walter/I-6034-2012
OI Rogan, Walter/0000-0002-9302-0160
FU NIH, National Institute of Environmental Health Sciences
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences.
NR 38
TC 18
Z9 19
U1 3
U2 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2047-6310
EI 2047-6302
J9 PEDIATR OBES
JI Pediatr. Obes.
PD APR
PY 2012
VL 7
IS 2
BP 101
EP 109
DI 10.1111/j.2047-6310.2011.00022.x
PG 9
WC Pediatrics
SC Pediatrics
GA 029SQ
UT WOS:000310516400008
PM 22434749
ER
PT J
AU Hall, KD
Heymsfield, SB
Kemnitz, JW
Klein, S
Schoeller, DA
Speakman, JR
AF Hall, Kevin D.
Heymsfield, Steven B.
Kemnitz, Joseph W.
Klein, Samuel
Schoeller, Dale A.
Speakman, John R.
TI Energy balance and its components: implications for body weight
regulation
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID PHYSICAL-ACTIVITY; METABOLIC-RATE; FOOD-INTAKE; EXPENDITURE; HUMANS;
MEN; OBESE; GAIN; AGE
C1 [Speakman, John R.] Univ Aberdeen, Inst Biol & Environm Sci, Aberdeen AB24 2TZ, Scotland.
[Hall, Kevin D.] NIDDKD, NIH, Bethesda, MD 20892 USA.
[Heymsfield, Steven B.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Kemnitz, Joseph W.] Univ Wisconsin, Inst Clin & Translat Res, Madison, WI USA.
[Klein, Samuel] Washington Univ, Sch Med, St Louis, MO USA.
RP Speakman, JR (reprint author), Univ Aberdeen, Inst Biol & Environm Sci, Aberdeen AB24 2TZ, Scotland.
EM j.speakman@abdn.ac.uk
RI John, Speakman/A-9494-2008
OI John, Speakman/0000-0002-2457-1823
FU ILSI North America; Intramural Research Program of the NIH, National
Institute of Diabetes and Digestive and Kidney Diseases
FX This work was supported in part by an educational grant from ILSI North
America; administrative support was provided by the ASN. This research
was supported in part by the Intramural Research Program of the NIH,
National Institute of Diabetes and Digestive and Kidney Diseases (KDH).
NR 22
TC 117
Z9 119
U1 13
U2 52
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 APR
PY 2012
VL 95
IS 4
BP 989
EP 994
DI 10.3945/ajcn.112.036350
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 033KQ
UT WOS:000310795300001
PM 22434603
ER
PT J
AU Masuda, T
Tsuda, M
Yoshinaga, R
Tozaki-Saitoh, H
Ozato, K
Tamura, T
Inoue, K
AF Masuda, Takahiro
Tsuda, Makoto
Yoshinaga, Ryohei
Tozaki-Saitoh, Hidetoshi
Ozato, Keiko
Tamura, Tomohiko
Inoue, Kazuhide
TI IRF8 Is a Critical Transcription Factor for Transforming Microglia into
a Reactive Phenotype
SO CELL REPORTS
LA English
DT Article
ID SEQUENCE BINDING-PROTEIN; CENTRAL-NERVOUS-SYSTEM; NEUROPATHIC PAIN;
SPINAL MICROGLIA; RECEPTORS; MACROPHAGES; EXPRESSION; BRAIN; CELLS;
ACTIVATION
AB Microglia become activated by multiple types of damage in the nervous system and play essential roles in neuronal pathologies. However, how microglia transform into reactive phenotypes is poorly understood. Here, we identify the transcription factor interferon regulatory factor 8 (IRF8) as a critical regulator of reactive microglia. Within the spinal cord, IRF8 expression was normally low; however, the expression was markedly upregulated in microglia, but not in neurons or astrocytes, after peripheral nerve injury (PNI). IRF8 overexpression in cultured microglia promoted the transcription of genes associated with reactive states; conversely, IRF8 deficiency prevented these gene expressions in the spinal cord following PNI. Furthermore, IRF8-deficient mice were resistant to neuropathic pain, a common sequela of PNI, and transferring IRF8-overexpressing microglia spinally to normal mice produced pain. Therefore, IRF8 may activate a program of gene expression that transforms microglia into a reactive phenotype. Our findings provide a newly observed mechanism for microglial activation.
C1 [Masuda, Takahiro; Tsuda, Makoto; Yoshinaga, Ryohei; Tozaki-Saitoh, Hidetoshi; Inoue, Kazuhide] Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Mol & Syst Pharmacol, Higashi Ku, Fukuoka 8128582, Japan.
[Ozato, Keiko] NICHHD, Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
[Tamura, Tomohiko] Yokohama City Univ, Grad Sch Med, Dept Immunol, Yokohama, Kanagawa 2360004, Japan.
RP Tsuda, M (reprint author), Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Mol & Syst Pharmacol, Higashi Ku, 3-1-1 Maidashi, Fukuoka 8128582, Japan.
EM tsuda@phar.kyushu-u.ac.jp; inoue@phar.kyushu-u.ac.jp
RI U-ID, Kyushu/C-5291-2016
FU JSPS through NEXT Program; MEXT of Japan; Core-to-Core program of JSPS
FX This work was supported by grants from the JSPS through the NEXT Program
initiated by the CSTP (M. T.) and the MEXT of Japan (T. M., M. T., K.
I.) and from the Core-to-Core program of JSPS (K. I.). We thank Ms.
Junko Kitano, Ms. Yukari Hasegawa, Dr. Shigeo Hasegawa and the Research
Support Center (Graduate School of Medical Sciences, Kyushu University)
for assisting with experiments, and Dr. Hiroyuki Miyoshi (RIKEN
BioResource Center) for providing the lentiviral vector and its
packaging plasmids. T. M. designed and performed most of the
experiments, analyzed the data, and wrote the manuscript. M. T.
conceived the study, supervised the overall project, performed
immunohistochemical experiments, and wrote the manuscript. R.Y. assisted
with the experiments. H.T.-S. optimized transduction of lentiviral
vectors into primary cultured microglia. K.O. and T. T. provided
critical materials including Irf8-/- mice and advice on data
interpretation. K. I. supervised the overall project and wrote the
manuscript.
NR 25
TC 65
Z9 68
U1 0
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REPORTS
JI Cell Reports
PD APR
PY 2012
VL 1
IS 4
BP 334
EP 340
DI 10.1016/j.celrep.2012.02.014
PG 7
WC Cell Biology
SC Cell Biology
GA 019BN
UT WOS:000309712000006
PM 22832225
ER
PT J
AU Sacks, DB
Arnold, M
Bakris, GL
Bruns, DE
Horvath, AR
Kirkman, MS
Lemmark, A
Metzger, BE
Nathan, DM
AF Sacks, David B.
Arnold, Mark
Bakris, George L.
Bruns, David E.
Horvath, Andrea Rita
Kirkman, M. Sue
Lemmark, Ake
Metzger, Boyd E.
Nathan, David M.
TI Practice Guides of the Clinical Laboratory Guides and recommendations
for the diagnosis and treatment of Diabetes Mellitus Chapters 1-6
SO ACTA BIOQUIMICA CLINICA LATINOAMERICANA
LA Spanish
DT Article
ID IMPAIRED FASTING GLUCOSE; NUTRITION EXAMINATION SURVEY;
COST-EFFECTIVENESS ANALYSIS; NEAR-INFRARED SPECTROSCOPY; LONG-TERM
COMPLICATIONS; CRITICALLY-ILL PATIENTS; PATHOLOGISTS Q-PROBES;
BLOOD-GLUCOSE; PLASMA-GLUCOSE; QUALITY SPECIFICATIONS
C1 [Sacks, David B.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
[Arnold, Mark] Univ Iowa, Dept Chem, Iowa City, IA 52242 USA.
[Bakris, George L.] Univ Chicago, Dept Med, Hypertens Dis Unit, Sect Endocrinol Diabet & Metab, Chicago, IL 60637 USA.
[Bruns, David E.] Univ Virginia, Sch Med, Dept Pathol, Charlottesville, VA 22908 USA.
[Horvath, Andrea Rita] Univ Sydney, Screening & Test Evaluat Program, Sch Publ Hlth, SEALS Dept Clin Chem,Prince Wales Hosp, Sydney, NSW 2006, Australia.
[Kirkman, M. Sue] Amer Diabet Assoc, Alexandria, VA USA.
[Lemmark, Ake] Lund Univ, Dept Clin Sci, CRC, Skane Univ Hosp Malmo, Malmo, Sweden.
[Metzger, Boyd E.] Northwestern Univ, Div Endocrinol, Feinberg Sch Med, Chicago, IL 60611 USA.
[Nathan, David M.] Univ Toronto, Toronto, ON M5S 1A1, Canada.
[Nathan, David M.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Nathan, David M.] Harvard Univ, Sch Med, Ctr Diabet, Boston, MA USA.
RP Sacks, DB (reprint author), NIH, Dept Lab Med, Bldg 10, Bethesda, MD 20892 USA.
NR 191
TC 0
Z9 0
U1 0
U2 2
PU FEDERACION BIOQUIMICA PROVINCIA BUENOS AIRES
PI LA PLATA, BUENOS AIRES
PA CALLE 6, NO. 1344, 1900 LA PLATA, BUENOS AIRES, ARGENTINA
SN 0325-2957
EI 1851-6114
J9 ACTA BIOQUIM CLIN L
JI Acta Bioquim. Clin. Latinoam.
PD APR-JUN
PY 2012
VL 46
IS 2
BP 303
EP 336
PG 34
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA 015DR
UT WOS:000309426200014
ER
PT J
AU Klionsky, DJ
Abdalla, FC
Abeliovich, H
Abraham, RT
Acevedo-Arozena, A
Adeli, K
Agholme, L
Agnello, M
Agostinis, P
Aguirre-Ghiso, JA
Ahn, HJ
Ait-Mohamed, O
Ait-Si-Ali, S
Akematsu, T
Akira, S
Al-Younes, HM
Al-Zeer, MA
Albert, ML
Albin, RL
Alegre-Abarrategui, J
Aleo, MF
Alirezaei, M
Almasan, A
Almonte-Becerril, M
Amano, A
Amaravadi, R
Amarnath, S
Amer, AO
Andrieu-Abadie, N
Anantharam, V
Ann, DK
Anoopkumar-Dukie, S
Aoki, H
Apostolova, N
Arancia, G
Aris, JP
Asanuma, K
Asare, NYO
Ashida, H
Askanas, V
Askew, DS
Auberger, P
Baba, M
Backues, SK
Baehrecke, EH
Bahr, BA
Bai, XY
Bailly, Y
Baiocchi, R
Baldini, G
Balduini, W
Ballabio, A
Bamber, BA
Bampton, ETW
Banhegyi, G
Bartholomew, CR
Bassham, DC
Bast, RC
Batoko, H
Bay, BH
Beau, I
Bechet, DM
Begley, TJ
Behl, C
Behrends, C
Bekri, S
Bellaire, B
Bendall, LJ
Benetti, L
Berliocchi, L
Bernardi, H
Bernassola, F
Besteiro, S
Bhatia-Kissova, I
Bi, XN
Biard-Piechaczyk, M
Blum, JS
Boise, LH
Bonaldo, P
Boone, DL
Bornhauser, BC
Bortoluci, KR
Bossis, I
Bost, F
Bourquin, JP
Boya, P
Boyer-Guittaut, M
Bozhkov, PV
Brady, NR
Brancolini, C
Brech, A
Brenman, JE
Brennand, A
Bresnick, EH
Brest, P
Bridges, D
Bristol, ML
Brookes, PS
Brown, EJ
Brumell, JH
Brunetti-Pierri, N
Brunk, UT
Bulman, DE
Bultman, SJ
Bultynck, G
Burbulla, LF
Bursch, W
Butchar, JP
Buzgariu, W
Bydlowski, SP
Cadwell, K
Cahova, M
Cai, DS
Cai, JY
Cai, Q
Calabretta, B
Calvo-Garrido, J
Camougrand, N
Campanella, M
Campos-Salinas, J
Candi, E
Cao, LZ
Caplan, AB
Carding, SR
Cardoso, SM
Carew, JS
Carlin, CR
Carmignac, V
Carneiro, LAM
Carra, S
Caruso, RA
Casari, G
Casas, C
Castino, R
Cebollero, E
Cecconi, F
Celli, J
Chaachouay, H
Chae, HJ
Chai, CY
Chan, DC
Chan, EY
Chang, RCC
Che, CM
Chen, CC
Chen, GC
Chen, GQ
Chen, M
Chen, Q
Chen, SSL
Chen, WL
Chen, X
Chen, XM
Chen, XQ
Chen, YG
Chen, YY
Chen, YQ
Chen, YJ
Chen, ZX
Cheng, A
Cheng, CHK
Cheng, Y
Cheong, H
Cheong, JH
Cherry, S
Chess-Williams, R
Cheung, ZH
Chevet, E
Chiang, HL
Chiarelli, R
Chiba, T
Chin, LS
Chiou, SH
Chisari, FV
Cho, CH
Cho, DH
Choi, AMK
Choi, D
Choi, KS
Choi, ME
Chouaib, S
Choubey, D
Choubey, V
Chu, CT
Chuang, TH
Chueh, SH
Chun, T
Chwae, YJ
Chye, ML
Ciarcia, R
Ciriolo, MR
Clague, MJ
Clark, RSB
Clarke, PGH
Clarke, R
Codogno, P
Coller, HA
Colombo, MI
Comincini, S
Condello, M
Condorelli, F
Cookson, MR
Coppens, GHCI
Corbalan, R
Cossart, P
Costelli, P
Costes, S
Coto-Montes, A
Couve, E
Coxon, FP
Cregg, JM
Crespo, JL
Cronje, MJ
Cuervo, AM
Cullen, JJ
Czaja, MJ
D'Amelio, M
Darfeuille-Michaud, A
Davids, LM
Davies, FE
De Felici, M
de Groot, JF
de Haan, CAM
De Martino, L
De Milito, A
De Tata, V
Debnath, J
Degterev, A
Dehay, B
Delbridge, LMD
Demarchi, F
Deng, YZ
Dengjel, J
Dent, P
Denton, D
Deretic, V
Desai, SD
Devenish, RJ
Di Gioacchino, M
Di Paolo, G
Di Pietro, C
Diaz-Araya, G
Diaz-Laviada, I
Diaz-Meco, MT
Diaz-Nido, J
Dikic, I
Dinesh-Kumar, SP
Ding, WX
Distelhorst, CW
Diwan, A
Djavaheri-Mergny, M
Dokudovskaya, S
Dong, Z
Dorsey, FC
Dosenko, V
Dowling, JJ
Doxsey, S
Dreux, M
Drew, ME
Duan, QH
Duchosal, MA
Duff, K
Dugail, I
Durbeej, M
Duszenko, M
Edelstein, CL
Edinger, AL
Egea, G
Eichinger, L
Eissa, NT
Ekmekcioglu, S
El-Deiry, WS
Elazar, Z
Elgendy, M
Ellerby, LM
Eng, KE
Engelbrecht, AM
Engelender, S
Erenpreisa, J
Escalante, R
Esclatine, A
Eskelinen, EL
Espert, L
Espina, V
Fan, HZ
Fan, J
Fan, QW
Fan, Z
Fang, SY
Fang, YQ
Fanto, M
Fanzani, A
Farkas, T
Farre, JC
Faure, M
Fechheimer, M
Feng, CG
Feng, J
Feng, QL
Feng, YJ
Fesus, L
Feuer, R
Figueiredo-Pereira, ME
Fimia, GM
Fingar, DC
Finkbeiner, S
Finkel, T
Finley, KD
Fiorito, F
Fisher, EA
Fisher, PB
Flajolet, M
Florez-McClure, ML
Florio, S
Fon, EA
Fornai, F
Fortunato, F
Fotedar, R
Fowler, DH
Fox, HS
Franco, R
Frankel, LB
Fransen, M
Fuentes, JM
Fueyo, J
Fujii, J
Fujisaki, K
Fujita, E
Fukuda, M
Furukawa, RH
Gaestel, M
Gailly, P
Gajewska, M
Galliot, B
Galy, V
Ganesh, S
Ganetzky, B
Ganley, IG
Gao, FB
Gao, GF
Gao, JM
Garcia, L
Garcia-Manero, G
Garcia-Marcos, M
Garmyn, M
Gartel, AL
Gatti, E
Gautel, M
Gawriluk, TR
Gegg, ME
Geng, JF
Germain, M
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Debnath, Jayanta
Degterev, Alexei
Dehay, Benjamin
Delbridge, Lea M. D.
Demarchi, Francesca
Deng, Yi Zhen
Dengjel, Joen
Dent, Paul
Denton, Donna
Deretic, Vojo
Desai, Shyamal D.
Devenish, Rodney J.
Di Gioacchino, Mario
Di Paolo, Gilbert
Di Pietro, Chiara
Diaz-Araya, Guillermo
Diaz-Laviada, Ines
Diaz-Meco, Maria T.
Diaz-Nido, Javier
Dikic, Ivan
Dinesh-Kumar, Savithramma P.
Ding, Wen-Xing
Distelhorst, Clark W.
Diwan, Abhinav
Djavaheri-Mergny, Mojgan
Dokudovskaya, Svetlana
Dong, Zheng
Dorsey, Frank C.
Dosenko, Victor
Dowling, James J.
Doxsey, Stephen
Dreux, Marlene
Drew, Mark E.
Duan, Qiuhong
Duchosal, Michel A.
Duff, Karen
Dugail, Isabelle
Durbeej, Madeleine
Duszenko, Michael
Edelstein, Charles L.
Edinger, Aimee L.
Egea, Gustavo
Eichinger, Ludwig
Eissa, N. Tony
Ekmekcioglu, Suhendan
El-Deiry, Wafik S.
Elazar, Zvulun
Elgendy, Mohamed
Ellerby, Lisa M.
Eng, Kai Er
Engelbrecht, Anna-Mart
Engelender, Simone
Erenpreisa, Jekaterina
Escalante, Ricardo
Esclatine, Audrey
Eskelinen, Eeva-Liisa
Espert, Lucile
Espina, Virginia
Fan, Huizhou
Fan, Jia
Fan, Qi-Wen
Fan, Zhen
Fang, Shengyun
Fang, Yongqi
Fanto, Manolis
Fanzani, Alessandro
Farkas, Thomas
Farre, Jean-Claude
Faure, Mathias
Fechheimer, Marcus
Feng, Carl G.
Feng, Jian
Feng, Qili
Feng, Youji
Fesues, Laszlo
Feuer, Ralph
Figueiredo-Pereira, Maria E.
Fimia, Gian Maria
Fingar, Diane C.
Finkbeiner, Steven
Finkel, Toren
Finley, Kim D.
Fiorito, Filomena
Fisher, Edward A.
Fisher, Paul B.
Flajolet, Marc
Florez-McClure, Maria L.
Florio, Salvatore
Fon, Edward A.
Fornai, Francesco
Fortunato, Franco
Fotedar, Rati
Fowler, Daniel H.
Fox, Howard S.
Franco, Rodrigo
Frankel, Lisa B.
Fransen, Marc
Fuentes, Jose M.
Fueyo, Juan
Fujii, Jun
Fujisaki, Kozo
Fujita, Eriko
Fukuda, Mitsunori
Furukawa, Ruth H.
Gaestel, Matthias
Gailly, Philippe
Gajewska, Malgorzata
Galliot, Brigitte
Galy, Vincent
Ganesh, Subramaniam
Ganetzky, Barry
Ganley, Ian G.
Gao, Fen-Biao
Gao, George F.
Gao, Jinming
Garcia, Lorena
Garcia-Manero, Guillermo
Garcia-Marcos, Mikel
Garmyn, Marjan
Gartel, Andrei L.
Gatti, Evelina
Gautel, Mathias
Gawriluk, Thomas R.
Gegg, Matthew E.
Geng, Jiefei
Germain, Marc
Gestwicki, Jason E.
Gewirtz, David A.
Ghavami, Saeid
Ghosh, Pradipta
Giammarioli, Anna M.
Giatromanolaki, Alexandra N.
Gibson, Spencer B.
Gilkerson, Robert W.
Ginger, Michael L.
Ginsberg, Henry N.
Golab, Jakub
Goligorsky, Michael S.
Golstein, Pierre
Gomez-Manzano, Candelaria
Goncu, Ebru
Gongora, Celine
Gonzalez, Claudio D.
Gonzalez, Ramon
Gonzalez-Estevez, Cristina
Gonzalez-Polo, Rosa Ana
Gonzalez-Rey, Elena
Gorbunov, Nikolai V.
Gorski, Sharon
Goruppi, Sandro
Gottlieb, Roberta A.
Gozuacik, Devrim
Granato, Giovanna Elvira
Grant, Gary D.
Green, Kim N.
Gregorc, Ales
Gros, Frederic
Grose, Charles
Grunt, Thomas W.
Gual, Philippe
Guan, Jun-Lin
Guan, Kun-Liang
Guichard, Sylvie M.
Gukovskaya, Anna S.
Gukovsky, Ilya
Gunst, Jan
Gustafsson, Asa B.
Halayko, Andrew J.
Hale, Amber N.
Halonen, Sandra K.
Hamasaki, Maho
Han, Feng
Han, Ting
Hancock, Michael K.
Hansen, Malene
Harada, Hisashi
Harada, Masaru
Hardt, Stefan E.
Harper, J. Wade
Harris, Adrian L.
Harris, James
Harris, Steven D.
Hashimoto, Makoto
Haspel, Jeffrey A.
Hayashi, Shin-ichiro
Hazelhurst, Lori A.
He, Congcong
He, You-Wen
Hebert, Marie-Josee
Heidenreich, Kim A.
Helfrich, Miep H.
Helgason, Gudmundur V.
Henske, Elizabeth P.
Herman, Brian
Herman, Paul K.
Hetz, Claudio
Hilfiker, Sabine
Hill, Joseph A.
Hocking, Lynne J.
Hofman, Paul
Hofmann, Thomas G.
Hoehfeld, Joerg
Holyoake, Tessa L.
Hong, Ming-Huang
Hood, David A.
Hotamisligil, Goekhan S.
Houwerzijl, Ewout J.
Hoyer-Hansen, Maria
Hu, Bingren
Hu, Chien-An A.
Hu, Hong-Ming
Hua, Ya
Huang, Canhua
Huang, Ju
Huang, Shengbing
Huang, Wei-Pang
Huber, Tobias B.
Huh, Won-Ki
Hung, Tai-Ho
Hupp, Ted R.
Hur, Gang Min
Hurley, James B.
Hussain, Sabah N. A.
Hussey, Patrick J.
Hwang, Jung Jin
Hwang, Seungmin
Ichihara, Atsuhiro
Ilkhanizadeh, Shirin
Inoki, Ken
Into, Takeshi
Iovane, Valentine
Iovanna, Juan L.
Ip, Nancy Y.
Isaka, Yoshitaka
Ishida, Hiroyuki
Isidoro, Ciro
Isobe, Ken-ichi
Iwasaki, Akiko
Izquierdo, Marta
Izumi, Yotaro
Jaakkola, Panu M.
Jaattela, Marja
Jackson, George R.
Jackson, William T.
Janji, Bassam
Jendrach, Marina
Jeon, Ju-Hong
Jeung, Eui-Bae
Jiang, Hong
Jiang, Hongchi
Jiang, Jean X.
Jiang, Ming
Jiang, Qing
Jiang, Xuejun
Jiang, Xuejun
Jimenez, Alberto
Jin, Meiyan
Jin, Shengkan
Joe, Cheol O.
Johansen, Terje
Johnson, Daniel E.
Johnson, Gail V. W.
Jones, Nicola L.
Joseph, Bertrand
Joseph, Suresh K.
Joubert, Annie M.
Juhasz, Gabor
Juillerat-Jeanneret, Lucienne
Jung, Chang Hwa
Jung, Yong-Keun
Kaarniranta, Kai
Kaasik, Allen
Kabuta, Tomohiro
Kadowaki, Motoni
Kagedal, Katarina
Kamada, Yoshiaki
Kaminskyy, Vitaliy O.
Kampinga, Harm H.
Kanamori, Hiromitsu
Kang, Chanhee
Kang, Khong Bee
Kang, Kwang Il
Kang, Rui
Kang, Yoon-A
Kanki, Tomotake
Kanneganti, Thirumala-Devi
Kanno, Haruo
Kanthasamy, Anumantha G.
Kanthasamy, Arthi
Karantza, Vassiliki
Kaushal, Gur P.
Kaushik, Susmita
Kawazoe, Yoshinori
Ke, Po-Yuan
Kehrl, John H.
Kelekar, Ameeta
Kerkhoff, Claus
Kessel, David H.
Khalil, Hany
Kiel, Jan A. K. W.
Kiger, Amy A.
Kihara, Akio
Kim, Deok Ryong
Kim, Do-Hyung
Kim, Dong-Hou
Kim, Eun-Kyoung
Kim, Hyung-Ryong
Kim, Jae-Sung
Kim, Jeong Hun
Kim, Jin Cheon
Kim, John K.
Kim, Peter K.
Kim, Seong Who
Kim, Yong-Sun
Kim, Yonghyun
Kimchi, Adi
Kimmelman, Alec C.
King, Jason S.
Kinsella, Timothy J.
Kirkin, Vladimir
Kirshenbaum, Lorrie A.
Kitamoto, Katsuhiko
Kitazato, Kaio
Klein, Ludger
Klimecki, Walter T.
Klucken, Jochen
Knecht, Erwin
Ko, Ben C. B.
Koch, Jan C.
Koga, Hiroshi
Koh, Jae-Young
Koh, Young Ho
Koike, Masato
Komatsu, Masaaki
Kominami, Eiki
Kong, Hee Jeong
Kong, Wei-Jia
Korolchuk, Viktor I.
Kotake, Yaichiro
Koukourakis, Michael I.
Flores, Juan B. Kouri
Kovacs, Attila L.
Kraft, Claudine
Krainc, Dimitri
Kraemer, Helmut
Kretz-Remy, Carole
Krichevsky, Anna M.
Kroemer, Guido
Krueger, Rejko
Krut, Oleg
Ktistakis, Nicholas T.
Kuan, Chia-Yi
Kucharczyk, Roza
Kumar, Ashok
Kumar, Raj
Kumar, Sharad
Kundu, Mondira
Kung, Hsing-Jien
Kurz, Tino
Kwon, Ho Jeong
La Spada, Albert R.
Lafont, Frank
Lamark, Trond
Landry, Jacques
Lane, Jon D.
Lapaquette, Pierre
Laporte, Jocelyn F.
Laszlo, Lajos
Lavandero, Sergio
Lavoie, Josee N.
Layfield, Robert
Lazo, Pedro A.
Le, Weidong
Le Cam, Laurent
Ledbetter, Daniel J.
Lee, Alvin J. X.
Lee, Byung-Wan
Lee, Gyun Min
Lee, Jongdae
Lee, Ju-Hyun
Lee, Michael
Lee, Myung-Shik
Lee, Sug Hyung
Leeuwenburgh, Christiaan
Legembre, Patrick
Legouis, Renaud
Lehmann, Michael
Lei, Huan-Yao
Lei, Qun-Ying
Leib, David A.
Leiro, Jose
Lemasters, John J.
Lemoine, Antoinette
Lesniak, Maciej S.
Lev, Dina
Levenson, Victor V.
Levine, Beth
Levy, Efrat
Li, Faqiang
Li, Jun-Lin
Li, Lian
Li, Sheng
Li, Weijie
Li, Xue-Jun
Li, Yan-bo
Li, Yi-Ping
Liang, Chengyu
Liang, Qiangrong
Liao, Yung-Feng
Liberski, Pawel P.
Lieberman, Andrew
Lim, Hyunjung J.
Lim, Kah-Leong
Lim, Kyu
Lin, Chiou-Feng
Lin, Fu-Cheng
Lin, Jian
Lin, Jiandie D.
Lin, Kui
Lin, Wan-Wan
Lin, Weei-Chin
Lin, Yi-Ling
Linden, Rafael
Lingor, Paul
Lippincott-Schwartz, Jennifer
Lisanti, Michael P.
Liton, Paloma B.
Liu, Bo
Liu, Chun-Feng
Liu, Kaiyu
Liu, Leyuan
Liu, Qiong A.
Liu, Wei
Liu, Young-Chau
Liu, Yule
Lockshin, Richard A.
Lok, Chun-Nam
Lonial, Sagar
Loos, Benjamin
Lopez-Berestein, Gabriel
Lopez-Otin, Carlos
Lossi, Laura
Lotze, Michael T.
Low, Peter
Lu, Binfeng
Lu, Bingwei
Lu, Bo
Lu, Zhen
Luciano, Frederic
Lukacs, Nicholas W.
Lund, Anders H.
Lynch-Day, Melinda A.
Ma, Yong
Macian, Fernando
MacKeigan, Jeff P.
Macleod, Kay F.
Madeo, Frank
Maiuri, Luigi
Maiuri, Maria Chiara
Malagoli, Davide
Malicdan, May Christine V.
Malorni, Walter
Man, Na
Mandelkow, Eva-Maria
Manon, Stephen
Manov, Irena
Mao, Kai
Mao, Xiang
Mao, Zixu
Marambaud, Philippe
Marazziti, Daniela
Marcel, Yves L.
Marchbank, Katie
Marchetti, Piero
Marciniak, Stefan J.
Marcondes, Mateus
Mardi, Mohsen
Marfe, Gabriella
Marino, Guillermo
Markaki, Maria
Marten, Mark R.
Martin, Seamus J.
Martinand-Mari, Camille
Martinet, Wim
Martinez-Vicente, Marta
Masini, Matilde
Matarrese, Paola
Matsuo, Saburo
Matteoni, Raffaele
Mayer, Andreas
Mazure, Nathalie M.
McConkey, David J.
McConnell, Melanie J.
McDermott, Catherine
McDonald, Christine
McInerney, Gerald M.
McKenna, Sharon L.
McLaughlin, BethAnn
McLean, Pamela J.
McMaster, Christopher R.
McQuibban, G. Angus
Meijer, Alfred J.
Meisler, Miriam H.
Melendez, Alicia
Melia, Thomas J.
Melino, Gerry
Mena, Maria A.
Menendez, Javier A.
Menna-Barreto, Rubem F. S.
Menon, Manoj B.
Menzies, Fiona M.
Mercer, Carol A.
Merighi, Adalberto
Merry, Diane E.
Meschini, Stefania
Meyer, Christian G.
Meyer, Thomas F.
Miao, Chao-Yu
Miao, Jun-Ying
Michels, Paul A. M.
Michiels, Carine
Mijaljica, Dalibor
Milojkovic, Ana
Minucci, Saverio
Miracco, Clelia
Miranti, Cindy K.
Mitroulis, Ioannis
Miyazawa, Keisuke
Mizushima, Noboru
Mograbi, Baharia
Mohseni, Simin
Molero, Xavier
Mollereau, Bertrand
Mollinedo, Faustino
Momoi, Takashi
Monastyrska, Iryna
Monick, Martha M.
Monteiro, Mervyn J.
Moore, Michael N.
Mora, Rodrigo
Moreau, Kevin
Moreira, Paula I.
Moriyasu, Yuji
Moscat, Jorge
Mostowy, Serge
Mottram, Jeremy C.
Motyl, Tomasz
Moussa, Charbel E. -H.
Mueller, Sylke
Muenger, Karl
Muenz, Christian
Murphy, Leon O.
Murphy, Maureen E.
Musaro, Antonio
Mysorekar, Indira
Nagata, Eiichiro
Nagata, Kazuhiro
Nahimana, Aimable
Nair, Usha
Nakagawa, Toshiyuki
Nakahira, Kiichi
Nakano, Hiroyasu
Nakataogawa, Hitoshi
Nanjundan, Meera
Naqvi, Naweed I.
Narendra, Derek P.
Narita, Masashi
Navarro, Miguel
Nawrocki, Steffan T.
Nazarko, Taras Y.
Nemchenko, Andriy
Netea, Mihai G.
Neufeld, Thomas P.
Ney, Paul A.
Nezis, Ioannis P.
Huu Phuc Nguyen
Nie, Daotai
Nishino, Ichizo
Nislow, Corey
Nixon, Ralph A.
Noda, Takeshi
Noegel, Angelika A.
Nogalska, Anna
Noguchi, Satoru
Notterpek, Lucia
Novak, Ivana
Nozaki, Tomoyoshi
Nukina, Nobuyuki
Nuernberger, Thorsten
Nyfeler, Beat
Obara, Keisuke
Oberley, Terry D.
Oddo, Salvatore
Ogawa, Michinaga
Ohashi, Toya
Okamoto, Koji
Oleinick, Nancy L.
Oliver, F. Javier
Olsen, Laura J.
Olsson, Stefan
Opota, Onya
Osborne, Timothy F.
Ostrander, Gary K.
Otsu, Kinya
Ou, Jing-hsiung James
Ouimet, Mireille
Overholtzer, Michael
Ozpolat, Bulent
Paganetti, Paolo
Pagnini, Ugo
Pallet, Nicolas
Palmer, Glen E.
Palumbo, Camilla
Pan, Tianhong
Panaretakis, Theocharis
Pandey, Udai Bhan
Papackova, Zuzana
Papassideri, Issidora
Paris, Irmgard
Park, Junsoo
Park, Ohkmae K.
Parys, Jan B.
Parzych, Katherine R.
Patschan, Susann
Patterson, Cam
Pattingre, Sophie
Pawelek, John M.
Peng, Jianxin
Perlmutter, David H.
Perrotta, Ida
Perry, George
Pervaiz, Shazib
Peter, Matthias
Peters, Godefridus J.
Petersen, Morten
Petrovski, Goran
Phang, James M.
Piacentini, Mauro
Pierre, Philippe
Pierrefite-Carle, Valerie
Pierron, Gerard
Pinkas-Kramarski, Ronit
Piras, Antonio
Piri, Natik
Platanias, Leonidas C.
Poeggeler, Stefanie
Poirot, Marc
Poletti, Angelo
Poues, Christian
Pozuelo-Rubio, Mercedes
Praetorius-Ibba, Mette
Prasad, Anil
Prescott, Mark
Priault, Muriel
Produit-Zengaffinen, Nathalie
Progulske-Fox, Ann
Proikas-Cezanne, Tassula
Przedborski, Serge
Przyklenk, Karin
Puertollano, Rosa
Puyal, Julien
Qian, Shu-Bing
Qin, Liang
Qin, Zheng-Hong
Quaggin, Susan E.
Raben, Nina
Rabinowich, Hannah
Rabkin, Simon W.
Rahman, Irfan
Rami, Abdelhaq
Ramm, Georg
Randall, Glenn
Randow, Felix
Rao, V. Ashutosh
Rathmell, Jeffrey C.
Ravikumar, Brinda
Ray, Swapan K.
Reed, Bruce H.
Reed, John C.
Reggiori, Fulvio
Regnier-Vigouroux, Anne
Reichert, Andreas S.
Reiners, John J., Jr.
Reiter, Russel J.
Ren, Jun
Revuelta, Jose L.
Rhodes, Christopher J.
Ritis, Konstantinos
Rizzo, Elizete
Robbins, Jeffrey
Roberge, Michel
Roca, Hernan
Roccheri, Maria C.
Rocchi, Stephane
Rodemann, H. Peter
de Cordoba, Santiago Rodriguez
Rohrer, Baerbel
Roninson, Igor B.
Rosen, Kirill
Rost-Roszkowska, Magdalena M.
Rouis, Mustapha
Rouschop, Kasper M. A.
Rovetta, Francesca
Rubin, Brian P.
Rubinsztein, David C.
Ruckdeschel, Klaus
Rucker, Edmund B., III
Rudich, Assaf
Rudolf, Emil
Ruiz-Opazo, Nelson
Russo, Rossella
Rusten, Tor Erik
Ryan, Kevin M.
Ryter, Stefan W.
Sabatini, David M.
Sadoshima, Junichi
Saha, Tapas
Saitoh, Tatsuya
Sakagami, Hiroshi
Sakai, Yasuyoshi
Salekdeh, Ghasem Hoseini
Salomoni, Paolo
Salvaterra, Paul M.
Salvesen, Guy
Salvioli, Rosa
Sanchez, Anthony M. J.
Sanchez-Alcazar, Jose A.
Sanchez-Prieto, Ricardo
Sandri, Marco
Sankar, Uma
Sansanwal, Poonam
Santambrogio, Laura
Saran, Shweta
Sarkar, Sovan
Sarwal, Minnie
Sasakawa, Chihiro
Sasnauskiene, Ausra
Sass, Miklos
Sato, Ken
Sato, Miyuki
Schapira, Anthony H. V.
Scharl, Michael
Schaetzl, Hermann M.
Scheper, Wiep
Schiaffino, Stefano
Schneider, Claudio
Schneider, Marion E.
Schneider-Stock, Regine
Schoenlein, Patricia V.
Schorderet, Daniel F.
Schueller, Christoph
Schwartz, Gary K.
Scorrano, Luca
Sealy, Linda
Seglen, Per O.
Segura-Aguilar, Juan
Seiliez, Iban
Seleverstov, Oleksandr
Sell, Christian
Seo, Jong Bok
Separovic, Duska
Setaluri, Vijayasaradhi
Setoguchi, Takao
Settembre, Carmine
Shacka, John J.
Shanmugam, Mala
Shapiro, Irving M.
Shaulian, Eitan
Shaw, Reuben J.
Shelhamer, James H.
Shen, Han-Ming
Shen, Wei-Chiang
Sheng, Zu-Hang
Shi, Yang
Shibuya, Kenichi
Shidoji, Yoshihiro
Shieh, Jeng-Jer
Shih, Chwen-Ming
Shimada, Yohta
Shimizu, Shigeomi
Shintani, Takahiro
Shirihai, Orian S.
Shore, Gordon C.
Sibirny, Andriy A.
Sidhu, Stan B.
Sikorska, Beata
Silva-Zacarin, Elaine C. M.
Simmons, Alison
Simon, Anna Katharina
Simon, Hans-Uwe
Simone, Cristiano
Simonsen, Anne
Sinclair, David A.
Singh, Rajat
Sinha, Debasish
Sinicrope, Frank A.
Sirko, Agnieszka
Siu, Parco M.
Sivridis, Efthimios
Skop, Vojtech
Skulachev, Vladimir P.
Slack, Ruth S.
Smaili, Soraya S.
Smith, Duncan R.
Soengas, Maria S.
Soldati, Thierry
Song, Xueqin
Sood, Anil K.
Soong, Tuck Wah
Sotgia, Federica
Spector, Stephen A.
Spies, Claudia D.
Springer, Wolfdieter
Srinivasula, Srinivasa M.
Stefanis, Leonidas
Steffan, Joan S.
Stendel, Ruediger
Stenmark, Harald
Stephanou, Anastasis
Stern, Stephan T.
Sternberg, Cinthya
Stork, Bjoern
Stralfors, Peter
Subauste, Carlos S.
Sui, Xinbing
Sulzer, David
Sun, Jiaren
Sun, Shi-Yong
Sun, Zhi-Jun
Sung, Joseph J. Y.
Suzuki, Kuninori
Suzuki, Toshihiko
Swanson, Michele S.
Swanton, Charles
Sweeney, Sean T.
Sy, Lai-King
Szabadkai, Gyorgy
Tabas, Ira
Taegtmeyer, Heinrich
Tafani, Marco
Takacs-Vellai, Krisztina
Takano, Yoshitaka
Takegawa, Kaoru
Takemura, Genzou
Takeshita, Fumihiko
Talbot, Nicholas J.
Tan, Kevin S. W.
Tanaka, Keiji
Tanaka, Kozo
Tang, Daolin
Tang, Dingzhong
Tanida, Isei
Tannous, Bakhos A.
Tavernarakis, Nektarios
Taylor, Graham S.
Taylor, Gregory A.
Taylor, J. Paul
Terada, Lance S.
Terman, Alexei
Tettamanti, Gianluca
Thevissen, Karin
Thompson, Craig B.
Thorburn, Andrew
Thumm, Michael
Tian, FengFeng
Tian, Yuan
Tocchini-Valentini, Glauco
Tolkovsky, Aviva M.
Tomino, Yasuhiko
Toenges, Lars
Tooze, Sharon A.
Tournier, Cathy
Tower, John
Towns, Roberto
Trajkovic, Vladimir
Travassos, Leonardo H.
Tsai, Ting-Fen
Tschan, Mario P.
Tsubata, Takeshi
Tsung, Allan
Turk, Boris
Turner, Lorianne S.
Tyagi, Suresh C.
Uchiyama, Yasuo
Ueno, Takashi
Umekawa, Midori
Umemiya-Shirafuji, Rika
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Valente, Enza Maria
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van Dyk, Linda F.
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Vandenabeele, Peter
Vandenberghe, Wim P.
Vanhorebeek, Ilse
Vaquero, Eva C.
Velasco, Guillermo
Vellai, Tibor
Vicencio, Jose Miguel
Vierstra, Richard D.
Vila, Miquel
Vindis, Cecile
Viola, Giampietro
Viscomi, Maria Teresa
Voitsekhovskaja, Olga V.
von Haefen, Clarissa
Votruba, Marcela
Wada, Keiji
Wade-Martins, Richard
Walker, Cheryl L.
Walsh, Craig M.
Walter, Jochen
Wan, Xiang-Bo
Wang, Aimin
Wang, Chenguang
Wang, Dawei
Wang, Fan
Wang, Fen
Wang, Guanghui
Wang, Haichao
Wang, Hong-Gang
Wang, Horng-Dar
Wang, Jin
Wang, Ke
Wang, Mei
Wang, Richard C.
Wang, Xinglong
Wang, Xuejun
Wang, Ying-Jan
Wang, Yipeng
Wang, Zhen
Wang, Zhigang Charles
Wang, Zhinong
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Ward, Diane M.
Watada, Hirotaka
Waters, Sarah L.
Webster, Paul
Wei, Lixin
Weihl, Conrad C.
Weiss, William A.
Welford, Scott M.
Wen, Long-Ping
Whitehouse, Caroline A.
Whitton, J. Lindsay
Whitworth, Alexander J.
Wileman, Tom
Wiley, John W.
Wilkinson, Simon
Willbold, Dieter
Williams, Roger L.
Williamson, Peter R.
Wouters, Bradly G.
Wu, Chenghan
Wu, Dao-Cheng
Wu, William K. K.
Wyttenbach, Andreas
Xavier, Ramnik J.
Xi, Zhijun
Xia, Pu
Xiao, Gengfu
Xie, Zhiping
Xie, Zhonglin
Xu, Da-zhi
Xu, Jianzhen
Xu, Liang
Xu, Xiaolei
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Yamashina, Shunhei
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Zhang, Jing-Pu
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Zhao, Yi-Fang
Zhao, Ying
Zhao, Zhizhuang J.
Zheng, Xiaoxiang
Zhivotovsky, Boris
Zhong, Qing
Zhou, Cong-Zhao
Zhu, Changlian
Zhu, Wei-Guo
Zhu, Xiao-Feng
Zhu, Xiongwei
Zhu, Yuangang
Zoladek, Teresa
Zong, Wei-Xing
Zorzano, Antonio
Zschocke, Juergen
Zuckerbraun, Brian
TI Guidelines for the use and interpretation of assays for monitoring
autophagy
SO AUTOPHAGY
LA English
DT Review
DE autolysosome; autophagosome; flux; LC3; lysosome; phagophore; stress;
vacuole
ID ACTIVATED PROTEIN-KINASE; CHAPERONE-MEDIATED AUTOPHAGY; PROGRAMMED
CELL-DEATH; ISOLATED RAT HEPATOCYTES; STARVATION-INDUCED AUTOPHAGY;
VACUOLE TARGETING PATHWAY; GLUCAGON-INDUCED AUTOPHAGY; BREAST-CANCER
CELLS; BETAINE HOMOCYSTEINE METHYLTRANSFERASE; ENDOPLASMIC-RETICULUM
STRESS
AB In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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[Chevet, Eric] Univ Bordeaux Segalen, Bordeaux, France.
[Chevet, Eric] INSERM, U1053, Bordeaux, France.
[Chiang, Hui-Ling] Penn State Univ, Coll Med, Dept Cellular & Mol Physiol, Hershey, PA USA.
[Chiba, Tomoki] Univ Tsukuba, Grad Sch Life & Environm Sci, Ibaraki, Japan.
[Chin, Lih-Shen; Li, Lian; Mao, Zixu] Emory Univ, Sch Med, Dept Pharmacol, Atlanta, GA 30322 USA.
[Chiou, Shih-Hwa] Natl Yang Ming Univ, Sch Med, Inst Pharmacol, Taipei 112, Taiwan.
[Cho, Chi Hin] Chinese Univ Hong Kong, Sch Biomed Sci, Hong Kong, Hong Kong, Peoples R China.
[Cho, Dong-Hyung] Kyung Hee Univ, Grad Sch EW Med Sci, Yongin, South Korea.
[Choi, Augustine M. K.; Haspel, Jeffrey A.; Henske, Elizabeth P.; Nakahira, Kiichi; Ryter, Stefan W.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Pulm & Crit Care Med, Boston, MA 02115 USA.
[Choi, DooSeok] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Obstet & Gynecol, Seoul, South Korea.
[Choi, Kyeong Sook] Ajou Univ, Sch Med, Inst Med Sci, Suwon 441749, South Korea.
[Choi, Mary E.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Med,Renal Div, Boston, MA 02115 USA.
[Chouaib, Salem] Inst Gustave Roussy, INSERM, U753 PR1, F-94805 Villejuif, France.
[Choubey, Divaker] Univ Cincinnati, Dept Environm Hlth, Cincinnati, OH USA.
[Choubey, Vinay; Kaasik, Allen] Univ Tartu, Dept Pharmacol, EE-50090 Tartu, Estonia.
[Chu, Charleen T.; Rabinowich, Hannah] Univ Pittsburgh, Sch Med, Dept Pathol, Pittsburgh, PA USA.
[Chu, Charleen T.] Univ Pittsburgh, Sch Med, Ctr Neurosci, Pittsburgh, PA USA.
[Chuang, Tsung-Hsien] Natl Hlth Res Inst, Immunol Res Ctr, Miaoli Cty, Taiwan.
[Chueh, Sheau-Huei] Natl Def Med Ctr, Dept Biochem, Taipei, Taiwan.
[Chun, Taehoon; Park, Ohkmae K.] Korea Univ, Sch Life Sci & Biotechnol, Seoul, South Korea.
[Chwae, Yong-Joon] Ajou Univ, Sch Med, Dept Microbiol, Suwon 441749, South Korea.
[Chye, Mee-Len] Univ Hong Kong, Sch Biol Sci, Pokfulam, Hong Kong, Peoples R China.
[Ciarcia, Roberto; Florio, Salvatore; Granato, Giovanna Elvira] Univ Naples Federico II, Dept Struct Funct & Biol Technol, Naples, Italy.
[Ciriolo, Maria R.] IRCCS San Raffaele, Rome, Italy.
[Clague, Michael J.] Univ Liverpool, Physiol Lab, Inst Translat Med, Liverpool L69 3BX, Merseyside, England.
[Clark, Robert S. B.] Safar Ctr Resuscitat Res, Pittsburgh, PA USA.
[Clarke, Peter G. H.; Puyal, Julien] Univ Lausanne, Dept Biol Cellulaire & Morphol, Lausanne, Switzerland.
[Clarke, Robert; Saha, Tapas] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC USA.
[Codogno, Patrice] Univ Paris S, INSERM, U984, Paris, France.
[Coller, Hilary A.] Princeton Univ, Dept Mol Biol, Princeton, NJ 08544 USA.
[Colombo, Maria I.] Univ Nacl Cuyo, CONICET, Inst Histol & Embriol, Lab Biol Celular & Mol, RA-5500 Mendoza, Argentina.
[Comincini, Sergio] Univ Pavia, Dept Genet & Microbiol, I-27100 Pavia, Italy.
[Condorelli, Fabrizio] Univ Piemonte Orientale, Fac Pharm, Novara, Italy.
[Cookson, Mark R.] NIA, Cell Biol & Gene Express Sect, NIH, Bethesda, MD 20892 USA.
[Corbalan, Ramon] Johns Hopkins Univ, Dept Mol Microbiol & Immunol, Baltimore, MD USA.
[Cossart, Pascale] Pontificia Univ Catolica Chile, Fac Med, Dept Enfermedades Cardiovasc, Santiago, Chile.
[Costelli, Paola] Inst Pasteur, Unite Interact Bacteries Cellules, Paris, France.
[Costelli, Paola] INSERM, INRA, U604, USC2020, Paris, France.
[Costes, Safia] Univ Turin, Dept Expt Med & Oncol, Turin, Italy.
[Coto-Montes, Ana] Univ Calif Los Angeles, David Geffen Sch Med, Larry Hillblom Islet Res Ctr, Los Angeles, CA 90095 USA.
[Couve, Eduardo] Univ Oviedo, Dept Morfol & Biol Celular, Oviedo, Spain.
[Coxon, Fraser P.] Univ Valparaiso, Fac Ciencias, Dept Biol & Cs Ambientales, Valparaiso, Chile.
[Cregg, James M.; Helfrich, Miep H.; Hocking, Lynne J.] Univ Aberdeen, Div Appl Med, Aberdeen, Scotland.
[Crespo, Jose L.] Keck Grad Inst Appl Sci, Claremont, CA USA.
[Cronje, Marianne J.] Univ Seville, CSIC, Inst Bioquim Vegetal Fotosintesis, Seville, Spain.
Univ Johannesburg, Dept Biochem, Johannesburg, South Africa.
[Kaushik, Susmita] Albert Einstein Coll Med, Dept Anat & Struct Biol, Bronx, NY 10467 USA.
[Kaushik, Susmita; Koga, Hiroshi] Albert Einstein Coll Med, Dept Dev & Mol Biol, Bronx, NY 10467 USA.
[D'Amelio, Marcello; Kaushik, Susmita; Koga, Hiroshi] Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Bronx, NY 10467 USA.
Univ Iowa, Dept Surg, Iowa City, IA 52242 USA.
[D'Amelio, Marcello] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
Santa Lucia Fdn, European Ctr Brain Res, Expt Neurol Unit, Rome, Italy.
Univ Campus Biomed, Rome, Italy.
[Cuervo, Ana Maria; Darfeuille-Michaud, Arlette] INRA, USC 2018, Clermont Ferrand, France.
[Cuervo, Ana Maria; Darfeuille-Michaud, Arlette] Univ Auvergne, INSERM, UMR 1071, Clermont Ferrand, France.
[Cullen, Joseph J.; Davids, Lester M.] Univ Cape Town, Dept Human Biol, ZA-7925 Cape Town, South Africa.
[Czaja, Mark J.; Davies, Faith E.] Inst Canc Res, Div Mol Pathol, Sutton, Surrey, England.
[Czaja, Mark J.; Davies, Faith E.] Royal Marsden Hosp, Sutton, Surrey, England.
[De Felici, Massimo] Univ Roma Tor Vergata, Dept Publ Hlth & Cell Biol, Rome, Italy.
[de Groot, John F.; Fueyo, Juan; Gomez-Manzano, Candelaria; Jiang, Hong] Univ Texas Houston, MD Anderson Canc Ctr, Dept Neurooncol, Houston, TX 77030 USA.
[de Haan, Cornelis A. M.; Monastyrska, Iryna] Univ Utrecht, Dept Infect Dis & Immunol, Div Virol, Utrecht, Netherlands.
[De Martino, Luisa; Fiorito, Filomena; Iovane, Valentine; Pagnini, Ugo] Univ Naples Federico II, Dept Pathol & Anim Hlth, Naples, Italy.
[De Milito, Angelo; Joseph, Bertrand; Panaretakis, Theocharis] Karolinska Inst, Dept Oncol Pathol, Canc Ctr Karolinska, Stockholm, Sweden.
[De Tata, Vincenzo] Univ Pisa, Sch Med, Dept Expt Pathol, I-56100 Pisa, Italy.
[Debnath, Jayanta] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94140 USA.
[Degterev, Alexei] Tufts Univ, Sch Med, Dept Biochem, Boston, MA 02111 USA.
[Dehay, Benjamin] Univ Bordeaux Segalen, Inst Malad Neurodegenerat, CNRS, UMR 5293, Bordeaux, France.
[Delbridge, Lea M. D.] Univ Melbourne, Dept Physiol, Parkville, Vic 3052, Australia.
[Demarchi, Francesca; Schneider, Claudio] Lab Nazl Consorzio Interuniv, Trieste, Italy.
[Deng, Yi Zhen; Naqvi, Naweed I.] Natl Univ Singapore, Temasek Life Sci Lab, Fungal Pathobiol Grp, Singapore 117548, Singapore.
[Dengjel, Joen] Freiburg Inst Adv Studies FRIAS, Sch Life Sci LifeNet, Freiburg, Germany.
[Dent, Paul] Virginia Commonwealth Univ, Sch Med, VCU Massey Canc Ctr, Dept Neurosurg,VCU Inst Moleular Med, Richmond, VA USA.
[Denton, Donna] SA Pathol, Ctr Canc Biol, Adelaide, SA, Australia.
[Denton, Donna] Univ Adelaide, Sch Mol & Biomed Sci, Adelaide, SA, Australia.
[Deretic, Vojo] Univ New Mexico, Hlth Sci Ctr, Dept Mol Genet & Microbiol, Albuquerque, NM 87131 USA.
[Desai, Shyamal D.] Louisiana State Univ, Hlth Sci Ctr, Sch Med, Dept Biochem & Mol Biol, New Orleans, LA USA.
[Devenish, Rodney J.; Mijaljica, Dalibor; Prescott, Mark; Ramm, Georg] Monash Univ, Dept Biochem & Mol Biol, Melbourne, Vic 3004, Australia.
[Devenish, Rodney J.] Monash Univ, ARC Ctr Excellence Struct & Funct Microbial Genom, Melbourne, Vic 3004, Australia.
[Di Gioacchino, Mario] Univ dAnnunzio Fdn, Ageing Res Ctr CeSI, Unit Allergy & Immunotoxicol, Chieti, Italy.
[Di Paolo, Gilbert; Duff, Karen; Yu, Wai Haung] Columbia Univ, Med Ctr, Taub Inst Alzheimers Dis Res, New York, NY USA.
[Di Paolo, Gilbert; Duff, Karen; Przedborski, Serge; Yamamoto, Ai; Yu, Wai Haung] Columbia Univ, Med Ctr, Dept Pathol & Cell Biol, New York, NY USA.
[Di Pietro, Chiara; Marazziti, Daniela; Matteoni, Raffaele; Tocchini-Valentini, Glauco] EMMA CNR, Inst Cell Biol & Neurobiol, Rome, Italy.
[Diaz-Araya, Guillermo] Univ Chile, Dept Pharmacol & Toxicol Chem, Santiago, Chile.
[Diaz-Laviada, Ines] Univ Alcala De Henares, Sch Med, Dept Biochem & Mol Biol, Madrid, Spain.
[Diaz-Meco, Maria T.; Fotedar, Rati; Hansen, Malene; Moscat, Jorge; Reed, John C.; Salvesen, Guy; Yang, Zhifen] Sanford Burnham Med Res Inst, La Jolla, CA USA.
[Diaz-Nido, Javier; Izquierdo, Marta] Univ Autonoma Madrid, UAM CSIC, Dept Biol Mol, Ctr Biol Mol Severo Ochoa, Madrid, Spain.
[Dikic, Ivan] Frankfurt Inst Mol Life Sci, Frankfurt, Germany.
[Dinesh-Kumar, Savithramma P.] Univ Calif Davis, Coll Biol Sci, Genome Ctr, Davis, CA 95616 USA.
[Dinesh-Kumar, Savithramma P.] Univ Calif Davis, Dept Plant Biol, Davis, CA 95616 USA.
[Ding, Wen-Xing] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, Kansas City, KS 66103 USA.
[Distelhorst, Clark W.; Subauste, Carlos S.] Case Western Reserve Univ, Univ Hosp Cleveland, Dept Med, Cleveland, OH 44106 USA.
[Distelhorst, Clark W.] Case Western Reserve Univ, Univ Hosp Cleveland, Dept Pharmacol, Cleveland, OH 44106 USA.
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[Diwan, Abhinav] Washington Univ, Sch Med, Cardiovasc Res Ctr, St Louis, MO USA.
[Diwan, Abhinav] Washington Univ, Sch Med, Dept Internal Med, St Louis, MO 63110 USA.
[Djavaheri-Mergny, Mojgan] Univ Bordeaux, INSERM, VINCO, U916, Bordeaux, France.
[Dokudovskaya, Svetlana] Univ Paris 11, CNRS, Inst Gustave Roussy, UMR 8126, Villejuif, France.
[Dong, Zheng] Georgia Hlth Sci Univ, Charlie Norwood VA Med Ctr, Department Cellular Biol & Anat, Augusta, GA USA.
[Dorsey, Frank C.] Eli Lilly & Co, Lilly Res Labs, Indianapolis, IN 46285 USA.
[Dosenko, Victor] Bogomoletz Inst Physiol, Gen & Mol Pathophysiol Dept, Kiev, Ukraine.
[Dowling, James J.] Univ Michigan, Sch Med, Dept Pediat & Communicable Dis, Ann Arbor, MI USA.
[Doxsey, Stephen] Univ Massachusetts, Sch Med, Dept Cell Biol, Worcester, MA 01655 USA.
[Dreux, Marlene] Ecole Normale Super Lyon, INSERM, Dept Human Virol, U758, F-69364 Lyon, France.
[Duan, Qiuhong] Huazhong Univ Techol & Sci, Tongji Med Coll, Dept Biochem & Mol Biol, Wuhan, Hubei, Peoples R China.
[Duchosal, Michel A.] Univ Lausanne Hosp, Div Hematol, Lausanne, Switzerland.
[Duchosal, Michel A.] Univ Lausanne Hosp, Cent Lab Hematol, Lausanne, Switzerland.
[Dugail, Isabelle; Maiuri, Maria Chiara] INSERM, Ctr Rech Cordeliers, Paris, France.
[Dugail, Isabelle] Univ Paris 06, Paris, France.
[Duszenko, Michael] Univ Tubingen, Dept Biochem, Tubingen, Germany.
[Edelstein, Charles L.] Univ Colorado Denver, Div Renal Dis & Hypertens, Aurora, CO USA.
[Edinger, Aimee L.] Univ Calif Irvine, Dept Dev & Cell Biol, Irvine, CA 92717 USA.
[Egea, Gustavo] Univ Barcelona, Fac Med, IDIBAPS, Dept Biol Celular Inmunol & Neurociencias, Barcelona 7, Spain.
[Eichinger, Ludwig; Noegel, Angelika A.] Univ Cologne, Fac Med, Inst Biochem 1, D-50931 Cologne, Germany.
[Eissa, N. Tony; Lin, Weei-Chin] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Ekmekcioglu, Suhendan] Univ Texas MD Anderson Canc Ctr, Dept Melanoma Med Oncol, Houston, TX 77030 USA.
[El-Deiry, Wafik S.] Penn State Coll Med, Penn State Hershey Med Ctr, Dept Med Hematol Oncol, Lab Translat Oncol & Expt Canc Therapeut, Hershey, PA USA.
[Elazar, Zvulun] Weizmann Inst Sci, Dept Biol Chem, IL-76100 Rehovot, Israel.
[Elgendy, Mohamed; Minucci, Saverio] Univ Milan, European Inst Oncol, Milan, Italy.
[Elgendy, Mohamed; Minucci, Saverio] Univ Milan, Dept Biomol Sci & Biotechnol, Milan, Italy.
[Ellerby, Lisa M.] Buck Inst Res Aging, Novato, CA USA.
[Eng, Kai Er; McInerney, Gerald M.] Karolinska Inst, Dept Microbiol Tumor & Cell Biol, Stockholm, Sweden.
[Engelbrecht, Anna-Mart; Loos, Benjamin] Univ Stellenbosch, Dept Physiol Sci, ZA-7600 Stellenbosch, South Africa.
[Engelender, Simone] Technion Israel Inst Technol, Bruce Rappaport Fac Med, Dept Pharmacol, IL-31096 Haifa, Israel.
[Erenpreisa, Jekaterina] Latvian Biomed Res & Study Ctr, Riga, Latvia.
[Eskelinen, Eeva-Liisa] Univ Helsinki, Dept Biosci, Helsinki, Finland.
[Espina, Virginia] George Mason Univ, Ctr Appl Prote & Mol Med, Manassas, VA USA.
[Fan, Huizhou] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Physiol & Biophys, Piscataway, NJ 08854 USA.
[Fan, Jia] Fudan Univ, Zhongshan Hosp, Liver Canc Inst, Shanghai 200433, Peoples R China.
[Fan, Qi-Wen; Ilkhanizadeh, Shirin; Weiss, William A.] Univ Calif San Francisco, Dept Neurol, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Fan, Qi-Wen; Ilkhanizadeh, Shirin; Weiss, William A.] Univ Calif San Francisco, Dept Pediat, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Fan, Qi-Wen; Ilkhanizadeh, Shirin; Weiss, William A.] Univ Calif San Francisco, Dept Neurol Surg, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Fan, Qi-Wen; Ilkhanizadeh, Shirin; Weiss, William A.] Univ Calif San Francisco, Brain Tumor Res Ctr, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA USA.
[Fang, Shengyun; Monteiro, Mervyn J.] Univ Maryland, Ctr Biomed Engn & Technol BioMET, Baltimore, MD 21201 USA.
[Fang, Shengyun] Univ Maryland, Dept Physiol, Baltimore, MD 21201 USA.
[Fang, Yongqi] Guangzhou Univ Chinese Med, Affiliated Hosp 1, Guangzhou, Guangdong, Peoples R China.
[Fanto, Manolis] Kings Coll London, MRC, Ctr Dev Neurobiol, London, England.
[Farkas, Thomas; Jaattela, Marja] Danish Canc Soc, Res Ctr, Copenhagen, Denmark.
[Farre, Jean-Claude; Nazarko, Taras Y.] Univ Calif San Diego, Div Biol Sci, Mol Biol Sect, La Jolla, CA 92093 USA.
[Faure, Mathias] Univ Lyon 1, F-69365 Lyon, France.
[Faure, Mathias] Univ Lyon, INSERM, U851, Lyon, France.
[Fechheimer, Marcus; Furukawa, Ruth H.] Univ Georgia, Dept Cellular Biol, Athens, GA 30602 USA.
[Feng, Carl G.] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Feng, Jian] SUNY Buffalo, Dept Physiol & Biophys, Buffalo, NY 14260 USA.
[Feng, Qili] S China Normal Univ, Sch Life Sci, Guangdong Prov Key Lab Biotechnol Plant Dev, Guangzhou, Guangdong, Peoples R China.
[Feng, Youji] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 1, Dept Obstet & Gynecol, Shanghai 200030, Peoples R China.
[Fesues, Laszlo] Univ Debrecen, Res Ctr Mol Med, Hungarian Acad Sci, Res Grp,Dept Biochem & Mol Biol, H-4012 Debrecen, Hungary.
[Fesues, Laszlo] Univ Debrecen, Res Ctr Mol Med, Hungarian Acad Sci, Res Grp,Dept Apoptosis & Genom, H-4012 Debrecen, Hungary.
[Feuer, Ralph] San Diego State Univ, Dept Biol, Cell & Mol Biol Joint Doctoral Program, San Diego, CA 92182 USA.
[Figueiredo-Pereira, Maria E.] CUNY, Hunter Coll, Dept Biol Sci, New York, NY 10021 USA.
[Fimia, Gian Maria] IRCCS L Spallanzani, Natl Inst Infect Dis, Rome, Italy.
[Fingar, Diane C.; Guan, Jun-Lin; Han, Ting; Lin, Jiandie D.] Univ Michigan, Sch Med, Dept Cell & Dev Biol, Ann Arbor, MI USA.
[Finkbeiner, Steven] Univ Calif San Francisco, Gladstone Inst, Taube Koret Ctr Huntingtons Dis, San Francisco, CA 94143 USA.
[Finkbeiner, Steven] Univ Calif San Francisco, Hellman Alzheimers Dis Program, San Francisco, CA 94143 USA.
[Finkel, Toren] NHLBI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Finley, Kim D.; Gottlieb, Roberta A.] San Diego State Univ, Biosci Ctr, San Diego, CA 92182 USA.
[Fisher, Edward A.] NYU, Sch Med, Dept Med, New York, NY USA.
[Fisher, Edward A.] NYU, Sch Med, Dept Cell Biol, Marc & Ruti Bell Program Vasc Biol, New York, NY 10016 USA.
[Fisher, Paul B.] Virginia Commonwealth Univ, Sch Med, VCU Inst Moleular Med, Dept Human & Mol Genet,VCU Massey Canc Ctr, Richmond, VA USA.
[Flajolet, Marc; Tian, Yuan] Rockefeller Univ, Lab Mol & Cellular Neurosci, New York, NY 10021 USA.
[Florez-McClure, Maria L.] Univ Colorado, Inst Behav Genet, Boulder, CO 80309 USA.
[Fon, Edward A.] McGill Univ, Dept Neurol & Neurosurg, McGill Parkinson Program, Montreal Neurol Inst, Montreal, PQ, Canada.
[Fornai, Francesco] Univ Pisa, Dept Human Morphol & Appl Biol, Pisa, Italy.
[Fornai, Francesco] IRCCS Neuromed, Pozzilli, Italy.
[Fortunato, Franco] Univ Heidelberg Hosp, Dept Surg, Res Lab, Heidelberg, Germany.
[Fox, Howard S.] Univ Nebraska, Med Ctr, Dept Pharmacol & Expt Neurosci, Omaha, NE USA.
[Franco, Rodrigo] Univ Nebraska, Sch Vet Med & Biomed Sci, Lincoln, NE USA.
[Franco, Rodrigo] Univ Nebraska, Redox Biol Ctr, Lincoln, NE USA.
[Frankel, Lisa B.; Lund, Anders H.] Univ Copenhagen, Biotech Res & Innovat Ctre, Copenhagen, Denmark.
[Fransen, Marc] Katholieke Univ Leuven, Dept Mol & Cellular Med, Louvain, Belgium.
[Fuentes, Jose M.; Gonzalez-Polo, Rosa Ana] Univ Extremadura, Dept Bioquim & Biol Mol Genet, EU Enfermeria, Ctr Invest Biomed Red Enfermedades Neurodegenerat, Caceres, Spain.
[Fujii, Jun] Kyushu Univ, Grad Sch Med Sci, Dept Bacteriol, Kagoshima, Japan.
[Fujisaki, Kozo; Umemiya-Shirafuji, Rika] Kyushu Univ, Dept Frontier Vet Med, Lab Emerging Infect Dis, Kagoshima, Japan.
[Fujita, Eriko] Jichi Med Univ, Dept Pediat, Shimotsuke, Tochigi, Japan.
[Fukuda, Mitsunori] Tohoku Univ, Grad Sch Life Sci, Dept Dev Biol & Neurosci, Sendai, Miyagi 980, Japan.
[Gaestel, Matthias; Menon, Manoj B.] Hannover Med Sch, Inst Physiol Chem, D-3000 Hannover, Germany.
[Gailly, Philippe] Univ Louvain, Lab Cell Physiol, Brussels, Belgium.
[Gajewska, Malgorzata; Motyl, Tomasz] Warsaw Univ Life Sci, Fac Vet Med, Dept Physiol Sci, Warsaw, Poland.
[Galy, Vincent] Univ Paris 06, CNRS, UMR 7622, Paris, France.
[Ganesh, Subramaniam] Indian Inst Technol, Dept Biol Sci & Bioengn, Kanpur 208016, Uttar Pradesh, India.
[Ganetzky, Barry] Univ Wisconsin, Genet Lab, Madison, WI 53706 USA.
[Ganley, Ian G.] Univ Dundee, Coll Life Sci, MRC, Prot Phosphorylat Unit, Dundee, Scotland.
[Gao, Fen-Biao] Univ Massachusetts, Sch Med, Dept Neurol, Worcester, MA USA.
[Gao, George F.] Chinese Acad Sci, Inst Microbiol, CAS Key Lab Pathogen Microbiol & Immunol, Beijing, Peoples R China.
[Gao, Jinming] UT SW Med Ctr, Dallas, TX USA.
[Garcia, Lorena; Lavandero, Sergio] Univ Chile, Fac Med, Santiago 7, Chile.
[Garcia, Lorena; Lavandero, Sergio] Univ Chile, Fac Ciencias Quim & Farmaceut, Ctr Estudios Mol Celula, Santiago 7, Chile.
[Garcia-Manero, Guillermo] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA.
[Garcia-Marcos, Mikel] Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA.
[Garmyn, Marjan] Katholieke Univ Leuven, Dept Oncol, Dermatol Lab, Louvain, Belgium.
[Gartel, Andrei L.] Univ Illinois, Dept Med, Chicago, IL USA.
[Gatti, Evelina; Golstein, Pierre; Pierre, Philippe] Univ Aix Marseille 2, Ctr Immunol Marseille Luminy, INSERM, UM2,U1104, F-13284 Marseille 07, France.
[Gatti, Evelina; Golstein, Pierre; Pierre, Philippe] CNRS, UMR7280, Marseille, France.
[Gautel, Mathias] Kings Coll London, Randall Div Cell & Mol Biophys, London WC2R 2LS, England.
[Gautel, Mathias] Kings Coll London, Div Cardiovasc, London WC2R 2LS, England.
[Gawriluk, Thomas R.; Hale, Amber N.; Ledbetter, Daniel J.; Rucker, Edmund B., III] Univ Kentucky, Dept Biol, Lexington, KY USA.
[Gegg, Matthew E.; Schapira, Anthony H. V.] UCL, Inst Neurol, Dept Clin Neurosci, London, England.
[Geng, Jiefei; Harper, J. Wade] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA USA.
[Germain, Marc; Slack, Ruth S.] Univ Ottawa, Dept Cellular Mol Med, Ottawa, ON, Canada.
[Gestwicki, Jason E.; Lieberman, Andrew; Lukacs, Nicholas W.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
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[Ghosh, Pradipta; Lee, Jongdae] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Giammarioli, Anna M.; Malorni, Walter] Ist Super Sanita, Dept Therapeut Res & Med Evaluat, I-00161 Rome, Italy.
[Giatromanolaki, Alexandra N.; Sivridis, Efthimios] Democritus Univ Thrace, Dept Pathol, Alexandroupolis, Greece.
[Giatromanolaki, Alexandra N.; Sivridis, Efthimios] Univ Gen Hosp Alexandroupolis, Alexandroupolis, Greece.
[Gibson, Spencer B.] Univ Manitoba, Manitoba Inst Cell Biol, Winnipeg, MB, Canada.
[Gilkerson, Robert W.; Przedborski, Serge; Sulzer, David; Yamamoto, Ai] Columbia Univ, Dept Neurol, Med Ctr, New York, NY USA.
[Ginger, Michael L.] Univ Lancaster, Sch Hlth & Med, Lancaster, England.
[Ginsberg, Henry N.; Tabas, Ira] Columbia Univ, Coll Phys & Surg, Dept Med, New York, NY USA.
[Golab, Jakub] Med Univ Warsaw, Dept Immunol, Warsaw, Poland.
[Goligorsky, Michael S.] New York Med Coll, Renal Res Inst, Valhalla, NY 10595 USA.
[Gomez-Manzano, Candelaria] Univ Texas MD Anderson Canc Ctr, Dept Genet, Houston, TX 77030 USA.
[Goncu, Ebru] Ege Univ, Fac Sci, Dept Biol, Izmir, Turkey.
[Gongora, Celine; Le Cam, Laurent; Legouis, Renaud; Pattingre, Sophie] Univ Montpellier I, INSERM, Inst Rech Cancerol Montpellier, U896, Montpellier, France.
[Gonzalez, Claudio D.; Vaccaro, Maira I.] Univ Buenos Aires, Dept Pathophysiol, Sch Pharm & Biochem, Buenos Aires, DF, Argentina.
[Gonzalez, Ramon] CSIC UR CAR, Inst Ciencias Vino, Logrono, Spain.
[Gonzalez-Estevez, Cristina] Univ Nottingham, Queens Med Ctr, Ctr Genet & Genom, Dept Dev Genet & Gene Control, Nottingham NG7 2RD, England.
[Gorbunov, Nikolai V.] Uniformed Serv Univ Hlth Sci, Henry M Jackson Fdn Adv Mil Med, Bethesda, MD 20814 USA.
[Gorski, Sharon] BC Canc Agcy, Genome Sci Ctr, Vancouver, BC, Canada.
[Goruppi, Sandro] Tufts Univ, Sch Med, Tufts Med Ctr, Mol Cardiol Res Inst, Boston, MA 02111 USA.
[Goruppi, Sandro] Tufts Univ, Sch Med, Dept Med, Boston, MA 02111 USA.
[Gozuacik, Devrim] Sabanci Univ, Biol Sci & Bioengn Program, Istanbul, Turkey.
[Green, Kim N.] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA USA.
[Gregorc, Ales] Agr Inst Slovenia, Ljubljana, Slovenia.
[Gros, Frederic] Univ Strasbourg, CNRS, Strasbourg, France.
[Grose, Charles] Univ Iowa, Dept Pediat, Childrens Hosp, Iowa City, IA 52242 USA.
[Grunt, Thomas W.] Med Univ Vienna, Ctr Comprehens Canc, Dept Med 1, Signaling Networks Program,Div Oncol, Vienna, Austria.
[Guan, Kun-Liang] Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA.
[Guan, Kun-Liang] Univ Calif San Diego, Moores Canc Ctr, La Jolla, CA 92093 USA.
[Gukovskaya, Anna S.; Gukovsky, Ilya] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Los Angeles, CA 90095 USA.
[Gunst, Jan; Van den Berghe, Greet; Vanhorebeek, Ilse] Katholieke Univ Leuven, Dept & Lab Intens Care Med, Louvain, Belgium.
[Gustafsson, Asa B.] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, San Diego, CA 92103 USA.
[Halayko, Andrew J.] Univ Manitoba, Manitoba Inst Child Hlth, Dept Internal Med, Winnipeg, MB, Canada.
[Halonen, Sandra K.] Montana State Univ, Dept Microbiol, Bozeman, MT 59717 USA.
[Hamasaki, Maho; Noda, Takeshi; Yoshimori, Tamotsu] Osaka Univ, Dept Genet, Grad Sch Med, Osaka, Japan.
[Han, Feng] Zhejiang Univ, Inst Pharmacol,Toxicol & Biochem Pharmaceut, Hangzhou 310003, Zhejiang, Peoples R China.
[Hancock, Michael K.] Life Technol, Discovery & ADMET TOX Syst, Madison, WI USA.
[Harada, Hisashi] Virginia Commonwealth Univ, Massey Canc Ctr, Dept Oral & Craniofacial Mol Biol, Richmond, VA USA.
[Harada, Masaru] Univ Occupat & Environm Hlth, Sch Med, Dept Internal Med 3, Kitakyushu, Fukuoka 807, Japan.
[Hardt, Stefan E.] Heidelberg Univ, Dept Cardiol Angiol & Pulmol, Heidelberg, Germany.
[Harris, Adrian L.] Univ Oxford, John Radcliffe Hosp, Weatherall Inst Mol Med, Mol Oncol Labs,Dept Oncol, Oxford OX3 9DU, England.
[Harris, James] Trinity Coll Dublin, Sch Biochem & Immunol, Immunol Res Ctr, Dublin, Ireland.
[Harris, Steven D.] Univ Nebraska, Ctr Plant Sci Innovat, Lincoln, NE USA.
[Hashimoto, Makoto] Tokyo Metropolitan Inst Med Sci, Div Sensory & Motor Syst, Tokyo 113, Japan.
[Haspel, Jeffrey A.] VA Boston Healthcare Syst, Boston, MA USA.
[Hayashi, Shin-ichiro] Natl Cerebral & Cardiovasc Ctr, Div Hypertens & Nephrol, Osaka, Japan.
[Hayashi, Shin-ichiro] Gifu Univ, Grad Sch Med, Dept Cell Signalling, Gifu, Japan.
[Hazelhurst, Lori A.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[He, Congcong; Levine, Beth; Terada, Lance S.] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA.
[He, Congcong; Levine, Beth; Terada, Lance S.] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA.
[He, You-Wen; Rathmell, Jeffrey C.; Taylor, Gregory A.] Duke Univ, Med Ctr, Dept Immunol, Durham, NC USA.
[Hebert, Marie-Josee] CRCHUM, Dept Nephrol, Montreal, PQ, Canada.
[Heidenreich, Kim A.] Univ Colorado, Sch Med, Dept Pharmacol, Aurora, CO USA.
[Helgason, Gudmundur V.; Holyoake, Tessa L.] Univ Glasgow, Inst Canc Sci, Coll Med Vet & Life Sci, Glasgow, Lanark, Scotland.
[Herman, Brian; Reiter, Russel J.] Univ Texas Hlth Sci Ctr San Antonio, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA.
[Herman, Paul K.] Ohio State Univ, Dept Mol Genet, Columbus, OH 43210 USA.
[Hetz, Claudio] Univ Chile, Fac Med, ICBM, Biomed Neurosci Inst, Santiago 7, Chile.
[Hilfiker, Sabine; Navarro, Miguel] CSIC, IPBLN, Inst Parasitol & Biomed Lopez Neyra, Dept Mol Biol, Granada, Spain.
[Hill, Joseph A.; Lavandero, Sergio; Nemchenko, Andriy] Univ Texas SW Med Ctr Dallas, Div Cardiol, Dallas, TX 75390 USA.
[Hofmann, Thomas G.] DKFZ ZMBH Alliance, German Canc Res Ctr, Cellular Senescence Grp A210, Heidelberg, Germany.
[Hoehfeld, Joerg] Univ Bonn, Inst Cell Biol, Bonn, Germany.
[Hong, Ming-Huang] Sun Yat Sen Univ, GCP Ctr, Guangzhou 510275, Guangdong, Peoples R China.
[Hood, David A.] York Univ, Sch Kinesiol & Hlth Sci, Toronto, ON M3J 2R7, Canada.
[Hotamisligil, Goekhan S.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Houwerzijl, Ewout J.] Univ Med Ctr Groningen, Dept Internal Med, NL-9713 AV Groningen, Netherlands.
[Hoyer-Hansen, Maria] LEO Pharma AS, Dept Mol Biomed, Ballerup, Denmark.
[Hu, Bingren] Univ Maryland, Sch Med, Shock Trauma & Anesthesiol Res Ctr, Baltimore, MD 21201 USA.
[Hu, Chien-An A.] Univ New Mexico, Sch Med, Dept Biochem & Mol Biol, Albuquerque, NM 87131 USA.
[Hu, Hong-Ming] Providence Portland Med Ctr, Earle A Chiles Res Inst, Lab Canc Immunobiol, Portland, OR USA.
[Hua, Ya] Univ Michigan, Dept Neurosurg, Ann Arbor, MI 48109 USA.
[Huang, Canhua; Liu, Bo] Sichuan Univ, State Key Lab Biotherapy, Chengdu 610064, Peoples R China.
[Huang, Shengbing; Sinicrope, Frank A.] Mayo Clin, Dept Med, Rochester, MN USA.
[Huang, Shengbing; Sinicrope, Frank A.] Mayo Canc Ctr, Rochester, MN USA.
[Huang, Wei-Pang] Natl Taiwan Univ, Dept Life Sci, Taipei 10764, Taiwan.
[Huang, Wei-Pang] Natl Taiwan Univ, Inst Zool, Taipei 10764, Taiwan.
[Huber, Tobias B.] Univ Freiburg, BIOSS Ctr Biol Signalling Studies, D-79106 Freiburg, Germany.
[Huber, Tobias B.] Univ Hosp Freiburg, Div Renal, Freiburg, Germany.
[Huh, Won-Ki] Seoul Natl Univ, Sch Biol Sci, Seoul, South Korea.
[Huh, Won-Ki] Seoul Natl Univ, Res Ctr Funct Cellul, Seoul, South Korea.
[Hung, Tai-Ho] Chang Gung Mem Hosp, Dept Obstet & Gynecol, Taipei 10591, Taiwan.
[Hupp, Ted R.] Univ Edinburgh, Dept Expt Canc Res, Inst Genet & Mol Med, Cell Signalling Unit, Edinburgh, Midlothian, Scotland.
[Hur, Gang Min] Chungnam Natl Univ, Coll Med, Dept Pharmacol, Infect Signaling Network,Res Ctr, Taejon, South Korea.
[Hurley, James B.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
[Hussain, Sabah N. A.] McGill Univ, Crit Care Dept, Montreal, PQ, Canada.
[Hussey, Patrick J.] Univ Durham, Sch Biol & Biomed Sci, Durham, England.
[Hwang, Jung Jin] Univ Ulsan, Coll Med, Inst Innovat Canc Res, Seoul, South Korea.
[Hwang, Jung Jin] Asan Med Ctr, Seoul, South Korea.
[Hwang, Seungmin] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
[Ichihara, Atsuhiro] Tokyo Womens Med Univ, Dept Med 2, Tokyo, Japan.
[Inoki, Ken] Univ Michigan, Sch Med, Dept Internal Med, Div Nephrol, Ann Arbor, MI USA.
[Inoki, Ken] Univ Michigan, Sch Med, Dept Mol & Integrat Physiol, Ann Arbor, MI USA.
[Into, Takeshi] Asahi Univ, Sch Dent, Dept Oral Microbiol, Div Oral Infect & Hlth Sci, Mizuho, Japan.
[Iovanna, Juan L.] Univ Aix Marseille 2, Marseille, France.
[Iovanna, Juan L.] INSERM, U624, F-13258 Marseille, France.
[Ip, Nancy Y.] Hong Kong Univ Sci & Technol, Div Life Sci, Hong Kong, Hong Kong, Peoples R China.
[Ip, Nancy Y.] Hong Kong Univ Sci & Technol, State Key Lab Mol Neurosci, Hong Kong, Hong Kong, Peoples R China.
[Isaka, Yoshitaka] Osaka Univ, Grad Sch Med, Dept Geriatr Med & Nephrol, Suita, Osaka, Japan.
[Ishida, Hiroyuki] Tohoku Univ, Grad Sch Agr Sci, Dept Appl Plant Sci, Sendai, Miyagi 980, Japan.
[Isobe, Ken-ichi] Nagoya Univ, Grad Sch Med, Dept Immunol, Nagoya, Aichi 4648601, Japan.
[Iwasaki, Akiko] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT USA.
[Izumi, Yotaro] Keio Univ, Sch Med, Divs Gen Thorac Surg, Tokyo, Japan.
[Jaakkola, Panu M.] Univ Turku, Ctr Biotechnol, Turku, Finland.
[Jackson, George R.] Univ Texas Med Branch, Dept Neurol, Galveston, TX USA.
[Jackson, William T.] Med Coll Wisconsin, Dept Microbiol & Mol Genet, Milwaukee, WI 53226 USA.
[Janji, Bassam] Publ Res Ctr Hlth CRP Sante, Dept Oncol, Lab Extpt Hematooncol, Luxembourg, Luxembourg.
[Jendrach, Marina] Goethe Univ Frankfurt, Dept Neurol, Univ Med Sch, Frankfurt, Germany.
[Jeon, Ju-Hong] Seoul Natl Univ, Coll Med, Dept Physiol, Seoul, South Korea.
[Jeung, Eui-Bae] Chungbuk Natl Univ, Coll Vet Med, Lab Vet Biochem & Mol Biol, Chonju, South Korea.
[Jiang, Hongchi; Ma, Yong; Wang, Dawei] Harbin Med Univ, Affiliated Hosp 1, Dept Gen Surg, Key Lab Hepatosplen Surg, Harbin, Peoples R China.
[Jiang, Jean X.] Univ Texas Hlth Sci Ctr San Antonio, Dept Biochem, San Antonio, TX 78229 USA.
[Jiang, Ming] Vanderbilt Univ, Med Ctr, Dept Urol Surg, Nashville, TN USA.
[Jiang, Qing] Purdue Univ, Dept Nutr Sci, W Lafayette, IN 47907 USA.
[Jiang, Xuejun; Overholtzer, Michael] Mem Sloan Kettering Canc Ctr, Dept Cell Biol, New York, NY 10021 USA.
[Jiang, Xuejun] Chinese Acad Sci, Inst Microbiol, State Key Lab Mycol, Beijing, Peoples R China.
[Jimenez, Alberto; Revuelta, Jose L.] Univ Salamanca, Dept Microbiol & Genet, E-37008 Salamanca, Spain.
[Jin, Shengkan] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pharmacol, Piscataway, NJ 08854 USA.
[Joe, Cheol O.; Lee, Gyun Min] Korea Adv Inst Sci & Technol, Dept Biol Sci, Taejon 305701, South Korea.
[Johansen, Terje; Lamark, Trond] Univ Tromso, Dept Biochem, Inst Med Biol, Tromso, Norway.
[Johnson, Daniel E.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Jones, Nicola L.] Univ Toronto, Dept Pediat, Cell Biol Program, Toronto, ON, Canada.
[Jones, Nicola L.] Univ Toronto, Dept Physiol, Toronto, ON, Canada.
[Joseph, Suresh K.] Thomas Jefferson Univ, Dept Pathol & Cell Biol, Philadelphia, PA 19107 USA.
[Joubert, Annie M.] Univ Pretoria, Dept Physiol, ZA-0002 Pretoria, South Africa.
[Juhasz, Gabor; Kovacs, Attila L.; Laszlo, Lajos; Low, Peter; Sass, Miklos] Eotvos Lorand Univ, Dept Anat Cell & Dev Biol, Budapest, Hungary.
[Juillerat-Jeanneret, Lucienne] CHUV Univ Lausanne, Univ Inst Pathol, Lausanne, Switzerland.
[Jung, Yong-Keun] Seoul Natl Univ, Dept Biol Sci, Seoul, South Korea.
[Kaarniranta, Kai] Univ Eastern Finland, Dept Ophthalmol, Kuopio, Finland.
[Kaarniranta, Kai] Kuopio Univ Hosp, SF-70210 Kuopio, Finland.
[Kabuta, Tomohiro; Wada, Keiji] Natl Ctr Neurol & Psychiat NCNP, Natl Inst Neurosci, Dept Degenerat Neurol Dis, Tokyo, Japan.
[Kadowaki, Motoni] Niigata Univ, Dept Appl Biol Chem, Niigata, Japan.
[Kagedal, Katarina] Linkoping Univ, Fac Hlth Sci, Dept Clin & Expt Med, Linkoping, Sweden.
[Kamada, Yoshiaki] Natl Inst Basic Biol, Lab Biol Divers, Okazaki, Aichi 444, Japan.
[Kaminskyy, Vitaliy O.; Zhivotovsky, Boris] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
[Kanamori, Hiromitsu; Takemura, Genzou] Gifu Univ, Grad Sch Med, Div Cardiol, Gifu, Japan.
[Kang, Chanhee] Harvard Univ, Brigham & Womens Hosp, Howard Hughes Med Inst, Div Genet,Med Sch, Boston, MA 02115 USA.
[Kang, Khong Bee] Natl Canc Ctr Singapore, Humphrey Oei Inst Canc Res, Div Med Sci, Singapore, Singapore.
[Kang, Kwang Il] Korea Adv Inst Sci & Technol, Korea Sci Acad, Dept Chem & Biol, Pusan, South Korea.
[Kang, Rui; Lotze, Michael T.; Tang, Daolin] Univ Pittsburgh, Inst Canc, Dept Surg, DAMP Lab,Hillman Canc Ctr, Pittsburgh, PA USA.
[Kanki, Tomotake] Kyushu Univ, Grad Sch Med Sci, Dept Clin Chem & Lab Med, Fukuoka 812, Japan.
[Kanneganti, Thirumala-Devi] St Jude Childrens Res Hosp, Dept Immunol, Memphis, TN 38105 USA.
[Kanno, Haruo] Tohoku Univ, Sch Med, Dept Orthopaed Surg, Sendai, Miyagi 980, Japan.
[Karantza, Vassiliki] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Internal Med, Div Med Oncol, Piscataway, NJ 08854 USA.
[Kaushal, Gur P.] Univ Arkansas Med Sci, Dept Med, Little Rock, AR 72205 USA.
[Kaushal, Gur P.] Univ Arkansas Med Sci, Cent Arkansas Vet Healthcare Syst, Little Rock, AR 72205 USA.
[Kawazoe, Yoshinori] Kyoto Univ, Inst Chem Res, Div Biochem, Kyoto 606, Japan.
[Ke, Po-Yuan] Chang Gung Univ, Coll Med, Dept Biochem & Mol Biol, Tao Yuan, Taiwan.
[Kehrl, John H.] NIAID, B Cell Mol Immunol Sect, Lab Immunoregulat, NIH, Bethesda, MD 20892 USA.
[Kelekar, Ameeta] Univ Minnesota, Dept Lab Med & Pathol, Ctr Canc, Minneapolis, MN 55455 USA.
[Kerkhoff, Claus] Fraunhofer Grp Extracorporeal Immune Modulat EXIM, Div Nephrol, Dept Internal Med, Rostock, Germany.
[Kessel, David H.] Wayne State Univ, Sch Med, Dept Pharmacol, Detroit, MI 48201 USA.
[Khalil, Hany] Menoufiya Univ, Genet Engn & Biotechnol Res Inst, Dept Mol Biol, El Sadat City, Egypt.
[Kiel, Jan A. K. W.; van der Klei, Ida J.] Univ Groningen, Groningen Biomol Sci & Biotechnol Inst GBB, Haren, Netherlands.
[Kiel, Jan A. K. W.; van der Klei, Ida J.] Univ Groningen, Kluyver Ctr Genom Ind Fermentat, Haren, Netherlands.
[Kiger, Amy A.] Univ Calif San Diego, Sect Cell & Dev Biol, La Jolla, CA 92093 USA.
[Kihara, Akio; Obara, Keisuke] Hokkaido Univ, Fac Pharmaceut Sci, Sapporo, Hokkaido 060, Japan.
[Kim, Deok Ryong] Gyeongsang Natl Univ, Sch Med, Inst Hlth Sci, Jinju, South Korea.
[Kim, Deok Ryong] Gyeongsang Natl Univ, Dept Biochem, Jinju, South Korea.
[Kim, Do-Hyung] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Minneapolis, MN USA.
[Kim, Dong-Hou; Yoon, Seung-Yong] Univ Ulsan, Coll Med, Dept Anat & Cell Biol, CDRC, Seoul, South Korea.
[Kim, Eun-Kyoung; Yu, Seong-Woon] Daegu Gyeongbuk Inst Sci & Technol, Dept Brain Sci, Taegu, South Korea.
[Kim, Hyung-Ryong] Wonkwang Univ, Coll Dent, Dept Dent Pharmacol, Chonbuk, South Korea.
[Kim, Jae-Sung] Univ Florida, Dept Surg, Gainesville, FL USA.
[Kim, Jeong Hun] Seoul Natl Univ, Coll Med, Dept Ophthalmol, Seoul, South Korea.
[Kim, Jeong Hun] Seoul Natl Univ, Clin Res Inst, Seoul, South Korea.
[Kim, Jin Cheon] Univ Ulsan, Coll Med, Dept Surg, Seoul, South Korea.
[Kim, John K.; Meisler, Miriam H.] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
[Kim, Peter K.; McQuibban, G. Angus] Univ Toronto, Dept Biochem, Toronto, ON, Canada.
[Kim, Seong Who] Univ Ulsan, Coll Med, Dept Biochem & Mol Biol, Seoul, South Korea.
[Kim, Yong-Sun; Koh, Young Ho] Hallym Univ, Coll Med, Ilsong Inst Life Sci, Chunchon, South Korea.
[Kim, Yong-Sun] Hallym Univ, Coll Med, Dept Microbiol, Chunchon, South Korea.
[Kim, Yonghyun; Marten, Mark R.] Univ Maryland Baltimore Cty, Dept Chem Biochem & Environm Engn, Baltimore, MD 21228 USA.
[Kimchi, Adi] Weizmann Inst Sci, Dept Mol Genet, IL-76100 Rehovot, Israel.
[Kimmelman, Alec C.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Radiat Oncol,Div Genom Stabil & DNA Repair, Boston, MA 02115 USA.
[King, Jason S.; Ryan, Kevin M.] Beatson Inst Canc Res, Tumor Cell Death Biol, Glasgow G61 1BD, Lanark, Scotland.
[Kinsella, Timothy J.] Brown Univ, Dept Radiat Oncol, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Kinsella, Timothy J.] Rhode Isl Hosp, Providence, RI USA.
[Kirkin, Vladimir] Merck KGaA, Merck Serono, Darmstadt, Germany.
[Kirshenbaum, Lorrie A.] Univ Manitoba, Dept Pharmacol & Therapeut, Inst Cardiovasc Sci, St Boniface Gen Hosp,Res Ctr, Winnipeg, MB, Canada.
[Kitamoto, Katsuhiko] Univ Tokyo, Dept Biotechnol, Tokyo, Japan.
[Kitazato, Kaio] Nagasaki Univ, Grad Sch Biomed Sci, Dept Mol Microbiol & Immunol, Nagasaka, Yamanashi, Japan.
[Klein, Ludger] Univ Munich, Inst Immunol, D-8000 Munich, Germany.
[Klimecki, Walter T.] Univ Arizona, Dept Pharmacol & Toxicol, Tucson, AZ 85721 USA.
[Klucken, Jochen] Univ Hosp, Div Mol Neurol, Erlangen, Germany.
[Knecht, Erwin] Ctr Invest Principe, Dept Cell Biol, Valencia, Spain.
[Ko, Ben C. B.] Chinese Univ Hong Kong, State Key Lab Oncol So China, Dept Anat & Cellular Pathol, Hong Kong, Hong Kong, Peoples R China.
[Koch, Jan C.; Lingor, Paul; Toenges, Lars] Univ Gottingen, Dept Neurol, D-3400 Gottingen, Germany.
[Koh, Jae-Young] Univ Ulsan, Coll Med, Dept Neurol, Seoul, South Korea.
[Koike, Masato; Uchiyama, Yasuo] Juntendo Univ, Sch Med, Dept Cell Biol & Neurosci, Tokyo 113, Japan.
[Komatsu, Masaaki; Tanaka, Keiji] Tokyo Metropolitan Inst Med Sci, Prot Metab Project, Tokyo 113, Japan.
[Kominami, Eiki; Ueno, Takashi] Juntendo Univ, Sch Med, Dept Biochem, Tokyo 113, Japan.
[Kong, Hee Jeong] Natl Fisheries Res & Dev Inst NFRDI, Biotechnol Res Div, Pusan, South Korea.
[Kong, Wei-Jia] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Otorhinolaryngol, Wuhan 430074, Peoples R China.
[Korolchuk, Viktor I.] Newcastle Univ, Inst Ageing & Hlth, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Kotake, Yaichiro] Hiroshima Univ, Grad Sch Biomed Sci, Hiroshima, Japan.
[Koukourakis, Michael I.] Democritus Univ Thrace, Dept Radiotherapy Oncol, Alexandroupolis, Greece.
Univ Vienna, Max Perutz Labs, Vienna, Austria.
[McLean, Pamela J.; Tannous, Bakhos A.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, MassGen Inst Neurodegenerat Dis, Charlestown, MA USA.
Univ Texas SW Med Ctr Dallas, Dept Neurosci, Dallas, TX 75390 USA.
Univ Texas SW Med Ctr Dallas, Dept Cell Biol, Dallas, TX 75390 USA.
Univ Lyon 1, CNRS, Ctr Genet & Physiol Mol & Cellulaire, UMR5534, F-69365 Lyon, France.
Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol, Boston, MA 02115 USA.
Univ Paris 05, Fac Med, Paris, France.
Univ Cologne, Inst Med Microbiol Immunol & Hyg, D-50931 Cologne, Germany.
Babraham Inst, Signaling Program, Cambridge, England.
Cincinnati Childrens Hosp Res Fdn, Div Dev Biol, Cincinnati, OH USA.
[Zoladek, Teresa] Polish Acad Sci, Inst Biochem & Biophys, Warsaw, Poland.
Univ Louisville, Sch Med, Dept Anat Sci & Neurobiol, Louisville, KY 40292 USA.
Commonwealth Med Coll, Dept Basic Sci, Scranton, PA USA.
St Jude Childrens Res Hosp, Dept Pathol, Memphis, TN 38105 USA.
Univ Calif Davis, Ctr Canc, Dept Biochem & Mol Med, Sacramento, CA 95817 USA.
Yonsei Univ, Coll Life Sci & Biotechnol, Dept Biotechnol, Seoul, South Korea.
Univ Calif San Diego, Dept Pediat, La Jolla, CA 92093 USA.
Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA.
Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA.
Univ Calif San Diego, Inst Genom Med, La Jolla, CA 92093 USA.
[Spector, Stephen A.] Rady Childrens Hosp, San Diego, CA USA.
[Lafont, Frank] Univ Lille Nord France, INSERM, Inst Pasteur Lille, Ctr Infect & Immun Lille,CNRS,UMR8204,U1019, Lille, France.
[Landry, Jacques; Lavoie, Josee N.] Univ Laval, Canc Res Ctr, Quebec City, PQ G1K 7P4, Canada.
[Lane, Jon D.] Univ Bristol, Sch Biochem, Bristol, Avon, England.
[Lapaquette, Pierre] Inst Pasteur, INSERM, Nucl Org & Oncogenesis Unit, U993, F-75724 Paris, France.
[Laporte, Jocelyn F.] Univ Strasbourg, CNRS, INSERM, Dept Translat Med,IGBMC,U964,UMR7104, Illkirch Graffenstaden, France.
[Layfield, Robert] Univ Nottingham, Queens Med Ctr, Sch Biomed Sci, Nottingham NG7 2RD, England.
[Lazo, Pedro A.; Mollinedo, Faustino] Univ Salamanca, CSIC, Inst Biol Mol & Celular Canc, E-37008 Salamanca, Spain.
[Le, Weidong; Legembre, Patrick] Shanghai Jiao Tong Univ, Chinese Acad Sci, Sch Med, Inst Hlth Sci, Shanghai 200030, Peoples R China.
[Le, Weidong; Legembre, Patrick; Li, Sheng] Chinese Acad Sci, Shanghai Inst Biol Sci, Shanghai, Peoples R China.
[Lee, Alvin J. X.; Swanton, Charles] Canc Res UK London Res Inst, Translat Canc Therapeut Lab, London, England.
[Lee, Byung-Wan] Yonsei Univ, Coll Med, Dept Internal Med, Seoul, South Korea.
[Lee, Ju-Hyun; Levy, Efrat; Nixon, Ralph A.; Yang, Dun-Sheng] NYU, Sch Med, Nathan S Kline Inst Psychiat Res, Dept Psychiat, Orangeburg, NY USA.
[Lee, Michael] Univ Incheon, Div Life Sci, Inchon, South Korea.
[Lee, Myung-Shik] Samsung Med Ctr, Dept Med, Seoul, South Korea.
[Lee, Sug Hyung] Catholic Univ Korea, Coll Med, Dept Pathobiol, Seoul, South Korea.
[Leeuwenburgh, Christiaan] Univ Florida, Dept Aging & Geriatr, Div Biol Aging, Gainesville, FL USA.
Univ Rennes 1, IRSET, INSERM, TeamDRaTE,U1085, Rennes, France.
Univ Paris 11, CNRS, Ctr Genet Mol, UPR3404, Gif Sur Yvette, France.
[Lehmann, Michael] Univ Arkansas, Dept Biol Sci, Fayetteville, AR 72701 USA.
[Lei, Huan-Yao] Natl Cheng Kung Univ, Coll Med, Dept Microbiol & Immunol, Tainan 70101, Taiwan.
[Lei, Qun-Ying] Fudan Univ, Shanghai Med Coll, Dept Biochem, Shanghai 200433, Peoples R China.
[Lei, Qun-Ying] Fudan Univ, Shanghai Med Coll, Dept Mol Biol, Shanghai 200433, Peoples R China.
[Lei, Qun-Ying] Fudan Univ, Shanghai Med Coll, Biomed Sci Inst, Shanghai 200433, Peoples R China.
[Leib, David A.] Dartmouth Med Sch, Dept Microbiol & Immunol, Lebanon, NH USA.
[Leiro, Jose] Univ Santiago Compostela, Inst Invest & Anal Alimentarios, Parasitol Lab, La Coruna, Spain.
[Lemasters, John J.] Med Univ S Carolina, Dept Pharmaceut & Biomed Sci, Charleston, SC 29425 USA.
[Lemasters, John J.] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
[Lemoine, Antoinette] Univ Paris 11, INSERM, APHP, Dept Biochem & Mol Biol,U1004, Villejuif, France.
[Lesniak, Maciej S.] Univ Chicago, Dept Surg & Canc Biol, Chicago, IL 60637 USA.
[Lev, Dina; McConkey, David J.] Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA.
[Levenson, Victor V.] Rush Univ, Med Ctr, Dept Radiat Oncol, Chicago, IL 60612 USA.
[Levy, Efrat] NYU, Sch Med, Nathan S Kline Inst Psychiat Res, Dept Pharmacol, Orangeburg, NY USA.
[Li, Faqiang; Vierstra, Richard D.] Univ Wisconsin, Dept Genet, Madison, WI 53706 USA.
[Li, Jun-Lin] Cent Hosp Yongzhou City, Dept Gen Surg, Yongzhou City, Hunan, Peoples R China.
[Li, Sheng] Inst Plant Physiol & Ecol, Key Lab Insect Dev & Evolutionary Biol, Shanghai, Peoples R China.
[Li, Weijie] Hanshan Normal Univ, Dept Chem, Chaozhou, Peoples R China.
[Li, Xue-Jun] Peking Univ, Dept Pharmacol, Sch Basic Med Sci, Beijing 100871, Peoples R China.
[Li, Yan-bo; Yin, Jia-jing] Harbin Med Univ, Affiliated Hosp 1, Dept Endocrinol, Harbin, Peoples R China.
[Li, Yi-Ping] Univ Texas Hlth Sci Ctr Houston, Dept Integrat Biol & Pharmacol, Houston, TX USA.
[Liang, Chengyu; Ou, Jing-hsiung James] Univ So Calif, Keck Sch Med, Dept Mol Microbiol & Immunol, Los Angeles, CA 90033 USA.
[Liang, Qiangrong] Univ S Dakota, Sanford Sch Med, Sioux Falls, SD USA.
[Liang, Qiangrong] Univ S Dakota, Sanford Res, Cardiovasc Hlth Res Ctr, Sioux Falls, SD USA.
[Liao, Yung-Feng] Acad Sinica, Inst Cellular & Organism Biol, Taipei 115, Taiwan.
[Liberski, Pawel P.; Sikorska, Beata] Med Univ Lodz, Dept Mol Pathol & Neuropathol, Lodz, Poland.
[Lim, Hyunjung J.] Konkuk Univ, Dept Biomed Sci & Technol, Seoul, South Korea.
[Lim, Kah-Leong; Pervaiz, Shazib; Soong, Tuck Wah] Natl Univ Singapore, Yong Loo Lin Sch Med, Dept Physiol, Singapore 117595, Singapore.
[Lim, Kyu] Chungnam Natl Univ, Coll Med, Dept Biochem, Canc Res Inst, Taejon, South Korea.
[Lim, Kyu] Chungnam Natl Univ, Coll Med, Infect Signaling Network Res Ctr, Taejon, South Korea.
[Lin, Chiou-Feng] Natl Cheng Kung Univ, Coll Med, Inst Clin Med, Tainan 70101, Taiwan.
[Lin, Fu-Cheng] Zhejiang Univ, Inst Biotechnol, Hangzhou 310003, Zhejiang, Peoples R China.
[Lin, Jian] Peking Univ, Coll Chem & Mol Engn, Beijing NMR Ctr, Beijing 100871, Peoples R China.
[Lin, Kui] Genentech Inc, Dept Canc Signaling, San Francisco, CA 94080 USA.
[Lin, Weei-Chin] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA.
[Linden, Rafael] Univ Fed Rio de Janeiro, Inst Biophys, Rio De Janeiro, Brazil.
[Lippincott-Schwartz, Jennifer] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, NIH, Bethesda, MD USA.
[Lisanti, Michael P.] Thomas Jefferson Univ, Kimmel Canc Ctr, Dept Stem Cell Biol, Philadelphia, PA 19107 USA.
[Lisanti, Michael P.] Univ Manchester, Breakthrough Breast Canc Res Unit, Manchester, Lancs, England.
[Liton, Paloma B.] Duke Univ, Dept Ophthalmol, Durham, NC USA.
[Liu, Chun-Feng] Soochow Univ, Dept Neurol, Affiliated Hosp 2, Suzhou, Peoples R China.
[Liu, Chun-Feng] Soochow Univ, Inst Neurosci, Suzhou, Peoples R China.
[Liu, Kaiyu] Cent China Normal Univ, Coll Life Sci, Wuhan, Peoples R China.
[Liu, Leyuan; Wang, Fen] Texas A&M Hlth Sci Ctr, Inst Biosci & Technol, Ctr Canc & StemCell Biol, Houston, TX USA.
[Liu, Qiong A.] SUNY Stony Brook, Dept Biochem & Cell Biol, Stony Brook, NY 11794 USA.
[Liu, Wei; Phang, James M.; Zabirnyk, Olga] NCI Frederick, Metab & Canc Susceptibil Sect, Basic Res Lab, Ctr Canc Res, Frederick, MD USA.
[Lockshin, Richard A.; Melendez, Alicia; Zakeri, Zahra] CUNY, Grad Ctr, Flushing, NY USA.
[Lockshin, Richard A.; Melendez, Alicia; Zakeri, Zahra] CUNY, Queens Coll, Dept Biol, Flushing, NY USA.
[Lopez-Otin, Carlos] Univ Oviedo, Dept Bioquim & Biol Mol, Inst Univ Oncol, Oviedo, Spain.
[Lossi, Laura; Merighi, Adalberto] Univ Turin, Turin, Italy.
[Lu, Binfeng] Univ Pittsburgh, Dept Immunol, Pittsburgh, PA USA.
[Lu, Bingwei] Stanford Univ, Dept Pathol, Sch Med, Stanford, CA 94305 USA.
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[Macian, Fernando; Santambrogio, Laura] Albert Einstein Coll Med, Dept Pathol, Bronx, NY 10467 USA.
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[Malorni, Walter] San Raffaele Sulmona Inst, Laquila, Italy.
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[Paris, Irmgard] Santo Tomas Univ, Vina Del Mar, Chile.
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[Peters, Godefridus J.] Vrije Univ Amsterdam, Med Ctr, Dept Med Oncol, Amsterdam, Netherlands.
[Petersen, Morten] Univ Copenhagen, Dept Biol, Copenhagen, Denmark.
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[Pierrefite-Carle, Valerie] Univ Nice Sophia Antipolis, Fac Med, CNRS, GePITOs,UMR 6235, Nice, France.
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[Pinkas-Kramarski, Ronit] Tel Aviv Univ, Dept Neurobiol, IL-69978 Tel Aviv, Israel.
[Piras, Antonio] Univ Turin, NICO, Orbassano, TO, Italy.
[Piri, Natik] Univ Calif Los Angeles, Jules Stein Eye Inst, Los Angeles, CA 90024 USA.
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[Poeggeler, Stefanie] Univ Gottingen, Inst Microbiol & Genet, Dept Genet Eukaryot Microogranisms, Gottingen, Germany.
[Poirot, Marc] Inst Claudius Regaud, Toulouse, France.
[Poletti, Angelo] Univ Milan, Dipartimento Endocrinol Fisiopatol & Biol Applica, Ctr Eccellenza Malattie Neurodegenerat, Milan, Italy.
[Poues, Christian] Univ Paris 11, EA4530, Chatenay Malabry, France.
[Pozuelo-Rubio, Mercedes] CSIC, Ctr Andaluz Biol Mol & Med Regenerat, E-41080 Seville, Spain.
[Praetorius-Ibba, Mette] Ohio State Univ, Dept Mol & Cellular Biochem, Columbus, OH 43210 USA.
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[Produit-Zengaffinen, Nathalie; Schorderet, Daniel F.] IRO, Sion, Switzerland.
[Progulske-Fox, Ann] Univ Florida, Dept Oral Biol, Gainesville, FL 32610 USA.
[Progulske-Fox, Ann] Univ Florida, Ctr Mol Microbiol, Gainesville, FL 32610 USA.
[Proikas-Cezanne, Tassula] Univ Tubingen, Dept Mol Biol, Tubingen, Germany.
[Przedborski, Serge] Columbia Univ, Ctr Motor Neuron Biol & Dis, New York, NY USA.
[Przyklenk, Karin] Wayne State Univ, Sch Med, Cardiovasc Res Inst, Detroit, MI USA.
[Przyklenk, Karin] Wayne State Univ, Sch Med, Dept Physiol, Detroit, MI 48201 USA.
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[Qian, Shu-Bing] Cornell Univ, Div Nutr Sci, Ithaca, NY 14853 USA.
[Qin, Liang] Chinese Acad Med Sci, Inst Basic Med Sci, Beijing 100730, Peoples R China.
[Qin, Liang] Chinese Acad Med Sci, Sch Basic Med, Beijing 100730, Peoples R China.
[Qin, Liang] Peking Union Med Coll, Dept Physiol, Beijing 100021, Peoples R China.
[Qin, Liang] Peking Union Med Coll, Dept Pathol, Beijing 100021, Peoples R China.
[Qin, Zheng-Hong; Wang, Guanghui; Zhang, Hui-Ling] Soochow Univ, Sch Pharmaceut Sci, Dept Pharmacol, Suzhou, Peoples R China.
[Quaggin, Susan E.] Univ Toronto, Samuel Lunenfeld Res Inst, Toronto, ON, Canada.
[Raben, Nina] NIAMSD, Arthrit & Rheumatism Branch, NIH, Bethesda, MD 20892 USA.
[Rabkin, Simon W.] Univ British Columbia, Dept Med, Vancouver, BC, Canada.
[Rahman, Irfan] Univ Rochester, Med Ctr, Dept Environm Med, Lung Biol & Dis Program, Rochester, NY 14642 USA.
[Rami, Abdelhaq] JWG Univ, Inst Cellular & Mol Anat, Frankfurt, Germany.
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[Randow, Felix; Williams, Roger L.] MRC, Mol Biol Lab, Cambridge CB2 2QH, England.
[Rao, V. Ashutosh] US FDA, Biochem Lab, Ctr Drug Evaluat & Res, Bethesda, MD 20014 USA.
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[Reed, Bruce H.] Univ Waterloo, Dept Biol, Waterloo, ON N2L 3G1, Canada.
[Regnier-Vigouroux, Anne] Johannes Gutenberg Univ Mainz, Dept Biol, Mainz, Germany.
[Regnier-Vigouroux, Anne] Johannes Gutenberg Univ Mainz, German Canc Res Ctr, Div Tumor Virol, Mainz, Germany.
[Reichert, Andreas S.] Goethe Univ Frankfurt, Zentrum Mol Med, Buchmann Inst Mol Life Sci, Frankfurt, Germany.
[Reiners, John J., Jr.] Wayne State Univ, Inst Environm Hlth Sci, Detroit, MI USA.
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[Roberge, Michel] Univ British Columbia, Dept Biochem & Mol Biol, Vancouver, BC V5Z 1M9, Canada.
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[Rocchi, Stephane] CHU Nice, Hop Archet 2, Serv Dermatol, Nice, France.
[de Cordoba, Santiago Rodriguez] Ctr Invest Biol CSIC & Ciber Enfermedades Raras, Madrid, Spain.
[Rohrer, Baerbel] Med Univ S Carolina, Div Ophthalmol, Charleston, SC 29425 USA.
[Rohrer, Baerbel] Med Univ S Carolina, Div Neurosci, Charleston, SC 29425 USA.
[Roninson, Igor B.] Univ S Carolina, S Carolina Coll Pharm, Dept Pharmaceut & Biomed Sci, Columbia, SC 29208 USA.
[Rost-Roszkowska, Magdalena M.] Univ Silesia, Dept Anim Histol & Embryol, Katowice, Poland.
[Rouis, Mustapha] UPMC, Unite Rech 04, Paris, France.
[Rouschop, Kasper M. A.] Maastricht Univ, GROW Sch Oncol & Dev Biol, Dept Radiat Oncol, Maastro Lab, Maastricht, Netherlands.
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[Ruckdeschel, Klaus] Univ Med Ctr Eppendorf, Inst Med Microbiol Virol & Hyg, Hamburg, Germany.
[Rudich, Assaf] Ben Gurion Univ Negev, Dept Clin Biochem, IL-84105 Beer Sheva, Israel.
[Rudich, Assaf] Ben Gurion Univ Negev, Natl Inst Biotechnol Negev, IL-84105 Beer Sheva, Israel.
[Rudolf, Emil] Charles Univ Prague, Fac Med Hradec Kralove, Dept Med Biol & Genet, Hradec Kralove, Czech Republic.
[Ruiz-Opazo, Nelson] Boston Univ, Sch Med, Sect Mol Med, Boston, MA 02118 USA.
[Russo, Rossella] Univ Calabria, Dept Pharmacol, Arcavacata Di Rende, Italy.
[Sabatini, David M.] MIT, Whitehead Inst, Dept Biol, Cambridge, MA 02139 USA.
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[Sakagami, Hiroshi] Meikai Univ, Sch Dent, Dept Diagnost & Therapeut Sci, Sakado, Saitama 35002, Japan.
[Sakai, Yasuyoshi] Kyoto Univ, Div Appl Life Sci, Grad Sch Agr, Kyoto, Japan.
[Sakai, Yasuyoshi] Kyoto Univ, Res Unit Physiol Chem, Ctr Promot Interdisciplinary Educ & Res, Kyoto, Japan.
[Salekdeh, Ghasem Hoseini] Agr Biotechnol Res Inst Iran, Dept Syst Biol, Karaj, Iran.
[Salomoni, Paolo] UCL Canc Inst, Samantha Dickson Brain Canc Unit, London, England.
[Salvaterra, Paul M.] City Hope Natl Med Ctr, Beckman Res Inst, Div Neurosci, Duarte, CA USA.
[Salvioli, Rosa] Ist Super Sanita, Dept Hematol Oncol & Mol Med, I-00161 Rome, Italy.
[Sanchez-Alcazar, Jose A.] Univ Pablo Olavide, Consejo Super Invest Cient Junta Andalucia, CABD, Seville, Spain.
[Sanchez-Prieto, Ricardo] Univ Castilla La Mancha, CRIB PcyTA, Lab Oncol Mol, Albacete, Spain.
[Sandri, Marco; Scorrano, Luca] Dulbecco Telethon Inst, Padua, Italy.
[Sandri, Marco; Schiaffino, Stefano] Venetian Inst Mol Med, Padua, Italy.
[Sankar, Uma] Univ Louisville, James Graham Brown Canc Ctr, Dept Pharmacol & Toxicol, Louisville, KY 40292 USA.
[Sankar, Uma] Univ Louisville, Owensboro Canc Res Program, Louisville, KY 40292 USA.
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[Scharl, Michael] Univ Zurich Hosp, Div Gastroenterol & Hepatol, CH-8091 Zurich, Switzerland.
[Schaetzl, Hermann M.] Univ Wyoming, Dept Vet Sci, Laramie, WY 82071 USA.
[Schaetzl, Hermann M.] Univ Wyoming, Dept Mol Biol, Laramie, WY 82071 USA.
[Scheper, Wiep] Univ Amsterdam, Acad Med Ctr, Dept Genome Anal, NL-1105 AZ Amsterdam, Netherlands.
[Scheper, Wiep] Univ Amsterdam, Acad Med Ctr, Dept Neurol, NL-1105 AZ Amsterdam, Netherlands.
[Schneider, Marion E.] Univ Ulm Klinikum, Sekt Expt Anasthesiol, Ulm, Germany.
[Schneider-Stock, Regine] Univ Erlangen Nurnberg, Inst Pathol, Erlangen, Germany.
[Schoenlein, Patricia V.] Med Coll Georgia, Dept Cellular Biol & Anat, Augusta, GA 30912 USA.
[Schueller, Christoph] Univ Nat Resources & Life Sci Vienna BOKU, Dept Appl Genet & Cell Biol, DAGZ, Vienna, Austria.
[Schwartz, Gary K.] Mem Sloan Kettering Canc Ctr, Mem Hosp Res Labs, New York, NY 10021 USA.
[Scorrano, Luca] Univ Geneva, Dept Cell Physiol & Med, Geneva, Switzerland.
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[Zorzano, Antonio] Univ Barcelona, Barcelona, Spain.
[Zorzano, Antonio] CIBERDEM, Inst Res Biomed, Barcelona, Spain.
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RP Klionsky, DJ (reprint author), Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
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Leonardo/G-1925-2012; Salekdeh, Ghasem Hosseini/R-8716-2016; Carra,
Serena/O-2835-2015; SHEN, Han-Ming/B-5942-2011; Martinez-Vicente,
Marta/K-4312-2014; Fransen, Marc/C-6262-2008; Dikic, Ivan/O-4650-2015;
MENENDEZ, JAVIER/C-6148-2016; Rouis, Mustapha/E-4993-2016; Gonzalez
Polo, Rosa-Ana/I-6076-2016; Menon, Manoj/P-1543-2015; Nakatogawa,
Hitoshi/D-5155-2015; di Ronza, Alberto/H-7674-2016; Butchar,
Jonathan/E-2825-2011; Musaro, Antonio/K-9598-2016; Escalante,
Ricardo/G-8272-2015; Choubey, Vinay/H-3170-2015; Wansink,
Derick/F-3404-2010; Soengas, Maria/H-6455-2015; Kaasik,
Allen/I-2738-2015; Martinet, Wim/I-7375-2015; Marchetti,
Piero/J-7439-2013; Sanchez-Alcazar, Jose A./L-4925-2014; Netea,
Mihai/N-5155-2014; Johansen, Terje/N-2971-2015; Koh,
Jae-Young/C-9014-2011; Koike, Masato/F-9584-2010; Tang,
Daolin/B-2905-2010; Votruba, Marcela/B-7306-2015; Nanotechnology
Characterization Lab, NCL/K-8454-2012; Pervaiz, Shazib/C-4188-2015;
Segura-Aguilar, Juan/H-8839-2013; wang, baocheng/B-7805-2008; Zhang,
Miqin/F-5537-2010; Lazo, Pedro /M-6435-2014; MESCHINI,
STEFANIA/E-9091-2015; Obara, Keisuke/A-3824-2012; Crespo,
Jose/L-3977-2014; Nguyen, Huu Phuc/F-5390-2015; Besteiro,
Sebastien/F-3622-2014; LICEND, CEMND/F-1296-2015; Hilfiker,
Sabine/L-6369-2014; Knecht, Erwin/K-2432-2014; Bornhauser,
Beat/M-4437-2014; FAURE, Mathias/M-5627-2014; Dreux,
Marlene/M-7295-2014; Sanchez-Prieto, Ricardo/B-6877-2008; Cheng,
Alan/M-9319-2013; Xie, Zhiping/A-1306-2015; Wang, Hong-Gang/A-3018-2015;
Thumm, Michael/A-8033-2015; Chen, Yongsheng/D-3256-2011; Navarro,
Miguel/C-3685-2009; Kabuta, Tomohiro/B-2948-2015; Thevissen,
Karin/B-7003-2015; Talbot, Nicholas/I-9584-2014; GROS,
Frederic/G-6332-2013; Fang, Shengyun/H-3802-2011; Petersen,
Morten/J-5023-2014; Muller, Sylviane/J-5319-2014; Gegg,
Matthew/B-4826-2011; Boya, Patricia/K-2911-2014; Rodriguez de Cordoba,
Santiago/K-6727-2014; Chu, Charleen/B-1601-2008; Yoshimori,
Tamotsu/K-9626-2014; GONZALEZ-REY, ELENA/L-3296-2014; Bortoluci, Karina
/C-6018-2012; Liu, Yule/E-5700-2010; Lane, Jon/A-9320-2011; Chuang,
Tsung-Hsien/F-9679-2010; Liao, Yung-Feng/A-9761-2011; Yoon,
Seung-Yong/E-9959-2012; Hwang, Jung Jin /F-3424-2014; Lund,
Anders/F-4786-2014; Kirshenbaum, Lorrie/F-5742-2014; Gorski,
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Stefan/H-2617-2014; Fuentes, Jose/H-9490-2014; Nezis,
Ioannis/I-4910-2014; Malagoli, Davide/I-5412-2014; Linden,
Rafael/F-2275-2011; Meyer, Thomas F./J-2485-2013; Wang,
Xuejun/K-8874-2013; Cardoso, Sandra/L-1962-2013; Diaz-Nido,
Javier/L-2371-2013; Andrieu-Abadie, Nathalie/N-6793-2013; Banhegyi,
Gabor/A-1476-2014; Golstein, Pierre/A-4954-2014; Walter,
Jochen/B-3677-2014; Knecht, Erwin/A-9366-2014; Yoshimoto,
Kohki/C-6322-2011; Bydlowski, Sergio/D-5171-2013; Lee, Myung
Shik/C-9606-2011; Brady, Nathan/H-2452-2013; zhu, wei-guo/E-1334-2012;
Hetz, Claudio/I-1900-2013; Joe, Cheol O/C-1917-2011; Lee, Gyun
Min/C-2020-2011; Yoo, Ook Joon/C-1860-2011; Galliot,
Brigitte/I-7051-2013; Voitsekhovskaja, Olga/B-8422-2013; laporte,
jocelyn/J-7008-2012; Michels, Paul/A-5637-2009; Mizushima,
Noboru/C-3635-2009; Yuzaki, Michisuke/K-5328-2013; Golab,
Jakub/K-6974-2013; Zhou, Cong-Zhao/E-9174-2011; Engelbrecht,
Anna-Mart/B-5846-2011;
OI Gonzalez, Ramon/0000-0001-7388-1660; Poletti,
Angelo/0000-0002-8883-0468; Poirot, Marc/0000-0002-5711-6624; Schapira,
Anthony/0000-0002-3018-3966; Codogno, Patrice/0000-0002-5492-3180;
Kanki, Tomotake/0000-0001-9646-5379; Juhasz, Gabor/0000-0001-8548-8874;
Velasco, Guillermo/0000-0002-1994-2386; Johnson,
David/0000-0001-5491-3460; Wu, William K.K./0000-0002-5662-5240;
Tavernarakis, Nektarios/0000-0002-5253-1466; Votruba,
Marcela/0000-0002-7680-9135; van Grunsven, Leo/0000-0002-0990-7034;
Bast, Robert/0000-0003-4621-8462; Smith, Duncan /0000-0002-6592-9852;
Sternberg, Cinthya/0000-0002-4760-6339; Johnson,
Gail/0000-0003-3464-0404; Wang, Haichao/0000-0002-0211-9000; Clarke,
Robert/0000-0002-9278-0854; Noda, Takeshi/0000-0003-3581-7961; Viola,
Giampietro/0000-0001-9329-165X; Willbold, Dieter/0000-0002-0065-7366;
Moreira, Paula/0000-0001-5177-6747; Yang, Shi Yu/0000-0001-8517-9238;
Stork, Bjorn/0000-0002-4167-7806; Skulachev,
Vladimir/0000-0003-4886-2243; Perry, George/0000-0002-6547-0172; Marino,
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Jason/0000-0003-0596-4506; Siu, Parco/0000-0002-3548-5058; Aris,
John/0000-0002-6475-064X; Hussey, Patrick/0000-0002-7349-8722;
Garcia-Marcos, Mikel/0000-0001-9513-4826; Cardoso, Sandra
M/0000-0002-2199-0555; Mollereau, Bertrand/0000-0003-4710-8185;
Djavaheri-Mergny, Mojgan/0000-0003-4893-6505; Apostolova,
Nadezda/0000-0002-4487-2471; Ledbetter, Daniel/0000-0002-5877-5904;
Aguirre-Ghiso, Julio/0000-0002-6694-6507; Gibson,
Spencer/0000-0003-0119-732X; Lee, Alvin/0000-0002-7427-9142; Franco,
Rodrigo/0000-0003-3241-8615; brest, patrick/0000-0002-1252-4747;
Revuelta, Jose/0000-0001-7838-5308; Jimenez,
Alberto/0000-0003-3685-6479; Zaffaroni, Nadia/0000-0002-4669-0890;
Novak, Ivana/0000-0003-0682-7052; AUBERGER, Patrick/0000-0002-2481-8275;
Rocchi, Stephane/0000-0002-0943-1304; Lopez-Otin,
Carlos/0000-0001-6964-1904; Chevet, Eric/0000-0001-5855-4522; Al-Younes,
Hesham/0000-0002-8210-9514; Tettamanti, Gianluca/0000-0002-0665-828X;
Fiorito, Filomena/0000-0002-6658-7807; Cho, Chi Hin/0000-0002-7658-3260;
SOLDATI, Thierry/0000-0002-2056-7931; KIHARA, AKIO/0000-0001-5889-0788;
McLaughlin, BethAnn/0000-0003-0228-6500; Travassos,
Leonardo/0000-0003-1323-3797; Carra, Serena/0000-0003-0939-0140; SHEN,
Han-Ming/0000-0001-7369-5227; Martinez-Vicente,
Marta/0000-0001-7053-2625; Dikic, Ivan/0000-0001-8156-9511; MENENDEZ,
JAVIER/0000-0001-8733-4561; Gonzalez Polo, Rosa-Ana/0000-0002-0163-2953;
Menon, Manoj/0000-0001-5859-0347; Nakatogawa,
Hitoshi/0000-0002-5828-0741; di Ronza, Alberto/0000-0002-9813-5143;
Musaro, Antonio/0000-0002-2944-9739; Escalante,
Ricardo/0000-0001-8547-531X; Soengas, Maria/0000-0003-0612-6299;
Marchetti, Piero/0000-0003-4907-0635; Sanchez-Alcazar, Jose
A./0000-0001-9705-1469; Johansen, Terje/0000-0003-1451-9578; Koh,
Jae-Young/0000-0002-4318-495X; Koike, Masato/0000-0002-3174-5684;
Votruba, Marcela/0000-0002-7680-9135; Segura-Aguilar,
Juan/0000-0002-1018-673X; wang, baocheng/0000-0002-8236-8014; Zhang,
Miqin/0000-0001-8974-1494; Lazo, Pedro /0000-0001-8997-3025; MESCHINI,
STEFANIA/0000-0001-9079-1181; Crespo, Jose/0000-0003-3514-1025; Nguyen,
Huu Phuc/0000-0001-6139-788X; Besteiro, Sebastien/0000-0003-1853-1494;
Hilfiker, Sabine/0000-0002-5167-7682; Knecht, Erwin/0000-0002-7208-3832;
Dreux, Marlene/0000-0002-6607-4796; Sanchez-Prieto,
Ricardo/0000-0003-0882-9780; Cheng, Alan/0000-0001-7897-4751; Xie,
Zhiping/0000-0001-5816-6159; Chen, Yongsheng/0000-0003-1448-8177;
Navarro, Miguel/0000-0003-2301-2699; Thevissen,
Karin/0000-0003-0275-9072; Talbot, Nicholas/0000-0001-6434-7757; GROS,
Frederic/0000-0002-6252-4323; Petersen, Morten/0000-0002-3035-5991;
Gegg, Matthew/0000-0001-8093-0723; Boya, Patricia/0000-0003-3045-951X;
Rodriguez de Cordoba, Santiago/0000-0001-6401-1874; Chu,
Charleen/0000-0002-5052-8271; Yoshimori, Tamotsu/0000-0001-9787-3788;
GONZALEZ-REY, ELENA/0000-0003-3917-9020; Bortoluci, Karina
/0000-0001-6780-5397; Liu, Yule/0000-0002-4423-6045; Yoon,
Seung-Yong/0000-0003-0325-9993; Gorski, Sharon/0000-0002-3821-8289;
Olsson, Stefan/0000-0003-1931-9081; Fuentes, Jose/0000-0001-6910-2089;
Nezis, Ioannis/0000-0003-0233-7574; Malagoli,
Davide/0000-0002-9857-8534; Linden, Rafael/0000-0003-3287-336X; Meyer,
Thomas F./0000-0002-6120-8679; Wang, Xuejun/0000-0001-9267-1343;
Diaz-Nido, Javier/0000-0002-0927-7925; Andrieu-Abadie,
Nathalie/0000-0003-2698-1970; Golstein, Pierre/0000-0003-1750-3483;
Yoshimoto, Kohki/0000-0003-3948-3751; Hetz, Claudio/0000-0001-7724-1767;
Voitsekhovskaja, Olga/0000-0003-0966-1270; Mizushima,
Noboru/0000-0002-6258-6444; Yuzaki, Michisuke/0000-0002-5750-3544;
Golab, Jakub/0000-0002-2830-5100; Kim, Do-Hyung/0000-0002-2924-4370;
Korolchuk, Viktor/0000-0002-4071-592X; Mottram,
Jeremy/0000-0001-5574-3766; Marazziti, Daniela/0000-0002-1582-9271;
SIMONE, Cristiano/0000-0002-2628-7658; Galliot,
Brigitte/0000-0001-7596-8284; Gozuacik, Devrim/0000-0001-7739-2346;
Fallon, Brian/0000-0003-1797-9713; Paris, Irmgard/0000-0003-2331-7513;
legembre, patrick/0000-0001-6649-8049; Parys, Jan/0000-0002-3591-4967;
HUANG, WEI-PANG/0000-0001-8410-6555; Marciniak,
Stefan/0000-0001-8472-7183; Ryan, Kevin M./0000-0002-1059-9681; Marten,
Mark/0000-0002-1863-8956; Brunetti-Pierri, Nicola/0000-0002-6895-8819;
Almasan, Alex/0000-0002-8916-6650; Zhang, Xu Dong/0000-0001-9457-8003;
Lee, Ju-hyun/0000-0002-0280-8375; Balduini, Walter/0000-0001-8438-9559;
Mograbi, Baharia/0000-0002-1025-3429; Frankel, Lisa/0000-0001-7249-3607;
Khalil, Hany/0000-0001-9738-4087; malorni, walter/0000-0002-1223-7000;
Hocking, Lynne J/0000-0002-2414-2826; Rouschop,
Kasper/0000-0002-4208-5415; Condorelli, Fabrizio/0000-0002-9943-0857;
Palumbo, Camilla/0000-0001-5087-7140; Panaretakis,
Theocharis/0000-0001-5754-6950; LIANG, CHENGYU/0000-0001-6082-2143;
D'Amelio, Marcello/0000-0001-6526-1832; Bozhkov,
Peter/0000-0002-8819-3884; Van der Klei, Ida J./0000-0001-7165-9679;
Sinclair, David/0000-0002-9936-436X; De Felici,
Massimo/0000-0001-8479-8264; Wang, Xinglong/0000-0001-8657-0159; Russo,
Rossella/0000-0001-8758-6523; CASARI, Giorgio/0000-0002-0115-8980;
gatti, evelina/0000-0002-0667-0799; Whitworth,
Alexander/0000-0002-1154-6629; Grant, Gary/0000-0002-2574-5442;
Berliocchi, Laura/0000-0002-3014-1838; FORNAI,
FRANCESCO/0000-0002-3883-5084; SETTEMBRE, Carmine/0000-0002-5829-8589;
Zhou, Cong-Zhao/0000-0002-6881-7151; CHEN,
CHING-CHOW/0000-0002-7810-0939; Hofman, Paul/0000-0003-0431-9353;
pierre, philippe/0000-0003-0863-8255; Ganley, Ian/0000-0003-1481-9407;
Ko, Ben Chi Bun/0000-0003-2027-5899; Fox, Howard/0000-0003-2032-374X;
McInerney, Gerald/0000-0003-2257-7241; Low, Peter/0000-0003-2450-7087;
De Milito, Angelo/0000-0003-2591-2914; Leiro Vidal, Jose
Manuel/0000-0001-6963-515X; Chisari, Francis/0000-0002-4832-1044;
Isidoro, Ciro/0000-0002-5494-3034; BRANCOLINI,
Claudio/0000-0002-6597-5373; Lavandero, Sergio/0000-0003-4258-1483;
holyoake, tessa/0000-0002-0608-6066; Kramer, Helmut/0000-0002-1167-2676;
Gaestel, Matthias/0000-0002-4944-4652; Cadwell, Ken/0000-0002-5860-0661;
Simon, Hans-Uwe/0000-0002-9404-7736; Espina,
Virginia/0000-0001-5080-5972; Lingor, Paul/0000-0001-9362-7096; Jung,
Yong-Keun/0000-0002-9686-3120; Hwang, Seungmin/0000-0003-0846-5462;
Clague, Michael/0000-0003-3355-9479; Scorrano, Luca/0000-0002-8515-8928;
Demarchi, Francesca/0000-0003-1565-3162; Ruiz-Opazo,
Nelson/0000-0001-8234-1332; Zhivotovsky, Boris/0000-0002-2238-3482;
Deretic, Vojo/0000-0002-3624-5208; COTO-MONTES, ANA/0000-0002-6609-6258;
Lund, Anders/0000-0002-7407-3398; Marambaud,
Philippe/0000-0002-8983-1497; BALLABIO, Andrea/0000-0003-1381-4604; YUN,
Cheol-Heui/0000-0002-0041-2887; Wu, Daocheng/0000-0002-6183-539X;
Simonsen, Anne/0000-0003-4711-7057; Tonges, Lars/0000-0001-6621-144X;
Liton, Paloma/0000-0002-1440-3762; Subauste, Carlos/0000-0002-5602-1439;
Cecconi, Francesco/0000-0002-5614-4359; Kanneganti,
Thirumala-Devi/0000-0002-6395-6443; Mostowy, Serge/0000-0002-7286-6503;
Nakano, Hiroyasu/0000-0003-4843-1427; Bultynck,
Geert/0000-0002-5968-4828; Ginger, Michael/0000-0002-9643-8482; Bechet,
Daniel/0000-0002-3812-8099; Lin, Wan Wan/0000-0002-3207-734X; Kehrl,
John/0000-0002-6526-159X; Macian, Fernando/0000-0003-2666-035X; Carding,
Simon/0000-0002-2383-9701; Piras, Antonio/0000-0003-3052-1715; Harris,
Adrian/0000-0003-1376-8409; Egea, Gustavo/0000-0001-5242-150X; MATTEONI,
RAFAELE/0000-0002-0314-5948; Kaminskyy, Vitaliy/0000-0002-8151-5270;
/0000-0003-3505-3674; Wouters, Bradly/0000-0002-8187-592X; Kaarniranta,
Kai/0000-0003-2600-8679; Kabuta, Tomohiro/0000-0002-3058-2596; Jaattela,
Marja/0000-0001-5950-7111; Kumar, Sharad/0000-0001-7126-9814; Weiss,
William/0000-0003-2230-9132; Tschan, Mario P./0000-0001-5897-3647;
Zacks, David/0000-0001-8592-5165; Nishino, Ichizo/0000-0001-9452-112X;
Kim, Yonghyun/0000-0001-6344-1258; Zhu, Wei-Guo/0000-0001-8385-6581;
Merighi, Adalberto/0000-0002-1140-3556; Engelbrecht,
Anna-Mart/0000-0003-1469-0148; Skop, Vojtech/0000-0002-4685-4429;
Batoko, Henri/0000-0002-8256-519X; Schiaffino,
Stefano/0000-0002-5607-6421; Munger, Karl/0000-0003-3288-9935; Chen,
Quan/0000-0001-7539-8728
FU National Institutes of Health Public Health Service [GM53396]
FX In a rapidly expanding and highly dynamic field such as autophagy, it is
possible that some authors who should have been included on this
manuscript have been missed. D.J.K. extends his apologies to researchers
in the field of autophagy who, due to oversight or any other reason,
could not be included. This work was supported by National Institutes of
Health Public Health Service grant GM53396 to D.J.K. Due to space and
other limitations, it is not possible to include all other sources of
financial support.
NR 884
TC 1731
Z9 1809
U1 266
U2 2286
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 1554-8627
EI 1554-8635
J9 AUTOPHAGY
JI Autophagy
PD APR
PY 2012
VL 8
IS 4
BP 445
EP 544
DI 10.4161/auto.19496
PG 100
WC Cell Biology
SC Cell Biology
GA 960QQ
UT WOS:000305403400002
PM 22966490
ER
PT J
AU Marotta, F
Naito, Y
Jain, S
Lorenzetti, A
Soresi, V
Kumari, A
Bastos, PC
Tomella, C
Yadav, H
AF Marotta, F.
Naito, Y.
Jain, S.
Lorenzetti, A.
Soresi, V.
Kumari, A.
Bastos, P. Carrera
Tomella, C.
Yadav, H.
TI IS THERE A POTENTIAL APPLICATION OF A FERMENTED NUTRACEUTICAL IN ACUTE
RESPIRATORY ILLNESSES? AN IN-VIVO PLACEBO-CONTROLLED, CROSS-OVER
CLINICAL STUDY IN DIFFERENT AGE GROUPS OF HEALTHY SUBJECTS
SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Article
DE fermented papaya preparation; epigenomic modification; nasal lavage
ID EXTRACELLULAR-SUPEROXIDE DISMUTASE; INFLUENZA-VIRUS INFECTION; PAPAYA
PREPARATION; NITRIC-OXIDE; OXIDATIVE DAMAGE; IMMUNOGLOBULIN-A; OXYGEN
RADICALS; LUNG; MICE; PATHOGENESIS
AB The role of oxidants in viral diseases is fairly complex because it includes metabolic regulation both of host metabolism and viral replication. However, a role for reactive oxygen species (ROS) and reactive nitrogen species (RNS) as mediators of virus-induced lung damage is supported by studies and antioxidants can thus be expected to act at many different levels. The aim of the present pilot study was to test an antioxidant nutraceutical approach on some relevant immunological parameters known to be affected in common seasonal respiratory tract infection. The study population consisted of 90 sedentary healthy patients, previously selected as being GSTM1-positive, divided into three groups: A) 20-40 years; B) 41-65 years; B) over 65 years. Each patients was administered a life style and dietary questionnaire. Subjects were supplemented for 6 weeks with either 9g/day (4.5g twice a day sublingually) of a fermented papaya preparation (Osato Research Institute, Gifu, Japan) or placebo. After a further month period of wash out, subjects were treated again in a crossover manner. Parameters checked were as fellows: routine blood tests with WBC formula, saliva flow rate and secretary IgA and lysozyme production and redox gene expression of Phase II enzyme and SOD from upper airways cells (from nasal lavage). Salivary secretion rate showed an age-related decline and was significantly increased by FPP supplementation only in the youngest age-group (p<0.05). Subjects treated with FPP showed a significantly higher lever of IgA and lisozyme production., irrespective of age group while their baseline production was significantly lower in the oldest age-group as compared to the youngest one (C vs A, p<0.05). FPP treatment brought about a significant upregulation of all phase II enzyme and SOD gene expression tested in nasal lavage cells. In conclusion, FPP supplementation during 1 month resulted in higher salivary IgA and increase in phase II and SOD enzyme expression, i.e the most important antioxidant in the respiratory tract. The biological significance of these effects i.e., whether it will help reducing the whole respiratory oxidative stress in the human airway and, hopefully, the incidence and/or severity of URTI remains to be demonstrated in longer clinical trials.
C1 [Marotta, F.; Lorenzetti, A.; Soresi, V.; Tomella, C.] ReGenera Res Grp Aging Intervent, Milan, Italy.
[Naito, Y.] Immunol Res Inst & Clin, Nagoya, Aichi, Japan.
[Jain, S.; Yadav, H.] NIDDK, NIH, Bethesda, MD USA.
[Kumari, A.] Univ Quebec, Ctr Eau Terre & Environm, Inst Natl Rech Sci, Quebec City, PQ, Canada.
[Bastos, P. Carrera] Lund Univ Malmo, Fac Med, Ctr Primary Hlth Care Res, Malmo, Sweden.
RP Marotta, F (reprint author), Piazza Firenze 12, I-20154 Milan, Italy.
EM fmarchimede@libero.it
NR 41
TC 7
Z9 7
U1 0
U2 3
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD APR-JUN
PY 2012
VL 26
IS 2
BP 285
EP 294
PG 10
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
Experimental; Physiology
SC Endocrinology & Metabolism; Immunology; Research & Experimental
Medicine; Physiology
GA 982HX
UT WOS:000307034900014
PM 22824755
ER
PT J
AU Pisetsky, DS
Ward, MM
AF Pisetsky, David S.
Ward, Michael M.
TI Advances in the treatment of inflammatory arthritis
SO BEST PRACTICE & RESEARCH IN CLINICAL RHEUMATOLOGY
LA English
DT Article
DE Rheumatoid arthritis; Spondyloarthritis; Ankylosing spondylitis
ID EARLY RHEUMATOID-ARTHRITIS; SOCIETY CLASSIFICATION CRITERIA; GENOME-WIDE
ASSOCIATION; ANKYLOSING-SPONDYLITIS; PSORIATIC-ARTHRITIS; SUSCEPTIBILITY
LOCI; AMERICAN-COLLEGE; DOUBLE-BLIND; BACK-PAIN; RHEUMATOLOGY/EUROPEAN
LEAGUE
AB The inflammatory arthritides are a diverse group of conditions characterised by joint inflammation which can lead to pain, deformity and disability. Of these diseases, rheumatoid arthritis (RA) and spondyloarthritis are two of the most common. While the clinical and demographic features of these diseases differ, the central role of inflammation in their pathogenesis has allowed the development of highly effective treatment strategies with wide applicability. These strategies include the use of biological agents which target the cytokine tumour necrosis factor (TNF), a key mediator of inflammation. With the advent of effective agents, therapy has become more aggressive, reducing disease activity and allowing, at least in RA, remission in many patients. While the array of available effective treatments is extensive, the use of objective measures of disease activity can guide treatment decisions (treat to target) and lead to improved outcomes. (C) 2012 Published by Elsevier Ltd.
C1 [Pisetsky, David S.] Durham VA Hosp, Med Res Serv, Durham, NC 27705 USA.
[Pisetsky, David S.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27705 USA.
[Ward, Michael M.] NIAMS, NIH, IRP, Bethesda, MD 20892 USA.
RP Pisetsky, DS (reprint author), Durham VA Hosp, Med Res Serv, 151G Durham VAMC,508 Fulton St, Durham, NC 27705 USA.
EM dpiset@duke.edu; wardm1@mail.nih.gov
FU VA Merit Review grant; NIH [AI083923]
FX These studies were supported by a VA Merit Review grant and NIH grant
AI083923.
NR 55
TC 10
Z9 13
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6942
J9 BEST PRACT RES CL RH
JI Best Pract. Res. Clin. Rheumatol.
PD APR
PY 2012
VL 26
IS 2
BP 251
EP 261
DI 10.1016/j.berh.2012.03.001
PG 11
WC Rheumatology
SC Rheumatology
GA 983RA
UT WOS:000307135200007
PM 22794097
ER
PT J
AU Tsujimoto, T
Sasai, H
Miyashita, M
Eto, M
So, RN
Ohkubo, H
Tanaka, K
AF Tsujimoto, Takehiko
Sasai, Hiroyuki
Miyashita, Masashi
Eto, Miki
So, Rina
Ohkubo, Hiroyuki
Tanaka, Kiyoji
TI Effect of weight loss on maximal fat oxidation rate in obese men
SO OBESITY RESEARCH & CLINICAL PRACTICE
LA English
DT Article
DE Obesity; Weight loss; Maximal fat oxidation rate
ID HUMAN SKELETAL-MUSCLE; INSULIN-RESISTANCE; EXERCISE INTENSITY; LIPID
OXIDATION; RESPIRATORY QUOTIENT; INDIRECT CALORIMETRY; SUBSTRATE
OXIDATION; PHYSICAL-ACTIVITY; BODY-COMPOSITION; GRADED-EXERCISE
AB Introduction: The hallmark features of obesity include insulin resistance and an impaired ability to oxidize lipids. As compared to exercise training, it remains relatively unclear if diet-induced weight loss can also induce fat metabolism. This study was undertaken to examine the effects of diet-induced weight loss on fat metabolism during a single session of exercise in middle-aged obese men. Methods: Fifteen obese men who were otherwise healthy (average age of 53.5 +/- 6.9 yr and average body mass index of 27.8 +/- 1.6 kg/m(2)) participated in a 12-wk weight loss program primarily consisting of dietary modification. Maximal fat oxidation (MFO) rates, MFO per lean body mass (MFOLBM) and insulin resistance (HOMA-IR) were measured before and after the program. Participants performed a 24-min graded exercise test on a cycle ergometer, with 15-W increments every 4 min. Expired gas analysis was performed by indirect calorimetry, and nonprotein respiratory quotient equations were used to calculate fat oxidation rates. Results: The weight (-8.3 +/- 3.8 kg), fat mass (-4.5 +/- 1.9 kg), and lean body mass (-3.8 +/- 2.4 kg) (P < 0.001 for all measurements) of the participants were decreased at the end of the 12-wk program. The MFO tended to increase by 19% (P = 0.08) and MFOLBM significantly increased by 28.8% (P = 0.02). Although insulin resistance also significantly decreased by 49% (P < 0.001), changes in fat oxidation variables did not correlate with changes in insulin resistance. Conclusion: Diet-induced weight loss improves fat metabolism with the improvement in insulin resistance. (C) 2011 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.
C1 [Tsujimoto, Takehiko; Eto, Miki; So, Rina; Ohkubo, Hiroyuki; Tanaka, Kiyoji] Univ Tsukuba, Grad Sch Comprehens Human Sci, Tsukuba, Ibaraki 3058577, Japan.
[Sasai, Hiroyuki] NIDDKD, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Sasai, Hiroyuki] Japan Soc Promot Sci, Tokyo, Japan.
[Miyashita, Masashi] Waseda Univ, Fac Sport Sci, Saitama, Japan.
RP Tsujimoto, T (reprint author), Univ Tsukuba, Grad Sch Comprehens Human Sci, 1-1-1 10-Nodai, Tsukuba, Ibaraki 3058577, Japan.
EM tsujimoto@stat.taiiku.tsukuba.ac.jp
OI Sasai, Hiroyuki/0000-0001-8120-6163
FU Japanese Ministry of Education, Culture, Sports, Science and Technology
FX This work was supported by a grant-in aid from the Japanese Ministry of
Education, Culture, Sports, Science and Technology (2008-2010, Tanaka
Project).
NR 46
TC 3
Z9 3
U1 1
U2 12
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1871-403X
J9 OBES RES CLIN PRACT
JI Obes. Res. Clin. Pract.
PD APR-JUN
PY 2012
VL 6
IS 2
BP E111
EP E119
DI 10.1016/j.orcp.2011.06.003
PG 9
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA 981HI
UT WOS:000306957200003
ER
PT J
AU Darlow, S
Goodman, MS
Stafford, JD
Lachance, CR
Kaphingst, KA
AF Darlow, Susan
Goodman, Melody S.
Stafford, Jewel D.
Lachance, Christina R.
Kaphingst, Kimberly A.
TI Weight Perceptions and Perceived Risk for Diabetes and Heart Disease
Among Overweight and Obese Women, Suffolk County, New York, 2008
SO PREVENTING CHRONIC DISEASE
LA English
DT Article
ID HEALTH LITERACY; UNITED-STATES; VITAL SIGN; US ADULTS; ASSOCIATION;
PREVALENCE; KNOWLEDGE; MORTALITY; OUTCOMES; TRENDS
AB Introduction
Many Americans fail to accurately identify themselves as overweight and underestimate their risk for obesity-related diseases. The purpose of this study was to investigate associations between weight perceptions and perceived risk for diabetes and heart disease among overweight or obese women.
Methods
We examined survey responses from 397 overweight or obese female health center patients on disease risk perceptions and weight perceptions. We derived odds ratios (ORs) and 95% confidence intervals (CIs) from multivariable logistic regression analyses to examine predictors of perceived risk for diabetes and heart disease. We further stratified results by health literacy.
Results
Perceiving oneself as overweight (OR, 2.78; 95% CI, 1.16-6.66), believing that being overweight is a personal health problem (OR, 2.46; 95% CI, 1.26-4.80), and family history of diabetes (OR, 3.22; 95% CI, 1.53-6.78) were associated with greater perceived risk for diabetes. Perceiving oneself as overweight (OR, 4.33; 95% CI, 1.26-14.86) and family history of heart disease (OR, 2.25; 95% CI, 1.08-4.69) were associated with greater perceived risk for heart disease. Among respondents with higher health literacy, believing that being overweight was a personal health problem was associated with greater perceived risk for diabetes (OR, 4.91; 95% CI, 1.68-14.35). Among respondents with lower health literacy, perceiving oneself as overweight was associated with greater perceived risk for heart disease (OR, 4.69; 95% CI, 1.02-21.62).
Conclusion
Our findings indicate an association between accurate weight perceptions and perceived risk for diabetes and heart disease in overweight or obese women. This study adds to research on disease risk perceptions in at-risk populations.
C1 [Goodman, Melody S.; Stafford, Jewel D.; Kaphingst, Kimberly A.] Washington Univ, Sch Med, St Louis, MO USA.
[Lachance, Christina R.] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Darlow, S (reprint author), Fox Chase Canc Ctr, Canc Prevent & Control Program, Room P4159,333 Cottman Ave, Philadelphia, PA 19111 USA.
EM susan.darlow@fccc.edu
RI Goodman, Melody/F-6768-2011
OI Goodman, Melody/0000-0001-8932-624X
FU National Human Genome Research Institute at the National Institutes of
Health; Barnes-Jewish Hospital Foundation
FX This research was funded by the National Human Genome Research Institute
at the National Institutes of Health. Drs Goodman and Kaphingst were
also supported by funding from the Barnes-Jewish Hospital Foundation.
NR 30
TC 2
Z9 2
U1 1
U2 13
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 APR
PY 2012
VL 9
AR 110185
DI 10.5888/pcd9.110185
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 977HL
UT WOS:000306647200002
ER
PT J
AU Geyer, CB
Saba, R
Kato, Y
Anderson, AJ
Chappell, VK
Saga, Y
Eddy, EM
AF Geyer, Christopher B.
Saba, Rie
Kato, Yuzuru
Anderson, Amy J.
Chappell, Vesna K.
Saga, Yumiko
Eddy, Edward M.
TI Rhox13 Is Translated in Premeiotic Germ Cells in Male and Female Mice
and Is Regulated by NANOS2 in the Male
SO BIOLOGY OF REPRODUCTION
LA English
DT Article
DE meiosis; NANOS2; retinoic acid; Rhox13; testis; translation
ID ACID GENE-8 STRA8; RETINOIC ACID; MEIOTIC INITIATION; CHROMOSOME
CONDENSATION; SPERMATOGENIC CELLS; SUPPRESSES MEIOSIS; HOMEOBOX GENE;
MOUSE; EXPRESSION; OOGENESIS
AB Male and female germ cells enter meiosis in response to an extrinsic cue by retinoic acid (RA), but the pathways downstream of RA signaling that regulate early gametogenesis remain uncertain. We identified a novel reproductive homeobox gene, Rhox13, transcribed in the prenatal ovary and testis beginning on Embryonic Day (E) 13.5. Translation of RHOX13 also begins in female germ cells on E13.5 but is suppressed in male germ cells until Postnatal Day 3. Translation of RHOX13 coincides with initiation of RA signaling in both male and female gonads in vivo but occurs precociously in neonatal testes exposed to RA in vitro or in fetal male germ cells when NANOS2 is absent in vivo. Conversely, RHOX13 translation in female germ cells is suppressed in the presence of ectopically induced NANOS2. These results strongly suggest that RHOX13 expression is regulated at a posttranscriptional step by direct interaction of NANOS2 with Rhox13 mRNA to suppress translation.
C1 [Geyer, Christopher B.; Chappell, Vesna K.] E Carolina Univ, Dept Anat & Cell Biol, Brody Sch Med, Greenville, NC 27834 USA.
[Geyer, Christopher B.; Anderson, Amy J.; Eddy, Edward M.] NIEHS, Gamete Biol Grp, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
[Saba, Rie; Kato, Yuzuru; Saga, Yumiko] Natl Inst Genet, Div Mammalian Dev, Mishima, Shizuoka 411, Japan.
RP Geyer, CB (reprint author), E Carolina Univ, Dept Anat & Cell Biol, Brody Sch Med, 600 Moye Blvd, Greenville, NC 27834 USA.
EM geyerc@ecu.edu
FU NIH, National Institute of Environmental Health Sciences [ZO1-ES070076];
Ministry of Education, Culture, Sports, Science and Technology, Japan
FX Supported in part by the Intramural Research Program of the NIH,
National Institute of Environmental Health Sciences (ZO1-ES070076, EME)
and in part by Grants-in-Aid for Scientific Research (S) of the Ministry
of Education, Culture, Sports, Science and Technology, Japan.
NR 45
TC 10
Z9 11
U1 0
U2 4
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 APR
PY 2012
VL 86
IS 4
AR 127
DI 10.1095/biolreprod.111.094938
PG 9
WC Reproductive Biology
SC Reproductive Biology
GA 975ZE
UT WOS:000306549500015
PM 22190708
ER
PT J
AU Subbaramaiah, K
Morris, PG
Zhou, XK
Morrow, M
Du, BH
Giri, D
Kopelovich, L
Hudis, CA
Dannenberg, AJ
AF Subbaramaiah, Kotha
Morris, Patrick G.
Zhou, Xi Kathy
Morrow, Monica
Du, Baoheng
Giri, Dilip
Kopelovich, Levy
Hudis, Clifford A.
Dannenberg, Andrew J.
TI Increased Levels of COX-2 and Prostaglandin E-2 Contribute to Elevated
Aromatase Expression in Inflamed Breast Tissue of Obese Women
SO CANCER DISCOVERY
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; ADIPOSE-TISSUE; GENE-EXPRESSION; POSTMENOPAUSAL
WOMEN; INSULIN-RESISTANCE; CANCER CELLS; FACTOR-ALPHA; CYCLOOXYGENASE-2;
INFLAMMATION; MACROPHAGES
AB Obesity is a risk factor for hormone receptor-positive breast cancer in post-menopausal women. Estrogen synthesis is catalyzed by aromatase, which is encoded by CYP19. We previously showed that aromatase expression and activity are increased in the breast tissue of overweight and obese women in the presence of characteristic inflammatory foci [crown-like structures of the breast (CLS-B)]. In preclinical studies, proinflammatory prostaglandin E-2 (PGE(2)) is a determinant of aromatase expression. We provide evidence that cyclooxygenase (COX)-2-derived PGE(2) stimulates the cyclic AMP (cAMP)-> PKA signal transduction pathway that activates CYP19 transcription, resulting in increased aromatase expression and elevated progesterone receptor levels in breast tissues from overweight and obese women. We further demonstrate that a measure of in-breast inflammation (CLS-B index) is a better correlate of these biologic end points than body mass index. The obesity -> inflammation -> aromatase axis is likely to contribute to the increased risk of hormone receptor-positive breast cancer and the worse prognosis of obese patients with breast cancer.
SIGNIFICANCE: We show that obesity-associated inflammatory foci in the human breast are associated with elevated COX-2 levels and activation of the PGE(2)-> cAMP -> PKA signal transduction pathway resulting in increased aromatase expression. These findings help to explain the link among obesity, low-grade chronic inflammation, and breast cancer with important clinical implications. Cancer Discov; 2(4); 356-65. (c) 2012 AACR.
C1 [Subbaramaiah, Kotha; Du, Baoheng; Hudis, Clifford A.; Dannenberg, Andrew J.] Weill Cornell Canc Ctr, Dept Med, New York, NY 10065 USA.
[Zhou, Xi Kathy] Weill Cornell Canc Ctr, Dept Publ Hlth, New York, NY 10065 USA.
[Morris, Patrick G.; Hudis, Clifford A.] Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10021 USA.
[Morrow, Monica] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10021 USA.
[Giri, Dilip] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Dannenberg, AJ (reprint author), Weill Cornell Canc Ctr, Dept Med, 525 E 68th St,Room F-206, New York, NY 10065 USA.
EM ksubba@med.cornell.edu; ajdannen@med.cornell.edu
FU National Cancer Institute [1R01CA154481, N01-CN-43302]; Breast Cancer
Research Foundation; Botwinick-Wolfensohn Foundation; Kochavi Breast
Cancer Prevention Fund; Metastasis Research Center of Memorial
Sloan-Kettering Cancer Center
FX This work was supported by National Cancer Institute 1R01CA154481 and
N01-CN-43302 (to A.J. Dannenberg), the Breast Cancer Research Foundation
(to A.J. Dannenberg and C.A. Hudis), the Botwinick-Wolfensohn Foundation
[in memory of Mr. and Mrs. Benjamin Botwinick (to A.J. Dannenberg)], the
Kochavi Breast Cancer Prevention Fund (to C.A. Hudis), and the
Metastasis Research Center of Memorial Sloan-Kettering Cancer Center (to
C.A. Hudis). The content is solely the responsibility of the authors and
does not necessarily represent the official views of the National Cancer
Institute or the NIH.
NR 40
TC 98
Z9 99
U1 0
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 2159-8274
J9 CANCER DISCOV
JI Cancer Discov.
PD APR
PY 2012
VL 2
IS 4
BP 356
EP 365
DI 10.1158/2159-8290.CD-11-0241
PG 10
WC Oncology
SC Oncology
GA 973BP
UT WOS:000306327000029
PM 22576212
ER
PT J
AU Blair, KS
Blair, RJR
AF Blair, Karina S.
Blair, R. J. R.
TI A Cognitive Neuroscience Approach to Generalized Anxiety Disorder and
Social Phobia
SO EMOTION REVIEW
LA English
DT Article
DE conditioning; emotion regulation; generalized anxiety disorder; social
phobia; social threat processing
ID AMYGDALA ACTIVATION; PREFRONTAL CORTEX; EMOTIONAL FACES; FACIAL
EXPRESSIONS; ANTERIOR CINGULATE; TREATMENT RESPONSE; BRAIN ACTIVATION;
ATTENTIONAL BIAS; FUNCTIONAL MRI; ANGRY
AB Generalized anxiety disorder (GAD) and social phobia (SP) are major anxiety disorders identified by the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV). They are comorbid, overlap in symptoms, yet present with distinct features (worry in GAD and fear of embarrassment in SP). Both have also been explained in terms of conditioning-based models. However, there is little reasoning currently to believe that GAD in adulthood reflects heightened conditionability or heightened threat processing-though patients with SP may show heightened processing of social threat stimuli. Moreover, the computational architectures that maintain these disorders in adulthood are different. For GAD this may reflect the development of an inefficient "worrying" strategy of emotional regulation. For SP this appears to reflect the atypical processing of self-referential information.
C1 [Blair, Karina S.; Blair, R. J. R.] NIMH, Mood & Anxiety Program, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Blair, KS (reprint author), NIMH, Mood & Anxiety Program, NIH, Dept Hlth & Human Serv, 15K North Dr,MSC 2670, Bethesda, MD 20892 USA.
EM peschark@mail.nih.gov
NR 56
TC 9
Z9 9
U1 17
U2 41
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1754-0739
J9 EMOT REV
JI Emot. Rev.
PD APR
PY 2012
VL 4
IS 2
BP 133
EP 138
DI 10.1177/1754073911430251
PG 6
WC Psychology, Multidisciplinary
SC Psychology
GA 972KN
UT WOS:000306276100004
ER
PT J
AU Wang, S
Xiong, W
Ma, WP
Chanock, S
Jedrychowski, W
Wu, RL
Perera, FP
AF Wang, Shuang
Xiong, Wei
Ma, Weiping
Chanock, Stephen
Jedrychowski, Wieslaw
Wu, Rongling
Perera, Frederica P.
TI Gene-Environment Interactions on Growth Trajectories
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE gene-environment interactions; growth curves; Wald test; parametric
bootstrap
ID POLYCYCLIC AROMATIC-HYDROCARBONS; PAH-DNA ADDUCTS; PRENATAL EXPOSURE;
CHILDREN; POLYMORPHISMS; INTELLIGENCE; FETAL; AGE; BENZO(A)PYRENE; LIFE
AB It has been suggested that children with larger brains tend to perform better on IQ tests or cognitive function tests. Prenatal head growth and head growth in infancy are two crucial periods for subsequent intelligence. Studies have shown that environmental exposure to air pollutants during pregnancy is associated with fetal growth reduction, developmental delay, and reduced IQ. Meanwhile, genetic polymorphisms may modify the effect of environment on head growth. However, studies on gene-environment or gene-gene interactions on growth trajectories have been quite limited partly due to the difficulty to quantitatively measure interactions on growth trajectories. Moreover, it is known that assessing the significance of gene-environment or gene-gene interactions on cross-sectional outcomes empirically using the permutation procedures may bring substantial errors in the tests. We proposed a score that quantitatively measures interactions on growth trajectories and developed an algorithm with a parametric bootstrap procedure to empirically assess the significance of the interactions on growth trajectories under the likelihood framework. We also derived a Wald statistic to test for interactions on growth trajectories and compared it to the proposed parametric bootstrap procedure. Through extensive simulation studies, we demonstrated the feasibility and power of the proposed testing procedures. We applied our method to a real dataset with head circumference measures from birth to age 7 on a cohort currently being conducted by the Columbia Center for Children's Environmental Health (CCCEH) in Krakow, Poland, and identified several significant gene-environment interactions on head circumference growth trajectories. Genet. Epidemiol. 36:206-213, 2012. (C) 2012 Wiley Periodicals, Inc.
C1 [Wang, Shuang; Xiong, Wei] Columbia Univ, Dept Biostat, Mailman Sch Publ Hlth, New York, NY 10032 USA.
[Ma, Weiping] Fudan Univ, Sch Math Sci, Shanghai 200433, Peoples R China.
[Chanock, Stephen] NCI, Bethesda, MD 20892 USA.
[Jedrychowski, Wieslaw] Jagiellonian Univ, Dept Epidemiol & Prevent Med, Coll Med, Krakow, Poland.
[Jedrychowski, Wieslaw; Perera, Frederica P.] Columbia Univ, Columbia Ctr Childrens Environm Hlth, Mailman Sch Publ Hlth, New York, NY 10032 USA.
[Wu, Rongling] Penn State Univ, Ctr Stat Genet, Hershey, PA USA.
RP Wang, S (reprint author), Columbia Univ, Dept Biostat, Mailman Sch Publ Hlth, 722 W 168th St,Room 630, New York, NY 10032 USA.
EM sw2206@columbia.edu
FU National Institute of Environmental Health Sciences [P01 ES09600, R01
ES08977, P50ES015905]
FX Contract grant sponsor: National Institute of Environmental Health
Sciences; Contract grant numbers: P01 ES09600, R01 ES08977, P50ES015905.
NR 29
TC 1
Z9 1
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD APR
PY 2012
VL 36
IS 3
BP 206
EP 213
DI 10.1002/gepi.21613
PG 8
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 932VX
UT WOS:000303319700004
PM 22311237
ER
PT J
AU Zheng, G
Wu, CO
Kwak, M
Jiang, W
Joo, J
Lima, JAC
AF Zheng, Gang
Wu, Colin O.
Kwak, Minjung
Jiang, Wenhua
Joo, Jungnam
Lima, Joao A. C.
TI Joint Analysis of Binary and Quantitative Traits With Data Sharing and
Outcome-Dependent Sampling
SO GENETIC EPIDEMIOLOGY
LA English
DT Article
DE case-control; continuous trait; F-test; missing data; Fisher's
combination; genome-wide ranking; polygenetic pleiotropy; scaled
chi-squared distribution; trend test
ID RHEUMATOID-ARTHRITIS; LINKAGE DISEQUILIBRIUM; P-VALUES; ASSOCIATION;
ANTIBODIES; TESTS; SIZE; LOCI
AB We study the analysis of a joint association between a genetic marker with both binary (case-control) and quantitative (continuous) traits, where the quantitative trait values are only available for the cases due to data sharing and outcome-dependent sampling. Data sharing becomes common in genetic association studies, and the outcome-dependent sampling is the consequence of data sharing, under which a phenotype of interest is not measured for some subgroup. The trend test (or Pearson's test) and F-test are often, respectively, used to analyze the binary and quantitative traits. Because of the outcome-dependent sampling, the usual F-test can be applied using the subgroup with the observed quantitative traits. We propose a modified F-test by also incorporating the genotype frequencies of the subgroup whose traits are not observed. Further, a combination of this modified F-test and Pearson's test is proposed by Fisher's combination of their P-values as a joint analysis. Because of the correlation of the two analyses, we propose to use a Gamma (scaled chi-squared) distribution to fit the asymptotic null distribution for the joint analysis. The proposed modified F-test and the joint analysis can also be applied to test single trait association (either binary or quantitative trait). Through simulations, we identify the situations under which the proposed tests are more powerful than the existing ones. Application to a real dataset of rheumatoid arthritis is presented. Genet. Epidemiol. 36:263-273, 2012. (C) 2012 Wiley Periodicals, Inc.
C1 [Zheng, Gang] NHLBI, Off Biostat Res, Bethesda, MD 20892 USA.
[Jiang, Wenhua; Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Joo, Jungnam] Natl Canc Ctr, Geonggi Do, South Korea.
RP Zheng, G (reprint author), NHLBI, Off Biostat Res, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM zhengg@nhlbi.nih.gov
FU National Institutes of Health [NO1-AR-2-2263, RO1-AR-44422]; National
Arthritis Foundation
FX This work is based on the data (GAW16) that were gathered with the
support of grants from the National Institutes of Health (NO1-AR-2-2263
and RO1-AR-44422, Peter K. Gregersen, PI), and the National Arthritis
Foundation. The use of the data was approved by GAW16. The authors would
like to thank Neal Jeffries for extracting some marker data from GAW16
that were used in the application and Jing Qin for some helpful
discussion. We also thank three reviewers for their insightful thoughts
and helpful suggestions that led to the current version. The authors
have no conflict of interest to declare.
NR 20
TC 12
Z9 12
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD APR
PY 2012
VL 36
IS 3
BP 263
EP 273
DI 10.1002/gepi.21619
PG 11
WC Genetics & Heredity; Mathematical & Computational Biology
SC Genetics & Heredity; Mathematical & Computational Biology
GA 932VX
UT WOS:000303319700010
PM 22460626
ER
PT J
AU Ward, JM
Rehg, JE
Morse, HC
AF Ward, Jerrold M.
Rehg, Jerold E.
Morse, Herbert C., III
TI Differentiation of Rodent Immune and Hematopoietic System Reactive
Lesions from Neoplasias
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE clonality; mice; hematopoietic system; immune system;
immunohistochemistry; lymph nodes; lymphoid; lymphoid hyperplasia;
lymphoma; lymphoproliferative disease; rats; spleen; Thymus
ID PLASMA-CELL NEOPLASMS; LYMPH-NODES; B-CELL; ENHANCED HISTOPATHOLOGY;
IMMUNODEFICIENCY SYNDROME; EXTENDED HISTOPATHOLOGY; BETHESDA PROPOSALS;
C-MYC; MICE; MOUSE
AB The immune and hematopoietic systems play an important role in the normal homeostasis of blood and blood cells and for immune responses to endogenous and exogenous processes and insults. In order to interpret histopathologic changes in the immune and hematopoietic systems, it is important to understand the normal anatomy and histology of the thymus, spleen, lymph nodes, bone marrow, and other tissues. The thymus, spleen, and lymph nodes can be categorized by anatomical compartments, each of which contributes to specific immune functions. Lesions may be diagnosed by interpretive or descriptive (semiquantitative) methods. The interpretation of these tissues by lesion in anatomical compartments should allow for better understanding of these reactions and more definitive pathologic findings. Proliferative lesions may be difficult to differentiate from lymphomas and leukemias. The use of immunohistochemistry, compartmental pathology, and methods for the evaluation of clonality will make interpretation easier.
C1 [Ward, Jerrold M.; Morse, Herbert C., III] NIAID, Immunopathol Lab, NIH, Bethesda, MD 20892 USA.
[Rehg, Jerold E.] St Jude Childrens Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Ward, Jerrold M.] Global VetPathol, Bethesda, MD USA.
RP Ward, JM (reprint author), NIAID, Immunopathol Lab, NIH, MSC 8152, Bethesda, MD 20892 USA.
EM globalvetpathology@gmail.com
OI Morse, Herbert/0000-0002-9331-3705
FU NIH, National Institute of Allergy and Infectious Diseases
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: in part, by
the Intramural Research Program of the NIH, National Institute of
Allergy and Infectious Diseases.
NR 62
TC 8
Z9 8
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD APR
PY 2012
VL 40
IS 3
BP 425
EP 434
DI 10.1177/0192623311431467
PG 10
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 961JS
UT WOS:000305461300002
PM 22215512
ER
PT J
AU Morgan, DL
Jokinen, MP
Price, HC
Gwinn, WM
Palmer, SM
Flake, GP
AF Morgan, Daniel L.
Jokinen, Micheal P.
Price, Herman C.
Gwinn, William M.
Palmer, Scott M.
Flake, Gordon P.
TI Bronchial and Bronchiolar Fibrosis in Rats Exposed to 2,3-Pentanedione
Vapors: Implications for Bronchiolitis Obliterans in Humans
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE 2,3-pentanedione; bronchiolitis obliterans; acetyl propionyl; butter
flavoring; diacetyl; nasal cavity; airways; rats; mice
ID C-REACTIVE PROTEIN; ONCOSTATIN-M; LUNG TRANSPLANTATION; DERMAL
FIBROBLASTS; EXPRESSION; DIACETYL; COLLAGEN; ALPHA; IDENTIFICATION;
EPITHELIUM
AB 2,3-Pentanedione (PD) is a component of artificial butter flavorings. The use of PD is increasing since diacetyl, a major butter flavorant, was associated with bronchiolitis obliterans (BO) in workers and has been removed from many products. Because the toxicity of inhaled PD is unknown, these studies were conducted to characterize the toxicity of inhaled PD across a range of concentrations in rodents. Male and female Wistar-Han rats and B6C3F1 mice were exposed to 0, 50, 100, or 200 ppm PD 6 h/d, 5 d/wk for up to 2 wk. Bronchoalveolar lavage fluid (BALF) was collected after 1, 3, 5, and 10 exposures, and histopathology was evaluated after 12 exposures. MCP-1, MCP-3, CRP, FGF-9, fibrinogen, and OSM were increased 2- to 9-fold in BALF of rats exposed for 5 and 10 days to 200 ppm. In mice, only fibrinogen was increased after 5 exposures to 200 ppm. The epithelium lining the respiratory tract was the site of toxicity in all mice and rats exposed to 200 ppm. Significantly, PD also caused both intraluminal and intramural fibrotic airway lesions in rats. The histopathological and biological changes observed in rats raise concerns that PD inhalation may cause BO in exposed humans.
C1 [Morgan, Daniel L.; Gwinn, William M.; Flake, Gordon P.] Natl Inst Environm Hlth Sci, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Jokinen, Micheal P.] Charles River Labs Pathol Associates, Durham, NC USA.
[Price, Herman C.] Alion Sci & Technol, Res Triangle Pk, NC USA.
[Palmer, Scott M.] Duke Univ, Med Ctr, Durham, NC USA.
RP Morgan, DL (reprint author), Natl Inst Environm Hlth Sci, Natl Toxicol Program, Mail Drop IF-00, Res Triangle Pk, NC 27709 USA.
EM morgan3@niehs.nih.gov
NR 42
TC 25
Z9 25
U1 0
U2 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
EI 1533-1601
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD APR
PY 2012
VL 40
IS 3
BP 448
EP 465
DI 10.1177/0192623311431946
PG 18
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 961JS
UT WOS:000305461300004
PM 22215510
ER
PT J
AU Ellis, JM
Paul, DS
DePetrillo, MA
Singh, BP
Malarkey, DE
Coleman, RA
AF Ellis, Jessica M.
Paul, David S.
DePetrillo, Michael A.
Singh, Bhanu P.
Malarkey, David E.
Coleman, Rosalind A.
TI Mice Deficient in Glycerol-3-Phosphate Acyltransferase-1 Have a Reduced
Susceptibility to Liver Cancer
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE hepatocellular carcinoma; glycerolipid synthesis; non-alcoholic fatty
liver disease; non-alcoholic steatohepatitis; diethylnitrosamine
ID HEPATOCELLULAR-CARCINOMA; HEPATIC STEATOSIS; PPAR-ALPHA; NONALCOHOLIC
STEATOHEPATITIS; TRIACYLGLYCEROL SYNTHESIS; PEROXISOME PROLIFERATOR;
INSULIN-RESISTANCE; HEPATOCARCINOGENESIS; MITOCHONDRIAL; IDENTIFICATION
AB The risk of hepatocellular carcinoma increases with the persistence of non-alcoholic fatty liver disease. Triacylglycerol synthesis is initiated by glycerol-3-phosphate acyltransferase (GPAT). Of four isoforms, GPAT1 contributes 30-50% of total liver GPAT activity, and we hypothesized that it might influence liver susceptibility to tumorigenesis. C57Bl/6 mice deficient in GPAT1 were backcrossed 6 times to C3H mice. After exposure to the carcinogen diethylnitrosamine (DEN) and the tumor promoter phenobarbital, male Gpat1(-/-) mice, compared with controls (Gpat1(+/+)), had 93% fewer macroscopically visible nodules per liver at 21 weeks of age and 39% fewer at 34 weeks of age. Microscopically, control mice had increased numbers of foci of altered hepatocytes, particularly the basophilic subtype, as well as more, and malignant, liver neoplasms than did the Gpat1(-/-) mice. At 21 weeks of age, 50% (4/8) of control mice (50%) had hepatocellular adenomas with an average multiplicity (tumors per tumor-bearing-animal) of 4.3, while none occurred in 8 Gpat1(-/-) mice. At 34 weeks of age, all 15 control mice (100%) had hepatocellular adenomas with an average multiplicity of 5.2 compared to an incidence of 93% in Gpat1(-/-) mice and multiplicity of 3.1. HCCs were observed in 13% of control mice and in only 6% of Gpat1(-/-) mice. These data show that alterations in the formation of complex lipids catalyzed by Gpat1 reduce susceptibility to DEN-induced liver tumorigenesis.
C1 [Ellis, Jessica M.; Paul, David S.; DePetrillo, Michael A.; Coleman, Rosalind A.] Univ N Carolina, Dept Nutr, Chapel Hill, NC 27599 USA.
[Ellis, Jessica M.] Johns Hopkins Univ, Sch Med, Ctr Metab & Obes Res, Dept Biol Chem, Baltimore, MD USA.
[Singh, Bhanu P.; Malarkey, David E.] Natl Inst Environm Hlth & Sci, Natl Toxicol Program, Cellular & Mol Pathol Branch, Res Triangle Pk, NC USA.
[Singh, Bhanu P.] Dupont Haskell Global Ctr Hlth & Environm Sci, Newark, DE USA.
RP Coleman, RA (reprint author), Univ N Carolina, Dept Nutr, CB 7461, Chapel Hill, NC 27599 USA.
EM rcoleman@unc.edu
FU NIH [DK056598]; predoctoral training grant in Integrative Vascular
Biology [HL069768]; American Heart Association-Mid-Atlantic Region [P30
DK034987, P30-ES010126, P30 DK056350]; NIH, National Institute of
Environmental Health Sciences
FX This work was supported by NIH grant DK056598 (RAC); a predoctoral
training grant HL069768 in Integrative Vascular Biology (JME); P30
DK034987, P30-ES010126, P30 DK056350, and a predoctoral fellowship from
the American Heart Association-Mid-Atlantic Region (JME). This research
was also supported in part by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences.
NR 46
TC 2
Z9 3
U1 0
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0192-6233
J9 TOXICOL PATHOL
JI Toxicol. Pathol.
PD APR
PY 2012
VL 40
IS 3
BP 513
EP 521
DI 10.1177/0192623311432298
PG 9
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 961JS
UT WOS:000305461300010
PM 22215515
ER
PT J
AU Lipsky, LM
Cheon, K
Nansel, TR
Albert, PS
AF Lipsky, Leah M.
Cheon, Kyeongmi
Nansel, Tonja R.
Albert, Paul S.
TI Candidate measures of whole plant food intake are related to biomarkers
of nutrition and health in the US population (National Health and
Nutrition Examination Survey 1999-2002)
SO NUTRITION RESEARCH
LA English
DT Article
DE Human; Nutrition indices; National Health and Nutrition Examination
Survey; Food plants; Biomarkers
ID CORONARY-HEART-DISEASE; CARDIOVASCULAR-DISEASE; DIETARY PATTERNS;
VEGETABLE INTAKE; RISK-FACTORS; GRAIN INTAKE; CANCER; WOMEN; QUALITY;
ADULTS
AB Indices of overall dietary patterns are used in epidemiologic research to examine the relationship between nutrition and health. The objective of this study was to develop and validate an interpretable summary measure of dietary intake of whole plant foods (WPF; whole grains, vegetables, whole fruit, legumes, nuts, seeds) because of their similar nutritional characteristics and health effects. Six candidate WPF measures were calculated using data from subjects (age >= 6 years) participating in the 1999-2000 and 2001-2002 National Health and Nutrition Examination Survey. Measures differed by the inclusion or exclusion of potatoes and whether they were expressed as total intake or as a proportion of energy (4180 kJ) or mass (kg) consumed. Both standard and nontruncated (allowed to vary proportionally with intake) Healthy Eating Index-2005 (HEI-2005) scores were calculated. Regression analysis examined the associations between WPF and HEI-2005 measures, and between all diet measures and serum carotenoid concentration, serum lipids, fasting glucose, insulin, C-peptide, and C-reactive protein. Mean total WPF intake was 3.6 cup/oz equivalents, or 1.7 cup/oz equivalents per 4180 kJ and per kg. The largest R-2 between WPF and HEI-2005 measures was found for energy-adjusted WPF including potatoes and nontruncated HEI-2005 (R-2 = 0.50). All diet measures were positively related to serum carotenoids (P <.001) and were similarly related to health indicators (R-2 range from 0.003 to 0.16, P <.045 for regressions, indicating significant associations between WPF measures and health indicators). Whole plant food measures are interpretable indicators of dietary intake that are significantly related to nutrition and health biomarkers and may be of public health use. Published by Elsevier Inc.
C1 [Lipsky, Leah M.; Cheon, Kyeongmi; Nansel, Tonja R.; Albert, Paul S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20852 USA.
RP Lipsky, LM (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20852 USA.
EM lipskylm@mail.nih.gov
OI Nansel, Tonja/0000-0002-8298-7595; Lipsky, Leah/0000-0003-2645-4388
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development
FX This research was funded by the intramural research program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development. The authors declare no conflicts of interest.
NR 37
TC 11
Z9 11
U1 0
U2 19
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0271-5317
J9 NUTR RES
JI Nutr. Res.
PD APR
PY 2012
VL 32
IS 4
BP 251
EP 259
DI 10.1016/j.nutres.2012.03.005
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 958TS
UT WOS:000305264200003
PM 22575037
ER
PT J
AU Kong, A
Beresford, SAA
Imayama, I
Duggan, C
Alfano, CM
Foster-Schubert, KE
Neuhouser, ML
Johnson, DB
Wang, CY
Xiao, LR
Bain, CE
McTiernan, A
AF Kong, Angela
Beresford, Shirley A. A.
Imayama, Ikuyo
Duggan, Catherine
Alfano, Catherine M.
Foster-Schubert, Karen E.
Neuhouser, Marian L.
Johnson, Donna B.
Wang, Ching-Yun
Xiao, Liren
Bain, Carolyn E.
McTiernan, Anne
TI Adoption of diet-related self-monitoring behaviors varies by
race/ethnicity, education, and baseline binge eating score among
overweight-to-obese postmenopausal women in a 12-month dietary weight
loss intervention
SO NUTRITION RESEARCH
LA English
DT Article
ID LOSS MAINTENANCE; RISK-FACTOR; TRIAL; QUESTIONNAIRE; LIFE; PARTICIPANTS;
PREVENTION; PROGRAM; GAIN; MEN
AB Recent research has identified self-monitoring behaviors as important strategies for both initial weight loss and weight loss maintenance, but relatively little is known about adopters and nonadopters of these behaviors. To test our hypothesis that key characteristics distinguish adopters from nonadopters, we examined the demographic characteristics and eating behaviors (eg, restrained, uncontrolled, emotional, and binge eating) associated with more frequent compared with less frequent use of these behaviors. Baseline demographic characteristics and eating behaviors as well as 12-month self-monitoring behaviors (ie, self-weighing, food journaling, monitoring energy intake) were assessed in 123 postmenopausal women enrolled in a dietary weight loss intervention. Logistic regression models were used to test associations of self-monitoring use with demographic characteristics and eating behaviors. Nonwhites, compared with non-Hispanic whites, were less likely to monitor energy intake regularly (adjusted odds ratio [OR], 0.36; 95% confidence interval [CI], 0.13-0.97; P < .05), controlling for intervention arm and baseline body mass index. Participants with a college degree or higher education were less likely to self-weigh daily (adjusted OR, 0.30; 95% CI, 0.13-0.67; P < .01) compared with individuals who attended some college or less. Those with higher baseline binge eating scores were less likely to monitor energy intake (adjusted OR, 0.84; 95% CI, 0.73-0.97; P < .01) compared with participants with lower binge eating scores. In summary, use of diet-related self-monitoring behaviors varied by race/ethnicity, education, and binge eating score in postmenopausal women who completed a year-long dietary weight loss intervention. Improved recognition of groups less likely to self-monitor may be helpful in promoting these behaviors in future interventions. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Beresford, Shirley A. A.; Imayama, Ikuyo; Duggan, Catherine; Foster-Schubert, Karen E.; Neuhouser, Marian L.; Wang, Ching-Yun; Xiao, Liren; Bain, Carolyn E.; McTiernan, Anne] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Beresford, Shirley A. A.; Neuhouser, Marian L.; Johnson, Donna B.; McTiernan, Anne] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
[Kong, Angela] Univ Illinois, Canc Educ & Career Dev Program, Chicago, IL 60608 USA.
[Alfano, Catherine M.] NCI, Off Canc Survivorship, Bethesda, MD 20892 USA.
[Foster-Schubert, Karen E.; McTiernan, Anne] Univ Washington, Sch Med, Seattle, WA 98195 USA.
RP McTiernan, A (reprint author), Fred Hutchinson Canc Res Ctr, POB 19024,Mail Stop M4-B874, Seattle, WA 98109 USA.
EM amctiem@fhcrc.org
RI Duggan, Catherine/F-9414-2015
OI Duggan, Catherine/0000-0001-7369-4021
FU National Cancer Institute [R01 CA105204-01A1, R25 CA094880,
2R25CA057699, U54 CA116847]; National Center for Research Resources [5
KL2 RR025015-03]
FX This study was supported by the National Cancer Institute (grants R01
CA105204-01A1, R25 CA094880, 2R25CA057699, and U54 CA116847) and
National Center for Research Resources (grant 5 KL2 RR025015-03).
NR 28
TC 5
Z9 5
U1 2
U2 17
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0271-5317
J9 NUTR RES
JI Nutr. Res.
PD APR
PY 2012
VL 32
IS 4
BP 260
EP 265
DI 10.1016/j.nutres.2012.03.001
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 958TS
UT WOS:000305264200004
PM 22575038
ER
PT J
AU Demple, B
Rao, KS
Bohr, VA
AF Demple, Bruce
Rao, Kalluri S.
Bohr, Vilhelm A.
TI Indo-US workshop on base excision DNA repair, brain function and aging
Preface
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Editorial Material
ID MITOCHONDRIAL-DNA; DAMAGE
C1 [Demple, Bruce] SUNY Stony Brook, Dept Pharmacol Sci, Sch Med, Stony Brook, NY 11790 USA.
[Rao, Kalluri S.] Jawaharlal Nehru Technol Univ, Inst Sci & Technol, Biotechnol Res Ctr, Hyderabad 500085, Andhra Pradesh, India.
[Rao, Kalluri S.] Jawaharlal Nehru Technol Univ, Inst Sci & Technol, Ctr Innovat Res, Hyderabad 500085, Andhra Pradesh, India.
[Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Demple, B (reprint author), SUNY Stony Brook, Dept Pharmacol Sci, Sch Med, Stony Brook, NY 11790 USA.
FU Intramural NIH HHS [Z99 AG999999]
NR 11
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD APR
PY 2012
VL 133
IS 4
SI SI
BP V
EP VI
DI 10.1016/S0047-6374(12)00063-2
PG 2
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 953TE
UT WOS:000304895300001
PM 22579128
ER
PT J
AU Sykora, P
Wilson, DM
Bohr, VA
AF Sykora, Peter
Wilson, David M., III
Bohr, Vilhelm A.
TI Repair of persistent strand breaks in the mitochondrial genome
SO MECHANISMS OF AGEING AND DEVELOPMENT
LA English
DT Article; Proceedings Paper
CT Indo-US Workshop on Base Excision DNA Repair, Brain Function and Aging
CY JAN, 2011
CL Hyderabad, INDIA
DE DNA repair; Mitochondria; Aging; Oxidative DNA damage
ID BASE EXCISION-REPAIR; DNA-LIGASE-III; ONSET SPINOCEREBELLAR ATAXIA;
DISEASE PROTEIN APRATAXIN; MAMMALIAN MITOCHONDRIA; OXIDATIVE STRESS;
GENETIC-DISEASE; XRCC1; MUTATIONS; DAMAGE
AB Oxidative DNA damage has been attributed to increased cancer incidence and premature aging phenotypes. Reactive oxygen species (ROS) are unavoidable byproducts of oxidative phosphorylation and are the major contributors of endogenous oxidative damage. To prevent the negative effects of ROS, cells have developed DNA repair mechanisms designed to specifically combat endogenous DNA modifications. The base excision repair (BER) pathway is primarily responsible for the repair of small non-helix distorting lesions and DNA single strand breaks. This repair pathway is found in all organisms, and in mammalian cells, consists of three related sub-pathways: short patch (SP-BER), long patch (LP-BER) and single strand break repair (SSBR). While much is known about nuclear BER, comparatively little is known about this pathway in the mitochondria, particularly the LP-BER and SSBR sub-pathways. There are a number of proteins that have recently been found to be involved in mitochondrial BER, including Cockayne syndrome proteins A and B (CSA and CSB), aprataxin (APTX), tryosyl-DNA phosphodiesterase 1 (TDP1), flap endonuclease 1 (FEN-1) and exonuclease G (EXOG). These significant advances in mitochondrial DNA repair may open new avenues in the management and treatment of a number of neurological disorders associated with mitochondrial dysfunction, and will be reviewed in further detail herein. (C) 2011 Published by Elsevier Ireland Ltd.
C1 [Sykora, Peter; Wilson, David M., III; Bohr, Vilhelm A.] NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIH, Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM sykorap@mail.nih.gov; wilsonda@mail.nih.gov; BohrV@grc.nia.nih.gov
FU Intramural NIH HHS [Z01 AG000733-12, ZIA AG000733-17]
NR 63
TC 27
Z9 27
U1 1
U2 9
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0047-6374
J9 MECH AGEING DEV
JI Mech. Ageing Dev.
PD APR
PY 2012
VL 133
IS 4
SI SI
BP 169
EP 175
DI 10.1016/j.mad.2011.11.003
PG 7
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 953TE
UT WOS:000304895300010
PM 22138376
ER
PT J
AU Briggs, JW
Ren, L
Nguyen, R
Chakrabarti, K
Cassavaugh, J
Rahim, S
Bulut, G
Zhou, M
Veenstra, TD
Chen, QR
Wei, JS
Khan, J
Uren, A
Khanna, C
AF Briggs, Joseph W.
Ren, Ling
Nguyen, Rachel
Chakrabarti, Kristi
Cassavaugh, Jessica
Rahim, Said
Bulut, Gulay
Zhou, Ming
Veenstra, Timothy D.
Chen, Qingrong
Wei, Jun S.
Khan, Javed
Uren, Aykut
Khanna, Chand
TI The Ezrin Metastatic Phenotype Is Associated with the Initiation of
Protein Translation
SO NEOPLASIA
LA English
DT Article
ID MESSENGER-RNA; EUKARYOTIC TRANSLATION; ERM PROTEINS; POLY(A)-BINDING
PROTEIN-1; PLASMA-MEMBRANE; GENE-EXPRESSION; CELL CARCINOMA;
OSTEOSARCOMA; CYTOSKELETON; RIBOSOME
AB We previously associated the cytoskeleton linker protein, Ezrin, with the metastatic phenotype of pediatric sarcomas, including osteosarcoma and rhabdomyosarcoma. These studies have suggested that Ezrin contributes to the survival of cancer cells after their arrival at secondary metastatic locations. To better understand this role in metastasis, we undertook two noncandidate analyses of Ezrin function including a microarray subtraction of high- and low-Ezrin-expressing cells and a proteomic approach to identify proteins that bound the N-terminus of Ezrin in tumor lysates. Functional analyses of these data led to a novel and unifying hypothesis that Ezrin contributes to the efficiency of metastasis through regulation of protein translation. In support of this hypothesis, we found Ezrin to be part of the ribonucleoprotein complex to facilitate the expression of complex messenger RNA in cells and to bind with poly A binding protein 1 (PABP1; PABPC1). The relevance of these findings was supported by our identification of Ezrin and components of the translational machinery in pseudopodia of highly metastatic cells during the process of cell invasion. Finally, two small molecule inhibitors recently shown to inhibit the Ezrin metastatic phenotype disrupted the Ezrin/PABP1 association. Taken together, these results provide a novel mechanistic basis by which Ezrin may contribute to metastasis.
C1 [Khanna, Chand] NCI, Tumor & Metastasis Biol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Rahim, Said; Bulut, Gulay; Uren, Aykut] Georgetown Univ, Lombardi Canc Ctr, Washington, DC USA.
[Zhou, Ming; Veenstra, Timothy D.] NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Chen, Qingrong; Wei, Jun S.; Khan, Javed] NCI, Oncogen Sect, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Khanna, C (reprint author), NCI, Tumor & Metastasis Biol Sect, Pediat Oncol Branch, Ctr Canc Res,NIH, 37 Convent Dr,Rm 2144, Bethesda, MD 20892 USA.
EM khannac@mail.nih.gov
RI Khan, Javed/P-9157-2014
OI Khan, Javed/0000-0002-5858-0488
NR 56
TC 16
Z9 17
U1 0
U2 7
PU NEOPLASIA PRESS
PI ANN ARBOR
PA 1150 W MEDICAL CENTER DR, MSRB III, RM 9303, ANN ARBOR, MI 48109-0648
USA
SN 1522-8002
J9 NEOPLASIA
JI Neoplasia
PD APR
PY 2012
VL 14
IS 4
BP 297
EP +
DI 10.1593/neo.111518
PG 16
WC Oncology
SC Oncology
GA 956EG
UT WOS:000305072100004
PM 22577345
ER
PT J
AU Orru, CD
Wilham, JM
Vascellari, S
Hughson, AG
Caughey, B
AF Orru, Christina D.
Wilham, Jason M.
Vascellari, Sarah
Hughson, Andrew G.
Caughey, Byron
TI New generation QuIC assays for prion seeding activity
SO PRION
LA English
DT Review
DE real time QuIC; prion detection; enhanced QuIC; prion diagnosis;
recombinant PMCA
ID CREUTZFELDT-JAKOB-DISEASE; IN-VITRO AMPLIFICATION; MISFOLDING CYCLIC
AMPLIFICATION; QUAKING-INDUCED CONVERSION; CHRONIC WASTING DISEASE;
SEEDED CONVERSION; SENSITIVE ASSAY; PROTEIN; SCRAPIE; BLOOD
AB The ability of abnormal TSE-associated forms of PrP to seed the formation of amyloid fibrils from recombinant PrPSen has served as the basis for several relatively rapid and highly sensitive tests for prion diseases. These tests include rPrP-PMCA (rPMCA), standard quaking-induced conversion (S-QuIC), amyloid seeding assay (ASA), real-time QuIC (RT-QuIC) and enhanced QuIC (eQuIC). Here, we summarize recent improvements in the RT-QuIC-based assays that enhance the practicality, sensitivity and quantitative attributes of assays QuIC and promote the detection of prion seeding activity in dilute, inhibitor-laden fluids such as blood plasma.
C1 [Orru, Christina D.; Wilham, Jason M.; Vascellari, Sarah; Hughson, Andrew G.; Caughey, Byron] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
RP Caughey, B (reprint author), NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT USA.
EM bcaughey@nih.gov
FU NIAID, NIH; Master and Back Program of the Regione Sardegna (Italy)
FX This work was supported by the Intramural Research Program of the NIAID,
NIH. S.V. was partially supported by the Master and Back Program of the
Regione Sardegna (Italy).
NR 44
TC 28
Z9 28
U1 0
U2 10
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1933-6896
J9 PRION
JI Prion
PD APR-JUN
PY 2012
VL 6
IS 2
BP 147
EP 152
DI 10.4161/pri.19430
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 948SW
UT WOS:000304523900009
ER
PT J
AU Avila, C
Huang, RJ
Stevens, MV
Aponte, AM
Tripodi, D
Kim, KY
Sack, MN
AF Avila, C.
Huang, R. J.
Stevens, M. V.
Aponte, A. M.
Tripodi, D.
Kim, K. Y.
Sack, M. N.
TI Platelet Mitochondrial Dysfunction is Evident in Type 2 Diabetes in
Association with Modifications of Mitochondrial Anti-Oxidant Stress
Proteins
SO EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
LA English
DT Article
DE mitochondria; platelets; reactive oxygen species; respiration; diabetes
ID SKELETAL-MUSCLE; INSULIN-RESISTANCE
AB Objective: Mitochondrial dysfunction and oxidative stress in insulin responsive tissues is implicated in the pathogenesis of type 2 diabetes. Whether these perturbations extend to other tissues and contribute to their pathophysiology is less well established. The objective of this study was to investigate platelet mitochondria to evaluate whether type 2 diabetes associated mitochondria( dysfunction is evident in circulating cells.
Method: A pilot study of mitochondrial respiratory function and proteomic changes comparing platelets extracted from insulin sensitive (n=8) and type 2 diabetic subjects (n=7).
Results: In-situ platelet mitochondria show diminished oxygen consumption and lower oxygen-dependent ATP synthesis in diabetic vs. control subjects. Mass spectrometric identification and confirmatory immunoblot analysis identifies induction of the mitochondrial anti-oxidant enzymes superoxide dismutase 2 and thioredoxin-dependent peroxide reductase 3 in platelets of diabetic subjects. As oxidative stress upregulates anti-oxidant enzymes we assessed mitochondrial protein carbonylation as an index of oxidative-stress. Platelets of diabetic subjects exhibit significantly increased protein carbonylation compared to controls.
Conclusions: As platelets are anuclear fragments of megakaryocytes, our data suggest that the bone marrow compartment in type 2 diabetic subjects is exposed to increased mitochondrial oxidative stress with upregulation of nuclear-encoded antioxidant mitochondrial enzymes. This 'stress-signature' in platelets of diabetic subjects is associated with a diminution of their mitochondrial contribution to energy production and support that mitochondrial perturbations in type 2 diabetes extends beyond the classical insulin responsive tissues. Platelets, as "accessible human tissue", may be useful to measure the mitochondrial modulatory effects of emerging anti-diabetic therapeutics.
C1 [Avila, C.; Huang, R. J.; Stevens, M. V.; Tripodi, D.; Kim, K. Y.; Sack, M. N.] NHLBI, Ctr Mol Med, NIH, Bethesda, MD 20892 USA.
[Aponte, A. M.] NHLBI, Prote Core Facil, NIH, Bethesda, MD 20892 USA.
RP Sack, MN (reprint author), NHLBI, Ctr Mol Med, NIH, Bldg 10-CRC,Room 5-3150,10 Ctr Dr, Bethesda, MD 20892 USA.
EM sackm@nhlbi.nih.gov
FU Division of Intramural Research of the NHLBI; NIH-Pfizer
FX This research is funded by the Division of Intramural Research of the
NHLBI. CA and RJH were funded by an NIH-Pfizer Clinical Research
Training Fellowship. We thank the NHLBI Flow Cytometry Core Facility for
assistance in the confirmation of platelet purity and Stephanie A
French, Darci Phillips and Dr. Marjan Gucek of the NHLBI for helpful
discussion regarding mitochondrial protein isolation and proteomic
analysis.
NR 15
TC 25
Z9 25
U1 2
U2 16
PU JOHANN AMBROSIUS BARTH VERLAG MEDIZINVERLAGE HEIDELBERG GMBH
PI STUTTGART
PA RUEDIGERSTR 14, D-70469 STUTTGART, GERMANY
SN 0947-7349
J9 EXP CLIN ENDOCR DIAB
JI Exp. Clin. Endocrinol. Diabet.
PD APR
PY 2012
VL 120
IS 4
BP 248
EP 251
DI 10.1055/s-0031-1285833
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 949NI
UT WOS:000304582500020
PM 21922457
ER
PT J
AU Felsenfeld, G
Dekker, J
AF Felsenfeld, Gary
Dekker, Job
TI Genome architecture and expression
SO CURRENT OPINION IN GENETICS & DEVELOPMENT
LA English
DT Editorial Material
C1 [Felsenfeld, Gary] NIDDK, Chem Phys Sect, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Dekker, Job] Univ Massachusetts, Sch Med, LRB 509, Worcester, MA 01605 USA.
RP Felsenfeld, G (reprint author), NIDDK, Chem Phys Sect, Mol Biol Lab, NIH, Bldg 5,Room 212,5 Mem Dr, Bethesda, MD 20892 USA.
EM garyf@intra.niddk.nih.gov
FU Intramural NIH HHS; NHGRI NIH HHS [R01 HG003143]
NR 0
TC 6
Z9 6
U1 2
U2 9
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-437X
J9 CURR OPIN GENET DEV
JI Curr. Opin. Genet. Dev.
PD APR
PY 2012
VL 22
IS 2
BP 59
EP 61
DI 10.1016/j.gde.2012.03.003
PG 3
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 946FX
UT WOS:000304338000001
PM 22483506
ER
PT J
AU Krivega, I
Dean, A
AF Krivega, Ivan
Dean, Ann
TI Enhancer and promoter interactions-long distance calls
SO CURRENT OPINION IN GENETICS & DEVELOPMENT
LA English
DT Review
ID BETA-GLOBIN LOCUS; RNA-POLYMERASE-II; MAJOR HISTOCOMPATIBILITY COMPLEX;
CCCTC-BINDING FACTOR; GENE-EXPRESSION; CONTROL REGION; NONCODING RNAS;
ERYTHROID-DIFFERENTIATION; INTERGENIC TRANSCRIPTION; CHROMATIN
ARCHITECTURE
AB In metazoans, enhancers of gene transcription must often exert their effects over tens of kilobases of DNA. Over the past decade it has become clear that to do this, enhancers come into close proximity with target promoters with the looping away of intervening sequences. In a few cases proteins that are involved in the establishment or maintenance of these loops have been revealed but how the proper gene target is selected remains mysterious. Chromatin insulators had been appreciated as elements that play a role in enhancer fidelity through their enhancer blocking or barrier activity. However, recent work suggests more direct participation of insulators in enhancer-gene interactions. The emerging view begins to incorporate transcription activation by distant enhancers with large scale nuclear architecture and subnuclear movement.
C1 [Krivega, Ivan; Dean, Ann] NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20982 USA.
RP Dean, A (reprint author), NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20982 USA.
EM anndean@helix.nih.gov
RI Krivega, Ivan/G-9247-2015
OI Krivega, Ivan/0000-0002-3473-4198
FU NIDDK, NIH
FX We would like to thank Dr. Gerd Blobel for helpful comments on the
manuscript and members of our laboratory for their suggestions. Work in
our laboratory is supported by the Intramural Program of NIDDK, NIH.
NR 64
TC 75
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U1 1
U2 19
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-437X
J9 CURR OPIN GENET DEV
JI Curr. Opin. Genet. Dev.
PD APR
PY 2012
VL 22
IS 2
BP 79
EP 85
DI 10.1016/j.gde.2011.11.001
PG 7
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 946FX
UT WOS:000304338000004
PM 22169023
ER
PT J
AU Reyes-Turcu, FE
Grewal, SIS
AF Reyes-Turcu, Francisca E.
Grewal, Shiv I. S.
TI Different means, same end - heterochromatin formation by RNAi and
RNAi-independent RNA processing factors in fission yeast
SO CURRENT OPINION IN GENETICS & DEVELOPMENT
LA English
DT Review
ID LONG NONCODING RNAS; HISTONE H3; HP1 PROTEINS;
SCHIZOSACCHAROMYCES-POMBE; SELECTIVE ELIMINATION; LYSINE-9 METHYLATION;
CHROMODOMAIN PROTEIN; EPIGENETIC CONTROL; CHP1 CHROMODOMAIN; UBIQUITIN
LIGASE
AB The assembly of heterochromatin in eukaryotic genomes is critical for diverse chromosomal events including regulation of gene expression, silencing of repetitive DNA elements, proper segregation of chromosomes and maintenance of genomic integrity. Previous studies have shown that noncoding RNAs and the RNA interference (RNAi) machinery promote the assembly of heterochromatin that serves as a multipurpose platform for targeting effectors involved in various chromosomal processes. Recent work has revealed that RNAi-independent mechanisms, involving RNA processing activities that utilize both noncoding and coding RNAs, operate in the assembly of heterochromatin. These findings have established that, in addition to coding for proteins, mRNAs also function as signaling molecules that modify chromatin structure by targeting heterochromatin assembly factors.
C1 [Reyes-Turcu, Francisca E.; Grewal, Shiv I. S.] NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Grewal, SIS (reprint author), NCI, Biochem & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM grewals@mail.nih.gov
FU National Institutes of Health, National Cancer Institute
FX We thank members of Grewal Laboratory for helpful discussions. We are
especially thankful to J. Barrowman, V. Chalamcharla and N. Lee comments
on the manuscript. Research in Grewal Laboratory is supported by the
Intramural Research Program of the National Institutes of Health,
National Cancer Institute.
NR 75
TC 39
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U1 1
U2 16
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-437X
J9 CURR OPIN GENET DEV
JI Curr. Opin. Genet. Dev.
PD APR
PY 2012
VL 22
IS 2
BP 156
EP 163
DI 10.1016/j.gde.2011.12.004
PG 8
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 946FX
UT WOS:000304338000014
PM 22243696
ER
PT J
AU Semba, RD
Chang, SS
Sun, K
Talegawkar, S
Ferrucci, L
Fried, LP
AF Semba, R. D.
Chang, S. S.
Sun, K.
Talegawkar, S.
Ferrucci, L.
Fried, L. P.
TI Serum carotenoids and pulmonary function in older community-dwelling
women
SO JOURNAL OF NUTRITION HEALTH & AGING
LA English
DT Article
DE Aging; carotenoids; lung function; women
ID LUNG-FUNCTION; BETA-CAROTENE; GENERAL-POPULATION; ALPHA-TOCOPHEROL;
DIETARY PATTERNS; VITAMIN-A; DISEASE; HEALTH; NUTRITION; FRUITS
AB Deterioration in pulmonary function is associated with greater disability and mortality in older adults. Dietary antioxidants are implicated in lung health, but the relationship between major dietary antioxidants, such as serum carotenoids, and pulmonary function have not been well characterized. Serum carotenoids are considered the most reliable indicator of fruit and vegetable intake.
We examined the relationship between serum alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein/zeaxanthin, and lycopene with pulmonary function (forced expiratory volume in one second [FEV1] and forced vital capacity [FVC]) in a population-based sample of 631 moderately to severely disabled community-dwelling older women (Women's Health and Aging Study I) in Baltimore, Maryland, USA.
Higher serum alpha-carotene and beta-carotene concentrations were positively associated with both FEV1 and FVC, respectively (all P < 0.05), in separate multivariate linear regression models adjusting for age, race, education, cognition, anemia, inflammation, and chronic diseases. Total serum carotenoids were associated with FEV1 (P = 0.08) and FVC (P = 0.06), respectively, in similar models. No association was found between beta-cryptoxanthin, lutein/zeaxanthin, and lycopene, and FEV1 or FVC.
Higher serum alpha-carotene and beta-carotene concentrations, which reflect greater intake of orange and dark green leafy fruits and vegetables, were associated with better pulmonary function among older community-dwelling women.function may lead to food avoidance and to a higher incidence of digestive complaints.
C1 [Semba, R. D.] Johns Hopkins Univ, Sch Med, Dept Ophthalmol, Baltimore, MD 21287 USA.
[Sun, K.] Yale Univ, Sch Med, Dept Internal Med, Sect Geriatr, New Haven, CT 06510 USA.
[Talegawkar, S.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Int Hlth, Ctr Human Nutr, Baltimore, MD USA.
[Ferrucci, L.] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
[Fried, L. P.] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
RP Semba, RD (reprint author), Johns Hopkins Univ, Sch Med, Dept Ophthalmol, Smith Bldg,M015,400 N Broadway, Baltimore, MD 21287 USA.
EM rdsemba@jhmi.edu
FU National Institute on Aging [R01 AG027012]; NIH-NCRR; OPD-GCRC
[RR00722]; NIA [N01-AG12112]; Johns Hopkins Older Americans'
Independence Center; National Institute on Aging, NIH
FX Grant Support: This work was supported by National Institute on Aging
Grant R01 AG027012, NIH-NCRR, OPD-GCRC grant RR00722, and NIA Contract
N01-AG12112, the Johns Hopkins Older Americans' Independence Center, and
the Intramural Research Program, National Institute on Aging, NIH.
NR 33
TC 3
Z9 3
U1 0
U2 3
PU SPRINGER FRANCE
PI PARIS
PA 22 RUE DE PALESTRO, PARIS, 75002, FRANCE
SN 1279-7707
J9 J NUTR HEALTH AGING
JI J. Nutr. Health Aging
PD APR
PY 2012
VL 16
IS 4
BP 291
EP 296
DI 10.1007/s12603-012-0034-z
PG 6
WC Geriatrics & Gerontology; Nutrition & Dietetics
SC Geriatrics & Gerontology; Nutrition & Dietetics
GA 943OT
UT WOS:000304134500003
PM 22499445
ER
PT J
AU Caughey, B
Orru, CD
Wilham, JM
Vascellari, S
Hughson, AG
Raymond, LD
Raymond, GJ
AF Caughey, Byron
Orru, Christina D.
Wilham, Jason M.
Vascellari, Sarah
Hughson, Andrew G.
Raymond, Lynne D.
Raymond, Gregory J.
TI Prion-seeded conversion of recombinant PrP: implications for prion
biology and diagnostics
SO PRION
LA English
DT Meeting Abstract
ID CEREBROSPINAL-FLUID
C1 [Caughey, Byron; Orru, Christina D.; Wilham, Jason M.; Vascellari, Sarah; Hughson, Andrew G.; Raymond, Lynne D.; Raymond, Gregory J.] NIAID, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
NR 7
TC 0
Z9 0
U1 0
U2 4
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1933-6896
J9 PRION
JI Prion
PD APR-JUN
PY 2012
VL 6
SU S
BP 11
EP 12
PG 2
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 944WK
UT WOS:000304234300024
ER
PT J
AU Blanco, RA
De Wolf, C
Tan, B
Agarwal, S
Orru, C
Caughey, B
Raeber, A
Gill, A
Manson, J
McCutcheon, S
AF Blanco, Richard Alejo
De Wolf, Christopher
Tan, Boon
Agarwal, Sonya
Orru, Christina
Caughey, Byron
Raeber, Alex
Gill, Andrew
Manson, Jean
McCutcheon, Sandra
TI Analysis of BSE-infected sheep tissues and plasma using the real-time
quaking induced conversion (RT-QuIC) assay
SO PRION
LA English
DT Meeting Abstract
C1 [Blanco, Richard Alejo; De Wolf, Christopher; Tan, Boon; Agarwal, Sonya; Gill, Andrew; Manson, Jean; McCutcheon, Sandra] Roslin Inst, Edinburgh, Midlothian, Scotland.
[Blanco, Richard Alejo; De Wolf, Christopher; Tan, Boon; Agarwal, Sonya; Gill, Andrew; Manson, Jean; McCutcheon, Sandra] R D SVS, Edinburgh, Midlothian, Scotland.
[Orru, Christina; Caughey, Byron] NIAID, NIH, Hamilton, MT USA.
[Raeber, Alex] Prionics AG, Zurich, Switzerland.
RI Gill, Andrew/A-5219-2009
NR 5
TC 2
Z9 2
U1 0
U2 2
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1933-6896
J9 PRION
JI Prion
PD APR-JUN
PY 2012
VL 6
SU S
BP 94
EP 94
PG 1
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 944WK
UT WOS:000304234300194
ER
PT J
AU Pick, CG
Rubovitch, V
Rachmany, L
Tweedie, D
Hoffer, BJ
Schreiber, S
Greig, NH
AF Pick, Chaim G. (Chagi)
Rubovitch, Vardit
Rachmany, Lital
Tweedie, David
Hoffer, Barry J.
Schreiber, Shaul
Greig, Nigel H.
TI Possible translational study to the clinic of a combat zone-like mouse
model of Blast Brain Injury
SO BRAIN INJURY
LA English
DT Meeting Abstract
C1 [Pick, Chaim G. (Chagi); Rubovitch, Vardit; Rachmany, Lital] Tel Aviv Univ, Sackler Sch Med, Dept Anat & Anthropol, IL-69978 Tel Aviv, Israel.
[Tweedie, David; Greig, Nigel H.] NIA, Neurosci Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
[Hoffer, Barry J.] NIDA, Cellular Neurobiol Branch, Intramural Res Program, Baltimore, MD USA.
[Schreiber, Shaul] Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Dept Psychiat, IL-69978 Tel Aviv, Israel.
[Schreiber, Shaul] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
RI Schreiber, Shaul/E-5821-2010
OI Schreiber, Shaul/0000-0002-2189-0693
NR 0
TC 0
Z9 0
U1 0
U2 4
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0269-9052
J9 BRAIN INJURY
JI Brain Inj.
PD APR-MAY
PY 2012
VL 26
IS 4-5
MA 0086
BP 340
EP 341
PG 2
WC Neurosciences; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 943EZ
UT WOS:000304104600064
ER
PT J
AU Zafonte, R
Ansel, B
Freidwald, W
Novack, T
Timmons, S
Eisenberg, H
Ricker, J
Merchant, R
Temkin, N
Jallo, J
Bagiella, E
AF Zafonte, Ross
Ansel, Beth
Freidwald, William
Novack, Thomas
Timmons, Shelly
Eisenberg, Howard
Ricker, Joe
Merchant, Randall
Temkin, Nancy
Jallo, Jack
Bagiella, Emilia
TI Results of the citicoline brain injury treatment (COBRIT) trial
SO BRAIN INJURY
LA English
DT Meeting Abstract
C1 NIH, Bethesda, MD 20892 USA.
Columbia Univ, NYC, New York, NY USA.
Univ Alabama Birmingham, Birmingham, AL USA.
Univ Maryland, Baltimore, MD 21201 USA.
Univ Pittsburgh, Pittsburgh, PA USA.
Virginia Commonwealth Univ, Richmond, VA USA.
Univ Washington, Seattle, WA 98195 USA.
Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
NYC, Mt Sinai Sch Med, New York, NY USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0269-9052
J9 BRAIN INJURY
JI Brain Inj.
PD APR-MAY
PY 2012
VL 26
IS 4-5
MA 0182
BP 389
EP 389
PG 1
WC Neurosciences; Rehabilitation
SC Neurosciences & Neurology; Rehabilitation
GA 943EZ
UT WOS:000304104600153
ER
PT J
AU Balasubbu, S
Krishnadas, SR
Jiao, XD
Hejtmancik, JF
Sundaresan, P
AF Balasubbu, Suganthalakshmi
Krishnadas, Subbaiah R.
Jiao, Xiaodong
Hejtmancik, J. Fielding
Sundaresan, Periasamy
TI Evaluation of SNPs on Chromosome 2p with Primary Open Angle Glaucoma in
the South Indian Cohort
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID GENOME-WIDE SCAN; BARBADOS; IDENTIFICATION; ASSOCIATION; POPULATION;
VARIANTS; DISEASE; RISK; GENE; POAG
AB PURPOSE. Glaucoma comprises a heterogeneous group of optic neuropathies with a complex genetic basis. It is the second leading cause of irreversible blindness in the world. This study investigates the association of SNPs on chromosome 2p with primary open angle glaucoma (POAG) in a Southern Indian population.
METHODS. Case-control analysis was performed using 220 unrelated POAG cases and 220 age-matched unaffected controls recruited through the Aravind Eye Hospital and its outlying clinics. Five SNPs (rs1533428, rs12994401, rs10202118, rs11125375, and rs11889995) on chromosome 2p were evaluated in these two groups and genotyped using Taq Man SNP genotyping assay. Statistical analysis was performed using the SVS program package by Golden Helix to identify the distributions of allele and genotype frequencies, Fisher exact test P values, and odds ratios and to check Hardy-Weinberg equilibrium.
RESULTS. Among the five SNPs screened, SNP rs10202118, showed a P = 0.026 for the basic allelic test, P = 0.004 for the genotypic test, and P = 0.0014 for the recessive model. The second suggestive marker was rs11125375, which also showed P = 0.033 for the recessive model. The associated SNPs formed a common disease haplotype. The remaining three SNPs showed insignificant association in this study population.
CONCLUSIONS. This was the first study to demonstrate the association of SNPs on chromosome 2p in patients with POAG in the Indian population. The two tagging SNPs (rs10202118 and rs11125375) on chromosome 2p are the most likely sites underlying the significant association with POAG in this study population. (Invest Ophthalmol Vis Sci. 2012;53:1861-1864) DOI:10.1167/iovs.11-8602
C1 [Balasubbu, Suganthalakshmi; Sundaresan, Periasamy] Aravind Eye Hosp, Dr G Venkataswamy Eye Res Inst, Dept Genet, Aravind Med Res Fdn, Madurai 625020, Tamil Nadu, India.
[Krishnadas, Subbaiah R.] Aravind Eye Hosp, Glaucoma Clin, Madurai 625020, Tamil Nadu, India.
[Jiao, Xiaodong; Hejtmancik, J. Fielding] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Rockville, MD USA.
RP Sundaresan, P (reprint author), Aravind Eye Hosp, Dr G Venkataswamy Eye Res Inst, Dept Genet, Aravind Med Res Fdn, 1 Anna Nagar, Madurai 625020, Tamil Nadu, India.
EM sundar@aravind.org
FU Alcon; Aravind Medical Research Foundation
FX Supported by Alcon, Aravind Medical Research Foundation.
NR 22
TC 4
Z9 4
U1 0
U2 0
PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC
PI ROCKVILLE
PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA
SN 0146-0404
J9 INVEST OPHTH VIS SCI
JI Invest. Ophthalmol. Vis. Sci.
PD APR
PY 2012
VL 53
IS 4
BP 1861
EP 1864
DI 10.1167/iovs.11-8602
PG 4
WC Ophthalmology
SC Ophthalmology
GA 937PC
UT WOS:000303669400021
PM 22410552
ER
PT J
AU Dauner, JG
Pan, YJ
Hildesheim, A
Kemp, TJ
Porras, C
Pinto, LA
AF Dauner, Joseph G.
Pan, Yuanji
Hildesheim, Allan
Kemp, Troy J.
Porras, Carolina
Pinto, Ligia A.
TI Development and application of a GuHCl-modified ELISA to measure the
avidity of anti-HPV L1 VLP antibodies in vaccinated individuals
SO MOLECULAR AND CELLULAR PROBES
LA English
DT Article
DE HPV vaccine; Antibody; Avidity
ID VIRUS-LIKE PARTICLES; HUMAN-PAPILLOMAVIRUS TYPE-16; IMMUNOGLOBULIN-G;
STREPTOCOCCUS-PNEUMONIAE; MONOCLONAL-ANTIBODIES; COMBINATION VACCINES;
THIOCYANATE ELUTION; CONJUGATE VACCINES; IMMUNE-RESPONSES; RHESUS
MACAQUES
AB Antibody responses against infectious agents are an important component in the prevention of disease. The avidity of antibodies for their antigens relates to their functional efficiency, and is a fundamental aspect in the investigation of humoral responses. Modified ELISAs are used to estimate avidity through the use of chaotropic agents and the measurement of the degree to which they disrupt the interaction between antibody and antigen. The theory behind the assay is the higher the avidity of an interaction the less susceptible it is to the effects of the chaotropic agent. The goal of this study was to generate a modified ELISA where a complex, multimeric coating-antigen, human papillomavirus (HPV) virus-like particles (VLP), was used to measure the avidity of anti-HPV antibodies generated following vaccination with HPV VLPs. A series of chaotropic agents were evaluated in the assay for their effectiveness in measuring avidity. Guanidine hydrochloride (GuHCl) was selected as a chaotropic reagent with the ability to disrupt antibody and antigen interactions, while not affecting the integrity of the plate-bound VLP. Two methods of determining the avidity index were assessed and shown to be comparable. This assay was then successfully applied to measure the avidity of anti-HPV VLP serum antibodies in samples from an HPV L1 VLP vaccine clinical trial. Overall, the assay was highly reproducible and captured a wide range of antibody avidities. Therefore, a GuHCl-modifiecl ELISA is an acceptable method that can be used to determine HPV-specific antibody avidity indices within a clinical trial setting. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Dauner, Joseph G.; Pan, Yuanji; Kemp, Troy J.; Pinto, Ligia A.] NCI, HPV Immunol Lab, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Hildesheim, Allan] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Pinto, LA (reprint author), NCI, HPV Immunol Lab, SAIC Frederick Inc, Bldg 469,Room 120, Frederick, MD 21702 USA.
EM pintol@mail.nih.gov
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU NCI; NCI, the National Institutes of Health Office for Research on
Women's Health (ORWH); GSK Bio [FDA BB-IND 7920]; National Cancer
Institute, National Institutes of Health [HHSN261200800001E]
FX The Costa Rica HPV Vaccine Trial is a long-standing collaboration
between investigators in Costa Rica and the NCI. The trial is sponsored
by the NCI, and conducted with support from the Ministry of Health of
Costa Rica. This project has been funded in part by the NCI Intramural
Research Program, the National Institutes of Health Office for Research
on Women's Health (ORWH). Vaccine was provided for our trial by
GlaxoSmithKline Biologicals (GSK Bio, Rixensart, Belgium), under a
Clinical Trials Agreement with the NCI. GSK Bio also provided support
for aspects of the trial associated with regulatory submission needs of
the company under grant FDA BB-IND 7920. Laboratory testing was
performed at the NCI-sponsored SAIC-Frederick, Inc. HPV Immunology
Laboratory in Frederick, MD. The NCI and Costa Rica investigators are
responsible for the design and conduct of the study; collection,
management, analysis, and interpretation of the data; and preparation of
the manuscript. The NCI and Costa Rica investigators make final
editorial decisions on this and subsequent publications; GSK Bio has the
right to review and comment.; This project has been funded in whole or
in part with federal funds from the National Cancer Institute, National
Institutes of Health, under Contract No. HHSN261200800001E. The content
of this publication does not necessarily reflect the views or policies
of the Department of Health and Human Services, nor does mention of
trade names, commercial products, or organizations imply endorsement by
the U.S. Government.
NR 39
TC 10
Z9 10
U1 0
U2 7
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0890-8508
J9 MOL CELL PROBE
JI Mol. Cell. Probes
PD APR
PY 2012
VL 26
IS 2
BP 73
EP 80
DI 10.1016/j.mcp.2012.01.002
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biotechnology & Applied Microbiology; Cell Biology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Cell Biology
GA 944UF
UT WOS:000304228600003
PM 22285687
ER
PT J
AU Boja, ES
Rodriguez, H
AF Boja, Emily S.
Rodriguez, Henry
TI Mass spectrometry-based targeted quantitative proteomics: Achieving
sensitive and reproducible detection of proteins
SO PROTEOMICS
LA English
DT Review
DE Biomarker verification; Multiple reaction monitoring mass spectrometry;
Posttranslational modifications; Protein quantitation; Systems biology;
Technology
ID ACTIVITY-BASED PROBES; STABLE-ISOTOPE DILUTION; ABSOLUTE QUANTIFICATION;
PEPTIDE ENRICHMENT; MULTIPLEXED ASSAYS; PLASMA PROTEOME; MAGNETIC BEADS;
CANCER; BIOMARKER; SERUM
AB Traditional shotgun proteomics used to detect a mixture of hundreds to thousands of proteins through mass spectrometric analysis, has been the standard approach in research to profile protein content in a biological sample which could lead to the discovery of new (and all) protein candidates with diagnostic, prognostic, and therapeutic values. In practice, this approach requires significant resources and time, and does not necessarily represent the goal of the researcher who would rather study a subset of such discovered proteins (including their variations or posttranslational modifications) under different biological conditions. In this context, targeted proteomics is playing an increasingly important role in the accurate measurement of protein targets in biological samples in the hope of elucidating the molecular mechanism of cellular function via the understanding of intricate protein networks and pathways. One such (targeted) approach, selected reaction monitoring (or multiple reaction monitoring) mass spectrometry (MRM-MS), offers the capability of measuring multiple proteins with higher sensitivity and throughput than shotgun proteomics. Developing and validating MRM-MS-based assays, however, is an extensive and iterative process, requiring a coordinated and collaborative effort by the scientific community through the sharing of publicly accessible data and datasets, bioinformatic tools, standard operating procedures, and well characterized reagents.
C1 [Boja, Emily S.; Rodriguez, Henry] NCI, Off Canc Clin Prote Res, NIH, Bethesda, MD 20892 USA.
RP Boja, ES (reprint author), NCI, Off Canc Clin Prote Res, NIH, 31 Ctr Dr,MS 2580, Bethesda, MD 20892 USA.
EM bojae@mail.nih.gov
NR 93
TC 76
Z9 77
U1 6
U2 79
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1615-9853
J9 PROTEOMICS
JI Proteomics
PD APR
PY 2012
VL 12
IS 8
BP 1093
EP 1110
DI 10.1002/pmic.201100387
PG 18
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 940UI
UT WOS:000303918200003
PM 22577011
ER
PT J
AU Barrett, J
Bollard, CM
AF Barrett, John
Bollard, Catherine M.
TI T-cell therapy for cancer
SO IMMUNOTHERAPY
LA English
DT Editorial Material
DE adoptive transfer; cytotoxic T cells; graft-versus-leukemia
ID HODGKIN-LYMPHOMA; LYMPHOPROLIFERATIVE DISEASE; METASTATIC MELANOMA;
ADOPTIVE TRANSFER; LYMPHOCYTES; EBV; TRANSPLANTATION; RESPONSES;
LEUKEMIA; HUMANS
C1 [Bollard, Catherine M.] Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
[Barrett, John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Bollard, CM (reprint author), Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
EM cmbollar@txch.org
NR 40
TC 2
Z9 2
U1 0
U2 0
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1750-743X
J9 IMMUNOTHERAPY-UK
JI Immunotherapy
PD APR
PY 2012
VL 4
IS 4
BP 347
EP 350
DI 10.2217/IMT.12.12
PG 4
WC Immunology
SC Immunology
GA 937VP
UT WOS:000303691400001
PM 22512624
ER
PT J
AU Nakashima, H
Husain, SR
Puri, RK
AF Nakashima, Hideyuki
Husain, Syed R.
Puri, Raj K.
TI IL-13 receptor-directed cancer vaccines and immunotherapy
SO IMMUNOTHERAPY
LA English
DT Review
DE combination therapy; DNA vaccine; IL-13 receptor alpha 2; immunotoxin;
myeloid-derived suppressor cells
ID MYELOID SUPPRESSOR-CELLS; REGULATORY T-CELLS; GLIOMA-ASSOCIATED
ANTIGENS; MURINE TUMOR-MODELS; INTERLEUKIN-13 RECEPTOR; ALPHA-2 CHAIN;
PSEUDOMONAS EXOTOXIN; SIGNAL-TRANSDUCTION; IMMUNE-RESPONSE; ANTICANCER
THERAPY
AB Many immunotherapy approaches including therapeutic cancer vaccines targeting specific tumor-associated antigens are at various stages of development. Although the significance of overexpression of (IL-13R alpha 2) in cancer is being actively investigated, we have reported that IL-13R alpha 2 is a novel tumor-associated antigen. The IL-13R alpha 2-directed cancer vaccine is one of the most promising approaches to tumor immunotherapy, because of the selective expression of IL-13R alpha 2 in various solid tumor types but not in normal tissues. In this article, we will summarize its present status and potential strategies to improve IL-13R alpha 2-directed cancer vaccines for an optimal therapy of cancer.
C1 [Nakashima, Hideyuki; Husain, Syed R.; Puri, Raj K.] US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
RP Puri, RK (reprint author), US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, NIH Bldg 29B,Room 2NN20,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM raj.puri@fda.hhs.gov
NR 79
TC 10
Z9 10
U1 0
U2 2
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1750-743X
J9 IMMUNOTHERAPY-UK
JI Immunotherapy
PD APR
PY 2012
VL 4
IS 4
BP 443
EP 451
DI 10.2217/IMT.12.28
PG 9
WC Immunology
SC Immunology
GA 937VP
UT WOS:000303691400017
PM 22512637
ER
PT J
AU Hamilton, JG
Lobel, M
AF Hamilton, Jada G.
Lobel, Marci
TI Passing years, changing fears? Conceptualizing and measuring risk
perceptions for chronic disease in younger and middle-aged women
SO JOURNAL OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Risk perception; Perceived vulnerability; Chronic disease; Women's
health; Structural equation modeling
ID BREAST-CANCER; PERCEIVED RISK; HEALTH BEHAVIOR; SUSCEPTIBILITY;
VICTIMIZATION; VULNERABILITY; PERSONALITY; PSYCHOLOGY; KNOWLEDGE
AB As is true for many behavioral theory constructs, no consensus exists on how best to measure perceived risk; therefore, it is unclear whether different measures of disease risk perception are conceptually equivalent and whether such measures are equally appropriate for people with different objective disease risk. To investigate these issues, we used four commonly utilized risk perception items (measuring beliefs about personal risk, others' risk, disease prevalence, and mortality) to assess susceptibility to cardiovascular disease, breast cancer, and lung cancer among 454 younger (ages 18-25) and 169 middle-aged (40-64) women. We examined age-and ethnicity-related differences in participants' responses to the items. We also used structural equation modeling to test whether these items reflect a multidimensional, disease-specific latent construct of risk perception; and to test whether consistency exists in participants' disease-specific risk perceptions. Despite differences in responses to individual items, hypothesized models of perceived risk fit both age groups, suggesting that risk perception can be conceptualized in younger and middle-aged women as a multidimensional construct that is specific to disease yet reflective of global risk-related beliefs.
C1 [Hamilton, Jada G.; Lobel, Marci] SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA.
RP Hamilton, JG (reprint author), NCI, Canc Prevent Fellowship Program, Ctr Canc Training, Proc Care Res,Branch Behav Res Program,Div Canc C, 6130 Execut Blvd,Room 4051C,MSC 7331, Bethesda, MD 20892 USA.
EM hamiltonjg@mail.nih.gov
NR 49
TC 3
Z9 3
U1 1
U2 8
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0160-7715
J9 J BEHAV MED
JI J. Behav. Med.
PD APR
PY 2012
VL 35
IS 2
BP 124
EP 138
DI 10.1007/s10865-011-9342-8
PG 15
WC Psychology, Clinical
SC Psychology
GA 940BP
UT WOS:000303865300002
PM 21487721
ER
PT J
AU Okano, J
Lichti, U
Mamiya, S
Aronova, M
Zhang, GF
Yuspa, SH
Hamada, H
Sakai, Y
Morasso, MI
AF Okano, Junko
Lichti, Ulrike
Mamiya, Satoru
Aronova, Maria
Zhang, Guofeng
Yuspa, Stuart H.
Hamada, Hiroshi
Sakai, Yasuo
Morasso, Maria I.
TI Increased retinoic acid levels through ablation of Cyp26b1 determine the
processes of embryonic skin barrier formation and peridermal development
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Retinoic acid; Cyp26b1; Periderm; Skin differentiation; Skin barrier
formation; Filaggrin
ID CORNIFIED ENVELOPE; EPIDERMAL BARRIER; TERMINAL DIFFERENTIATION;
ATOPIC-DERMATITIS; INTEGRATED VIEW; CLEFT-PALATE; EXPRESSION; MICE;
GENE; FILAGGRIN
AB The process by which the periderm transitions to stratified epidermis with the establishment of the skin barrier is unknown. Understanding the cellular and molecular processes involved is crucial for the treatment of human pathologies, where abnormal skin development and barrier dysfunction are associated with hypothermia and perinatal dehydration. For the first time, we demonstrate that retinoic acid (RA) levels are important for periderm desquamation, embryonic skin differentiation and barrier formation. Although excess exogenous RA has been known to have teratogenic effects, little is known about the consequences of elevated endogenous retinoids in skin during embryogenesis. Absence of cytochrome P450, family 26, subfamily b, polypeptide 1 (Cyp26b1), a retinoic-acid-degrading enzyme, results in aberrant epidermal differentiation and filaggrin expression, defective cornified envelopes and skin barrier formation, in conjunction with peridermal retention. We show that these alterations are RA dependent because administration of exogenous RA in vivo and to organotypic skin cultures phenocopy Cyp26b1(-/-) skin abnormalities. Furthermore, utilizing the Flaky tail (Ft/Ft) mice, a mouse model for human ichthyosis, characterized by mutations in the filaggrin gene, we establish that proper differentiation and barrier formation is a prerequisite for periderm sloughing. These results are important in understanding pathologies associated with abnormal embryonic skin development and barrier dysfunction.
C1 [Okano, Junko; 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.
[Mamiya, Satoru; Hamada, Hiroshi] Osaka Univ, Grad Sch Frontier Biosci, Dev Genet Grp, Suita, Osaka 5650871, Japan.
[Aronova, Maria; Zhang, Guofeng] NIBIB, Lab Bioengn & Phys Sci, NIH, Bethesda, MD 20892 USA.
[Sakai, Yasuo] Osaka Univ, Sch Med, Dept Plast Surg, Suita, Osaka 5650871, Japan.
RP Morasso, MI (reprint author), NIAMS, Dev Skin Biol Sect, NIH, Bethesda, MD 20892 USA.
EM morasso@nih.gov
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases,
National Institutes of Health
FX This study was supported by an Intramural Research Program of the
National Institute of Arthritis and Musculoskeletal and Skin Diseases,
National Institutes of Health. Deposited in PMC for release after 12
months.
NR 56
TC 11
Z9 11
U1 1
U2 6
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD APR 1
PY 2012
VL 125
IS 7
BP 1827
EP 1836
DI 10.1242/jcs.101550
PG 10
WC Cell Biology
SC Cell Biology
GA 940RR
UT WOS:000303911300022
PM 22366455
ER
PT J
AU Riley, BD
Culver, JO
Skrzynia, C
Senter, LA
Peters, JA
Costalas, JW
Callif-Daley, F
Grumet, SC
Hunt, KS
Nagy, RS
McKinnon, WC
Petrucelli, NM
Bennett, RL
Trepanier, AM
AF Riley, Bronson D.
Culver, Julie O.
Skrzynia, Cecile
Senter, Leigha A.
Peters, June A.
Costalas, Josephine W.
Callif-Daley, Faith
Grumet, Sherry C.
Hunt, Katherine S.
Nagy, Rebecca S.
McKinnon, Wendy C.
Petrucelli, Nancie M.
Bennett, Robin L.
Trepanier, Angela M.
TI Essential Elements of Genetic Cancer Risk Assessment, Counseling, and
Testing: Updated Recommendations of the National Society of Genetic
Counselors
SO JOURNAL OF GENETIC COUNSELING
LA English
DT Article
DE Cancer genetic counseling; Risk assessment; Genetic testing; Family
history; Psychosocial assessment; Hereditary cancer; Informed consent
ID BRCA2 MUTATION CARRIERS; POLICY STATEMENT UPDATE; BREAST-CANCER;
LYNCH-SYNDROME; OVARIAN-CANCER; HEREDITARY CANCER; FAMILY-HISTORY;
PREDISPOSITION SYNDROMES; PSYCHOLOGICAL IMPACT; AMERICAN-SOCIETY
AB Updated from their original publication in 2004, these cancer genetic counseling recommendations describe the medical, psychosocial, and ethical ramifications of counseling at-risk individuals through genetic cancer risk assessment with or without genetic testing. They were developed by members of the Practice Issues Subcommittee of the National Society of Genetic Counselors Familial Cancer Risk Counseling Special Interest Group. The information contained in this document is derived from extensive review of the current literature on cancer genetic risk assessment and counseling as well as the personal expertise of genetic counselors specializing in cancer genetics. The recommendations are intended to provide information about the process of genetic counseling and risk assessment for hereditary cancer disorders rather than specific information about individual syndromes. Essential components include the intake, cancer risk assessment, genetic testing for an inherited cancer syndrome, informed consent, disclosure of genetic test results, and psychosocial assessment. These recommendations should not be construed as dictating an exclusive course of management, nor does use of such recommendations guarantee a particular outcome. These recommendations do not displace a health care provider's professional judgment based on the clinical circumstances of a client.
C1 [Riley, Bronson D.] SE Nebraska Canc Ctr, Lincoln, NE USA.
[Culver, Julie O.] City Hope Natl Med Ctr, Div Clin Canc Genet, Duarte, CA USA.
[Skrzynia, Cecile] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Skrzynia, Cecile] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Senter, Leigha A.] Ohio State Univ, Div Human Genet, Columbus, OH 43210 USA.
[Peters, June A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Costalas, Josephine W.] St Mary Reg Canc Ctr, Langhorne, PA USA.
[Callif-Daley, Faith] Childrens Med Ctr Dayton, Dept Med Genet, Dayton, OH USA.
[Grumet, Sherry C.] Monmouth Med Ctr, Leon Hess Canc Ctr, Long Branch, NJ USA.
[Hunt, Katherine S.] Mayo Coll Med, Scottsdale, AZ USA.
[Nagy, Rebecca S.] Ohio State Univ, Clin Canc Genet Program, James Canc Hosp, Columbus, OH 43210 USA.
[Nagy, Rebecca S.] Ohio State Univ, Solove Res Inst, Columbus, OH 43210 USA.
[McKinnon, Wendy C.] Fletcher Allen Hlth Care, Vermont Reg Genet Ctr, Dept Pediat, Burlington, VT USA.
[Petrucelli, Nancie M.] Karmanos Canc Inst, Detroit, MI USA.
[Bennett, Robin L.] Univ Washington, Div Med Genet, Med Ctr, Seattle, WA 98195 USA.
[Trepanier, Angela M.] Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI USA.
RP Riley, BD (reprint author), SE Nebraska Canc Ctr, Lincoln, NE USA.
EM bronsonr@leadingcancercare.com
RI Shrigley Nagy, Rebecca/E-4088-2011
NR 79
TC 83
Z9 87
U1 4
U2 15
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1059-7700
J9 J GENET COUNS
JI J. Genet. Couns.
PD APR
PY 2012
VL 21
IS 2
BP 151
EP 161
DI 10.1007/s10897-011-9462-x
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 940LC
UT WOS:000303890000001
PM 22134580
ER
PT J
AU Yoshinaga, K
AF Yoshinaga, Koji
TI Two Concepts on the Immunological Aspect of Blastocyst Implantation
SO JOURNAL OF REPRODUCTION AND DEVELOPMENT
LA English
DT Review
DE Blastocyst implantation; Concepts; Immune aspect
ID LEUKEMIA INHIBITORY FACTOR; HUMAN CHORIONIC-GONADOTROPIN;
COLONY-STIMULATING FACTOR; FACTOR GENE-EXPRESSION; ENDOMETRIAL
EPITHELIAL-CELLS; PREIMPLANTATION MOUSE EMBRYO; DECAY-ACCELERATING
FACTOR; UTERINE RECEPTIVITY; CANNABINOID RECEPTOR; DENDRITIC CELLS
AB The process of blastocyst implantation is a series of interactions between the blastocyst and maternal tissues. The purpose of this process is (1) to provide nourishment to the embryo for developmental growth in appropriate physiological and endocrinological environment until a placenta is established, and (2) to protect the (semi-)allogeneic embryo from any attacks from the maternal immune system. To facilitate successful implantation, therefore, these two aspects of the embryonic demand must be satisfied in the embryo-maternal interface throughout the entire process of implantation. The first concept I present in this paper is that blastocyst implantation essential factors (BIEFs) have dual functions: one, for structural and functional modification of the endometrium to accommodate the developing embryo and provide nourishment and suitable environment for its development, and the other, for modulation, directly or indirectly, of the maternal immune system to prevent attacks by the maternal immune system. The second concept is that BIEFs convert the endometrium (or uterus) from an immunologically non-privileged site to a privileged site. This endometrial (uterine) conversion is the immunological aspect of the blastocyst implantation process. When the endometrium has become receptive for blastocyst implantation, it signifies that the immunological conversion of the endometrium by BIEFs has been sufficiently attained to let the embryo start contacting maternal tissues. During the early stages of placentation, as the trophoblast cells differentiate and make their way to the maternal blood vessels to establish the placenta, BIEFs continuously provide nourishment and immunological protection to the developing embryo. The immunological protection or the embryo/fetus from potential attacks by the maternal immune system appears to reach a peak at the time of establishment of the placenta. Thus, clarification of the roles of BIEFs in both the physiological/endocrinological aspect as well as the immunological aspect is essential for understanding the biological process of implantation.
C1 NICHD, Reprod Sci Branch, NIH, DHHS, Bethesda, MD 20892 USA.
RP Yoshinaga, K (reprint author), NICHD, Reprod Sci Branch, NIH, DHHS, Bethesda, MD 20892 USA.
EM ky6a@nih.gov
NR 99
TC 9
Z9 10
U1 1
U2 7
PU SOCIETY REPRODUCTION & DEVELOPMENT-SRD
PI TSUKUBA
PA C/O KAZUHIRO KIKUCHI, PHD DVM, NATL INST AGROBIOLOGICAL SCIENCES
KANNONDAI 2-1-2, TSUKUBA, IBARAKI 305-8602, JAPAN
SN 0916-8818
J9 J REPROD DEVELOP
JI J. Reprod. Dev.
PD APR
PY 2012
VL 58
IS 2
BP 196
EP 203
PG 8
WC Agriculture, Dairy & Animal Science; Reproductive Biology
SC Agriculture; Reproductive Biology
GA 939BV
UT WOS:000303782800005
PM 22738903
ER
PT J
AU Aschebrook-Kilfoy, B
Ward, MH
Zheng, TZ
Holford, TR
Boyle, P
Leaderer, B
Zhang, YW
AF Aschebrook-Kilfoy, Briseis
Ward, Mary H.
Zheng, Tongzhang
Holford, Theodore R.
Boyle, Peter
Leaderer, Brian
Zhang, Yawei
TI Dietary Nitrate and Nitrite Intake and Non-Hodgkin Lymphoma Survival
SO NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL
LA English
DT Article
ID N-NITROSO COMPOUNDS; UNITED-STATES; CANCER; CLASSIFICATION; SUBTYPE
AB Nitrate and nitrite are precursors in the formation of N-nitroso compounds. We recently found a 40% increased risk of NHL with higher dietary nitrite intake and significant increases in risk for follicular and T-cell lymphoma. It is possible that these compounds also affect NHL prognosis by enhancing cancer progression in addition to development by further impairing immune system function. To test the hypothesis that nitrate and nitrite intake affects NHL survival, we evaluated the association in study participants that have been followed post-disease diagnosis in a population-based case-control study among women in Connecticut. We did not observe a significant increasing trend of mortality for NHL overall or by subtype for nitrate or nitrite intake for deaths from NHL or death from any cause, although a borderline significant protective trend was observed for follicular lymphoma with increasing nitrate intake. We did not identify a difference in overall survival for nitrate (P = 0.39) or for nitrite (P = 0.66) or for NHL specific survival for nitrate (P = 0.96) or nitrite (P = 0.17). Thus, our null findings do not confer support for the possibility that dietary nitrate and nitrite intake impacts NHL survival by promoting immune unresponsiveness.
C1 [Aschebrook-Kilfoy, Briseis] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
[Ward, Mary H.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD USA.
[Zheng, Tongzhang; Holford, Theodore R.; Leaderer, Brian; Zhang, Yawei] Yale Univ, Yale Sch Publ Hlth, New Haven, CT USA.
[Boyle, Peter] Int Prevent Res Inst, Lyon, France.
RP Aschebrook-Kilfoy, B (reprint author), Univ Chicago, Dept Hlth Studies, 5841 S Maryland Ave,N101B, Chicago, IL 60637 USA.
EM brisa@uchicago.edu
RI Boyle, Peter/A-4380-2014
OI Boyle, Peter/0000-0001-6251-0610
FU Yale Cancer Center [22067A]; National Cancer Institute (NCI) [CA62006];
NCI, National Institutes of Health (NIH); NIH [1D43TW008323-01,
1D43TW007864-01]; CTSA from the National Center for Research Resources
(NCRR), NIH [UL1 RR024139]; NHL roadmap for medical research
FX This research was supported by Hull Argall and Anna Grant 22067A from
the Yale Cancer Center, Grant CA62006 from the National Cancer Institute
(NCI), the Intramural Research Program of the NCI, National Institutes
of Health (NIH), and Fogarty Training Grant 1D43TW008323-01 and
1D43TW007864-01 from the NIH. This publication was made possible by CTSA
Grant UL1 RR024139 from the National Center for Research Resources
(NCRR), a component of the NIH, and NHL roadmap for medical research.
Its contents are solely the responsibility of the authors and do not
necessarily represent the official view of NCRR. This research was
approved by the DPH HIC. Certain data used in this study were obtained
from the Connecticut Department of Public Health. The authors assume
full responsibility for analyses and interpretation of these data.
NR 17
TC 3
Z9 3
U1 0
U2 1
PU LAWRENCE ERLBAUM ASSOC INC-TAYLOR & FRANCIS
PI PHILADELPHIA
PA 325 CHESTNUT STREET, STE 800, PHILADELPHIA, PA 19106 USA
SN 0163-5581
J9 NUTR CANCER
JI Nutr. Cancer
PD APR
PY 2012
VL 64
IS 3
BP 488
EP 492
DI 10.1080/01635581.2012.658136
PG 5
WC Oncology; Nutrition & Dietetics
SC Oncology; Nutrition & Dietetics
GA 937ZL
UT WOS:000303702600015
PM 22420290
ER
PT J
AU Kelly, RJ
Robey, RW
Chen, CC
Draper, D
Luchenko, V
Barnett, D
Oldham, RK
Caluag, Z
Frye, AR
Steinberg, SM
Fojo, T
Bates, SE
AF Kelly, Ronan J.
Robey, Robert W.
Chen, Clara C.
Draper, Deborah
Luchenko, Victoria
Barnett, Daryl
Oldham, Robert K.
Caluag, Zinnah
Frye, A. Robin
Steinberg, Seth M.
Fojo, Tito
Bates, Susan E.
TI A Pharmacodynamic Study of the P-glycoprotein Antagonist CBT-1 (R) in
Combination With Paclitaxel in Solid Tumors
SO ONCOLOGIST
LA English
DT Article
AB Background: This pharmacodynamic trial evaluated the effect of CBT-1 (R) on efflux by the ATP binding cassette (ABC) multidrug transporter P-glycoprotein (Pgp/MDR1/ABCB1) in normal human cells and tissues. CBT-1 (R) is an orally administered bisbenzylisoquinoline Pgp inhibitor being evaluated clinically. Laboratory studies showed potent and durable inhibition of Pgp, and in phase I studies CBT-1 (R) did not alter the pharmacokinetics of paclitaxel or doxorubicin.
Methods: CBT-1 (R) was dosed at 500 mg/m(2) for 7 days; a 3-hour infusion of paclitaxel at 135 mg/m2 was administered on day 6. Peripheral blood mononuclear cells (PBMCs) were obtained prior to CBT-1 (R) administration and on day 6 prior to the paclitaxel infusion. Tc-99m-sestamibi imaging was performed on the same schedule. The area under the concentration-time curve from 0-3 hours (AUC(0-3)) was determined for Tc-99m-sestamibi.
Results: Twelve patients were planned and enrolled. Toxicities were minimal and related to paclitaxel (grade 3 or 4 neutropenia in 18% of cycles). Rhodamine efflux from CD56(+) PBMCs was a statistically significant 51%-100% lower (p < .0001) with CBT-1 (R). Among 10 patients who completed imaging, the Tc-99m-sestamibi AUC(0-3) for liver (normalized to the AUC(0-3) of the heart) increased from 34.7% to 100.8% (median, 71.9%; p < .0001) after CBT-1 (R) administration. Lung uptake was not changed.
Conclusion: CBT-1 (R) is able to inhibit Pgp-mediated efflux from PBMCs and normal liver to a degree observed with Pgp inhibitors studied in earlier clinical trials. Combined with its ease of administration and lack of toxicity, the data showing inhibition of normal tissue Pgp support further studies with CBT-1 (R) to evaluate its ability to modulate drug uptake in tumor tissue.
Discussion: Although overexpression of ABCB1 and other ABC transporters has been linked with poor outcome following chemotherapy efforts to negate that through pharmacologic inhibition have generally failed. This is thought to be a result of several factors, including (a) failure to select patients with tumors in which ABCB1 is a dominant resistance mechanism; (b) inhibitors that were not potent, or that impaired drug clearance; and (c) the existence of other mechanisms of drug resistance, including other ABC transporters. Although an animal model for Pgp has been lacking, recent studies have exploited a Brca1(-/-); p53(-/-) mouse model of hereditary breast cancer that develops sporadic tumors similar to cancers in women harboring BRCA1 mutations. Treatment with doxorubicin, docetaxel, or the poly(ADP-ribose) polymerase inhibitor olaparib brings about shrinkage, but resistance eventually emerges. Overexpression of the Abcb1a gene, the mouse ortholog of human ABCB1, has been shown to be a mechanism of resistance in a subset of these tumors. Treating mice with resistant tumors with olaparib plus the Pgp inhibitor tariquidar resensitized the tumors to olaparib. Although results in this animal model support a new look at Pgp as a target, in this era of "targeted therapies," trial designs that directly assess modulation of drug uptake, including quantitative nuclear imaging, should be pursued before clinical efficacy assessments are undertaken. Such assessment should be performed with compounds that inhibit tissue Pgp without altering the pharmacokinetics of chemotherapeutic agents. This pharmacodynamic study demonstrated that CBT-1 (R),inhibits Pgp-mediated efflux from PBMCs and normal liver.
C1 [Kelly, Ronan J.; Robey, Robert W.; Draper, Deborah; Luchenko, Victoria; Frye, A. Robin; Fojo, Tito; Bates, Susan E.] NIH, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NIH, Biostat & Data Management Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Chen, Clara C.] NIH, Dept Nucl Med, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Chen, Clara C.] NIH, Dept Radiol, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Barnett, Daryl; Oldham, Robert K.; Caluag, Zinnah] CBA Res, Lexington, KY USA.
RP Bates, SE (reprint author), 9000 Rockville Pike,Bldg 10,Room 12N226, Bethesda, MD 20892 USA.
EM sebates@helix.nih.gov
NR 0
TC 19
Z9 20
U1 0
U2 3
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 1083-7159
J9 ONCOLOGIST
JI Oncologist
PD APR
PY 2012
VL 17
IS 4
BP 512
EP 512
DI 10.1634/theoncologist.2012-0080
PG 1
WC Oncology
SC Oncology
GA 940FA
UT WOS:000303874200009
PM 22416063
ER
PT J
AU Giorgobiani, E
Lawyer, PG
Babuadze, G
Dolidze, N
Jochim, RC
Tskhvaradze, L
Kikaleishvili, K
Kamhawi, S
AF Giorgobiani, Ekaterina
Lawyer, Phillip G.
Babuadze, Giorgi
Dolidze, Nato
Jochim, Ryan C.
Tskhvaradze, Lamzira
Kikaleishvili, Konstantin
Kamhawi, Shaden
TI Incrimination of Phlebotomus kandelakii and Phlebotomus balcanicus as
Vectors of Leishmania infantum in Tbilisi, Georgia
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID VISCERAL LEISHMANIASIS; SEQUENCE ALIGNMENT; TRANSMISSION; PSYCHODIDAE;
DIPTERA; FOCUS
AB A survey of potential vector sand flies was conducted in the neighboring suburban communities of Vake and Mtatsminda districts in an active focus of visceral Leishmaniasis (VL) in Tbilisi, Georgia. Using light and sticky-paper traps, 1,266 male and 1,179 female sand flies were collected during 2006-2008. Five Phlebotomus species of three subgenera were collected: Phlebotomus balcanicus Theodor and Phlebotomus halepensis Theodor of the subgenus Adlerius; Phlebotomus kandelakii Shchurenkova and Phlebotomus wenyoni Adler and Theodor of the subgenus Larroussius; Phlebotomus sergenti Perfil'ev of the subgenus Paraphlebotomus. Phlebotomus sergenti (35.1%) predominated in Vake, followed by P. kandelakii (33.5%), P. balcanicus (18.9%), P. halepensis (12.2%), and P. wenyoni (0.3%). In Mtatsminda, P. kandelakii (76.8%) comprised over three fourths of collected sand flies, followed by P. sergenti (12.6%), P. balcanicus (5.8%), P. halepensis (3.7%), and P. wenyoni (1.1%). The sand fly season in Georgia is exceptionally short beginning in early June, peaking in July and August, then declining to zero in early September. Of 659 female sand flies examined for Leishmania, 12 (1.8%) specimens without traces of blood were infected including 10 of 535 P. kandelakii (1.9%) and two of 40 P. balcanicus (5.0%). Six isolates were successfully cultured and characterized as Leishmania by PCR. Three isolates from P. kandelakii (2) and P. balcanicus (1) were further identified as L. infantum using sequence alignment of the 70 kDa heat-shock protein gene. Importantly, the sand fly isolates showed a high percent identity (99.8%-99.9%) to human and dog isolates from the same focus, incriminating the two sand fly species as vectors. Blood meal analysis showed that P. kandelakii preferentially feeds on dogs (76%) but also feeds on humans. The abundance, infection rate and feeding behavior of P. kandelakii and the infection rate in P. balcanicus establish these species as vectors in the Tbilisi VL focus.
C1 [Giorgobiani, Ekaterina; Babuadze, Giorgi; Dolidze, Nato; Tskhvaradze, Lamzira; Kikaleishvili, Konstantin] Natl Ctr Dis Control & Publ Hlth, Tbilisi, Rep of Georgia.
[Lawyer, Phillip G.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Jochim, Ryan C.; Kamhawi, Shaden] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
RP Giorgobiani, E (reprint author), Natl Ctr Dis Control & Publ Hlth, Tbilisi, Rep of Georgia.
EM egiorgobiani@yahoo.com; skamhawi@niaid.nih.gov
RI Jochim, Ryan/C-6756-2013
FU United States Department of Health and Human Services through the
International Science and Technology Center [ISTC G-1081/BTEP N89];
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases
FX This study was supported by the United States Department of Health and
Human Services Biotechnology Engagement Program through the
International Science and Technology Center (grant ISTC G-1081/BTEP N89)
and by the Division of Intramural Research, 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 29
TC 12
Z9 12
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 APR
PY 2012
VL 6
IS 4
AR e1609
DI 10.1371/journal.pntd.0001609
PG 10
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 935CP
UT WOS:000303496800025
PM 22509422
ER
PT J
AU Gomes, R
Teixeira, C
Oliveira, F
Lawyer, PG
Elnaiem, DE
Meneses, C
Goto, Y
Bhatia, A
Howard, RF
Reed, SG
Valenzuela, JG
Kamhawi, S
AF Gomes, Regis
Teixeira, Clarissa
Oliveira, Fabiano
Lawyer, Phillip G.
Elnaiem, Dia-Eldin
Meneses, Claudio
Goto, Yasuyuki
Bhatia, Ajay
Howard, Randall F.
Reed, Steven G.
Valenzuela, Jesus G.
Kamhawi, Shaden
TI KSAC, a Defined Leishmania Antigen, plus Adjuvant Protects against the
Virulence of L. major Transmitted by Its Natural Vector Phlebotomus
duboscqi
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID CANINE VISCERAL LEISHMANIASIS; CUTANEOUS LEISHMANIASIS; LEISH-F1+MPL-SE
VACCINE; POLYPROTEIN VACCINE; CLINICAL-TRIAL; SAND FLIES; T-CELLS;
MEGLUMINE ANTIMONIATE; IMMUNOGENICITY; EVALUATE
AB Background: Recombinant KSAC and L110f are promising Leishmania vaccine candidates. Both antigens formulated in stable emulsions (SE) with the natural TLR4 agonist MPL (R) and L110f with the synthetic TLR4 agonist GLA in SE protected BALB/c mice against L. major infection following needle challenge. Considering the virulence of vector-transmitted Leishmania infections, we vaccinated BALB/c mice with either KSAC+GLA-SE or L110f+GLA-SE to assess protection against L. major transmitted via its vector Phlebotomus duboscqi.
Methods: Mice receiving the KSAC or L110f vaccines were challenged by needle or L. major-infected sand flies. Weekly disease progression and terminal parasite loads were determined. Immunological responses to KSAC, L110f, or soluble Leishmania antigen (SLA) were assessed throughout vaccination, three and twelve weeks after immunization, and one week post-challenge.
Results: Following sand fly challenge, KSAC-vaccinated mice were protected while L110f-vaccinated animals showed partial protection. Protection correlated with the ability of SLA to induce IFN-gamma-producing CD4(+)CD62L(low)CCR7(low) effector memory T cells pre- and post-sand fly challenge.
Conclusions: This study demonstrates the protective efficacy of KSAC+GLA-SE against sand fly challenge; the importance of vector-transmitted challenge in evaluating vaccine candidates against Leishmania infection; and the necessity of a rapid potent Th1 response against Leishmania to attain true protection.
C1 [Gomes, Regis; Teixeira, Clarissa; Oliveira, Fabiano; Meneses, Claudio; Valenzuela, Jesus G.; Kamhawi, Shaden] NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Lawyer, Phillip G.] NIAID, Parasit Dis Lab, NIH, Rockville, MD USA.
[Elnaiem, Dia-Eldin] Eastern Shore Univ, Dept Zool, Eastern Shore Maryland, MD USA.
[Goto, Yasuyuki; Bhatia, Ajay; Howard, Randall F.; Reed, Steven G.] Infect Dis Res Inst, Seattle, WA USA.
RP Gomes, R (reprint author), NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
EM jvalenzuela@niaid.nih.gov; skamhawi@niaid.nih.gov
RI Goto, Yasuyuki/E-9028-2011; Oliveira, Fabiano/B-4251-2009
OI Goto, Yasuyuki/0000-0002-8654-7888; Oliveira,
Fabiano/0000-0002-7924-8038
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases (NIAID); NIAID [AI-25038]
FX The study was funded by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases (NIAID) and supported in
part by a grant from NIAID to SGR (AI-25038). The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 34
TC 14
Z9 14
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD APR
PY 2012
VL 6
IS 4
AR e1610
DI 10.1371/journal.pntd.0001610
PG 9
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 935CP
UT WOS:000303496800026
PM 22509423
ER
PT J
AU Sehba, FA
Hou, J
Pluta, RM
Zhang, JH
AF Sehba, Fatima A.
Hou, Jack
Pluta, Ryszard M.
Zhang, John H.
TI The importance of early brain injury after subarachnoid hemorrhage
SO PROGRESS IN NEUROBIOLOGY
LA English
DT Review
DE Subarachnoid hemorrhage; Vasospasm; Early brain injury; Animal models;
Therapy failure
ID CEREBRAL-BLOOD-FLOW; NITRIC-OXIDE SYNTHASE; INTERCELLULAR-ADHESION
MOLECULE-1; ISCHEMIC NEUROLOGICAL DEFICITS; BARRIER PERMEABILITY
CHANGES; SUB-ARACHNOID HEMORRHAGE; NEURON-SPECIFIC ENOLASE; CANINE
BASILAR ARTERY; C-REACTIVE PROTEIN; ENDOTHELIUM-DEPENDENT RELAXATION
AB Aneurysmal subarachnoid hemorrhage (aSAH) is a medical emergency that accounts for 5% of all stroke cases. Individuals affected are typically in the prime of their lives (mean age 50 years). Approximately 12% of patients die before receiving medical attention, 33% within 48 h and 50% within 30 days of aSAH. Of the survivors 50% suffer from permanent disability with an estimated lifetime cost more than double that of an ischemic stroke. Traditionally, spasm that develops in large cerebral arteries 3-7 days after aneurysm rupture is considered the most important determinant of brain injury and outcome after aSAH. However, recent studies show that prevention of delayed vasospasm does not improve outcome in aSAH patients. This finding has finally brought in focus the influence of early brain injury on outcome of aSAH. A substantial amount of evidence indicates that brain injury begins at the aneurysm rupture, evolves with time and plays an important role in patients' outcome. In this manuscript we review early brain injury after aSAH. Due to the early nature, most of the information on this injury comes from animals and few only from autopsy of patients who died within days after aSAH. Consequently, we began with a review of animal models of early brain injury, next we review the mechanisms of brain injury according to the sequence of their temporal appearance and finally we discuss the failure of clinical translation of therapies successful in animal models of aSAH. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Sehba, Fatima A.] Mt Sinai Sch Med, Dept Neurosurg, New York, NY 10029 USA.
[Sehba, Fatima A.] Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA.
[Pluta, Ryszard M.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Hou, Jack; Zhang, John H.] Loma Linda Univ, Med Ctr, Dept Neurosurg, Loma Linda, CA USA.
RP Sehba, FA (reprint author), Mt Sinai Sch Med, Dept Neurosurg, New York, NY 10029 USA.
EM fatima.sehba@mssm.edu
OI Zhang, John H./0000-0002-4319-4285
FU American Heart Organization [10GRNT4570012]; National Institutes of
Health National Center for Research Resources [RO1 NS050576, NS053407];
National Institute of Neurological Disorders and Stroke
FX This work was supported by American Heart Organization Grant
[10GRNT4570012 (FAS)] and the National Institutes of Health National
Center for Research Resources [RO1 NS050576 (FAS); NS053407 (JHZ)]; and
by the Intramural Research Program (RMP) of the National Institute of
Neurological Disorders and Stroke.
NR 519
TC 130
Z9 144
U1 4
U2 34
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0301-0082
J9 PROG NEUROBIOL
JI Prog. Neurobiol.
PD APR
PY 2012
VL 97
IS 1
BP 14
EP 37
DI 10.1016/j.pneurobio.2012.02.003
PG 24
WC Neurosciences
SC Neurosciences & Neurology
GA 939UY
UT WOS:000303845600002
PM 22414893
ER
PT J
AU Akhter, I
Simon, T
Khan, S
Matthews, I
Sheikh, Y
AF Akhter, Ijaz
Simon, Tomas
Khan, Sohaib
Matthews, Iain
Sheikh, Yaser
TI Bilinear Spatiotemporal Basis Models
SO ACM TRANSACTIONS ON GRAPHICS
LA English
DT Article
DE Algorithms; Theory; Measurement; Bilinear models; spatiotemporal; motion
data; motion capture
ID ACTIVE SHAPE MODELS; HUMAN MOTION; CARDIAC MR; ANIMATION; CAPTURE;
TRACKING; SPACES; STYLE
AB A variety of dynamic objects, such as faces, bodies, and cloth, are represented in computer graphics as a collection of moving spatial landmarks. Spatiotemporal data is inherent in a number of graphics applications including animation, simulation, and object and camera tracking. The principal modes of variation in the spatial geometry of objects are typically modeled using dimensionality reduction techniques, while concurrently, trajectory representations like splines and autoregressive models are widely used to exploit the temporal regularity of deformation. In this article, we present the bilinear spatiotemporal basis as a model that simultaneously exploits spatial and temporal regularity while maintaining the ability to generalize well to new sequences. This factorization allows the use of analytical, predefined functions to represent temporal variation (e.g., B-Splines or the Discrete Cosine Transform) resulting in efficient model representation and estimation. The model can be interpreted as representing the data as a linear combination of spatiotemporal sequences consisting of shape modes oscillating over time at key frequencies. We apply the bilinear model to natural spatiotemporal phenomena, including face, body, and cloth motion data, and compare it in terms of compaction, generalization ability, predictive precision, and efficiency to existing models. We demonstrate the application of the model to a number of graphics tasks including labeling, gap-filling, denoising, and motion touch-up.
C1 [Akhter, Ijaz] Disney Res Pittsburgh, LUMS Sch Sci & Engn, Pittsburgh, PA USA.
[Simon, Tomas; Matthews, Iain] Carnegie Mellon Univ, Disney Res Pittsburgh, Pittsburgh, PA 15213 USA.
[Khan, Sohaib] Lahore Univ Management Sci, LUMS Sch Sci & Engn, Lahore, Pakistan.
[Sheikh, Yaser] Carnegie Mellon Univ, Dept Comp Sci, Pittsburgh, PA 15213 USA.
RP Akhter, I (reprint author), Disney Res Pittsburgh, LUMS Sch Sci & Engn, Pittsburgh, PA USA.
EM akhter@lums.edu.pk; tsimon@cmu.edu; sohaib@lums.edu.pk;
iainm@disneyresearch.com; yaser@cs.cmu.edu
NR 58
TC 7
Z9 7
U1 1
U2 5
PU ASSOC COMPUTING MACHINERY
PI NEW YORK
PA 2 PENN PLAZA, STE 701, NEW YORK, NY 10121-0701 USA
SN 0730-0301
J9 ACM T GRAPHIC
JI ACM Trans. Graph.
PD APR
PY 2012
VL 31
IS 2
AR 17
DI 10.1145/2159516.2159523
PG 12
WC Computer Science, Software Engineering
SC Computer Science
GA 934IJ
UT WOS:000303437400006
ER
PT J
AU Ramaswamy, B
Fiskus, W
Cohen, B
Pellegrino, C
Hershman, DL
Chuang, E
Luu, T
Somlo, G
Goetz, M
Swaby, R
Shapiro, CL
Stearns, V
Christos, P
Espinoza-Delgado, I
Bhalla, K
Sparano, JA
AF Ramaswamy, B.
Fiskus, W.
Cohen, B.
Pellegrino, C.
Hershman, D. L.
Chuang, E.
Luu, Thehang
Somlo, G.
Goetz, M.
Swaby, R.
Shapiro, C. L.
Stearns, V.
Christos, P.
Espinoza-Delgado, I.
Bhalla, K.
Sparano, J. A.
TI Phase I-II study of vorinostat plus paclitaxel and bevacizumab in
metastatic breast cancer: evidence for vorinostat-induced tubulin
acetylation and Hsp90 inhibition in vivo
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article; Proceedings Paper
CT 100th Annual Meeting of the American-Association-for-Cancer-Research
(AACR)
CY APR 18-22, 2009
CL Denver, CO
SP Amer Assoc Canc Res (AACR)
DE Metastatic breast cancer; Paclitaxel; Bevacizumab; Vorinostat; HDAC
inhibitors
ID SUBEROYLANILIDE HYDROXAMIC ACID; HISTONE DEACETYLASE INHIBITORS; CELLS;
TRIAL; HEAT-SHOCK-PROTEIN-90; HER-2
AB In preclinical models, the histone deacetylase inhibitor vorinostat sensitizes breast cancer cells to tubulin-polymerizing agents and to anti-vascular endothelial growth factor-directed therapies. We sought to determine the safety and efficacy of vorinostat plus paclitaxel and bevacizumab as first-line therapy in metastatic breast cancer (MBC), and the biological effects of vorinostat in vivo. For this purpose of this study, 54 patients with measurable disease and no prior chemotherapy for MBC received vorinostat (200 or 300 mg PO BID) on days 1-3, 8-10, and 15-17, plus paclitaxel (90 mg/m(2)) on days 2, 9, 16, and bevacizumab (10 mg/kg) on days 2 and 16 every 28 days. The primary objective of the phase I study was to determine the recommended phase II dose (RPTD) of vorinostat, and for the phase II to detect an improvement of response rate from 40 to 60% (alpha = 0.10, beta = 0.10). No dose limiting toxicities were observed, and the RPTD of vorinostat was 300 mg BID. For the primary efficacy analysis in 44 patients at the RPTD, we observed 24 objective responses (55%, 95% confidence intervals (C.I) 39%, 70%). The adverse event profile was consistent with paclitaxel-bevacizumab, with the exception of increased diarrhea with the addition of vorinostat. Analysis of serial tumor biopsies in seven patients showed increased acetylation of Hsp90 and alpha-tubulin following vorinostat. Vorinostat induces histone and alpha tubulin acetylation and functional inhibition of Hsp90 in breast cancer in vivo and can be safely combined with paclitaxel and bevacizumab.
C1 [Ramaswamy, B.; Shapiro, C. L.] Ohio State Univ, Columbus, OH 43210 USA.
[Fiskus, W.; Bhalla, K.] Univ Kansas, Ctr Canc, Kansas City, KS USA.
[Cohen, B.; Pellegrino, C.; Sparano, J. A.] Montefiore Med Ctr, Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Hershman, D. L.] New York Presbyterian Hosp, New York, NY USA.
[Chuang, E.; Christos, P.] Weill Cornell Med Coll, New York, NY USA.
[Luu, Thehang; Somlo, G.] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Goetz, M.] Mayo Clin, Rochester, MN USA.
[Swaby, R.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Stearns, V.] Johns Hopkins, Sidney Kimmel Canc Ctr, Baltimore, MD USA.
[Espinoza-Delgado, I.] NCI, Bethesda, MD 20892 USA.
RP Ramaswamy, B (reprint author), Ohio State Univ, Columbus, OH 43210 USA.
EM Bhuvaneswari.ramaswamy@osumc.edu
RI Ramaswamy, Bhuvaneswari/E-3919-2011
FU NCI NIH HHS [N01-CM-62207, N01CM62204, N01-CM-62204, N01 CM62205,
N01CM62207, N01 CM062205]
NR 26
TC 27
Z9 30
U1 1
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD APR
PY 2012
VL 132
IS 3
SI SI
BP 1063
EP 1072
DI 10.1007/s10549-011-1928-x
PG 10
WC Oncology
SC Oncology
GA 933RL
UT WOS:000303379800028
PM 22200869
ER
PT J
AU Patterson, E
Webb, R
Weisbrod, A
Bian, B
He, M
Zhang, L
Holloway, AK
Krishna, R
Nilubol, N
Pacak, K
Kebebew, E
AF Patterson, E.
Webb, R.
Weisbrod, A.
Bian, B.
He, M.
Zhang, L.
Holloway, A. K.
Krishna, R.
Nilubol, N.
Pacak, K.
Kebebew, E.
TI The microRNA expression changes associated with malignancy and SDHB
mutation in pheochromocytoma
SO ENDOCRINE-RELATED CANCER
LA English
DT Article
ID GERMLINE MUTATIONS; GENE-MUTATIONS; PARAGANGLIOMAS; CANCER; HEREDITARY;
TARGETS; BENIGN
AB Currently, the diagnosis of malignant pheochromocytoma can only be made when there is clinical evidence of metastasis or extensive local invasion. Thus, there is a need for new diagnostic marker(s) to identify tumors with malignant potential. The purpose of this study was to identify microRNAs (miRNAs) that are differentially expressed between benign and malignant pheochromocytomas and assess their diagnostic accuracy. Toward this aim, we analyzed miRNA expression in benign and malignant pheochromocytoma tumor samples using whole genome microarray profiling. Microarray analysis identified eight miRNAs that were significantly differentially expressed between benign and malignant pheochromocytomas. We measured a subset of these miRNAs directly by RT-PCR and found that miR-483-5p, miR-183, and miR-101 had significantly higher expression in malignant tumors as compared to their benign counterparts. Area under the receiver operating curve (AUC) analysis indicated that miR-483-5p, miR-101, and miR-183 could be useful diagnostic markers for distinguishing malignant from benign pheochromocytomas. In addition, these miRNAs could be detected in pheochromocytoma patient serum. Overall our data suggest that misexpression of miR-483-5p, miR-101, and miR-183 is associated with malignant pheochromocytoma. Endocrine-Related Cancer (2012) 19 157-166
C1 [Patterson, E.; Webb, R.; Weisbrod, A.; Bian, B.; He, M.; Zhang, L.; Krishna, R.; Nilubol, N.; Kebebew, E.] NCI, Endocrine Oncol Sect, Surg Branch, NIH,Hatfield Clin Res Ctr, Bethesda, MD 20892 USA.
[Holloway, A. K.] Univ Calif San Francisco, Gladstone Inst, San Francisco, CA 94158 USA.
[Pacak, K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP Kebebew, E (reprint author), NCI, Endocrine Oncol Sect, Surg Branch, NIH,Hatfield Clin Res Ctr, Room 4-5952,10 Ctr Dr, Bethesda, MD 20892 USA.
EM kebebewe@mail.nih.gov
RI Holloway, Alisha/H-9574-2013
OI Holloway, Alisha/0000-0001-9810-389X
FU NIH, National Cancer Institute, Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 23
TC 22
Z9 24
U1 1
U2 3
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 1351-0088
J9 ENDOCR-RELAT CANCER
JI Endocr.-Relat. Cancer
PD APR
PY 2012
VL 19
IS 2
BP 157
EP 166
DI 10.1530/ERC-11-0308
PG 10
WC Oncology; Endocrinology & Metabolism
SC Oncology; Endocrinology & Metabolism
GA 935SE
UT WOS:000303539700008
PM 22241719
ER
PT J
AU Valent, P
Gleich, GJ
Reiter, A
Roufosse, F
Weller, PF
Hellmann, A
Metzgeroth, G
Leiferman, KM
Arock, M
Sotlar, K
Butterfield, JH
Cerny-Reiterer, S
Mayerhofer, M
Vandenberghe, P
Haferlach, T
Bochner, BS
Gotlib, J
Horny, HP
Simon, HU
Klion, AD
AF Valent, Peter
Gleich, Gerald J.
Reiter, Andreas
Roufosse, Florence
Weller, Peter F.
Hellmann, Andrzej
Metzgeroth, Georgia
Leiferman, Kristin M.
Arock, Michel
Sotlar, Karl
Butterfield, Joseph H.
Cerny-Reiterer, Sabine
Mayerhofer, Matthias
Vandenberghe, Peter
Haferlach, Torsten
Bochner, Bruce S.
Gotlib, Jason
Horny, Hans-Peter
Simon, Hans-Uwe
Klion, Amy D.
TI Pathogenesis and classification of eosinophil disorders: a review of
recent developments in the field
SO EXPERT REVIEW OF HEMATOLOGY
LA English
DT Review
DE classification; eosinophilic leukemia; FIP1L1-PDGFRA; hypereosinophilia;
hypereosinophilic syndromes; targeted therapy
ID IDIOPATHIC HYPEREOSINOPHILIC SYNDROME; HUMAN PERIPHERAL-BLOOD; VASCULAR
ENDOTHELIAL-CELLS; GROWTH-FACTOR RECEPTOR; CHURG-STRAUSS-SYNDROME;
CHRONIC MYELOPROLIFERATIVE DISEASES; RECOMBINANT HUMAN INTERLEUKIN-5;
COLONY-STIMULATING FACTOR; MAJOR BASIC-PROTEIN; IN-VITRO
AB Eosinophils and their products play an essential role in the pathogenesis of various reactive and neoplastic disorders. Depending on the underlying disease, molecular defect and involved cytokines, hypereosinophilia may develop and may lead to organ damage. In other patients, persistent eosinophilia is accompanied by typical clinical findings, but the causative role and impact of eosinophilia remain uncertain. For patients with eosinophil-mediated organ pathology, early therapeutic intervention with agents reducing eosinophil counts can be effective in limiting or preventing irreversible organ damage. Therefore, it is important to approach eosinophil disorders and related syndromes early by using established criteria, to perform all appropriate staging investigations, and to search for molecular targets of therapy. In this article, we review current concepts in the pathogenesis and evolution of eosinophilia and eosinophil-related organ damage in neoplastic and non-neoplastic conditions. In addition, we discuss classifications of eosinophil disorders and related syndromes as well as diagnostic algorithms and standard treatment for various eosinophil-related disorders.
C1 [Valent, Peter; Cerny-Reiterer, Sabine] Med Univ Vienna, Dept Med 1, Div Hematol & Hemostaseol, Vienna, Austria.
[Valent, Peter; Cerny-Reiterer, Sabine] Ludwig Boltzmann Cluster Oncol, Vienna, Austria.
[Gleich, Gerald J.; Leiferman, Kristin M.] Univ Utah, Dept Dermatol, Salt Lake City, UT USA.
[Reiter, Andreas; Metzgeroth, Georgia] Univ Med Mannheim, Med Univ Klin, Mannheim, Germany.
[Roufosse, Florence] Univ Libre Brussels, Dept Internal Med, Erasme Hosp, Brussels, Belgium.
[Weller, Peter F.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Boston, MA 02215 USA.
[Hellmann, Andrzej] Med Univ Gdansk, Dept Hematol, Gdansk, Poland.
[Arock, Michel] Ecole Normale Super, LBPA, CNRS, UMR8113, Cachan, France.
[Sotlar, Karl; Horny, Hans-Peter] Univ Munich, Inst Pathol, D-8000 Munich, Germany.
[Butterfield, Joseph H.] Mayo Clin Rochester, Div Allerg Dis, Rochester, MN USA.
[Mayerhofer, Matthias] Med Univ Vienna, Dept Lab Med, Vienna, Austria.
[Vandenberghe, Peter] Katholieke Univ Leuven, Ctr Human Genet, Louvain, Belgium.
[Vandenberghe, Peter] Univ Hosp Leuven, Louvain, Belgium.
[Haferlach, Torsten] MLL Munchner Leukamielab, Munich, Germany.
[Bochner, Bruce S.] Johns Hopkins Univ, Sch Med, Dept Med, Div Allergy & Clin Immunol, Baltimore, MD 21205 USA.
[Gotlib, Jason] Stanford Univ, Sch Med, Stanford Canc Ctr, Stanford, CA 94305 USA.
[Simon, Hans-Uwe] Univ Bern, Inst Pharmacol, CH-3012 Bern, Switzerland.
[Klion, Amy D.] NIAID, Eosinophil Pathol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Valent, P (reprint author), Med Univ Vienna, Dept Med 1, Div Hematol & Hemostaseol, Vienna, Austria.
EM peter.valent@meduniwien.ac.at
OI Vandenberghe, Peter/0000-0003-4719-1935; Simon,
Hans-Uwe/0000-0002-9404-7736; Klion, Amy/0000-0002-4986-5326
FU Novartis; BMS; NIAID, NIH; GSK; Medical University of Vienna; Division
of Intramural Research, NIAID, NIH, Bethesda, MD, USA
FX P Valent has received a Research Grant from Novartis and a Research
Grant from BMS, as well as honoraria from Novartis and BMS. AD Klein is
supported by the Intramural Program of the NIAID, NIH. KM Leiferman, HU
Simon and GJ Gleich have been supported by grants from GSK. M Arock
received honorarium from Novartis. P Vandenberghe is a Senior Clinical
Investigator of FWO-Vlaanderen. T Haferlach is part owner of the Munich
Leukemia Laboratory. A Reiter received Honoraria from Novartis and BMS.
BS Bochner is a co-author on existing and pending Siglec-8-related
patents. If Siglec-8-related products are developed in the future, BS
Bochner may be entitled to a share of royalties received by Johns
Hopkins University on the potential sales of such products. The terms of
this arrangement are being managed by Johns Hopkins University in
accordance with its conflict of interest policies. This study was
supported by a research grant of the Medical University of Vienna and by
the Division of Intramural Research, NIAID, NIH, Bethesda, MD, USA. 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 182
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U1 0
U2 7
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1747-4086
J9 EXPERT REV HEMATOL
JI Expert Rev. Hematol.
PD APR
PY 2012
VL 5
IS 2
BP 157
EP 176
DI 10.1586/EHM.11.81
PG 20
WC Hematology
SC Hematology
GA 936ZS
UT WOS:000303629400013
PM 22475285
ER
PT J
AU Sincan, M
Simeonov, DR
Adams, D
Markello, TC
Pierson, TM
Toro, C
Gahl, WA
Boerkoel, CF
AF Sincan, Murat
Simeonov, Dimitre R.
Adams, David
Markello, Thomas C.
Pierson, Tyler M.
Toro, Camilo
Gahl, William A.
Boerkoel, Cornelius F.
CA NIH Undiagnosed Dis Program
TI VAR-MD: A tool to analyze whole exome-genome variants in small human
pedigrees with mendelian inheritance
SO HUMAN MUTATION
LA English
DT Article
DE exome; next generation sequencing; variant filtering; Mendelian
ID MUTATIONS; FORM; DISEASES; GENE
AB The analysis of variants generated by exome sequencing (ES) of families with rare Mendelian diseases is a time-consuming, manual process that represents one barrier to applying the technology routinely. To address this issue, we have developed a software tool, VAR-MD (), for analyzing the DNA sequence variants produced by human ES. VAR-MD generates a ranked list of variants using predicted pathogenicity, Mendelian inheritance models, genotype quality, and population variant frequency data. VAR-MD was tested using two previously solved data sets and one unsolved data set. In the solved cases, the correct variant was listed at the top of VAR-MD's variant ranking. In the unsolved case, the correct variant was highly ranked, allowing for subsequent identification and validation. We conclude that VAR-MD has the potential to enhance mutation identification using family based, annotated next generation sequencing data. Moreover, we predict an incremental advancement in software performance as the reference databases, such as Single Nucleotide Polymorphism Database and Human Gene Mutation Database, continue to improve. Hum Mutat 33:593598, 2012. (c) 2012 Wiley Periodicals, Inc.* This article is a US Government work and, as such, is in the public domain of the United States of America.
C1 [Sincan, Murat; Adams, David; Pierson, Tyler M.; Gahl, William A.] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Markello, Thomas C.; Gahl, William A.] NHGRI, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Simeonov, Dimitre R.; Adams, David; Markello, Thomas C.; Toro, Camilo; Gahl, William A.; Boerkoel, Cornelius F.] NIH, Undiagnosed Dis Program, Bethesda, MD 20892 USA.
[Pierson, Tyler M.] Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA.
[Pierson, Tyler M.] NINDS, Neurogenet Branch, Bethesda, MD 20892 USA.
RP Sincan, M (reprint author), NHGRI, Med Genet Branch, NIH, 10 Ctr Dr,MSC 1851,Bldg 10,Room 3C-716, Bethesda, MD 20892 USA.
EM sincanm@mail.nih.gov
FU Office of Rare Diseases Research; NIH Clinical Center; National Human
Genome Research Institute; National Institute of Neurological Disorders
and Stroke
FX Contract grant sponsors: Office of Rare Diseases Research (Dr. Stephen
Groft); the NIH Clinical Center ( Dr. John Gallin); and the Intramural
Research Programs of the National Human Genome Research Institute and
the National Institute of Neurological Disorders and Stroke.
NR 32
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U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PD APR
PY 2012
VL 33
IS 4
BP 593
EP 598
DI 10.1002/humu.22034
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 906IP
UT WOS:000301338900004
PM 22290570
ER
PT J
AU Adams, DR
Sincan, M
Fajardo, KF
Mullikin, JC
Pierson, TM
Toro, C
Boerkoel, CF
Tifft, CJ
Gahl, WA
Markello, TC
AF Adams, David R.
Sincan, Murat
Fajardo, Karin Fuentes
Mullikin, James C.
Pierson, Tyler M.
Toro, Camilo
Boerkoel, Cornelius F.
Tifft, Cynthia J.
Gahl, William A.
Markello, Tom C.
CA NIH Undiagnosed Dis Program
TI Analysis of DNA sequence variants detected by high-throughput sequencing
SO HUMAN MUTATION
LA English
DT Article
DE genomics; next generation sequencing; exome; molecular diagnosis
ID AMINO-ACID SUBSTITUTIONS; SPLICE-SITE PREDICTION; UNDIAGNOSED DISEASES;
PROTEIN FAMILIES; GENOME ANALYSIS; MESSENGER-RNA; HEARING-LOSS;
MUTATIONS; DATABASE; GENE
AB The Undiagnosed Diseases Program at the National Institutes of Health uses high-throughput sequencing (HTS) to diagnose rare and novel diseases. HTS techniques generate large numbers of DNA sequence variants, which must be analyzed and filtered to find candidates for disease causation. Despite the publication of an increasing number of successful exome-based projects, there has been little formal discussion of the analytic steps applied to HTS variant lists. We present the results of our experience with over 30 families for whom HTS sequencing was used in an attempt to find clinical diagnoses. For each family, exome sequence was augmented with high-density SNP-array data. We present a discussion of the theory and practical application of each analytic step and provide example data to illustrate our approach. The article is designed to provide an analytic roadmap for variant analysis, thereby enabling a wide range of researchers and clinical genetics practitioners to perform direct analysis of HTS data for their patients and projects. Hum Mutat 33:599608, 2012. (c) 2012 Wiley Periodicals, Inc.
C1 [Adams, David R.; Sincan, Murat; Gahl, William A.] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Adams, David R.; Fajardo, Karin Fuentes; Pierson, Tyler M.; Toro, Camilo; Boerkoel, Cornelius F.; Tifft, Cynthia J.; Gahl, William A.] NIH, Undiagnosed Dis Program, Bethesda, MD 20892 USA.
[Tifft, Cynthia J.; Gahl, William A.; Markello, Tom C.] NHGRI, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Pierson, Tyler M.] NINDS, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
[Mullikin, James C.] NHGRI, Intramural Sequencing Ctr, NIH, Bethesda, MD 20892 USA.
RP Adams, DR (reprint author), NHGRI, Med Genet Branch, NIH, 10 Ctr Dr,MSC 1851,10-10C-103, Bethesda, MD 20892 USA.
EM david.adams@nih.gov
FU Intramural division of the National Human Genome Research Institute;
National Institute of Neurological Disorders and Stroke; NIH Clinical
Center; NIH Office of the Director
FX Contract grant sponsors: Intramural division of the National Human
Genome Research Institute; the National Institute of Neurological
Disorders and Stroke; the NIH Clinical Center; and the NIH Office of the
Director.
NR 70
TC 21
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U1 1
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PD APR
PY 2012
VL 33
IS 4
BP 599
EP 608
DI 10.1002/humu.22035
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 906IP
UT WOS:000301338900005
PM 22290882
ER
PT J
AU Fajardo, KVF
Adams, D
Mason, CE
Sincan, M
Tifft, C
Toro, C
Boerkoel, CF
Gahl, W
Markello, T
AF Fajardo, Karin V. Fuentes
Adams, David
Mason, Christopher E.
Sincan, Murat
Tifft, Cynthia
Toro, Camilo
Boerkoel, Cornelius F.
Gahl, William
Markello, Thomas
CA NISC Comparative Sequencing
NIH Undiagnosed Dis Program
TI Detecting false-positive signals in exome sequencing
SO HUMAN MUTATION
LA English
DT Article
DE Exome sequencing; inherited disease; false positives; next generation
sequencing; genomics; Illumina; sequencing errors; alignment errors;
WES; SureSelect Human All Exon
ID HARDY-WEINBERG EQUILIBRIUM; UNDIAGNOSED DISEASES; EXACT TESTS;
MUTATIONS; GENOME; ACCURATE; GENE; CHALLENGES; DISCOVERY; ALIGNMENT
AB Disease gene discovery has been transformed by affordable sequencing of exomes and genomes. Identification of disease-causing mutations requires sifting through a large number of sequence variants. A subset of the variants are unlikely to be good candidates for disease causation based on one or more of the following criteria: (1) being located in genomic regions known to be highly polymorphic, (2) having characteristics suggesting assembly misalignment, and/or (3) being labeled as variants based on misleading reference genome information. We analyzed exome sequence data from 118 individuals in 29 families seen in the NIH Undiagnosed Diseases Program (UDP) to create lists of variants and genes with these characteristics. Specifically, we identified several groups of genes that are candidates for provisional exclusion during exome analysis: 23,389 positions with excess heterozygosity suggestive of alignment errors and 1,009 positions in which the hg18 human genome reference sequence appeared to contain a minor allele. Exclusion of such variants, which we provide in supplemental lists, will likely enhance identification of disease-causing mutations using exome sequence data. Hum Mutat 33:609613, 2012. (c) 2012 Wiley Periodicals, Inc.
C1 [Markello, Thomas] NHGRI, Med Genet Branch, Off Clin Director, NIH, Bethesda, MD 20892 USA.
[Fajardo, Karin V. Fuentes; Adams, David; Tifft, Cynthia; Toro, Camilo; Boerkoel, Cornelius F.; Gahl, William] NIH Off Rare Dis Res, NIH Undiagnosed Dis Program, Bethesda, MD USA.
[NISC Comparative Sequencing] NIH, Intramural Sequencing Ctr, Bethesda, MD 20892 USA.
[Mason, Christopher E.] Cornell Univ, Weill Med Coll, Dept Physiol & Biophys, New York, NY 10021 USA.
[Mason, Christopher E.] Cornell Univ, Weill Med Coll, HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsau, New York, NY 10021 USA.
RP Markello, T (reprint author), NHGRI, Med Genet Branch, Off Clin Director, NIH, 10 Ctr Dr,Bldg 10-10C103, Bethesda, MD 20892 USA.
EM markellot@mail.nih.gov
FU NHGRI; UDP through the office of the Director NIH
FX Contract grant sponsors: NHGRI intramural funding; UDP program through
the office of the Director NIH.
NR 48
TC 50
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U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1059-7794
EI 1098-1004
J9 HUM MUTAT
JI Hum. Mutat.
PD APR
PY 2012
VL 33
IS 4
BP 609
EP 613
DI 10.1002/humu.22033
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 906IP
UT WOS:000301338900006
ER
PT J
AU Dias, C
Sincan, M
Cherukuri, PF
Rupps, R
Huang, Y
Briemberg, H
Selby, K
Mullikin, JC
Markello, TC
Adams, DR
Gahl, WA
Boerkoel, CF
AF Dias, Cristina
Sincan, Murat
Cherukuri, Praveen F.
Rupps, Rosemarie
Huang, Yan
Briemberg, Hannah
Selby, Kathryn
Mullikin, James C.
Markello, Thomas C.
Adams, David R.
Gahl, William A.
Boerkoel, Cornelius F.
TI An analysis of exome sequencing for diagnostic testing of the genes
associated with muscle disease and spastic paraplegia
SO HUMAN MUTATION
LA English
DT Review
DE CAPN3; exome; LGMD; HSP; neuromuscular disorders; clinical genetic
testing
ID CONGENITAL MUSCULAR-DYSTROPHY; FIBER-TYPE DISPROPORTION; INCLUSION-BODY
MYOPATHY; HEREDITARY HEARING-LOSS; X-LINKED GENE; NEMALINE MYOPATHY;
BINDING-PROTEIN; ABNORMAL GLYCOSYLATION; CENTRONUCLEAR MYOPATHY; DILATED
CARDIOMYOPATHY
AB In this study, we assess exome sequencing (ES) as a diagnostic alternative for genetically heterogeneous disorders. Because ES readily identified a previously reported homozygous mutation in the CAPN3 gene for an individual with an undiagnosed limb girdle muscular dystrophy, we evaluated ES as a generalizable clinical diagnostic tool by assessing the targeting efficiency and sequencing coverage of 88 genes associated with muscle disease (MD) and spastic paraplegia (SPG). We used three exome-capture kits on 125 individuals. Exons constituting each gene were defined using the UCSC and CCDS databases. The three exome-capture kits targeted 4792% of bases within the UCSC-defined exons and 9799% of bases within the CCDS-defined exons. An average of 61.299.5% and 19.199.5% of targeted bases per gene were sequenced to 20X coverage within the CCDS-defined MD and SPG coding exons, respectively. Greater than 9599% of targeted known mutation positions were sequenced to =1X coverage and 5587% to =20X coverage in every exome. We conclude, therefore, that ES is a rapid and efficient first-tier method to screen for mutations, particularly within the CCDS annotated exons, although its application requires disclosure of the extent of coverage for each targeted gene and supplementation with second-tier Sanger sequencing for full coverage. Hum Mutat 33:614626, 2012. (c) 2012 Wiley Periodicals, Inc.
C1 [Boerkoel, Cornelius F.] NHGRI, UDP Translat Lab, NIH, Bethesda, MD 20892 USA.
[Dias, Cristina; Rupps, Rosemarie; Boerkoel, Cornelius F.] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada.
[Dias, Cristina; Rupps, Rosemarie; Boerkoel, Cornelius F.] Childrens & Womens Hlth Ctr British Columbia, Child & Family Res Inst, Vancouver, BC, Canada.
[Briemberg, Hannah] Univ British Columbia, Dept Med, Div Neurol, Vancouver, BC V6T 1W5, Canada.
[Selby, Kathryn] Univ British Columbia, Dept Pediat, Div Pediat Neurol, Vancouver, BC V6T 1W5, Canada.
[Mullikin, James C.] NHGRI, NIH, Intramural Sequencing Ctr, Bethesda, MD 20892 USA.
[Sincan, Murat; Cherukuri, Praveen F.; Huang, Yan; Markello, Thomas C.; Adams, David R.; Gahl, William A.] NIH, Undiagnosed Dis Program, Bethesda, MD 20892 USA.
RP Boerkoel, CF (reprint author), NHGRI, UDP Translat Lab, NIH, 9 Mem Dr,Bldg 9,Rm 1E100, Bethesda, MD 20892 USA.
EM boerkoelcf@mail.nih.gov
OI Selby, Kathryn/0000-0001-9239-1704; Dias, Cristina/0000-0001-5411-4984
FU Rare Disease Foundation; National Human Genome Research Institute; Child
and Family Research Institute; Canadian Child Health Clinician Scientist
Program
FX Contract grant sponsors: This study was supported in part by the Rare
Disease Foundation and by the Intramural Research Program of the
National Human Genome Research Institute. CD is funded by the Child and
Family Research Institute and the Canadian Child Health Clinician
Scientist Program.
NR 117
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U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PD APR
PY 2012
VL 33
IS 4
BP 614
EP 626
DI 10.1002/humu.22032
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 906IP
UT WOS:000301338900007
PM 22311686
ER
PT J
AU Mou, HW
Li, ZM
Kong, Y
Deng, B
Qian, LH
Wang, JM
Le, YY
AF Mou, Haiwei
Li, Zongmeng
Kong, Yan
Deng, Bo
Qian, Lihua
Wang, Ji Ming
Le, Yingying
TI Proinflammatory Stimulants Promote the Expression of a Promiscuous G
Protein-Coupled Receptor, mFPR2, in Microvascular Endothelial Cells
SO INFLAMMATION
LA English
DT Article
DE lipopolysaccharide; interleukin-1 beta; murine formylpeptide receptor 2;
endothelial cell; MAP kinase; NF-kappa B
ID FORMYL-PEPTIDE RECEPTOR; CEREBRAL-AMYLOID-ANGIOPATHY; MURINE MICROGLIAL
CELLS; SIGNAL-TRANSDUCTION; DENDRITIC CELLS; UP-REGULATION;
MATRIX-METALLOPROTEINASE-9; ANGIOGENESIS; INFLAMMATION; MACROPHAGES
AB Human formylpeptide receptor 2 (FPR2) and its mouse homologue mFPR2 belong to the G protein-coupled, seven-transmembrane receptor superfamily. Both FPR2 and mFPR2 recognize a variety of exogenous and host-derived chemotactic peptides associated with proinflammatory conditions. Since endothelial cells actively participate in inflammation, we investigated whether microvascular endothelial cells express mFPR2 and its regulation by proinflammatory factors. We found that resting primary mouse microvascular endothelial cells and a cell line bEnd.3 expressed low levels of mFPR2 at both mRNA and protein levels, which was markedly enhanced by two key proinflammatory stimulants, lipopolysaccharide (LPS) and interleukin (IL)-1 beta. While the inductive effect of LPS was dependent on the JNK MAP kinase, both JNK and ERK MAP kinases were utilized by IL-1 beta to enhance mFPR2 expression. Overexpression of dominant-negative I kappa B alpha attenuated LPS- and IL-1 beta-induced mFPR2 expression, indicating an essential role for NF-kappa B in regulating mFPR2 expression in endothelial cells by proinflammatory stimulants. Our results suggest that upregulated mFPR2 in vascular endothelial cells under inflammatory conditions may mediate cell responses in diseases in which mFPR2 agonists are elevated.
C1 [Mou, Haiwei; Li, Zongmeng; Kong, Yan; Deng, Bo; Qian, Lihua; Le, Yingying] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, Shanghai, Peoples R China.
[Wang, Ji Ming] Natl Canc Inst Frederick, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD USA.
[Mou, Haiwei; Li, Zongmeng; Kong, Yan; Deng, Bo; Qian, Lihua; Le, Yingying] Chinese Acad Sci, Grad Sch, Shanghai, Peoples R China.
RP Le, YY (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutr Sci, Key Lab Nutr & Metab, Shanghai, Peoples R China.
EM yyle@sibs.ac.cn
FU National Basic Research Program of China (973 Program) [2010CB529701];
Science and Technology Commission of Shanghai Municipality
[09ZR1436700]; National Natural Science Foundation of China [30870931]
FX We thank R. Lin (McGill University, Montreal, QC, Canada) for providing
plasmid DN-I kappa B alpha and control vector flag-zeo, and M. Li (Sun
Yat-sen University, Guangzhou, China) for providing plasmid c-Jun DN.
This work was supported by research grants from: the National Basic
Research Program of China (973 Program) (2010CB529701); the Science and
Technology Commission of Shanghai Municipality (09ZR1436700), and the
National Natural Science Foundation of China (30870931) to Y. Le.
NR 31
TC 3
Z9 4
U1 0
U2 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0360-3997
J9 INFLAMMATION
JI Inflammation
PD APR
PY 2012
VL 35
IS 2
BP 656
EP 664
DI 10.1007/s10753-011-9358-9
PG 9
WC Cell Biology; Immunology
SC Cell Biology; Immunology
GA 933SG
UT WOS:000303382200030
PM 21761148
ER
PT J
AU Singh, GK
Siahpush, M
Williams, SD
AF Singh, Gopal K.
Siahpush, Mohammad
Williams, Shanita D.
TI Changing Urbanization Patterns in US Lung Cancer Mortality, 1950-2007
SO JOURNAL OF COMMUNITY HEALTH
LA English
DT Article
DE Urbanization; Metropolitan; Nonmetropolitan; Lung cancer mortality;
Deprivation; Age; Sex; Time trend
ID AREA SOCIOECONOMIC PATTERNS; INEQUALITIES; DEPRIVATION
AB This study examined disparities in lung cancer mortality rates among US men and women in metropolitan and non-metropolitan areas from 1950 through 2007. Annual age-adjusted mortality rates were calculated for men and women in metropolitan and non-metropolitan areas, and differences in mortality rates were tested for statistical significance. Log-linear regression was used to model annual rates of change in mortality over time, while Poisson regression was used to estimate relative risk after adjusting for age, sex, deprivation, and urbanization levels. Urbanization patterns in lung cancer mortality changed dramatically between 1950 and 2007. Compared to men in metropolitan areas, men aged 25-64 years in non-metropolitan areas had significantly lower lung cancer mortality rates from 1950 to 1977 and men aged >= 65 years in non-metropolitan areas had lower mortality rates from 1950 to 1985. Differentials began to reverse and widen by the mid-1980s for men and by the mid-1990s for younger women. In 2007, compared to their metropolitan counterparts, men aged 25-64 and >= 65 years in non-metropolitan areas had 49 and 19% higher lung cancer mortality and women aged 25-64 and >= 65 years in non-metropolitan areas had 32 and 4% higher lung cancer mortality, respectively. Although adjustment for deprivation levels reduced excess lung cancer mortality risk among those in non-metropolitan areas, significant rural-urban differences remained. Rural-urban patterns reversed because of faster and earlier reductions in lung cancer mortality among men and women in metropolitan areas. Temporal trends in rural-urban disparities in lung cancer mortality appear to be consistent with those in smoking.
C1 [Singh, Gopal K.] Maternal & Child Hlth Bur, US Dept HHS, Hlth Resources & Serv Adm, Rockville, MD 20857 USA.
[Siahpush, Mohammad] Univ Nebraska Med Ctr, Dept Hlth Promot Social & Behav Hlth, Omaha, NE 68198 USA.
[Williams, Shanita D.] Natl Inst Minor Hlth & Hlth Dispar, NIH, Bethesda, MD 20892 USA.
RP Singh, GK (reprint author), Maternal & Child Hlth Bur, US Dept HHS, Hlth Resources & Serv Adm, 5600 Fishers Lane,Room 18-41, Rockville, MD 20857 USA.
EM gsingh@hrsa.gov; msiahpush@unmc.edu; shanita@mail.nih.gov
NR 26
TC 10
Z9 10
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0094-5145
J9 J COMMUN HEALTH
JI J. Community Health
PD APR
PY 2012
VL 37
IS 2
BP 412
EP 420
DI 10.1007/s10900-011-9458-3
PG 9
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 936KY
UT WOS:000303590500020
PM 21858690
ER
PT J
AU Abdoler, E
Wendler, D
AF Abdoler, Emily
Wendler, David
TI USING DATA TO IMPROVE SURROGATE CONSENT FOR CLINICAL RESEARCH WITH
INCAPACITATED ADULTS
SO JOURNAL OF EMPIRICAL RESEARCH ON HUMAN RESEARCH ETHICS
LA English
DT Article
DE capacity; consent; research
ID RESEARCH ADVANCE DIRECTIVES; DEMENTIA RESEARCH; RESEARCH PARTICIPATION;
ALZHEIMERS-DISEASE; INFORMED CONSENT; DECISION-MAKERS; PROXY CONSENT;
CARE RESEARCH; PREFERENCES; WILLINGNESS
AB CURRENT PRACTICE RELIES ON surrogates to enroll incapacitated adults in research. Yet, it is unclear to what extent this practice protects adults who have lost the ability to consent for themselves. To address this question, we conducted two literature searches to identify articles which report empirical data on three issues central to protecting adults who have lost the ability to consent: (1) adults' willingness to participate in research should they lose the ability to consent; (2) adults' willingness to allow a surrogate to make research decisions for them; and (3) the extent to which surrogates' enrollment decisions are consistent with their charges' preferences and values. These searches identified 21 articles, representing 20 distinct datasets. The data indicate that many adults are willing to participate in research should they lose the ability to consent, and many are willing to allow their family members to make research decisions for them if they become incapacitated. The data also raise concern that surrogates may be making research enrollment decisions that, in some cases, are inconsistent with their charges' preferences and values. These findings suggest that modifications to current practice should be considered to better protect adults who have lost the ability to consent. One option would be to require, in addition to surrogate permission and subject assent, sufficient evidence that enrollment is consistent with the individual's preferences and values.
C1 [Wendler, David] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
RP Wendler, D (reprint author), NIH, Dept Bioeth, Ctr Clin, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM dwendler@nih.gov
FU NIH
FX Thanks to Marion Danis, NIH, Annette Rid, NIH, and Rebecca Wolitz, NIH,
for their helpful comments on previous drafts of the manuscript; to
Seema Shah, NIH, for her important input; and to Karen Smith MLS, NIH
Library, for assistance with the literature search. This research was
supported by the Intramural Research Program of the NIH.
NR 33
TC 3
Z9 3
U1 0
U2 0
PU UNIV CALIFORNIA PRESS
PI BERKELEY
PA C/O JOURNALS & DIGITAL PUBLISHING DIVISION, 2000 CENTER ST, STE 303,
BERKELEY, CA 94704-1223 USA
SN 1556-2646
J9 J EMPIR RES HUM RES
JI J. Empir. Res. Hum. Res. Ethics
PD APR
PY 2012
VL 7
IS 2
BP 37
EP 50
DI 10.1525/jer.2012.7.2.37
PG 14
WC Ethics; Medical Ethics
SC Social Sciences - Other Topics; Medical Ethics
GA 937CW
UT WOS:000303637600005
PM 22565582
ER
PT J
AU Fraum, TJ
Barak, S
Pack, S
Lonser, RR
Fine, HA
Quezado, M
Iwamoto, FM
AF Fraum, Tyler J.
Barak, Stephanie
Pack, Svetlana
Lonser, Russell R.
Fine, Howard A.
Quezado, Martha
Iwamoto, Fabio M.
TI Spinal cord glioneuronal tumor with neuropil-like islands with 1p/19q
deletion in an adult with low-grade cerebral oligodendroglioma
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article
DE Glioneuronal tumor with neuropil-like islands (GTNI); 1p/19q deletion;
Oligodendroglioma; Astrocytoma
ID GLIOMAS; FEATURES; NODULES; 19Q; 1P
AB Glioneuronal tumor with neuropil-like islands (GTNI) is considered a rare variant of astrocytoma, characterized by discrete aggregates of cells expressing neuronal markers that punctuate a GFAP-positive glial background. Of the 24 published GTNI cases, only two occurred in adult spinal cords; none occurred concurrent with another CNS tumor; and none of those tested exhibited the 1p/19q deletion typical of oligodendroglioma. A 48-year-old man without significant past medical history was diagnosed with a WHO grade II oligodendroglioma by stereotactic biopsy of a lesion discovered after the patient suffered a generalized tonic-clonic seizure. By FISH analysis, this tumor exhibited the 1p/19q deletion present in up to 80% of oligodendrogliomas. The patient received 14 monthly cycles of temozolomide, and his cerebral tumor had a minor response. When the patient subsequently reported progressive paresthesias of his lower extremities, an MRI revealed an enhancing, cystic tumor of the thoracic spinal cord that was diagnosed as GTNI by histological analysis. By FISH analysis, this lesion exhibited the same 1p/19q deletion present in the concurrent cerebral oligodendroglioma. This case of a spinal cord GTNI with 1p/19q deletions constitutes the third report of a spinal cord GTNI in an adult patient; the first report of a GTNI in an individual with a separate CNS neoplasm; and the first report of a GTNI with 1p/19q deletions. This case establishes a potential genetic kinship between GTNI and oligodendroglioma that warrants further investigation.
C1 [Fraum, Tyler J.; Fine, Howard A.; Iwamoto, Fabio M.] NIH, Neurooncol Branch, Bethesda, MD 20892 USA.
[Fraum, Tyler J.] Duke Univ, Sch Med, Durham, NC USA.
[Barak, Stephanie; Pack, Svetlana; Quezado, Martha] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Lonser, Russell R.] Natl Inst Neurol Disorders & Stroke, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Iwamoto, FM (reprint author), NIH, Neurooncol Branch, 9030 Old Georgetown Rd,Room 221, Bethesda, MD 20892 USA.
EM tyler.fraum@duke.edu; stephanie.barak@nih.gov; spack@mail.nih.gov;
lonserr@ninds.nih.gov; hfine@mail.nih.gov; quezadom@mail.nih.gov;
iwamotofm@mail.nih.gov
RI Pack, Svetlana/C-2020-2014
FU NIH [1ZIABC011347-01, 1ZIABC011348-01]; Pfizer Inc; National Cancer
Institute
FX NIH Intramural Research Program (1ZI-DBC011098-02). T.J.F. is a Fellow
in the Clinical Research Training Program, a public-private partnership
supported jointly by the NIH and Pfizer Inc (via a grant to the
Foundation for NIH from Pfizer Inc). F. M. I. is supported by the
National Cancer Institute's Clinical Investigator Development Program
and the NIH Intramural Program (1ZIABC011347-01 and 1ZIABC011348-01).
NR 23
TC 5
Z9 7
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD APR
PY 2012
VL 107
IS 2
BP 421
EP 426
DI 10.1007/s11060-011-0760-9
PG 6
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 934TG
UT WOS:000303469000024
PM 22083647
ER
PT J
AU Obregon, D
Hou, HY
Deng, J
Giunta, B
Tian, J
Darlington, D
Shahaduzzaman, M
Zhu, YY
Mori, T
Mattson, MP
Tan, J
AF Obregon, Demian
Hou, Huayan
Deng, Juan
Giunta, Brian
Tian, Jun
Darlington, Donna
Shahaduzzaman, Md
Zhu, Yuyuan
Mori, Takashi
Mattson, Mark P.
Tan, Jun
TI Soluble amyloid precursor protein-alpha modulates beta-secretase
activity and amyloid-beta generation
SO NATURE COMMUNICATIONS
LA English
DT Article
ID ALZHEIMERS-DISEASE; GAMMA-SECRETASE; OXIDATIVE STRESS; CLEAVING ENZYME;
CHRONIC HYPOXIA; A-BETA; BACE1; APP; CLEAVAGE; MICE
AB In sporadic age-related forms of Alzheimer's disease (AD), it is unclear why amyloid-beta (A beta) peptides accumulate. Here we show that soluble amyloid precursor protein-alpha (sAPP-alpha) decreases A beta generation by directly associating with beta-site APP-converting enzyme (BACE) 1, thereby modulating APP processing. Whereas specifically targeting sAPP-alpha using antibodies enhances A beta production; in transgenic mice with AD-like pathology, sAPP-alpha overexpression decreases beta-amyloid plaques and soluble A beta. In support, immunoneutralization of sAPP-alpha increases APP amyloidogenic processing in these mice. Given our current findings, and because a number of risk factors for sporadic AD serve to lower levels of sAPP-alpha in brains of AD patients, inadequate sAPP-alpha levels may be sufficient to polarize APP processing towards the amyloidogenic, A beta-producing route. Therefore, restoration of sAPP-alpha or enhancement of its association with BACE may be viable strategies to ameliorate imbalances in APP processing that can lead to AD pathogenesis.
C1 [Obregon, Demian; Hou, Huayan; Deng, Juan; Giunta, Brian; Tian, Jun; Darlington, Donna; Shahaduzzaman, Md; Zhu, Yuyuan; Tan, Jun] Univ S Florida, Rashid Lab Dev Neurobiol, Silver Child Dev Ctr, Dept Psychiat & Behav Neurosci,Morsani Coll Med, Tampa, FL 33613 USA.
[Obregon, Demian; Tan, Jun] James A Haley Vet Hosp, Tampa, FL 33612 USA.
[Giunta, Brian] Univ S Florida, Dept Psychiat & Behav Neurosci, Morsani Coll Med, Neuroimmunol Lab, Tampa, FL 33613 USA.
[Shahaduzzaman, Md] Univ S Florida, Ctr Aging & Brain Repair, Morsani Coll Med, Dept Neurosurg & Brain Repair, Tampa, FL 33613 USA.
[Mori, Takashi] Saitama Med Ctr, Dept Biomed Sci, Kawagoe, Saitama 3508550, Japan.
[Mori, Takashi] Saitama Med Ctr, Dept Pathol, Kawagoe, Saitama 3508550, Japan.
[Mori, Takashi] Saitama Med Univ, Kawagoe, Saitama 3508550, Japan.
[Mattson, Mark P.] NIA, Lab Neurosci, Intramural Res Program, Baltimore, MD 21224 USA.
RP Tan, J (reprint author), Univ S Florida, Rashid Lab Dev Neurobiol, Silver Child Dev Ctr, Dept Psychiat & Behav Neurosci,Morsani Coll Med, Tampa, FL 33613 USA.
EM jtan@health.usf.edu
RI Mattson, Mark/F-6038-2012; Giunta, Brian/H-3817-2011
FU NIH/NIA [R01AG032432, R42AG031586]; National Institute on Aging;
Department of Veterans Affairs, Veterans Health Administration, Office
of Research and Development, Medical Research Service
FX This work was supported by the NIH/NIA [R01AG032432 and R42AG031586
(J.T.)], and the National Institute on Aging Intramural Research
Program. This work was also supported in part by the Department of
Veterans Affairs, Veterans Health Administration, Office of Research and
Development, Medical Research Service through a Veterans Affairs Merit
grant (J.T.). We would like to thank Terrence Town and Song Min for
helpful discussion.
NR 59
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U1 0
U2 8
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 APR
PY 2012
VL 3
AR 777
DI 10.1038/ncomms1781
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 934PB
UT WOS:000303455200014
PM 22491325
ER
PT J
AU Singh, A
Mishra, AK
Ylaya, K
Hewitt, SM
Sharma, KC
Saxena, S
AF Singh, Avninder
Mishra, Ashwani Kumar
Ylaya, Kris
Hewitt, Stephen M.
Sharma, Karam Chand
Saxena, Sunita
TI Wilms Tumor-1, Claudin-1 and Ezrin Are Useful Immunohistochemical
Markers That Help to Distinguish Schwannoma from Fibroblastic Meningioma
SO PATHOLOGY & ONCOLOGY RESEARCH
LA English
DT Article
DE Biomarkers; Fibroblastic meningioma; Immunohistochemistry; Schwannoma;
Tissue microarray
ID EPITHELIAL MEMBRANE ANTIGEN; SOLITARY FIBROUS TUMOR; MENINGEAL
HEMANGIOPERICYTOMA; TISSUE MICROARRAY; EXPRESSION; PROGESTERONE;
RECEPTORS; DIAGNOSIS; PATHOLOGY; PROTEIN
AB The aim of this study is to identify immunohistochemical (IHC) markers that can reliably separate schwannoma (SCHW) and fibroblastic meningioma (FM). We selected 106 cases of intracranial SCHW (n=56) and FM (n=50) and constructed a tissue microarray (TMA) of core diameter of 1.0 mm from archival formalin-fixed paraffin-embedded tissue. ATMA-IHC was performed using 14 antibodies. After IHC staining, 98 cores were found suitable for evaluation. The IHC staining was scored as 0-2+ (0, negative; 1+, weak and/or focal 2+ strong and/or diffuse positive). A discriminant analysis (DA) (Wilks'Lambda test) was performed to assess the relative importance of these biomarkers in classifying the two groups FM and SCHW. It showed that WT-1 (Wilks'lambda 0.085, p<0.001), EMA (Wilks'lambda 0.253, p<0.001), S100 (Wilks'lambda 0.487, p<0.001), Claudin-1 (Wilks' lambda 0.57, p<0.001) and Ezrin (Wilks'lambda 0.656, p<0.001), SPARC (Wilks'lambda 0.751, p<0.01), NP-Y (Wilks'lambda, 0.819, p<0.001) and EGFR (Wilks'lambda 0.845, p=0.026) were some of the statistically significant markers that discriminated SCHW and FM. For sensitivity and specificity for SCHW the significant markers [Area under the curve (95% CI), p-value] by ROC analysis were WT-1 [ 0.990(0.000, 1.000), <0.001], S100 [0.880(0.808, 0.951), <0.001] while for diagnosing FM the most sensitive and specific markers were EMA [0.957(0.914, 1.000), <.001], Claudin-1 [0.857(0.782, 0.932), <0.001] and ezrin [0.792(0.700,0.884),<0.001]. WT-1, Claudin-1 and Ezrin may be potentially useful immunohistochemical adjuncts to EMA and S100 that differentiate SCHW from FM
C1 [Singh, Avninder; Mishra, Ashwani Kumar; Saxena, Sunita] Natl Inst Pathol ICMR, New Delhi 110029, India.
[Ylaya, Kris; Hewitt, Stephen M.] Natl Canc Inst, Natl Inst Hlth, TARP Lab, Bethesda, MD USA.
[Sharma, Karam Chand] Safdarjang Hosp, Dept Neurosurg, New Delhi, India.
RP Singh, A (reprint author), Natl Inst Pathol ICMR, Safdarjung Hosp Campus,Room 602,6th floor, New Delhi 110029, India.
EM dravninder@yahoo.co.in
OI Hewitt, Stephen/0000-0001-8283-1788
FU Indo-US Science and Technology forum, Department of Science and
Technology, Government of India
FX The authors wish to thank the Indo-US Science and Technology forum,
Department of Science and Technology, Government of India for the IUSSTF
Research fellowship to Dr Avninder Singh to visit the TARP Lab, NCI,
NIH, USA for construction of TMA. The authors also wish to thank Ms
Preet Sayal for typing the manuscript and Mr JS Sayal for the adobe
photoshop work
NR 28
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U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1219-4956
J9 PATHOL ONCOL RES
JI Pathol. Oncol. Res.
PD APR
PY 2012
VL 18
IS 2
BP 383
EP 389
DI 10.1007/s12253-011-9456-x
PG 7
WC Oncology; Pathology
SC Oncology; Pathology
GA 935RP
UT WOS:000303538200034
PM 21909685
ER
PT J
AU Bellan, SE
Pulliam, JRC
Scott, JC
Dushoff, J
AF Bellan, Steve E.
Pulliam, Juliet R. C.
Scott, James C.
Dushoff, Jonathan
CA MMED Organizing Comm
TI How to Make Epidemiological Training Infectious
SO PLOS BIOLOGY
LA English
DT Article
ID ECO-EPIDEMIOLOGY; BLACK-BOX; DYNAMICS; TRACHOMA; ELIMINATION; DISEASE;
MODELS
AB Modern infectious disease epidemiology builds on two independently developed fields: classical epidemiology and dynamical epidemiology. Over the past decade, integration of the two fields has increased in research practice, but training options within the fields remain distinct with few opportunities for integration in the classroom. The annual Clinic on the Meaningful Modeling of Epidemiological Data (MMED) at the African Institute for Mathematical Sciences has begun to address this gap. MMED offers participants exposure to a broad range of concepts and techniques from both epidemiological traditions. During MMED 2010 we developed a pedagogical approach that bridges the traditional distinction between classical and dynamical epidemiology and can be used at multiple educational levels, from high school to graduate level courses. The approach is hands-on, consisting of a real-time simulation of a stochastic outbreak in course participants, including realistic data reporting, followed by a variety of mathematical and statistical analyses, stemming from both epidemiological traditions. During the exercise, dynamical epidemiologists developed empirical skills such as study design and learned concepts of bias while classical epidemiologists were trained in systems thinking and began to understand epidemics as dynamic nonlinear processes. We believe this type of integrated educational tool will prove extremely valuable in the training of future infectious disease epidemiologists. We also believe that such interdisciplinary training will be critical for local capacity building in analytical epidemiology as Africa continues to produce new cohorts of well-trained mathematicians, statisticians, and scientists. And because the lessons draw on skills and concepts from many fields in biology-from pathogen biology, evolutionary dynamics of host-pathogen interactions, and the ecology of infectious disease to bioinformatics, computational biology, and statistics-this exercise can be incorporated into a broad array of life sciences courses.
C1 [Bellan, Steve E.] Univ Calif Berkeley, Dept Environm Sci Policy & Management, Berkeley, CA 94720 USA.
[Pulliam, Juliet R. C.] Natl Inst Hlth, Fogarty Int Ctr, Bethesda, MD USA.
[Pulliam, Juliet R. C.] Univ Florida, Dept Biol, Gainesville, FL USA.
[Pulliam, Juliet R. C.] Univ Florida, Emerging Pathogens Inst, Gainesville, FL USA.
[Scott, James C.] Colby Coll, Dept Math & Stat, Waterville, ME 04901 USA.
[Dushoff, Jonathan] McMaster Univ, Dept Biol, Hamilton, ON, Canada.
RP Bellan, SE (reprint author), Univ Calif Berkeley, Dept Environm Sci Policy & Management, Berkeley, CA 94720 USA.
EM steve.bellan@gmail.com
RI Bellan, Steve/D-6368-2013; Pulliam, Juliet/A-6516-2008;
OI Bellan, Steve/0000-0002-4110-272X; Pulliam, Juliet/0000-0003-3314-8223;
Delva, Wim/0000-0001-8054-1904
FU National Institute of Health [R24TW008822, GM83863]; Henry Wheeler
Center for Emerging and Neglected Diseases; African Biomathematics
Initiative (National Science Foundation) [DMS-829652]; NSF-NIH Ecology
of Infectious Diseases [1134964]; Center for Discrete Mathematics and
Theoretical Computer Science; African Institute for Mathematical
Sciences; South African Centre for Excellence in Epidemiological
Modelling and Analysis; Chang-Lin Tien Environmental Fellowship; Andrew
Fellowship; University of California; Mary Thompson Rocca Fellowship;
Berkeley Environmental Science, Policy & Management and Entomology
Society; National Institute of Health Ecology of Infectious Disease
[GM83863]; Research and Policy in Infectious Disease Dynamics (RAPIDD)
of the Science and Technology Directorate; Department of Homeland
Security; Fogarty International Center, National Institutes of Health
FX The Meaningful Modeling of Epidemiological Data Clinics have been
generously funded by the National Institute of Health Framework Programs
for Global Health Innovations (R24TW008822 to Lee Riley), the Henry
Wheeler Center for Emerging and Neglected Diseases, the African
Biomathematics Initiative (National Science Foundation grant DMS-829652
awarded to Fred S. Roberts and Avner Friedman), the NSF-NIH Ecology of
Infectious Diseases program (NSF award 1134964 to J.R.C.P.), the Center
for Discrete Mathematics and Theoretical Computer Science, the African
Institute for Mathematical Sciences, and the South African Centre for
Excellence in Epidemiological Modelling and Analysis. This work was also
partially supported by Chang-Lin Tien Environmental Fellowship, Andrew
and Mary Thompson Rocca Fellowships, University of California, Berkeley
Environmental Science, Policy & Management and Entomology Society Travel
Grants to S. E. B., and National Institute of Health Ecology of
Infectious Disease grant (GM83863) to Wayne M. Getz. J.R.C.P is
supported by the Research and Policy in Infectious Disease Dynamics
(RAPIDD) Program of the Science and Technology Directorate, Department
of Homeland Security, and Fogarty International Center, National
Institutes of Health. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 29
TC 3
Z9 4
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1545-7885
J9 PLOS BIOL
JI PLoS. Biol.
PD APR
PY 2012
VL 10
IS 4
AR e1001295
DI 10.1371/journal.pbio.1001295
PG 8
WC Biochemistry & Molecular Biology; Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics
GA 935SV
UT WOS:000303541800001
PM 22509129
ER
PT J
AU Hao, H
Kim, DS
Klocke, B
Johnson, KR
Cui, KR
Gotoh, N
Zang, CZ
Gregorski, J
Gieser, L
Peng, WQ
Fann, Y
Seifert, M
Zhao, KJ
Swaroop, A
AF Hao, Hong
Kim, Douglas S.
Klocke, Bernward
Johnson, Kory R.
Cui, Kairong
Gotoh, Norimoto
Zang, Chongzhi
Gregorski, Janina
Gieser, Linn
Peng, Weiqun
Fann, Yang
Seifert, Martin
Zhao, Keji
Swaroop, Anand
TI Transcriptional Regulation of Rod Photoreceptor Homeostasis Revealed by
In Vivo NRL Targetome Analysis
SO PLOS GENETICS
LA English
DT Article
ID NUCLEAR RECEPTOR NR2E3; S-CONE SYNDROME; GENE-EXPRESSION;
LEUCINE-ZIPPER; DIFFERENTIATION FACTOR; RETINAL DEVELOPMENT; PROMOTER
ANALYSIS; PRECURSOR CELLS; SUBUNIT GENE; MOUSE RETINA
AB A stringent control of homeostasis is critical for functional maintenance and survival of neurons. In the mammalian retina the basic motif leucine zipper transcription factor NRL determines rod versus cone photoreceptor cell fate and activates the expression of many rod-specific genes. Here, we report an integrated analysis of NRL-centered gene regulatory network by coupling chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-Seq) data from Illumina and ABI platforms with global expression profiling and in vivo knockdown studies. We identified approximately 300 direct NRL target genes. Of these, 22 NRL targets are associated with human retinal dystrophies, revealed an enrichment of distinct sets whereas 95 mapped to regions of as yet uncloned retinal disease loci. In analysis of NRL ChIP-Seq peak sequences of transcription factor binding sites. Specifically, we discovered that genes involved in photoreceptor function include binding sites for both NRL and homeodomain protein CRX. Evaluation of 26 ChIP-Seq regions validated their enhancer functions in reporter assays. in vivo knockdown of 16 NRL target genes resulted in death or abnormal morphology of rod photoreceptors, suggesting their importance in maintaining retinal function. We also identified histone demethylase Kdm5b as a novel secondary node in NRL transcriptional hierarchy. Exon array analysis of flow-sorted photoreceptors in which Kdm5b was knocked down by shRNA indicated its role in regulating rod-expressed genes. Our studies identify candidate genes for retinal dystrophies, define cis-regulatory module(s) for photoreceptor-expressed genes and provide a framework for decoding transcriptional regulatory networks that dictate rod homeostasis.
C1 [Hao, Hong; Kim, Douglas S.; Gotoh, Norimoto; Gregorski, Janina; Gieser, Linn; Swaroop, Anand] NEI, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
[Klocke, Bernward; Seifert, Martin] Genomatix GmbH, Munich, Germany.
[Johnson, Kory R.; Fann, Yang] NINDS, Informat Technol & Bioinformat Program, NIH, Bethesda, MD 20892 USA.
[Cui, Kairong; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Zang, Chongzhi; Peng, Weiqun] George Washington Univ, Dept Phys, Washington, DC 20052 USA.
RP Hao, H (reprint author), NEI, Neurobiol Neurodegenerat & Repair Lab, NIH, Bethesda, MD 20892 USA.
EM swaroopa@nei.nih.gov
RI Zang, Chongzhi/D-1445-2011;
OI Swaroop, Anand/0000-0002-1975-1141
FU National Eye Institute of the National Institutes of Health; National
Institute of Neurological Disorders and Stroke of the National
Institutes of Health; National Heart, Lung and Blood Institute of the
National Institutes of Health
FX This research was supported by intramural programs of the National Eye
Institute, National Institute of Neurological Disorders and Stroke, and
National Heart, Lung and Blood Institute, 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 77
TC 43
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U1 1
U2 7
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 APR
PY 2012
VL 8
IS 4
BP 380
EP 394
AR e1002649
DI 10.1371/journal.pgen.1002649
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 934KA
UT WOS:000303441800028
PM 22511886
ER
PT J
AU Kanel, DP
Shusterman, M
Rong, YK
McVey, M
AF Kanel, Daniel P.
Shusterman, Michael
Rong, Yikang
McVey, Mitch
TI Competition between Replicative and Translesion Polymerases during
Homologous Recombination Repair in Drosophila
SO PLOS GENETICS
LA English
DT Article
ID DOUBLE-STRAND-BREAK; DNA-POLYMERASES; SACCHAROMYCES-CEREVISIAE; REV1
PROTEIN; IN-VIVO; POL32 SUBUNIT; GAP REPAIR; DELTA; BYPASS; ROLES
AB In metazoans, the mechanism by which DNA is synthesized during homologous recombination repair of double-strand breaks is poorly understood. Specifically, the identities of the polymerase(s) that carry out repair synthesis and how they are recruited to repair sites are unclear. Here, we have investigated the roles of several different polymerases during homologous recombination repair in Drosophila melanogaster. Using a gap repair assay, we found that homologous recombination is impaired in Drosophila lacking DNA polymerase zeta and, to a lesser extent, polymerase eta. In addition, the Pol32 protein, part of the polymerase delta complex, is needed for repair requiring extensive synthesis. Loss of Rev1, which interacts with multiple translesion polymerases, results in increased synthesis during gap repair. Together, our findings support a model in which translesion polymerases and the polymerase delta complex compete during homologous recombination repair. In addition, they establish Rev1 as a crucial factor that regulates the extent of repair synthesis.
C1 [Kanel, Daniel P.; Shusterman, Michael; McVey, Mitch] Tufts Univ, Dept Biol, Medford, MA 02155 USA.
[Rong, Yikang] NCI, Bethesda, MD 20892 USA.
[McVey, Mitch] Tufts Sackler Sch Grad Biomed Sci, Genet Program, Boston, MA USA.
RP Kanel, DP (reprint author), Tufts Univ, Dept Biol, Medford, MA 02155 USA.
EM mitch.mcvey@tufts.edu
FU National Science Foundation [MCB-0643253]; National Institutes of Health
[R01GM092866]; National Cancer Institute
FX This research was supported by grants from the National Science
Foundation (MCB-0643253) and the National Institutes of Health
(R01GM092866) to MM. Research in the YR lab is supported by the
intramural research program of the National Cancer Institute. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 44
TC 23
Z9 23
U1 0
U2 1
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 APR
PY 2012
VL 8
IS 4
BP 447
EP 455
AR e1002659
DI 10.1371/journal.pgen.1002659
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 934KA
UT WOS:000303441800034
PM 22532806
ER
PT J
AU Kulkarni, M
Shakes, DC
Guevel, K
Smith, HE
AF Kulkarni, Madhura
Shakes, Diane C.
Guevel, Katie
Smith, Harold E.
TI SPE-44 Implements Sperm Cell Fate
SO PLOS GENETICS
LA English
DT Article
ID SEX-DETERMINING GENE; NEMATODE CAENORHABDITIS-ELEGANS; GLUCOCORTICOID
MODULATORY ELEMENT; FERTILIZATION-DEFECTIVE MUTANTS; GATA-FACTOR ELT-1;
C-ELEGANS; PROTEIN PHOSPHATASE; SAND DOMAIN; MONOCLONAL-ANTIBODIES;
TRANSCRIPTION FACTOR
AB The sperm/oocyte decision in the hermaphrodite germline of Caenorhabditis elegans provides a powerful model for the characterization of stem cell fate specification and differentiation. The germline sex determination program that governs gamete fate has been well studied, but direct mediators of cell-type-specific transcription are largely unknown. We report the identification of spe-44 as a critical regulator of sperm gene expression. Deletion of spe-44 causes sperm-specific defects cytokinesis, cell cycle progression, and organelle assembly resulting in sterility. Expression of spe-44 correlates precisely with spermatogenesis and is regulated by the germline sex determination pathway. spe-44 is required for the appropriate expression of several hundred sperm-enriched genes. The SPE-44 protein is restricted to the sperm-producing germline where it localizes to the autosomes (which contain sperm genes) but is excluded from the transcriptionally silent. X chromosome (which does not). The orthologous gene in other Caenorhabditis species is similarly expressed in a sex-biased manner, and the protein likewise exhibits autosome-specific localization in developing sperm, strongly suggestive of an evolutionarily conserved role in sperm gene expression. Our analysis represents the first identification of a transcriptional regulator whose primary function is the control of gamete-type-specific transcription in this system.
C1 [Shakes, Diane C.; Guevel, Katie] Coll William & Mary, Dept Biol, Williamsburg, VA 23185 USA.
[Smith, Harold E.] NIDDK, NIH, Bethesda, MD USA.
[Kulkarni, Madhura] Univ Maryland, Dept Cell Biol & Mol Genet, College Pk, MD 20742 USA.
RP Kulkarni, M (reprint author), Natl Univ Singapore, Canc Sci Inst Singapore, Singapore 117548, Singapore.
EM smithhe2@niddk.nih.gov
FU National Science Foundation [0445684]; Jeffress Memorial Trust [J-840];
National Institutes of Health [R15 5GM096309]; Howard Hughes Medical
Institute (HHMI)
FX This work was supported in part by National Science Foundation grant
number 0445684 to HES and grants from the Jeffress Memorial Trust
(J-840) and the National Institutes of Health (R15 5GM096309) to DCS. KG
received support from the Howard Hughes Medical Institute (HHMI) through
the Undergraduate Biological Sciences Education Program to the College
of William and Mary. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 81
TC 10
Z9 17
U1 1
U2 11
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 APR
PY 2012
VL 8
IS 4
BP 587
EP 600
AR e1002678
DI 10.1371/journal.pgen.1002678
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 934KA
UT WOS:000303441800044
PM 22570621
ER
PT J
AU Pastrana, DV
Brennan, DC
Cuburu, N
Storch, GA
Viscidi, RP
Randhawa, PS
Buck, CB
AF Pastrana, Diana V.
Brennan, Daniel C.
Cuburu, Nicolas
Storch, Gregory A.
Viscidi, Raphael P.
Randhawa, Parmjeet S.
Buck, Christopher B.
TI Neutralization Serotyping of BK Polyomavirus Infection in Kidney
Transplant Recipients
SO PLOS PATHOGENS
LA English
DT Article
ID VIRUS-LIKE PARTICLES; RENAL-TRANSPLANTATION; INTRAVENOUS IMMUNOGLOBULIN;
INTERSTITIAL NEPHRITIS; ALLOGRAFT RECIPIENTS; HEMORRHAGIC CYSTITIS;
NEPHROPATHY; IDENTIFICATION; ANTIBODY; VACCINE
AB BK polyomavirus (BKV or BKPyV) associated nephropathy affects up to 10% of kidney transplant recipients (KTRs). BKV isolates are categorized into four genotypes. It is currently unclear whether the four genotypes are also serotypes. To address this issue, we developed high-throughput serological assays based on antibody-mediated neutralization of BKV genotype I and IV reporter vectors (pseudoviruses). Neutralization-based testing of sera from mice immunized with BKV-I or BKV-IV virus-like particles (VLPs) or sera from naturally infected human subjects revealed that BKV-I specific serum antibodies are poorly neutralizing against BKV-IV and vice versa. The fact that BKV-I and BKV-IV are distinct serotypes was less evident in traditional VLP-based ELISAs. BKV-I and BKV-IV neutralization assays were used to examine BKV type-specific neutralizing antibody responses in KTRs at various time points after transplantation. At study entry, sera from 5% and 49% of KTRs showed no detectable neutralizing activity for BKV-I or BKV-IV neutralization, respectively. By one year after transplantation, all KTRs were neutralization seropositive for BKV-I, and 43% of the initially BKV-IV seronegative subjects showed evidence of acute seroconversion for BKV-IV neutralization. The results suggest a model in which BKV-IV-specific seroconversion reflects a de novo BKV-IV infection in KTRs who initially lack protective antibody responses capable of neutralizing genotype IV BKVs. If this model is correct, it suggests that pre-vaccinating prospective KTRs with a multivalent VLP-based vaccine against all BKV serotypes, or administration of BKV-neutralizing antibodies, might offer protection against graft loss or dysfunction due to BKV associated nephropathy.
C1 [Pastrana, Diana V.; Cuburu, Nicolas; Buck, Christopher B.] NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA.
[Brennan, Daniel C.; Storch, Gregory A.] Washington Univ, Sch Med, St Louis, MO USA.
[Viscidi, Raphael P.] Johns Hopkins Med Ctr, Dept Pediat, Baltimore, MD USA.
[Randhawa, Parmjeet S.] Univ Pittsburgh, Dept Pathol, Med Ctr, Pittsburgh, PA USA.
RP Pastrana, DV (reprint author), NCI, Cellular Oncol Lab, Bethesda, MD 20892 USA.
EM BuckC@mail.nih.gov
OI Buck, Christopher/0000-0003-3165-8094
FU NIH [K24-DK002886, P-30 DK079333, R01-51227, R01-63360]; Center for
Cancer Research; NCI
FX This work was funded in part by the Intramural Research Program of the
NIH, with support from the Center for Cancer Research and the NCI
Director's Intramural Innovation Award Program, and in part by NIH
grants K24-DK002886 and P-30 DK079333 (DCP) and R01-51227 and R01-63360
(PSR). The funders had no role in study design, data collection and
analysis, decision to publish or preparation of the manuscript.
NR 62
TC 31
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U1 1
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD APR
PY 2012
VL 8
IS 4
AR e1002650
DI 10.1371/journal.ppat.1002650
PG 11
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 934KY
UT WOS:000303444200042
PM 22511874
ER
PT J
AU Schelhaas, M
Shah, B
Holzer, M
Blattmann, P
Kuhling, L
Day, PM
Schiller, JT
Helenius, A
AF Schelhaas, Mario
Shah, Bhavin
Holzer, Michael
Blattmann, Peter
Kuehling, Lena
Day, Patricia M.
Schiller, John T.
Helenius, Ari
TI Entry of Human Papillomavirus Type 16 by Actin-Dependent, Clathrin- and
Lipid Raft-Independent Endocytosis
SO PLOS PATHOGENS
LA English
DT Article
ID VIRUS-LIKE PARTICLES; SURFACE HEPARAN-SULFATE; SEMLIKI-FOREST-VIRUS;
HUMAN KERATINOCYTES; INFECTIOUS ENTRY; CAPSID PROTEIN; HOST-CELLS;
CALMODULIN ANTAGONISTS; PHOSPHOLIPASE-C; PATHWAY
AB Infectious endocytosis of incoming human papillomavirus type 16 (HPV-16), the main etiological agent of cervical cancer, is poorly characterized in terms of cellular requirements and pathways. Conflicting reports attribute HPV-16 entry to clathrin-dependent and -independent mechanisms. To comprehensively describe the cell biological features of HPV-16 entry into human epithelial cells, we compared HPV-16 pseudovirion (PsV) infection in the context of cell perturbations (drug inhibition, siRNA silencing, overexpression of dominant mutants) to five other viruses (influenza A virus, Semliki Forest virus, simian virus 40, vesicular stomatitis virus, and vaccinia virus) with defined endocytic requirements. Our analysis included infection data, i.e. GFP expression after plasmid delivery by HPV-16 PsV, and endocytosis assays in combination with electron, immunofluorescence, and video microscopy. The results indicated that HPV-16 entry into HeLa and HaCaT cells was clathrin-, caveolin-, cholesterol- and dynamin-independent. The virus made use of a potentially novel ligand-induced endocytic pathway related to macropinocytosis. This pathway was distinct from classical macropinocytosis in regards to vesicle size, cholesterol-sensitivity, and GTPase requirements, but similar in respect to the need for tyrosine kinase signaling, actin dynamics, Na+/H+ exchangers, PAK-1 and PKC. After internalization the virus was transported to late endosomes and/or endolysosomes, and activated through exposure to low pH.
C1 [Schelhaas, Mario; Shah, Bhavin; Kuehling, Lena] Univ Munster, Emmy Noether Grp Virus Endocytosis, Inst Mol Virol & Med Biochem, Munster, Germany.
[Schelhaas, Mario; Holzer, Michael; Blattmann, Peter; Helenius, Ari] ETH, Inst Biochem, Zurich, Switzerland.
[Day, Patricia M.; Schiller, John T.] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
RP Schelhaas, M (reprint author), Univ Munster, Emmy Noether Grp Virus Endocytosis, Inst Mol Virol & Med Biochem, Munster, Germany.
EM schelhaas@uni-muenster.de
RI Blattmann, Peter/D-2880-2012
OI Blattmann, Peter/0000-0001-9105-6381
FU ETH Zurich; German Science Foundation (DFG) [SCHE 1552/2-1, SFB629A16];
Swiss National Science Foundation (SNF); European Research Council (ERC)
FX MS was supported by ETH Zurich (www.ethz.ch) and the German Science
Foundation (DFG, www.dfg.de, grants SCHE 1552/2-1, SFB629A16). AH was
supported by the ETH Zurich (www.ethz.ch), and by grants from the Swiss
National Science Foundation (SNF, www.snf.ch) and the European Research
Council (ERC, erc.europa.eu). The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 81
TC 99
Z9 101
U1 1
U2 28
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 APR
PY 2012
VL 8
IS 4
AR e1002657
DI 10.1371/journal.ppat.1002657
PG 21
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 934KY
UT WOS:000303444200046
PM 22536154
ER
PT J
AU Smith, DL
Battle, KE
Hay, SI
Barker, CM
Scott, TW
McKenzie, FE
AF Smith, David L.
Battle, Katherine E.
Hay, Simon I.
Barker, Christopher M.
Scott, Thomas W.
McKenzie, F. Ellis
TI Ross, Macdonald, and a Theory for the Dynamics and Control of
Mosquito-Transmitted Pathogens
SO PLOS PATHOGENS
LA English
DT Review
ID A-PRIORI PATHOMETRY; MALARIA TRANSMISSION; VECTORIAL CAPACITY;
MATHEMATICAL-MODELS; GENERAL PART; EPIDEMIOLOGY; PROBABILITIES;
INTERRUPTION; ERADICATION; ENTOMOLOGY
AB Ronald Ross and George Macdonald are credited with developing a mathematical model of mosquito-borne pathogen transmission. A systematic historical review suggests that several mathematicians and scientists contributed to development of the Ross-Macdonald model over a period of 70 years. Ross developed two different mathematical models, Macdonald a third, and various "Ross-Macdonald'' mathematical models exist. Ross-Macdonald models are best defined by a consensus set of assumptions. The mathematical model is just one part of a theory for the dynamics and control of mosquito-transmitted pathogens that also includes epidemiological and entomological concepts and metrics for measuring transmission. All the basic elements of the theory had fallen into place by the end of the Global Malaria Eradication Programme (GMEP, 1955-1969) with the concept of vectorial capacity, methods for measuring key components of transmission by mosquitoes, and a quantitative theory of vector control. The Ross-Macdonald theory has since played a central role in development of research on mosquito-borne pathogen transmission and the development of strategies for mosquito-borne disease prevention.
C1 [Smith, David L.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Smith, David L.] Johns Hopkins Bloomberg Sch Publ Hlth, Malaria Res Inst, Baltimore, MD USA.
[Smith, David L.; Hay, Simon I.; Barker, Christopher M.; Scott, Thomas W.; McKenzie, F. Ellis] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Battle, Katherine E.; Hay, Simon I.] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford OX1 3PS, England.
[Barker, Christopher M.] Univ Calif Davis, Ctr Vectorborne Dis, Davis, CA 95616 USA.
[Barker, Christopher M.] Univ Calif Davis, Dept Pathol Microbiol & Immunol, Sch Vet Med, Davis, CA 95616 USA.
[Scott, Thomas W.] Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
RP Smith, DL (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
EM dlsmith@jhsph.edu
RI Smith, David/L-8850-2013; Hay, Simon/F-8967-2015;
OI Smith, David/0000-0003-4367-3849; Hay, Simon/0000-0002-0611-7272;
Battle, Katherine/0000-0003-2401-2615
FU NIH/NIAID [U19AI089674]; Bill & Melinda Gates Foundation [49446,
OPP52250]; US Centers for Disease Control and Prevention [5 U01
EH000418]; Wellcome Trust [079091]; Wellcome Trust, UK
FX FEM and DLS began assembling the bibliography at the Fogarty
International Center NIH. DLS acknowledges funding from NIH/NIAID
(U19AI089674) and the Bill & Melinda Gates Foundation (49446). CMB
acknowledges funding from the US Centers for Disease Control and
Prevention (5 U01 EH000418). SIH is funded by a Senior Research
Fellowship from the Wellcome Trust (079091), which also supported KB.
This work forms part of the output of the Malaria Atlas Project (MAP,
http://www.map.ox.ac.uk), principally funded by the Wellcome Trust, UK
(http://www.wellcome.ac.uk). TWS acknowledges funding from the Bill &
Melinda Gates Foundation (OPP52250). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 113
TC 119
Z9 122
U1 4
U2 44
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD APR
PY 2012
VL 8
IS 4
AR e1002588
DI 10.1371/journal.ppat.1002588
PG 13
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 934KY
UT WOS:000303444200003
PM 22496640
ER
PT J
AU Vassena, L
Miao, HY
Cimbro, R
Malnati, MS
Cassina, G
Proschan, MA
Hirsch, VM
Lafont, BA
Morre, M
Fauci, AS
Lusso, P
AF Vassena, Lia
Miao, Huiyi
Cimbro, Raffaello
Malnati, Mauro S.
Cassina, Giulia
Proschan, Michael A.
Hirsch, Vanessa M.
Lafont, Bernard A.
Morre, Michel
Fauci, Anthony S.
Lusso, Paolo
TI Treatment with IL-7 Prevents the Decline of Circulating CD4(+) T Cells
during the Acute Phase of SIV Infection in Rhesus Macaques
SO PLOS PATHOGENS
LA English
DT Article
ID SIMIAN IMMUNODEFICIENCY VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; ACUTE
HIV-1 INFECTION; GASTROINTESTINAL-TRACT; APOPTOSIS INDUCTION;
NONHUMAN-PRIMATES; VIRAL REPLICATION; ANTIVIRAL THERAPY; TYPE-1
INFECTION; LYMPHOID-TISSUE
AB Although treatment with interleukin-7 (IL-7) was shown to transiently expand the naive and memory T-cell pools in patients with chronic HIV-1 infection receiving antiretroviral therapy (ART), it is uncertain whether a full immunologic reconstitution can be achieved. Moreover, the effects of IL-7 have never been evaluated during acute HIV-1 (or SIV) infection, a critical phase of the disease in which the most dramatic depletion of CD4(+) T cells is believed to occur. In the present study, recombinant, fully glycosylated simian IL-7 (50 mu g/kg, s.c., once weekly for 7 weeks) was administered to 6 rhesus macaques throughout the acute phase of infection with a pathogenic SIV strain (mac251); 6 animals were infected at the same time and served as untreated controls. Treatment with IL-7 did not cause clinically detectable side effects and, despite the absence of concomitant ART, did not induce significant increases in the levels of SIV replication except at the earliest time point tested (day 4 post-infection). Strikingly, animals treated with IL-7 were protected from the dramatic decline of circulating naive and memory CD4(+) T-cells that occurred in untreated animals. Treatment with IL-7 induced only transient T-cell proliferation, but it was associated with sustained increase in the expression of the anti-apoptotic protein Bcl-2 on both CD4(+) and CD8(+) T cells, persistent expansion of all circulating CD8(+) T-cell subsets, and development of earlier and stronger SIV Tat-specific T-cell responses. However, the beneficial effects of IL-7 were not sustained after treatment interruption. These data demonstrate that IL-7 administration is effective in protecting the CD4(+) T-cell pool during the acute phase of SIV infection in macaques, providing a rationale for the clinical evaluation of this cytokine in patients with acute HIV-1 infection.
C1 [Vassena, Lia; Miao, Huiyi; Cimbro, Raffaello; Fauci, Anthony S.; Lusso, Paolo] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Vassena, Lia; Malnati, Mauro S.; Cassina, Giulia] DIBIT HSR, Human Virol Unit, Milan, Italy.
[Proschan, Michael A.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Hirsch, Vanessa M.] NIAID, Mol Med Lab, NIH, Bethesda, MD 20892 USA.
[Lafont, Bernard A.] NIAID, Mol Microbiol Lab, NIH, Bethesda, MD 20892 USA.
[Morre, Michel] Cytheris, Issy Les Moulineaux, France.
RP Vassena, L (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM plusso@niaid.nih.gov
RI Lafont, Bernard/B-7236-2014;
OI Cimbro, Raffaello/0000-0002-6251-5160
FU NIAID; NIH
FX This research was supported by the Intramural Research Program of the
NIAID, NIH. The funder had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
NR 45
TC 14
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U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD APR
PY 2012
VL 8
IS 4
AR e1002636
DI 10.1371/journal.ppat.1002636
PG 11
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 934KY
UT WOS:000303444200029
PM 22511868
ER
PT J
AU Klassen, AC
Creswell, J
Clark, VLP
Smith, KC
Meissner, HI
AF Klassen, Ann C.
Creswell, John
Clark, Vicki L. Plano
Smith, Katherine Clegg
Meissner, Helen I.
TI Best practices in mixed methods for quality of life research
SO QUALITY OF LIFE RESEARCH
LA English
DT Editorial Material
ID METHODS DESIGNS
C1 [Klassen, Ann C.] Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19104 USA.
[Creswell, John] John Univ Nebraska, Lincoln, NE USA.
[Clark, Vicki L. Plano] Univ Nebraska, Lincoln, NE USA.
[Smith, Katherine Clegg] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Meissner, Helen I.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
RP Klassen, AC (reprint author), Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19104 USA.
EM ack57@drexel.edu; creswell@unlserve.unl.edu; vpc@unlserve.unl.edu;
kasmith@jhsph.edu; meissneh@mail.nih.gov
NR 15
TC 18
Z9 18
U1 2
U2 22
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-9343
J9 QUAL LIFE RES
JI Qual. Life Res.
PD APR
PY 2012
VL 21
IS 3
BP 377
EP 380
DI 10.1007/s11136-012-0122-x
PG 4
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 933ZB
UT WOS:000303405100002
PM 22311251
ER
PT J
AU Wallen, GR
Baker, K
Stolar, M
Miller-Davis, C
Ames, N
Yates, J
Bolle, J
Pereira, D
St Germain, D
Handel, D
Berger, A
AF Wallen, Gwenyth R.
Baker, Karen
Stolar, Marilyn
Miller-Davis, Claiborne
Ames, Nancy
Yates, Jan
Bolle, Jacques
Pereira, Donna
St Germain, Diane
Handel, Daniel
Berger, Ann
TI Palliative care outcomes in surgical oncology patients with advanced
malignancies: a mixed methods approach
SO QUALITY OF LIFE RESEARCH
LA English
DT Article
DE Cancer malignancies; Palliative care; Pain management; Symptom
management; Mixed methods
ID OF-LIFE MEASURES; SOCIAL SUPPORT; PAIN; INTERVENTION; CHALLENGES;
NEUROPATHY; CANCER; MODELS; TRIAL; SCALE
AB Purpose To prospectively compare outcomes and processes of hospital-based early palliative care with standard care in surgical oncology patients (N = 152).
Methods A randomized, mixed methods, longitudinal study evaluated the effectiveness of a hospital-based Pain and Palliative Care Service (PPCS). Interviews were conducted presurgically and at follow-up visits up to 1 year. Primary outcome measures included the Gracely Pain Intensity and Unpleasantness Scales and the Symptom Distress Scale. Qualitative interviews assessed social support, satisfaction with care, and communication with providers. Survival analysis methods explored factors related to treatment crossover and study discontinuation. Models for repeated measures within subjects over time explored treatment and covariate effects on patient-reported pain and symptom distress.
Results None of the estimated differences achieved statistical significance; however, for those who remained on study for 12 months, the PPCS group performed better than their standard of care counterparts. Patients identified consistent communication, emotional support, and pain and symptom management as positive contributions delivered by the PPCS.
Conclusions It is unclear whether lower pain perceptions despite greater symptom distress were clinically meaningful; however, when coupled with the patients' perceptions of their increased resources and alternatives for pain control, one begins to see the value of an integrated PPCS.
C1 [Wallen, Gwenyth R.; Baker, Karen; Handel, Daniel; Berger, Ann] NIH, Pain & Palliat Care Serv, Ctr Clin, Bethesda, MD 20892 USA.
[Stolar, Marilyn] United BioSource Corp, Lexington, MA 02420 USA.
[Yates, Jan] Shenandoah Univ, Martinsburg, WV 25403 USA.
[Bolle, Jacques] NIH, Ctr Clin, Chevy Chase, MD 20815 USA.
[Pereira, Donna] George Washington Univ Hosp, Palliat Care Dept, Washington, DC 20037 USA.
[St Germain, Diane] NCI, NIH, Bethesda, MD 20892 USA.
RP Wallen, GR (reprint author), NIH, Pain & Palliat Care Serv, Ctr Clin, Bldg 10,Room 2B14,10 Ctr Dr, Bethesda, MD 20892 USA.
EM gwallen@cc.nih.gov
FU Intramural NIH HHS [ZIA CL001136-10]
NR 43
TC 10
Z9 10
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-9343
J9 QUAL LIFE RES
JI Qual. Life Res.
PD APR
PY 2012
VL 21
IS 3
BP 405
EP 415
DI 10.1007/s11136-011-0065-7
PG 11
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 933ZB
UT WOS:000303405100005
PM 22101861
ER
PT J
AU Gershon, RC
Lai, JS
Bode, R
Choi, S
Moy, C
Bleck, T
Miller, D
Peterman, A
Cella, D
AF Gershon, Richard C.
Lai, Jin Shei
Bode, Rita
Choi, Seung
Moy, Claudia
Bleck, Tom
Miller, Deborah
Peterman, Amy
Cella, David
TI Neuro-QOL: quality of life item banks for adults with neurological
disorders: item development and calibrations based upon clinical and
general population testing
SO QUALITY OF LIFE RESEARCH
LA English
DT Article
DE Outcome measures; Quality of life; Neurological disorders; Computerized
adaptive testing; item banking
ID INFORMATION-SYSTEM PROMIS; OUTCOMES MEASUREMENT; PARALLEL ANALYSIS
AB Purpose Neuro-QOL provides a clinically relevant and psychometrically robust health-related quality of life (HRQL) assessment tool for both adults and children with common neurological disorders. We now report the psychometric results for the adult tools.
Methods An extensive research, survey and consensus process was used to produce a list of 5 priority adult neurological conditions (stroke, multiple sclerosis, Parkinson's disease, epilepsy and ALS). We identified relevant health related quality of life (HRQL) domains through multiple methods and data sources including a comprehensive review of the literature and literature search, expert interviews and surveys and patient and caregiver focus groups. The final domain framework consisted of 17 domains of Physical, Mental and Social health. There were five phases of item development: (1) identification of 3,482 extant items, (2) item classification and selection, (3) item review and revision, (4) cognitive interviews with 63 patients to assess their understanding of individual items and (5) field testing of 432 representative items. Participants and Procedures Participants were drawn from the US general population and clinical settings, and included both English and Spanish speaking subjects (N = 3,246). Confirmatory factor analysis (CFA) was used to evaluate the dimensionality of unidimensional domains. Where the domain structure was previously unknown, the dataset was split and first analyzed with exploratory factor analysis and then CFA. Samejima's graded response model (GRM) was used to calculate IRT parameters. We further evaluated differential item functioning (DIF) on gender, education and age.
Results Thirteen unidimensional calibrated item banks consisting of 297 items were developed. All of the tested item banks had high reliability and few or no locally dependent items. The range of item slopes and thresholds with good information are reported for each of the item banks. The banks can support CAT and the development of short forms.
Conclusion The Neuro-QOL measurement system provides item banks and short forms that enable PRO measurement in neurological research, minimizes patient burden and can be used to create multiple instrument types minimizing standard error. The 17 adult measures include 13 calibrated item banks, 3 item pools available for calibration work by others, and 1 stand-alone scale (index). The Neuro-QOL instruments provide a "common metric" of representative concepts for use across patient groups in different studies.
C1 [Gershon, Richard C.; Lai, Jin Shei; Bode, Rita; Choi, Seung; Cella, David] Northwestern Univ, Chicago, IL 60611 USA.
[Moy, Claudia] Natl Inst Neurol Disorders & Stroke, Bethesda, MD USA.
[Bleck, Tom] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Miller, Deborah] Cleveland Clin, Cleveland, OH 44106 USA.
[Peterman, Amy] Univ N Carolina, Charlotte, NC 28223 USA.
RP Gershon, RC (reprint author), Northwestern Univ, Chicago, IL 60611 USA.
EM gershon@northwestern.edu
OI Bleck, Thomas/0000-0002-8267-9787
FU NINDS NIH HHS [N01 NS042360]
NR 22
TC 57
Z9 58
U1 4
U2 23
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0962-9343
J9 QUAL LIFE RES
JI Qual. Life Res.
PD APR
PY 2012
VL 21
IS 3
BP 475
EP 486
DI 10.1007/s11136-011-9958-8
PG 12
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 933ZB
UT WOS:000303405100011
PM 21874314
ER
PT J
AU Gonnord, P
Blouin, CM
Lamaze, C
AF Gonnord, Pauline
Blouin, Cedric M.
Lamaze, Christophe
TI Membrane trafficking and signaling: Two sides of the same coin
SO SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
LA English
DT Review
DE Trafficking; Signaling; Endocytosis; Imaging; Clustering
ID T-CELL-ACTIVATION; CLATHRIN-INDEPENDENT ENDOCYTOSIS; SINGLE-MOLECULE
TRACKING; PLASMA-MEMBRANE; IMMUNOLOGICAL SYNAPSE; LIVING CELLS; MEDIATED
ENDOCYTOSIS; EGF RECEPTOR; DEPENDENT ENDOCYTOSIS; FRET MICROSCOPY
AB Recent findings on clathrin-dependent and non clathrin-dependent endocytic routes are currently changing our classical view of endocytosis. Originally seen as a way for the cell to internalize membrane, receptors or various soluble molecules, this process is in fact directly linked to complex signaling pathways. Here, we review new insights in endocytosis and present latest development in imaging techniques that allow us to visualize and follow the dynamics of membrane-associated signaling events at the plasma membrane and other intracellular compartments. The immune synapse is taken as an illustration of the importance of membrane reorganization and proteins clustering to initiate and maintain signaling. Future challenges include understanding the crosslink between traffic and signaling and how all compartmentalized signals are integrated inside the cell at a higher level. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Lamaze, Christophe] Inst Curie, CNRS, Lab Traf Signalisat & Ciblage Intracellulaires, UMR 144,Ctr Rech, F-75248 Paris, France.
[Gonnord, Pauline] NIAID, Lab Cellular & Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Blouin, Cedric M.; Lamaze, Christophe] CNRS, UMR144, F-75700 Paris, France.
RP Lamaze, C (reprint author), Inst Curie, CNRS, Lab Traf Signalisat & Ciblage Intracellulaires, UMR 144,Ctr Rech, F-75248 Paris, France.
EM christophe.lamaze@curie.fr
OI Blouin, Cedric/0000-0003-0800-0948
NR 119
TC 37
Z9 39
U1 2
U2 32
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1084-9521
J9 SEMIN CELL DEV BIOL
JI Semin. Cell Dev. Biol.
PD APR
PY 2012
VL 23
IS 2
BP 154
EP 164
DI 10.1016/j.semcdb.2011.11.002
PG 11
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 935UP
UT WOS:000303547400004
PM 22085846
ER
PT J
AU Benninghoff, J
van der Ven, A
Schloesser, RJ
Moessner, R
Moller, HJ
Rujescu, D
AF Benninghoff, Jens
van der Ven, Amelie
Schloesser, Robert J.
Moessner, Rainald
Moeller, Hans Juergen
Rujescu, Dan
TI The complex role of the serotonin transporter in adult neurogenesis and
neuroplasticity. A critical review
SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY
LA English
DT Review
DE Serotonin; serotonin transporter; antidepressants; neuroplasticity;
neurogenesis
ID NEURAL STEM-CELLS; IN-VIVO MICRODIALYSIS; KNOCK-OUT MICE; EXTRACELLULAR
SEROTONIN; MAJOR DEPRESSION; HIPPOCAMPAL NEUROGENESIS; DEFICIENT MICE;
BEHAVIORAL-RESPONSES; MONOAMINE-OXIDASE; 5-HT1A RECEPTORS
AB Objectives. Studies on the serotonin transporter (SERT) with regard to neurogenesis and neuroplastic effects on the adult brain are scarce. This is intriguing since neurogenesis is believed to play a decisive role in modulating the effect of selective serotonin reuptake inhibitors (SSRI), which are targeting SERT. Methods. Therefore, we reviewed the current scientific literature about the influence of serotonin on neurogenesis with particular emphasis on SERT in various settings, both in vivo and in vitro. Results. Experiments using SERT KO (knock-out) animal models showed that SERT does not directly or indirectly influence neurogenesis in vitro, whereas compensatory mechanism seem to participate in vivo. Conclusion. At least with regard to adult neural stem cells, the impact of serotonin (5-HT) on neuroplasticity and neurogenesis is not due to SERT-mediated effcts. Instead, serotonergic fine-tuning may be exerted by a number of other different mechanisms including endogenous production of 5-HT in adult neural stem cells, uptake of 5-HT into adult neural stem cells by other monoamine transporters, and actions of the 5-HT1A receptors present on these cells.
C1 [Benninghoff, Jens; van der Ven, Amelie; Moeller, Hans Juergen; Rujescu, Dan] LMU Univ Munich, Dept Psychiat, D-80336 Munich, Germany.
[Schloesser, Robert J.] NIMH, Mol Pathophysiol Lab, Mood & Anxiety Disorders Programme, NIH, Bethesda, MD 20892 USA.
[Moessner, Rainald] Univ Bonn, Dept Psychiat, Bonn, Germany.
RP Benninghoff, J (reprint author), LMU Univ Munich, Dept Psychiat, D-80336 Munich, Germany.
EM jens.benninghoff@med.uni-muenchen.de
NR 73
TC 8
Z9 9
U1 2
U2 25
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1562-2975
J9 WORLD J BIOL PSYCHIA
JI World J. Biol. Psychiatry
PD APR
PY 2012
VL 13
IS 4
BP 240
EP 247
PG 8
WC Psychiatry
SC Psychiatry
GA 933VG
UT WOS:000303391400002
PM 22409535
ER
PT J
AU Canto, AJ
Kiefe, CI
Goldberg, RJ
Rogers, WJ
Peterson, ED
Wenger, NK
Vaccarino, V
Frederick, PD
Sopko, G
Zheng, ZJ
Canto, JG
AF Canto, Andrew J.
Kiefe, Catarina I.
Goldberg, Robert J.
Rogers, William J.
Peterson, Eric D.
Wenger, Nanette K.
Vaccarino, Viola
Frederick, Paul D.
Sopko, George
Zheng, Zhi-Jie
Canto, John G.
CA NRMI Investigators
TI Differences in symptom presentation and hospital mortality according to
type of acute myocardial infarction
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID ACUTE CORONARY SYNDROMES; CHEST-PAIN; REGISTRY
AB Background Chest pain/discomfort (CP) is the hallmark symptom of acute myocardial infarction (MI), but some patients with MI present without CP. We hypothesized that MI type (ST-segment elevation MI [STEMI] or non-STEMI [NSTEMI]) may be associated with the presence or absence of CP.
Methods We investigated the association between CP at presentation and MI type, hospital care, and mortality among 1,143,513 patients with MI in the National Registry of Myocardial Infarction (NRMI) from 1994 to 2006.
Results Overall, 43.6% of patients with NSTEMI and 27.1% of patients with STEMI presented without CP. For both MI type, patients without CP were older, were more frequently female, had more diabetes or history of heart failure, were more likely to delay hospital arrival, and were less likely to receive evidence-based medical therapies and invasive cardiac procedures. Multivariable analysis indicated that NSTEMI (vs STEMI) was the strongest predictor of atypical symptoms (adjusted odds ratio [95% CI], 1.93 [1.91-1.95]). Within the 4 CP/MI type categories, hospital mortality was highest for no CP/STEMI (27.8%), followed by no CP/NSTEMI (15.3%) and CP/STEMI (9.6%), and was lowest for CP/NSTEMI (5.4%). The adjusted odds ratio of mortality was 1.38 (1.35-1.41) for no CP (vs CP) in the STEMI group and 1.31 (1.28-1.34) in the NSTEMI group.
Conclusions Hospitalized patients with NSTEMI were nearly 2-fold more likely to present without CP than patients with STEMI. Patients with MI without CP were less quickly diagnosed and treated and had higher adjusted odds of hospital mortality, regardless of whether they had ST-segment elevation. (Am Heart J 2012; 163:572-9.)
C1 [Canto, John G.] Watson Clin, Lakeland, FL 33805 USA.
[Canto, John G.] Lakeland Reg Med Ctr, Lakeland, FL USA.
[Canto, Andrew J.] Int Baccalaureate Sch, Bartow, FL USA.
[Kiefe, Catarina I.; Goldberg, Robert J.] Univ Massachusetts, Sch Med, Dept Quantitat Hlth Sci, Worcester, MA USA.
[Rogers, William J.] Univ Alabama, Med Ctr, Birmingham, AL 35294 USA.
[Peterson, Eric D.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC USA.
[Wenger, Nanette K.; Vaccarino, Viola] Emory Sch Med, Dept Med, Div Cardiol, San Francisco, CA USA.
[Vaccarino, Viola] Emory Univ, Dept Epidemiol, Rollins Sch Publ Hlth, San Francisco, CA USA.
[Frederick, Paul D.] ICON Late Phase & Outcomes Res, San Francisco, CA USA.
[Sopko, George] NHLBI, Bethesda, MD 20892 USA.
[Zheng, Zhi-Jie] Shanghai Jiao Tong Univ, Sch Publ Hlth, Shanghai 200030, Peoples R China.
RP Canto, JG (reprint author), Watson Clin, 1600 Lakeland Hill Blvd, Lakeland, FL 33805 USA.
EM jcanto@watsonclinic.com
OI Frederick, Paul/0000-0002-7936-5488
FU pharmaceutical industry; Genentech, Inc
FX Paul D. Frederick is an employee of ICON, a contract research
organization that receives research funding from the pharmaceutical
industry. He was paid by Genentech, Inc, to provide biostatistical and
analytic services. George Sopko is an employee of the Health and Human
Services, National Institutes of Health, and National Heart, Lung, and
Blood Institute, and the material presented should not be taken as
representing the viewpoint of these organizations.
NR 9
TC 19
Z9 20
U1 0
U2 7
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD APR
PY 2012
VL 163
IS 4
BP 572
EP 579
DI 10.1016/j.ahj.2012.01.020
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 930AD
UT WOS:000303106800017
PM 22520522
ER
PT J
AU Magnani, JW
Moser, CB
Murabito, JM
Nelson, KP
Fontes, JD
Lubitz, SA
Sullivan, LM
Ellinor, PT
Benjamin, EJ
AF Magnani, Jared W.
Moser, Carlee B.
Murabito, Joanne M.
Nelson, Kerrie P.
Fontes, Joao D.
Lubitz, Steven A.
Sullivan, Lisa M.
Ellinor, Patrick T.
Benjamin, Emelia J.
TI Age of natural menopause and atrial fibrillation: The Framingham Heart
Study
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID C-REACTIVE PROTEIN; CARDIOVASCULAR RISK-FACTORS; POSTMENOPAUSAL WOMEN;
CARDIAC ELECTROPHYSIOLOGY; GENDER-DIFFERENCES; ESTROGEN-RECEPTOR;
DISEASE RISK; MORTALITY; FAILURE; HYPERTENSION
AB Background Early menopausal age is associated with risk of cardiovascular events including myocardial infraction, stroke, and increased mortality. Relations between menopausal age and atrial fibrillation (AF) have not been investigated. We examined the association between menopausal age and AF.
Methods Framingham Heart Study women >= 60 years old without prevalent AF and natural menopause were followed up for 10 years or until incident AF. Menopausal age was modeled as a continuous variable and by categories (<45, 45-53, and >53 years). We used Cox proportional hazards regression to determine associations between menopausal age and AF risk.
Results In 1,809 Framingham women (2,662 person-examinations, mean baseline age 71.4 +/- 7.6 years, menopausal age 49.8 +/- 3.6 years), there were 273 unique participants with incident AF. We did not identify a significant association between the SD of menopausal age (3.6 years) and AF (hazard ratio [HR] per SD 0.94, 95% CI 0.83-1.06; P = .29). In a multivariable model with established risk factors for AF, menopausal age was not associated with incident AF (HR per SD 0.97, 95% CI 0.86-1.09; P = .60). Examining categorical menopausal age, earlier menopausal age (<45 years) was not significantly associated with increased AF risk compared with older menopausal age >53 years (HR 1.20, 95% CI 0.74-1.94; P = .52) or menopausal age 45 to 53 years (HR 1.38, 95% CI 0.93-2.04; P = .11).
Conclusion In our moderate-sized, community-based sample, we did not identify menopausal age as significantly increasing AF risk. However, future larger studies will need to examine whether there is a small effect of menopausal age on AF risk. (Am Heart J 2012;163:729-34.)
C1 [Magnani, Jared W.] Boston Univ, Sch Med, Sect Cardiovasc Med, Dept Med, Boston, MA 02118 USA.
[Magnani, Jared W.; Murabito, Joanne M.; Fontes, Joao D.; Benjamin, Emelia J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Magnani, Jared W.; Murabito, Joanne M.; Fontes, Joao D.; Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Moser, Carlee B.; Nelson, Kerrie P.; Sullivan, Lisa M.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Murabito, Joanne M.] Boston Univ, Gen Internal Med Sect, Dept Med, Boston, MA 02215 USA.
[Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Charlestown, MA USA.
[Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Prevent Med Sect, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
RP Magnani, JW (reprint author), Boston Univ, Sch Med, Sect Cardiovasc Med, Dept Med, 88 E Newton St, Boston, MA 02118 USA.
EM jmagnani@bu.edu
OI Murabito, Joanne/0000-0002-0192-7516; Sullivan,
Lisa/0000-0003-0726-7149; Benjamin, Emelia/0000-0003-4076-2336
FU American Heart Association [09FTF219028]; NIH [HL092577, RO1AG028321,
RC1-HL01056, 1R01HL102214, 5R21DA027021, 1RO1HL104156, 1K24HL105780,
6R01-NS17950, N01-HC25195]; Evans Center for Interdisciplinary
Biomedical Research ARC
FX Dr. Magnani is supported by American Heart Association Award
09FTF219028. This work was supported by grants from the NIH to Drs.
Benjamin and Ellinor (HL092577), Dr. Benjamin (RO1AG028321, RC1-HL01056,
1R01HL102214) and Dr. Ellinor (5R21DA027021, 1RO1HL104156, 1K24HL105780)
and 6R01-NS17950, N01-HC25195. This work was partially supported by the
Evans Center for Interdisciplinary Biomedical Research ARC on "Atrial
Fibrillation at Boston University
(http://www.bumc.bu.edu/evanscenteribr/).
NR 47
TC 4
Z9 4
U1 1
U2 7
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-8703
J9 AM HEART J
JI Am. Heart J.
PD APR
PY 2012
VL 163
IS 4
BP 729
EP 734
DI 10.1016/j.ahj.2012.01.010
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 930AD
UT WOS:000303106800036
PM 22520541
ER
PT J
AU Cashion, AK
Zeimetz, M
AF Cashion, Ann K.
Zeimetz, Marie
TI IOM's Clarion Call for Health Care Transformation: The Role of Nursing
Science
SO BIOLOGICAL RESEARCH FOR NURSING
LA English
DT Editorial Material
C1 [Cashion, Ann K.] Univ Tennessee, Ctr Hlth Sci, Coll Nursing, Memphis, TN 38163 USA.
[Zeimetz, Marie] NINR, NIH, Bethesda, MD 20892 USA.
RP Cashion, AK (reprint author), Univ Tennessee, Ctr Hlth Sci, Coll Nursing, 920 Madison,Suite 507, Memphis, TN 38163 USA.
EM acashion@uthsc.edu
NR 6
TC 1
Z9 1
U1 0
U2 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1099-8004
J9 BIOL RES NURS
JI Biol. Res. Nurs.
PD APR
PY 2012
VL 14
IS 2
BP 113
EP 114
DI 10.1177/1099800412439746
PG 2
WC Nursing
SC Nursing
GA 930HL
UT WOS:000303128200001
PM 22529184
ER
PT J
AU Insel, KC
Merkle, CJ
Hsiao, CP
Vidrine, AN
Montgomery, DW
AF Insel, Kathleen C.
Merkle, Carrie J.
Hsiao, Chao-Pin
Vidrine, Amy N.
Montgomery, David W.
TI Biomarkers for Cognitive Aging Part I: Telomere Length, Blood Pressure
and Cognition Among Individuals with Hypertension
SO BIOLOGICAL RESEARCH FOR NURSING
LA English
DT Article
DE telomere length; biological age; RT-qPCR; cognitive processes; blood
pressure; hypertension
ID OLDER; AGE; MORTALITY; WOMEN; ATHEROSCLEROSIS; ASSOCIATION; DEMENTIA;
DECLINE; DISEASE; STRESS
AB Chronological age is used as a marker for age-associated changes in cognitive function. However, there is great interindividual variability in cognitive ability among people of the same age. Physiological age rather than chronological age should be more closely associated with age-related cognitive changes because these changes are not universal and are likely dependent on several factors in addition to the number of years lived. Cognitive function is associated with successful self-management, and a biological marker that reflects physiological age and is associated with cognitive function could be used to identify risk for failure to self-manage. The purpose of this study was to investigate the association between telomere length, a known biomarker of age; blood pressure; cognitive assessments; and adherence to antihypertensive medication among community-dwelling middle-aged and older adults. The authors administered a battery of cognitive assessments to 42 participants (M = 69 years of age), collected blood samples, and isolated peripheral blood mononuclear leukocytes for genomic DNA. The authors determined relative telomere length using Cawthon's method for real-time quantitative polymerase chain reaction (RT-qPCR) and measured medication adherence using an electronic medication monitoring system (MEMS by Aardex) over 8 weeks. Findings indicate that telomere length was inversely associated with systolic blood pressure (r = -.38, p < .01) and diastolic blood pressure (r = -.42, p < .01) but not with cognitive assessments or adherence. The authors discuss the nonsignificant findings between telomere length and cognitive assessments including the potential modifying role of gender.
C1 [Insel, Kathleen C.; Merkle, Carrie J.; Vidrine, Amy N.; Montgomery, David W.] Univ Arizona, Coll Nursing, Tucson, AZ 85721 USA.
[Hsiao, Chao-Pin] NINR, Symptom Management Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Insel, KC (reprint author), Univ Arizona, Coll Nursing, POB 210203, Tucson, AZ 85721 USA.
EM insel@email.arizona.edu
FU National Institutes of Health [R03 NR010010-01, P20 NR007794]
FX The authors disclosed receipt of the following financial support for the
research and/or authorship of this article: This research was supported
by the National Institutes of Health, R03 NR010010-01 and P20 NR007794.
NR 52
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Z9 8
U1 0
U2 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1099-8004
J9 BIOL RES NURS
JI Biol. Res. Nurs.
PD APR
PY 2012
VL 14
IS 2
BP 124
EP 132
DI 10.1177/1099800411406433
PG 9
WC Nursing
SC Nursing
GA 930HL
UT WOS:000303128200003
PM 21586494
ER
PT J
AU Feng, LZ
Shay, DK
Jiang, Y
Zhou, H
Chen, X
Zheng, YD
Jiang, LL
Zhang, QJ
Lin, H
Wang, SJ
Ying, YY
Xu, YJ
Wang, ND
Feng, ZJ
Viboud, C
Yang, WZ
Yu, HJ
AF Feng, Luzhao
Shay, David K.
Jiang, Yong
Zhou, Hong
Chen, Xin
Zheng, Yingdong
Jiang, Lili
Zhang, Qingjun
Lin, Hong
Wang, Shaojie
Ying, Yanyan
Xu, Yanjun
Wang, Nanda
Feng, Zijian
Viboud, Cecile
Yang, Weizhong
Yu, Hongjie
TI Influenza-associated mortality in temperate and subtropical Chinese
cities, 2003-2008
SO BULLETIN OF THE WORLD HEALTH ORGANIZATION
LA English
DT Article
ID OF-DEATH STATISTICS; SEASONAL INFLUENZA; EXCESS MORTALITY;
UNITED-STATES; TROPICAL SINGAPORE; PNEUMONIA; EPIDEMIC; IMPACT;
HOSPITALIZATION; VACCINATION
AB Objective To estimate influenza-associated mortality in urban China.
Methods Influenza-associated excess mortality for the period 2003-2008 was estimated in three cities in temperate northern China and five cities in the subtropical south of the country. The estimates were derived from models based on negative binomial regressions, vital statistics and the results of weekly influenza virus surveillance.
Findings Annual influenza-associated excess mortality, for all causes, was 18.0 (range: 10.9-32.7) deaths per 100 000 population in the northern cities and 11.3 (range: 7.3-1.7.8) deaths per 100000 in the southern cities. Excess mortality for, respiratory and circulatory disease was 12.4 (range: 7.4-22.2) and 8.8 (range: 5.5-13.6) deaths per 100 000 people in the northern and southern cities, respectively. Most (86%) deaths occurred among people aged 65 years. Influenza-associated excess mortality was higher in B-virus-dominant seasons than in seasons when A(H3N2) or A(H1N1) predominated, and more than half of all influenza-associated mortality was associated with influenza B virus.
Conclusion Between 2003 and 2008, seasonal influenza, particularly that caused by the influenza B virus, was associated with substantial mortality in three cities in the temperate north of China and five cities in the subtropical south of the country:
C1 [Jiang, Yong; Yu, Hongjie] Chinese Ctr Dis Control & Prevent, Natl Ctr Chron & Noncommunicable Dis Control & Pr, Beijing 102206, Peoples R China.
[Shay, David K.; Zhou, Hong] Ctr Dis Control & Prevent, Natl Ctr Immunizat & Resp Dis, Atlanta, GA USA.
[Zheng, Yingdong] Peking Univ, Sch Publ Hlth, Beijing 100871, Peoples R China.
[Jiang, Lili] Shanghai Municipal Ctr Dis Control & Prevent, Shanghai, Peoples R China.
[Zhang, Qingjun] Hubei Prov Ctr Dis Control & Prevent, Wuhan, Peoples R China.
[Lin, Hong] Dalian Ctr Dis Control & Prevent, Dalian, Peoples R China.
[Wang, Shaojie] Qingdao Ctr Dis Control & Prevent, Qingdao, Peoples R China.
[Ying, Yanyan] Ningbo Ctr Dis Control & Prevent, Ningbo, Zhejiang, Peoples R China.
[Xu, Yanjun] Guangdong Prov Ctr Dis Control & Prevent, Guangzhou, Guangdong, Peoples R China.
[Wang, Nanda] Zhaoyuan Ctr Dis Control & Prevent, Yantai, Peoples R China.
[Viboud, Cecile] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Yu, HJ (reprint author), Chinese Ctr Dis Control & Prevent, Natl Ctr Chron & Noncommunicable Dis Control & Pr, 155 Changbai Rd, Beijing 102206, Peoples R China.
EM yuhj@chinacdc.cn
FU China-US Collaborative Program on Emerging and Re-emerging Infectious
Diseases
FX This study was supported by the China-US Collaborative Program on
Emerging and Re-emerging Infectious Diseases.
NR 34
TC 41
Z9 50
U1 1
U2 8
PU WORLD HEALTH ORGANIZATION
PI GENEVA 27
PA MARKETING AND DISSEMINATION, CH-1211 GENEVA 27, SWITZERLAND
SN 0042-9686
J9 B WORLD HEALTH ORGAN
JI Bull. World Health Organ.
PD APR
PY 2012
VL 90
IS 4
BP 279
EP 288
DI 10.2471/BLT.11.096958
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 932EL
UT WOS:000303273100018
PM 22511824
ER
PT J
AU Gudmundsson, LS
Scher, AI
AF Gudmundsson, Larus S.
Scher, Ann I.
TI High migraine prevalence in Parma: Why?
SO CEPHALALGIA
LA English
DT Editorial Material
ID SOCIOECONOMIC-STATUS; UNITED-STATES; HEADACHE; POPULATION;
CLASSIFICATION; RISK; AURA; MORTALITY; CRITERIA; BURDEN
C1 [Gudmundsson, Larus S.; Scher, Ann I.] Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, Bethesda, MD 20814 USA.
[Gudmundsson, Larus S.; Scher, Ann I.] NIA, Lab Epidemiol Demog & Biometry, NIH, Bethesda, MD 20892 USA.
RP Gudmundsson, LS (reprint author), Uniformed Serv Univ Hlth Sci, Dept Prevent Med & Biometr, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM larus.gudmundsson@usuhs.edu
NR 34
TC 2
Z9 2
U1 0
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0333-1024
J9 CEPHALALGIA
JI Cephalalgia
PD APR
PY 2012
VL 32
IS 5
BP 355
EP 357
DI 10.1177/0333102412439799
PG 3
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 929LQ
UT WOS:000303065700001
PM 22436372
ER
PT J
AU Klotz, L
Chetner, M
Chin, J
Finelli, T
Fleshner, N
Fradet, Y
Goldenberg, L
Nickel, JC
Siemens, R
So, A
Sugar, L
Zlotta, A
Klein, E
Parnes, H
Penson, D
AF Klotz, Laurence
Chetner, Michael
Chin, Joseph
Finelli, Tony
Fleshner, Neil
Fradet, Yves
Goldenberg, Larry
Nickel, J. Curtis
Siemens, Robert
So, Alan
Sugar, Linda
Zlotta, Alexandre
Klein, Eric
Parnes, Howard
Penson, David
TI Canadian Consensus Conference: The FDA decision on the use of 5ARIs
SO CUAJ-CANADIAN UROLOGICAL ASSOCIATION JOURNAL
LA English
DT Article
ID PROSTATE-CANCER PREVENTION; TRIAL; DUTASTERIDE; ANTIGEN; MEN
C1 [Klotz, Laurence; Zlotta, Alexandre] Univ Toronto, Sunnybrook Hlth Sci Ctr, Dept Urol, Toronto, ON M4N 3M5, Canada.
[Chetner, Michael] Univ Alberta Hosp, Div Urol, Edmonton, AB T6G 2B7, Canada.
[Chin, Joseph] Western Univ, Div Urol Surg, London, ON, Canada.
[Finelli, Tony] Princess Margaret Hosp, Div Urol Minimally Invas Surg, Dept Surg Oncol, Toronto, ON M4X 1K9, Canada.
[Fleshner, Neil] Univ Hlth Network, Div Urol, Toronto, ON, Canada.
[Fradet, Yves] Univ Laval, Dept Urol, Quebec City, PQ, Canada.
[Goldenberg, Larry; So, Alan] Univ British Columbia, Dept Urol Sci, Vancouver, BC, Canada.
[Nickel, J. Curtis; Siemens, Robert] Queens Univ, Dept Urol, Kingston, ON, Canada.
[Sugar, Linda] Sunnybrook Hlth Sci Ctr, Dept Pathol, Toronto, ON M4N 3M5, Canada.
[Klein, Eric] Glickman Urol & Kidney Inst, Cleveland, OH USA.
[Parnes, Howard] NCI, Prostate & Urol Canc Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
[Penson, David] Vanderbilt Univ, Med Ctr, Div Urol, Nashville, TN USA.
RP Klotz, L (reprint author), Univ Toronto, Sunnybrook Hlth Sci Ctr, Dept Urol, 2075 Bayview Ave,Room MG 204, Toronto, ON M4N 3M5, Canada.
EM laurence.klotz@sunnybrook.ca
RI Zlotta, Alexandre/K-8285-2015
NR 11
TC 3
Z9 3
U1 0
U2 1
PU CANADIAN UROLOGICAL ASSOCIATION
PI DORVAL
PA 185 DORVAL AVENUE, STE 401, DORVAL, QC H9S 5J9, CANADA
SN 1911-6470
J9 CUAJ-CAN UROL ASSOC
JI CUAJ-Can. Urol. Assoc. J.
PD APR
PY 2012
VL 6
IS 2
BP 83
EP 88
DI 10.5489/cuaj.12058
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 932LE
UT WOS:000303291800003
PM 22511412
ER
PT J
AU Xiong, YM
Bosselut, R
AF Xiong, Yumei
Bosselut, Remy
TI CD4-CD8 differentiation in the thymus: connecting circuits and building
memories
SO CURRENT OPINION IN IMMUNOLOGY
LA English
DT Review
ID T-CELL LINEAGE; DOUBLE-POSITIVE THYMOCYTES; HELPER TYPE-1 CELLS;
TRANSCRIPTION FACTORS; GENE-EXPRESSION; CD4 EXPRESSION;
CYTOTOXIC-LINEAGE; RUNX PROTEINS; NKT CELLS; THPOK
AB The proper choice of the CD4-helper or CD8-cytotoxic lineages by developing T cells is crucial for the generation of an antigen-responsive and functionally fit T cell repertoire. Here we present a brief overview of the transcr ptional control of this process, with emphasis on two issues. The study of Cd4 expression, that had previously generated important paradigms for transcriptional regulation in eukaryotic cells, now brings new twists to the concept of 'epigenetic memory'. And connections are emerging between transcriptional regulators critical for commitment to either lineage. The present review attempts to integrate these findings and d scusses the still elusive mechanisms that match CD4-CD8 lineage differentiation to MHC specificity.
C1 [Xiong, Yumei; Bosselut, Remy] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Bosselut, R (reprint author), NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM remy@helix.nih.gov
FU National Cancer Institute, Center for Cancer Research
FX We thank A. Gegonne, P. Love and M. Vacchio for reading the manuscript
and apologize to colleagues whose work could not be discussed because of
space limitations. Research work in the authors' laboratory is supported
by the Intramural Research Program or the National Cancer Institute,
Center for Cancer Research.
NR 61
TC 17
Z9 18
U1 1
U2 6
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0952-7915
J9 CURR OPIN IMMUNOL
JI Curr. Opin. Immunol.
PD APR
PY 2012
VL 24
IS 2
BP 139
EP 145
DI 10.1016/j.coi.2012.02.002
PG 7
WC Immunology
SC Immunology
GA 931AY
UT WOS:000303187600003
PM 22387323
ER
PT J
AU Aggarwal, M
Brosh, RM
AF Aggarwal, Monika
Brosh, Robert M., Jr.
TI Functional analyses of human DNA repair proteins important for aging and
genomic stability using yeast genetics
SO DNA REPAIR
LA English
DT Review
DE Aging; DNA repair; Yeast; Genetics; Genomic stability
ID BASE EXCISION-REPAIR; NONPOLYPOSIS COLORECTAL-CANCER; HEMATOPOIETIC
STEM-CELLS; CHRONOLOGICAL LIFE-SPAN; WERNER-SYNDROME PROTEIN;
SACCHAROMYCES-CEREVISIAE; MISMATCH REPAIR; FLAP ENDONUCLEASE-1; RECQ
HELICASES; P53 MUTANTS
AB Model systems have been extremely useful for studying various theories of aging. Studies of yeast have been particularly helpful to explore the molecular mechanisms and pathways that affect aging at the cellular level in the simple eukaryote. Although genetic analysis has been useful to interrogate the aging process, there has been both interest and debate over how functionally conserved the mechanisms of aging are between yeast and higher eukaryotes, especially mammalian cells. One area of interest has been the importance of genomic stability for age-related processes, and the potential conservation of proteins and pathways between yeast and human. Translational genetics have been employed to examine the functional roles of mammalian proteins using yeast as a pliable model system. In the current review recent advancements made in this area are discussed, highlighting work which shows that the cellular functions of human proteins in DNA repair and maintenance of genomic stability can be elucidated by genetic rescue experiments performed in yeast. Published by Elsevier B.V.
C1 [Aggarwal, Monika; Brosh, Robert M., Jr.] NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Brosh, RM (reprint author), NIA, Lab Mol Gerontol, NIH, NIH Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM broshr@mail.nih.gov
FU NIH, National Institute on Aging
FX This work was supported by the Intramural Research program of the NIH,
National Institute on Aging. We wish to thank Dr. Avvaru Suhasini and
Dr. Jian Lu, Laboratory of Molecular Gerontology, NIA-NIH for critical
reading of the manuscript.
NR 163
TC 3
Z9 3
U1 2
U2 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD APR 1
PY 2012
VL 11
IS 4
BP 335
EP 348
DI 10.1016/j.dnarep.2012.01.013
PG 14
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 929XS
UT WOS:000303099600002
PM 22349084
ER
PT J
AU Hanssen-Bauer, A
Solvang-Garten, K
Gilljam, KM
Torseth, K
Wilson, DM
Akbari, M
Otterlei, M
AF Hanssen-Bauer, Audun
Solvang-Garten, Karin
Gilljam, Karin Margaretha
Torseth, Kathrin
Wilson, David M., III
Akbari, Mansour
Otterlei, Marit
TI The region of XRCC1 which harbours the three most common nonsynonymous
polymorphic variants, is essential for the scaffolding function of XRCC1
SO DNA REPAIR
LA English
DT Article
DE XRCC1 Arg194Trp; XRCC1 Arg280His; XRCC1 Arg399GIn; DNA repair complexes;
Micro-irradiation
ID STRAND-BREAK REPAIR; DNA-LIGASE-III; BASE EXCISION-REPAIR;
SISTER-CHROMATID EXCHANGE; POLYMERASE-BETA; CANCER RISK;
POLY(ADP-RIBOSE) POLYMERASE; PROTEIN; DAMAGE; REPLICATION
AB XRCC1 functions as a non-enzymatic, scaffold protein in single strand break repair (SSBR) and base excision repair (BER). Here, we examine different regions of XRCC1 for their contribution to the scaffolding functions of the protein. We found that the central BRCT1 domain is essential for recruitment of XRCC1 to sites of DNA damage and DNA replication. Also, we found that ectopic expression of the region from residue 166-436 partially rescued the methyl methanesulfonate (MMS) hypersensitivity of XRCC1-deficient EM9 cells, suggesting a key role for this region in mediating DNA repair. The three most common amino acid variants of XRCC1, Argl 94Trp, Arg280His and Arg399G1n, are located within the region comprising the NLS and BRCT1 domains, and these variants may be associated with increased incidence of specific types of cancer. While we could not detect differences in the intra-nuclear localization or the ability to support recruitment of POL beta or PNKP to micro-irradiated sites for these variants relative to the conservative protein, we did observe lower foci intensity after micro-irradiation and a reduced stability of the foci with the Arg280His and Arg399GIn variants, respectively. Furthermore, when challenged with MMS or hydrogen peroxide, we detected small but consistent differences in the repair profiles of cells expressing these two variants in comparison to the conservative protein. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Hanssen-Bauer, Audun; Solvang-Garten, Karin; Gilljam, Karin Margaretha; Torseth, Kathrin; Akbari, Mansour; Otterlei, Marit] Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, Fac Med, N-7006 Trondheim, Norway.
[Wilson, David M., III] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
RP Otterlei, M (reprint author), Norwegian Univ Sci & Technol, Dept Canc Res & Mol Med, Fac Med, NO-7489 Trondheim, Norway.
EM marit.otterlei@ntnu.no
OI Akbari, Mansour/0000-0002-6490-7766
FU St. Olavs Hospital, Trondheim, Norway; Liaison Committee; Norwegian
Research Council; Norwegian Cancer Society; NIH, National Institute on
Aging, USA
FX We would like to thank Nina-Beate Liabakk for technical assistance. This
work is supported by The Cancer Fund at St. Olavs Hospital, Trondheim,
Norway, The Liaison Committee between the Central Norway Regional Health
Authority (RHA) and the Norwegian University of Science and Technology
(NTNU), Norway, The Norwegian Research Council program FUGE, The
Norwegian Cancer Society, and the Intramural Research Program of the
NIH, National Institute on Aging, USA.
NR 50
TC 13
Z9 13
U1 0
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD APR 1
PY 2012
VL 11
IS 4
BP 357
EP 366
DI 10.1016/j.dnarep.2012.01.001
PG 10
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 929XS
UT WOS:000303099600004
PM 22281126
ER
PT J
AU Karata, K
Vaisman, A
Goodman, MF
Woodgate, R
AF Karata, Kiyonobu
Vaisman, Alexandra
Goodman, Myron F.
Woodgate, Roger
TI Simple and efficient purification of Escherichia coli DNA polymerase V:
Cofactor requirements for optimal activity and processivity in vitro
SO DNA REPAIR
LA English
DT Article
DE UmuC; UmuD '; SOS mutagenesis; Y-family DNA polymerase; Mutagenesis;
Translesion DNA synthesis
ID SINGLE-STRANDED-DNA; MEDIATED TRANSLESION SYNTHESIS; UV-MUTAGENESIS;
RECA PROTEIN; POL V; PROOFREADING FUNCTION; CYCLOBUTANE DIMER; SOS
MUTAGENESIS; GROE MUTANTS; BETA-CLAMP
AB Most damage induced mutagenesis in Escherichia coli is dependent upon the UmuD'C-2 protein complex, which comprises DNA polymerase V (pol V). Biochemical characterization of pol V has been hindered by the fact that the enzyme is notoriously difficult to purify, largely because overproduced UmuC is insoluble. Here, we report a simple and efficient protocol for the rapid purification of milligram quantities of pol V from just 4 L of bacterial culture. Rather than over producing the UmuC protein, it was expressed at low basal levels, while UmuD'(2) was expressed in trans from a high copy-number plasmid with an inducible promoter. We have also developed strategies to purify the beta-clamp and gamma-clamp loader free from contaminating polymerases. Using these highly purified proteins, we determined the cofactor requirements for optimal activity of pol V in vitro and found that pol V shows robust activity on an SSB-coated circular DNA template in the presence of the beta/gamma-complex and a RecA nucleoprotein filament (RecA*) formed in trans. This strong activity was attributed to the unexpectedly high processivity of pol V Mut (UmuD'C-2 . RecA . ATP), which was efficiently recruited to a primer terminus by SSB. Published by Elsevier B.V.
C1 [Karata, Kiyonobu; Vaisman, Alexandra; 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 Woodgate, R (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 Institutes of Health/National Institute of Child Health and
Human Development; National Institutes of Health [GM21422, ESO12259];
Japan Society for the Promotion of Science
FX We thank Toshifumi Tomoyasu for providing us pBB280 and Charles McHenry
for plasmids pTGCP.1.7 and pSJS9. This work was supported in part, by
funds from the National Institutes of Health/National Institute of Child
Health and Human Development Intramural Research Program to RW and
National Institutes of Health [GM21422, ESO12259] to MFG. K.K. was also
a recipient of a research fellowship from the Japan Society for the
Promotion of Science.
NR 48
TC 17
Z9 17
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
EI 1568-7856
J9 DNA REPAIR
JI DNA Repair
PD APR 1
PY 2012
VL 11
IS 4
BP 431
EP 440
DI 10.1016/j.dnarep.2012.01.012
PG 10
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 929XS
UT WOS:000303099600012
PM 22341652
ER
PT J
AU Izawa, K
Hijikata, A
Tanaka, N
Kawai, T
Saito, MK
Goldbach-Mansky, R
Aksentijevich, I
Yasumi, T
Nakahata, T
Heike, T
Nishikomori, R
Ohara, O
AF Izawa, Kazushi
Hijikata, Atsushi
Tanaka, Naoko
Kawai, Tomoki
Saito, Megumu K.
Goldbach-Mansky, Raphaela
Aksentijevich, Ivona
Yasumi, Takahiro
Nakahata, Tatsutoshi
Heike, Toshio
Nishikomori, Ryuta
Ohara, Osamu
TI Detection of Base Substitution-Type Somatic Mosaicism of the NLRP3 Gene
with > 99.9% Statistical Confidence by Massively Parallel Sequencing
SO DNA RESEARCH
LA English
DT Article
DE next generation sequencing; mosaicism; DNA diagnosis; chronic infantile
neurological cutaneous and articular syndrome
ID MULTISYSTEM INFLAMMATORY DISEASE; ARTICULAR SYNDROME; CIAS1 MUTATIONS;
GENOME; DEATH; CELLS
AB Chronic infantile neurological cutaneous and articular syndrome (CINCA), also known as neonatal-onset multisystem inflammatory disease (NOMID), is a dominantly inherited systemic autoinflammatory disease and is caused by a heterozygous germline gain-of-function mutation in the NLRP3 gene. We recently found a high incidence of NLRP3 somatic mosaicism in apparently mutation-negative CINCA/NOMID patients using subcloning and subsequent capillary DNA sequencing. It is important to rapidly diagnose somatic NLRP3 mosaicism to ensure proper treatment. However, this approach requires large investments of time, cost, and labour that prevent routine genetic diagnosis of low-level somatic NLRP3 mosaicism. We developed a routine pipeline to detect even a low-level allele of NLRP3 with statistical significance using massively parallel DNA sequencing. To address the critical concern of discriminating a low-level allele from sequencing errors, we first constructed error rate maps of 14 polymerase chain reaction products covering the entire coding NLRP3 exons on a Roche 454 GS-FLX sequencer from 50 control samples without mosaicism. Based on these results, we formulated a statistical confidence value for each sequence variation in each strand to discriminate sequencing errors from real genetic variation even in a low-level allele, and thereby detected base substitutions at an allele frequency as low as 1% with 99.9% or higher confidence.
C1 [Izawa, Kazushi; Tanaka, Naoko; Kawai, Tomoki; Yasumi, Takahiro; Heike, Toshio; Nishikomori, Ryuta] Kyoto Univ, Dept Pediat, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan.
[Hijikata, Atsushi; Ohara, Osamu] RIKEN Yokohama Inst, RIKEN Res Ctr Allergy & Immunol, Lab Immunogenom, Tarumi Ku, Yokohama, Kanagawa 2300045, Japan.
[Saito, Megumu K.; Nakahata, Tatsutoshi] Kyoto Univ, Ctr iPS Cell Res & Applicat CiRA, Clin Applicat Dept, Kyoto, Japan.
[Goldbach-Mansky, Raphaela] NIAMS, Translat Autoinflammatory Dis Sect, NIH, Bethesda, MD USA.
[Aksentijevich, Ivona] NHGRI, Bethesda, MD 20892 USA.
[Ohara, Osamu] Kazusa DNA Res Inst, Dept Human Genome Res, Kisarazu, Chiba 2920818, Japan.
RP Nishikomori, R (reprint author), Kyoto Univ, Dept Pediat, Grad Sch Med, Sakyo Ku, 54 Shogoin, Kyoto 6068507, Japan.
EM rnishiko@kuhp.kyoto-u.ac.jp; ohara@kazusa.or.jp
RI Ohara, Osamu/G-5448-2015
OI Ohara, Osamu/0000-0002-3328-9571
FU Japanese Ministry of Education, Science, Sports, and Culture; Japanese
Ministry of Health, Labor, and Welfare
FX This study was supported by the Japanese Ministry of Education, Science,
Sports, and Culture, and the Japanese Ministry of Health, Labor, and
Welfare.
NR 28
TC 17
Z9 17
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1340-2838
J9 DNA RES
JI DNA Res.
PD APR
PY 2012
VL 19
IS 2
BP 143
EP 152
DI 10.1093/dnares/dsr047
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 932KN
UT WOS:000303290100004
PM 22279087
ER
PT J
AU Sun, HM
Tawa, G
Wallqvist, A
AF Sun, Hongmao
Tawa, Gregory
Wallqvist, Anders
TI Classification of scaffold-hopping approaches
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID CAMBRIDGE STRUCTURAL DATABASE; ANGIOTENSIN-II; RECEPTOR ANTAGONISTS;
BIOLOGICAL-ACTIVITIES; DRUG DISCOVERY; COMBINATORIAL LIBRARIES;
SIMILARITY SEARCHES; MEDICINAL CHEMISTRY; KINASE INHIBITORS;
CRYSTAL-STRUCTURE
AB The general goal of drug discovery is to identify novel compounds that are active against a preselected biological target with acceptable pharmacological properties defined by marketed drugs. Scaffold hopping has been widely applied by medicinal chemists to discover equipotent compounds with novel backbones that have improved properties. In this article we classify scaffold hopping into four major categories, namely heterocycle replacements, ring opening or closure, peptidomimetics and topology-based hopping. We review the structural diversity of original and final scaffolds with respect to each category. We discuss the advantages and limitations of small, medium and large-step scaffold hopping. Finally, we summarize software that is frequently used to facilitate different kinds of scaffold-hopping methods.
C1 [Sun, Hongmao; Tawa, Gregory; Wallqvist, Anders] US Army Med Res & Mat Command, Biotechnol HPC Software Applicat Inst, Telemed & Adv Technol Res Ctr, Frederick, MD 21702 USA.
RP Sun, HM (reprint author), NIH, NIH Ctr Translat Therapeut, 9800 Med Ctr Dr, Bethesda, MD 20892 USA.
EM hongmao.sun@nih.gov
OI wallqvist, anders/0000-0002-9775-7469
FU U.S. Department of Defense Threat Reduction Agency [TMTI0004_09_BH_T];
Department of Defense Biotechnology High Performance Computing Software
Applications Institute
FX Funding of this research was provided by the U.S. Department of Defense
Threat Reduction Agency Grant TMTI0004_09_BH_T and the Department of
Defense Biotechnology High Performance Computing Software Applications
Institute. The opinions or assertions contained herein are the private
views of the authors and are not to be construed as official or as
reflecting the views of the U.S. Army or of the U.S. Department of
Defense.
NR 120
TC 65
Z9 65
U1 5
U2 44
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD APR
PY 2012
VL 17
IS 7-8
BP 310
EP 324
DI 10.1016/j.drudis.2011.10.024
PG 15
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 929XV
UT WOS:000303099900006
PM 22056715
ER
PT J
AU Fishman, P
Bar-Yehuda, S
Liang, BT
Jacobson, KA
AF Fishman, Pnina
Bar-Yehuda, Sara
Liang, Bruce T.
Jacobson, Kenneth A.
TI Pharmacological and therapeutic effects of A(3) adenosine receptor
agonists
SO DRUG DISCOVERY TODAY
LA English
DT Review
ID NF-KAPPA-B; TUMOR-GROWTH INHIBITION; COLON-CARCINOMA GROWTH;
RHEUMATOID-ARTHRITIS; IB-MECA; BIOCHEMICAL-CHARACTERIZATION;
MYOCARDIAL-ISCHEMIA; REPERFUSION INJURY; ENDOTOXEMIC MICE;
CANCER-THERAPY
AB The A(3) adenosine receptor (A(3)AR) coupled to G(i) (inhibitory regulative guanine nucleotide-binding protein) mediates anti-inflammatory, anticancer and anti-ischemic protective effects. The receptor is overexpressed in inflammatory and cancer cells, while low expression is found in normal cells, rendering the A(3)AR as a potential therapeutic target. Highly selective A(3)AR agonists have been synthesized and molecular recognition in the binding site has been characterized. In this article, we summarize preclinical and clinical human studies that demonstrate that A(3)AR agonists induce specific antiinflammatory and anticancer effects through a molecular mechanism that entails modulation of the Wnt and the NF-kappa B signal transduction pathways. At present, A(3)AR agonists are being developed for the treatment of inflammatory diseases, including rheumatoid arthritis (RA) and psoriasis; ophthalmic diseases such as dry eye syndrome and glaucoma; liver diseases such as hepatocellular carcinoma and hepatitis.
C1 [Jacobson, Kenneth A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Fishman, Pnina; Bar-Yehuda, Sara] Can Fite BioPharma Ltd, Kiryat Matalon, IL-49170 Petah Tiqwa, Israel.
[Liang, Bruce T.] Univ Connecticut, Pat & Jim Calhoun Cardiol Ctr, Ctr Hlth, Farmington, CT 06030 USA.
RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bldg 8A,Rm B1A-19, Bethesda, MD 20892 USA.
EM kajacobs@helix.nih.gov
RI Ji, Haofeng/G-6206-2012; Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU Intramural NIH HHS [ZIA DK031117-24]
NR 77
TC 73
Z9 74
U1 3
U2 19
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1359-6446
J9 DRUG DISCOV TODAY
JI Drug Discov. Today
PD APR
PY 2012
VL 17
IS 7-8
BP 359
EP 366
DI 10.1016/j.drudis.2011.10.007
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 929XV
UT WOS:000303099900011
PM 22033198
ER
PT J
AU Iyer, MR
Lee, YS
Deschamps, JR
Dersch, CM
Rothman, RB
Jacobson, AE
Rice, KC
AF Iyer, Malliga R.
Lee, Yong Sok
Deschamps, Jeffrey R.
Dersch, Christina M.
Rothman, Richard B.
Jacobson, Arthur E.
Rice, Kenner C.
TI Probes for narcotic receptor mediated phenomena. 44. Synthesis of an
N-substituted 4-hydroxy-5-(3-hydroxyphenyl)morphan with high affinity
and selective mu-antagonist activity
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Osmium tetroxide mediated oxidation; Opioid receptor affinity; Opioid
receptor efficacy;
5-(3-Hydroxyphenyl)-2-phenethyl-2-azabicyclo[3.3.1]nonan-4-ol synthesis;
Energy minimization for molecular overlay; X-ray crystallographic
structure
ID AGONIST; 5-(3-HYDROXYPHENYL)-N-PHENYLETHYLMORPHAN; DERIVATIVES; MORPHINE
AB A simple three-step synthesis of 5-(3-hydroxyphenyl)-2-methyl-2-azabicyclo[3.3.1]nonan-4-ol (3a) was achieved using an osmium tetroxide mediated oxidation of the known intermediate 6. A pyrrolidine-ring variant of 3a (3-(7-(hydroxymethyl)-6-methyl-6-azabicyclo[3.2.1]octan-1-yl)phenol (5)) was isolated when other routes were used. The epimeric hydroxy analogue 4a was synthesized by simple inversion of the stereochemistry at C-4. Both N-methyl (3a and 4a) and N-phenethyl (3b and 4b) derivatives were synthesized. The compounds were examined for their opioid receptor affinity and the N-phenethyl analogue 3b was found to have relatively weak affinity for the mu-opioid receptor (K-i = 74 nM). However, the N-phenethyl analogue of the C-4 epimer, 4b, had about 15 fold higher affinity than 3b and was selective for the mu-opioid receptor (K-i = 4.6 nM). Compound 4b was a moderately potent mu-opioid antagonist (K-e = 12 nM), as determined by [S-35]GTP-gamma-S assays. Compounds 3b and 4b were energy minimized at the level of B3LYP/6-31G*, and then overlaid onto the 5-phenylmorphan, the (1R,5R,9S)-(-)-enantiomer of 2b (Fig. 1) with the alpha or beta-OH group at the C-9 position. The spatial orientation of the hydroxyl moiety in 3b, 4b, 2a, and 2b is proposed to be the structural requirement for high p-opioid receptor binding affinity and their agonist or antagonist activity. The modest change in spatial position of the hydroxyl moiety, and not the N-substituent, induced the change from potent agonist to an antagonist of moderate potency. Published by Elsevier Masson SAS.
C1 [Iyer, Malliga R.; Jacobson, Arthur E.; Rice, Kenner C.] NIDA, Drug Design & Synth Sect, Chem Biol Res Branch, Bethesda, MD 20892 USA.
[Iyer, Malliga R.; Jacobson, Arthur E.; Rice, Kenner C.] NIAAA, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Lee, Yong Sok] NIH, Ctr Mol Modeling, Div Computat Biosci, CIT,DHHS, Bethesda, MD 20892 USA.
[Deschamps, Jeffrey R.] USN, Res Lab, Ctr Biomol Sci & Engn, Washington, DC 20375 USA.
[Dersch, Christina M.; Rothman, Richard B.] NIDA, Clin Psychopharmacol Sect, Chem Biol Res Branch, Addict Res Ctr,NIH,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
RP Rice, KC (reprint author), NIDA, Drug Design & Synth Sect, Chem Biol Res Branch, 5625 Fishers Lane,Room 4N03, Bethesda, MD 20892 USA.
EM kr21f@nih.gov
OI Deschamps, Jeffrey/0000-0001-5845-0010
FU NIH of the National Institute on Drug Abuse (NIDA); National Institute
of Alcohol Abuse and Alcoholism; NIH through the Center for Information
Technology; NIDA through Naval Research Laboratory (NRL) [Y1-DA1101]
FX The work of the Drug Design and Synthesis Section, CBRB, NIDA, & NIAAA,
was supported by the NIH Intramural Research Programs of the National
Institute on Drug Abuse (NIDA) and the National Institute of Alcohol
Abuse and Alcoholism. The Clinical Psychopharmacology Section, CBRB,
NIDA, was supported by the NIH Intramural Research Program of the
National Institute on Drug Abuse (NIDA). We also thank Dr. Klaus
Gawrisch and Dr. Walter Teague (Laboratory of Membrane Biochemistry and
Biophysics. NIAAA, for NMR spectral data. The authors also express their
thanks to Noel Whittaker and Dr. Herman Yeh, Laboratory of Analytical
Chemistry, NIDDK, for mass spectral data and 1H NMR spectral
data. The quantum chemical study utilized PC/LINUX clusters at the
Center for Molecular Modeling of the NIH (http://cit.nih.gov), and this
research was supported by the NIH Intramural Research Program through
the Center for Information Technology. The X-ray crystallographic work
was supported by NIDA through an Interagency Agreement #Y1-DA1101 with
the Naval Research Laboratory (NRL).
NR 13
TC 5
Z9 5
U1 0
U2 5
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0223-5234
J9 EUR J MED CHEM
JI Eur. J. Med. Chem.
PD APR
PY 2012
VL 50
BP 44
EP 54
DI 10.1016/j.ejmech.2012.01.025
PG 11
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 932IP
UT WOS:000303284400006
PM 22341895
ER
PT J
AU Villalba, JM
de Cabo, R
Alcain, FJ
AF Villalba, Jose M.
de Cabo, Rafael
Alcain, Francisco J.
TI A patent review of sirtuin activators: an update
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Review
DE aging; metabolic diseases; resveratrol; sirtuin activators; sirtuins
ID SMALL-MOLECULE ACTIVATORS; NICOTINAMIDE ADENINE-DINUCLEOTIDE; CALORIE
RESTRICTION; LIFE-SPAN; HISTONE DEACETYLASE; GENE-EXPRESSION;
SACCHAROMYCES-CEREVISIAE; MODIFIED RESVERATROL; MAMMALIAN-CELLS;
SKELETAL-MUSCLE
AB Introduction: Reversible acetylation is a key post-translational modification of target proteins. Sirtuin deacetylases represent the homolog of the yeast silent information regulator (SIR2). Although seven sirtuins have been found in mammals, all sirtuin activators described to date act through SIRT1.
Areas covered: Areas covered in this paper include a review of the patent literature associated with SIRT1 activators, with a focus on therapeutic applications, primarily related to the use of pharmaceuticals and nutraceuticals containing resveratrol (RSV), and the development of second-generation activators unrelated to RSV. Also discussed is the current controversy over whether or not these molecules are actual SIRT1 activators.
Expert opinion: Developing effective strategies to protect against diet-induced metabolic imbalance is necessary to fight against current obesity rates. The hypothalamus is a candidate for developing drugs that suppress SIRT1 degradation, as a strategy for treating metabolic syndrome. Deciphering the basic mechanism of activators is essential to develop effective strategies to alter sirtuin activity. This is true regardless of the apparent controversy of whether in vitro activation of SIRT1 is direct or not, depending on the experimental design, and whether sirtuins may play a major role in longevity. The numerous studies on their positive effects against age-related diseases, obesity and other metabolic disorders are still valid, promising to positively influence the development of treatments to improve human health.
C1 [Alcain, Francisco J.] Univ Castilla La Mancha, Dept Ciencias Med, Fac Med, E-13071 Ciudad Real, Spain.
[Villalba, Jose M.] Univ Cordoba, Fac Ciencias, Dept Biol Celular Fisiol & Inmunol, Cordoba 14014, Spain.
[de Cabo, Rafael] NIA, NIH, Lab Expt Gerontol, Baltimore, MD 21224 USA.
RP Alcain, FJ (reprint author), Univ Castilla La Mancha, Dept Ciencias Med, Fac Med, Campus Ciudad Real, E-13071 Ciudad Real, Spain.
EM franciscoj.alcain@uclm.es
RI de Cabo, Rafael/J-5230-2016; Alcain, Francisco /N-7503-2016;
OI de Cabo, Rafael/0000-0002-3354-2442; Alcain, Francisco
/0000-0002-6833-7940; , rafael/0000-0003-2830-5693
FU Universidad de Castilla la Mancha [GE20112221]; Junta de Comunidades de
Castilla la Mancha [PPII11-0318-2669]; NIH [1R01AG028125-01A1];
Ministerio de Ciencia e Innovacion [BFU2011-23578]; Junta de Andalucia
Proyectos de Excelencia [P09-CVI-4887]; Junta de Andalucia Proyectos
Internacionales; Junta de Andalucia and University of Cordoba [BIO-276];
NIH/NIA
FX Authors' work is supported by Grants: Universidad de Castilla la Mancha
GE20112221, Junta de Comunidades de Castilla la Mancha PPII11-0318-2669
to Dr FJ Alcain and NIH 1R01AG028125-01A1, Ministerio de Ciencia e
Innovacion BFU2011-23578, Junta de Andalucia Proyectos de Excelencia
P09-CVI-4887, Junta de Andalucia Proyectos Internacionales and BIO-276
(Junta de Andalucia and University of Cordoba) to JM Villalba. Funding
to R de Cabo was provided by the NIH/NIA Intramural Research Program.
Rafael de Cabo has a cooperative research and development agreement with
Sirtris/GSK.
NR 98
TC 14
Z9 14
U1 0
U2 27
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1354-3776
J9 EXPERT OPIN THER PAT
JI Expert Opin. Ther. Patents
PD APR
PY 2012
VL 22
IS 4
BP 355
EP 367
DI 10.1517/13543776.2012.669374
PG 13
WC Chemistry, Medicinal; Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 921DK
UT WOS:000302458000002
PM 22475539
ER
PT J
AU Wang, WX
Corrigan-Cummins, M
Hudson, J
Maric, I
Simakova, O
Neelapu, SS
Kwak, LW
Janik, JE
Gause, B
Jaffe, ES
Calvo, KR
AF Wang, Weixin
Corrigan-Cummins, Meghan
Hudson, Justin
Maric, Irina
Simakova, Olga
Neelapu, Sattva S.
Kwak, Larry W.
Janik, John E.
Gause, Barry
Jaffe, Elaine S.
Calvo, Katherine R.
TI MicroRNA profiling of follicular lymphoma identifies microRNAs related
to cell proliferation and tumor response
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Article
DE follicular lymphoma; miRNA; lymphomagenesis; tumor response
ID GENE-EXPRESSION; DNA-DAMAGE; B-LYMPHOCYTES; TRANSLOCATION T(14/18);
MALIGNANT-LYMPHOMA; CROSS-TALK; IN-VIVO; DIFFERENTIATION; ACTIVATION;
TARGET
AB Background
MicroRNAs can play an important role in tumorigenesis through post-transcriptional regulation of gene expression, and are not well characterized in follicular lymphoma.
Design and Methods
MicroRNA profiles of enriched follicular lymphoma tumor cells from 16 patients were generated by assaying 851 human microRNAs. Tandem gene expression profiles were obtained for predicting microRNA targets.
Results
The expression of 133 microRNAs was significantly different (> 2-fold; P<0.05) between follicular lymphoma and follicular hyperplasia. Forty-four microRNAs in three groups generated a unique follicular lymphoma signature. Of these, ten microRNAs were increased (miR-193a-5p, -193b*, -345, -513b, -574-3p, -584, -663, -1287, -1295, and -1471), 11 microRNAs were decreased (miR-17*, -30a, -33a, -106a*, -141, -202, -205, -222, -301b, -431*, and -570), and 23 microRNAs formed a group that was increased in most cases of follicular lymphoma but showed lower expression in a subset of cases (let-7a, let-7f, miR-7-1*, -9, -9*, -20a, -20b, -30b, -96, -98, -194, -195, -221*, -374a, -374b, -451, -454, -502-3p, -532-3p, -664*, -1274a, -1274b, and -1260). Higher expression of this last group was associated with improved response to chemotherapy. Gene expression analysis revealed increased expression of MAPK1, AKT1, PRKCE, IL4R and DROSHA and decreased expression of CDKN1A/p21, SOCS2, CHEK1, RAD51, KLF4, BLIMP1 and IRF4 in follicular lymphoma. Functional studies indicated that CDKN1A/p21 and SOCS2 expression is directly regulated by miR-20a/-20b and miR-194, respectively.
Conclusions
Follicular lymphoma is characterized by a unique microRNA signature, containing a subset of microRNAs whose expression correlate with response to chemotherapy. miR-20a/b and miR-194 target CDKN1A and SOCS2 in follicular lymphoma, potentially contributing to tumor cell proliferation and survival.
C1 [Wang, Weixin; Corrigan-Cummins, Meghan; Maric, Irina; Simakova, Olga; Calvo, Katherine R.] NIH, Dept Lab Med, Hematol Sect, Ctr Clin, Bethesda, MD 20892 USA.
[Hudson, Justin] Howard Univ, Coll Med, Washington, DC USA.
[Neelapu, Sattva S.; Kwak, Larry W.] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Lymphoma & Myeloma, Houston, TX 77030 USA.
[Janik, John E.] NCI, Metab Branch, Bethesda, MD 20892 USA.
[Gause, Barry] NCI, SAIC, Frederick, MD 21701 USA.
[Jaffe, Elaine S.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RP Calvo, KR (reprint author), NIH, Dept Lab Med, Hematol Sect, Ctr Clin, 10 Ctr Dr,Bldg 10-2C306, Bethesda, MD 20892 USA.
EM calvok@mail.nih.gov
RI Calvo, Katherine/A-8109-2009;
OI Calvo, Katherine/0000-0002-0771-4191; Jaffe, Elaine/0000-0003-4632-0301
FU NIH Clinical Center; Center for Cancer Research, NCI
FX this work was supported by the Intramural Research Program of the NIH
Clinical Center and the Center for Cancer Research, NCI.
NR 52
TC 43
Z9 44
U1 0
U2 11
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD APR
PY 2012
VL 97
IS 4
BP 586
EP 594
DI 10.3324/haematol.2011.048132
PG 9
WC Hematology
SC Hematology
GA 931TG
UT WOS:000303241600021
PM 22102710
ER
PT J
AU Calvo, KR
Hickstein, DD
Holland, SM
AF Calvo, Katherine R.
Hickstein, Dennis D.
Holland, Steven M.
TI MonoMAC and GATA2 deficiency: overlapping clinical and pathological
features with aplastic anemia and idiopathic CD4+ lymphocytopenia. Reply
to Haematologica. 2012;97(4):058669
SO HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
LA English
DT Letter
DE MonoMac; GATA2; deficiency; diagnosis; aplastic anemia; ICL
ID ACUTE MYELOID-LEUKEMIA; SPORADIC MONOCYTOPENIA; AUTOSOMAL-DOMINANT;
PRIMARY LYMPHEDEMA; EMBERGER SYNDROME; MUTATIONS; MYELODYSPLASIA; CELL
C1 [Calvo, Katherine R.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Hickstein, Dennis D.] NCI, Bethesda, MD 20892 USA.
[Holland, Steven M.] NIAID, Bethesda, MD 20892 USA.
RP Calvo, KR (reprint author), NIH, Dept Lab Med, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
EM calvok@mail.nih.gov
RI Calvo, Katherine/A-8109-2009
NR 13
TC 2
Z9 2
U1 0
U2 1
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOL-HEMATOL J
JI Haematol-Hematol. J.
PD APR
PY 2012
VL 97
IS 4
BP E12
EP E13
DI 10.3324/haematol.2012.063396
PG 2
WC Hematology
SC Hematology
GA 931TG
UT WOS:000303241600002
ER
PT J
AU Adams, DK
Nowakowski, NM
Angerer, LA
AF Adams, D. K.
Nowakowski, N. M.
Angerer, L. A.
TI Evolution of food-induced developmental plasticity in echinoids
SO INTEGRATIVE AND COMPARATIVE BIOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Integrative-and-Comparative-Biology
(SICB)
CY JAN 03-07, 2012
CL Charleston, SC
SP Soc Integrat & Comparat Biol (SICB)
C1 NIH, Bethesda, MD 20892 USA.
American Univ, Washington, DC 20016 USA.
EM adamsdi@mail.nih.gov
RI Adams, Diane/E-7831-2015
OI Adams, Diane/0000-0001-6638-5781
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 1540-7063
J9 INTEGR COMP BIOL
JI Integr. Comp. Biol.
PD APR
PY 2012
VL 52
SU 1
BP E202
EP E202
PG 1
WC Zoology
SC Zoology
GA 930TV
UT WOS:000303165001273
ER
PT J
AU Adams, DK
Sewell, MA
Nowakowski, NM
Angerer, LM
AF Adams, D. K.
Sewell, M. A.
Nowakowski, N. M.
Angerer, L. M.
TI Mechanism underlying developmental plasticity in echinoid larval form
SO INTEGRATIVE AND COMPARATIVE BIOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Integrative-and-Comparative-Biology
(SICB)
CY JAN 03-07, 2012
CL Charleston, SC
SP Soc Integrat & Comparat Biol (SICB)
C1 NIH, Bethesda, MD 20892 USA.
Univ Auckland, Auckland 1, New Zealand.
American Univ, Washington, DC 20016 USA.
EM adamsdi@mail.nih.gov
RI Adams, Diane/E-7831-2015
OI Adams, Diane/0000-0001-6638-5781
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 1540-7063
J9 INTEGR COMP BIOL
JI Integr. Comp. Biol.
PD APR
PY 2012
VL 52
SU 1
BP E1
EP E1
PG 1
WC Zoology
SC Zoology
GA 930TV
UT WOS:000303165000005
ER
PT J
AU Browne, WE
Schnitzler, CE
Gildea, D
Nguyen, AD
Maxwell, E
Ryan, JF
Baxevanis, AD
AF Browne, W. E.
Schnitzler, C. E.
Gildea, D.
Nguyen, A-D
Maxwell, E.
Ryan, J. F.
Baxevanis, A. D.
TI The Early Embryo: Genomic analysis of gene expression in an early
diverging lineage of metazoans, the Ctenophora
SO INTEGRATIVE AND COMPARATIVE BIOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Integrative-and-Comparative-Biology
(SICB)
CY JAN 03-07, 2012
CL Charleston, SC
SP Soc Integrat & Comparat Biol (SICB)
C1 [Browne, W. E.; Schnitzler, C. E.; Gildea, D.; Nguyen, A-D; Maxwell, E.; Ryan, J. F.; Baxevanis, A. D.] Univ Miami, NHGRI, NIH, Coral Gables, FL 33124 USA.
EM wbrowne@bio.miami.edu
RI Schnitzler, Christine/G-8733-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1540-7063
J9 INTEGR COMP BIOL
JI Integr. Comp. Biol.
PD APR
PY 2012
VL 52
SU 1
BP E21
EP E21
PG 1
WC Zoology
SC Zoology
GA 930TV
UT WOS:000303165000083
ER
PT J
AU Haspel, G
Schwartz, A
Soares, D
AF Haspel, G.
Schwartz, A.
Soares, D.
TI Unique mechanosensory adaptation to extreme environments in cavefish
SO INTEGRATIVE AND COMPARATIVE BIOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Integrative-and-Comparative-Biology
(SICB)
CY JAN 03-07, 2012
CL Charleston, SC
SP Soc Integrat & Comparat Biol (SICB)
C1 [Haspel, G.; Schwartz, A.; Soares, D.] Univ Maryland, NINDS, College Pk, MD 20742 USA.
EM daphne.soares@gmail.com
NR 0
TC 0
Z9 0
U1 0
U2 6
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1540-7063
J9 INTEGR COMP BIOL
JI Integr. Comp. Biol.
PD APR
PY 2012
VL 52
SU 1
BP E259
EP E259
PG 1
WC Zoology
SC Zoology
GA 930TV
UT WOS:000303165001501
ER
PT J
AU Ryan, JF
Pang, K
Schnitzler, CE
Nguyen, AD
Moreland, RT
Havlak, P
Putnam, NH
Nisc
Wolfsberg, TG
Mullikin, JC
Martindale, MQ
Baxevanis, AD
AF Ryan, J. F.
Pang, K.
Schnitzler, C. E.
Nguyen, A-D
Moreland, R. T.
Havlak, P.
Putnam, N. H.
Nisc
Wolfsberg, T. G.
Mullikin, J. C.
Martindale, M. Q.
Baxevanis, A. D.
TI The Genome of the Ctenophore, Mnemiopsis leidyi: Insights into the
Origins of Morphological Complexity
SO INTEGRATIVE AND COMPARATIVE BIOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the Society-for-Integrative-and-Comparative-Biology
(SICB)
CY JAN 03-07, 2012
CL Charleston, SC
SP Soc Integrat & Comparat Biol (SICB)
C1 NHGRI, NIH, Bethesda, MD 20892 USA.
Univ Hawaii, Honolulu, HI 96822 USA.
Rice Univ, Houston, TX 77251 USA.
EM andy@mail.nih.gov
RI Schnitzler, Christine/G-8733-2013
NR 0
TC 0
Z9 0
U1 0
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1540-7063
J9 INTEGR COMP BIOL
JI Integr. Comp. Biol.
PD APR
PY 2012
VL 52
SU 1
BP E150
EP E150
PG 1
WC Zoology
SC Zoology
GA 930TV
UT WOS:000303165001068
ER
PT J
AU Grespan, R
Lemos, HP
Carregaro, V
Verri, WA
Souto, FO
de Oliveira, CJF
Teixeira, C
Ribeiro, JM
Valenzuela, JG
Cunha, FQ
AF Grespan, Renata
Lemos, Henrique P.
Carregaro, Vanessa
Verri, Waldiceu A., Jr.
Souto, Fabricio O.
de Oliveira, Carlo J. F.
Teixeira, Clarissa
Ribeiro, Jose Marcos
Valenzuela, Jesus G.
Cunha, Fernando Q.
TI The protein LJM 111 from Lutzomyia longipalpis Salivary Gland Extract
(SGE) accounts for the SGE-inhibitory effects upon inflammatory
parameters in experimental arthritis model
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE LJM 111 protein; Salivary gland extract; Arthritis; Chemotaxis
ID TUMOR-NECROSIS-FACTOR; COLLAGEN-INDUCED ARTHRITIS; ANTIGEN-INDUCED
ARTHRITIS; SAND FLY SALIVA; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS;
COUPLED RECEPTOR KINASES; NF-KAPPA-B; DENDRITIC CELLS;
RHEUMATOID-ARTHRITIS; FACTOR-ALPHA
AB Several studies have pointed out the immunomodulatory properties of the Salivary Gland Extract (SGE) from Lutzomyia longipalpis. We aimed to identify the SGE component (s) responsible for its effect on ovalbumin (OVA)-induced neutrophil migration (NM) and to evaluate the effect of SGE and components in the antigen-induced arthritis (AIA) model. We tested the anti-arthritic activities of SGE and the recombinant LJM111 salivary protein (rLJM111) by measuring the mechanical hypernociception and the NM into synovial cavity. Furthermore, we measured IL-17, TNF-alpha and IFN-gamma released by lymph nodes cells stimulated with mBSA or anti-CD3 using enzyme-linked immunosorbent assay (ELISA). Additionally, we tested the effect of SGE and rLJM111 on co-stimulatory molecules expression (MHC-II and CD-86) by flow cytometry. TNF-alpha and IL-10 production (ELISA) of bone marrow-derived dendritic cells (BMDCs) stimulated with LPS, chemotaxis and actin polymerization from neutrophils. Besides, the effect of SGE on CXCR2 and GRK-2 expression on neutrophils was investigated. We identified one plasmid expressing the protein LJM111 that prevented NM in OVA-challenged immunized mice. Furthermore, both SGE and rLJM111 inhibited NM and pain sensitivity in AIA and reduced IL-17, TNF-alpha and IFN-gamma. SGE and rLJM111 also reduced MHC-II and CD-86 expression and TNF-alpha whereas increased IL-10 release by LPS-stimulated BMDCs. SGE, but not LJM 111, inhibited neutrophils chemotaxis and actin polymerization. Additionally, SGE reduced neutrophil CXCR2 expression and increased GRK-2. Thus, rLJM111 is partially responsible for SGE mechanisms by diminishing DC function and maturation but not chemoattraction of neutrophils. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Grespan, Renata; Lemos, Henrique P.; Verri, Waldiceu A., Jr.; Cunha, Fernando Q.] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Pharmacol, Ribeirao Preto, SP, Brazil.
[Carregaro, Vanessa; Souto, Fabricio O.; de Oliveira, Carlo J. F.] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Immunol & Biochem, Ribeirao Preto, SP, Brazil.
[Verri, Waldiceu A., Jr.] Univ Estadual Londrina, Ctr Biol Sci, Dept Pathol, Londrina, PR, Brazil.
[Teixeira, Clarissa; Ribeiro, Jose Marcos; Valenzuela, Jesus G.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
RP Grespan, R (reprint author), Univ Sao Paulo, Dept Pharmacol, Fac Med Ribeirao Preto, Ave Bandeirantes 3900, BR-14049900 Sao Paulo, Brazil.
EM r_grespan@yahoo.com.br
RI Carregaro, Vanessa/D-2913-2012; Souto, Fabricio/I-3071-2013; Ribeiro,
Jose/J-7011-2015; Verri, Waldiceu/I-1330-2013; Cunha,
Fernando/M-3090-2014;
OI Souto, Fabricio/0000-0002-2392-8499; Verri,
Waldiceu/0000-0003-2756-9283; Cunha, Fernando
Queiroz/0000-0003-4755-1670; Ribeiro, Jose/0000-0002-9107-0818
FU Intramural NIH HHS [ZIA AI000932-09]
NR 68
TC 6
Z9 6
U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD APR
PY 2012
VL 12
IS 4
BP 603
EP 610
DI 10.1016/j.intimp.2012.02.004
PG 8
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA 930MP
UT WOS:000303143800009
PM 22366405
ER
PT J
AU Dale, W
Mohile, SG
Eldadah, BA
Trimble, EL
Schilsky, RL
Cohen, HJ
Muss, HB
Schmader, KE
Ferrell, B
Extermann, M
Nayfield, SG
Hurria, A
AF Dale, William
Mohile, Supriya G.
Eldadah, Basil A.
Trimble, Edward L.
Schilsky, Richard L.
Cohen, Harvey J.
Muss, Hyman B.
Schmader, Kenneth E.
Ferrell, Betty
Extermann, Martine
Nayfield, Susan G.
Hurria, Arti
CA Canc & Aging Res Grp
TI Biological, Clinical, and Psychosocial Correlates at the Interface of
Cancer and Aging Research
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID COMPREHENSIVE GERIATRIC ASSESSMENT; ACUTE MYELOID-LEUKEMIA;
QUALITY-OF-LIFE; OLDER-ADULTS; BREAST-CANCER; PROSTATE-CANCER;
UNITED-STATES; ADJUVANT CHEMOTHERAPY; CELLULAR SENESCENCE; PERFORMANCE
STATUS
AB In September 2010, the Cancer and Aging Research Group, in collaboration with the National Cancer Institute and the National Institute on Aging, conducted the first of three planned conferences to discuss research methodology to generate the highest quality research in older adults with cancer and then disseminate these findings among those working in the fields of cancer and aging. Conference speakers discussed the current level of research evidence in geriatric oncology, outlined the current knowledge gaps, and put forth principles for research designs and strategies that would address these gaps within the next 10 years. It was agreed that future oncology research trials that enroll older adults should include: 1) improved standardized geriatric assessment of older oncology patients, 2) substantially enhanced biological assessment of older oncology patients, 3) specific trials for the most vulnerable and/or those older than 75 years, and 4) research infrastructure that specifically targets older adults and substantially strengthened geriatrics and oncology research collaborations. This initial conference laid the foundation for the next two meetings, which will address the research designs and collaborations needed to enhance therapeutic and intervention trials in older adults with cancer.
C1 [Hurria, Arti] City Hope Natl Med Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA.
[Dale, William] Univ Chicago, Dept Med, Sect Geriatr & Palliat Med, Chicago, IL 60637 USA.
[Schilsky, Richard L.] Univ Chicago, Sect Hematol Oncol, Chicago, IL 60637 USA.
[Mohile, Supriya G.] Univ Rochester, James P Wilmot Canc Ctr, Dept Med Hematol Oncol, Rochester, NY USA.
[Eldadah, Basil A.] NIA, Div Geriatr & Clin Gerontol, Bethesda, MD 20892 USA.
[Trimble, Edward L.] NCI, Ctr Global Hlth, Bethesda, MD 20892 USA.
[Nayfield, Susan G.] Univ Florida, Dept Aging & Geriatr Res, Gainesville, FL USA.
[Cohen, Harvey J.] Duke Univ, Ctr Study Aging & Human Dev, Durham, NC USA.
[Schmader, Kenneth E.] Duke Univ, Dept Geriatr Med, Durham, NC USA.
[Muss, Hyman B.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
[Muss, Hyman B.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Ferrell, Betty] Durham Vet Affairs Med, Geriatr Res Educ Ctr, Durham, NC USA.
[Ferrell, Betty] Durham Vet Affairs Med, Clin Ctr, Durham, NC USA.
[Extermann, Martine] Univ S Florida, H Lee Moffitt Canc Ctr, Senior Adult Oncol Program, Tampa, FL 33682 USA.
RP Hurria, A (reprint author), City Hope Natl Med Ctr, Dept Med Oncol & Therapeut Res, Duarte, CA 91010 USA.
EM ahurria@coh.org
FU NCATS NIH HHS [UL1 TR000064]; NCI NIH HHS [7U10-CA31946-29]; NCRR NIH
HHS [KL2 RR024136]; NIA NIH HHS [R01 AG037037, U13 AG038151]
NR 57
TC 31
Z9 31
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD APR
PY 2012
VL 104
IS 8
BP 581
EP 589
DI 10.1093/jnci/djs145
PG 9
WC Oncology
SC Oncology
GA 930TE
UT WOS:000303162400008
PM 22457474
ER
PT J
AU Schlom, J
AF Schlom, Jeffrey
TI Therapeutic Cancer Vaccines: Current Status and Moving Forward
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Review
ID COLONY-STIMULATING FACTOR; CELL LUNG-CANCER; RESISTANT PROSTATE-CANCER;
LONG-TERM SURVIVAL; REGULATORY T-CELLS; CYCLOOXYGENASE-2 INHIBITOR
CELECOXIB; METASTATIC COLORECTAL-CANCER; TUMOR-ASSOCIATED ANTIGENS;
CHRONIC VIRAL-INFECTION; HIGH-DOSE INTERLEUKIN-2
AB Concurrent with US Food and Drug Administration (FDA) approval of the first therapeutic cancer vaccine, a wide spectrum of other cancer vaccine platforms that target a diverse range of tumor-associated antigens is currently being evaluated in randomized phase II and phase III trials. The profound influence of the tumor microenvironment and other immunosuppressive entities, however, can limit the effectiveness of these vaccines. Numerous strategies are currently being evaluated both preclinically and clinically to counteract these immunosuppressive entities, including the combined use of vaccines with immune checkpoint inhibitors, certain chemotherapeutics, small-molecule targeted therapies, and radiation. The potential influence of the appropriate patient population and clinical trial endpoint in vaccine therapy studies is discussed, as well as the potential importance of biomarkers in future directions of this field.
C1 NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Schlom, J (reprint author), NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, 10 Ctr Dr,Rm 8B09, Bethesda, MD 20892 USA.
EM js141c@nih.gov
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health
FX This study was supported by the Intramural Research Program of the
Center for Cancer Research, National Cancer Institute, National
Institutes of Health.
NR 208
TC 124
Z9 129
U1 4
U2 46
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD APR
PY 2012
VL 104
IS 8
BP 599
EP 613
DI 10.1093/jnci/djs033
PG 15
WC Oncology
SC Oncology
GA 930TE
UT WOS:000303162400010
PM 22395641
ER
PT J
AU Kane, JM
Hill, LD
Kinon, BJ
Potter, WZ
Rapaport, MH
Schooler, NR
AF Kane, John M.
Hill, Lauren D.
Kinon, Bruce J.
Potter, William Z.
Rapaport, Mark H.
Schooler, Nina R.
TI New Clinical Drug Evaluation Unit (NCDEU) Annual Meeting: A Great
Opportunity for Early Career Psychiatrists
SO JOURNAL OF CLINICAL PSYCHIATRY
LA English
DT Editorial Material
C1 [Kane, John M.] Zucker Hillside Hosp, Glen Oaks, NY 11004 USA.
[Kane, John M.] Hofstra N Shore LIJ Sch Med, Glen Oaks, NY USA.
[Hill, Lauren D.] NIMH, Div Serv & Intervent Res, Bethesda, MD 20892 USA.
[Kinon, Bruce J.] Eli Lilly & Co, Indianapolis, IN 46285 USA.
[Rapaport, Mark H.] Emory Univ, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA.
[Schooler, Nina R.] Georgetown Univ, Dept Psychiat, Washington, DC USA.
[Schooler, Nina R.] Vet Affairs Capitol Hlth Care Network, Mental Illness Res Educ & Clin Ctr, Washington, DC USA.
RP Kane, JM (reprint author), Zucker Hillside Hosp, 75-59 263rd St,Kaufmann Bldg,Ste 103, Glen Oaks, NY 11004 USA.
EM psychiatry@nshs.edu
NR 0
TC 0
Z9 0
U1 0
U2 0
PU PHYSICIANS POSTGRADUATE PRESS
PI MEMPHIS
PA P O BOX 752870, MEMPHIS, TN 38175-2870 USA
SN 0160-6689
J9 J CLIN PSYCHIAT
JI J. Clin. Psychiatry
PD APR
PY 2012
VL 73
IS 4
BP 504
EP 505
DI 10.4088/JCP.12com07750
PG 2
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA 932PU
UT WOS:000303303800016
PM 22579149
ER
PT J
AU Matos, A
Duque, V
Luxo, C
Melico-Silvestre, A
Major, EO
AF Matos, Ana
Duque, Vitor
Luxo, Cristina
Melico-Silvestre, Antonio
Major, Eugene O.
TI Individuals infected with JC polyomavirus do not present detectable JC
virus DNA in oropharyngeal fluids
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; EPSTEIN-BARR-VIRUS;
BK-VIRUS; CYTOMEGALOVIRUS-INFECTION; HUMAN-POPULATIONS; HEALTHY-ADULTS;
URBAN SEWAGE; TRANSMISSION; EXCRETION; PREVALENCE
AB JC virus (JCV) is ubiquitous in the human population. Primary infection normally occurs during childhood and is followed by a lifelong persistent infection. The main mode of transmission remains unknown. Several authors have hypothesized that JCV transmission occurs through the respiratory route, and that respiratory secretions could represent a possible source of viral particles. The present study intended to evaluate oropharyngeal fluids from patients infected with JCV, in order to ascertain if respiratory secretions could indeed constitute a source of exposure to this polyomavirus. Oropharyngeal washing samples from 25 patients co-infected with JCV and human immunodeficiency virus type 1 were evaluated for the presence of JCV DNA. Regardless of the titre of antibodies or the presence of viral urinary excretion, JCV genome was not detected in oropharyngeal samples collected from any of the patients infected with JCV included in this study, which may suggest that oropharyngeal fluids are an unlikely source for JCV infection.
C1 [Matos, Ana; Luxo, Cristina] Univ Coimbra, Ctr Pharmaceut Studies, Fac Pharm, Coimbra, Portugal.
[Duque, Vitor; Melico-Silvestre, Antonio] Coimbras Univ Hosp, Virol Lab, Dept Infect Dis, Coimbra, Portugal.
[Major, Eugene O.] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
RP Matos, A (reprint author), Univ Coimbra, Ctr Pharmaceut Studies, Fac Pharm, Coimbra, Portugal.
EM anamatos@ci.uc.pt
OI Matos, Ana Miguel/0000-0001-5764-0023; Luxo Maia, Paula
Cristina/0000-0002-4676-5258
FU Center for Pharmaceutical Studies of the Portuguese Foundation for
Science and Technology through POCTI (FEDER)
FX The authors are grateful to the Center for Pharmaceutical Studies of the
Portuguese Foundation for Science and Technology through POCTI (FEDER)
for financial support.
NR 45
TC 3
Z9 3
U1 2
U2 5
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
EI 1465-2099
J9 J GEN VIROL
JI J. Gen. Virol.
PD APR
PY 2012
VL 93
BP 692
EP 697
DI 10.1099/vir.0.036798-0
PN 4
PG 6
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 929OF
UT WOS:000303074500002
PM 22158878
ER
PT J
AU Brooke, CB
Schafer, A
Matsushima, GK
White, LJ
Johnston, RE
AF Brooke, Christopher B.
Schaefer, Alexandra
Matsushima, Glenn K.
White, Laura J.
Johnston, Robert E.
TI Early activation of the host complement system is required to restrict
central nervous system invasion and limit neuropathology during
Venezuelan equine encephalitis virus infection
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID WEST-NILE-VIRUS; INDUCED DISEASE; SINDBIS VIRUS; HUMORAL RESPONSES;
DENDRITIC CELLS; CDNA-CLONE; IN-VITRO; RECEPTOR; CLEARANCE; PATHOGENESIS
AB Venezuelan equine encephalitis virus (VEEV) is a mosquito-borne RNA virus of the genus Alpha virus, family Togaviridae, that is responsible for sporadic outbreaks in human and equid populations in Central and South America. In order to ascertain the role that complement plays in resolving VEEV-induced disease, complement-deficient C3(-/-) were infected with a VEEV mutant (V3533) that caused mild, transient disease in immunocompetent mice. In the absence of a functional complement system, peripheral inoculation with V3533 induced much more severe encephalitis. This enhanced pathology was associated with a delay in clearance of infectious virus from the serum and more rapid invasion of the central nervous system in C3(-/-) mice. If V3533 was inoculated directly into the brain, however, disease outcome in C3(-/-) and wild-type mice was identical. These findings indicate that complement-dependent enhancement of peripheral virus clearance is critical for protecting against the development of severe VEEV-induced encephalitis.
C1 [Brooke, Christopher B.; Schaefer, Alexandra; Matsushima, Glenn K.; White, Laura J.; Johnston, Robert E.] Univ N Carolina, Dept Microbiol & Immunol, Chapel Hill, NC 27599 USA.
[Brooke, Christopher B.; Schaefer, Alexandra; White, Laura J.; Johnston, Robert E.] Univ N Carolina, Carolina Vaccine Inst, Chapel Hill, NC 27599 USA.
[Matsushima, Glenn K.] Univ N Carolina, UNC Neurosci Ctr, Chapel Hill, NC 27599 USA.
RP Brooke, CB (reprint author), NIAID, Cell Biol Sect, Viral Dis Lab, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM brookecb@niaid.nih.gov
FU NIH [U01AI070976, 5T32AI007419]
FX This research was supported by NIH research grant U01AI070976. C. B. B.
was supported by NIH training grant 5T32AI007419. We thank members of
the Carolina Vaccine Institute for helpful discussions. We also thank
Janice Weaver at the LCCC/DLAM University of North Carolina at Chapel
Hill histopathology core facility.
NR 58
TC 3
Z9 3
U1 0
U2 2
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
J9 J GEN VIROL
JI J. Gen. Virol.
PD APR
PY 2012
VL 93
BP 797
EP 806
DI 10.1099/vir.0.038281-0
PN 4
PG 10
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 929OF
UT WOS:000303074500014
PM 22205717
ER
PT J
AU Lam, TTY
Zhu, HC
Smith, DK
Guan, Y
Holmes, EC
Pybus, OG
AF Lam, Tommy Tsan-Yuk
Zhu, Huachen
Smith, David K.
Guan, Yi
Holmes, Edward C.
Pybus, Oliver G.
TI The recombinant origin of emerging human norovirus GII.4/2008:
intra-genotypic exchange of the capsid P2 domain
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID ACUTE GASTROENTERITIS; VARIANT; EMERGENCE; CHILDREN; VIRUS; KOREA;
ALGORITHM; EVOLUTION; STRAINS; SEASONS
AB GII.4 noroviruses are a major cause of acute gastroenteritis in humans. A new variant of GII.4, the 2008 variant, has recently increased its prevalence on a global scale. A previous study of this variant in Japan suggested that it might be of recombinant origin, with a breakpoint at the ORF1-ORF2 junction. Here, examination of the evolutionary origin of the 2008 variant based on a larger sample of worldwide GII.4 norovirus sequences revealed a more complex pattern of recombination between the 2006a- and 2006b-like variants of genotype GII.4, involving the P2 antigenic domain. Double (termed '2008i' and triple (termed '2008ii') recombinant forms of 2008 variants were identified. This study highlights the possible importance of intra-genotypic recombination over antigenic regions in driving norovirus evolution, and is suggestive of a process analogous to the antigenic shift of influenza A virus by reassortment.
C1 [Lam, Tommy Tsan-Yuk; Pybus, Oliver G.] Univ Oxford, Dept Zool, Oxford OX1 3PS, England.
[Lam, Tommy Tsan-Yuk; Zhu, Huachen; Smith, David K.; Guan, Yi] Shantou Univ Med Coll, Int Inst Infect & Immun, Shantou, Guangdong, Peoples R China.
[Lam, Tommy Tsan-Yuk; Zhu, Huachen; Smith, David K.; Guan, Yi] Univ Hong Kong, State Key Lab Emerging Infect Dis, Li Ka Shing Fac Med, Hong Kong, Hong Kong, Peoples R China.
[Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis, University Pk, PA 16802 USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Lam, TTY (reprint author), Univ Oxford, Dept Zool, S Parks Rd, Oxford OX1 3PS, England.
EM tylam.tommy@gmail.com
RI Lam, Tommy Tsan-Yuk/D-4837-2012; Zhu, Huachen/A-8252-2017;
OI Zhu, Huachen/0000-0003-2711-0501; Pybus, Oliver/0000-0002-8797-2667;
Holmes, Edward/0000-0001-9596-3552
FU Royal Society; Li Ka Shing Foundation; Research Grant Council of Hong
Kong SAR [HKU 765809M]; Royal Society, UK
FX T. T.-Y. L. is supported by Newton International Fellowship from Royal
Society. H. Z., D. K. S. and Y. G. are supported by Li Ka Shing
Foundation and Research Grant Council of Hong Kong SAR (HKU 765809M). O.
G. P. is supported by Royal Society, UK. Additional bioinformatic and
computational resources were provided by the Computer Centre at The
University of Hong Kong (HKU). We thank the two anonymous reviewers for
useful suggestions. We also thank W. K. Kwan, Frankie Cheung and Lilian
Chan (HKU) for technical support.
NR 36
TC 11
Z9 11
U1 0
U2 2
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
J9 J GEN VIROL
JI J. Gen. Virol.
PD APR
PY 2012
VL 93
BP 817
EP 822
DI 10.1099/vir.0.039057-0
PN 4
PG 6
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 929OF
UT WOS:000303074500016
PM 22238233
ER
PT J
AU Barrett, L
Trehanpati, N
Poonia, S
Sarin, SK
Polis, MA
Masur, H
Kottilil, S
AF Barrett, L.
Trehanpati, N.
Poonia, S.
Sarin, S. K.
Polis, M. A.
Masur, H.
Kottilil, S.
TI HEPATIC COMPARTMENTALIZATION OF EXHAUSTED REGULATORY CELLS IN CHRONIC
HEPATITIS C PATIENTS
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Barrett, L.; Poonia, S.; Polis, M. A.; Masur, H.; Kottilil, S.] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Trehanpati, N.; Sarin, S. K.] ILBS, New Delhi, India.
EM barrettl@niaid.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 821
BP S321
EP S321
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241301381
ER
PT J
AU Fuchs, C
Claudel, T
Kumari, P
Stojakovic, T
Halilbasic, E
Spindelboek, W
Gonzalez, F
Trauner, M
AF Fuchs, C.
Claudel, T.
Kumari, P.
Stojakovic, T.
Halilbasic, E.
Spindelboek, W.
Gonzalez, F.
Trauner, M.
TI FXR IS A KEY PLAYER IN NAFLD DEVELOPMENT BY CONTROLLING CHOP EXPRESSION
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Fuchs, C.; Claudel, T.; Kumari, P.; Halilbasic, E.; Trauner, M.] Med Univ Vienna, Vienna, Austria.
[Stojakovic, T.] Med Univ Graz, Clin Inst Med & Chem Lab Diagnost, Graz, Austria.
[Gonzalez, F.] NCI, Lab Metab, Bethesda, MD 20892 USA.
EM claudia.fuchs@stud.medunigraz.at
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 1236
BP S490
EP S490
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241302343
ER
PT J
AU Ghabril, M
Bonkovsky, H
Kum, C
Davern, T
Kleiner, D
Serrano, J
Hayashi, P
Fontana, R
Bonacini, M
AF Ghabril, M.
Bonkovsky, H.
Kum, C.
Davern, T.
Kleiner, D.
Serrano, J.
Hayashi, P.
Fontana, R.
Bonacini, M.
CA DILIN Coinvestigators
TI LIVER INJURY FOLLOWING ANTI-TNF-ALPHA PEPTIDES: EXPERIENCE OF THE US
DRUG-INDUCED LIVER INJURY NETWORK (DILIN) AND CRITICAL REVIEW OF
PUBLISHED REPORTS
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Ghabril, M.] Indiana Univ, Indianapolis, IN 46204 USA.
[Bonkovsky, H.] Carolinas Med Ctr, Charlotte, NC 28203 USA.
[Kum, C.; Davern, T.] CPMC, San Francisco, CA USA.
[Kleiner, D.; Serrano, J.] NIH, Bethesda, MD 20892 USA.
[Hayashi, P.] UNC, Chapel Hill, NC USA.
[Fontana, R.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Bonacini, M.] Calif Pacific Med Ctr, San Francisco, CA USA.
EM bonacim@sutterhealth.org
NR 0
TC 0
Z9 1
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 1342
BP S528
EP S528
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241303017
ER
PT J
AU Govaere, O
Komuta, M
Spee, B
Durnez, A
Vander Borght, S
Verslype, C
Aerts, R
Topal, B
Pirenne, J
Nevens, F
Desmet, VJ
Roberts, LR
Thorgeirsson, SS
Roskams, T
AF Govaere, O.
Komuta, M.
Spee, B.
Durnez, A.
Vander Borght, S.
Verslype, C.
Aerts, R.
Topal, B.
Pirenne, J.
Nevens, F.
Desmet, V. J.
Roberts, L. R.
Thorgeirsson, S. S.
Roskams, T.
TI KERATIN19: A KEY ROLE PLAYER IN THE INVASION OF HUMAN HEPATOCELLULAR
CARCINOMAS WITH PROGENITOR CELL FEATURES
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Govaere, O.; Komuta, M.; Spee, B.; Durnez, A.; Vander Borght, S.; Desmet, V. J.; Roskams, T.] Katholieke Univ Leuven Hosp, Dept Morphol & Mol Pathol, Louvain, Belgium.
[Verslype, C.; Nevens, F.] Katholieke Univ Leuven Hosp, Dept Hepatol, Louvain, Belgium.
[Aerts, R.; Topal, B.] Katholieke Univ Leuven Hosp, Dept Abdominal Surg, Louvain, Belgium.
[Pirenne, J.] Katholieke Univ Leuven Hosp, Dept Abdominal Transplant Surg, Louvain, Belgium.
[Roberts, L. R.] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA.
[Thorgeirsson, S. S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM olivier.govaere@uzleuven.be
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 113
BP S50
EP S50
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241300114
ER
PT J
AU Guedj, J
Rotman, Y
Schmidt, P
Albrecht, J
Haynes-Williams, V
Liang, JT
Hoofnagle, JH
Heller, T
Dahari, H
AF Guedj, J.
Rotman, Y.
Schmidt, P.
Albrecht, J.
Haynes-Williams, V.
Liang, J. T.
Hoofnagle, J. H.
Heller, T.
Dahari, H.
TI MODELING HDV KINETICS DURING PEGYLATED INTERFERON-ALFA TREATMENT
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Guedj, J.; Dahari, H.] Los Alamos Natl Lab, Los Alamos, NM USA.
[Rotman, Y.; Haynes-Williams, V.; Liang, J. T.; Hoofnagle, J. H.; Heller, T.] NIDDK, Liver Dis Branch, NIH, Bethesda, MD USA.
[Schmidt, P.; Albrecht, J.] Natl Inst Genet, Los Angeles, CA USA.
[Dahari, H.] Univ Illinois, Chicago, IL USA.
EM daharih@uic.edu
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 507
BP S200
EP S200
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241301067
ER
PT J
AU Kohli, A
Funk, E
Burbelo, P
Shivakumar, B
Polis, M
Masur, H
Kottilil, S
AF Kohli, A.
Funk, E.
Burbelo, P.
Shivakumar, B.
Polis, M.
Masur, H.
Kottilil, S.
TI A NOVEL HCV-PROTEOME-WIDE LUCIFERASE IMMUNOPRECIPITATION ASSAY
PREDICTIVE OF HCV TREATMENT OUTCOME
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Kohli, A.; Funk, E.; Shivakumar, B.; Polis, M.; Kottilil, S.] NIAID, Bethesda, MD 20892 USA.
[Burbelo, P.] NIDCR, Bethesda, MD USA.
[Masur, H.] NIH, CCMD CC, Bethesda, MD 20892 USA.
EM kohlia@niaid.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 1127
BP S444
EP S444
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241302234
ER
PT J
AU Marquardt, JU
Maass, T
Krupp, M
Staib, F
Gasier, T
Andersen, JB
Galle, PR
Thorgeirsson, SS
Teufel, A
AF Marquardt, J. U.
Maass, T.
Krupp, M.
Staib, F.
Gasier, T.
Andersen, J. B.
Galle, P. R.
Thorgeirsson, S. S.
Teufel, A.
TI MOLECULAR STAGES OF PDGFB DRIVEN LIVER FIBROSIS: LESONS FROM A
TRANSGENIC MOUSE MODEL
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Marquardt, J. U.; Maass, T.; Krupp, M.; Staib, F.; Galle, P. R.; Teufel, A.] Johannes Gutenberg Univ Mainz, Dept Med 1, D-6500 Mainz, Germany.
[Marquardt, J. U.; Andersen, J. B.; Thorgeirsson, S. S.] NCI, Lab Expt Carcinogenesis, CCR, NIH, Bethesda, MD 20892 USA.
[Gasier, T.] Univ Mannheim, Dept Pathol, Mannheim, Germany.
EM marquarj@uni-mainz.de
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 385
BP S155
EP S155
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241300383
ER
PT J
AU Marquardt, JU
Fischer, K
Krupp, M
Teufel, A
Thorgeirsson, SS
Galle, PR
Strand, S
AF Marquardt, J. U.
Fischer, K.
Krupp, M.
Teufel, A.
Thorgeirsson, S. S.
Galle, P. R.
Strand, S.
TI INTEGRATIVE ANALYSIS OF SIRT6 REGULATED GENE NETWORKS IN THE DEVELOPMENT
AND PROGRESSION OF HUMAN HEPATOCELLULAR CARCINOMA
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Marquardt, J. U.; Fischer, K.; Krupp, M.; Teufel, A.; Galle, P. R.; Strand, S.] Johannes Gutenberg Univ Mainz, Dept Med 1, D-6500 Mainz, Germany.
[Marquardt, J. U.; Thorgeirsson, S. S.] NCI, Expt Carcinogenesis Lab, CCR, NIH, Bethesda, MD 20892 USA.
EM marquarj@uni-mainz.de
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 290
BP S120
EP S120
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241300289
ER
PT J
AU Navarro, VJ
Barnhart, HX
Bonkovsky, HL
Reddy, KR
Seeff, L
Serrano, J
Talwalkar, JA
Vega, M
Vuppalanchi, R
AF Navarro, V. J.
Barnhart, H. X.
Bonkovsky, H. L.
Reddy, K. R.
Seeff, L.
Serrano, J.
Talwalkar, J. A.
Vega, M.
Vuppalanchi, R.
CA DILIN Investigators
TI DIAGNOSING HEPATOTOXICITY ATTRIBUTABLE TO HERBAL & DIETARY SUPPLEMENTS
(HDS): TEST-RETEST RELIABILITY OF A NOVEL CAUSALITY ASSESSMENT TOOL
SO JOURNAL OF HEPATOLOGY
LA English
DT Meeting Abstract
CT 47th Annual Meeting of the
European-Association-for-the-Study-of-the-Liver (EASL)
CY APR 18-22, 2012
CL Barcelona, SPAIN
SP European Assoc Study Liver (EASL)
C1 [Navarro, V. J.; Vega, M.] Thomas Jefferson Univ, Div Gastroenterol & Hepatol, Philadelphia, PA 19107 USA.
[Barnhart, H. X.] Duke Clin Res Inst, Dept Biostat & Bioinformat, Durham, NC USA.
[Bonkovsky, H. L.] Carolinas Med Ctr & HealthCare Syst, Charlotte, NC USA.
[Reddy, K. R.] Univ Penn, Div Gastroenterol & Hepatol, Philadelphia, PA 19104 USA.
[Seeff, L.] US FDA, Silver Spring, MD USA.
[Serrano, J.] NIDDK, Div Digest Dis & Nutr, Bethesda, MD USA.
[Talwalkar, J. A.] Mayo Clin, Rochester, MN USA.
[Vuppalanchi, R.] Indiana Univ, Div Gastroenterol & Hepatol, Indianapolis, IN 46204 USA.
EM victor.navarro@jefferson.edu
NR 0
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-8278
J9 J HEPATOL
JI J. Hepatol.
PD APR
PY 2012
VL 56
SU 2
MA 1364
BP S536
EP S536
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 931TD
UT WOS:000303241303039
ER
PT J
AU Boos, TL
Cheng, KJ
Greiner, E
Deschamps, JR
Jacobson, AE
Rice, KC
AF Boos, Terrence L.
Cheng, Kejun
Greiner, Elisabeth
Deschamps, Jeffrey R.
Jacobson, Arthur E.
Rice, Kenner C.
TI Configurational Reassignment and Improved Preparation of the Competitive
IL-6 Receptor Antagonist 20R,21R-Epoxyresibufogenin-3-formate
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID BUFADIENOLIDES; INTERLEUKIN-6; RESIBUFOGENIN
AB 20R,21R-Epoxyresibufogenin-3-formate (1) and 20S,21S-epoxyresibufogenin-3-formate (2) were synthesized from commercial resibufogenin (3) using known procedures. The major product (1) was dextrorotatory, as was the major product from the reported synthesis of epoxyresibufogenin-3-formate; however, the literature (+)-compound was assigned the 20S,21S-configuration on the basis of NMR data. We have now unequivocally determined, using single-crystal X-ray structure analyses of the major and minor products of the synthesis and of their derivatives, that the major product from the synthesis was (+)-20R,21R-epoxyresibufogenin-3-formate (1). Our minor synthetic product was determined to have the (-)-20S,21S-configuration (2). The (+)-20R,21R-compound 1 has been found to have high affinity for the IL-6 receptor and to act as an IL-6 antagonist. A greatly improved synthesis of 1 was achieved through oxidation of preformed resibufogenin-3-formate. This has enabled us to prepare, from the very expensive commercial resibufogenin, considerably larger quantities of 1, the only known nonpeptide small-molecule IL-6 antagonist.
C1 [Boos, Terrence L.; Cheng, Kejun; Greiner, Elisabeth; Jacobson, Arthur E.; Rice, Kenner C.] NIDA, Drug Design & Synth Sect, Chem Biol Res Branch, Bethesda, MD 20892 USA.
[Boos, Terrence L.; Cheng, Kejun; Greiner, Elisabeth; Jacobson, Arthur E.; Rice, Kenner C.] NIAAA, NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Deschamps, Jeffrey R.] USN, Ctr Biomol Sci & Engn, Res Lab, Washington, DC 20375 USA.
RP Rice, KC (reprint author), NIDA, Drug Design & Synth Sect, Chem Biol Res Branch, 5625 Fishers Lane,Room 4N03, Bethesda, MD 20892 USA.
EM kr21f@nih.gov
OI Deschamps, Jeffrey/0000-0001-5845-0010
FU NIH of the National Institute of Diabetes and Digestive and Kidney
Diseases; National Institute on Drug Abuse [Y1-DA1101]; National
Institute of Alcohol Abuse and Alcoholism, NIH, DHHS; Naval Research
Laboratory (NRL)
FX This research was supported by the NIH Intramural Research Programs of
the National Institute of Diabetes and Digestive and Kidney Diseases,
the National Institute on Drug Abuse, and the National Institute of
Alcohol Abuse and Alcoholism, NIH, DHHS. We thank N. Whittaker and Dr.
J. Lloyd (Mass Spectrometry Facility, NIDDK) for the MS data and Drs. K.
Gawrisch and W. Teague (Laboratory of Membrane Biochemistry and
Biophysics, NIAAA) for NMR spectroscopic data. The X-ray
crystallographic work was supported by NIDA through Interagency
Agreement #Y1-DA1101 with the Naval Research Laboratory (NRL).
NR 22
TC 3
Z9 3
U1 0
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD APR
PY 2012
VL 75
IS 4
BP 661
EP 668
DI 10.1021/np2008957
PG 8
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 931LD
UT WOS:000303220500022
PM 22360661
ER
PT J
AU Li, J
Fronczek, FR
Ferreira, D
Burandt, CL
Setola, V
Roth, BL
Zjawiony, JK
AF Li, Jun
Fronczek, Frank R.
Ferreira, Daneel
Burandt, Charles L., Jr.
Setola, Vincent
Roth, Bryan L.
Zjawiony, Jordan K.
TI Bis-spirolabdane Diterpenoids from Leonotis nepetaefolia
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID LABDANE DITERPENOIDS; LEONURUS-SIBIRICUS; CONSTITUENTS; PERSICUS
AB Ten new bis-spirolabdane diterpenoids, leonepetaefolins A-E (1, 3, 5, 7, 9) and 15-epi-leonepetaefolins A-E (2, 4, 6, 8, 10), together with eight known labdane diterpenoids (11-18) as well as two known flavonoids, apigenin and cirsiliol, were isolated from the leaves of Leonotis nepetaefolia. The structures of the new compounds were determined on the basis of ID- and 2D-NMR experiments including H-1, C-13, DEPT, H-1-H-1 COSY, HSQC, HMBC, and NOESY. The absolute configuration of an epimeric mixture of 1 and 2 was determined by X-ray crystallographic analysis. The compounds - isolated were evaluated for their binding propensity in several CNS G-protein-coupled receptor assays in vitro.
C1 [Li, Jun; Ferreira, Daneel; Zjawiony, Jordan K.] Univ Mississippi, Sch Pharm, Dept Pharmacognosy, University, MS 38677 USA.
[Ferreira, Daneel; Zjawiony, Jordan K.] Univ Mississippi, Sch Pharm, Res Inst Pharmaceut Sci, University, MS 38677 USA.
[Fronczek, Frank R.] Louisiana State Univ, Dept Chem, Baton Rouge, LA 70803 USA.
[Setola, Vincent; Roth, Bryan L.] Univ N Carolina, Sch Med, Dept Pharmacognosy, Chapel Hill, NC 27599 USA.
[Setola, Vincent; Roth, Bryan L.] Univ N Carolina, NIMH Psychoact Drug Screening Program, Chapel Hill, NC 27599 USA.
[Burandt, Charles L., Jr.] Univ Mississippi, Natl Ctr Nat Prod Res, University, MS 38677 USA.
RP Zjawiony, JK (reprint author), Univ Mississippi, Sch Pharm, Dept Pharmacognosy, University, MS 38677 USA.
EM jordan@olemiss.edu
RI Roth, Bryan/F-3928-2010; Li, Jun /M-9884-2016
OI Li, Jun /0000-0001-8243-5267
FU National Institutes of Health [R03DA023491]; NIMH
FX The project was financially supported by a grant from the National
Institutes of Health (R03DA023491) and by the NIMH Psychoactive Drug
Screening Program. The authors are grateful to Ms. B. Wang at the
Department of Pharmacognosy for running the HRESIMS experiments.
NR 37
TC 9
Z9 9
U1 0
U2 12
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0163-3864
J9 J NAT PROD
JI J. Nat. Prod.
PD APR
PY 2012
VL 75
IS 4
BP 728
EP 734
DI 10.1021/np3000156
PG 7
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 931LD
UT WOS:000303220500032
PM 22475308
ER
PT J
AU Negus, SS
Rosenberg, MB
Altarifi, AA
O'Connell, RH
Folk, JE
Rice, KC
AF Negus, S. Stevens
Rosenberg, Marisa B.
Altarifi, Ahmad A.
O'Connell, Robert H.
Folk, John E.
Rice, Kenner C.
TI Effects of the Delta Opioid Receptor Agonist SNC80 on Pain-Related
Depression of Intracranial Self-Stimulation (ICSS) in Rats
SO JOURNAL OF PAIN
LA English
DT Article
DE Pain; depression; delta opioid receptor; SNC80; ARM390
ID SPRAGUE-DAWLEY RATS; RHESUS-MONKEYS; ANTIDEPRESSANT-LIKE; MODEL;
TOLERANCE; MORPHINE; MICE; INFLAMMATION; ANALGESICS; DEPENDENCE
AB The delta opioid receptor agonist SNC80 produces both antinociceptive and antidepressant effects in rodents. This profile suggests that SNC80 may also reverse prodepressant effects of pain. Accordingly, this study compared SNC80 effects in complementary assays of pain-stimulated and pain-depressed behavior in rats. Intraperitoneal injection of dilute acid served as an acute noxious visceral stimulus in rats to stimulate abdominal stretching (a pain-stimulated behavior) or depress intracranial self-stimulation of the medial forebrain bundle (ICSS; a pain-depressed behavior). When administered once per week to minimize acute tolerance, SNC80 (1-10 mg/kg IP) decreased acid-stimulated stretching but had little effect on acid-induced depression of ICSS. More frequent SNC80 administration produced tolerance to SNC80 effects on acid-stimulated stretching, but unmasked antinociception in the assay of acid-depressed ICSS. SNC80 did not facilitate ICSS in the absence of pain, and effects of SNC80 were not duplicated by ARM390, a reputed delta agonist congener of SNC80 that does not internalize delta receptors. These findings support continued consideration of delta agonists as candidate analgesics to treat prodepressant effects of pain and illustrate the potential for diametrically opposite effects of drug treatments on preclinical measures of pain-stimulated and pain-depressed behavior.
Perspective: The delta opioid agonist SNC80 blocked pain-related depression of intracranial self-stimulation in rats, suggesting that delta agonists may be useful to treat prodepressant effects of pain. Repeated SNC80 produced tolerance to SNC80 antinociception in a conventional assay of pain-stimulated behavior but unmasked SNC80 antinociception in an assay of pain-depressed behavior. (c) 2012 by the American Pain Society. Published by Elsevier Inc. All rights reserved
C1 [Negus, S. Stevens; Rosenberg, Marisa B.; Altarifi, Ahmad A.; O'Connell, Robert H.] Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, Richmond, VA 23220 USA.
[Folk, John E.; Rice, Kenner C.] Natl Inst Drug Abuse, Chem Biol Res Branch, Bethesda, MD USA.
[Folk, John E.; Rice, Kenner C.] NIAAA, NIH, DHHS, Bethesda, MD USA.
RP Negus, SS (reprint author), Virginia Commonwealth Univ, Dept Pharmacol & Toxicol, 410 N 12th St, Richmond, VA 23220 USA.
EM ssnegus@vcu.edu
FU National Institute on Drug Abuse [R01-DA11460]; National Institute of
Neurological Disorders and Stroke [R01-NS070715]; National Institute on
Alcohol Abuse and Alcoholism
FX Supported in part by R01-DA11460 from the National Institute on Drug
Abuse and R01-NS070715 from the National Institute of Neurological
Disorders and Stroke. A portion of this work was also supported by the
Intramural Research Programs of the National Institute on Drug Abuse and
the National Institute on Alcohol Abuse and Alcoholism.
NR 44
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Z9 16
U1 0
U2 7
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1526-5900
J9 J PAIN
JI J. Pain
PD APR
PY 2012
VL 13
IS 4
BP 317
EP 327
DI 10.1016/j.jpain.2011.12.003
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 932CK
UT WOS:000303267800002
PM 22424913
ER
PT J
AU Carlson-Bremer, D
Johnson, CK
Miller, RH
Gulland, FMD
Conrad, PA
Wasmuth, JD
Colegrove, KM
Grigg, ME
AF Carlson-Bremer, Daphne
Johnson, Christine K.
Miller, Robin H.
Gulland, Frances M. D.
Conrad, Patricia A.
Wasmuth, James D.
Colegrove, Kathleen M.
Grigg, Michael E.
TI IDENTIFICATION OF TWO NOVEL COCCIDIAN SPECIES SHED BY CALIFORNIA SEA
LIONS (ZALOPHUS CALIFORNIANUS)
SO JOURNAL OF PARASITOLOGY
LA English
DT Article
ID EIMERIA-PHOCAE; HARBOR SEALS; TOXOPLASMA-GONDII; VITULINA; APICOMPLEXA;
EVOLUTION; SPOROZOA; OOCYSTS; MANATEE; SIRENIA
AB Routine fecal examination revealed novel coccidian oocysts in asymptomatic California sea lions (Zalophus californianus) in a rehabilitation facility. Coccidian oocysts were observed in fecal samples collected from 15 of 410 California sea lions admitted to The Marine Mammal Center between April 2007 and October 2009. Phylogenetic analysis using the full ITS-1 region, partial small subunit 18S rDNA sequence, and the Apicomplexa rpoB region identified 2 distinct sequence clades, referred to as Coccidia A and Coccidia B, and placed them in the Sarcocystidae, grouped with the tissue-cyst forming coccidia. Both sequence clades resolved as individual taxa at ITS-1 and rpoB and were most closely related to Neospora caninum. Coccidia A was identified in 11 and Coccidia B in 4 of 12 sea lion oocyst samples successfully sequenced (3 of those sea lions were co-infected with both parasites). Shedding of Coccidia A oocysts was not associated with age class, sex, or stranding location, but yearlings represented the majority of shedders (8/15). This is the first study to use molecular phylogenetics to identify and describe coccidian parasites shed by a marine mammal.
C1 [Carlson-Bremer, Daphne; Johnson, Christine K.; Miller, Robin H.; Gulland, Frances M. D.; Conrad, Patricia A.; Wasmuth, James D.; Colegrove, Kathleen M.; Grigg, Michael E.] Univ Calif Davis, Wildlife Hlth Ctr, Sch Vet Med, Davis, CA 95616 USA.
RP Grigg, ME (reprint author), NIAID, Mol Parasitol Unit, Parasit Dis Lab, NIH, 4 Ctr Dr,Room B1-06, Bethesda, MD 20892 USA.
EM griggm@niaid.nih.gov
FU NSF-EID from the Ocean Sciences Division [OCE-1065990]; NIH [T32
RR07038]; NIAID; Canadian Institute for Advanced Research (CIFAR);
Wildlife Health Center, School of Veterinary Medicine, University of
California, Davis; The Marine Mammal Center
FX This work was supported and funded in part by an NSF-EID grant from the
Ocean Sciences Division, OCE-1065990, NIH Training Grant T32 RR07038,
the Intramural Research Program of the NIH and NIAID, the Canadian
Institute for Advanced Research (CIFAR) Integrated Microbial
Biodiversity Program (MEG), the Wildlife Health Center, School of
Veterinary Medicine, University of California, Davis, and The Marine
Mammal Center. We would like to thank Liz Wheeler, Emily Andrews, Denise
Greig, and all the volunteers at The Marine Mammal Center for their
assistance in sample collection and transport. We also gratefully
acknowledge Ann C. Melli, Andrea Packham, Samantha Hunt, and Aiko Adell
for their assistance in the laboratory processing of samples. All
samples used in this study were authorized by the National Marine
Fisheries Service Research and Enhancement Permit to Take Marine Mammals
(Permit No. 932-1489-08). Sarcocystis neurona monoclonal antibody was
provided by Dr. Antoinette Marsh, University of Missouri College of
Veterinary Medicine, Columbia, Missouri. Neospora caninum polyclonal
antibody was obtained from the California Animal Health and Food Safety
Laboratory, University of California, Davis, California.
NR 37
TC 5
Z9 6
U1 0
U2 10
PU AMER SOC PARASITOLOGISTS
PI LAWRENCE
PA 810 EAST 10TH STREET, LAWRENCE, KS 66044 USA
SN 0022-3395
J9 J PARASITOL
JI J. Parasitol.
PD APR
PY 2012
VL 98
IS 2
BP 347
EP 354
DI 10.1645/GE-2752.1
PG 8
WC Parasitology
SC Parasitology
GA 932FL
UT WOS:000303275700019
PM 22091999
ER
PT J
AU Klumpers, F
Denys, D
Kenemans, JL
Grillon, C
van der Aart, J
Baas, JMP
AF Klumpers, Floris
Denys, Damiaan
Kenemans, J. Leon
Grillon, Christian
van der Aart, Jasper
Baas, Johanna M. P.
TI Testing the effects of Delta 9-THC and D-cycloserine on extinction of
conditioned fear in humans
SO JOURNAL OF PSYCHOPHARMACOLOGY
LA English
DT Article
DE Delta 9-THC; d-cycloserine; extinction; fear conditioning;
fear-potentiated startle; human
ID OBSESSIVE-COMPULSIVE DISORDER; RANDOMIZED CONTROLLED-TRIAL; SOCIAL
ANXIETY DISORDER; AGONIST D-CYCLOSERINE; POTENTIATED STARTLE; EXPOSURE
THERAPY; ENDOCANNABINOID SYSTEM; HEALTHY-VOLUNTEERS; MEMORY;
FACILITATION
AB Preclinical evidence implicates several neurotransmitter systems in the extinction of conditioned fear. These results are of great interest, because the reduction of acquired fear associations is critical in therapies for anxiety disorders. We tested whether findings with respect to the N-methyl-D-aspartate (NMDA) and cannabinoid receptor (CB) systems in animals carry over to healthy human subjects. To that end, we administered selected doses of D-cycloserine (partial NMDA receptor agonist, 250 mg), delta-9-tetrahydrocannabinol (THC, CB1 receptor agonist, 10 mg), or placebo prior to the extinction session of a 3-day conditioning protocol. D-cycloserine did not affect within-session extinction, or the retention of extinction in healthy human participants, in contrast with patient data but in line with previous reports in healthy volunteers. During extinction training, Delta 9-THC reduced conditioned skin conductance responses, but not fear-potentiated startle. This effect was not retained at the retention test 2 days later, suggesting it was dependent on acute effects of the drug. Our findings implicate that facilitation of the CB1 or NMDA system with the substances used in this study does not affect conditioned fear extinction lastingly in healthy humans. The apparent discrepancy between these findings and the results from (pre-)clinical trials is discussed in terms of room for improvement in these systems in healthy volunteers, and the lack of specificity of THC as a CB1 agonist.
C1 [Baas, Johanna M. P.] Univ Utrecht, Dept Expt Psychol, Fac Social Sci, Helmholtz Inst, NL-3584 CS Utrecht, Netherlands.
[Klumpers, Floris; Kenemans, J. Leon; Baas, Johanna M. P.] Univ Utrecht, Utrecht Inst Pharmaceut Sci, NL-3584 CS Utrecht, Netherlands.
[Denys, Damiaan] Univ Amsterdam, Acad Med Ctr, Dept Psychiat, NL-1105 AZ Amsterdam, Netherlands.
[Denys, Damiaan] Inst Neurosci, Amsterdam, Netherlands.
[Grillon, Christian] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
RP Baas, JMP (reprint author), Univ Utrecht, Dept Expt Psychol, Fac Social Sci, Helmholtz Inst, Van Unnik Bldg,Heidelberglaan 2, NL-3584 CS Utrecht, Netherlands.
EM j.m.p.baas@uu.nl
RI Klumpers, Floris/J-2857-2012
FU NWO; NIMH
FX This work was supported by a NWO Veni-grant awarded to JMPB, and by the
NIMH Intramural Research Program (CG).
NR 57
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U1 3
U2 8
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0269-8811
J9 J PSYCHOPHARMACOL
JI J. Psychopharmacol.
PD APR
PY 2012
VL 26
IS 4
BP 471
EP 478
DI 10.1177/0269881111431624
PG 8
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 930GQ
UT WOS:000303126100005
PM 22351380
ER
PT J
AU Baranowski, T
Islam, N
Baranowski, J
Martin, S
Beltran, A
Dadabhoy, H
Adame, SH
Watson, KB
Thompson, D
Cullen, KW
Subar, AF
AF Baranowski, Tom
Islam, Noemi
Baranowski, Janice
Martin, Shelby
Beltran, Alicia
Dadabhoy, Hafza
Adame, Su-heyla
Watson, Kathleen B.
Thompson, Debbe
Cullen, Karen W.
Subar, Amy F.
TI Comparison of a Web-Based versus Traditional Diet Recall among Children
SO JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS
LA English
DT Article
DE Diet assessment; Computer; 24-hour recall; Children
ID 13-YEAR-OLD CHILDREN; FOOD-INTAKE; ACCURACY; NUTRITION; VALIDITY
AB Self-administered instruments offer a low-cost diet assessment method for use in adult and pediatric populations. This study tested whether 8- to 13-year-old children could complete an early version of the Automated Self Administered 24-hour diet recall (ASA24) and how this compared to an interviewer-administered 24-hour diet recall. One-hundred twenty 8- to 13-year-old children were recruited in Houston from June through August 2009 and randomly assigned to complete either the ASA24 or an interviewer-administered 24-hour diet recall, followed by the other recall mode covering the same time interval. Multivariate analysis of variance, testing for differences by age, sex, and ethnic/racial group, were applied to percentages of food matches, intrusions, and omissions between reports on the ASA24 and the interviewer-administered 24-hour diet recall. For the ASA24, qualitative findings were reported regarding ease of use. Overall matches between interviewer-administered and ASA24 self-administered 24-hour diet recall was 47.8%. Matches were significantly lower among younger (8- to 9-year-old) compared with older (10- to 13-year-old) children. Omissions on ASA24 (18.9% overall) were most common among 8-year-olds and intermediate among 9-year-olds. Eight- and 9-year-olds had substantial difficulties and often required aid in completing ASA24. Findings from this study suggest that a simpler version of an Internet-based diet recall program would be easier for children to use. J Acad Nutr Diet. 2012;112:527-532.
C1 [Baranowski, Tom; Islam, Noemi; Baranowski, Janice; Martin, Shelby; Beltran, Alicia; Dadabhoy, Hafza; Adame, Su-heyla; Watson, Kathleen B.; Thompson, Debbe; Cullen, Karen W.] Baylor Coll Med, USDA ARS, Childrens Nutr Res Ctr, Houston, TX 77030 USA.
[Subar, Amy F.] NCI, Div Canc Control & Populat Sci, Appl Res Program, Risk Factor Monitoring & Methods Branch EPN, Bethesda, MD 20892 USA.
RP Baranowski, T (reprint author), Baylor Coll Med, USDA ARS, Childrens Nutr Res Ctr, 1100 Bates St, Houston, TX 77030 USA.
EM tbaranow@bcm.edu
OI Baranowski, Tom/0000-0002-0653-2222
FU National Cancer Institute [5 U01 CA130762-04]; USDA/ARS [58-6250-6001]
FX This research was primarily funded by a grant from the National Cancer
Institute (5 U01 CA130762-04). This work is also a publication of the
United States Department of Agriculture (USDA/ARS) Children's Nutrition
Research Center, Department of Pediatrics, Baylor College of Medicine,
Houston, TX, and had been funded in part with federal funds from the
USDA/ARS under Cooperative Agreement No. 58-6250-6001. The contents of
this publication do not necessarily reflect the views or policies of the
USDA, nor does mention of trade names, commercial products, or
organizations imply endorsement from the US government.
NR 24
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U1 0
U2 16
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 2212-2672
J9 J ACAD NUTR DIET
JI J. Acad. Nutr. Diet.
PD APR
PY 2012
VL 112
IS 4
BP 527
EP 532
DI 10.1016/j.jada.2011.10.002
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 930WR
UT WOS:000303175900010
PM 22717216
ER
PT J
AU Amiri-Kordestani, L
Fojo, T
AF Amiri-Kordestani, Laleh
Fojo, Tito
TI Why Do Phase III Clinical Trials in Oncology Fail so Often?
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID DRUG DEVELOPMENT; TARGETED AGENTS; STABLE DISEASE; END-POINT;
CHEMOTHERAPY; SURVIVAL; CANCER; BENEFIT; DESIGNS
C1 [Amiri-Kordestani, Laleh; Fojo, Tito] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Fojo, T (reprint author), NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bldg 10,Rm 12N226,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM fojot@mail.nih.gov
NR 19
TC 17
Z9 17
U1 1
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD APR
PY 2012
VL 104
IS 8
BP 568
EP 569
DI 10.1093/jnci/djs180
PG 2
WC Oncology
SC Oncology
GA 930TE
UT WOS:000303162400001
PM 22491346
ER
PT J
AU Lee, C
Kim, KP
Long, DJ
Bolch, WE
AF Lee, Choonsik
Kim, Kwang Pyo
Long, Daniel J.
Bolch, Wesley E.
TI Organ doses for reference pediatric and adolescent patients undergoing
computed tomography estimated by Monte Carlo simulation
SO MEDICAL PHYSICS
LA English
DT Article
ID HYBRID COMPUTATIONAL PHANTOMS; TUBE CURRENT MODULATION; CT EXAMINATIONS;
FEMALE; FEASIBILITY; DOSIMETRY; MODELS
AB Purpose: To establish an organ dose database for pediatric and adolescent reference individuals undergoing computed tomography (CT) examinations by using Monte Carlo simulation. The data will permit rapid estimates of organ and effective doses for patients of different age, gender, examination type, and CT scanner model.
Methods: The Monte Carlo simulation model of a Siemens Sensation 16 CT scanner previously published was employed as a base CT scanner model. A set of absorbed doses for 33 organs/tissues normalized to the product of 100 mAs and CTDIvol (mGy/100 mAs mGy) was established by coupling the CT scanner model with age-dependent reference pediatric hybrid phantoms. A series of single axial scans from the top of head to the feet of the phantoms was performed at a slice thickness of 10 mm, and at tube potentials of 80, 100, and 120 kVp. Using the established CTDIvol- and 100 mAs-normalized dose matrix, organ doses for different pediatric phantoms undergoing head, chest, abdomen-pelvis, and chest-abdomen-pelvis (CAP) scans with the Siemens Sensation 16 scanner were estimated and analyzed. The results were then compared with the values obtained from three independent published methods: CT-Expo software, organ dose for abdominal CT scan derived empirically from patient abdominal circumference, and effective dose per dose-length product (DLP).
Results: Organ and effective doses were calculated and normalized to 100 mAs and CTDIvol for different CT examinations. At the same technical setting, dose to the organs, which were entirely included in the CT beam coverage, were higher by from 40 to 80% for newborn phantoms compared to those of 15-year phantoms. An increase of tube potential from 80 to 120 kVp resulted in 2.5-2.9-fold greater brain dose for head scans. The results from this study were compared with three different published studies and/or techniques. First, organ doses were compared to those given by CT-Expo which revealed dose differences up to several-fold when organs were partially included in the scan coverage. Second, selected organ doses from our calculations agreed to within 20% of values derived from empirical formulae based upon measured patient abdominal circumference. Third, the existing DLP-to-effective dose conversion coefficients tended to be smaller than values given in the present study for all examinations except head scans.
Conclusions: A comprehensive organ/effective dose database was established to readily calculate doses for given patients undergoing different CT examinations. The comparisons of our results with the existing studies highlight that use of hybrid phantoms with realistic anatomy is important to improve the accuracy of CT organ dosimetry. The comprehensive pediatric dose data developed here are the first organ-specific pediatric CT scan database based on the realistic pediatric hybrid phantoms which are compliant with the reference data from the International Commission on Radiological Protection (ICRP). The organ dose database is being coupled with an adult organ dose database recently published as part of the development of a user-friendly computer program enabling rapid estimates of organ and effective dose doses for patients of any age, gender, examination types, and CT scanner model. (C) 2012 American Association of Physicists in Medicine. [http://dx.doi.org/10.1118/1.3693052]
C1 [Lee, Choonsik] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20852 USA.
[Kim, Kwang Pyo] Kyung Hee Univ, Dept Nucl Engn, Gyeonggi Do 446906, South Korea.
[Long, Daniel J.; Bolch, Wesley E.] Univ Florida, J Crayton Pruitt Family Dept Biomed Engn, Gainesville, FL 32611 USA.
RP Lee, C (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20852 USA.
EM leechoonsik@mail.nih.gov
RI Lee, Choonsik/C-9023-2015
OI Lee, Choonsik/0000-0003-4289-9870
FU Radiation Epidemiology Branch of the National Cancer Institute
[HHS-N2612-0090-0098P, HHS-N2612-0100-0692P, HHS-N2612-0090-0177P]
FX This work was supported by Contract Nos. HHS-N2612-0090-0098P,
HHS-N2612-0100-0692P, and HHS-N2612-0090-0177P with the Radiation
Epidemiology Branch of the National Cancer Institute.
NR 28
TC 39
Z9 40
U1 1
U2 8
PU AMER ASSOC PHYSICISTS MEDICINE AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0094-2405
J9 MED PHYS
JI Med. Phys.
PD APR
PY 2012
VL 39
IS 4
BP 2129
EP 2146
DI 10.1118/1.3693052
PG 18
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 919ZY
UT WOS:000302371900042
PM 22482634
ER
PT J
AU Ashizawa, T
Perlman, S
Gomez, C
Wilmot, G
Schmahmann, J
Ying, S
Zesiewicz, T
Paulson, H
Shakkottai, V
Bushara, K
Mazzoni, P
Kuo, SH
Pulst, S
Figueroa, K
Xia, GB
Krischer, J
Cuthbertson, D
Holbert, AR
Ferguson, J
Galpern, W
Subramony, S
AF Ashizawa, Tetsuo
Perlman, Susan
Gomez, Christopher
Wilmot, George
Schmahmann, Jeremy
Ying, Sarah
Zesiewicz, Theresa
Paulson, Henry
Shakkottai, Vikram
Bushara, Khalaf
Mazzoni, Pietro
Kuo, Sheng-Han
Pulst, Stefan
Figueroa, Karla
Xia, Guangbin
Krischer, Jeffrey
Cuthbertson, David
Holbert, Amy Roberts
Ferguson, John
Galpern, Wendy
Subramony, S.
TI Clinical Characteristics of Spinocerebellar Ataxias 1, 2, 3 and 6
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Ashizawa, Tetsuo] Univ Florida, McKnight Brain Inst UF, Gainesville, FL USA.
[Perlman, Susan] Univ Calif Los Angeles, Sherman Oaks, CA USA.
[Gomez, Christopher] Univ Chicago, Chicago, IL 60637 USA.
[Wilmot, George] Emory Univ, Atlanta, GA 30322 USA.
[Zesiewicz, Theresa; Krischer, Jeffrey; Cuthbertson, David; Holbert, Amy Roberts] Univ S Florida, Tampa, FL USA.
[Pulst, Stefan; Figueroa, Karla] Univ Utah, Salt Lake City, UT USA.
[Paulson, Henry; Shakkottai, Vikram] Univ Michigan, Ann Arbor, MI 48109 USA.
[Schmahmann, Jeremy] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Ying, Sarah] Jons Hopkins Univ, Baltimore, MD USA.
[Bushara, Khalaf] Univ Minnesota, Minneapolis, MN USA.
[Mazzoni, Pietro; Kuo, Sheng-Han] Columbia Univ, New York, NY USA.
[Ferguson, John] NIH, Off Rare Dis, Bethesda, MD 20892 USA.
[Galpern, Wendy] NINDS, Bethesda, MD 20892 USA.
NR 0
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PU LIPPINCOTT WILLIAMS & WILKINS
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PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
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J9 NEUROLOGY
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PY 2012
VL 78
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GA 931GQ
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ER
PT J
AU Benninger, D
Dukart, J
Von Meyenburg, J
Thees, S
Bassetti, C
Waldvogel, D
Kollias, S
Iseki, K
Draganski, B
AF Benninger, David
Dukart, Juergen
Von Meyenburg, Jan
Thees, Sebastian
Bassetti, Claudio
Waldvogel, Daniel
Kollias, Spyridon
Iseki, Kazumi
Draganski, Bogdan
TI Progressive Cortical Degeneration in Parkinson's Disease
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Benninger, David] CHUV, Dept Neurol, Lausanne, Switzerland.
[Von Meyenburg, Jan; Thees, Sebastian] Inst Neuroradiol, Zurich, Switzerland.
[Bassetti, Claudio] Neuroctr Svizzera Italiana, Lugano, Switzerland.
[Waldvogel, Daniel] Univ Zurich Hosp, Dept Neurol, CH-8091 Zurich, Switzerland.
[Kollias, Spyridon] Dept Neuroradiol, Zurich, Switzerland.
[Iseki, Kazumi] NINDS, Bethesda, MD 20892 USA.
RI Kollias, Spyros/J-9276-2012; Dukart, Juergen/E-5459-2011; Benninger,
David/A-8157-2015; Draganski, Bogdan/C-3096-2016
OI Benninger, David/0000-0002-1049-9533; Draganski,
Bogdan/0000-0002-5159-5919
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
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PD APR
PY 2012
VL 78
SU 1
MA P01214
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WC Clinical Neurology
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GA 931GQ
UT WOS:000303204800316
ER
PT J
AU Bette, S
Liaghat, J
De la Plata, CM
Diaz-Arrastia, R
AF Bette, Sagari
Liaghat, John
De la Plata, Carlos Marquez
Diaz-Arrastia, Ramon
TI Examination of Functional Connectivity Networks in Traumatic Brain
Injury
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Bette, Sagari; Liaghat, John; De la Plata, Carlos Marquez] UT SW Med Ctr, Dallas, TX USA.
[Diaz-Arrastia, Ramon] NIH, Rockville, 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 0028-3878
J9 NEUROLOGY
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PD APR
PY 2012
VL 78
SU 1
MA P01181
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WC Clinical Neurology
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GA 931GQ
UT WOS:000303204800259
ER
PT J
AU Bette, S
Liaghat, J
De la Plata, CM
Diaz-Arrastia, R
AF Bette, Sagari
Liaghat, John
De la Plata, Carlos Marquez
Diaz-Arrastia, Ramon
TI Examination of Functional Connectivity Networks in Traumatic Brain
Injury
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Bette, Sagari; Liaghat, John; De la Plata, Carlos Marquez] UT SW Med Ctr, Dallas, TX USA.
[Diaz-Arrastia, Ramon] NIH, Rockville, MD 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN61007
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WC Clinical Neurology
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GA 931GQ
UT WOS:000303204800108
ER
PT J
AU Bhanushali, M
Kranick, S
Inati, S
Freeman, A
Battiwalla, M
Nath, A
AF Bhanushali, Minal
Kranick, Sarah
Inati, Sara
Freeman, Alexandra
Battiwalla, Minoo
Nath, Avindra
TI Herpes Virus Infections of the Brain Complicating Allogeneic
Hematopoietic Stem Cell Transplantation (SCT)
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Bhanushali, Minal; Inati, Sara] NINDS, NIH, Bethesda, MD 20892 USA.
[Kranick, Sarah] NINDS, NIH, Brookeville, MD USA.
[Freeman, Alexandra] NIAID, NIH, Bethesda, MD 20892 USA.
[Battiwalla, Minoo] NHLBI, NIH, Bethesda, MD 20892 USA.
[Nath, Avindra] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S57001
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803199
ER
PT J
AU Bosch, EP
Tracy, J
Goodman, B
Dyck, PJB
Toro, C
Giannini, C
AF Bosch, E. Peter
Tracy, Jennifer
Goodman, Brent
Dyck, P. James B.
Toro, Camilo
Giannini, Caterina
TI Facial Onset Sensory and Motor Neuronopathy: A Neurodegenerative TDP-43
Proteinopathy?
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Bosch, E. Peter; Goodman, Brent] Mayo Clin Arizona, Scottsdale, AZ USA.
[Tracy, Jennifer; Dyck, P. James B.; Giannini, Caterina] Mayo Clin, Rochester, MN USA.
[Toro, Camilo] NHGRI, NIH, Frederick, 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
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J9 NEUROLOGY
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PD APR
PY 2012
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GA 931GQ
UT WOS:000303204803064
ER
PT J
AU Bosch, EP
Tracy, J
Goodman, B
Dyck, PJB
Toro, C
Giannini, C
AF Bosch, E. Peter
Tracy, Jennifer
Goodman, Brent
Dyck, P. James B.
Toro, Camilo
Giannini, Caterina
TI Facial Onset Sensory and Motor Neuronopathy: A Neurodegenerative TDP-43
Proteinopathy?
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Bosch, E. Peter; Goodman, Brent] Mayo Clin Arizona, Scottsdale, AZ USA.
[Tracy, Jennifer; Dyck, P. James B.; Giannini, Caterina] Mayo Clin, Rochester, MN USA.
[Toro, Camilo] NHGRI, NIH, Frederick, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P03183
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801287
ER
PT J
AU Calvo, A
Borghero, G
Cannas, A
Marrosu, M
Murru, M
Floris, G
Traynor, B
Renton, A
Moglia, C
Canosa, A
Ilardi, A
Cammarosano, S
Brunetti, M
Ossola, I
Restagno, G
Chio, A
AF Calvo, Andrea
Borghero, Giuseppe
Cannas, Antonino
Marrosu, Maria
Murru, Maria
Floris, Gianluca
Traynor, Bryan
Renton, Alan
Moglia, Cristina
Canosa, Antonio
Ilardi, Antonio
Cammarosano, Stefania
Brunetti, Maura
Ossola, Irene
Restagno, Gabriella
Chio, Adriano
TI An ALS-FTD Patient Carrying a Double Pathogenetic Mutation of C9ORF72
and TARDBP: Case Report
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Calvo, Andrea; Moglia, Cristina; Canosa, Antonio; Ilardi, Antonio; Cammarosano, Stefania] Univ Turin, Turin, Italy.
[Borghero, Giuseppe; Cannas, Antonino; Marrosu, Maria; Murru, Maria; Floris, Gianluca] Univ Cagliari, Cagliari, Italy.
[Traynor, Bryan; Renton, Alan] NIH, Bethesda, MD 20892 USA.
[Brunetti, Maura; Ossola, Irene; Restagno, Gabriella] OIRM S Anna, Turin, Italy.
[Chio, Adriano] Univ Torino, Biella, Italy.
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 0028-3878
J9 NEUROLOGY
JI Neurology
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PY 2012
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MA IN91006
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WC Clinical Neurology
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GA 931GQ
UT WOS:000303204803068
ER
PT J
AU Calvo, A
Borghero, G
Cannas, A
Marrosu, M
Murru, M
Floris, G
Traynor, B
Renton, A
Moglia, C
Canosa, A
Ilardi, A
Cammarosano, S
Brunetti, M
Ossola, I
Restagno, G
Chio, A
AF Calvo, Andrea
Borghero, Giuseppe
Cannas, Antonino
Marrosu, Maria
Murru, Maria
Floris, Gianluca
Traynor, Bryan
Renton, Alan
Moglia, Cristina
Canosa, Antonio
Ilardi, Antonio
Cammarosano, Stefania
Brunetti, Maura
Ossola, Irene
Restagno, Gabriella
Chio, Adriano
TI An ALS-FTD Patient Carrying a Double Pathogenetic Mutation of C9ORF72
and TARDBP: Case Report
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Calvo, Andrea; Moglia, Cristina; Canosa, Antonio; Ilardi, Antonio; Cammarosano, Stefania] Univ Turin, Turin, Italy.
[Borghero, Giuseppe; Cannas, Antonino; Marrosu, Maria; Murru, Maria; Floris, Gianluca] Univ Cagliari, Cagliari, Italy.
[Traynor, Bryan; Renton, Alan] NIH, Bethesda, MD 20892 USA.
[Brunetti, Maura; Ossola, Irene; Restagno, Gabriella] OIRM S Anna, Turin, Italy.
[Chio, Adriano] Univ Torino, Biella, Italy.
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P01100
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800143
ER
PT J
AU Chio, A
Borghero, G
Sabatelli, M
Corbo, M
Mora, G
Giannini, F
Conforti, F
Penco, S
Calvo, A
Pugliatti, M
Sotgiu, A
Logroscino, G
Traynor, B
Renton, A
Majounie, E
Lauria, G
Caponnetto, C
Mandrioli, J
Salvi, F
Volanti, P
La Bella, V
Monsurro, M
Zollino, M
Ossola, I
Brunetti, M
Restagno, G
AF Chio, Adriano
Borghero, Giuseppe
Sabatelli, Mario
Corbo, Massimo
Mora, Gabriele
Giannini, Fabio
Conforti, Francesca
Penco, Silvana
Calvo, Andrea
Pugliatti, Maura
Sotgiu, Alessandra
Logroscino, Giancarlo
Traynor, Bryan
Renton, Alan
Majounie, Elisa
Lauria, Giuseppe
Caponnetto, Claudia
Mandrioli, Jessica
Salvi, Fabrizio
Volanti, Paolo
La Bella, Vincenzo
Monsurro, Maria
Zollino, Marcella
Ossola, Irene
Brunetti, Maura
Restagno, Gabriella
TI C9ORF72 in a Large Series of Italian and Sardinian Familial and Sporadic
ALS Patients
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Chio, Adriano; Calvo, Andrea; Ossola, Irene; Brunetti, Maura] Univ Turin, Turin, Italy.
[Borghero, Giuseppe] Univ Cagliari, Cagliari, Italy.
[Sabatelli, Mario] Univ Cattolica Sacro Cuore, Rome, Italy.
[Corbo, Massimo] NEMO Ctr, Milan, Italy.
[Mora, Gabriele] Fdn Maugeri, Milan, Italy.
[Giannini, Fabio] Univ Siena, I-53100 Siena, Italy.
[Conforti, Francesca] CNR, Cosenza, Italy.
[Penco, Silvana] Osped Niguarda Ca Granda, Milan, Italy.
[Pugliatti, Maura; Sotgiu, Alessandra] Univ Sassari, Milan, Italy.
[Logroscino, Giancarlo] Univ Bari, Bari, Italy.
[Traynor, Bryan; Renton, Alan; Majounie, Elisa] NIH, Bethesda, MD 20892 USA.
[Lauria, Giuseppe] Ist Neurol Besta, Milan, Italy.
[Caponnetto, Claudia] Univ Genoa, Genoa, Italy.
[Mandrioli, Jessica] Univ Modena, I-41100 Modena, Italy.
[Salvi, Fabrizio] Osped Bellaria, Cesena, FC, Italy.
[Volanti, Paolo] Fdn Maugeri, Mistretta, Italy.
[La Bella, Vincenzo] Univ Palermo, Palermo, Italy.
[Monsurro, Maria] Univ Naples Federico II, Naples, Italy.
[Zollino, Marcella] Catholic Hosp, Rome, Italy.
[Restagno, Gabriella] OIRM SantAnna Hosp, Turin, Italy.
RI La Bella, Vincenzo/H-4532-2012
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN91003
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803071
ER
PT J
AU Chio, A
Restagno, G
Brunetti, M
Ossola, I
Calvo, A
Moglia, C
Traynor, B
Renton, A
Majounie, E
Corrado, L
D'Alfonso, S
Mora, G
Mazzini, L
AF Chio, Adriano
Restagno, Gabriella
Brunetti, Maura
Ossola, Irene
Calvo, Andrea
Moglia, Cristina
Traynor, Bryan
Renton, Alan
Majounie, Elisa
Corrado, Lucia
D'Alfonso, Sandra
Mora, Gabriele
Mazzini, Letizia
CA PARALS Study Grp
TI Genetics of ALS in Italy: A Population-Based Study
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Chio, Adriano] Unviers Torino, Biella, Italy.
[Restagno, Gabriella; Brunetti, Maura; Ossola, Irene] ASO OIRM SantAnna, Turin, Italy.
[Brunetti, Maura; Ossola, Irene] Dept Neurosci, Turin, Italy.
[Calvo, Andrea; Moglia, Cristina] Univ Turin, Turin, Italy.
[Traynor, Bryan; Renton, Alan; Majounie, Elisa] NIH, Bethesda, MD 20892 USA.
[Corrado, Lucia; D'Alfonso, Sandra; Mazzini, Letizia] Univ Piemonte Orientale, Novara, Italy.
[Mora, Gabriele] Fdn Maugeri, Milan, Italy.
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN91007
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WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803067
ER
PT J
AU Chio, A
Borghero, G
Sabatelli, M
Corbo, M
Mora, G
Giannini, F
Conforti, F
Penco, S
Calvo, A
Pugliatti, M
Sotgiu, A
Logroscino, G
Traynor, B
Renton, A
Majounie, E
Lauria, G
Caponnetto, C
Mandrioli, J
Salvi, F
Volanti, P
La Bella, V
Monsurro, M
Zollino, M
Ossola, I
Brunetti, M
Restagno, G
AF Chio, Adriano
Borghero, Giuseppe
Sabatelli, Mario
Corbo, Massimo
Mora, Gabriele
Giannini, Fabio
Conforti, Francesca
Penco, Silvana
Calvo, Andrea
Pugliatti, Maura
Sotgiu, Alessandra
Logroscino, Giancarlo
Traynor, Bryan
Renton, Alan
Majounie, Elisa
Lauria, Giuseppe
Caponnetto, Claudia
Mandrioli, Jessica
Salvi, Fabrizio
Volanti, Paolo
La Bella, Vincenzo
Monsurro, Maria
Zollino, Marcella
Ossola, Irene
Brunetti, Maura
Restagno, Gabriella
TI C9ORF72 in a Large Series of Italian and Sardinian Familial and Sporadic
ALS Patients
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Chio, Adriano; Calvo, Andrea; Ossola, Irene; Brunetti, Maura] Univ Turin, Turin, Italy.
[Borghero, Giuseppe] Univ Cagliari, Cagliari, Italy.
[Sabatelli, Mario] Univ Cattolica Sacro Cuore, Rome, Italy.
[Corbo, Massimo] NEMO Ctr, Milan, Italy.
[Mora, Gabriele] Fdn Maugeri, Milan, Italy.
[Giannini, Fabio] Univ Siena, I-53100 Siena, Italy.
[Conforti, Francesca] CNR Cosenza, Cosenza, Italy.
[Penco, Silvana] Osped Niguarda Ca Granda, Milan, Italy.
[Pugliatti, Maura] Univ Sassari, Milan, Italy.
[Sotgiu, Alessandra] Univ Sassari, I-07100 Sassari, Italy.
[Logroscino, Giancarlo] Univ Bari, Bari, Italy.
[Traynor, Bryan; Renton, Alan; Majounie, Elisa] NIH, Bethesda, MD 20892 USA.
[Lauria, Giuseppe] Ist Neurol Besta, Milan, Italy.
[Caponnetto, Claudia] Univ Genoa, Genoa, Italy.
[Mandrioli, Jessica] Univ Modena, I-41100 Modena, Italy.
[Salvi, Fabrizio] Osped Bellaria, Cesena, FC, Italy.
[Volanti, Paolo] Fdn Maugeri, Mistretta, Italy.
[La Bella, Vincenzo] Univ Palermo, Palermo, Italy.
[Monsurro, Maria] Univ Naples Federico II, Naples, Italy.
[Zollino, Marcella] Catholic Hosp, Rome, Italy.
[Restagno, Gabriella] OIRM St Anna Hosp, Turin, Italy.
RI LOGROSCINO, GIANCARLO/K-5148-2016
OI LOGROSCINO, GIANCARLO/0000-0003-0423-3242
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P05161
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802407
ER
PT J
AU Chio, A
Restagno, G
Brunetti, M
Ossola, I
Calvo, A
Moglia, C
Traynor, B
Renton, A
Majounie, E
Corrado, L
D'Alfonso, S
Mora, G
Mazzini, L
AF Chio, Adriano
Restagno, Gabriella
Brunetti, Maura
Ossola, Irene
Calvo, Andrea
Moglia, Cristina
Traynor, Bryan
Renton, Alan
Majounie, Elisa
Corrado, Lucia
D'Alfonso, Sandra
Mora, Gabriele
Mazzini, Letizia
CA PARALS Study Grp
TI Genetics of ALS in Italy: A Population-Based Study
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Chio, Adriano] Univ Turin, Biella, Italy.
[Restagno, Gabriella; Brunetti, Maura; Ossola, Irene] ASO OIRM St Anna, Turin, Italy.
[Brunetti, Maura; Ossola, Irene] Dept Neurosci, Turin, Italy.
[Calvo, Andrea; Moglia, Cristina] Univ Turin, Turin, Italy.
[Traynor, Bryan; Renton, Alan; Majounie, Elisa] NIH, Bethesda, MD 20892 USA.
[Corrado, Lucia; D'Alfonso, Sandra; Mazzini, Letizia] Univ Piemonte Orientale, Novara, Italy.
[Mora, Gabriele] Fdn Maugeri, Milan, Italy.
RI D'Alfonso, Sandra/K-7295-2014
OI D'Alfonso, Sandra/0000-0002-3983-9925
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S05005
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800412
ER
PT J
AU Czarnecki, K
Kranick, S
Horovitz, S
Voon, V
Ostuni, J
Hallett, M
AF Czarnecki, Kathrin
Kranick, Sarah
Horovitz, Silvina
Voon, Valerie
Ostuni, John
Hallett, Mark
TI Voxel-Based Morphometry (VBM) and Cortical Thickness in Motor Conversion
Disorders
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Czarnecki, Kathrin] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
[Kranick, Sarah] NINDS, NIH, Brookeville, MD USA.
[Voon, Valerie] Behav & Clin Neurosci Inst, Dept Expt Psychol, Cambridge, England.
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P03124
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801480
ER
PT J
AU De Jesus-Acosta, C
Rosado, N
Hechavarria, R
Miguel, LS
Serrano, L
Nath, A
Wojna, V
AF De Jesus-Acosta, Carolina
Rosado, Noel
Hechavarria, Rosa
Miguel, Liza San
Serrano, Luis
Nath, Avindra
Wojna, Valerie
TI Thinning of Retinal Nerve Fiber Layer Is Associated with Neurocognitive
Impairment in HIV Infected Women
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [De Jesus-Acosta, Carolina] Duke Med Ctr Neuromuscular Med Fellowship, Durham, NC USA.
[Rosado, Noel] Duke Med Ctr Cornea Fellowship, Duke Eye Ctr, Durham, NC USA.
[Hechavarria, Rosa; Wojna, Valerie] Univ Puerto Rico, NeuroAIDS Program, San Juan, PR 00936 USA.
[Miguel, Liza San; Wojna, Valerie] Univ Puerto Rico, Div Neurol, San Juan, PR 00936 USA.
[Nath, Avindra] NINDS, Sect Infect Nervous Syst, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P01263
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800230
ER
PT J
AU Ellenstein, A
Karabanov, A
Song, SB
Sigman, L
Martinez, V
Hallett, M
AF Ellenstein, Aviva
Karabanov, Anke
Song, Sunbin
Sigman, Lauren
Martinez, Valeria
Hallett, Mark
TI Motor Sequence Learning Via the Mirror Neuron System
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Ellenstein, Aviva; Karabanov, Anke; Martinez, Valeria; Hallett, Mark] Natl Inst Neurol Disorders & Stroke, Human Motor Control Sect, NIH, Bethesda, MD USA.
[Sigman, Lauren] Boston Univ, Sch Med, Boston, MA 02118 USA.
[Song, Sunbin] Natl Inst Neurol Disorders & Stroke, Human Cort Physiol & Stroke Neurorehabil Unit, NIH, Bethesda, MD 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P04026
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802229
ER
PT J
AU Gaitan, M
de Alwis, M
Sati, P
Reich, D
AF Gaitan, Maria
de Alwis, Manori
Sati, Pascal
Reich, Daniel
TI Multiple Sclerosis Changes the Size of Intralesional and Extralesional
Parenchymal Veins
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Gaitan, Maria; Sati, Pascal; Reich, Daniel] NIH, Neuroimmunol Branch, Bethesda, MD 20892 USA.
[de Alwis, Manori] Cornell Univ, New York, NY 10021 USA.
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P03040
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801516
ER
PT J
AU Gao, JJ
Staub, H
Zhao, EJ
Chen, HL
AF Gao, Jianjun
Staub, Heidi
Zhao, Edward J.
Chen, Honglei
TI Head Injury and Parkinson's Disease
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Gao, Jianjun; Zhao, Edward J.; Chen, Honglei] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Staub, Heidi] Social & Sci Syst, Durham, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P07134
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204804153
ER
PT J
AU Gao, JJ
Nalls, M
Shi, M
Joubert, B
Hernandez, D
Huang, XM
Hollenbeck, A
Singleton, A
Chen, HL
AF Gao, Jianjun
Nalls, Michael
Shi, Min
Joubert, Bonnie
Hernandez, Dena
Huang, Xuemei
Hollenbeck, Albert
Singleton, Andrew
Chen, Honglei
TI An Exploratory Analysis on Gene-Environment Interactions for Parkinson
Disease
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Gao, Jianjun; Joubert, Bonnie] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Nalls, Michael; Hernandez, Dena; Singleton, Andrew] NIA, Neurogenet Lab, Bethesda, MD 20892 USA.
[Shi, Min] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Huang, Xuemei] Penn State Univ, Milton S Hershey Med Ctr, Dept Neurol, Hershey, PA 17033 USA.
[Hollenbeck, Albert] AARP, Washington, DC USA.
RI Singleton, Andrew/C-3010-2009
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA PD4.003
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802095
ER
PT J
AU Goldman, S
Kamel, F
Bhudhikanok, G
Korell, M
Meng, C
Comyns, K
Umbach, D
Hoppin, J
Ross, W
Marras, C
Kasten, M
Chade, A
Sandler, D
Blair, A
Langston, J
Tanner, C
AF Goldman, Samuel
Kamel, Freya
Bhudhikanok, Grace
Korell, Monica
Meng, Cheryl
Comyns, Kathleen
Umbach, David
Hoppin, Jane
Ross, Web
Marras, Connie
Kasten, Meike
Chade, Anabel
Sandler, Dale
Blair, Aaron
Langston, J.
Tanner, Caroline
TI Paraquat Use Modifies the Association of Head Injury and Parkinson's
Disease
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Goldman, Samuel; Bhudhikanok, Grace; Korell, Monica; Meng, Cheryl; Comyns, Kathleen; Langston, J.] Parkinsons Inst, Sunnyvale, CA USA.
[Umbach, David] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Hoppin, Jane; Sandler, Dale] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Ross, Web] Vet Affairs Pacific Isl Hlth Care Syst, Honolulu, HI USA.
[Marras, Connie] Toronto Western Hosp, Toronto, ON M5T 2S8, Canada.
[Kasten, Meike] Univ Lubeck, Lubeck, Germany.
[Chade, Anabel] Favaloro Univ, Inst Neurosci, Buenos Aires, DF, Argentina.
[Chade, Anabel] Favaloro Univ, Inst Cognit Neurol INECO, Buenos Aires, DF, Argentina.
[Blair, Aaron] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Tanner, Caroline] TPI, Sunnyvale, CA 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S42003
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803105
ER
PT J
AU Gudmundsson, L
Scher, A
Aspelund, T
Sigurdsson, S
Vidal, JS
Gudnason, V
Launer, L
AF Gudmundsson, Larus
Scher, Ann
Aspelund, Thor
Sigurdsson, Sigurdur
Vidal, Jean-Sebastien
Gudnason, Vilmundur
Launer, Lenore
TI The Joint Association of Migraine and Depression with Brain Volume: The
AGES-Reykjavik Study
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Gudmundsson, Larus; Scher, Ann] PMB Uniformed Serv Univ, Bethesda, MD USA.
[Aspelund, Thor; Sigurdsson, Sigurdur; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Vidal, Jean-Sebastien; Launer, Lenore] NIA, NIH, Bethesda, MD 20892 USA.
RI Aspelund, Thor/C-5983-2008; Gudnason, Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S36003
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802043
ER
PT J
AU Han, SP
Salgado, A
Alfahad, T
Bielekova, B
AF Han, Sungpil
Salgado, Alan
Alfahad, Tariq
Bielekova, Bibiana
TI Flow Cytometric Immunophenotyping of the Blood and CSF of Patients with
Multiple Sclerosis
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Han, Sungpil; Salgado, Alan; Bielekova, Bibiana] NIH, Neuroimmunol Branch, Bethesda, MD 20892 USA.
[Alfahad, Tariq] NIH, Neuroimmunol Branch, Arlington, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P02.081
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801211
ER
PT J
AU Harrison, D
Oh, J
Jones, C
Hua, J
Wood, E
Calabresi, P
Van Zijl, P
Reich, D
AF Harrison, Daniel
Oh, Jiwon
Jones, Craig
Hua, Jun
Wood, Emily
Calabresi, Peter
Van Zijl, Peter
Reich, Daniel
TI A Method for Analysis of Cortical Lesions on 7-Tesla MRI in Multiple
Sclerosis
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Harrison, Daniel; Oh, Jiwon; Wood, Emily; Calabresi, Peter] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Hua, Jun] Kennedy Krieger Inst, FM Kirby Res Ctr, Dept Radiol, Baltimore, MD USA.
[Reich, Daniel] Natl Inst Neurol Disorders & Stroke, Neuroimmunol Branch, Bethesda, MD USA.
RI Hua, Jun/F-7879-2012; Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P03064
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801531
ER
PT J
AU Herman, M
Wu, TX
Bielekova, B
AF Herman, Matthew
Wu, Tianxia
Bielekova, Bibiana
TI Cerebrospinal Fluid IL-12p40 Is a Biomarker of Intrathecal Inflammation
in Multiple Sclerosis
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Herman, Matthew; Wu, Tianxia; Bielekova, Bibiana] NINDS, Neuroimmunol Branch, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S40006
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802063
ER
PT J
AU Hernandez, D
Merino, J
Freeman, J
Luby, M
Warach, S
Latour, L
AF Hernandez, Daymara
Merino, Jose
Freeman, Jason
Luby, Marie
Warach, Steven
Latour, Lawrence
TI Gradient-Echo and Segmented-EPI Imaging Comparison in Thrombolytic
Treated Patients
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Hernandez, Daymara; Merino, Jose; Freeman, Jason; Luby, Marie; Warach, Steven; Latour, Lawrence] NINDS, Sect Stroke Diagnost & Therapeut, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S23003
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801552
ER
PT J
AU Hernandez, D
Merino, J
Freeman, J
Luby, M
Warach, S
Latour, L
AF Hernandez, Daymara
Merino, Jose
Freeman, Jason
Luby, Marie
Warach, Steven
Latour, Lawrence
TI Gradient-Echo and Segmented-EPI Imaging Comparison in Thrombolytic
Treated Patients
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Hernandez, Daymara; Merino, Jose; Freeman, Jason; Luby, Marie; Warach, Steven; Latour, Lawrence] Natl Inst Neurol Disorders & Stroke, Sect Stroke Diagnost & Therapeut, Bethesda, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN21004
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800028
ER
PT J
AU Kamel, F
Richardson, G
Umbach, D
Richards, M
Bhudhikanok, G
Blair, A
Chade, A
Comyns, K
Goldman, S
Hoppin, J
Kasten, M
Korell, M
Marras, C
Meng, C
Ross, G
Langston, J
Sandler, D
Tanner, C
AF Kamel, Freya
Richardson, Gina
Umbach, David
Richards, Marie
Bhudhikanok, Grace
Blair, Aaron
Chade, Anabel
Comyns, Kathleen
Goldman, Samuel
Hoppin, Jane
Kasten, Meike
Korell, Monica
Marras, Connie
Meng, Cheryl
Ross, G.
Langston, J.
Sandler, Dale
Tanner, Caroline
TI Risk of Parkinson's Disease (PD) Associated with the Herbicide Paraquat
Is Attenuated by High Dietary Intake of Polyunsaturated Fatty Acids
(PUFAs)
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Kamel, Freya; Richardson, Gina; Umbach, David; Hoppin, Jane; Sandler, Dale] NIEHS, Res Triangle Pk, NC 27709 USA.
[Richards, Marie] Westat Corp, Durham, NC USA.
[Bhudhikanok, Grace; Comyns, Kathleen; Goldman, Samuel; Korell, Monica; Meng, Cheryl; Langston, J.; Tanner, Caroline] Parkinsons Inst, Sunnyvale, CA USA.
[Blair, Aaron] NCI, Rockville, MD USA.
[Chade, Anabel] Favaloro Univ, Buenos Aires, DF, Argentina.
[Kasten, Meike] Univ Lubeck, Lubeck, Germany.
[Marras, Connie] Univ Toronto, Toronto, ON, Canada.
[Ross, G.] VA Pacific Isl Hlth Care Syst, Honolulu, HI USA.
NR 0
TC 0
Z9 0
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S42004
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803106
ER
PT J
AU Kapogiannis, D
Reiter, D
AF Kapogiannis, Dimitrios
Reiter, David
TI Precuneus Glutamate and GABA Predict Default Mode Network Activity
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Kapogiannis, Dimitrios; Reiter, David] NIA, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA PD7005
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803233
ER
PT J
AU Kapogiannis, D
Reiter, D
AF Kapogiannis, Dimitrios
Reiter, David
TI Precuneus Glutamate and GABA Predict Default Mode Network Activity
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Kapogiannis, Dimitrios; Reiter, David] NIA, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN41001
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800082
ER
PT J
AU Kranick, S
Holland, S
Uzel, G
Nath, A
AF Kranick, Sarah
Holland, Steven
Uzel, Gulbu
Nath, Avindra
TI CNS Complications in Immunodeficiency Syndromes Due to Mutations in
Transcription Factors STAT-1 and GATA-2
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Kranick, Sarah] Natl Inst Neurol Disorders & Stroke, Neurol Consult Serv, NIH, Bethesda, MD USA.
[Holland, Steven; Uzel, Gulbu] NIAID, Lab Clin Infect Dis, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S57003
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803197
ER
PT J
AU Kreisl, W
Brown, A
Lyoo, CH
Zhang, Y
Morse, C
Jenko, K
Clark, D
Zoghbi, S
Esposito, D
Mbeo, G
Creighton, J
Pike, V
Innis, R
McArthur, J
AF Kreisl, William
Brown, Amira
Lyoo, Chul Hyoung
Zhang, Yi
Morse, Cheryl
Jenko, Kimberly
Clark, David
Zoghbi, Sami
Esposito, Deneen
Mbeo, Gilbert
Creighton, Jason
Pike, Victor
Innis, Robert
McArthur, Justin
TI Mild Neurocognitive Impairment in HIV Infection Is Associated with
Neuroinflammation on Positron Emission Tomography
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Kreisl, William; Brown, Amira; Lyoo, Chul Hyoung; Zhang, Yi; Morse, Cheryl; Jenko, Kimberly; Clark, David; Zoghbi, Sami; Pike, Victor; Innis, Robert] NIMH, Bethesda, MD 20892 USA.
[Esposito, Deneen; Mbeo, Gilbert; Creighton, Jason; McArthur, Justin] Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S37003
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802072
ER
PT J
AU Kreisl, W
Brown, A
Lyoo, CH
Zhang, Y
Morse, C
Jenko, K
Clark, D
Zoghbi, S
Esposito, D
Mbeo, G
Creighton, J
Pike, V
Innis, R
McArthur, J
AF Kreisl, William
Brown, Amira
Lyoo, Chul Hyoung
Zhang, Yi
Morse, Cheryl
Jenko, Kimberly
Clark, David
Zoghbi, Sami
Esposito, Deneen
Mbeo, Gilbert
Creighton, Jason
Pike, Victor
Innis, Robert
McArthur, Justin
TI Mild Neurocognitive Impairment in HIV Infection Is Associated with
Neuroinflammation on Positron Emission Tomography
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Kreisl, William; Brown, Amira; Lyoo, Chul Hyoung; Zhang, Yi; Morse, Cheryl; Jenko, Kimberly; Clark, David; Zoghbi, Sami; Pike, Victor; Innis, Robert] NIMH, Bethesda, MD 20892 USA.
[Esposito, Deneen; Mbeo, Gilbert; Creighton, Jason; McArthur, Justin] Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN31008
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800069
ER
PT J
AU Lee, P
Xu, QG
Herman, M
Reich, D
Bielekova, B
AF Lee, Paul
Xu, Quangang
Herman, Matthew
Reich, Daniel
Bielekova, Bibiana
TI Distinct Phenotype of Immortalized CSF B-Cells in Multiple Sclerosis
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Herman, Matthew] NIH, Neuroimmunol Branch, Bethesda, MD 20892 USA.
[Xu, Quangang] Chinese Peoples Liberat Army Gen Hosp, Beijing, Peoples R China.
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S30007
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802027
ER
PT J
AU Leishear, K
Boudreau, R
Studenski, S
Ferrucci, L
Rosano, C
de Rekeneire, N
Houston, D
Kritchevsky, S
Schwartz, A
Vinik, A
Hogervorst, E
Yaffe, K
Harris, T
Newman, A
Strotmeyer, E
AF Leishear, Kira
Boudreau, Robert
Studenski, Stephanie
Ferrucci, Luigi
Rosano, Caterina
de Rekeneire, Nathalie
Houston, Denise
Kritchevsky, Stephen
Schwartz, Ann
Vinik, Aaron
Hogervorst, Eva
Yaffe, Kristine
Harris, Tamara
Newman, Anne
Strotmeyer, Elsa
TI Vitamin B12 and Neurological Function: Is There a Threshold Level?
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Leishear, Kira; Boudreau, Robert; Studenski, Stephanie; Rosano, Caterina; Newman, Anne; Strotmeyer, Elsa] Univ Pittsburgh, Pittsburgh, PA USA.
[Ferrucci, Luigi] NIA, Baltimore, MD 21224 USA.
[de Rekeneire, Nathalie] Yale Univ, Sch Med, New Haven, CT USA.
[Houston, Denise; Kritchevsky, Stephen] Wake Forest Sch Med, Winston Salem, NC USA.
[Schwartz, Ann; Yaffe, Kristine] UCSF, San Francisco, CA USA.
[Vinik, Aaron] EVMS Strelitz Diabet Res Ctr, Norfolk, VA USA.
[Hogervorst, Eva] Univ Loughborough, Loughborough, Leics, England.
[Harris, Tamara] NIA, Bethesda, MD 20892 USA.
RI Newman, Anne/C-6408-2013; Strotmeyer, Elsa/F-3015-2014
OI Newman, Anne/0000-0002-0106-1150;
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P02059
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801006
ER
PT J
AU Lewis, J
Wassermann, E
AF Lewis, Jeffrey
Wassermann, Eric
TI Anhedonia in Combat Veterans with Penetrating Head Injury
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Lewis, Jeffrey; Wassermann, Eric] NINDS, Behav Neurol Unit, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P01180
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800260
ER
PT J
AU Lewis, J
Wassermann, E
AF Lewis, Jeffrey
Wassermann, Eric
TI Anhedonia in Combat Veterans with Penetrating Head Injury
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Lewis, Jeffrey; Wassermann, Eric] NINDS, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN41009
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800090
ER
PT J
AU Lill, C
Meissner, E
Schjeide, L
Schjeide, BM
Liebsch, M
Roehr, J
Rouleau, G
Hardiman, O
Traynor, B
Van den Berg, L
Al-Chalabi, A
Bertram, L
AF Lill, Christina
Meissner, Esther
Schjeide, Leif
Schjeide, Brit-Maren
Liebsch, Maria
Roehr, Johannes
Rouleau, Guy
Hardiman, Orla
Traynor, Bryan
Van den Berg, Leonard
Al-Chalabi, Ammar
Bertram, Lars
TI Comprehensive Research Synopsis and Systematic Meta-Analyses in ALS
Genetics: The ALSGene Database
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Lill, Christina; Meissner, Esther; Schjeide, Leif; Schjeide, Brit-Maren; Liebsch, Maria; Roehr, Johannes; Bertram, Lars] Max Planck Inst Mol Genet, Dept Vertebrate Genom, D-14195 Berlin, Germany.
[Rouleau, Guy] CHUM Res Ctr, Montreal, PQ, Canada.
[Hardiman, Orla] Trinity Coll Dublin, Dublin, Ireland.
[Hardiman, Orla] Beaumont Hosp, Dublin 9, Ireland.
[Traynor, Bryan] NIA, Bethesda, MD 20892 USA.
[Van den Berg, Leonard] Univ Utrecht, Rudolf Magnus Inst, Utrecht, Netherlands.
[Al-Chalabi, Ammar] Kings Coll London, London WC2R 2LS, England.
RI Al-Chalabi, Ammar/E-5361-2010
OI Al-Chalabi, Ammar/0000-0002-4924-7712
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P01095
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800148
ER
PT J
AU Lublin, F
Cofield, S
Cutter, G
Conwit, R
Narayana, P
Nelson, F
Gustafson, T
Wolinsky, J
AF Lublin, Fred
Cofield, Stacey
Cutter, Gary
Conwit, Robin
Narayana, Ponnada
Nelson, Flavia
Gustafson, Tarah
Wolinsky, Jerry
CA CombiRx Investigators
TI The CombiRx Trial: A Multi-Center, Double-Blind, Randomized Study
Comparing the Combined Use of Interferon Beta-1a and Glatiramer Acetate
to Either Agent Alone in Participants with Relapsing-Remitting Multiple
Sclerosis - Clinical Outcomes
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Lublin, Fred; Gustafson, Tarah; CombiRx Investigators] Mt Sinai Sch Med, New York, NY USA.
[Cofield, Stacey; Cutter, Gary] Univ Alabama Birmingham, Birmingham, AL USA.
[Conwit, Robin] NINDS, NIH, Lutherville Timonium, MD USA.
[Narayana, Ponnada; Nelson, Flavia; Wolinsky, Jerry] Univ Texas Hlth Sci Ctr Houston, Houston, TX 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA PL02003
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204804243
ER
PT J
AU Masdeu, J
Mattay, V
Chen, Q
Kohn, P
Muse, J
Kolachana, B
Nichols, L
Weinberger, D
Berman, K
AF Masdeu, Joseph
Mattay, Venkata
Chen, Qiang
Kohn, Philip
Muse, John
Kolachana, Bhaskar
Nichols, Lisa
Weinberger, Daniel
Berman, Karen
TI Age-Related Effect of APOE Genotype on Brain Functional Connectivity
during Episodic Memory Encoding
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Masdeu, Joseph; Chen, Qiang; Kohn, Philip; Muse, John; Kolachana, Bhaskar; Nichols, Lisa; Weinberger, Daniel; Berman, Karen] NIH, Bethesda, MD 20892 USA.
[Mattay, Venkata] Intramural Natl Inst Hlth, Mclean, VA USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P03084
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801300
ER
PT J
AU Nair, G
Inati, S
Kranick, S
Quezado, M
Sereti, I
Sheikh, V
Reich, D
Nath, A
AF Nair, Govind
Inati, Souheil
Kranick, Sarah
Quezado, Martha
Sereti, Irini
Sheikh, Virginia
Reich, Daniel
Nath, Avindra
TI Postmortem MRI in Progressive Multifocal Leukoencephalopathy
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Nair, Govind; Reich, Daniel] NINDS, NIH, Bethesda, MD 20892 USA.
[Inati, Souheil] NIMH, NIH, Bethesda, MD 20892 USA.
[Kranick, Sarah] NIH, Brookeville, MD USA.
[Quezado, Martha] NCI, NIH, Bethesda, MD 20892 USA.
[Sereti, Irini; Sheikh, Virginia] NIAID, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P02272
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801104
ER
PT J
AU Nath, A
Choi, E
Wang, TG
AF Nath, Avindra
Choi, Elliot
Wang, Tongguang
TI Direct Conversion to Neurons from Adult Human Fibroblasts and
Hematopoietic Stem Cells In Vitro
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Nath, Avindra; Choi, Elliot; Wang, Tongguang] NINDS, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN81003
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801542
ER
PT J
AU Nath, A
Choi, E
Wang, TG
AF Nath, Avindra
Choi, Elliot
Wang, Tongguang
TI Direct Conversion to Neurons from Adult Human Fibroblasts and
Hematopoietic Stem Cells In Vitro
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Nath, Avindra; Choi, Elliot; Wang, Tongguang] NINDS, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P02014
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801135
ER
PT J
AU Nath, A
Major, E
Aksamit, A
Calabrese, L
Sejvar, J
Kotton, C
Barhams, M
AF Nath, Avindra
Major, Eugene
Aksamit, Allen
Calabrese, Leonard
Sejvar, James
Kotton, Camille
Barhams, Maria
TI Establishment of a Registry To Identify Cases of PML Using Uniform
Diagnostic Criteria
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Nath, Avindra; Major, Eugene; Barhams, Maria] NINDS, NIH, Bethesda, MD 20892 USA.
[Aksamit, Allen] Mayo Clin, Rochester, MN USA.
[Calabrese, Leonard] Cleveland Clin, Cleveland, OH 44106 USA.
[Sejvar, James] CDC, Decatur, GA USA.
[Kotton, Camille] Massachusetts Gen Hosp, Boston, MA 02114 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S08002
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800420
ER
PT J
AU Nayak, L
Scott, J
Bauchet, L
Fraum, T
Cooper, A
Chao, S
Suh, J
Abrey, L
Peereboom, D
Zouaoui, S
Fabbro-Peray, P
Taillandier, L
Rigao, V
Vogelbaum, M
Mathieu-Daude, H
DeAngelis, L
Shih, J
Iwamoto, F
AF Nayak, Lakshmi
Scott, Jacob
Bauchet, Luc
Fraum, Tyler
Cooper, Anna
Chao, Samuel
Suh, John
Abrey, Lauren
Peereboom, David
Zouaoui, Sonia
Fabbro-Peray, Pascale
Taillandier, Luc
Rigao, Valerie
Vogelbaum, Michael
Mathieu-Daude, Helene
DeAngelis, Lisa
Shih, Joanna
Iwamoto, Fabio
TI Recursive Partitioning Analysis Identifies Prognostic Groups for
Glioblastoma Patients Aged 70 Years or Older
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Nayak, Lakshmi] Dana Farber Canc Inst, Ctr Neurooncol, Boston, MA 02115 USA.
[Scott, Jacob] Univ S Florida, H Lee Moffitt Canc Ctr, Dept Radiat Oncol, Tampa, FL 33682 USA.
[Bauchet, Luc; Zouaoui, Sonia] Hop St Eloi Gui de Chauliac, Dept Neurosurg, Montpellier, France.
[Bauchet, Luc; Zouaoui, Sonia] Hop St Eloi Gui de Chauliac, INSERM, U583, Montpellier, France.
[Fraum, Tyler] Duke Univ, Sch Med, Durham, NC USA.
[Cooper, Anna] Univ Rochester, Sch Med & Dent, Rochester, NY USA.
[Vogelbaum, Michael] Cleveland Clin Fdn, Brain Tumor & Neurooncol Ctr, Cleveland, OH 44195 USA.
[Abrey, Lauren] F Hoffmann La Roche Ltd, Basel, Switzerland.
[Fabbro-Peray, Pascale] Inst Univ Rech Clin, Montpellier, France.
[Taillandier, Luc] Hop Neurol, Nancy, France.
[Rigao, Valerie] Hop Gui de Chauliac, Dept Pathl, Ctr Hosp Univ, Montpellier, France.
[Mathieu-Daude, Helene] Languedoc Roussillon Registre Tumeurs Herault, Grp Neurooncol, Montpellier, France.
[DeAngelis, Lisa] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Shih, Joanna] NCI, Biometr Res Branch, Div Canc Treatment & Diag, NIH, Rockville, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P07109
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204804095
ER
PT J
AU Oh, J
Zackowski, K
Chen, M
Newsome, S
Smith, S
Prince, J
Calabresi, P
Reich, D
AF Oh, Jiwon
Zackowski, Kathleen
Chen, Min
Newsome, Scott
Smith, Seth
Prince, Jerry
Calabresi, Peter
Reich, Daniel
TI Diffusion Tensor and Magnetization Transfer Imaging Correlates of Motor
Dysfunction in the Spinal Cord in Multiple Sclerosis
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Oh, Jiwon] Johsn Hopkins Univ, Baltimore, MD USA.
[Zackowski, Kathleen] Johns Hopkins Univ, Kennedy Krieger Inst, Baltimore, MD USA.
[Newsome, Scott] Johns Hopkins Univ, Abingdon, MD USA.
[Smith, Seth] Vanderbilt Univ, Nashville, TN USA.
[Reich, Daniel] NINDS, Translat Neuroradiol Unit, Bethesda, MD 20892 USA.
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S21002
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801568
ER
PT J
AU Rinaldi, C
Grunseich, C
Sevrioukova, I
Schindler, A
Ghezzi, D
Zeviani, M
Fischbeck, K
AF Rinaldi, Carlo
Grunseich, Christopher
Sevrioukova, Irina
Schindler, Alice
Ghezzi, Daniele
Zeviani, Massimo
Fischbeck, Kenneth
TI X-Linked Recessive Axonal Neuropathy with Deafness and Cognitive
Impairment (Cowchock Syndrome) Is Associated with Mutation in AIFM1
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Rinaldi, Carlo; Grunseich, Christopher; Schindler, Alice; Fischbeck, Kenneth] NINDS, Neurogenet Branch, Bethesda, MD 20892 USA.
[Sevrioukova, Irina] Univ Calif Irvine, Irvine, CA USA.
[Ghezzi, Daniele; Zeviani, Massimo] Natl Neurol Inst Carlo Besta, Unit Mol Neurogenet, Milan, Italy.
RI Ghezzi, Daniele/J-7873-2016
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S07007
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800422
ER
PT J
AU Ross, W
Duda, J
Abbott, R
Petrovitch, H
Tanner, C
Masaki, K
Uyehara-Lock, J
Launer, L
White, L
AF Ross, Web
Duda, John
Abbott, Robert
Petrovitch, Helen
Tanner, Caroline
Masaki, Kamal
Uyehara-Lock, Jane
Launer, Lenore
White, Lon
TI Association of Coffee and Caffeine Consumption with Brain Lewy Pathology
in the Honolulu-Asia Aging Study
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Ross, Web] VA Pacific Isl Hlth Care Syst, Honolulu, HI USA.
[Duda, John] Philadelphia VA Med Ctr, Philadelphia, PA USA.
[Abbott, Robert] Univ Virginia, Sch Med, Charlottesville, VA 22908 USA.
[Petrovitch, Helen] Pacific Hlth Res & Educ Inst, Kailua, HI USA.
[Tanner, Caroline] Parkinsons Inst, Sunnyvale, CA USA.
[Masaki, Kamal] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96822 USA.
[Launer, Lenore] NIA, NIH, Washington, DC USA.
[White, Lon] Kuakini Med Ctr, Honolulu, HI USA.
[Uyehara-Lock, Jane] U Hawaii John A Burns Sch Med, Honolulu, HI 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S42005
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204803107
ER
PT J
AU Scharf, J
Yu, DM
Mathews, C
Neale, B
Stewart, E
Fagerness, J
Evans, P
Gamazon, E
Service, S
Osiecki, L
Illmann, C
Cath, D
King, R
Dion, Y
Sandor, P
Barr, C
Budman, C
Lyon, G
Grados, M
Singer, H
Jankovic, J
Gilbert, D
Hoekstra, P
Heiman, G
Tischfield, J
State, M
Robertson, M
Kurlan, R
Ophoff, R
Gibbs, JR
Cookson, M
Hardy, J
Singleton, A
Ruiz-Linares, A
Rouleau, G
Heutink, P
Oostra, B
McMahon, W
Freimer, N
Cox, N
Pauls, D
AF Scharf, Jeremiah
Yu, Dongmei
Mathews, Carol
Neale, Benjamin
Stewart, Evelyn
Fagerness, Jes
Evans, Patrick
Gamazon, Eric
Service, Susan
Osiecki, Lisa
Illmann, Cornelia
Cath, Danielle
King, Robert
Dion, Yves
Sandor, Paul
Barr, Cathy
Budman, Cathy
Lyon, Gholson
Grados, Marco
Singer, Harvey
Jankovic, Joseph
Gilbert, Donald
Hoekstra, Pieter
Heiman, Gary
Tischfield, Jay
State, Matthew
Robertson, Mary
Kurlan, Roger
Ophoff, Roel
Gibbs, J. Raphael
Cookson, Mark
Hardy, John
Singleton, Andrew
Ruiz-Linares, Andres
Rouleau, Guy
Heutink, Peter
Oostra, Ben
McMahon, William
Freimer, Nelson
Cox, Nancy
Pauls, David
TI Genome-Wide Association Study of Gilles de la Tourette Syndrome
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Yu, Dongmei; Neale, Benjamin] Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, Boston, MA USA.
[Stewart, Evelyn] Univ British Columbia, Vancouver, BC V5Z 1M9, Canada.
[Fagerness, Jes; Osiecki, Lisa] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Mathews, Carol] Psychiat UCSF, San Francisco, CA USA.
[Evans, Patrick; Gamazon, Eric; Cox, Nancy] Univ Chicago, Chicago, IL 60637 USA.
[Service, Susan; Ophoff, Roel; Freimer, Nelson] Univ Calif Los Angeles, Los Angeles, CA USA.
[Illmann, Cornelia] MGH, Boston, MA USA.
[Cath, Danielle] Univ Utrecht, Utrecht, Netherlands.
[State, Matthew] Yale Univ, Sch Med, New Haven, CT USA.
[Dion, Yves; Rouleau, Guy] Univ Montreal, Montreal, PQ, Canada.
[Dion, Yves; Sandor, Paul] Univ Toronto, Toronto, ON, Canada.
[Budman, Cathy] N Shore LIJ Med Ctr, Manhasset, NY USA.
[Lyon, Gholson] Childrens Hosp Philadephia, Philadelphia, PA USA.
[Grados, Marco] Johns Hopkins Univ, Baltimore, MD USA.
[Jankovic, Joseph] Baylor Coll Med, Houston, TX 77030 USA.
[Gilbert, Donald] Cincinnati Childrens Med Ctr, Cincinnati, OH USA.
[Hoekstra, Pieter] Univ Groningen, Groningen, Netherlands.
[Heiman, Gary; Tischfield, Jay] Rutgers State Univ, Piscataway, NJ USA.
[Robertson, Mary] St George Hosp, London, England.
[Kurlan, Roger] Atlantic Neurosci Inst, Summit, NJ USA.
[Gibbs, J. Raphael; Cookson, Mark; Singleton, Andrew] NIH, Bethesda, MD 20892 USA.
[Hardy, John; Ruiz-Linares, Andres] UCL, London, England.
[Heutink, Peter] Dept Clin Genet, Amsterdam, Netherlands.
[Oostra, Ben] Erasmus Univ, Dept Clin Genet, NL-3000 DR Rotterdam, Netherlands.
[McMahon, William] Univ Utah, Salt Lake City, UT 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN101002
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204804240
ER
PT J
AU Scharf, J
Yu, DM
Mathews, C
Neale, B
Stewart, E
Fagerness, J
Evans, P
Gamazon, E
Service, S
Osiecki, L
Illmann, C
Cath, D
King, R
Dion, Y
Sandor, P
Barr, C
Budman, C
Lyon, G
Grados, M
Singer, H
Jankovic, J
Gilbert, D
Hoekstra, P
Heiman, G
Tischfield, J
State, M
Robertson, M
Kurlan, R
Ophoff, R
Gibbs, JR
Cookson, M
Hardy, J
Singleton, A
Ruiz-Linares, A
Rouleau, G
Heutink, P
Oostra, B
McMahon, W
Freimer, N
Cox, N
Pauls, D
AF Scharf, Jeremiah
Yu, Dongmei
Mathews, Carol
Neale, Benjamin
Stewart, Evelyn
Fagerness, Jes
Evans, Patrick
Gamazon, Eric
Service, Susan
Osiecki, Lisa
Illmann, Cornelia
Cath, Danielle
King, Robert
Dion, Yves
Sandor, Paul
Barr, Cathy
Budman, Cathy
Lyon, Gholson
Grados, Marco
Singer, Harvey
Jankovic, Joseph
Gilbert, Donald
Hoekstra, Pieter
Heiman, Gary
Tischfield, Jay
State, Matthew
Robertson, Mary
Kurlan, Roger
Ophoff, Roel
Gibbs, J. Raphael
Cookson, Mark
Hardy, John
Singleton, Andrew
Ruiz-Linares, Andres
Rouleau, Guy
Heutink, Peter
Oostra, Ben
McMahon, William
Freimer, Nelson
Cox, Nancy
Pauls, David
TI Genome-Wide Association Study of Gilles de la Tourette Syndrome
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Yu, Dongmei; Neale, Benjamin; Pauls, David] Ctr Human Genet Res, Psychiat & Neurodev Genet Unit, Boston, MA USA.
[Mathews, Carol] Psychiat UCSF, San Francisco, CA USA.
[Stewart, Evelyn] Univ British Columbia, Vancouver, BC, Canada.
[Fagerness, Jes; Osiecki, Lisa; Illmann, Cornelia] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Evans, Patrick; Gamazon, Eric; Cox, Nancy] Univ Chicago, Chicago, IL 60637 USA.
[Service, Susan; Ophoff, Roel; Freimer, Nelson] Univ Calif Los Angeles, Los Angeles, CA USA.
[Cath, Danielle] Univ Utrecht, Utrecht, Netherlands.
[State, Matthew] Yale Univ, Sch Med, New Haven, CT USA.
[Dion, Yves; Rouleau, Guy] Univ Montreal, Montreal, PQ, Canada.
[Sandor, Paul; Barr, Cathy] Univ Toronto, Toronto, ON, Canada.
[Budman, Cathy] N Shore LIJ Med Ctr, Manhasset, NY USA.
[Lyon, Gholson] Childrens Hosp Philadephia, Philadelphia, MA USA.
[Grados, Marco] Johns Hopkins Univ, Baltimore, MD USA.
[Singer, Harvey] Johns Hopkins, Baltimore, MD USA.
[Jankovic, Joseph] Baylor Coll Med, Houston, TX 77030 USA.
[Gilbert, Donald] Cincinnati Childrens Med Ctr, Cincinnati, OH USA.
[Hoekstra, Pieter] Univ Groningen, Groningen, Netherlands.
[Heiman, Gary; Tischfield, Jay] Rutgers State Univ, Piscataway, NJ USA.
[Robertson, Mary] St George Hosp, London, England.
[Kurlan, Roger] Atlantic Neurosci Inst, Summit, NJ USA.
[Gibbs, J. Raphael; Cookson, Mark; Singleton, Andrew] NIH, Bethesda, MD 20892 USA.
[Hardy, John; Ruiz-Linares, Andres] UCL, London, England.
[Heutink, Peter] Dept Clin Genet, Amsterdam, Netherlands.
[Oostra, Ben] Erasmus Univ, Dept Clin Genet, NL-3000 DR Rotterdam, Netherlands.
[McMahon, William] Univ Utah, Salt Lake City, UT USA.
RI Hardy, John/C-2451-2009; Singleton, Andrew/C-3010-2009; Stewart,
Evelyn/K-6961-2014
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S32006
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802034
ER
PT J
AU Scher, A
Eiriksdottir, G
Feit, P
Smith, A
Roecklein, K
Gudmundsson, L
Gudnason, V
Launer, L
AF Scher, Ann
Eiriksdottir, Gudny
Feit, Preethy
Smith, Albert
Roecklein, Kathryn
Gudmundsson, Larus
Gudnason, Vilmundur
Launer, Lenore
TI Selective Survival and Late-Life Risk Factor Studies
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Scher, Ann; Feit, Preethy; Gudmundsson, Larus] Uniformed Serv Univ Hlth Sci, Bethesda, MD USA.
[Eiriksdottir, Gudny; Smith, Albert; Gudnason, Vilmundur] Iceland Heart Assoc, Kopavogur, Iceland.
[Roecklein, Kathryn] Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA.
[Launer, Lenore] NIA, Washington, DC USA.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P04246
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802210
ER
PT J
AU Sheth, K
Koch, S
Elkind, M
Sung, G
Kittner, S
Frankel, M
Rosand, J
Langefeld, C
Comeau, M
Waddy, S
Osborne, J
Woo, D
AF Sheth, Kevin
Koch, Sebastian
Elkind, Mitchell
Sung, Gene
Kittner, Steven
Frankel, Michael
Rosand, Jonathan
Langefeld, Carl
Comeau, Mary
Waddy, Salina
Osborne, Jennifer
Woo, Daniel
CA ERICH Investigators
TI Anti-Epileptic Drug Use and Outcome in the Ethnic and Racial Variations
in Intracerebral Hemorrhage (ERICH) Study
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Sheth, Kevin] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
[Koch, Sebastian] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Elkind, Mitchell] Columbia Univ, New York, NY USA.
[Sung, Gene] Univ So Calif, Los Angeles, CA USA.
[Frankel, Michael] Emory Univ, Sch Med, Atlanta, GA USA.
[Rosand, Jonathan] MGH, Boston, MA USA.
[Langefeld, Carl] Wake Forest Sch Med, Winston Salem, NC USA.
[Comeau, Mary] Wake Forest Publ Hlth Sci, Winston Salem, NC USA.
[Waddy, Salina] NIH, Washington, DC USA.
[Osborne, Jennifer; Woo, Daniel; ERICH Investigators] Univ Cincinnati, Cincinnati, OH 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S23005
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801554
ER
PT J
AU Sweeney, E
Shinohara, R
Shea, C
Reich, D
Crainiceanu, C
AF Sweeney, Elizabeth
Shinohara, Russell
Shea, Colin
Reich, Daniel
Crainiceanu, Ciprian
TI Lesion Incidence Estimation and Detection Using Multi-Modality
Longitudinal MRIs
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Sweeney, Elizabeth; Shinohara, Russell; Crainiceanu, Ciprian] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
[Shea, Colin; Reich, Daniel] Natl Inst Neurol Disorder & Stroke, Bethesda, MD USA.
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P03069
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801526
ER
PT J
AU Theodore, W
Dustin, I
Khan, O
Hodgkinson, C
Akhtar, L
Goldman, D
AF Theodore, William
Dustin, Irene
Khan, Omar
Hodgkinson, Coiln
Akhtar, Longina
Goldman, David
TI Reduced Serotonin Transporter Promoter Activity in Mesial Temporal
Sclerosis and Temporal Lobe Epilepsy
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Theodore, William; Dustin, Irene; Khan, Omar] NIH, Bethesda, MD 20892 USA.
[Hodgkinson, Coiln; Akhtar, Longina; Goldman, David] NIH, Rockville, MD 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S26007
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204801570
ER
PT J
AU Theodore, W
Dustin, I
Khan, O
Hodgkinson, C
Akhtar, L
Goldman, D
AF Theodore, William
Dustin, Irene
Khan, Omar
Hodgkinson, Coiln
Akhtar, Longina
Goldman, David
TI Reduced Serotonin Transporter Promoter Activity in Mesial Temporal
Sclerosis and Temporal Lobe Epilepsy
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Theodore, William; Dustin, Irene; Khan, Omar] NIH, Bethesda, MD 20892 USA.
[Hodgkinson, Coiln; Akhtar, Longina; Goldman, David] NIH, Rockville, MD 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA IN52001
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800042
ER
PT J
AU Vanderver, A
Tonduti, D
Lebon, P
Blau, N
Loewenstein, J
Gahl, W
Toro, C
Hyland, K
AF Vanderver, Adeline
Tonduti, Davide
Lebon, Pierre
Blau, Nenad
Loewenstein, Johanna
Gahl, William
Toro, Camilo
Hyland, Keith
TI Neurotransmitter Abnormalities and Response to L-Dopa in SPG11
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Vanderver, Adeline; Loewenstein, Johanna] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Tonduti, Davide] IRCCS C Mondino Inst Neurol Fdn, Pavia, Italy.
[Lebon, Pierre] Univ Paris 05, Hop Cochin Paris, Paris, France.
[Blau, Nenad] Zurich ZH, Zurich, Switzerland.
[Gahl, William] NHGRI, NIH, Bethesda, MD 20892 USA.
[Toro, Camilo] NINDS, NIH, Frederick, MD USA.
RI tonduti, davide/K-1673-2016
OI tonduti, davide/0000-0001-9371-7454
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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P05133
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802487
ER
PT J
AU Wojna, V
Curry, T
Haughey, N
Bandaru, V
Skolasky, R
Hachavarria, R
Mayo, R
Bryant, C
Anderson, C
Fernandez, M
Velez, J
Nath, A
AF Wojna, Valerie
Curry, Thomas
Haughey, Norman
Bandaru, Veera
Skolasky, Richard
Hachavarria, Rosa
Mayo, Raul
Bryant, Carole
Anderson, Carole
Fernandez, Mayra
Velez, Joyce
Nath, Avindra
TI Gonadal Hormone Dysfunction Modulates CSF Oxidative Stress Markers in
HIV-Seropositive Women with Cognitive Impairment
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Wojna, Valerie] Univ Puerto Rico, Div Neurol, San Juan, PR 00936 USA.
[Wojna, Valerie; Hachavarria, Rosa; Mayo, Raul; Fernandez, Mayra; Velez, Joyce] Univ Puerto Rico, NeuroAIDS Program, San Juan, PR 00936 USA.
[Curry, Thomas; Bryant, Carole] Univ Kentucky, Div Reprod Endocrinol, Lexington, KY USA.
[Haughey, Norman; Bandaru, Veera] Johns Hopkins Univ, Dept Neurol, Baltimore, MD 21218 USA.
[Skolasky, Richard] Johns Hopkins Univ, Dept Orthopaed, Baltimore, MD USA.
[Anderson, Carole; Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Baltimore, MD 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S37002
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204802073
ER
PT J
AU Wolinsky, J
Narayana, P
Nelson, F
Datta, S
Cofield, S
Cutter, G
Conwit, R
Gustafson, T
Lublin, F
AF Wolinsky, Jerry
Narayana, Ponnada
Nelson, Flavia
Datta, Sushmita
Cofield, Stacey
Cutter, Gary
Conwit, Robin
Gustafson, Tarah
Lublin, Fred
CA CombiRx Investigators
TI The CombiRx Trial: A Multi-Center, Double-Blind, Randomized Study
Comparing the Combined Use of Interferon Beta-1a and Glatiramer Acetate
to Either Agent Alone in Participants with Relapsing Remitting Multiple
Sclerosis - MRI Outcomes
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Wolinsky, Jerry; Narayana, Ponnada; Nelson, Flavia; Datta, Sushmita] Univ Texas Hlth Sci Ctr Texas, Houston, TX USA.
[Cofield, Stacey; Cutter, Gary] Univ Alabama Birmingham, Birmingham, AL USA.
[Conwit, Robin] NINDS, NIH, Lutherville Timonium, MD USA.
[Gustafson, Tarah; Lublin, Fred; CombiRx Investigators] Mt Sinai Sch Med, New York, 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 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA S11002
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204804260
ER
PT J
AU Zhuang, P
Hallett, M
Dong, S
Zhang, XH
Zhang, YQ
Li, JY
Li, YJ
AF Zhuang, Ping
Hallett, Mark
Dong, Sheng
Zhang, Xiaohua
Zhang, Yuqing
Li, Jianyu
Li, Yongjie
TI Electrode Contact Location Correlates with the Location of Tic-Related
Neuronal Activity in the Globus Pallidus Internus in Patients with Tics
SO NEUROLOGY
LA English
DT Meeting Abstract
CT 64th Annual Meeting of the American-Academy-of-Neurology (AAN)
CY APR 21-28, 2012
CL New Orleans, LA
SP Amer Acad Neurol (AAN)
C1 [Zhuang, Ping; Dong, Sheng; Zhang, Xiaohua; Zhang, Yuqing; Li, Jianyu; Li, Yongjie] Capital Med Univ, Xuanwu Hosp, Beijing Inst Funct Neurosurg, Beijing, Peoples R China.
[Hallett, Mark] NINDS, Human Motor Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
SU 1
MA P01.189
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 931GQ
UT WOS:000303204800217
ER
PT J
AU Fernandez, MA
Rueda, C
Peddada, SD
AF Fernandez, Miguel A.
Rueda, Cristina
Peddada, Shyamal D.
TI Identification of a core set of signature cell cycle genes whose
relative order of time to peak expression is conserved across species
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID REGULATED GENES; FISSION YEAST; SACCHAROMYCES-CEREVISIAE;
EXPONENTIAL-FAMILIES; RESTRICTIONS; ARABIDOPSIS; CHECKPOINTS; NETWORK;
DAMAGE; POMBE
AB A cell division cycle is a well-coordinated process in eukaryotes with cell cycle genes exhibiting a periodic expression over time. There is considerable interest among cell biologists to determine genes that are periodic in multiple organisms and whether such genes are also evolutionarily conserved in their relative order of time to peak expression. Interestingly, periodicity is not well-conserved evolutionarily. A conservative estimate of a number of periodic genes common to fission yeast (Schizosaccharomyces pombe) and budding yeast (Saccharomyces cerevisiae) ('core set FB') is 35, while those common to fission yeast and humans (Homo sapiens) ('core set FH') is 24. Using a novel statistical methodology, we discover that the relative order of peak expression is conserved in similar to 80% of FB genes and in similar to 40% of FH genes. We also discover that the order is evolutionarily conserved in six genes which are potentially the core set of signature cell cycle genes. These include ace2 (a transcription factor) and polo-kinase plo1, which are well-known hubs of early M-phase clusters, cdc18 a key component of pre-replication complexes, mik1 which is critical for the establishment and maintenance of DNA damage check point, and histones hhf1 and hta2.
C1 [Peddada, Shyamal D.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Fernandez, Miguel A.; Rueda, Cristina] Univ Valladolid, Dept Stat & Operat Res, E-47005 Valladolid, Spain.
RP Peddada, SD (reprint author), NIEHS, Biostat Branch, Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM peddada@niehs.nih.gov
RI Peddada, Shyamal/D-1278-2012; Fernandez, Miguel/I-2874-2015
OI Fernandez, Miguel/0000-0002-1272-8950
FU Spanish Ministerio de Ciencia e Innovacion [MTM2009-11161]; National
Institutes of Health, National Institute of Environmental Health
Sciences [Z01 ES101744-04]; Biostatistics Branch, NIEHS, National
Institutes of Health
FX Spanish Ministerio de Ciencia e Innovacion (MTM2009-11161 to M.A.F. and
C.R.); Intramural Research Program of the National Institutes of Health,
National Institute of Environmental Health Sciences (Z01 ES101744-04).
Funding for open access charge: Biostatistics Branch, NIEHS, National
Institutes of Health.
NR 31
TC 10
Z9 10
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD APR
PY 2012
VL 40
IS 7
BP 2823
EP 2832
DI 10.1093/nar/gkr1077
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 930TQ
UT WOS:000303164400009
PM 22135306
ER
PT J
AU Kidder, BL
Palmer, S
AF Kidder, Benjamin L.
Palmer, Stephen
TI HDAC1 regulates pluripotency and lineage specific transcriptional
networks in embryonic and trophoblast stem cells
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID HISTONE DEACETYLASE 1; GENE-EXPRESSION; CHROMATIN-STRUCTURE;
POLYCOMB-GROUP; SELF-RENEWAL; DIFFERENTIATION; OCT4; REVEALS; COMPLEX;
NANOG
AB Epigenetic regulation of gene expression is important in maintaining self-renewal of embryonic stem (ES) and trophoblast stem (TS) cells. Histone deacetylases (HDACs) negatively control histone acetylation by removing covalent acetylation marks from histone tails. Because histone acetylation is a known mark for active transcription, HDACs presumably associate with inactive genes. Here, we used genome-wide chromatin immunoprecipitation to investigate targets of HDAC1 in ES and TS cells. Through evaluation of genes associated with acetylated histone H3 marks, and global expression analysis of Hdac1 knockout ES and trichostatin A-treated ES and TS cells, we found that HDAC1 occupies mainly active genes, including important regulators of ES and TS cells self-renewal. We also observed occupancy of methyl-CpG binding domain protein 3 (MBD3), a subunit of the nucleosome remodeling and histone deacetylation (NuRD) complex, at a subset of HDAC1-occupied sequences in ES cells, including the pluripotency regulators Oct4, Nanog and Kfl4. By mapping HDAC1 targets on a global scale, our results describe further insight into epigenetic mechanisms of ES and TS cells self-renewal.
C1 [Kidder, Benjamin L.; Palmer, Stephen] EMD Serono Res Inst, Billerica, MA 01821 USA.
[Kidder, Benjamin L.] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
RP Kidder, BL (reprint author), EMD Serono Res Inst, Billerica, MA 01821 USA.
EM Benjamin.kidder@nih.gov
FU EMD Serono Research Institute, Inc.; EMD Serono Research Institute
FX This work was funded by an internal grant at EMD Serono Research
Institute, Inc. Funding for open access charge: EMD Serono Research
Institute.
NR 44
TC 51
Z9 51
U1 0
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD APR
PY 2012
VL 40
IS 7
BP 2925
EP 2939
DI 10.1093/nar/gkr1151
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 930TQ
UT WOS:000303164400017
PM 22156375
ER
PT J
AU Kirby, TW
DeRose, EF
Cavanaugh, NA
Beard, WA
Shock, DD
Mueller, GA
Wilson, SH
London, RE
AF Kirby, Thomas W.
DeRose, Eugene F.
Cavanaugh, Nisha A.
Beard, William A.
Shock, David D.
Mueller, Geoffrey A.
Wilson, Samuel H.
London, Robert E.
TI Metal-induced DNA translocation leads to DNA polymerase conformational
activation
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID HIV-1 REVERSE-TRANSCRIPTASE; BASE EXCISION-REPAIR; NUCLEOTIDE
INCORPORATION; MAGNETIC-RESONANCE; MITOCHONDRIAL-DNA; GASTRIC-CANCER;
ABASIC SITE; IN-VITRO; BETA; MECHANISM
AB Binding of the catalytic divalent ion to the ternary DNA polymerase beta/gapped DNA/dNTP complex is thought to represent the final step in the assembly of the catalytic complex and is consequently a critical determinant of replicative fidelity. We have analyzed the effects of Mg2+ and Zn2+ on the conformational activation process based on NMR measurements of [methyl-C-13]methionine DNA polymerase beta. Unexpectedly, both divalent metals were able to produce a template base-dependent conformational activation of the polymerase/1-nt gapped DNA complex in the absence of a complementary incoming nucleotide, albeit with different temperature thresholds. This conformational activation is abolished by substituting Glu295 with lysine, thereby interrupting key hydrogen bonds necessary to stabilize the closed conformation. These and other results indicate that metal-binding can promote: translocation of the primer terminus base pair into the active site; expulsion of an unpaired pyrimidine, but not purine, base from the template-binding pocket; and motions of polymerase subdomains that close the active site. We also have performed pyrophosphorolysis studies that are consistent with predictions based on these results. These findings provide new insight into the relationships between conformational activation, enzyme activity and polymerase fidelity.
C1 [Kirby, Thomas W.; DeRose, Eugene F.; Cavanaugh, Nisha A.; Beard, William A.; Shock, David D.; Mueller, Geoffrey A.; Wilson, Samuel H.; London, Robert E.] NIEHS, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
RP London, RE (reprint author), NIEHS, Struct Biol Lab, POB 12233, Res Triangle Pk, NC 27709 USA.
EM london@niehs.nih.gov
FU National Institute of Environmental Health Sciences, National Institutes
of Health [Z01-ES050147, Z01-ES050158]; association with National
Institutes of Health [1U19CA105010]; National Institute of Environmental
Health Sciences
FX Intramural research program of the National Institute of Environmental
Health Sciences, National Institutes of Health, under projects
(Z01-ES050147 to R.E.L.) and (Z01-ES050158 to S.H.W.), in association
with National Institutes of Health (Grant 1U19CA105010). Funding for
open access charge: Research Project Numbers (Z01-ES050147 to R.E.L. and
Z01-ES050158 to S.H.W.). National Institute of Environmental Health
Sciences.
NR 42
TC 15
Z9 15
U1 1
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD APR
PY 2012
VL 40
IS 7
BP 2974
EP 2983
DI 10.1093/nar/gkr1218
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 930TQ
UT WOS:000303164400021
PM 22169953
ER
PT J
AU Chen, B
Zuo, XB
Wang, YX
Dayie, TK
AF Chen, Bin
Zuo, Xiaobing
Wang, Yun-Xing
Dayie, T. Kwaku
TI Multiple conformations of SAM-II riboswitch detected with SAXS and NMR
spectroscopy
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID X-RAY-SCATTERING; GLYCINE-DEPENDENT RIBOSWITCH; MESSENGER-RNA ELEMENT;
S-MK BOX; INDUCED FIT; SENSING RIBOSWITCH; GENE-EXPRESSION; APTAMER
DOMAIN; BIOLOGICAL MACROMOLECULES; ADAPTIVE RECOGNITION
AB Riboswitches are a newly discovered large family of structured functional RNA elements that specifically bind small molecule targets out of a myriad of cellular metabolites to modulate gene expression. Structural studies of ligand-bound riboswitches by X-ray crystallography and nuclear magnetic resonance (NMR) spectroscopy have provided insights into detailed RNA-ligand recognition and interactions. However, the structures of ligand-free riboswitches remain poorly characterized. In this study, we have used a variety of biochemical, biophysical and computational techniques including small-angle X-ray scattering and NMR spectroscopy to characterize the ligand-free and ligand-bound forms of SAM-II riboswitch. Our data demonstrate that the RNA adopts multiple conformations along its folding pathway and suggest that the RNA undergoes marked conformational changes upon Mg2+ compaction and S-adenosylmethionine (SAM) metabolite binding. Further studies indicated that Mg2+ ion is not essential for the ligand binding but can stabilize the complex by facilitating loop/stem interactions. In the presence of millimolar concentration of Mg2+ ion, the RNA samples a more compact conformation. This conformation is near to, but distinct from, the native fold and competent to bind the metabolite. We conclude that the formation of various secondary and tertiary structural elements, including a pseudoknot, occur to sequester the putative Shine-Dalgarno sequence of the RNA only after metabolite binding.
C1 [Chen, Bin; Dayie, T. Kwaku] Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA.
[Zuo, Xiaobing; Wang, Yun-Xing] NCI, Prot Nucle Acid Interact Sect, Struct Biophys Lab, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
RP Dayie, TK (reprint author), Univ Maryland, Dept Chem & Biochem, College Pk, MD 20742 USA.
EM dayie@umd.edu
RI Zuo, Xiaobing/F-1469-2010; Dayie, T Kwaku/E-6868-2011
OI Dayie, T Kwaku/0000-0002-7119-4362
FU US DOE; University of Maryland; National Institutes of Health [GM077326]
FX National Cancer Institute and Beamline 12-ID at Argonne National
Laboratory. The authors also thank Dr Robert T. Batey for kindly
providing the plasmid. DE-AC02-06CH11357). The authors thank X-ray
scattering beam time resource through PUP-21086/22978 between Office of
Science by Argonne National Laboratory, was supported by the US DOE
(under Contract No. Use of the Advanced Photon Source, an Office of
Science User Facility operated for the US Department of Energy (DOE).;
University of Maryland Nano-Biotechnology Award (partial); National
Institutes of Health grant (GM077326 to T. K. D., partial). Funding for
open access charge: NIH.
NR 80
TC 32
Z9 33
U1 2
U2 28
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD APR
PY 2012
VL 40
IS 7
BP 3117
EP 3130
DI 10.1093/nar/gkr1154
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 930TQ
UT WOS:000303164400033
PM 22139931
ER
PT J
AU Freudenberg, JM
Ghosh, S
Lackford, BL
Yellaboina, S
Zheng, XF
Li, RF
Cuddapah, S
Wade, PA
Hu, G
Jothi, R
AF Freudenberg, Johannes M.
Ghosh, Swati
Lackford, Brad L.
Yellaboina, Sailu
Zheng, Xiaofeng
Li, Ruifang
Cuddapah, Suresh
Wade, Paul A.
Hu, Guang
Jothi, Raja
TI Acute depletion of Tet1-dependent 5-hydroxymethylcytosine levels impairs
LIF/Stat3 signaling and results in loss of embryonic stem cell identity
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID ACTIVE DNA DEMETHYLATION; MOUSE ES CELLS; CHROMATIN REMODELING COMPLEX;
SELF-RENEWAL; TET PROTEINS; RNAI SCREEN; TRANSCRIPTIONAL NETWORK;
MYELOID CANCERS; MAMMALIAN DNA; HUMAN GENOME
AB The TET family of FE(II) and 2-oxoglutarate-dependent enzymes (Tet1/2/3) promote DNA demethylation by converting 5-methylcytosine to 5-hydroxymethylcytosine (5hmC), which they further oxidize into 5-formylcytosine and 5-carboxylcytosine. Tet1 is robustly expressed in mouse embryonic stem cells (mESCs) and has been implicated in mESC maintenance. Here we demonstrate that, unlike genetic deletion, RNAi-mediated depletion of Tet1 in mESCs led to a significant reduction in 5hmC and loss of mESC identity. The differentiation phenotype due to Tet1 depletion positively correlated with the extent of 5hmC loss. Meta-analyses of genomic data sets suggested interaction between Tet1 and leukemia inhibitory factor (LIF) signaling. LIF signaling is known to promote self-renewal and pluripotency in mESCs partly by opposing MAPK/ERK-mediated differentiation. Withdrawal of LIF leads to differentiation of mESCs. We discovered that Tet1 depletion impaired LIF-dependent Stat3-mediated gene activation by affecting Stat3's ability to bind to its target sites on chromatin. Nanog overexpression or inhibition of MAPK/ERK signaling, both known to maintain mESCs in the absence of LIF, rescued Tet1 depletion, further supporting the dependence of LIF/Stat3 signaling on Tet1. These data support the conclusion that analysis of mESCs in the hours/days immediately following efficient Tet1 depletion reveals Tet1's normal physiological role in maintaining the pluripotent state that may be subject to homeostatic compensation in genetic models.
C1 [Lackford, Brad L.; Zheng, Xiaofeng; Li, Ruifang; Wade, Paul A.; Hu, Guang] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Freudenberg, Johannes M.; Ghosh, Swati; Yellaboina, Sailu; Jothi, Raja] NIEHS, Syst Biol Sect, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Cuddapah, Suresh] NYU, Sch Med, Dept Environm Med, Tuxedo Pk, NY 10987 USA.
RP Jothi, R (reprint author), NIEHS, Syst Biol Sect, Biostat Branch, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM hug4@niehs.nih.gov; jothi@mail.nih.gov
RI Waha, Andreas/J-2950-2014; Jothi, Raja/G-3780-2015; Hu,
Guang/E-7474-2016
OI Hu, Guang/0000-0003-0437-4723
FU NIH, National Institute of Environmental Health Sciences
[1ZIAES102625-03, 1ZIAES102745-02, 1ZIAES101965-07]
FX Funding for open access charge: The Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences
[1ZIAES102625-03 (to R.J.), 1ZIAES102745-02 (to G.H.) and
1ZIAES101965-07 (to P.A.W.)].
NR 79
TC 49
Z9 50
U1 0
U2 14
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD APR
PY 2012
VL 40
IS 8
BP 3364
EP 3377
DI 10.1093/nar/gkr1253
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 933BF
UT WOS:000303333500014
PM 22210859
ER
PT J
AU Hudson, RS
Yi, M
Esposito, D
Watkins, SK
Hurwitz, AA
Yfantis, HG
Lee, DH
Borin, JF
Naslund, MJ
Alexander, RB
Dorsey, TH
Stephens, RM
Croce, CM
Ambs, S
AF Hudson, Robert S.
Yi, Ming
Esposito, Dominic
Watkins, Stephanie K.
Hurwitz, Arthur A.
Yfantis, Harris G.
Lee, Dong H.
Borin, James F.
Naslund, Michael J.
Alexander, Richard B.
Dorsey, Tiffany H.
Stephens, Robert M.
Croce, Carlo M.
Ambs, Stefan
TI MicroRNA-1 is a candidate tumor suppressor and prognostic marker in
human prostate cancer
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; DOWN-REGULATION; MESSENGER-RNAS;
EXPRESSION; CELLS; GENE; ADENOCARCINOMA; SIGNATURES; PROFILES; MOUSE
AB We previously reported that miR-1 is among the most consistently down-regulated miRs in primary human prostate tumors. In this follow-up study, we further corroborated this finding in an independent data set and made the novel observation that miR-1 expression is further reduced in distant metastasis and is a candidate predictor of disease recurrence. Moreover, we performed in vitro experiments to explore the tumor suppressor function of miR-1. Cell-based assays showed that miR-1 is epigenetically silenced in human prostate cancer. Overexpression of miR-1 in these cells led to growth inhibition and down-regulation of genes in pathways regulating cell cycle progression, mitosis, DNA replication/repair and actin dynamics. This observation was further corroborated with protein expression analysis and 3'-UTR-based reporter assays, indicating that genes in these pathways are either direct or indirect targets of miR-1. A gene set enrichment analysis revealed that the miR-1-mediated tumor suppressor effects are globally similar to those of histone deacetylase inhibitors. Lastly, we obtained preliminary evidence that miR-1 alters the cellular organization of F-actin and inhibits tumor cell invasion and filipodia formation. In conclusion, our findings indicate that miR-1 acts as a tumor suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell proliferation and motility.
C1 [Hudson, Robert S.; Dorsey, Tiffany H.; Ambs, Stefan] NCI, Human Carcinogenesis Lab, CCR, NIH, Bethesda, MD 20892 USA.
[Yi, Ming; Stephens, Robert M.] SAIC Frederick Inc, Adv Biomed Comp Ctr, Frederick, MD USA.
[Esposito, Dominic] SAIC Frederick Inc, Prot Express Lab, Adv Technol Program, Frederick, MD USA.
[Watkins, Stephanie K.; Hurwitz, Arthur A.] NCI Frederick, Mol Immunoregulat Lab, Frederick, MD USA.
[Yfantis, Harris G.; Lee, Dong H.] Univ Maryland, Baltimore Vet Affairs Med Ctr, Baltimore, MD 21201 USA.
[Borin, James F.; Naslund, Michael J.; Alexander, Richard B.] Univ Maryland, Urol & Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
[Croce, Carlo M.] Ohio State Univ, Ctr Comprehens Canc, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
RP Ambs, S (reprint author), NCI, Human Carcinogenesis Lab, CCR, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM ambss@mail.nih.gov
RI Jackson, Benjamin/C-4297-2012;
OI Borin, James/0000-0002-1217-1566
FU National Institutes of Health (NIH), National Cancer Institute, Center
for Cancer Research; Center for Cancer Research, NIH; University of
Maryland, Departments of Pathology and Epidemiology
FX Intramural Research Program of the National Institutes of Health (NIH),
National Cancer Institute, Center for Cancer Research. Funding for open
access charge: Center for Cancer Research, NIH.; We would like to thank
Barbara J. Taylor at the NCI FACS Core Laboratory and Judith A. Welsh at
the Laboratory of Human Carcinogenesis for technical help. We would also
like to thank staff at the University of Maryland, Departments of
Pathology and Epidemiology for their support with the collection of
human tissue samples.
NR 58
TC 65
Z9 74
U1 2
U2 15
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD APR
PY 2012
VL 40
IS 8
BP 3689
EP 3703
DI 10.1093/nar/gkr1222
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 933BF
UT WOS:000303333500039
PM 22210864
ER
PT J
AU Jonsson, H
Aspelund, T
Eiriksdottir, G
Tamm, A
Kisand, K
Franzson, L
Hauksdottir, AM
Harris, TB
Launer, LL
Gudnason, V
AF Jonsson, H.
Aspelund, T.
Eiriksdottir, G.
Tamm, A.
Kisand, K.
Franzson, L.
Hauksdottir, A. M.
Harris, T. B.
Launer, L. Lenore
Gudnason, V.
TI LOW SERUM CONCENTRATIONS OF SERUM VEGF-R2 IN ELDERLY FEMALES WITH THUMB
BASE OSTEOARTHRITIS: THE AGES-REYKJAVIK STUDY.
SO OSTEOARTHRITIS AND CARTILAGE
LA English
DT Meeting Abstract
CT World Congress on Osteoarthritis
CY APR 26-29, 2012
CL Barcelona, SPAIN
C1 [Jonsson, H.; Franzson, L.] Univ Iceland, Landspitalinn, Reykjavik, Iceland.
[Aspelund, T.; Eiriksdottir, G.; Hauksdottir, A. M.; Gudnason, V.] Iceland Heart Assoc, Kopavogur, Iceland.
[Aspelund, T.; Gudnason, V.] Univ Iceland, Reykjavik, Iceland.
[Tamm, A.; Kisand, K.] Univ Tartu, EE-50090 Tartu, Estonia.
[Harris, T. B.; Launer, L. Lenore] NIA, Bethesda, MD 20892 USA.
RI Aspelund, Thor/C-5983-2008; Gudnason, Vilmundur/K-6885-2015; Kisand,
Kalle/S-5958-2016
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084; Kisand, Kalle/0000-0002-7789-5565
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1063-4584
J9 OSTEOARTHR CARTILAGE
JI Osteoarthritis Cartilage
PD APR
PY 2012
VL 20
SU 1
BP S93
EP S94
PG 2
WC Orthopedics; Rheumatology
SC Orthopedics; Rheumatology
GA 931MF
UT WOS:000303223300203
ER
PT J
AU Glasgow, RE
Kurz, D
King, D
Dickman, JM
Faber, AJ
Halterman, E
Woolley, T
Toobert, DJ
Strycker, LA
Estabrooks, PA
Osuna, D
Ritzwoller, D
AF Glasgow, Russell E.
Kurz, Deanna
King, Diane
Dickman, Jennifer M.
Faber, Andrew J.
Halterman, Eve
Woolley, Tim
Toobert, Deborah J.
Strycker, Lisa A.
Estabrooks, Paul A.
Osuna, Diego
Ritzwoller, Debra
TI Twelve-month outcomes of an Internet-based diabetes self-management
support program
SO PATIENT EDUCATION AND COUNSELING
LA English
DT Article
DE Diabetes; Self-management; RCT; Internet intervention; Pragmatic trial;
Multiple behavior change
ID PHYSICAL-ACTIVITY; PRIMARY-CARE; WEIGHT-LOSS; FOLLOW-UP; INTERVENTIONS;
BEHAVIOR; TRIAL; ADULTS; RECRUITMENT; PREVENTION
AB Objective: Internet-based programs offer potential for practical, cost-effective chronic illness self-management programs.
Methods: We report 12-month results of an Internet-based diabetes self-management program, with and without additional support, compared to enhanced usual care in a 3-arm practical randomized trial. Patients (n = 463) were randomized: 77.3% completed 12-month follow-up. Primary outcomes were changes in health behaviors of healthy eating, physical activity, and medication taking. Secondary outcomes were hemoglobin A1c, body mass index, lipids, blood pressure, and psychosocial factors.
Results: Internet conditions improved health behaviors significantly vs. usual care over the 12-month period (d for effect size = .09-.16). All conditions improved moderately on biological and psychosocial outcomes. Latinos, lower literacy, and higher cardiovascular disease risk patients improved as much as other participants.
Conclusions: The Internet intervention meets the reach and feasibility criteria for a potentially broad public health impact. However, 12-month magnitude of effects was small, suggesting that different or more intensive approaches are necessary to support long-term outcomes. Research is needed to understand the linkages between intervention and maintenance processes and downstream outcomes.
Practice implications: Automated self-management interventions should be tailored and integrated into primary care; maintenance of patient self-management can be enhanced through links to community resources. Published by Elsevier Ireland Ltd.
C1 [Glasgow, Russell E.] NCI, Div Canc Control & Populat Sci, Rockville, MD 20852 USA.
[Glasgow, Russell E.; Kurz, Deanna; King, Diane; Dickman, Jennifer M.; Faber, Andrew J.; Halterman, Eve; Osuna, Diego; Ritzwoller, Debra] Kaiser Permanente Colorado, Inst Hlth Res, Denver, CO USA.
[Toobert, Deborah J.; Strycker, Lisa A.] Oregon Res Inst, Eugene, OR 97403 USA.
[Woolley, Tim] InterVis Media, Eugene, OR USA.
[Estabrooks, Paul A.] Virginia Polytech Inst & State Univ, Roanoke, VA USA.
RP Glasgow, RE (reprint author), NCI, Div Canc Control & Populat Sci, 6130 Execut Blvd,Room 6144, Rockville, MD 20852 USA.
EM glasgowre@mail.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases
[DK35524]
FX This study was supported by grant DK35524 from the National Institute of
Diabetes and Digestive and Kidney Diseases.
NR 53
TC 62
Z9 62
U1 4
U2 27
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0738-3991
J9 PATIENT EDUC COUNS
JI Patient Educ. Couns.
PD APR
PY 2012
VL 87
IS 1
BP 81
EP 92
DI 10.1016/j.pec.2011.07.024
PG 12
WC Public, Environmental & Occupational Health; Social Sciences,
Interdisciplinary
SC Public, Environmental & Occupational Health; Social Sciences - Other
Topics
GA 930YX
UT WOS:000303182000014
PM 21924576
ER
PT J
AU Beral, V
Hermon, C
Peto, R
Reeves, G
Brinton, L
Marchbanks, P
Negri, E
Ness, R
Peeters, PHM
Vessey, M
Calle, EE
Gapstur, SM
Patel, AV
Dal Maso, L
Talamini, R
Chetrit, A
Hirsh-Yechezkel, G
Lubin, F
Sadetzki, S
Allen, N
Bull, D
Callaghan, K
Crossley, B
Gaitskell, K
Goodill, A
Green, J
Key, T
Moser, K
Collins, R
Doll, R
Gonzalez, CA
Lee, N
Ory, HW
Peterson, HB
Wingo, PA
Martin, N
Pardthaisong, T
Silpisornkosol, S
Theetranont, C
Boosiri, B
Chutivongse, S
Jimakorn, P
Virutamasen, P
Wongsrichanalai, C
Tjonneland, A
Titus-Ernstoff, L
Byers, T
Rohan, T
Mosgaard, BJ
Yeates, D
Freudenheim, JL
Chang-Claude, J
Kaaks, R
Anderson, KE
Folsom, A
Robien, K
Rossing, MA
Thomas, DB
Weiss, NS
Riboli, E
Clavel-Chapelon, F
Cramer, D
Hankinson, SE
Tworoger, SS
Franceschi, S
La Vecchia, C
Magnusson, C
Riman, T
Weiderpass, E
Wolk, A
Schouten, LJ
van den Brandt, PA
Chantarakul, N
Koetsawang, S
Rachawat, D
Palli, D
Black, A
de Gonzalez, AB
Freedman, DM
Hartge, P
Hsing, AW
Lacey, JV
Hoover, RN
Schairer, C
Graff-Iversen, S
Selmer, R
Bain, CJ
Green, AC
Purdie, DM
Siskind, V
Webb, PM
McCann, SE
Hannaford, P
Kay, C
Binns, CW
Lee, AH
Zhang, M
Ness, RB
Nasca, P
Coogan, PF
Palmer, JR
Rosenberg, L
Kelsey, J
Paffenbarger, R
Whittemore, A
Katsouyanni, K
Trichopoulou, A
Trichopoulos, D
Tzonou, A
Dabancens, A
Martinez, L
Molina, R
Salas, O
Goodman, MT
Lurie, G
Carney, ME
Wilkens, LR
Hartman, L
Manjer, J
Olsson, H
Grisso, JA
Morgan, M
Wheeler, JE
Casagrande, J
Pike, MC
Ross, RK
Wu, AH
Miller, AB
Kumle, M
Lund, E
McGowan, L
Shu, XO
Zheng, W
Farley, TMM
Holck, S
Meirik, O
Risch, HA
AF Beral, V.
Hermon, C.
Peto, R.
Reeves, G.
Brinton, L.
Marchbanks, P.
Negri, E.
Ness, R.
Peeters, P. H. M.
Vessey, M.
Calle, E. E.
Gapstur, S. M.
Patel, A. V.
Dal Maso, L.
Talamini, R.
Chetrit, A.
Hirsh-Yechezkel, G.
Lubin, F.
Sadetzki, S.
Allen, N.
Bull, D.
Callaghan, K.
Crossley, B.
Gaitskell, K.
Goodill, A.
Green, J.
Key, T.
Moser, K.
Collins, R.
Doll, R.
Gonzalez, C. A.
Lee, N.
Ory, H. W.
Peterson, H. B.
Wingo, P. A.
Martin, N.
Pardthaisong, T.
Silpisornkosol, S.
Theetranont, C.
Boosiri, B.
Chutivongse, S.
Jimakorn, P.
Virutamasen, P.
Wongsrichanalai, C.
Tjonneland, A.
Titus-Ernstoff, L.
Byers, T.
Rohan, T.
Mosgaard, B. J.
Yeates, D.
Freudenheim, J. L.
Chang-Claude, J.
Kaaks, R.
Anderson, K. E.
Folsom, A.
Robien, K.
Rossing, M. A.
Thomas, D. B.
Weiss, N. S.
Riboli, E.
Clavel-Chapelon, F.
Cramer, D.
Hankinson, S. E.
Tworoger, S. S.
Franceschi, S.
La Vecchia, C.
Magnusson, C.
Riman, T.
Weiderpass, E.
Wolk, A.
Schouten, L. J.
van den Brandt, P. A.
Chantarakul, N.
Koetsawang, S.
Rachawat, D.
Palli, D.
Black, A.
de Gonzalez, A. Berrington
Freedman, D. M.
Hartge, P.
Hsing, A. W.
Lacey, J. V., Jr.
Hoover, R. N.
Schairer, C.
Graff-Iversen, S.
Selmer, R.
Bain, C. J.
Green, A. C.
Purdie, D. M.
Siskind, V.
Webb, P. M.
McCann, S. E.
Hannaford, P.
Kay, C.
Binns, C. W.
Lee, A. H.
Zhang, M.
Ness, R. B.
Nasca, P.
Coogan, P. F.
Palmer, J. R.
Rosenberg, L.
Kelsey, J.
Paffenbarger, R.
Whittemore, A.
Katsouyanni, K.
Trichopoulou, A.
Trichopoulos, D.
Tzonou, A.
Dabancens, A.
Martinez, L.
Molina, R.
Salas, O.
Goodman, M. T.
Lurie, G.
Carney, M. E.
Wilkens, L. R.
Hartman, L.
Manjer, J.
Olsson, H.
Grisso, J. A.
Morgan, M.
Wheeler, J. E.
Casagrande, J.
Pike, M. C.
Ross, R. K.
Wu, A. H.
Miller, A. B.
Kumle, M.
Lund, E.
McGowan, L.
Shu, X. O.
Zheng, W.
Farley, T. M. M.
Holck, S.
Meirik, O.
Risch, H. A.
CA Collaborative Grp Epidemiol Studie
TI Ovarian Cancer and Body Size: Individual Participant Meta-Analysis
Including 25,157 Women with Ovarian Cancer from 47 Epidemiological
Studies
SO PLOS MEDICINE
LA English
DT Article
ID ORAL-CONTRACEPTIVE USE; REQUIRING PROLONGED OBSERVATION; EPITHELIAL
OVARIAN; MASS INDEX; ANTHROPOMETRIC MEASURES; PROSPECTIVE COHORT;
UNITED-STATES; RISK-FACTORS; POSTMENOPAUSAL WOMEN; HORMONAL FACTORS
AB Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships.
Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p<0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p<0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p<0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy.
Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ovarian cancer incidence per decade.
C1 [Beral, V.; Hermon, C.; Reeves, G.; Allen, N.; Bull, D.; Callaghan, K.; Crossley, B.; Gaitskell, K.; Goodill, A.; Green, J.; Key, T.; Moser, K.] Canc Epidemiol Unit, Oxford, England.
[Calle, E. E.; Gapstur, S. M.; Patel, A. V.] Amer Canc Soc, Atlanta, GA 30329 USA.
[Dal Maso, L.; Talamini, R.] Aviano Canc Ctr, Pordenone, Italy.
[Chetrit, A.; Hirsh-Yechezkel, G.; Lubin, F.; Sadetzki, S.] Gertner Inst, Canc & Radiat Epidemiol Unit, Tel Hashomer, Israel.
[Peto, R.; Collins, R.; Doll, R.] Canc Res UK MRC BHF Clin Trial Serv Unit, Oxford, England.
[Peto, R.; Collins, R.; Doll, R.] Epidemiol Studies Unit, Oxford, England.
[Gonzalez, C. A.] Catalan Inst Oncol, Barcelona, Spain.
[Marchbanks, P.; Lee, N.; Ory, H. W.; Peterson, H. B.; Wingo, P. A.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Martin, N.; Pardthaisong, T.; Silpisornkosol, S.; Theetranont, C.] Chiang Mai Univ, Chiang Mai 50000, Thailand.
[Boosiri, B.; Chutivongse, S.; Jimakorn, P.; Virutamasen, P.; Wongsrichanalai, C.] Chulalongkorn Univ, Bangkok, Thailand.
[Tjonneland, A.] Danish Canc Soc, Inst Canc Epidemiol, Copenhagen, Denmark.
[Titus-Ernstoff, L.] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Hanover, NH 03756 USA.
[Byers, T.] Colorado Sch Publ Hlth, Dept Epidemiol, Denver, CO USA.
[Rohan, T.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Mosgaard, B. J.] Herlev Univ Hosp, Dept Obstet & Gynaecol, Copenhagen, Denmark.
[Vessey, M.; Yeates, D.] Dept Publ Hlth, Oxford, England.
[Freudenheim, J. L.] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
[Chang-Claude, J.; Kaaks, R.] German Canc Res Ctr, Div Canc Epidemiol, Heidelberg, Germany.
[Anderson, K. E.; Folsom, A.; Robien, K.] Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA.
[Rossing, M. A.; Thomas, D. B.; Weiss, N. S.] Univ Washington, Fred Hutchinson Canc Res Ctr, Seattle, WA 98195 USA.
[Riboli, E.] Univ London Imperial Coll Sci Technol & Med, London, England.
[Clavel-Chapelon, F.] Paris S Univ, UMRS 1018, Inst Cancerol Gustave Roussy, Villejuif, France.
[Clavel-Chapelon, F.] INSERM, U1018, Villejuif, France.
[Cramer, D.] Harvard Univ, Sch Med, Brigham & Womens Hosp, Cambridge, MA 02138 USA.
[Hankinson, S. E.; Tworoger, S. S.] Harvard Univ, Sch Med, Channing Lab Nurses Hlth Study, Cambridge, MA 02138 USA.
[Franceschi, S.] Int Agcy Res Canc, F-69372 Lyon, France.
[Negri, E.; La Vecchia, C.] Univ Milan, Ist Ric Farmacol Mario Negri, Milan, Italy.
[Magnusson, C.; Riman, T.; Weiderpass, E.; Wolk, A.] Karolinska Inst, Stockholm, Sweden.
[Schouten, L. J.; van den Brandt, P. A.] Maastricht Univ, Maastricht, Netherlands.
[Chantarakul, N.; Koetsawang, S.; Rachawat, D.] Mahidol Univ, Bangkok 10700, Thailand.
[Palli, D.] Canc Res & Prevent Inst, Mol & Nutr Epidemiol Unit, Florence, Italy.
[Brinton, L.; Black, A.; de Gonzalez, A. Berrington; Freedman, D. M.; Hartge, P.; Hsing, A. W.; Lacey, J. V., Jr.; Hoover, R. N.; Schairer, C.] NCI, Bethesda, MD 20892 USA.
[Graff-Iversen, S.; Selmer, R.] Norwegian Inst Publ Hlth, Oslo, Norway.
[Bain, C. J.; Green, A. C.; Purdie, D. M.; Siskind, V.; Webb, P. M.] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Bain, C. J.; Green, A. C.; Purdie, D. M.; Siskind, V.; Webb, P. M.] Univ Queensland, Brisbane, Qld 4072, Australia.
[McCann, S. E.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Hannaford, P.; Kay, C.] Royal Coll Gen Practitioners Oral Contracept Stud, London, England.
[Binns, C. W.; Lee, A. H.; Zhang, M.] Curtin Univ Technol, Sch Publ Hlth, Perth, WA, Australia.
[Ness, R. B.] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
[Nasca, P.] Univ Massachusetts, Sch Publ Hlth & Hlth Sci, Boston, MA 02125 USA.
[Coogan, P. F.; Palmer, J. R.; Rosenberg, L.] Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA.
[Kelsey, J.; Paffenbarger, R.; Whittemore, A.] Stanford Univ, Stanford, CA 94305 USA.
[Katsouyanni, K.; Trichopoulou, A.; Trichopoulos, D.; Tzonou, A.] Univ Athens, Sch Med, GR-11527 Athens, Greece.
[Dabancens, A.; Martinez, L.; Molina, R.; Salas, O.] Univ Chile, Santiago, Chile.
[Goodman, M. T.; Lurie, G.; Carney, M. E.; Wilkens, L. R.] Univ Hawaii, Honolulu, HI 96822 USA.
[Hartman, L.; Manjer, J.; Olsson, H.] Univ Hosp, Lund, Sweden.
[Grisso, J. A.; Morgan, M.; Wheeler, J. E.] Univ Penn, Philadelphia, PA 19104 USA.
[Peeters, P. H. M.] Univ Med Ctr Utrecht, Utrecht, Netherlands.
[Casagrande, J.; Pike, M. C.; Ross, R. K.; Wu, A. H.] Univ So Calif, Los Angeles, CA USA.
[Miller, A. B.] Univ Toronto, Toronto, ON, Canada.
[Kumle, M.; Lund, E.] Univ Tromso, Tromso, Norway.
[McGowan, L.] George Washington Univ, Washington, DC USA.
[Shu, X. O.; Zheng, W.] Vanderbilt Univ, Nashville, TN USA.
[Farley, T. M. M.; Holck, S.; Meirik, O.] WHO, UNDP, UNFPA, World Bank Special Programme Res Dev & Res Traini, CH-1211 Geneva, Switzerland.
[Risch, H. A.] Yale Univ, Sch Publ Hlth, New Haven, CT 06520 USA.
RP Beral, V (reprint author), Canc Epidemiol Unit, Oxford, England.
RI Schouten, Leo/G-3713-2012; Beral, Valerie/B-2979-2013; Binns,
Colin/A-6012-2008; Negri, Eva/B-7244-2013; Webb, Penelope/D-5736-2013;
Clavel-Chapelon, Francoise/G-6733-2014; Gonzalez, Carlos A/O-4651-2014;
Brinton, Louise/G-7486-2015; Weiderpass, Elisabete/M-4029-2016;
OI dal maso, luigino/0000-0001-6163-200X; La Vecchia,
Carlo/0000-0003-1441-897X; PALLI, Domenico/0000-0002-5558-2437; Robien,
Kim/0000-0002-2120-2280; Negri, Eva/0000-0001-9712-8526; Webb,
Penelope/0000-0003-0733-5930; Gonzalez, Carlos A/0000-0003-2822-9715;
Brinton, Louise/0000-0003-3853-8562; Weiderpass,
Elisabete/0000-0003-2237-0128; Tworoger, Shelley/0000-0002-6986-7046;
Magnusson, Cecilia/0000-0002-8567-6725
FU Cancer Research UK
FX Funding for this collaborative reanalyis of original data was provided
by Cancer Research UK. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 66
TC 5
Z9 5
U1 0
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1549-1277
J9 PLOS MED
JI PLos Med.
PD APR
PY 2012
VL 9
IS 4
AR e1001200
DI 10.1371/journal.pmed.1001200
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 933VZ
UT WOS:000303393800003
ER
PT J
AU Krishna, MC
Matsumoto, S
Yasui, H
Saito, K
Devasahayam, N
Subramanian, S
Mitchell, JB
AF Krishna, Murali C.
Matsumoto, Shingo
Yasui, Hironobu
Saito, Keita
Devasahayam, Nallathamby
Subramanian, Sankaran
Mitchell, James B.
TI Electron Paramagnetic Resonance Imaging of Tumor pO(2)
SO RADIATION RESEARCH
LA English
DT Article
ID ALLOSTERIC HEMOGLOBIN MODIFIER; HYPOXIA-INDUCIBLE FACTOR-1; TISSUE
OXYGEN-TENSION; TRANSIENT HYPOXIA; CANCER-THERAPY; MURINE TUMORS;
BRAIN-TUMORS; SOLID TUMORS; EPR OXIMETRY; BLOOD-FLOW
AB Electron paramagnetic resonance imaging (EPRI) can be used to noninvasively and quantitatively obtain three-dimensional maps of tumor PO,. The paramagnetic tracer triarylmethyl (TAM), a substituted trityl radical moiety, is not toxic to animals and provides narrow isotropic spectra, which is ideal for in vivo EPR imaging experiments. From the oxygen-induced spectral broadening of TAM, pO(2) maps can be derived using EPRI. The instrumentation consists of an EPRI spectrometer and 7T magnetic resonance imaging (MRI) system both operating at a common radiofrequency of 300 MHz. Anatomic images obtained by MRI can be overlaid with pO(2) maps obtained from EPRI. With imaging times of less than 3 min, it was possible to monitor the dynamics of oxygen changes in tumor and distinguish chronically hypoxic regions from acutely hypoxic regions. In this article, the principles of pO(2) imaging with EPR and some relevant examples of tumor imaging are reviewed. (C) 2012 by Radiation Research Society
C1 [Krishna, Murali C.; Matsumoto, Shingo; Yasui, Hironobu; Saito, Keita; Devasahayam, Nallathamby; Subramanian, Sankaran; Mitchell, James B.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Krishna, MC (reprint author), NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bldg 10,Room B3-B69,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM murali@helix.nih.gov
FU Center for Cancer Research, National Cancer Institute, NIH
FX This research was supported by the Intramural Research Program of the
Center for Cancer Research, National Cancer Institute, NIH.
NR 59
TC 16
Z9 16
U1 3
U2 21
PU RADIATION RESEARCH SOC
PI LAWRENCE
PA 810 E TENTH STREET, LAWRENCE, KS 66044 USA
SN 0033-7587
J9 RADIAT RES
JI Radiat. Res.
PD APR
PY 2012
VL 177
IS 4
SI SI
BP 376
EP 386
DI 10.1667/RR2622.1
PG 11
WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging
SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology,
Nuclear Medicine & Medical Imaging
GA 929WZ
UT WOS:000303097700005
PM 22332927
ER
PT J
AU Marotta, F
Kumari, A
Catanzaro, R
Solimene, U
Jain, S
Minelli, E
Harada, M
AF Marotta, Francesco
Kumari, Archana
Catanzaro, Roberto
Solimene, Umberto
Jain, Shalini
Minelli, Emilio
Harada, Masatoshi
TI A Phytochemical Approach to Experimental Metabolic Syndrome-Associated
Renal Damage and Oxidative Stress
SO REJUVENATION RESEARCH
LA English
DT Article
ID CARDIOVASCULAR-DISEASE; KIDNEY-DISEASE; FRUCTOSE; HYPERTENSION;
NOTOGINSENG; MORTALITY; EXTRACTS; ADULTS; RATS
AB The aim of this study was to evaluate the effect of DTS-phytocompound on oxidant-antioxidant balance and protein damage in the kidneys of rats administered high doses of fructose. Adult male Wistar rats were divided into four groups. Group A received a control diet, whereas groups B and C were fed a high-fructose diet (60 g/100 g), the latter with additional DTS (50 mg/kg per day) for 60 days. Lipo-and nitro-peroxidation together with alpha-smooth muscle actin (alpha-SMA) expression in the glomerular and interstitial tissue of the kidneys were measured after 60 days. Fructose-fed rats showed significantly higher lipoperoxidation, 2,4-dinitrophenol and 3-nitrotyrosine protein adducts, and upregulation of alpha-SMA in the kidney. DTS significantly decreased such redox unbalance in renal tissue, while partially downregulating alpha-SMA (p < 0.01). These data suggest the potential clinical benefit of DTS in protecting the kidneys from metabolic syndrome-associated changes; gender-related analysis is under way.
C1 [Marotta, Francesco] ReGenera Res Grp Aging Intervent, I-20154 Milan, Italy.
[Kumari, Archana] Univ Quebec, Inst Natl Rech Sci, Ctr Eau Terre & Environm, Quebec City, PQ, Canada.
[Catanzaro, Roberto] Univ Catania, Dept Internal Med, Gastroenterol Unit, Catania, Italy.
[Solimene, Umberto; Minelli, Emilio] Univ Milan, WHO Ctr Biotechnol & Tradit Med, Milan, Italy.
[Jain, Shalini] NIDDK, NIH, Bethesda, MD USA.
[Harada, Masatoshi] MCH Hosp, Saitama, Japan.
RP Marotta, F (reprint author), ReGenera Res Grp Aging Intervent, Piazza Firenze 12, I-20154 Milan, Italy.
EM fmarchimede@libero.it
NR 21
TC 0
Z9 0
U1 1
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1549-1684
J9 REJUV RES
JI Rejuv. Res.
PD APR
PY 2012
VL 15
IS 2
BP 153
EP 156
DI 10.1089/rej.2011.1266
PG 4
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 933SS
UT WOS:000303383600010
PM 22533421
ER
PT J
AU Marotta, F
Kumari, A
Yadav, H
Polimeni, A
Soresi, V
Lorenzetti, A
Naito, Y
Jain, S
AF Marotta, Francesco
Kumari, Archana
Yadav, Hariom
Polimeni, Ascanio
Soresi, Vincenzo
Lorenzetti, Aldo
Naito, Yasuhiro
Jain, Shalini
TI Biomarine Extracts Significantly Protect from Ultraviolet A-Induced Skin
Photoaging: An Ex Vivo Study
SO REJUVENATION RESEARCH
LA English
DT Article
ID MATRIX METALLOPROTEINASES; IN-VITRO; RADIATION; PURIFICATION; MECHANISMS
AB We tested the activity of the marine nutraceutical CL-1222 added with a coenzyme Q10 (CoQ10)-lutein-selenium component (Celergen (R), Laboratoires-Dom, Switzerland) to protect human fibroblasts against ultraviolet A (UVA)-induced photoaging. Cells obtained from 22- to 39-year-old healthy donors were pretreated with CL-1222 before UV irradiation, as compared with same quantity of the CoQ10-lutein-selenium component. As compared to untreated control, UVA-irradiated samples exhibited a significant increase of secreted matrix metalloproteinase-1 (MMP-1) (p < 0.001) with over four-fold MMP-1 upregulation (p < 0.001). Samples treated with CL-1222, but not with the CoQ10-lutein-selenium component, showed a significant decrease of MMP-1 secretion (p < 0.01) and expression decrease (> 60%, p < 0.01) with > 54% elastase activity inhibition (p < 0.01). This preliminary study shows that such marine nutraceuticals can significantly protect against UV-irradiation irrespective of the CoQ10-lutein-selenium component with a specific protective gene expression modulation amenable to novel clinical applications.
C1 [Marotta, Francesco; Polimeni, Ascanio; Lorenzetti, Aldo] Regenera Res Grp Aging Intervent, I-20154 Milan, Italy.
[Kumari, Archana] Univ Quebec, Inst Natl Rech Sci, Ctr Eau Terre & Environm, Quebec City, PQ, Canada.
[Yadav, Hariom; Jain, Shalini] NIDDK, NIH, Bethesda, MD USA.
[Soresi, Vincenzo] Octopus Sci Assoc Bioprevent, Milan, Italy.
[Naito, Yasuhiro] Immunol Res Inst & Clin, Nagoya, Aichi, Japan.
RP Marotta, F (reprint author), Regenera Res Grp Aging Intervent, Viazza Firenze 12, I-20154 Milan, Italy.
EM fmarchimede@libero.it
OI Yadav, Hariom/0000-0003-4504-1597
NR 16
TC 1
Z9 1
U1 0
U2 4
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1549-1684
J9 REJUV RES
JI Rejuv. Res.
PD APR
PY 2012
VL 15
IS 2
BP 157
EP 160
DI 10.1089/rej.2011.1267
PG 4
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 933SS
UT WOS:000303383600011
PM 22533422
ER
PT J
AU Marotta, F
Polimeni, A
Solimene, U
Lorenzetti, A
Minelli, E
Jain, S
Rastmanesh, R
Sedriep, S
Soresi, V
AF Marotta, Francesco
Polimeni, Ascanio
Solimene, Umberto
Lorenzetti, Aldo
Minelli, Emilio
Jain, Shalini
Rastmanesh, Reza
Sedriep, Sonia
Soresi, Vincenzo
TI Beneficial Modulation from a High-Purity Caviar-Derived Homogenate on
Chronological Skin Aging
SO REJUVENATION RESEARCH
LA English
DT Article
ID OXIDATIVE STRESS; AGED SKIN; FIBROBLASTS; DISEASE; SALMON
AB This study tested the activity of LD-1227, which contains a caviar-derived homogenate added with coenzyme Q(10) (CoQ(10))-selenium component (CaviarLieri (R), Lab-Dom, Switzerland), in aged human skin and its potential role on skin mitochondria function. Human dermal fibroblasts were obtained from healthy donors over 70 years old and treated with LD-1227 for 72 hr. As compared to baseline, LD-1227 caused a robust (> 67%) collagen type I synthesis (p < 0.001) and decreased fibronectin synthesis (p < 0.05) with significant fibronectin messenger RNA (mRNA) downregulation (p < 0.05, r = 0.78). A significant collagen mRNA overexpression occurred with LD-1227 treatment (p < 0.05). Mitochondria cytosolic adenosine triphosphate (ATP) level decreased in aged skin samples (p < 0.05 vs. young control), but this phenomenon was reversed by LD-1227 (p < 0.01). These data show that LD-1227 may modify the extracellular matrix milieu in aged skin and also beneficially affect mitochondrial function.
C1 [Marotta, Francesco; Polimeni, Ascanio; Lorenzetti, Aldo; Sedriep, Sonia] ReGenera Res Grp Aging Intervent, I-20154 Milan, Italy.
[Solimene, Umberto; Minelli, Emilio] Univ Milan, WHO Ctr Biotechnol & Tradit Med, Milan, Italy.
[Jain, Shalini] NIDDK, NIH, Bethesda, MD USA.
[Rastmanesh, Reza] Shahid Beheshti Univ Med Sci, Fac Nutr Sci & Food Technol, Dept Clin Nutr & Dietet, Natl Nutr & Food Technol Res Inst, Tehran, Iran.
[Soresi, Vincenzo] Octopus Sci Assoc Bioprevent, Milan, Italy.
RP Marotta, F (reprint author), ReGenera Res Grp Aging Intervent, Piazza Firenze 12, I-20154 Milan, Italy.
EM fmarchimede@libero.it
NR 20
TC 2
Z9 2
U1 0
U2 6
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1549-1684
J9 REJUV RES
JI Rejuv. Res.
PD APR
PY 2012
VL 15
IS 2
BP 174
EP 177
DI 10.1089/rej.2011.1274
PG 4
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 933SS
UT WOS:000303383600015
PM 22533426
ER
PT J
AU Marotta, F
Yadav, H
Kumari, A
Catanzaro, R
Jain, S
Polimeni, A
Lorenzetti, A
Soresi, V
AF Marotta, Francesco
Yadav, Hariom
Kumari, Archana
Catanzaro, Roberto
Jain, Shalini
Polimeni, Ascanio
Lorenzetti, Aldo
Soresi, Vincenzo
TI Cardioprotective Effect of a Biofermented Nutraceutical on Endothelial
Function in Healthy Middle-Aged Subjects
SO REJUVENATION RESEARCH
LA English
DT Article
ID FERMENTED PAPAYA PREPARATION; ASYMMETRIC DIMETHYLARGININE; DYSFUNCTION;
ATHEROSCLEROSIS; MACROPHAGES
AB We tested a biofermented nutraceutical (FPP) that has been previously shown to positively modulate nitric oxide (NO). Forty-two healthy middle-aged subjects were given 3 grams of FPP three times a day for 6 weeks, and tests were repeated at 3 and 6 weeks; the control group was given a placebo. Flow-mediated dilation (FMD) was measured together with NO compounds (nitrogen oxides [NOx]: NO2- + NO3-) plasma levels and asymmetrical dimethylarginine (ADMA). In the interventional group, overall FMD significantly increased from 4.2% to 7.3% (p < 0.05 vs. placebo). A significant increase in plasma NO and a decrease in ADMA were detected after consumption of FPP (p < 0.01). Although larger studies are awaited, it appears that, at least in healthy individuals, such nutraceutical intervention by positively acting on significant cardiovascular parameters can be considered in the armamentarium of a proactive age-management strategy.
C1 [Marotta, Francesco; Polimeni, Ascanio; Lorenzetti, Aldo] ReGenera Res Grp Aging Intervent, I-20154 Milan, Italy.
[Yadav, Hariom; Jain, Shalini] NIDDK, NIH, Bethesda, MD USA.
[Kumari, Archana] Univ Quebec, Inst Natl Rech Sci, Ctr Eau Terre & Environm, Quebec City, PQ, Canada.
[Catanzaro, Roberto] Univ Catania, Dept Internal Med, Gastroenterol Unit, Catania, Italy.
[Soresi, Vincenzo] Octopus Sci Assoc Bioprevent, Milan, Italy.
RP Marotta, F (reprint author), ReGenera Res Grp Aging Intervent, Piazza Firenze 12, I-20154 Milan, Italy.
EM fmarchimede@libero.it
OI Yadav, Hariom/0000-0003-4504-1597
NR 21
TC 3
Z9 3
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1549-1684
J9 REJUV RES
JI Rejuv. Res.
PD APR
PY 2012
VL 15
IS 2
BP 178
EP 181
DI 10.1089/rej.2011.1276
PG 4
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 933SS
UT WOS:000303383600016
PM 22533427
ER
PT J
AU Sempos, CT
Vesper, HW
Phinney, KW
Thienpont, LM
Coates, PM
AF Sempos, Christopher T.
Vesper, Hubert W.
Phinney, Karen W.
Thienpont, Linda M.
Coates, Paul M.
CA VDSP
TI Vitamin D status as an international issue: National surveys and the
problem of standardization
SO SCANDINAVIAN JOURNAL OF CLINICAL & LABORATORY INVESTIGATION
LA English
DT Article
DE 25-hydroxyvitamin D; 3-epi-25-hydroxyvitamin D; Calibration;
Commutability; CAP; DEQAS; Harmonization; NIST; CLSI; Standardization;
Traceability
ID TANDEM MASS-SPECTROMETRY; 25-HYDROXYVITAMIN D-3; HUMAN SERUM; ADULTS
AB Wide spread variation in measurement results of total 25-hydroxyvitamin D (25(OH)D) confounds international efforts to develop evidence-based clinical guidelines. Accordingly, NIH Office of Dietary Supplements (ODS) in collaboration with CDC National Center for Environmental Health (NCEH), National Institute of Standards and Technology (NIST) and Ghent University established the Vitamin D Standardization Program (VDSP) in November 2010. VDSP objectives include: (1) standardize 25(OH)D concentration measurements in national health surveys around the world, (2) evaluate survey differences, (3) extend standardization efforts to assay manufacturers, and to clinical, commercial, and research laboratories, (4) promote standardization of emerging metabolites of vitamin D status, and (5) enable the use of standardized data in patient care and public health. An interlaboratory comparison study is being conducted to assess measurement variability among current assays. Participants include national health surveys from Australia, Canada, Germany, Ireland, Mexico, South Korea, UK and USA, 15 assay manufacturers, and two external quality assurance programs. CDC will implement a formal laboratory certification program. Standardization activities will use single-donor, fresh-frozen serum collected using the CLSI C37 protocol. Initial assay performance criteria, based on biological variability data, are <= 10 % imprecision and <= 5 % bias in relation to the reference values. An ancillary study on commutability of NIST SRM 972a, external quality assurance testing materials is included. To increase the comparability of existing data from different national surveys, master equations will be developed to facilitate the conversion of already existing national survey data to the NIST-Ghent University reference measurement procedures.
C1 [Sempos, Christopher T.; Coates, Paul M.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
[Vesper, Hubert W.] Ctr Dis Control & Prevent, Natl Ctr Environm Hlth, Atlanta, GA USA.
[Phinney, Karen W.] Natl Inst Stand & Technol, Div Analyt Chem, Gaithersburg, MD 20899 USA.
[Thienpont, Linda M.] Univ Ghent, Fac Pharmaceut Sci, Analyt Chem Lab, B-9000 Ghent, Belgium.
RP Sempos, CT (reprint author), NIH, Off Dietary Supplements, 6100 Execut Blvd,Rm 3B01, Bethesda, MD 20892 USA.
EM semposch@mail.nih.gov; hvesper@cdc.gov
RI Mensink, Gert/B-2447-2009;
OI Mensink, Gert/0000-0001-6268-5998; Young, Ian/0000-0003-3890-3152; Van
Uytfanghe, Katleen/0000-0001-8195-150X; Flynn,
Albert/0000-0002-7072-4202
FU Medical Research Council [MC_U105960371, MC_U105960384]
NR 28
TC 82
Z9 82
U1 0
U2 11
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0036-5513
J9 SCAND J CLIN LAB INV
JI Scand. J. Clin. Lab. Invest.
PD APR
PY 2012
VL 72
SU 243
BP 32
EP 40
DI 10.3109/00365513.2012.681935
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 931VV
UT WOS:000303248300006
PM 22536760
ER
PT J
AU Lee, YS
Simeon, FG
Briard, E
Pike, VW
AF Lee, Yong-Sok
Simeon, Fabrice G.
Briard, Emmanuelle
Pike, Victor W.
TI Solution Structures of the Prototypical 18 kDa Translocator Protein
Ligand, PK 11195, Elucidated with H-1/C-13 NMR Spectroscopy and Quantum
Chemistry
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Article
DE PK 11195; dynamic H-1/C-13 NMR; TSPO; rotamer; variable temperature;
energetics; quantum chemistry; structure
ID PERIPHERAL BENZODIAZEPINE-RECEPTOR; NUCLEAR-MAGNETIC-RESONANCE;
BINDING-SITE; IN-VIVO; AMIDES; ROTATION; DERIVATIVES; BOND;
N,N-DIMETHYLFORMAMIDE; NEUROINFLAMMATION
AB Eighteen kilodalton translocator protein (TSPO) is an important target for drug discovery and for clinical molecular imaging of brain and peripheral inflammatory processes. PK 11195 [1a; 1-(2-chlorophenyl)-N-methyl-(1-methylpropyl)-3-isoquinoline carboxamide) is the major prototypical high-affinity ligand for TSPO. Elucidation of the solution structure of la is of interest for understanding small-molecule ligand interactions with the lipophilic binding site of TSPO. Dynamic H-1/C-13 NMR spectroscopy of 1a revealed four quite stable but interconverting rotamers, due to amide bond and 2-chlorophenyl group rotation. These rotamers have been neglected in previous descriptions of the structure of la and of the binding of 1a to TSPO. Here, we used quantum chemistry at the level of B3LYP/6-311+G(2d,p) to calculate C-13 and H-1 chemical shifts for the rotamers of 1a and for the very weak TSPO ligand, N-desmethyl-PK 11195 (1b). These data, plus experimental NMR data, were then used to characterize the structures of rotamers of 1a and 1b in organic solution. Energy barriers for both the amide bond and 2'-chlorophenyl group rotation of 1a were determined from dynamic H-1 NMR to be similar (ca.17 to 18 kcal/mol), and they compared well with those calculated at the level of B3LYP/6-31G*. Furthermore, the computed barrier for Z to E rotation is considerably lower in 1a (18.7 kcal/mol) than in 1b (25.4 kcal/mol). NMR (NOE) unequivocally demonstrated that the E rotamer of 1a is the more stable in solution by about 0.4 kcal/mol. These detailed structural findings will aid future TSPO ligand design and support the notion that TSPO prefers to bind ligands as amide E-rotamers.
C1 [Simeon, Fabrice G.; Briard, Emmanuelle; Pike, Victor W.] NIMH, PET Radiopharmaceut Sci Sect, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Lee, Yong-Sok] NIH, Ctr Mol Modeling, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Pike, VW (reprint author), NIMH, PET Radiopharmaceut Sci Sect, Mol Imaging Branch, NIH, Bldg 10,Room B3 C346A,10 Ctr Dr, Bethesda, MD 20892 USA.
EM pikev@mail.nih.gov
FU National Institutes of Health (CIT); National Institutes of Health
(NIMH)
FX This research was supported by the Intramural Research Program of the
National Institutes of Health (CIT and NIMH).
NR 50
TC 8
Z9 8
U1 2
U2 8
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1948-7193
J9 ACS CHEM NEUROSCI
JI ACS Chem. Neurosci.
PD APR
PY 2012
VL 3
IS 4
BP 325
EP 335
DI 10.1021/cn3000108
PG 11
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA 927BH
UT WOS:000302881400010
PM 22860199
ER
PT J
AU Algin, O
Turkbey, B
AF Algin, O.
Turkbey, B.
TI Evaluation of Aqueductal Stenosis by 3D Sampling Perfection with
Application-Optimized Contrasts Using Different Flip Angle Evolutions
Sequence: Preliminary Results with 3T MR Imaging
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Article
ID CISTERNOGRAPHY; 3D-CISS
AB BACKGROUND AND PURPOSE: Diagnosis of AS and periaqueductal abnormalities by routine MR imaging sequences is challenging for neuroradiologists. The aim of our study was to evaluate the utility of the 3D-SPACE sequence with VFAM in patients with suspected AS.
MATERIALS AND METHODS: PC-MRI and 3D-SPACE images were obtained in 21 patients who had hydrocephalus on routine MR imaging scans and had clinical suspicion of AS, as well as in 12 control subjects. Aqueductal patency was visually scored (grade 0, normal; grade 1, partial obstruction; grade 2, complete stenosis) by 2 experienced radiologists on PC-MRI (plus routine T1-weighted and T2-weighted images) and 3D-SPACE images. Two separate scores were statistically compared with each other as well as with the consensus scores obtained from general agreement of both radiologists.
RESULTS: There was an excellent correlation between 3D-SPACE and PC-MRI scores (kappa = 0.828). The correlation between 3D-SPACE scorings and consensus-based scorings was higher compared with the correlation between PC-MRI and consensus-based scorings (r = 1, P < .001 and r = 0.966, P < .001, respectively).
CONCLUSIONS: 3D-SPACE sequence with VFAM alone can be used for adequate and successful evaluation of the aqueductal patency without the need for additional sequences and examinations. Noninvasive evaluation of the whole cranium is possible in a short time with high resolution by using 3D-SPACE.
C1 [Algin, O.] Ataturk Training & Res Hosp, Dept Radiol, Ankara, Turkey.
[Turkbey, B.] NCI, NIH, Bethesda, MD USA.
RP Algin, O (reprint author), Ataturk Training & Res Hosp, Dept Radiol, Ankara, Turkey.
EM droktayalgin@gmail.com
NR 20
TC 16
Z9 16
U1 1
U2 4
PU AMER SOC NEURORADIOLOGY
PI OAK BROOK
PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA
SN 0195-6108
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD APR
PY 2012
VL 33
IS 4
BP 740
EP 746
DI 10.3174/ajnr.A2833
PG 7
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 926PI
UT WOS:000302842900027
PM 22173764
ER
PT J
AU Lizunov, VA
Stenkula, KG
Lisinski, I
Gavrilova, O
Yver, DR
Chadt, A
Al-Hasani, H
Zimmerberg, J
Cushman, SW
AF Lizunov, Vladimir A.
Stenkula, Karin G.
Lisinski, Ivonne
Gavrilova, Oksana
Yver, Dena R.
Chadt, Alexandra
Al-Hasani, Hadi
Zimmerberg, Joshua
Cushman, Samuel W.
TI Insulin stimulates fusion, but not tethering, of GLUT4 vesicles in
skeletal muscle of HA-GLUT4-GFP transgenic mice
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE hemagglutinin; glucose transporter 4; green fluorescent protein;
insulin; fusion
ID GTPASE-ACTIVATING-PROTEIN; RAT ADIPOSE-CELLS; LIVING MICE; GLUCOSE
TRANSPORTERS; PLASMA-MEMBRANE; TRANSLOCATION; TRAFFICKING; FIBERS;
AS160; CONTRACTION
AB Insulin stimulates fusion, but not tethering, of GLUT4 vesicles in skeletal muscle of HA-GLUT4-GFP transgenic mice. Am J Physiol Endocrinol Metab 302: E950-E960, 2012. First published January 31, 2012; doi:10.1152/ajpendo.00466.2011.-Insulin regulates glucose uptake into fat and muscle by modulating the subcellular distribution of GLUT4 between the cell surface and intracellular compartments. However, quantification of these translocation processes in muscle by classical subcellular fractionation techniques is confounded by contaminating microfibrillar protein; dynamic studies at the molecular level are almost impossible. In this study, we introduce a muscle-specific transgenic mouse model in which HA-GLUT4-GFP is expressed under the control of the MCK promoter. HA-GLUT4-GFP was found to translocate to the plasma membrane and T-tubules after insulin stimulation, thus mimicking endogenous GLUT4. To investigate the dynamics of GLUT4 trafficking in skeletal muscle, we quantified vesicles containing HA-GLUT4-GFP near the sarcolemma and T-tubules and analyzed insulin-stimulated exocytosis at the single vesicle level by total internal reflection fluorescence and confocal microscopy. We found that only 10% of the intracellular GLUT4 pool comprised mobile vesicles, whereas most of the GLUT4 structures remained stationary or tethered at the sarcolemma or T-tubules. In fact, most of the insulin-stimulated exocytosis emanated from pretethered vesicles, whereas the small pool of mobile GLUT4 vesicles was not significantly affected by insulin. Our data strongly suggest that the mobile pool of GLUT4 vesicles is not a major site of insulin action but rather locally distributed. Most likely, pretethered GLUT4 structures are responsible for the initial phase of insulin-stimulated exocytosis.
C1 [Stenkula, Karin G.; Lisinski, Ivonne; Yver, Dena R.; Cushman, Samuel W.] NIDDK, Expt Diabet Metab & Nutr Sect, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
[Gavrilova, Oksana] NIDDK, Mouse Metab Core Lab, NIH, Bethesda, MD USA.
[Stenkula, Karin G.] Lund Univ, Lund, Sweden.
[Lizunov, Vladimir A.; Zimmerberg, Joshua] NICHHD, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Chadt, Alexandra; Al-Hasani, Hadi] German Inst Human Nutr, Potsdam, Germany.
[Al-Hasani, Hadi] Univ Dusseldorf, German Diabet Ctr, D-40225 Dusseldorf, Germany.
RP Cushman, SW (reprint author), NIDDK, Expt Diabet Metab & Nutr Sect, Diabet Endocrinol & Obes Branch, NIH, Bethesda, MD 20892 USA.
EM samc@mail.nih.gov
FU Swedish Research Council; National Institute of Diabetes and Digestive
and Kidney Diseases; National Institute of Child Health and Human
Development, National Institutes of Health
FX This work was supported in part by a Postdoctoral Fellowship to K.
Stenkula from the Swedish Research Council and by the intramural
research programs of National Institute of Diabetes and Digestive and
Kidney Diseases and National Institute of Child Health and Human
Development, National Institutes of Health.
NR 37
TC 13
Z9 14
U1 0
U2 4
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1849
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD APR
PY 2012
VL 302
IS 8
BP E950
EP E960
DI 10.1152/ajpendo.00466.2011
PG 11
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 924ZU
UT WOS:000302730600006
PM 22297303
ER
PT J
AU Tahlan, K
Wilson, R
Kastrinsky, DB
Arora, K
Nair, V
Fischer, E
Barnes, SW
Walker, JR
Alland, D
Barry, CE
Boshoff, HI
AF Tahlan, Kapil
Wilson, Regina
Kastrinsky, David B.
Arora, Kriti
Nair, Vinod
Fischer, Elizabeth
Barnes, S. Whitney
Walker, John R.
Alland, David
Barry, Clifton E., III
Boshoff, Helena I.
TI SQ109 Targets MmpL3, a Membrane Transporter of Trehalose Monomycolate
Involved in Mycolic Acid Donation to the Cell Wall Core of Mycobacterium
tuberculosis
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID DRUG DISCOVERY; ISONIAZID RESISTANCE; OUTER-MEMBRANE; IN-VITRO;
ETHAMBUTOL; BIOSYNTHESIS; BIOGENESIS; ENVELOPE; ARABINOGALACTAN;
IDENTIFICATION
AB SQ109, a 1,2-diamine related to ethambutol, is currently in clinical trials for the treatment of tuberculosis, but its mode of action remains unclear. Here, we demonstrate that SQ109 disrupts cell wall assembly, as evidenced by macromolecular incorporation assays and ultrastructural analyses. SQ109 interferes with the assembly of mycolic acids into the cell wall core of Mycobacterium tuberculosis, as bacilli exposed to SQ109 show immediate inhibition of trehalose dimycolate (TDM) production and fail to attach mycolates to the cell wall arabinogalactan. These effects were not due to inhibition of mycolate synthesis, since total mycolate levels were unaffected, but instead resulted in the accumulation of trehalose monomycolate (TMM), the precursor of TDM and cell wall mycolates. In vitro assays using purified enzymes showed that this was not due to inhibition of the secreted Ag85 mycolyltransferases. We were unable to achieve spontaneous generation of SQ109-resistant mutants; however, analogs of this compound that resulted in similar shutdown of TDM synthesis with concomitant TMM accumulation were used to spontaneously generate resistant mutants that were also cross-resistant to SQ109. Whole-genome sequencing of these mutants showed that these all had mutations in the essential mmpL3 gene, which encodes a transmembrane transporter. Our results suggest that MmpL3 is the target of SQ109 and that MmpL3 is a transporter of mycobacterial TMM.
C1 [Tahlan, Kapil; Kastrinsky, David B.; Arora, Kriti; Barry, Clifton E., III; Boshoff, Helena I.] NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Wilson, Regina; Alland, David] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Med, Div Infect Dis, Newark, NJ 07103 USA.
[Wilson, Regina; Alland, David] Univ Med & Dent New Jersey, New Jersey Med Sch, Ruy V Lourenco Ctr Study Emerging & Reemerging Pa, Newark, NJ 07103 USA.
[Nair, Vinod; Fischer, Elizabeth] NIAID, Res Technol Branch, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Barnes, S. Whitney; Walker, John R.] Novartis Res Fdn, Genom Inst, San Diego, CA USA.
RP Boshoff, HI (reprint author), NIAID, TB Res Sect, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM hboshoff@niaid.nih.gov
RI Barry, III, Clifton/H-3839-2012
FU NIAID; NIH; UNCF/Merck
FX This study was funded (in part) by the Intramural Research Program of
NIAID, NIH (to C.E.B.), and in part by a UNCF/Merck Postdoctoral Science
Research Fellowship (to R.W.).
NR 74
TC 156
Z9 161
U1 4
U2 43
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0066-4804
J9 ANTIMICROB AGENTS CH
JI Antimicrob. Agents Chemother.
PD APR
PY 2012
VL 56
IS 4
BP 1797
EP 1809
DI 10.1128/AAC.05708-11
PG 13
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 913SU
UT WOS:000301898500017
PM 22252828
ER
PT J
AU Becker, KG
AF Becker, Kevin G.
TI Male Gender Bias in Autism and Pediatric Autoimmunity
SO AUTISM RESEARCH
LA English
DT Review
DE autoimmune; immunology; molecular genetics; pediatrics; developmental
neurobiology
ID REGULATORY T-CELLS; SPECTRUM DISORDERS; MULTIPLE-SCLEROSIS;
SEX-DIFFERENCES; LEUKOTRIENE BIOSYNTHESIS; FAMILIAL AUTOIMMUNITY;
INCREASED PREVALENCE; DIABETES-MELLITUS; PUBERTAL STAGE; X-CHROMOSOME
AB Male bias in both autism and pediatric autoimmune disease is thought to involve hormonal perturbations in pregnancy or early childhood in the context of genetic control. These early molecular events, at a time of rapid development, are intimately linked to concurrent development in the brain and immune system. It is suggested here that these early regulatory events may overlap between autism and autoimmunity in determining male sex bias and may provide evidence of an etiological link among autism, immune dysregulation, and autoimmune disease. Autism Res 2012,:. Published 2012 International Society for Autism Research, Wiley Periodicals, Inc.dagger
C1 NIA, Biomed Res Ctr, NIH, Gene Express & Genom Unit, Baltimore, MD 21224 USA.
RP Becker, KG (reprint author), NIA, Biomed Res Ctr, NIH, Gene Express & Genom Unit, Suite 100,Room 4B122,251 Bayview Blvd, Baltimore, MD 21224 USA.
EM beckerk@grc.nia.nih.gov
OI Becker, Kevin/0000-0002-6794-6656
FU NIH, National Institute on Aging
FX The author would like to thank Drs. Andrea Wurster, Larry Brant, and
Bronwen Martin for helpful comments in editing the manuscript. This
research was supported entirely by the Intramural Research Program of
the NIH, National Institute on Aging.
NR 101
TC 3
Z9 3
U1 4
U2 19
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD APR
PY 2012
VL 5
IS 2
BP 77
EP 83
DI 10.1002/aur.1227
PG 7
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 927KK
UT WOS:000302906100001
PM 22431266
ER
PT J
AU Raznahan, A
Lee, Y
Vaituzis, C
Tran, L
Mackie, S
Tiemeier, H
Clasen, L
Lalonde, F
Greenstein, D
Pierson, R
Giedd, JN
AF Raznahan, Armin
Lee, Yohan
Vaituzis, Catherine
Tran, Lan
Mackie, Susan
Tiemeier, Henning
Clasen, Liv
Lalonde, Francois
Greenstein, Dede
Pierson, Ron
Giedd, Jay N.
TI Allelic Variation Within the Putative Autism Spectrum Disorder Risk Gene
Homeobox A1 and Cerebellar Maturation in Typically Developing Children
and Adolescents
SO AUTISM RESEARCH
LA English
DT Article
DE autism; HOXA1; cerebellum; gene; brain; MRI
ID HOXA1 A218G POLYMORPHISM; BRAIN-STEM; CORTICAL DEVELOPMENT;
INFANTILE-AUTISM; CELL-DEATH; ASSOCIATION; VARIANTS; MR; GROWTH; HOXB1
AB Homeobox A1 (HOXA1) has been proposed as a candidate gene for autism spectrum disorder (ASD) as it regulates embryological patterning of hind-brain structures implicated in autism neurobiology. In line with this notion, a nonsynonymous single nucleotide polymorphism within a highly conserved domain of HOXA1A218G (rs10951154)has been linked to both ASD risk, and cross-sectional differences in superior posterior lobar cerebellar anatomy in late adulthood. Despite evidence for early onset and developmentally dynamic cerebellar involvement in ASD, little is known of the relationship between A218G genotype and maturation of the cerebellum over early development. We addressed this issue using 296 longitudinally acquired structural magnetic resonance imaging brain scans from 116 healthy individuals between 5 and 23 years of age. Mixed models were used to compare the relationship between age and semi-automated measures of cerebellar volume in A-homozygotes (AA) and carriers of the G allele (Gcar). Total cerebellar volume increased between ages of 5 and 23 years in both groups. However, this was accelerated in the Gcar relative to the AA group (Genotype-by-age interaction term, P?=?0.03), and driven by genotype-dependent differences in the rate of bilateral superior posterior lobar volume change with age (P?=?0.002). Resultantly, although superior posterior lobar volume did not differ significantly between genotype groups at age 5 (P?=?0.9), by age 23 it was 12% greater in Gcar than AA (P?=?0.002). Our results suggest that common genetic variation within this putative ASD risk gene has the capacity to modify the development of cerebellar systems implicated in ASD neurobiology.
C1 [Raznahan, Armin; Lee, Yohan; Vaituzis, Catherine; Tran, Lan; Mackie, Susan; Tiemeier, Henning; Clasen, Liv; Lalonde, Francois; Greenstein, Dede; Pierson, Ron; Giedd, Jay N.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Raznahan, Armin] Kings Coll London, Inst Psychiat, Child Psychiat Dept, London WC2R 2LS, England.
RP Raznahan, A (reprint author), NIMH, Child Psychiat Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM raznahana@mail.nih.gov
RI Raznahan, Armin/F-4534-2012; Giedd, Jay/B-7302-2012; Giedd,
Jay/J-9644-2015;
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978;
Tiemeier, Henning/0000-0002-4395-1397
FU UK Medical Research Council [G0701370]
FX A.R. was funded by the UK Medical Research Council Fellowship (G0701370)
while carrying out aspects of this work. A.R. would like to thanks
Professors Patrick Bolton, Declan Murphy, and Gareth Barker for their
helpful comments on earlier versions of this article.
NR 55
TC 7
Z9 7
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD APR
PY 2012
VL 5
IS 2
BP 93
EP 100
DI 10.1002/aur.238
PG 8
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 927KK
UT WOS:000302906100003
PM 22359339
ER
PT J
AU Anderlini, P
Tolar, J
Deeg, H
Arai, S
Horwitz, M
Antin, J
McCarty, J
Adams, R
Ewell, M
Leifer, E
Gersten, I
Carter, S
Horowitz, M
Confer, D
Nakamura, R
Pulsipher, M
DiFronzo, N
Eapen, M
AF Anderlini, P.
Tolar, J.
Deeg, H.
Arai, S.
Horwitz, M.
Antin, J.
McCarty, J.
Adams, R.
Ewell, M.
Leifer, E.
Gersten, I.
Carter, S.
Horowitz, M.
Confer, D.
Nakamura, R.
Pulsipher, M.
DiFronzo, N.
Eapen, M.
TI Fludarabine-based conditioning for allogeneic marrow transplantation
from unrelated donors in severe aplastic anaemia: serious and unexpected
adverse events in pre-defined cyclophosphamide dose levels
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Anderlini, P.] UTMDACC, Houston, TX USA.
[Tolar, J.] Univ Minnesota, Masonic Canc Ctr, Minneapolis, MN USA.
[Deeg, H.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Arai, S.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Horwitz, M.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Antin, J.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[McCarty, J.] Virginia Commonwealth Univ Med Coll Virginia, Richmond, VA USA.
[Adams, R.] Mayo Clin, Scottsdale, AZ USA.
[Ewell, M.; Gersten, I.; Carter, S.] EMMES Corp, Rockville, MD USA.
[Leifer, E.; DiFronzo, N.] NHLBI, Bethesda, MD 20892 USA.
[Horowitz, M.; Eapen, M.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Confer, D.] Natl Marrow Donor Program, Minneapolis, MN USA.
[Pulsipher, M.] Univ Utah, Med Ctr, Salt Lake City, UT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S219
EP S220
PG 2
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749201275
ER
PT J
AU Barrett, J
Ito, S
Pophali, P
Fahle, G
Koklanaris, E
Superata, J
Childs, R
Battiwalla, M
AF Barrett, J.
Ito, S.
Pophali, P.
Fahle, G.
Koklanaris, E.
Superata, J.
Childs, R.
Battiwalla, M.
TI Cytomegalovirus reactivation is associated with a lower incidence of
relapse after allogeneic stem cell transplantation for chronic
myelogenous leukaemia
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Barrett, J.; Ito, S.; Pophali, P.; Koklanaris, E.; Superata, J.; Childs, R.; Battiwalla, M.] NHLBI, Bethesda, MD 20892 USA.
[Fahle, G.] NIH, Bethesda, MD 20892 USA.
RI Pophali, Priyanka/P-8646-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S427
EP S428
PG 2
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749201699
ER
PT J
AU Barrett, J
Pophali, P
Battiwalla, M
AF Barrett, J.
Pophali, P.
Battiwalla, M.
TI Sustained increased risk of cardiovascular disease in the second decade
post-transplant in male long-term survivors of allogeneic haematopoietic
stem cell transplantation
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Barrett, J.; Pophali, P.; Battiwalla, M.] NHLBI, Bethesda, MD 20892 USA.
RI Pophali, Priyanka/P-8646-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S54
EP S54
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749200116
ER
PT J
AU Bollard, C
Cruz, C
Savoldo, B
Krance, R
Kamble, R
Barrett, A
Hosing, C
Shpall, E
Heslop, H
Leen, A
Rooney, C
Brenner, M
Dotti, G
AF Bollard, C.
Cruz, C.
Savoldo, B.
Krance, R.
Kamble, R.
Barrett, A.
Hosing, C.
Shpall, E.
Heslop, H.
Leen, A.
Rooney, C.
Brenner, M.
Dotti, G.
TI Outcomes of CD19-directed multivirus specific cytotoxic T lymphocyte
therapy for patients with relapsed B cell malignancies after allogeneic
haematopoietic stem cell transplantation
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Bollard, C.; Cruz, C.; Savoldo, B.; Krance, R.; Kamble, R.; Heslop, H.; Leen, A.; Rooney, C.; Brenner, M.; Dotti, G.] Baylor Coll Med, Houston, TX 77030 USA.
[Barrett, A.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Hosing, C.; Shpall, E.] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 2
Z9 2
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S56
EP S56
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749200120
ER
PT J
AU de Latour, RP
Calado, R
Busson, M
Abrams, J
Robin, M
Larghero, J
Xhaard, A
Dhedin, N
Clave, E
Charron, D
Toubert, A
Loiseau, P
Socie, G
Young, N
AF de Latour, R. Peffault
Calado, R.
Busson, M.
Abrams, J.
Robin, M.
Larghero, J.
Xhaard, A.
Dhedin, N.
Clave, E.
Charron, D.
Toubert, A.
Loiseau, P.
Socie, G.
Young, N.
TI Age-adjusted recipient pre transplant telomere length and
treatment-related mortality after haematopoietic stem cell
transplantation
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [de Latour, R. Peffault; Busson, M.; Robin, M.; Larghero, J.; Xhaard, A.; Dhedin, N.; Clave, E.; Charron, D.; Toubert, A.; Loiseau, P.; Socie, G.] Hop St Louis, Paris, France.
[Calado, R.; Abrams, J.; Young, N.] NIH, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S28
EP S28
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749200053
ER
PT J
AU Grkovic, L
Pulanic, D
Steinberg, SM
Williams, KM
Baird, K
Mitchell, SA
Cowen, EW
Datiles, MB
Aria, D
Bassim, C
Joe, G
Comis, L
Baruffaldi, J
Zhang, D
Sportes, C
Fowler, DH
Hakim, F
Gress, RE
Pavletic, SZ
AF Grkovic, L.
Pulanic, D.
Steinberg, S. M.
Williams, K. M.
Baird, K.
Mitchell, S. A.
Cowen, E. W.
Datiles, M. B., III
Aria, D.
Bassim, C.
Joe, G.
Comis, L.
Baruffaldi, J.
Zhang, D.
Sportes, C.
Fowler, D. H.
Hakim, F.
Gress, R. E.
Pavletic, S. Z.
TI NIH lung score components are associated with clinical outcomes,
Bronchiolitis obliterans syndrome and survival in chronic GvHD
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Grkovic, L.; Pulanic, D.] Clin Hosp Ctr Zagreb, Zagreb, Croatia.
[Steinberg, S. M.; Williams, K. M.; Baird, K.; Mitchell, S. A.; Cowen, E. W.; Datiles, M. B., III; Aria, D.; Bassim, C.; Joe, G.; Comis, L.; Baruffaldi, J.; Zhang, D.; Sportes, C.; Fowler, D. H.; Hakim, F.; Gress, R. E.; Pavletic, S. Z.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S61
EP S61
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749200132
ER
PT J
AU Hanley, P
Martinez, C
Melenhorst, J
Leung, K
Savoldo, B
Leen, A
Dotti, G
Gee, A
Rooney, C
Heslop, H
Krance, R
Barrett, A
Shpall, E
Bollard, C
AF Hanley, P.
Martinez, C.
Melenhorst, J.
Leung, K.
Savoldo, B.
Leen, A.
Dotti, G.
Gee, A.
Rooney, C.
Heslop, H.
Krance, R.
Barrett, A.
Shpall, E.
Bollard, C.
TI Administration of cord blood (CB)-derived virus-specific cytotoxic T
lymphocytes to prevent CMV, adenovirus, and EBV infection after CB
transplant
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Hanley, P.; Martinez, C.; Melenhorst, J.; Leung, K.; Savoldo, B.; Leen, A.; Dotti, G.; Gee, A.; Rooney, C.; Heslop, H.; Krance, R.; Bollard, C.] Baylor Coll Med, Houston, TX 77030 USA.
[Barrett, A.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Shpall, E.] Univ Texas Houston, MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S56
EP S56
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749200119
ER
PT J
AU Kirsch, M
Mitchell, SA
Halter, J
Stussi, G
Dobbels, F
Basch, E
De Geest, S
AF Kirsch, M.
Mitchell, S. A.
Halter, J.
Stussi, G.
Dobbels, F.
Basch, E.
De Geest, S.
TI Development of a Patient Reported Outcome instrument for assessing
symptoms of late effects in survivors after allogeneic stem cell
transplantation: PROVIVO - a mixed methods study
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Kirsch, M.; De Geest, S.] Univ Basel, Inst Nursing Sci, Basel, Switzerland.
[Mitchell, S. A.] NCI, Bethesda, MD 20892 USA.
[Halter, J.] Univ Basel Hosp, CH-4031 Basel, Switzerland.
[Stussi, G.] Oncol Inst So Switzerland, Bellinzona, Switzerland.
[Dobbels, F.] Katholieke Univ Leuven, Louvain, Belgium.
[Basch, E.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S462
EP S462
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749202012
ER
PT J
AU Williams, K
Pavletic, S
Lee, S
Hakim, F
Mitchell, S
Manning-Geist, BL
Gea-Banacloche, J
Comis, L
Cowen, E
Baird, K
Shelhamer, J
Blacklock-Schuver, B
Avila, D
Zulchinski, D
Gress, R
AF Williams, K.
Pavletic, S.
Lee, S.
Hakim, F.
Mitchell, S.
Manning-Geist, B. L.
Gea-Banacloche, J.
Comis, L.
Cowen, E.
Baird, K.
Shelhamer, J.
Blacklock-Schuver, B.
Avila, D.
Zulchinski, D.
Gress, R.
TI Preliminary results of a phase II trial of montelukast for the treatment
of Bronchiolitis obliterans syndrome after HSCT and implications for
immunobiology of disease
SO BONE MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
European-Group-for-Blood-and-Marrow-Transplantation (EBMT)
CY APR 01-04, 2012
CL Geneva, SWITZERLAND
SP European Grp Blood & Marrow Transplantat (EBMT)
C1 [Williams, K.; Pavletic, S.; Hakim, F.; Mitchell, S.; Manning-Geist, B. L.; Gea-Banacloche, J.; Comis, L.; Cowen, E.; Baird, K.; Blacklock-Schuver, B.; Avila, D.; Zulchinski, D.; Gress, R.] NCI, Bethesda, MD 20892 USA.
[Lee, S.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Shelhamer, J.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD APR
PY 2012
VL 47
SU 1
BP S61
EP S61
PG 1
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA 925GN
UT WOS:000302749200131
ER
PT J
AU Cramer, SC
AF Cramer, Steven C.
TI Reply: Harnessing neuroplasticity for clinical applications
SO BRAIN
LA English
DT Letter
C1 [Cramer, Steven C.] NIMH, Neurodev Disorders Res Branch, Bethesda, MD 20892 USA.
RP Cramer, SC (reprint author), Univ Calif Irvine, UC Irvine Med Ctr, 101 City Dr S,Bldg 53,Room 203, Orange, CA 92868 USA.
EM scramer@uci.edu
NR 0
TC 0
Z9 0
U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD APR
PY 2012
VL 135
AR e216
DI 10.1093/brain/aws018
PN 4
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 927ZH
UT WOS:000302948700006
ER
PT J
AU Fukuto, JM
Carrington, SJ
Tantillo, DJ
Harrison, JG
Ignarro, LJ
Freeman, BA
Chen, A
Wink, DA
AF Fukuto, Jon M.
Carrington, Samantha J.
Tantillo, Dean J.
Harrison, Jason G.
Ignarro, Louis J.
Freeman, Bruce A.
Chen, Andrew
Wink, David A.
TI Small Molecule Signaling Agents: The Integrated Chemistry and
Biochemistry of Nitrogen Oxides, Oxides of Carbon, Dioxygen, Hydrogen
Sulfide, and Their Derived Species
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Review
ID CYSTATHIONINE-BETA-SYNTHASE; BOND-DISSOCIATION ENERGIES;
HYPOXIA-INDUCIBLE FACTOR-1-ALPHA; METAL-NITROSYL COMPLEXES; HUMAN
SERUM-ALBUMIN; NITRIC-OXIDE; SUPEROXIDE-DISMUTASE; AQUEOUS-SOLUTION;
REACTIVE OXYGEN; S-NITROSOTHIOLS
AB Several small molecule species formally known primarily as toxic gases have, over the past 20 years, been shown to be endogenously generated signaling molecules. The biological signaling associated with the small molecules NO, CO, H2S (and the nonendogenously generated O-2), and their derived species have become a topic of extreme interest. It has become increasingly clear that these small molecule signaling agents form an integrated signaling web that affects/regulates numerous physiological processes. The chemical interactions between these species and each other or biological targets is an important factor in their roles as signaling agents. Thus, a fundamental understanding of the chemistry of these molecules is essential to understanding their biological/physiological utility. This review focuses on this chemistry and attempts to establish the chemical basis for their signaling functions.
C1 [Fukuto, Jon M.; Carrington, Samantha J.; Chen, Andrew] Sonoma State Univ, Dept Chem, Rohnert Pk, CA 94928 USA.
[Tantillo, Dean J.; Harrison, Jason G.] Univ Calif Davis, Dept Chem, Davis, CA 95616 USA.
[Ignarro, Louis J.] UCLA Sch Med, Ctr Hlth Sci, Dept Mol & Med Pharmacol, Los Angeles, CA 90095 USA.
[Freeman, Bruce A.] Univ Pittsburgh, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15261 USA.
[Wink, David A.] NCI, Tumor Biol Sect, Radiat Biol Branch, Bethesda, MD 20892 USA.
RP Fukuto, JM (reprint author), Sonoma State Univ, Dept Chem, Rohnert Pk, CA 94928 USA.
EM jon.fukuto@sonoma.edu
RI Freeman, Bruce/H-9342-2012; Carrington, Samantha/F-5848-2014
FU NHLBI NIH HHS [R01 HL058115, R01 HL064937, R37 HL058115]
NR 183
TC 89
Z9 90
U1 5
U2 74
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0893-228X
J9 CHEM RES TOXICOL
JI Chem. Res. Toxicol.
PD APR
PY 2012
VL 25
IS 4
BP 769
EP 793
DI 10.1021/tx2005234
PG 25
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA 926JA
UT WOS:000302826000001
PM 22263838
ER
PT J
AU Insel, TR
AF Insel, Thomas R.
TI Invited Response to: Preparedness of the CTSA's Structural and
Scientific Assets to Support the Mission of the National Center for
Advancing Translational Sciences (NCATS)
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Article
C1 [Insel, Thomas R.] NCATS, Bethesda, MD USA.
[Insel, Thomas R.] NIMH, Bethesda, MD 20892 USA.
RP Insel, TR (reprint author), NCATS, Bethesda, MD USA.
EM tinsel@mail.nih.gov
NR 2
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1752-8054
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD APR
PY 2012
VL 5
IS 2
BP 130
EP 131
DI 10.1111/j.1752-8062.2012.00408.x
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 926VT
UT WOS:000302860700006
PM 22507117
ER
PT J
AU Meyers, FJ
Begg, MD
Fleming, M
Merchant, C
AF Meyers, Frederick J.
Begg, Melissa D.
Fleming, Michael
Merchant, Carol
TI Strengthening the Career Development of Clinical Translational Scientist
Trainees: A Consensus Statement of the Clinical Translational Science
Award (CTSA) Research Education and Career Development Committees
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Article
DE Clinical and Translational Science Award (CTSA); Education and Career
Development (EdCD) key function committee; interdisciplinary;
competencies; mentoring
ID RESEARCH MENTORS; INTERDISCIPLINARY RESEARCH; SCHOLARS
AB The challenges for scholars committed to successful careers in clinical and translational science are increasingly well recognized. The Education and Career Development (EdCD) of the national Clinical and Translational Science Award consortium gathered thought leaders to propose sustainable solutions and an agenda for future studies that would strengthen the infrastructure across the spectrum of pre- and postdoctoral, MD and PhD, scholars. Six consensus statements were prepared that include: (1) the requirement for career development of a qualitatively different investigator; (2) the implications of interdisciplinary science for career advancement including institutional promotion and tenure actions that were developed for discipline-specific accomplishments; (3) the need for long-term commitment of institutions to scholars; (4) discipline-specific curricula are still required but curricula designed to promote team work and interdisciplinary training will promote innovation; (5) PhD trainees have many pathways to career satisfaction and success; and (6) a centralized infrastructure to enhance and reward mentoring is required. Several themes cut across all of the recommendations including team science, innovation, and sustained institutional commitment. Implied themes include an effective and diverse job force and the requirement for a well-crafted public policy that supports continued investments in science education. Clin Trans Sci 2012; Volume #: 16
C1 [Meyers, Frederick J.] Univ Calif Davis, Sch Med, Sacramento, CA 95817 USA.
[Begg, Melissa D.] Mailman Sch Publ Hlth, New York, NY USA.
[Begg, Melissa D.] Irving Inst Clin & Translat Res, New York, NY USA.
[Fleming, Michael] Feinberg Sch Med, Chicago, IL USA.
[Merchant, Carol] NIH, Natl Ctr Res Resources, Bethesda, MD 20892 USA.
RP Meyers, FJ (reprint author), Univ Calif Davis, Sch Med, Sacramento, CA 95817 USA.
EM fred.meyers@ucdmc.ucdavis.edu
FU Clinical Translational Science award; [UC Davis UL1RR024146];
[Columbia UL1RR024156]; [Northwestern UL1RR025741]
FX This work was supported by Clinical Translational Science award and
Grants: UC Davis UL1RR024146, Columbia UL1RR024156, and Northwestern
UL1RR025741.
NR 34
TC 21
Z9 21
U1 1
U2 15
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1752-8054
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD APR
PY 2012
VL 5
IS 2
BP 132
EP 137
DI 10.1111/j.1752-8062.2011.00392.x
PG 6
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 926VT
UT WOS:000302860700007
PM 22507118
ER
PT J
AU Rubio, DM
Sufian, M
Trochim, WM
AF Rubio, Doris McGartland
Sufian, Meryl
Trochim, William M.
TI Strategies for a National Evaluation of the Clinical and Translational
Science Awards
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Article
ID MODEL
C1 [Rubio, Doris McGartland] Univ Pittsburgh, Sch Med, Dept Med, Ctr Res Hlth Care Data Ctr,Div Gen Internal Med, Pittsburgh, PA 15260 USA.
[Rubio, Doris McGartland] Univ Pittsburgh, Clin & Translat Sci Inst, Pittsburgh, PA USA.
[Sufian, Meryl] NIH, Off Sci & Policy, Natl Ctr Res Resources, Bethesda, MD 20892 USA.
[Trochim, William M.] Cornell Univ, Dept Policy Anal & Management, Ithaca, NY USA.
[Trochim, William M.] Weill Cornell Med Coll, Clin & Translat Sci Ctr, New York, NY USA.
RP Rubio, DM (reprint author), Univ Pittsburgh, Sch Med, Dept Med, Ctr Res Hlth Care Data Ctr,Div Gen Internal Med, Pittsburgh, PA 15260 USA.
EM rubiodm@upmc.edu
FU National Center for Research Resources (NCRR); National Institutes of
Health (NIH); NCRR/NIH CTSA [UL1 RR024153, UL1 RR024996]
FX The project reported here was supported in part by the National Center
for Research Resources (NCRR) and the National Institutes of Health
(NIH) through the Clinical and Translational Science Award (CTSA)
Program. The NCRR/NIH CTSA funding was awarded to the University of
Pittsburgh (UL1 RR024153) and Cornell University (UL1 RR024996).
NR 7
TC 5
Z9 6
U1 1
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1752-8054
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD APR
PY 2012
VL 5
IS 2
BP 138
EP 139
DI 10.1111/j.1752-8062.2011.00381.x
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 926VT
UT WOS:000302860700008
PM 22507119
ER
PT J
AU Zarin, DA
AF Zarin, Deborah A.
TI Factual Errors about ClinicalTrials.gov and Other Federal Mandates in
Special Report by Shuster
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Letter
C1 Natl Lib Med, ClinicalTrials Gov, Bethesda, MD 20894 USA.
RP Zarin, DA (reprint author), Natl Lib Med, ClinicalTrials Gov, Bethesda, MD 20894 USA.
EM dzarin@mail.nih.gov
NR 3
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1752-8054
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD APR
PY 2012
VL 5
IS 2
BP 217
EP 217
DI 10.1111/j.1752-8062.2012.00411.x
PG 1
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 926VT
UT WOS:000302860700011
PM 22507123
ER
PT J
AU Shechner, T
Britton, JC
Perez-Edgar, K
Bar-Haim, Y
Ernst, M
Fox, NA
Leibenluft, E
Pine, DS
AF Shechner, Tomer
Britton, Jennifer C.
Perez-Edgar, Koraly
Bar-Haim, Yair
Ernst, Monique
Fox, Nathan A.
Leibenluft, Ellen
Pine, Daniel S.
TI Attention biases, anxiety, and development: toward or away from threats
or rewards?
SO DEPRESSION AND ANXIETY
LA English
DT Review
DE attention bias; anxiety; brain-behavior; attention training
ID POSTTRAUMATIC-STRESS-DISORDER; PREFRONTAL CORTEX ACTIVATION; ANTICIPATED
PEER EVALUATION; MAJOR DEPRESSIVE DISORDER; GENERALIZED-ANXIETY;
BEHAVIORAL-INHIBITION; SELECTIVE ATTENTION; SOCIAL ANXIETY; ANGRY FACES;
EMOTIONAL INFORMATION
AB Research on attention provides a promising framework for studying anxiety pathophysiology and treatment. The study of attention biases appears particularly pertinent to developmental research, as attention affects learning and has down-stream effects on behavior. This review summarizes recent findings about attention orienting in anxiety, drawing on findings in recent developmental psychopathology and affective neuroscience research. These findings generate specific insights about both development and therapeutics. The review goes beyond a traditional focus on biased processing of threats and considers biased processing of rewards. Building on this work, we then turn to the treatment of pediatric anxiety, where manipulation of attention to threat and/or reward may serve a therapeutic role as a component of Attention Bias Modification Therapy. Depression and Anxiety 0:113, 2011. (C) 2011 Wiley Periodicals, Inc.
C1 [Shechner, Tomer] NIMH, Sect Dev Affect Neurosci, Bethesda, MD 20892 USA.
[Perez-Edgar, Koraly] George Mason Univ, Dept Psychol, Arlington, VA USA.
[Bar-Haim, Yair] Tel Aviv Univ, Dept Psychol, IL-69978 Tel Aviv, Israel.
[Fox, Nathan A.] Univ Maryland, Dept Human Dev, College Pk, MD 20742 USA.
RP Shechner, T (reprint author), NIMH, Sect Dev Affect Neurosci, 9000 Rockville Pike,Bldg 15K,Rm 208, Bethesda, MD 20892 USA.
EM shechnert@mail.nih.gov
RI Britton, Jennifer/J-4501-2013;
OI Perez-Edgar, Koraly/0000-0003-4051-9563
FU National Institutes of Mental Heatlh
FX The authors disclose the following financial relationships within the
past 3 years: The paper was supported in part by the Intramural Research
Program of the National Institutes of Mental Heatlh.
NR 77
TC 67
Z9 68
U1 10
U2 87
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1091-4269
J9 DEPRESS ANXIETY
JI Depress. Anxiety
PD APR
PY 2012
VL 29
IS 4
BP 282
EP 294
DI 10.1002/da.20914
PG 13
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 927KG
UT WOS:000302905600005
PM 22170764
ER
PT J
AU Cawley, NX
Wetsel, WC
Murthy, SRK
Park, JJ
Pacak, K
Loh, YP
AF Cawley, Niamh X.
Wetsel, William C.
Murthy, Saravana R. K.
Park, Joshua J.
Pacak, Karel
Loh, Y. Peng
TI New Roles of Carboxypeptidase E in Endocrine and Neural Function and
Cancer
SO ENDOCRINE REVIEWS
LA English
DT Review
ID NEUROPEPTIDE-PROCESSING ENZYME; REGULATED SECRETORY PATHWAY;
CENTRAL-NERVOUS-SYSTEM; DIFFERENTIAL GENE-EXPRESSION; ACTIVITY-DEPENDENT
SECRETION; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; H-3
GUANIDINOETHYLMERCAPTOSUCCINIC ACID; VESICULAR ACETYLCHOLINE
TRANSPORTER; CPE(FAT/FAT) MOUSE HYPOTHALAMUS; SINGLE NUCLEOTIDE
POLYMORPHISM
AB Carboxypeptidase E (CPE) or carboxypeptidase H was first discovered in 1982 as an enkephalin-convertase that cleaved a C-terminal basic residue from enkephalin precursors to generate enkephalin. Since then, CPE has been shown to be a multifunctional protein that subserves many essential nonenzymatic roles in the endocrine and nervous systems. Here, we review the phylogeny, structure, and function of CPE in hormone and neuropeptide sorting and vesicle transport for secretion, alternative splicing of the CPE transcript, and single nucleotide polymorphisms in humans. With this and the analysis of mutant and knockout mice, the data collectively support important roles for CPE in the modulation of metabolic and glucose homeostasis, bone remodeling, obesity, fertility, neuroprotection, stress, sexual behavior, mood and emotional responses, learning, and memory. Recently, a splice variant form of CPE has been found to be an inducer of tumor growth and metastasis and a prognostic biomarker for metastasis in endocrine and nonendocrine tumors. (Endocrine Reviews 33: 216-253, 2012)
C1 [Cawley, Niamh X.; Murthy, Saravana R. K.; Loh, Y. Peng] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cellular Neurobiol Sect, Program Dev Neurosci, NIH, Bethesda, MD 20892 USA.
[Wetsel, William C.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC 27710 USA.
[Wetsel, William C.] Duke Univ, Med Ctr, Dept Cell Biol, Durham, NC 27710 USA.
[Wetsel, William C.] Duke Univ, Med Ctr, Dept Med Endocrinol, Durham, NC 27710 USA.
[Wetsel, William C.] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA.
[Park, Joshua J.] Univ Toledo, Coll Med, Dept Neurosci, Toledo, OH 43614 USA.
[Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
RP Loh, YP (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cellular Neurobiol Sect, Program Dev Neurosci, NIH, 49 Convent Dr,Bldg 49,Room 5A-22, Bethesda, MD 20892 USA.
EM lohp@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD); NICHD
FX Research in the authors' laboratories was supported in part by the
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD) (to N.X.C., S.
R. K. M., and K. P.), and NICHD K22 and American Recovery and
Reinvestment Act grants (to J.J.P.).
NR 365
TC 41
Z9 43
U1 1
U2 8
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0163-769X
EI 1945-7189
J9 ENDOCR REV
JI Endocr. Rev.
PD APR
PY 2012
VL 33
IS 2
BP 216
EP 253
DI 10.1210/er.2011-1039
PG 38
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 925PZ
UT WOS:000302774700003
PM 22402194
ER
PT J
AU Mao, WM
Rubin, JS
Anoruo, N
Wordinger, RJ
Clark, AF
AF Mao, Weiming
Rubin, Jeffrey S.
Anoruo, Nancy
Wordinger, Robert J.
Clark, Abbot F.
TI SFRP1 promoter methylation and expression in human trabecular meshwork
cells
SO EXPERIMENTAL EYE RESEARCH
LA English
DT Article
DE glaucoma; intraocular pressure; trabecular meshwork; SFRP1; DNA
methylation; 5-aza-2 '-deoxycytidine
ID ELEVATES INTRAOCULAR-PRESSURE; FRIZZLED-RELATED PROTEINS; AQUEOUS-HUMOR;
EPIGENETIC INACTIVATION; GLAUCOMATOUS EYES; DNA METHYLATION;
GASTRIC-CANCER; CURVE ANALYSIS; WNT; GREMLIN
AB Glaucoma is a leading cause of blindness worldwide. In primary open angle glaucoma (POAG) patients, impaired trabecular meshwork (TM) function results in elevated intraocular pressure (IOP), which is the primary risk factor of developing optic neuropathy. Our previous studies showed that Wnt signaling pathway components are expressed in the human TM (HTM), and the Wnt inhibitor, secreted frizzled-related protein 1 (SFRP1) is elevated in the glaucomatous TM (GTM). Elevated SFRP1 increased IOP in mice eyes and in perfusion cultured anterior segments of the human eye. However, the cause of elevated SFRP1 in the GTM remains unknown. Promoter methylation plays a key role in regulating SFRP1 expression in certain cancer cells. In light of this, we studied whether promoter methylation is also involved in SFRP1 differential expression in the TM. Two normal TM (NTM) and two GTM cell strains were cultured for an additional 7 days after they were confluent. RNA and genomic DNA (gDNA) were isolated simultaneously to compare SFRP1 expression levels by quantitative PCR (qPCR) and to determine SFRP1 promoter methylation status by bisulfite conversion and methylation-sensitive high resolution melting analysis (MS-HRM). To study whether DNA methylation inhibitors affect SFRP1 expression in TM cells, the four TM cell strains were treated with or without 2 mu M 5-aza-2'-deoxycytidine (AZA-dC) for 4 days. RNA was isolated to compare SFRP1 expression by qPCR. In addition, a human cancer cell line, NCI-H460, was used as a positive control. We found that the two GTM cell strains had significantly higher expression levels of SFRP1 than the two NTM cell strains. However, the SFRP1 promoter of all four TM cell strains was unmethylated. In addition, AZA-dC treatment did not affect SFRP1 expression in any of the TM cell strains (n = 3, p > 0.05). In contrast, the hypermethylated SFRP1 promoter of NCI-H460 cells was partially demethylated by the same treatment. AZA-dC treatment also elevated SFRP1 expression by approximately two fold in NCI-H460 cells (n = 3, p < 0.01). Our data suggest that the differential expression of SFRP1 in HTM cells is not due to differential promoter methylation. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Mao, Weiming; Wordinger, Robert J.; Clark, Abbot F.] Univ N Texas, Hlth Sci Ctr, Dept Cell Biol & Anat, N Texas Eye Res Inst, Ft Worth, TX 76107 USA.
[Rubin, Jeffrey S.; Anoruo, Nancy] NCI, Cellular & Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Mao, WM (reprint author), Univ N Texas, Hlth Sci Ctr, Dept Cell Biol & Anat, N Texas Eye Res Inst, CBH440, Ft Worth, TX 76107 USA.
EM weiming.mao@unthsc.edu
OI Wordinger, Robert/0000-0002-2861-8967
NR 39
TC 7
Z9 9
U1 1
U2 6
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0014-4835
J9 EXP EYE RES
JI Exp. Eye Res.
PD APR
PY 2012
VL 97
IS 1
BP 130
EP 136
DI 10.1016/j.exer.2012.01.003
PG 7
WC Ophthalmology
SC Ophthalmology
GA 929QU
UT WOS:000303081400015
PM 22248913
ER
PT J
AU Young, NS
AF Young, Neal S.
TI Bone marrow failure and the new telomere diseases: practice and research
SO HEMATOLOGY
LA English
DT Article
DE Cirrhosis; Pulmonary fibrosis; Aplastic anemia; Genetics
ID DYSKERATOSIS-CONGENITA; LENGTH
AB The telomeropathies are a newly described group of human diseases based on the genetics and molecular biology of the telomeres, the ends of chromosomes. Telomeres are repeated hexanucleotides and their associated proteins; the protect chromosomes from recognition as damaged DNA, and their inevitable gradual loss with DNA replication is harmless as they are noncoding. However, when telomeres become critically short in a cell, senescence, apoptosis, or, rarely malignant transformation results. In individuals with mutations in genes involved in telomere repair, especially the enzymatic telomerase complex, telomere attrition is accelerated. Severe deficiencies result in dyskeratosis congenita, a congenital aplastic anemia with associated mucocutaneous abnormalities. Mutations in TERT, the catalytic component, and TERC, the RNA template, can behave as risk factors for the development of bone marrow failure, pulmonary fibrosis, and hepatic cirrhosis. Both penetrance and organ specificity are variable and not well understood. Chromosome instability is a result of critical shortening of telomeres and cancer. For example, short telomeres are the major prognostic risk factor for clonal evolution to myelodysplasia and acute leukemia. Practically, hematologists need to recognize the multisystem presentation of telomere disease, implications for outcomes, and options for therapy.
C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Young, NS (reprint author), NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
EM youngns@nhlbi.nih.gov
NR 11
TC 14
Z9 16
U1 0
U2 9
PU MANEY PUBLISHING
PI LEEDS
PA STE 1C, JOSEPHS WELL, HANOVER WALK, LEEDS LS3 1AB, W YORKS, ENGLAND
SN 1024-5332
J9 HEMATOLOGY
JI Hematology
PD APR
PY 2012
VL 17
SU 1
BP S18
EP S21
DI 10.1179/102453312X13336169155132
PG 4
WC Hematology
SC Hematology
GA 927OA
UT WOS:000302916200006
PM 22507770
ER
PT J
AU McCarthy, AM
Wehby, GL
Barron, S
Aylward, GP
Castilla, EE
Javois, LC
Goco, N
Murray, JC
AF McCarthy, Ann Marie
Wehby, George L.
Barron, Sheila
Aylward, Glen P.
Castilla, Eduardo E.
Javois, Lorette C.
Goco, Norman
Murray, Jeffrey C.
TI Application of neurodevelopmental screening to a sample of South
American infants: The Bayley Infant Neurodevelopmental Screener (BINS)
SO INFANT BEHAVIOR & DEVELOPMENT
LA English
DT Article
DE Developmental screening; Infants; South America; Bayley Infant
Neurodevelopmental; Screener
ID COGNITIVE-DEVELOPMENT; YOUNG-CHILDREN; HEALTH; RISK; BORN
AB Objective: To evaluate the utility of the Bayley Infant Neurodevelopmental Screener (BINS), standardized in the US, for South American infants, 3-24 months of age.
Methods: Thirty-five physicians administered the BINS to 2471 South American infants recruited during routine well-child visits, 578 (23%) from Brazil and 1893 (77%) from six other South American countries. The BINS was translated into Spanish and Portuguese and participating physicians were trained to administer the BINS. Physician inter-rater agreement with training tapes was 84.4%; test-retest reliability for age item sets ranged from 0.80 to 0.93 (Pearson's r). Infants were classified into being at low, moderate, or high risk for developmental delay or neurological impairment based on their total BINS score. The sample was stratified by infant's age, sex and language (Spanish and Portuguese). The BINS scores were compared to the scores of the US infant sample used to standardize the BINS.
Results: Female infants performed higher than male at 16-20 months and 21-24 months: male infant scores were more variable at 5-6 months. Scores on only two items were significantly different between Spanish and Portuguese speaking participants. South American scores were typically significantly higher than the US sample, and a lower proportion of infants were classified as being at high risk in the South American sample than in the US standardization sample.
Conclusion: Overall, the results of this study indicate that the BINS is feasible and appropriate for neurodevelopmental screening in South America. Further studies are needed to confirm the BINS utility in South America, including its use with a clinical sample. (C) 2012 Elsevier Inc. All rights reserved.
C1 [McCarthy, Ann Marie] Univ Iowa, Coll Nursing, Iowa City, IA 52242 USA.
[Wehby, George L.] Univ Iowa, Coll Publ Hlth, Iowa City, IA 52242 USA.
[Barron, Sheila] Univ Iowa, Stat Outreach Ctr, Coll Educ, Iowa City, IA 52242 USA.
[Aylward, Glen P.] So Illinois Univ, Sch Med, Div Dev & Behav Pediat Psychol, Springfield, IL USA.
[Castilla, Eduardo E.] CEMIC, Inst Nacl Genet Med Populac INAGEMP, Buenos Aires, DF, Argentina.
[Castilla, Eduardo E.] Fundacao Oswald Cruz, Inst Oswaldo Cruz, Lab Epidemiol Malformacees Congenitas, Rio De Janeiro, Brazil.
[Javois, Lorette C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Dev Biol Genet & Teratol Branch, Ctr Dev Biol & Perinatal Med, NIH, Bethesda, MD USA.
[Goco, Norman] RTI Int, Res Triangle Pk, NC USA.
[Murray, Jeffrey C.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
RP McCarthy, AM (reprint author), Univ Iowa, Coll Nursing, 50 Newton Rd,CNB 344, Iowa City, IA 52242 USA.
EM ann-mccarthy@uiowa.edu
RI Inagemp, Inct/J-9451-2013
FU NICHD NIH HHS [1U01 HD-40561-05S2, U01 HD040561, U01 HD040561-05S2, U01
HD040636]
NR 28
TC 7
Z9 7
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0163-6383
EI 1879-0453
J9 INFANT BEHAV DEV
JI Infant Behav. Dev.
PD APR
PY 2012
VL 35
IS 2
BP 280
EP 294
DI 10.1016/j.infbeh.2011.12.003
PG 15
WC Psychology, Developmental
SC Psychology
GA 929AN
UT WOS:000303033700011
PM 22244313
ER
PT J
AU Maalouf, FT
Porta, G
Vitiello, B
Emslie, G
Mayes, T
Clarke, G
Wagner, KD
Asarnow, JR
Spirito, A
Keller, M
Birmaher, B
Ryan, N
Shamseddeen, W
Iyengar, S
Brent, D
AF Maalouf, Fadi T.
Porta, Giovanna
Vitiello, Benedetto
Emslie, Graham
Mayes, Taryn
Clarke, Gregory
Wagner, Karen D.
Asarnow, Joan Rosenbaum
Spirito, Anthony
Keller, Martin
Birmaher, Boris
Ryan, Neal
Shamseddeen, Wael
Iyengar, Satish
Brent, David
TI Do sub-syndromal manic symptoms influence outcome in treatment resistant
depression in adolescents? A latent class analysis from the TORDIA study
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE TORDIA; Trajectories; Latent class analysis; Depression; Adolescent
ID COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED CONTROLLED-TRIAL; BIPOLAR
SPECTRUM DISORDERS; TREATMENT RESPONSE; OLDER ADOLESCENTS; COMMUNITY
SAMPLE; RATING-SCALE; PREDICTORS; CHILDREN; REMISSION
AB Background: To identify distinct depressive symptom trajectories in the TORDIA study and determine their correlates.
Methods: Latent Class Growth Analysis (LCGA) using the Children's Depression Rating Scale Revised (CDRS-R) through 72 weeks from intake.
Results: 3 classes were identified: (1) little change in symptomatic status ("NO"), comprising 24.9% of participants, with a 72-week remission rate of 25.3%; (2) slow, steady improvement ("SLOW"), comprising 47.9% of participants, with a remission rate of 60.0%, and (3) rapid symptom response ("GO"), comprising 27.2% of participants, with a remission rate of 85.7%. Higher baseline CDRS-R (p<0.001) and poorer functioning (p = 0.03) were the strongest discriminators between NO and GO. Higher baseline CDRS (p<0.001) and scores on the Mania Rating Scale (MRS) (p = 0.01) were the strongest discriminators between SLOW and GO. Other variables differentiating GO from both NO and from SLOW, were better baseline functioning, lower hopelessness, and lower family conflict. Both NO and SLOW showed increases on the MRS over time compared to GO (ps <= 0.04), and increasing MRS was strongly associated with lack of remission by 72 weeks (p = 0.02).
Limitations: High rate of open treatment by the end of the follow-up period creates difficulty in drawing clear inferences about the long-term impact of initial randomization.
Conclusion: Along with depressive severity, sub-syndromal manic symptoms, at baseline, and over time emerged as important predictors and correlates of poor outcome in this sample. Further research is needed on the treatment of severe depression, and on the assessment and management of sub-syndromal manic symptoms in treatment resistant depression. (C) 2011 Published by Elsevier B.V.
C1 [Maalouf, Fadi T.] Amer Univ Beirut, Beirut, Lebanon.
[Maalouf, Fadi T.; Porta, Giovanna; Birmaher, Boris; Ryan, Neal; Iyengar, Satish; Brent, David] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Vitiello, Benedetto] NIMH, Bethesda, MD 20892 USA.
[Wagner, Karen D.] Univ Texas Galveston, Galveston, TX USA.
[Asarnow, Joan Rosenbaum] Univ Calif Los Angeles, Los Angeles, CA USA.
[Spirito, Anthony; Keller, Martin] Brown Univ, Providence, RI 02912 USA.
[Shamseddeen, Wael] Rosalind Franklin Univ Med & Sci, N Chicago, IL USA.
RP Brent, D (reprint author), Western Psychiat Inst & Clin, 3811 OHara St,Rm 311 Bellefield Towers, Pittsburgh, PA 15213 USA.
EM brentda@upmc.edu
FU Phillip Morris; Pfizer; National Institute of Mental Health: is a
consultant for Schering Plough; Random House, Inc. (New Hope for
Children and Teens with Bipolar Disorder); Lippincott Williams & Wilkins
(Treating Child and Adolescent Depression); Guilford Press; UpToDate
Psychiatry; NIMH [MH61835, MH6185E, MH61864, MH61869, MH61958, MH62014];
Advanced Center for Early-Onset Mood and Anxiety Disorders [MH66371];
Hikma pharmaceuticals; Biobehavioral Diagnostics; Eli Lilly; Forest
Laboratories; GlaxoSmithKline; Somerset
FX Dr. Asarnow reports receiving unrestricted research support from Phillip
Morris and consulting on cognitive-behavior therapy and depression
quality improvement.; Dr. Keller is currently a professor of Psychiatry
and Human Behavior at Brown University School of Medicine, has been a
consultant and received honoraria from CENEREX, Medtronic, Sierra
Neuropharmaceuticals, and has received grant funding from Pfizer.; Dr.
Birmaher is currently employed by the University of Pittsburgh and the
University of Pittsburgh Medical Center/Western Psychiatric Institute
and Clinic; has received research funding from the National Institute of
Mental Health: is a consultant for Schering Plough; and has received
royalties from Random House, Inc. (New Hope for Children and Teens with
Bipolar Disorder) and Lippincott Williams & Wilkins (Treating Child and
Adolescent Depression).; Dr. Brent is currently employed by the
University of Pittsburgh, School of Medicine and the University of
Pittsburgh Medical Center, Western Psychiatric Institute and Clinic; has
received research support from the National Institute of Mental Health;
receives royalties from Guilford Press; and serves as UpToDate
Psychiatry Editor.; Funded by NIMH grants MH61835 (Pittsburgh); MH6185E
(Galveston); MH61864 (UCLA); MH61869 (Portland); MH61958 (Dallas); and
MH62014 (Brown), and the Advanced Center for Early-Onset Mood and
Anxiety Disorders (MH66371, PI: David Brent, MD). The NIMH had no
further role in study design; in the collection, analysis and
interpretation of data; in the writing of the report; and in the
decision to submit the paper for publication.; Dr. Maalouf is on the
Speaker's Bureau of Eli Lilly and participated in a meeting sponsored by
Hikma pharmaceuticals.; Dr. Emslie has received research support from
Biobehavioral Diagnostics, Eli Lilly, Forest Laboratories,
GlaxoSmithKline, and Somerset. He has served as a consultant for
Biobehavioral Diagnostics, Eli Lilly, Forest Laboratories,
GlaxoSmithKline, Pfizer, and Wyeth Pharmaceuticals.
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PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0327
J9 J AFFECT DISORDERS
JI J. Affect. Disord.
PD APR
PY 2012
VL 138
IS 1-2
BP 86
EP 95
DI 10.1016/j.jad.2011.12.021
PG 10
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 928IJ
UT WOS:000302976100012
PM 22284022
ER
PT J
AU Valiengo, LL
Soeiro-De-Souza, MG
Marques, AH
Moreno, DH
Juruena, MF
Andreazza, AC
Gattaz, WF
Machado-Vieira, R
AF Valiengo, Leandro L.
Soeiro-de-Souza, Marcio G.
Marques, Andrea H.
Moreno, Doris H.
Juruena, Mario F.
Andreazza, Ana Cristina
Gattaz, Wagner F.
Machado-Vieira, Rodrigo
TI Plasma cortisol in first episode drug-naive mania: Differential levels
in euphoric versus irritable mood
SO JOURNAL OF AFFECTIVE DISORDERS
LA English
DT Article
DE Cortisol; Bipolar disorder; Mania; Depression; Stress; Dimensional
ID PITUITARY-ADRENAL AXIS; DEXAMETHASONE-SUPPRESSION TEST; BIPOLAR
DISORDER; ADRENOCORTICAL FUNCTION; DEPRESSIVE SYMPTOMS; HORMONE TEST;
STRESS; LITHIUM; SCHIZOPHRENIA; ILLNESS
AB Background: Dysregulation of HPA axis has been widely described in subjects with bipolar disorder (BD), including changes in cortisol levels during mood episodes and euthymia. However, most of the studies were done with medicated BD patients with variable length of illness, which was shown to interfere on peripheral cortisol levels. Therefore, the present study aims to evaluate plasma cortisol levels in drug-naive BD subjects during the first manic episode, as well as investigate the relationship between plasma cortisol levels and manic symptomatology.
Methods: Twenty-six drug-naive patients were enrolled meeting criteria for a first manic episode in bipolar I disorder. Severity of mania was assessed using the Young Mania Rating Scale (YMRS). The control group included 27 healthy subjects matched by age and gender. Cortisol was quantified using a direct radioimmunoassay.
Results: Plasma cortisol levels were decreased during first manic episode compared to healthy controls. Higher cortisol levels were positively associated with the presence of irritability (dysphoria), while elated mania showed lower cortisol levels compared to controls.
Limitation: Data including larger samples are lacking.
Conclusion: Higher cortisol in dysphoric mania compared to predominantly elated/euphoric mania may indicate a clinical and neurobiological polymorphic phenomenon, potentially involving a higher biological sensitivity to stress in the presence of irritable mood. The present findings highlight the importance to add a dimensional approach to the traditional categorical diagnosis for future neurobiological studies in BD. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Valiengo, Leandro L.; Gattaz, Wagner F.; Machado-Vieira, Rodrigo] Univ Sao Paulo, Lab Neurosci, Inst & Dept Psychiat, BR-01060970 Sao Paulo, Brazil.
[Soeiro-de-Souza, Marcio G.; Moreno, Doris H.] Univ Sao Paulo HC FMUSP, Mood Disorders Unit GRUDA, Dept & Inst Psychiat, Sch Med, Sao Paulo, Brazil.
[Marques, Andrea H.] NIMH, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
[Juruena, Mario F.] Univ Sao Paulo, Dept Neurosci & Behav Sci, Ribeirao Preto, SP, Brazil.
[Andreazza, Ana Cristina] Univ Toronto, Dept Psychiat, Toronto, ON, Canada.
[Andreazza, Ana Cristina] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
RP Machado-Vieira, R (reprint author), Univ Sao Paulo, Inst Psychiat, LIM 27,Rua Ovidio Pires de Campos,785, BR-01060970 Sao Paulo, Brazil.
EM machadovieirar@gmail.com
RI Gattaz, Wagner/C-4456-2012; MACHADO-VIEIRA, RODRIGO/D-8293-2012;
Juruena, Mario/D-5571-2009;
OI MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190; Juruena,
Mario/0000-0001-8558-3396; Juruena, Mario F./0000-0002-4063-2278
FU Sao Paulo Research Foundation, Fapesp Brazil [2009/14891-9]; Fapesp
[2009/14891-9]; Associacao Beneficente Alzira Denise Hertzog da Silva
(ABADHS)
FX This study was funded by Sao Paulo Research Foundation, Fapesp
(2009/14891-9), Brazil.; We thank Fapesp (2009/14891-9) and Associacao
Beneficente Alzira Denise Hertzog da Silva (ABADHS).
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PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0327
J9 J AFFECT DISORDERS
JI J. Affect. Disord.
PD APR
PY 2012
VL 138
IS 1-2
BP 149
EP 152
DI 10.1016/j.jad.2011.11.046
PG 4
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 928IJ
UT WOS:000302976100020
PM 22305430
ER
PT J
AU Rosen, CJ
Abrams, SA
Aloia, JF
Brannon, PM
Clinton, SK
Durazo-Arvizu, RA
Gallagher, JC
Gallo, RL
Jones, G
Kovacs, CS
Manson, JE
Mayne, ST
Ross, AC
Shapses, SA
Taylor, CL
AF Rosen, Clifford J.
Abrams, Steven A.
Aloia, John F.
Brannon, Patsy M.
Clinton, Steven K.
Durazo-Arvizu, Ramon A.
Gallagher, J. Christopher
Gallo, Richard L.
Jones, Glenville
Kovacs, Christopher S.
Manson, JoAnn E.
Mayne, Susan T.
Ross, A. Catharine
Shapses, Sue A.
Taylor, Christine L.
TI IOM Committee Members Respond to Endocrine Society Vitamin D Guideline
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID D SUPPLEMENTATION; CALCIUM-ABSORPTION; BONE TURNOVER; D DEFICIENCY;
WOMEN; PREECLAMPSIA; PREVENTION; PREVALENCE; PREGNANCY; MOTHERS
AB In early 2011, a committee convened by the Institute of Medicine issued a report on the Dietary Reference Intakes for calcium and vitamin D. The Endocrine Society Task Force in July 2011 published a guideline for the evaluation, treatment, and prevention of vitamin D deficiency. Although these reports are intended for different purposes, the disagreements concerning the nature of the available data and the resulting conclusions have caused confusion for clinicians, researchers, and the public. In this commentary, members of the Institute of Medicine committee respond to aspects of The Endocrine Society guideline that are not well supported and in need of reconsideration. These concerns focus on target serum 25-hydroxyvitamin D levels, the definition of vitamin D deficiency, and the question of who constitutes a population at risk vs. the general population. (J Clin Endocrinol Metab 97: 1146-1152, 2012)
C1 [Rosen, Clifford J.] Maine Med Ctr Res Inst, Scarborough, ME 04074 USA.
Baylor Coll Med, Houston, TX 77030 USA.
SUNY Stony Brook, Mineola, NY 11501 USA.
Winthrop Univ Hosp, Mineola, NY 11501 USA.
Cornell Univ, Ithaca, NY 14853 USA.
Ohio State Univ, Columbus, OH 43210 USA.
Loyola Univ Chicago, Maywood, IL 60153 USA.
Creighton Univ, Med Ctr, Omaha, NE 68131 USA.
Univ Calif San Diego, San Diego, CA 92161 USA.
Queens Univ, Kingston, ON K7L 3N6, Canada.
Mem Univ Newfoundland, St John, NF A1B 3V6, Canada.
Harvard Univ, Sch Med, Boston, MA 02215 USA.
Yale Univ, Sch Publ Hlth, New Haven, CT 06520 USA.
Penn State Univ, University Pk, PA 16802 USA.
Rutgers State Univ, New Brunswick, NJ 08901 USA.
[Taylor, Christine L.] NIH, Off Dietary Supplements, Bethesda, MD 20892 USA.
RP Rosen, CJ (reprint author), Maine Med Ctr Res Inst, 81 Res Dr, Scarborough, ME 04074 USA.
EM crofen@gmail.com
OI Gallo, Richard/0000-0002-1401-7861; Abrams, Steven/0000-0003-4972-9233;
Kovacs, Christopher/0000-0002-5219-9993
FU NCI NIH HHS [R01 CA090214]
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PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD APR
PY 2012
VL 97
IS 4
BP 1146
EP 1152
DI 10.1210/jc.2011-2218
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 925US
UT WOS:000302787800039
PM 22442278
ER
PT J
AU Harlow, SD
Gass, M
Hall, JE
Lobo, R
Maki, P
Rebar, RW
Sherman, S
Sluss, PM
de Villiers, TJ
AF Harlow, Sioban D.
Gass, Margery
Hall, Janet E.
Lobo, Roger
Maki, Pauline
Rebar, Robert W.
Sherman, Sherry
Sluss, Patrick M.
de Villiers, Tobie J.
CA STRAW 10 Collaborative Grp
TI Executive Summary of the Stages of Reproductive Aging Workshop+10:
Addressing the Unfinished Agenda of Staging Reproductive Aging
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID FOLLICLE-STIMULATING-HORMONE; ANTI-MULLERIAN HORMONE; EARLY MENOPAUSAL
TRANSITION; POLYCYSTIC-OVARY-SYNDROME; MIDDLE-AGED WOMEN; REGULAR
MENSTRUAL CYCLES; INHIBIN-B; ANTIMULLERIAN HORMONE; LONGITUDINAL
CHANGES; DEPRESSIVE SYMPTOMS
AB Objective: The aim of this article is to summarize the recommended updates to the 2001 Stages of Reproductive Aging Workshop (STRAW) criteria. The 2011 STRAW + 10 reviewed advances in understanding of the critical changes in hypothalamic-pituitary-ovarian function that occur before and after the final menstrual period.
Methods: Scientists from five countries and multiple disciplines evaluated data from cohort studies of midlife women and in the context of chronic illness and endocrine disorders on change in menstrual, endocrine, and ovarian markers of reproductive aging including antimullerian hormone, inhibin-B, follicle-stimulating hormone, and antral follicle count. Modifications were adopted by consensus.
Results: STRAW + 10 simplified bleeding criteria for the early and late menopausal transition, recommended modifications to criteria for the late reproductive stage (Stage -3) and the early postmenopause stage (Stage +1), provided information on the duration of the late transition (Stage-1) and early postmenopause (Stage + 1), and recommended application regardless of women's age, ethnicity, body size, or lifestyle characteristics.
Conclusions: STRAW + 10 provides a more comprehensive basis for assessing reproductive aging in research and clinical contexts. Application of the STRAW + 10 staging system should improve comparability of studies of midlife women and facilitate clinical decision making. Nonetheless, important knowledge gaps persist, and seven research priorities are identified. (J Clin Endocrinol Metab 97: 1159-1168, 2012)
C1 [Harlow, Sioban D.] Univ Michigan, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Gass, Margery] N Amer Menopause Soc, Mayfield Hts, OH USA.
[Hall, Janet E.] Harvard Univ, Sch Med, Dept Med, Endocrine Soc, Boston, MA USA.
[Lobo, Roger] Columbia Univ, Dept Obstet & Gynecol, New York, NY USA.
[Maki, Pauline] Univ Illinois, Dept Psychiat & Psychol, Chicago, IL USA.
[Rebar, Robert W.] Amer Soc Reprod Med, Birmingham, AL USA.
[Sherman, Sherry] NIA, Bethesda, MD 20892 USA.
[Sluss, Patrick M.] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA.
[de Villiers, Tobie J.] Int Menopause Soc, Cape Town, South Africa.
RP Harlow, SD (reprint author), Univ Michigan, Dept Epidemiol, 1415 Washington Hts, Ann Arbor, MI 48109 USA.
EM harlow@umich.edu
FU National Institutes of Health (NIH); Department of Health and Human
Services (DHHS), through the National Institute on Aging (NIA)
[AG039961]; NIH Office of Research on Women's Health (ORWH); North
American Menopause Society (NAMS); American Society for Reproductive
Medicine (ASRM); International Menopause Society (IMS); Endocrine
Society; National Institute on Aging (NIA); Eunice Kennedy Shriver
National Institute of Child Health and Human Development(NICHD);
National Institute on Mental Health (NIMH); National Institute of
Allergy and Infectious Diseases (NIAID); National Institute on Drug
Abuse (NIDA); Royal Ottawa Foundation for Mental Health; Mayo Clinic;
Baycrest; Northwestern University; ASRM; Adcock Ingram; Pfizer; Servier
FX This article is being simultaneously published in the journals
Climacteric, Fertility and Sterility, the Journal of Clinical
Endocrinology and Metabolism, and Menopause Funding/support: The Stages
of Reproductive Aging Workshop (STRAW) + 10 had grant support from the
National Institutes of Health (NIH), Department of Health and Human
Services (DHHS), through the National Institute on Aging (NIA)
(AG039961), and the NIH Office of Research on Women's Health (ORWH) as
well as from The North American Menopause Society (NAMS), the American
Society for Reproductive Medicine (ASRM), the International Menopause
Society (IMS), and the Endocrine Society.; Financial
disclosure/conflicts of interest: P.M.S. and S.S. declare no conflict of
interest. M.G. receives salary support from The North American Menopause
Society (NAMS). S.D.H. has grant support from the National Institute on
Aging (NIA) and Eunice Kennedy Shriver National Institute of Child
Health and Human Development(NICHD) and receives travel support from
NAMS. J.E.H. has grant support from NIA and receives travel support from
the Endocrine Society. R.L. is past president of the American Society
for Reproductive Medicine (ASRM). P.M. receives grant support from the
National Institute on Mental Health (NIMH), the NIA, the National
Institute of Allergy and Infectious Diseases (NIAID), and the National
Institute on Drug Abuse (NIDA); is on the Board of Trustees for NAMS;
and has previously consulted for Noven Pharmaceuticals, received lecture
fees from the Royal Ottawa Foundation for Mental Health, the Mayo
Clinic, Baycrest, and Northwestern University and received travel
support from the Society for Women's Health Research, the International
Menopause Society, Pfizer, the Australasian Pacific Menopause Society,
Virginia Commonwealth University Institute for Women's Health. R.W.R.
receives salary support from ASRM. T.J.d.V. declares no direct conflict
of interest as regards the submitted article but has in the past
received consultancy fees from Adcock Ingram and Pfizer; speaker's fees
from Servier; and travel support from Amgen, Pfizer, and Bayer.
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PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD APR
PY 2012
VL 97
IS 4
BP 1159
EP 1168
DI 10.1210/jc.2011-3362
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 925US
UT WOS:000302787800041
PM 22344196
ER
PT J
AU Semba, RD
Sun, K
Egan, JM
Crasto, C
Carlson, OD
Ferrucci, L
AF Semba, Richard D.
Sun, Kai
Egan, Josephine M.
Crasto, Candace
Carlson, Olga D.
Ferrucci, Luigi
TI Relationship of Serum Fibroblast Growth Factor 21 with Abnormal Glucose
Metabolism and Insulin Resistance: The Baltimore Longitudinal Study of
Aging
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID DENSITY-LIPOPROTEIN CHOLESTEROL; CHINESE SUBJECTS; FGF21; PLASMA;
TOLERANCE; REGULATOR; OBESITY; CARBOHYDRATE; SENSITIVITY; MUSCLE
AB Context: The relationship of fibroblast growth factor 21 (FGF21) with glucose metabolism and insulin resistance has not been well characterized in community-dwelling adults.
Objective: The objective of the study was to examine the relationship of FGF21 with glucose metabolism and insulin resistance.
Design: Serum FGF21, fasting plasma glucose (FPG), glucose tolerance, and insulin resistance were measured in a cross-sectional study, 2002-2007.
Setting: The study was the Baltimore Longitudinal Study of Aging, a natural history cohort study of aging in community-dwelling men and women.
Participants: Seven hundred adults, mean age 63.3 yr, participated in the study.
Main Outcome Measures: FPG, 2-h plasma glucose, homeostasis model of insulin resistance, whole-body insulin sensitivity (Matsuda index), glucose area under the curve (AUC), and insulin AUC were measured.
Results: Overall, the median (25th and 75th percentiles) FGF21 concentration was 225 (126, 370) pg/ml. The proportion of adults with normal, impaired, and diabetic FPG was 77.0, 21.4, and 1.6%, and those with normal, impaired, and diabetic 2-h plasma glucose was 76.7, 19.1, and 4.1%, respectively. Log serum FGF21 (picograms per milliliter), per 1 SD increase, was associated with an FPG (odds ratio 1.43, 95% confidence interval 1.15, 1.77, P = 0.001) and with 2-h plasma glucose (odds ratio 1.39, 95% confidence interval 1.12, 1.73, P = 0.003), in respective multivariate, ordered logistic regression models, adjusted for potential confounders. Serum FGF21 (picograms per milliliter) was associated with the homeostasis model of insulin resistance, the Matsuda index, glucose AUC, and insulin AUC (all P < 0.0001) in respective multivariable linear regression models adjusted for potential confounders.
Conclusions: Higher serum FGF21 concentrations were associated with abnormal glucose metabolism and insulin resistance in community-dwelling adults. (J Clin Endocrinol Metab 97: 1375-1382, 2012)
C1 [Semba, Richard D.; Sun, Kai; Crasto, Candace] Johns Hopkins Univ, Sch Med, Dept Ophthalmol, Baltimore, MD 21287 USA.
[Egan, Josephine M.; Carlson, Olga D.] NIA, Clin Invest Lab, Baltimore, MD 21225 USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21225 USA.
RP Semba, RD (reprint author), Johns Hopkins Sch Med, Smith Bldg,400 N Broadway,M015, Baltimore, MD 21287 USA.
EM rdsemba@jhmi.edu
FU National Institutes of Health [R01 AG027012, R01 AG029148, R01
HL094507]; National Institute on Aging, National Institutes of Health
FX This work was supported by National Institutes of Health Grants R01
AG027012, R01 AG029148, and R01 HL094507 and the Intramural Research
Program, National Institute on Aging, National Institutes of Health.
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PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD APR
PY 2012
VL 97
IS 4
BP 1375
EP 1382
DI 10.1210/jc.2011-2823
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 925US
UT WOS:000302787800069
PM 22344195
ER
PT J
AU Almeida, MQ
Azevedo, MF
Xekouki, P
Bimpaki, EI
Horvath, A
Collins, MT
Karaviti, LP
Jeha, GS
Bhattacharyya, N
Cheadle, C
Watkins, T
Bourdeau, I
Nesterova, M
Stratakis, CA
AF Almeida, Madson Q.
Azevedo, Monalisa F.
Xekouki, Paraskevi
Bimpaki, Eirini I.
Horvath, Anelia
Collins, Michael T.
Karaviti, Lefkothea P.
Jeha, George S.
Bhattacharyya, Nisan
Cheadle, Chris
Watkins, Tonya
Bourdeau, Isabelle
Nesterova, Maria
Stratakis, Constantine A.
TI Activation of Cyclic AMP Signaling Leads to Different Pathway
Alterations in Lesions of the Adrenal Cortex Caused by Germline PRKAR1A
Defects versus Those due to Somatic GNAS Mutations
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID DAVID BIOINFORMATICS RESOURCES; LARGE GENE LISTS; ADRENOCORTICAL
HYPERPLASIA; PHOSPHODIESTERASE 11A; MICRORNA SIGNATURE; KINASE;
EXPRESSION; TUMORS; SUBUNIT; DISEASE
AB Context: The overwhelming majority of benign lesions of the adrenal cortex leading to Cushing syndrome are linked to one or another abnormality of the cAMP or protein kinase pathway. PRKAR1A-inactivating mutations are responsible for primary pigmented nodular adrenocortical disease, whereas somatic GNAS activating mutations cause macronodular disease in the context of McCune-Albright syndrome, ACTH-independent macronodular hyperplasia, and, rarely, cortisol-producing adenomas.
Objective and Design: The whole-genome expression profile (WGEP) of normal (pooled) adrenals, PRKAR1A-(3) and GNAS-mutant (3) was studied. Quantitative RT-PCR and Western blot were used to validate WGEP findings.
Results: MAPK and p53 signaling pathways were highly overexpressed in all lesions against normal tissue. GNAS-mutant tissues were significantly enriched for extracellular matrix receptor interaction and focal adhesion pathways when compared with PRKAR1A-mutant (fold enrichment 3.5, P < 0.0001 and 2.1, P < 0.002, respectively). NFKB, NFKBIA, and TNFRSF1A were higher inGNAS-mutant tumors (P < 0.05). Genes related to the Wntsignaling pathway(CCND1, CTNNB1, LEF1, LRP5, WISP1, and WNT3) were overexpressed in PRKAR1A-mutant lesions.
Conclusion: WGEP analysis revealed that not all cAMP activation is the same: adrenal lesions harboring PRKAR1A or GNAS mutations share the downstream activation of certain oncogenic signals (such as MAPK and some cell cycle genes) but differ substantially in their effects on others. (J Clin Endocrinol Metab 97: E687-E693, 2012)
C1 [Almeida, Madson Q.; Azevedo, Monalisa F.; Xekouki, Paraskevi; Bimpaki, Eirini I.; Horvath, Anelia; Bourdeau, Isabelle; Nesterova, Maria; Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet PDEGEN, Bethesda, MD 20892 USA.
[Stratakis, Constantine A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Endocrinol Interinst Training Program, Bethesda, MD 20892 USA.
[Collins, Michael T.; Bhattacharyya, Nisan] Natl Inst Dent & Craniofacial Res, Skeletal Clin Studies Unit, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD 20892 USA.
[Karaviti, Lefkothea P.; Jeha, George S.] Texas Childrens Hosp, Baylor Coll Med, Dept Pediat Endocrinol & Metab, Houston, TX 77030 USA.
[Cheadle, Chris; Watkins, Tonya] Johns Hopkins Univ, Sch Med, Div Allergy & Clin Immunol, Baltimore, MD 21224 USA.
[Bourdeau, Isabelle] Ctr Hosp Univ Montreal, Div Endocrinol, Dept Med, Res Ctr, Montreal, PQ H3T 1C5, Canada.
RP Stratakis, CA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet, CRC,NIH, Bldg 10,Room 1-3330,10 Ctr Dr,MSC1103, Bethesda, MD 20892 USA.
EM stratakc@mail.nih.gov
RI Levesque, Isabelle/A-1899-2012;
OI Jeha, George/0000-0002-3531-5059
FU National Institutes of Health, Eunice Kennedy Shriver National Institute
of Child Health and Human Development [Z01-HD-000642-04]
FX This work was supported by Intramural Project Grant Z01-HD-000642-04
from the National Institutes of Health, Eunice Kennedy Shriver National
Institute of Child Health and Human Development (to C.A.S.).
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PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD APR
PY 2012
VL 97
IS 4
BP E687
EP E693
DI 10.1210/jc.2011-3000
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 925US
UT WOS:000302787800026
PM 22259056
ER
PT J
AU Weisbrod, AB
Kitano, M
Gesuwan, K
Millo, C
Herscovitch, P
Nilubol, N
Linehan, WM
Kebebew, E
AF Weisbrod, Allison B.
Kitano, Mio
Gesuwan, Krisana
Millo, Corina
Herscovitch, Peter
Nilubol, Naris
Linehan, W. Marston
Kebebew, Electron
TI Clinical Utility of Functional Imaging with F-18-FDOPA in Von
Hippel-Lindau Syndrome
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID POSITRON-EMISSION-TOMOGRAPHY; NEUROENDOCRINE TUMORS; ENDOCRINE TUMORS;
PET; DISEASE; PHEOCHROMOCYTOMA; SCINTIGRAPHY
AB Context: Von Hippel-Lindau (VHL) syndrome is an inherited cancer syndrome in which patients are at risk of developing multiple tumors in different organs. 6-L-F-18-fluorodihydroxyphenylalanine (F-18-FDOPA) positron emission tomography (PET) is a relatively new metabolic imaging tracer proposed for the use of localizing sites of neuroendocrine tumors. There are limited data on the clinical utility of using F-18-FDOPA PET for identifying neuroendocrine tumors in a high-risk population such as VHL.
Objective: The aim of this prospective study was to evaluate the clinical utility of F-18-FDOPA PET in patients with VHL-related tumors.
Design: Radiological findings were prospectively collected from four imaging modalities: computed tomography, magnetic resonance imaging (MRI), F-18-fluorodeoxyglucose PET, and (18)FFDOPA PET. F-18-FDOPA PET findings were compared with those from other imaging modalities, as well as with clinical and laboratory data, and pathology findings if patients underwent an operation.
Results: In 52 patients with VHL, 390 lesions were identified by computed tomography (n = 139), MRI (n = 117), F-18-fluorodeoxyglucose PET (n = 94), and F-18-FDOPA PET (n = 40). F-18-FDOPA PET identified 20 pancreatic and 20 extrapancreatic tumors, including lesions in the adrenal gland (n = 11), kidney (n = 3), liver (n = 4), lung (n = 1), and cervical paraganglioma (n = 1). These tumor sites were not seen by conventional imaging studies in 9.6% of patients and 4.4% of lesions. Seven of eight patients who had an F-18-FDOPA PET-positive lesion underwent resection, and pathology showed a neuroendocrine tumor. Four of 10 patients with positive adrenal uptake had elevated catecholamine levels, and six of 10 patients had a discrete mass on axial imaging.
Conclusions: F-18-FDOPA PET is a useful complementary imaging study to detect neuroendocrine tumors in patients with VHL undergoing surveillance, especially in those suspected to have adrenal pheochromocytoma or unusual ectopic locations. (J Clin Endocrinol Metab 97: E613-E617, 2012)
C1 [Kebebew, Electron] NCI, Endocrine Oncol Sect, Surg Branch, NIH,Clin Res Ctr, Bethesda, MD 20892 USA.
[Millo, Corina; Herscovitch, Peter] NIH, Dept Nucl Med, Positron Emiss Tomog Imaging Sect, Bethesda, MD 20892 USA.
[Linehan, W. Marston] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
RP Kebebew, E (reprint author), NCI, Endocrine Oncol Sect, Surg Branch, NIH,Clin Res Ctr, Bldg 10-CRC,Room 3-3940,10 Ctr Dr,MSC 1201, Bethesda, MD 20892 USA.
EM kebebewe@mail.nih.gov
FU Center for Cancer Research, National Cancer Institute, National
Institutes of Health
FX This research was supported by the intramural research program of the
Center for Cancer Research, National Cancer Institute, National
Institutes of Health.
NR 19
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U1 1
U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0021-972X
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD APR
PY 2012
VL 97
IS 4
BP E613
EP E617
DI 10.1210/jc.2011-2626
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 925US
UT WOS:000302787800013
PM 22259055
ER
PT J
AU Newbold, RR
AF Newbold, R. R.
TI Prenatal exposure to diethylstilbestrol and long-term impact on the
breast and reproductive tract in humans and mice
SO JOURNAL OF DEVELOPMENTAL ORIGINS OF HEALTH AND DISEASE
LA English
DT Review
DE breast cancer; critical windows; epigenetics; fibroids; hormonal
carcinogenesis
ID MAMMARY-GLAND DEVELOPMENT; ENDOCRINE-DISRUPTING CHEMICALS; BISPHENOL-A
ALTERS; DEVELOPMENTAL EXPOSURE; PERINATAL EXPOSURE; CANCER-RISK;
IN-UTERO; ESTROGEN-RECEPTORS; GENE-EXPRESSION; NEONATAL MICE
AB The term 'developmental origins of health and disease' (DOHaD) originally referred to delayed effects of altered maternal factors (e.g. smoking or poor nutrition) on the developing offspring, but it now also encompasses early life exposure to environmental chemicals, which can cause an unhealthy prenatal environment that endangers the fetus and increases its susceptibility to disease later in life. Prenatal exposure to the pharmaceutical diethylstilbestrol (DES) is a well-known DOHaD example as it was associated in the 1970s with vaginal cancer in daughters who were exposed to this potent synthetic estrogen before birth. Subsequently, numerous long-term effects have been described in breast and reproductive tissues of DES-exposed humans and experimental animals. Data reviewed suggest that the prenatal DES-exposed population should continue to be monitored for potential-increased disease risks as they age. Knowledge of sensitive developmental periods, and the mechanisms of DES-induced toxicities, provides useful information in predicting potential adverse effects of other environmental estrogens.
C1 NIEHS, Natl Toxicol Program, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Newbold, RR (reprint author), NIEHS, Natl Toxicol Program, NIH, DHHS, POB 12233,Mail Drop K2-15, Res Triangle Pk, NC 27709 USA.
EM newbold1@niehs.nih.gov
NR 72
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Z9 4
U1 1
U2 15
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 2040-1744
J9 J DEV ORIG HLTH DIS
JI J. Dev. Orig. Health Dis.
PD APR
PY 2012
VL 3
IS 2
BP 73
EP 82
DI 10.1017/S2040174411000754
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 929KQ
UT WOS:000303061700002
PM 25101917
ER
PT J
AU Schisler, RE
Groninger, H
Rosielle, DA
AF Schisler, Randall E.
Groninger, Hunter
Rosielle, Drew A.
TI Counseling Patients on Side Effects and Driving When Starting Opioids
#248
SO JOURNAL OF PALLIATIVE MEDICINE
LA English
DT Editorial Material
ID CANCER PAIN
C1 [Groninger, Hunter] NIH, Pain & Palliat Care Serv, Ctr Clin, Bethesda, MD 20892 USA.
[Rosielle, Drew A.] Univ Minnesota, Palliat Care Program, Sch Med, Minneapolis, MN 55455 USA.
[Rosielle, Drew A.] Med Coll Wisconsin, End Life Palliat Educ Resource Ctr, Milwaukee, WI USA.
RP Groninger, H (reprint author), NIH, Pain & Palliat Care Serv, Ctr Clin, Bldg 10,Room 2-1733, Bethesda, MD 20892 USA.
EM hunter.groninger@nih.gov
OI Rosielle, Drew/0000-0003-3942-3791
NR 11
TC 3
Z9 3
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1096-6218
J9 J PALLIAT MED
JI J. Palliat. Med.
PD APR
PY 2012
VL 15
IS 4
BP 484
EP 485
DI 10.1089/jpm.2012.9596
PG 2
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 926TM
UT WOS:000302854700019
PM 22500484
ER
PT J
AU Greenberg, SJ
AF Greenberg, Stephen J.
TI The Plague in Print: Essential Elizabethan Sources, 1558-1603
SO JOURNAL OF THE HISTORY OF MEDICINE AND ALLIED SCIENCES
LA English
DT Book Review
C1 [Greenberg, Stephen J.] NIH, Hist Med Div, Natl Lib Med, US Dept HHS, Bethesda, MD 20894 USA.
RP Greenberg, SJ (reprint author), NIH, Hist Med Div, Natl Lib Med, US Dept HHS, Bethesda, MD 20894 USA.
NR 1
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 0022-5045
J9 J HIST MED ALL SCI
JI J. Hist. Med. Allied Sci.
PD APR
PY 2012
VL 67
IS 2
BP 328
EP 329
DI 10.1093/jhmas/jrr052
PG 2
WC Health Care Sciences & Services; History & Philosophy Of Science
SC Health Care Sciences & Services; History & Philosophy of Science
GA 927FH
UT WOS:000302892000006
ER
PT J
AU Reznick, JS
AF Reznick, Jeffrey S.
TI War, Politics, and Philanthropy: The History of Rehabilitation Medicine
SO JOURNAL OF THE HISTORY OF MEDICINE AND ALLIED SCIENCES
LA English
DT Book Review
C1 [Reznick, Jeffrey S.] NIH, Hist Med Div, US Natl Lib Med, Bethesda, MD 20894 USA.
RP Reznick, JS (reprint author), NIH, Hist Med Div, US Natl Lib Med, Bethesda, MD 20894 USA.
NR 1
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 0022-5045
J9 J HIST MED ALL SCI
JI J. Hist. Med. Allied Sci.
PD APR
PY 2012
VL 67
IS 2
BP 335
EP 337
DI 10.1093/jhmas/jrr062
PG 3
WC Health Care Sciences & Services; History & Philosophy Of Science
SC Health Care Sciences & Services; History & Philosophy of Science
GA 927FH
UT WOS:000302892000010
ER
PT J
AU Wolfe, LL
Kocisko, DA
Caughey, B
Miller, MW
AF Wolfe, Lisa L.
Kocisko, David A.
Caughey, Byron
Miller, Michael W.
TI Assessment of Prospective Preventive Therapies for Chronic Wasting
Disease in Mule Deer
SO JOURNAL OF WILDLIFE DISEASES
LA English
DT Article
ID PRION PROTEIN-FORMATION; SCRAPIE; INHIBITION
AB We compared prion infection rates among mule deer (Odocoileus hemionus) receiving pentosan polysulfate, tannic acid, tetracycline HCl, or no treatment 14 days before to 14 days after (dpi) oral inoculation with tonsil tissue homogenate. All deer were infected, but the rapid disease course (230-603 dpi) suggested our challenge was overwhelming.
C1 [Wolfe, Lisa L.; Miller, Michael W.] Wildlife Res Ctr, Colorado Div Wildlife, Ft Collins, CO 80526 USA.
[Kocisko, David A.; Caughey, Byron] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Wolfe, LL (reprint author), Wildlife Res Ctr, Colorado Div Wildlife, 317 W Prospect Rd, Ft Collins, CO 80526 USA.
EM lisa.wolfe@state.co.us
FU Colorado Division of Wildlife; National Institutes of Health
FX We thank the Colorado Division of Wildlife and the National Institutes
of Health for support, and T. M. Davis, E. S. Williams, and many others
for their assistance over the course of this study.
NR 15
TC 1
Z9 1
U1 0
U2 4
PU WILDLIFE DISEASE ASSOC, INC
PI LAWRENCE
PA 810 EAST 10TH ST, LAWRENCE, KS 66044-8897 USA
SN 0090-3558
J9 J WILDLIFE DIS
JI J. Wildl. Dis.
PD APR
PY 2012
VL 48
IS 2
BP 530
EP 533
PG 4
WC Veterinary Sciences
SC Veterinary Sciences
GA 922ZZ
UT WOS:000302589000038
PM 22493139
ER
PT J
AU Vatsalya, V
Coe, MA
Ramchandani, VA
Karch, R
AF Vatsalya, Vatsalya
Coe, Marion A.
Ramchandani, Vijay A.
Karch, Robert
TI Sex and Age Variations in Quality of Life Indices Among Alcohol Drinking
Population
SO JOURNAL OF WOMENS HEALTH
LA English
DT Meeting Abstract
C1 [Vatsalya, Vatsalya; Karch, Robert] Amer Univ DC, Washington, DC USA.
[Vatsalya, Vatsalya; Coe, Marion A.; Ramchandani, Vijay A.] NIAAA, SHP LCTS, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD APR
PY 2012
VL 21
IS 4
MA P139
BP 53
EP 53
PG 1
WC Public, Environmental & Occupational Health; Medicine, General &
Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
Medicine; Obstetrics & Gynecology; Women's Studies
GA 926UE
UT WOS:000302856600140
ER
PT J
AU Grkovic, L
Baird, K
Steinberg, SM
Williams, KM
Pulanic, D
Cowen, EW
Mitchell, SA
Hakim, FT
Martires, KJ
Avila, DN
Taylor, TN
Salit, RB
Rowley, SD
Zhang, D
Fowler, DH
Bishop, MR
Gress, RE
Pavletic, SZ
AF Grkovic, L.
Baird, K.
Steinberg, S. M.
Williams, K. M.
Pulanic, D.
Cowen, E. W.
Mitchell, S. A.
Hakim, F. T.
Martires, K. J.
Avila, D. N.
Taylor, T. N.
Salit, R. B.
Rowley, S. D.
Zhang, D.
Fowler, D. H.
Bishop, M. R.
Gress, R. E.
Pavletic, S. Z.
TI Clinical laboratory markers of inflammation as determinants of chronic
graft-versus-host disease activity and NIH global severity
SO LEUKEMIA
LA English
DT Article
DE chronic graft-versus-host disease; inflammation; activity; CRP;
platelets
ID C-REACTIVE PROTEIN; STEM-CELL TRANSPLANTATION;
BONE-MARROW-TRANSPLANTATION; CONSENSUS DEVELOPMENT PROJECT; WORKING
GROUP-REPORT; NEPHROTIC SYNDROME; RHEUMATOID-ARTHRITIS;
SYSTEMIC-SCLEROSIS; CHRONIC GVHD; INTERLEUKIN-6
AB Chronic graft-versus-host disease (cGVHD) remains a major cause of non-relapse morbidity and mortality after allogeneic hematopoietic stem cell transplantation. Currently there are no accepted measures of cGVHD activity to aid in clinical management and disease staging. We analyzed clinical markers of inflammation in the sera of patients with established cGVHD and correlated those with definitions of disease activity. In all, 189 adults with cGVHD (33% moderate and 66% severe according to National Institutes of Health (NIH) global scoring) were consecutively enrolled onto a cross-sectional prospective cGVHD natural history study. At the time of evaluation, 80% were receiving systemic immunosuppression and failed a median of four prior systemic therapies (PST) for their cGVHD. Lower albumin (P < 0.0001), higher C-reactive protein (P = 0.043), higher platelets (P = 0.030) and higher number of PST (P < 0.0001) were associated with active disease defined as clinician's intention to intensify or alter systemic therapy due to the lack of response. Higher platelet count (P = 0.021) and higher number of PST (P < 0.0001) were associated with more severe diseased defined by NIH global score. This study identified common laboratory indicators of inflammation that can serve as markers of cGVHD activity and severity. Leukemia (2012) 26, 633-643; doi:10.1038/leu.2011.254; published online 18 October 2011
C1 [Grkovic, L.; Williams, K. M.; Hakim, F. T.; Avila, D. N.; Taylor, T. N.; Salit, R. B.; Fowler, D. H.; Bishop, M. R.; Gress, R. E.; Pavletic, S. Z.] NCI, Graft Versus Host & Autoimmun Unit, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Grkovic, L.; Pulanic, D.] Clin Hosp Ctr Zagreb, Dept Internal Med, Div Hematol, Zagreb, Croatia.
[Baird, K.] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Steinberg, S. M.; Zhang, D.] NCI, Biostat & Data Management Sect, Off Clin Director, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Cowen, E. W.; Martires, K. J.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Mitchell, S. A.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Rowley, S. D.] Hackensack Univ, Med Ctr, John Theurer Canc Ctr, Hackensack, NJ USA.
RP Pavletic, SZ (reprint author), NCI, Graft Versus Host & Autoimmun Unit, Expt Transplantat & Immunol Branch, NIH, 10 Ctr Dr,Bldg 10,Room CRC 3-3330, Bethesda, MD 20892 USA.
EM pavletis@mail.nih.gov
FU National Institutes of Health, Center for Cancer Research and National
Cancer Institute; Clinical Research Training Program; NIH; Pfizer Inc.
FX This study was supported by the Intramural Research Program of the
National Institutes of Health, Center for Cancer Research and National
Cancer Institute. We thank Dr N Rehak, Dr Katherine Calvo and Dr Irina
Maric, Department of Laboratory Medicine, Clinical Center, NIH for
providing the clinical laboratory methods information. Lana Grkovic is a
participant in the NIH Graduate Partnership Program and a post-graduate
student at the Division of Hematology, University of Zagreb, School of
Medicine, Zagreb, Croatia. Kathryn J Martires was supported by the
Clinical Research Training Program, a public-private partnership
supported jointly by the NIH and Pfizer Inc. (via a grant to the
Foundation for NIH from Pfizer Inc.).
NR 52
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U1 1
U2 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD APR
PY 2012
VL 26
IS 4
BP 633
EP 643
DI 10.1038/leu.2011.254
PG 11
WC Oncology; Hematology
SC Oncology; Hematology
GA 925UX
UT WOS:000302788300009
PM 22005783
ER
PT J
AU Calado, RT
Cooper, JN
Padilla-Nash, HM
Sloand, EM
Wu, CO
Scheinberg, P
Ried, T
Young, NS
AF Calado, R. T.
Cooper, J. N.
Padilla-Nash, H. M.
Sloand, E. M.
Wu, C. O.
Scheinberg, P.
Ried, T.
Young, N. S.
TI Short telomeres result in chromosomal instability in hematopoietic cells
and precede malignant evolution in human aplastic anemia
SO LEUKEMIA
LA English
DT Article
DE telomere; chromosome instability; aplastic anemia; myelodysplasia;
cancer
ID DYSKERATOSIS-CONGENITA; CYTOGENETIC ABNORMALITIES; CANCER; DYSFUNCTION;
LENGTH; MICE; MUTATIONS; GENE; ASSOCIATION; COMPONENT
AB In cell and animal models, telomere erosion promotes chromosomal instability via breakage-fusion-bridge cycles, contributing to the early stages of tumorigenesis. However, evidence involving short telomeres in cancer development in humans is scarce, epidemiological and indirect. Here we directly implicate telomere shortening as a critical molecular event for malignant evolution in aplastic anemia (AA). Patients' telomere lengths at diagnosis of AA, while comparable to age-matched controls, inversely correlated with the probability of developing a cytogenetically abnormal clone. A significantly increased number of telomere signal-free chromosomal ends and chromosomal numerical and structural abnormalities were observed in bone marrow cells of patients with shorter telomeres in comparison with patients with longer telomeres and healthy subjects. The proportion of monosomy-7 cells in the bone marrow at diagnosis of AA inversely correlated with telomere length, years before the emergence of an autonomous and clinically detectable abnormal clone. Marrow cells of clinically healthy individuals carrying loss-of-function telomerase mutations and with extremely short telomeres also showed chromosomal instability in vitro. These results provide the first clinical direct evidence in humans that short telomeres in hematopoietic cells are dysfunctional, mediate chromosomal instability and predispose to malignant transformation in a human disease. Leukemia (2012) 26, 700-707; doi:10.1038/leu.2011.272; published online 18 October 2011
C1 [Calado, R. T.; Cooper, J. N.; Sloand, E. M.; Scheinberg, P.; Young, N. S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Cooper, J. N.] NIH, Clin Res Training Program, Bethesda, MD 20892 USA.
[Padilla-Nash, H. M.; Ried, T.] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
[Wu, C. O.] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RP Calado, RT (reprint author), Univ Sao Paulo, Sch Med, Dept Internal Med, Hematol Lab,Subsolo HCRP, Av Bandeirantes 3900,Bloco G, BR-14049900 Ribeirao Preto, SO, Brazil.
EM calador@nhlbi.nih.gov
RI Calado, Rodrigo/G-2619-2011;
OI Scheinberg, Phillip/0000-0002-9047-4538
FU NIH; Pfizer
FX This work was entirely supported by the NIH Intramural Research Program.
Dr Cooper's research year was made possible through the Clinical
Research Training Program (CRTP), a public-private partnership supported
jointly by the NIH and Pfizer (grant to the Foundation for NIH from
Pfizer). EMS is deceased. We are grateful to Olga Nunez, RN and Barbara
Weinstein, RN for patient care and sample collection.
NR 41
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U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD APR
PY 2012
VL 26
IS 4
BP 700
EP 707
DI 10.1038/leu.2011.272
PG 8
WC Oncology; Hematology
SC Oncology; Hematology
GA 925UX
UT WOS:000302788300016
PM 22005790
ER
PT J
AU Landgren, O
Ma, W
Kyle, RA
Rajkumar, SV
Korde, N
Albitar, M
AF Landgren, O.
Ma, W.
Kyle, R. A.
Rajkumar, S. V.
Korde, N.
Albitar, M.
TI Polymorphism of the erythropoietin gene promotor and the development of
myelodysplastic syndromes subsequent to multiple myeloma
SO LEUKEMIA
LA English
DT Letter
ID ACUTE-LEUKEMIA; MELPHALAN; CHEMOTHERAPY; ASSOCIATION; NEOPLASMS
C1 [Landgren, O.; Korde, N.] NCI, Multiple Myeloma Sect, Med Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Ma, W.; Albitar, M.] Quest Diagnost Nicols Inst, Dept Hematol Oncol, San Juan Capistrano, CA USA.
[Kyle, R. A.; Rajkumar, S. V.] Mayo Clin, Div Hematol, Rochester, MN USA.
RP Landgren, O (reprint author), NCI, Multiple Myeloma Sect, Med Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
EM landgreo@mail.nih.gov
OI Rajkumar, S. Vincent/0000-0002-5862-1833
NR 9
TC 7
Z9 7
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0887-6924
J9 LEUKEMIA
JI Leukemia
PD APR
PY 2012
VL 26
IS 4
BP 844
EP 845
DI 10.1038/leu.2011.262
PG 3
WC Oncology; Hematology
SC Oncology; Hematology
GA 925UX
UT WOS:000302788300037
PM 21926963
ER
PT J
AU Kapetanovic, IM
AF Kapetanovic, Izet M.
TI Comment on Resveratrol in human cancer chemoprevention- choosing the
right' dose'
SO MOLECULAR NUTRITION & FOOD RESEARCH
LA English
DT Letter
C1 NCI, NIH, Canc Prevent Div, Chemoprevent Agent Dev Res Grp, Bethesda, MD 20892 USA.
RP Kapetanovic, IM (reprint author), NCI, NIH, Canc Prevent Div, Chemoprevent Agent Dev Res Grp, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1613-4125
J9 MOL NUTR FOOD RES
JI Mol. Nutr. Food Res.
PD APR
PY 2012
VL 56
IS 4
BP 523
EP 523
DI 10.1002/mnfr.2012700024
PG 1
WC Food Science & Technology
SC Food Science & Technology
GA 924WH
UT WOS:000302721500001
PM 22495980
ER
PT J
AU Waubant, E
Pelletier, D
Mass, M
Cohen, JA
Kita, M
Cross, A
Bar-Or, A
Vollmer, T
Racke, M
Stuve, O
Schwid, S
Goodman, A
Kachuck, N
Preiningerova, J
Weinstock-Guttman, B
Calabresi, PA
Miller, A
Mokhtarani, M
Ikle, D
Murphy, S
Kopetskie, H
Ding, L
Rosenberg, E
Spencer, C
Zamvil, SS
AF Waubant, E.
Pelletier, D.
Mass, M.
Cohen, J. A.
Kita, M.
Cross, A.
Bar-Or, A.
Vollmer, T.
Racke, M.
Stueve, O.
Schwid, S.
Goodman, A.
Kachuck, N.
Preiningerova, J.
Weinstock-Guttman, B.
Calabresi, P. A.
Miller, A.
Mokhtarani, M.
Ikle, D.
Murphy, S.
Kopetskie, H.
Ding, L.
Rosenberg, E.
Spencer, C.
Zamvil, S. S.
CA ITN STAyCIS Study Grp
TI Randomized controlled trial of atorvastatin in clinically isolated
syndrome The STAyCIS study
SO NEUROLOGY
LA English
DT Article
ID REMITTING MULTIPLE-SCLEROSIS; INTRAMUSCULAR INTERFERON BETA-1A;
SIMVASTATIN TREATMENT; STATINS; THERAPY; CELLS; AUTOIMMUNITY;
COMBINATION; PARALYSIS; DISEASE
AB Objective: To test efficacy and safety of atorvastatin in subjects with clinically isolated syndrome (CIS).
Methods: Subjects with CIS were enrolled in a phase II, double-blind, placebo-controlled, 14-center randomized trial testing 80 mg atorvastatin on clinical and brain MRI activity. Brain MRIs were performed quarterly. The primary endpoint (PEP) was development of >= 3new T2 lesions, or one clinical relapse within 12months. Subjects meeting the PEP were offered additional weekly interferon beta-1a (IFN beta-1a).
Results: Due to slow recruitment, enrollment was discontinued after 81 of 152 planned subjects with CIS were randomized and initiated study drug. Median (interquartile range) numbers of T2 and gadolinium-enhancing (Gd) lesions were 15.0(22.0) and 0.0 (0.0) at baseline. A total of 53.1% of atorvastatin recipients (n = 26/49) met PEP compared to 56.3% of placebo recipients (n = 18/ 32) (p = 0.82). Eleven atorvastatin subjects (22.4%) and 7 placebo subjects (21.9%) met the PEP by clinical criteria. Proportion of subjects who did not develop new T2 lesions up to month 12 or to starting IFN beta-1a was 55.3% in the atorvastatin and 27.6% in the placebo group (p = 0.03). Likelihood of remaining free of new T2 lesions was significantly greater in the atorvastatin group compared with placebo (odds ratio [OR] = 4.34, p = 0.01). Likelihood of remaining free of Gd lesions tended to be higher in the atorvastatin group (OR = 2.72, p = 0.11). Overall, atorvastatin was well tolerated. No clear antagonistic effect of atorvastatin plus IFN beta-1a was observed on MRI measures.
Conclusion: Atorvastatin treatment significantly decreased development of new brain MRI T2 lesion activity, although it did not achieve the composite clinical and imaging PEP.
Classification of Evidence: This study provided Class II evidence that atorvastatin did not reduce the proportion of patients with CIS meeting imaging and clinical criteria for starting immunomodulating therapy after 12 months, compared to placebo. In an analysis of a secondary endpoint (Class III), atorvastatin was associated with a reduced risk for developing new T2 lesions. Neurology (R) 2012;78:1171-1178
C1 [Waubant, E.; Pelletier, D.; Spencer, C.; Zamvil, S. S.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Mass, M.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Cohen, J. A.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Kita, M.] Virginia Mason MS Ctr, Seattle, WA USA.
[Cross, A.] Washington Univ, MS Ctr, St Louis, MO USA.
[Bar-Or, A.] McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada.
[Vollmer, T.] Barrow Neurol Inst, Phoenix, AZ 85013 USA.
[Racke, M.; Stueve, O.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Schwid, S.; Goodman, A.] Univ Rochester, Rochester, NY USA.
[Kachuck, N.] Univ So Calif, Keck Sch Med, MS Ctr, Los Angeles, CA 90033 USA.
[Preiningerova, J.] Yale MS Res Ctr, New Haven, CT USA.
[Weinstock-Guttman, B.] Jacobs Neurol Inst, Buffalo, NY USA.
[Calabresi, P. A.] Johns Hopkins Univ, Baltimore, MD USA.
[Miller, A.] Mt Sinai Sch Med, New York, NY USA.
[Mokhtarani, M.] Immune Tolerance Network, Seattle, WA USA.
[Ikle, D.; Murphy, S.; Kopetskie, H.] Rho Inc, Chapel Hill, NC USA.
[Ding, L.; Rosenberg, E.] NIAID, Bethesda, MD 20892 USA.
RP Zamvil, SS (reprint author), Univ Calif San Francisco, San Francisco, CA 94143 USA.
EM zamvil@ucsf.neuroimmunol.org
FU Immune Tolerance Network [ITN020AI, N01-AI-15416]; National Institute of
Allergy and Infectious Diseases; Nancy Davis Foundation; National
Institutes of Health [RO1 AI059709]; Maisin Foundation
FX This research was performed as a project of the Immune Tolerance Network
(ITN020AI, ITN contract number N01-AI-15416), a clinical research
consortium sponsored by the National Institute of Allergy and Infectious
Diseases. Pfizer provided atorvastatin, placebo, and grant support.
Biogen Idec provided IFN beta-1a IM and grant support. E.W. is also
supported by the Nancy Davis Foundation. S.S.Z. was also supported for
this study by the National Institutes of Health (RO1 AI059709) and the
Maisin Foundation.
NR 23
TC 23
Z9 23
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD APR
PY 2012
VL 78
IS 15
BP 1171
EP 1178
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 925WH
UT WOS:000302792200014
PM 22459680
ER
PT J
AU Carlo, WA
McDonald, SA
Fanaroff, AA
Vohr, BR
Stoll, BJ
Ehrenkranz, RA
Andrews, WW
Wallace, D
Das, A
Bell, EF
Walsh, MC
Laptook, AR
Shankaran, S
Poindexter, BB
Hale, EC
Newman, NS
Davis, AS
Schibler, K
Kennedy, KA
Sanchez, PJ
Van Meurs, KP
Goldberg, RN
Watterberg, KL
Faix, RG
Frantz, ID
Higgins, RD
AF Carlo, Waldemar A.
McDonald, Scott A.
Fanaroff, Avroy A.
Vohr, Betty R.
Stoll, Barbara J.
Ehrenkranz, Richard A.
Andrews, William W.
Wallace, Dennis
Das, Abhik
Bell, Edward F.
Walsh, Michele C.
Laptook, Abbot R.
Shankaran, Seetha
Poindexter, Brenda B.
Hale, Ellen C.
Newman, Nancy S.
Davis, Alexis S.
Schibler, Kurt
Kennedy, Kathleen A.
Sanchez, Pablo J.
Van Meurs, Krisa P.
Goldberg, Ronald N.
Watterberg, Kristi L.
Faix, Roger G.
Frantz, Ivan D., III
Higgins, Rosemary D.
CA Eunice Kennedy Shriver Natl Inst
TI Association of Antenatal Corticosteroids With Mortality and
Neurodevelopmental Outcomes Among Infants Born at 22 to 25 Weeks'
Gestation EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
AB The benefits of antenatal corticosteroids in mothers with preterm labor from 24 to 34 weeks' gestational age are well established. Because of ethical issues related to periviability and the limited availability of data on the effectiveness of antenatal corticosteroids in infants born before 24 weeks' gestation, antenatal corticosteroids are not recommended for these premature infants. However, suggestions have been made that antenatal use of these agents should be considered before 24 weeks because such infants are at high risk of severe neurodevelopmental impairment, and many are receiving intensive care.
This cohort study investigated whether the use of antenatal corticosteroids in mothers of infants born at 22 and 23 weeks of gestation was associated with improvement in major outcomes. Data were obtained prospectively from 10,541 infants with a birth weight between 401 and 1000 g (n = 10,541) born at 22 to 25 weeks' gestation between 1993 and 2009, at 23 academic perinatal centers. A total of 4924 (86.5%) of these infants who survived to 18 to 22 months had follow-up examinations performed by certified examiners unaware of exposure to antenatal corticosteroids. Logistic regression analysis was used to assess the relationship between antenatal exposure to corticosteroids or no exposure and outcomes, adjusting for maternal and neonatal confounding variables. The main study outcome measure was death or neurodevelopmental impairment at an 18- to 22-month follow-up.
Death or neurodevelopmental impairment occurred significantly less frequently among infants who had been exposed to antenatal corticosteroids and were born at 23 weeks' gestation (exposure: 83.4% vs. no exposure: 90.5%; adjusted odds ratio [aOR], 0.58 [95% confidence interval{CI}, 0.42-0.80]), at 24 weeks' gestation (exposure: 68.4% vs. no exposure: 80.3%; aOR, 0.62 [95% CI, 0.49-0.78]), and at 25 weeks' gestation (exposure: 52.7% vs. no exposure: 67.9%; aOR, 0.61 [95% CI, 0.50-0.74]). There was no difference in outcomes for infants born at 22 weeks' gestation (90.2% with exposure vs. 93.1% without exposure; aOR, 0.80 [95% CI, 0.29-2.21]). Events occurring significantly less among infants who were born at 23, 24, and 25 weeks' gestation and exposed to antenatal corticosteroids were the following: death by 18 to 22 months, hospital death, the composite of death, intraventricular hemorrhage or periventricular leukomalacia, and the composite of death or necrotizing enterocolitis. The only outcome that occurred significantly less among infants born at 22 weeks' gestation was the composite of death or necrotizing enterocolitis (exposure: 73.5% vs. no exposure: 84.5%; the aOR was 0.54, with a 95% CI of 0.30 to 0.97.
These findings show that antenatal exposure of infants born at 23 to 25 weeks' gestation to corticosteroids was associated with a lower rate of death or neurodevelopmental impairment at 18 to 22 months compared with nonexposure.
C1 [Carlo, Waldemar A.] Univ Alabama, Dept Pediat, Birmingham, AL USA.
Childrens Hosp Alabama, Birmingham, AL USA.
RTI Int, Stat & Epidemiol Unit, Res Triangle Pk, NC USA.
Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Dept Pediat, Cleveland, OH 44106 USA.
Brown Univ, Women & Infants Hosp, Dept Pediat, Providence, RI 02908 USA.
Emory Univ, Sch Med, Dept Pediat, Atlanta, GA USA.
Childrens Hlth Care Atlanta, Atlanta, GA USA.
Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06510 USA.
RTI Int, Stat & Epidemiol Unit, Rockville, MD USA.
Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
Indiana Univ Sch Med, Dept Pediat, Indianapolis, IN USA.
Stanford Univ, Sch Med, Dept Pediat, Div Neonatal & Dev Med, Palo Alto, CA 94304 USA.
Lucile Packard Childrens Hosp, Palo Alto, CA USA.
Univ Cincinnati, Dept Pediat, Cincinnati, OH 45221 USA.
Univ Texas Med Sch, Dept Pediat, Houston, TX USA.
Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
Duke Univ, Dept Pediat, Durham, NC 27706 USA.
Univ New Mexico, Dept Pediat, Hlth Sci Ctr, Albuquerque, NM 87131 USA.
Univ Utah, Sch Med, Dept Pediat, Div Neonatol, Salt Lake City, UT USA.
Floating Hosp Children, Tufts Med Ctr, Dept Pediat, Div Newborn Med, Boston, MA USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Carlo, WA (reprint author), Univ Alabama, Dept Pediat, Birmingham, AL USA.
NR 2
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7828
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD APR
PY 2012
VL 67
IS 4
BP 215
EP 217
DI 10.1097/OGX.0b013e31825021ef
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 925WO
UT WOS:000302793000005
ER
PT J
AU Bukowski, R
Carpenter, M
Conway, D
Coustan, D
Dudley, DJ
Goldenberg, RL
Hogue, CJR
Koch, MA
Parker, CB
Pinar, H
Reddy, UM
Saade, GR
Silver, RM
Stoll, BJ
Varner, MW
Willinger, M
AF Bukowski, Radek
Carpenter, Marshall
Conway, Deborah
Coustan, Donald
Dudley, Donald J.
Goldenberg, Robert L.
Hogue, Carol J. Rowland
Koch, Matthew A.
Parker, Corette B.
Pinar, Halit
Reddy, Uma M.
Saade, George R.
Silver, Robert M.
Stoll, Barbara J.
Varner, Michael W.
Willinger, Marian
CA Stillbirth Collaborative Res
TI Causes of Death Among Stillbirths EDITORIAL COMMENT
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
AB The stillbirth rate in the United States is higher than that of other developed countries. Since 2003, the rate has stagnated at 6.2 stillbirths per 1000 births.
There is a lack of information on causes of stillbirth. Strategies to reduce the stillbirth rate will require systematic investigation into the cause of death. The stillbirth rate among non-Hispanic black women is 2.3-fold higher than that of non-Hispanic white women. This racial disparity is largely unexplained.
This multicenter population-based case-control study determined the causes of death among stillbirths and stratified the causes according to race/ethnicity. All stillbirths that occurred at 20 weeks or later between 2006 and 2008 were examined in data from 59 tertiary care and community hospitals that had access to at least 90% of the stillbirth and live birth deliveries in 5 catchment areas defined by state and county boundaries. Data on deliveries resulting from termination of a live fetus were excluded. Several outcome measures were evaluated to systematically assign causes of death. Standardized perinatal postmortem examination and placental pathology evaluation were performed at delivery. Other outcome measures included medical history, karyotype, and other laboratory tests.
Of the 663 women with stillbirth enrolled, 500 (75.4%) allowed a complete postmortem examination of their 512 stillborn neonates. Among the stillbirths, a probable cause of death was found for 312 cases (60.9%; 95% confidence interval [CI], 56.5%-65.2%) and possible or probable cause for 390 (76.2%; 95% CI, 72.2%-79.8%). The most common causes of death were the following: obstetric complications (29.3%; 95% CI, 25.4%-33.5%), placental abnormalities (23.6%; 95% CI, 20.1%-27.6%), fetal genetic/structural abnormalities (13.7%; 95% CI, 10.9%-17.0%), infection (12.9%; 95% CI, 10.2%-16.2%), umbilical cord abnormalities (10.4%; 95% CI, 7.9%-13.4%), hypertensive disorders (9.2%; 95% CI, 6.9%-12.1%), and other maternal medical complications (7.8%; 95% CI, 5.7%-10.6%). Compared with non-Hispanic white women and all Hispanics, non-Hispanic black women had a higher proportion of stillbirths associated with obstetric complications (43.5% vs. 23.7%; difference: 19.8%; 95% CI, 9.7%-29.9%; P < 0.001) and infections (25.2% vs. 7.8%; difference: 17.4%; 95% CI, 9.0%-25.8%; P < 0.001). Intrapartum and early in gestation stillbirths were more common among non-Hispanic black women. The most likely sources contributing to identifying a probable or possible cause of death were placental histology (52.3%; 95% CI, 47.9%-56.7%), perinatal postmortem examination (31.4%; 95% CI, 27.5%-35.7%), and karyotype (9%; 95% CI, 6.3%-12.5%).
These findings show that a systematic and thorough evaluation of a population-based cohort led to a probable or possible cause of death for the majority of cases of stillbirth. Causes were differentially distributed by race/ethnicity.
C1 [Bukowski, Radek] Univ Texas Med Branch, Dept Obstet & Gynecol, Galveston, TX 77555 USA.
Brown Univ, Sch Med, Div Maternal Fetal Med, Dept Obstet & Gynecol, Providence, RI 02912 USA.
Univ Texas Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, Div Maternal Fetal Med, San Antonio, TX 78229 USA.
Drexel Univ, Sch Med, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA.
Emory Univ, Womens & Childrens Ctr, Atlanta, GA 30322 USA.
RTI Int, Stat & Epidemiol Unit, Div Hlth Sci, Res Triangle Pk, NC USA.
Brown Univ, Sch Med, Dept Pathol & Lab Med, Div Perinatal & Pediat Pathol, Providence, RI 02912 USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, NIH, Bethesda, MD USA.
Univ Utah, Sch Med, Dept Obstet & Gynecol, Div Maternal Fetal Med, Salt Lake City, UT 84132 USA.
Intermt Healthcare, Maternal Fetal Med, Salt Lake City, UT USA.
Emory Univ, Sch Med, Atlanta, GA 30322 USA.
Childrens Healthcare Atlanta, Dept Pediat, Atlanta, GA USA.
RP Bukowski, R (reprint author), Univ Texas Med Branch, Dept Obstet & Gynecol, Galveston, TX 77555 USA.
RI Hogue, Carol/H-5442-2012
NR 5
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7828
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD APR
PY 2012
VL 67
IS 4
BP 223
EP 225
DI 10.1097/OGX.0b013e3182502211
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 925WO
UT WOS:000302793000009
ER
PT J
AU Lu, C
Zhu, X
Willingham, MC
Cheng, SY
AF Lu, C.
Zhu, X.
Willingham, M. C.
Cheng, S-Y
TI Activation of tumor cell proliferation by thyroid hormone in a mouse
model of follicular thyroid carcinoma
SO ONCOGENE
LA English
DT Article
DE thyroid hormone; follicular thyroid carcinoma; animal model; protein
kinase B/AKT; PTEN
ID BETA-CATENIN; PHOSPHATIDYLINOSITOL 3-KINASE; GENETIC ALTERATIONS;
RECEPTOR-BETA; TRANSCRIPTIONAL ACTIVITY; METASTATIC SPREAD; TRANSFORMING
GENE; PROTEIN-KINASE; GROWTH-FACTOR; CANCER
AB Thyroid cancers are the most common malignancy of the endocrine system in humans. To understand the molecular genetic events underlying thyroid carcinogenesis, we have generated a mouse model that spontaneously develops follicular thyroid carcinoma similar to human thyroid cancer (Thrb(PV/PV) mouse). This mutant mouse harbors a dominant-negative mutated thyroid hormone receptor beta (denoted PV). The PV mutation was identified in a patient with resistance to thyroid hormone (TH). Thrb(PV/PV) mice exhibit highly elevated serum thyroid-stimulating hormone levels and increased TH. We have previously shown that thyroid-stimulating hormone is required, but not sufficient to induce metastatic follicular thyroid cancer in Thrb(PV/PV) mice. However, whether the elevated TH also contributes to the thyroid carcinogenesis of Thrb(PV/PV) mice was not elucidated. To understand the role of TH in thyroid carcinogenesis, we blocked the production of TH by treating Thrb(PV/PV) mice with propylthiouracil (Thrb(PV/PV)-PTU mice) and compared the development of thyroid cancer in Thrb(PV/PV)-PTU and untreated ThrbPV/PV mice. We found that thyroid tumor growth was reduced by similar to 42% in Thrb(PV/PV)-PTU mice as compared with Thrb(PV/PV) mice. Analysis by bromodeoxyuridine-nuclear labeling showed decreased incorporation of bromodeoxyuridine in thyroid tumor cells of Thrb(PV/PV)-PTU mice, indicative of decreased tumor cell proliferation. However, cleaved-caspase 3 staining showed no apparent changes in apoptosis of tumor cells in Thrb(PV/PV)-PTU mice. Molecular studies identified a marked attenuation of the PI3K-AKT-beta-catenin signaling pathway that led to decreased protein levels of cyclin D2, thereby decreasing tumor cell proliferation in Thrb(PV/PV)-PTU mice. Furthermore, matrix metalloproteinase-2, a downstream target of beta-catenin and a key regulator during tumor invasion and metastasis, was also decreased. Thus, the present study uncovers a critical role of TH in promoting the thyroid carcinogenesis of Thrb(PV/PV) mice via membrane signaling events. Importantly, these findings suggest that anti-thyroid drugs could be considered as possible therapeutic agents of thyroid cancer. Oncogene (2012) 31, 2007-2016; doi: 10.1038/onc.2011.390; published online 12 September 2011
C1 [Lu, C.; Zhu, X.; Cheng, S-Y] NCI, Mol Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Willingham, M. C.] Wake Forest Univ, Dept Pathol, Winston Salem, NC 27109 USA.
RP Cheng, SY (reprint author), NCI, Mol Biol Lab, Ctr Canc Res, 37 Convent Dr,Room 5128, Bethesda, MD 20892 USA.
EM chengs@mail.nih.gov
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX This research was supported by the Intramural Research Program of
National Institutes of Health, National Cancer Institute, Center for
Cancer Research.
NR 50
TC 6
Z9 7
U1 2
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD APR
PY 2012
VL 31
IS 16
BP 2007
EP 2016
DI 10.1038/onc.2011.390
PG 10
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 928TP
UT WOS:000303008600002
PM 21909131
ER
PT J
AU Chu, IM
Michalowski, AM
Hoenerhoff, M
Szauter, KM
Luger, D
Sato, M
Flanders, K
Oshima, A
Csiszar, K
Green, JE
AF Chu, I. M.
Michalowski, A. M.
Hoenerhoff, M.
Szauter, K. M.
Luger, D.
Sato, M.
Flanders, K.
Oshima, A.
Csiszar, K.
Green, J. E.
TI GATA3 inhibits lysyl oxidase-mediated metastases of human basal
triple-negative breast cancer cells
SO ONCOGENE
LA English
DT Article
DE GATA3; basal triple-negative breast cancer; lysyl oxidase;
differentiation; gene expression profiling
ID GENE-EXPRESSION; MESENCHYMAL TRANSITION; ENZYME-ACTIVITY; MAMMARY-GLAND;
DIFFERENTIATION; GROWTH; MORPHOGENESIS; PROPEPTIDE; MIGRATION; SUBTYPES
AB Discovery of mechanisms that impede the aggressive and metastatic phenotype of human basal triple-negative-type breast cancers (BTNBCs) could provide novel targets for therapy for this form of breast cancer that has a relatively poor prognosis. Previous studies have demonstrated that expression of GATA3, the master transcriptional regulator of mammary luminal differentiation, can reduce the tumorigenicity and metastatic propensity of the human BTNBC MDA-MB-231 cell line (MB231), although the mechanism for reduced metastases was not elucidated. We demonstrate through gene expression profiling that GATA3 expression in 231 cells resulted in the dramatic reduction in the expression of lysyl oxidase (LOX), a metastasis-promoting, matrix-remodeling protein, in part, through methylation of the LOX promoter. Suppression of LOX expression by GATA3 was further confirmed in the BTNBC Hs578T cell line. Conversely, reduction of GATA3 expression by small interfering RNA in luminal BT474 cells increased LOX expression. Reconstitution of LOX expression in 231-GATA3 cells restored metastatic propensity. A strong inverse association between LOX and GATA3 expression was confirmed in a panel of 51 human breast cancer cell lines. Similarly, human breast cancer microarray data demonstrated that high LOX/low GATA3 expression is associated with the BTNBC subtype of breast cancer and poor patient prognosis. Expression of GATA3 reprograms BTNBCs to a less aggressive phenotype and inhibits a major mechanism of metastasis through inhibition of LOX. Induction of GATA3 in BTNBC cells or novel approaches that inhibit LOX expression or activity could be important strategies for treating BTNBCs. Oncogene (2012) 31, 2017-2027; doi: 10.1038/onc.2011.382; published online 5 September 2011
C1 [Green, J. E.] NCI, Transgen Oncogenesis & Genom Sect, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
[Hoenerhoff, M.] NIEHS, Cellular & Mol Pathol Branch, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Szauter, K. M.; Csiszar, K.] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96822 USA.
RP Green, JE (reprint author), NCI, Transgen Oncogenesis & Genom Sect, Lab Canc Biol & Genet, Bldg 37,Room 4054,37 Convent Dr, Bethesda, MD 20892 USA.
EM jegreen@nih.gov
FU Center for Cancer Research, NCI, NIH; Department of Defense
[W81XWH-10-2-0030]
FX We thank Drs Lalage Wakefield and Li Yang for helpful scientific
discussions. We also thank Lara El-Touny, Dalit Barkan, Zi-Yao Liu,
TingHu Qiu, Anthony Vieira, Christina Bennett, Christine Tomlinson,
Steven Austin, Christian Mustroph and Wei-Chu Lai for technical
assistance; Paul Meltzer for sharing unpublished data; the LRBGE
Fluorescence Imaging Core and Chand Khanna for the use of fluorescence
microscopy equipment; and Julie Foley and Norris Flagler for technical
assistance with image analysis. This research was supported in part by
the Intramural Research Program, Center for Cancer Research, NCI, NIH.
IMC acknowledges support from the Department of Defense Breast Cancer
Research Program (W81XWH-10-2-0030).
NR 34
TC 15
Z9 15
U1 3
U2 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD APR
PY 2012
VL 31
IS 16
BP 2017
EP 2027
DI 10.1038/onc.2011.382
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 928TP
UT WOS:000303008600003
PM 21892208
ER
PT J
AU Zhang, YH
Qi, YW
Li, J
Liu, SF
Hong, LX
Lin, TL
Long, C
Su, XZ
AF Zhang, Yanhui
Qi, Yanwei
Li, Jian
Liu, Shengfa
Hong, Lingxian
Lin, Tianlong
Long, Carole
Su, Xin-zhuan
TI A new malaria antigen produces partial protection against Plasmodium
yoelii challenge
SO PARASITOLOGY RESEARCH
LA English
DT Article
ID IMMUNE ADULT MEN; FALCIPARUM MALARIA; VACCINE; PARASITE; INFECTION;
SELECTION; EFFICACY; GAMBIA; GENE
AB Of all the parasitic diseases, malaria is the number one killer. Despite tremendous efforts in disease control and research, nearly a million people, primarily children, still die from the disease each year, partly due to drug resistance and the lack of an effective vaccine. Many parasite antigens have been identified and evaluated for vaccine development; however, none has been approved for human use. Antigenic variation, complex life cycle, and inadequate understanding of the mechanisms of parasite-host interaction and of host immune response all contribute to the lack of an effective vaccine for malaria control. In a recent search of genome-wide polymorphism in Plasmodium falciparum, several molecules were found to be recognized by sera from patients infected with the P. falciparum parasite. Here, we have expressed a 350-amino acid N terminus from one of the homologous candidate antigen genes from the rodent malaria parasite Plasmodium yoelii (Py01157, a putative dentin phosphorin) in bacteria and evaluated the immune response and protection generated after immunization with the recombinant protein. We showed that the recombinant protein was recognized by sera from both mice and humans infected with malaria parasites. Partial protection was observed after challenge with non-lethal P. yoelii 17XNL but not with the lethal P. yoelii 17XL parasite. Further tests using a full-length protein or the conserved C terminus may provide additional information on whether this protein has the potential for being a malaria vaccine.
C1 [Zhang, Yanhui; Long, Carole; Su, Xin-zhuan] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Zhang, Yanhui; Qi, Yanwei; Li, Jian; Liu, Shengfa; Hong, Lingxian] Xiamen Univ, State Key Lab Stress Cell Biol, Xiamen 361005, Fujian, Peoples R China.
[Lin, Tianlong] Fujian Acad Agr Sci, Fuzhou 350003, Fujian, Peoples R China.
RP Su, XZ (reprint author), NIAID, Lab Malaria & Vector Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM xsu@niaid.nih.gov
OI Su, Xinzhuan/0000-0003-3246-3248
FU 973 Program of China [2007CB513103]; Science Planning Program of Fujian
Province [2010J1008]; 111 Project of Education of China [B06016];
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work is supported by grants from the 973 Program 2007CB513103 of
China, the Science Planning Program of Fujian Province (2010J1008), 111
Project of Education of China (no. B06016), and by the Intramural
Research Program of the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health. We thank NIAID intramural editor Brenda Rae Marshall for
assistance.
NR 23
TC 2
Z9 2
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0932-0113
J9 PARASITOL RES
JI Parasitol. Res.
PD APR
PY 2012
VL 110
IS 4
BP 1337
EP 1345
DI 10.1007/s00436-011-2630-y
PG 9
WC Parasitology
SC Parasitology
GA 926EQ
UT WOS:000302814500004
PM 21915626
ER
PT J
AU Simmons, WK
Martin, A
AF Simmons, W. Kyle
Martin, Alex
TI Spontaneous resting-state BOLD fluctuations reveal persistent
domain-specific neural networks
SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
LA English
DT Article
DE social cognition; tools; resting-state functional connectivity;
posterior superior temporal sulcus; middle temporal gyrus
ID ANTERIOR TEMPORAL-LOBES; FUSIFORM FACE AREA; FUNCTIONAL CONNECTIVITY;
MANIPULATABLE OBJECTS; SOCIAL COGNITION; DEFAULT MODE; BIOLOGICAL
MOTION; SEMANTIC MEMORY; BRAIN ACTIVITY; CORTEX
AB Resting-state functional connectivity MRI (rs-fcMRI) analyses have identified intrinsic neural networks supporting domain-general cognitive functions including language, attention, executive control and memory. The brain, however, also has a domain-specific organization, including regions that contribute to perceiving and knowing about others (the 'social' system) or manipulable objects designed to perform specific functions (the 'tool' system). These 'social' and 'tool' systems, however, might not constitute intrinsic neural networks per se, but rather only come online as needed to support retrieval of domain-specific information during social- or tool-related cognitive tasks. To address this issue, we functionally localized two regions in lateral temporal cortex activated when subjects perform social- and tool conceptual tasks. We then compared the strength of the correlations with these seed regions during rs-fcMRI. Here, we show that the 'social' and 'tool' neural networks are maintained even when subjects are not engaged in social- and tool-related information processing, and so constitute intrinsic domain-specific neural networks.
C1 [Simmons, W. Kyle] Laureate Inst Brain Res, Tulsa, OK 74136 USA.
[Simmons, W. Kyle; Martin, Alex] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
RP Simmons, WK (reprint author), Laureate Inst Brain Res, 6655 S Yale Ave, Tulsa, OK 74136 USA.
EM wksimmons@laureateinstitute.org
RI martin, alex/B-6176-2009; Simmons, William/K-8925-2015
OI Simmons, William/0000-0002-0399-9003
FU National Institute of Mental Health Division of Intramural Research,
National Institutes of Health
FX This work was supported by the National Institute of Mental Health
Division of Intramural Research, National Institutes of Health.
NR 56
TC 26
Z9 26
U1 0
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1749-5016
J9 SOC COGN AFFECT NEUR
JI Soc. Cogn. Affect. Neurosci.
PD APR
PY 2012
VL 7
IS 4
BP 467
EP 475
DI 10.1093/scan/nsr018
PG 9
WC Neurosciences; Psychology; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 926CF
UT WOS:000302808200011
PM 21586527
ER
PT J
AU Danis, M
Pesce, J
AF Danis, Marion
Pesce, Julianna
TI Prospects for acknowledging and addressing the socioeconomic
determinants of health in the United States: A response to Goldberg
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Editorial Material
DE Health status disparities; Factors, socioeconomic; USA; Health policy,
national; Public opinion; Expert opinions
ID POLICY
C1 [Danis, Marion] NIH, Dept Clin Bioeth, Bethesda, MD 20892 USA.
[Pesce, Julianna] Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA.
RP Danis, M (reprint author), NIH, Dept Clin Bioeth, Bldg 10,Room 1C118,10 Ctr Dr MSC 1156, Bethesda, MD 20892 USA.
EM mdanis@nih.gov; juliannapesce@ucla.edu
NR 14
TC 0
Z9 0
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD APR
PY 2012
VL 74
IS 8
BP 1143
EP 1145
DI 10.1016/j.socscimed.2011.11.041
PG 3
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 928JE
UT WOS:000302978200002
ER
PT J
AU Shindo, S
Sakuma, T
Negishi, M
Squires, J
AF Shindo, Sawako
Sakuma, Tsutomu
Negishi, Masahiko
Squires, James
TI Phosphorylation of serine 212 confers novel activity to human estrogen
receptor alpha
SO STEROIDS
LA English
DT Article
DE Estrogen receptor; Phosphorylation; DNA binding domain; Gene expression;
Nuclear receptor CAR
ID CAR
AB Estrogen receptor alpha (ER alpha) can be phosphorylated at various residues, one of which is serine 212 in the DNA binding domain. The majority of human nuclear receptors conserves, as a motif, this serine residue within their DNA binding domain. Among these nuclear receptors, phosphorylation of the corresponding threonine 38 in the nuclear receptor CAR is essential for determining its activity [9]. Here, we have investigated the role of phosphorylated serine 212 in the regulation of ER alpha activity by comparing it with serine 236, another potential phosphorylation site within the DNA binding domain, and demonstrated that phosphorylation of serine 212 confers upon ER alpha a distinct activity regulating gene expression in Huh-7 cells. In Western blot analysis, wild type ER alpha and mutants ER alpha S212A, ER alpha S212D, ER alpha S236A and ER alpha S236D were equally expressed in the nucleus, thus indicating that phosphorylation does not determine nuclear localization of ER alpha. ER alpha S212D, but not ER alpha S236D, retained its capability of activating an ERE-reporter gene in luciferase assays. Similar results were also obtained for human ER beta: the ER beta S176D mutant retained its trans-activation activity, but the ER beta S200D mutant did not. cDNA microarray and Ingenuity Pathway Analysis, employed on Huh-7 cells ectopically expressing either ER alpha S212A or ER alpha S212D, revealed that phosphorylation of serine 212 enabled ER alpha to regulate a unique set of genes and cellular functions. Published by Elsevier Inc.
C1 [Shindo, Sawako; Sakuma, Tsutomu; Negishi, Masahiko; Squires, James] Natl Inst Environm Hlth Sci, Pharmacogenet Sect, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
RP Negishi, M (reprint author), Natl Inst Environm Hlth Sci, Pharmacogenet Sect, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
EM negishi@niehs.nih.gov
FU National Institute of Environmental Health Sciences [Z01ES1005-01]
FX We thank the laboratory of Dr. Ken Korach at NIEHS for kindly providing
us with human ER alpha and ER beta plasmids as well as for useful
suggestions. We also thank Dr. Kosuke Saito for ANOVA analysis and the
DNA sequencing and cDNA microarray cores of NIEHS for their assistance.
This research was supported by the Intramural Research Program of
National Institute of Environmental Health Sciences, Z01ES1005-01.
NR 12
TC 4
Z9 4
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0039-128X
J9 STEROIDS
JI Steroids
PD APR
PY 2012
VL 77
IS 5
BP 448
EP 453
DI 10.1016/j.steroids.2012.01.001
PG 6
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 929RU
UT WOS:000303084000013
PM 22266331
ER
PT J
AU Valeri, CR
Veech, RL
AF Valeri, C. Robert
Veech, Richard L.
TI The unrecognized effects of the volume and composition of the
resuscitation fluid used during the administration of blood products
SO TRANSFUSION AND APHERESIS SCIENCE
LA English
DT Article
ID KETONE-BODIES; INSULIN; CELLS
AB Background: Recent publications have reported the severe adverse events associated with blood products but have not considered the effect of the volume and composition of the resuscitative fluids infused with the blood products.
Methods: Injury leads to cellular reaction characterized by insulin resistance during which glucose cannot enter muscle and fat cells. In all cells, mitochondrial pyruvate dehydrogenase activity is decreased during insulin deficiency leaving cells deficient in substrates needed to power the Krebs cycle and make ATP.
Results: D-beta-Hydroxybutyrate, a normal ketone body metabolite, enters cells on the monocarboxylate transport mimicking the action of insulin and bypassing the enzymatic block at PDH. Metabolism of ketone bodies increases efficiency of mitochondrial energy production and cellular ATP level.
Conclusion: Infusion of 250 ml of 600 mM Na D-beta-hydroxybutyrate solution, with the same osmotic strength as the hypertonic NaCl solution currently being used, would correct insulin resistance, provide energy substrates for cells to produce ATP, correct the tendency of injured tissue to swell due to decreased energy of ionic gradients and correct acidosis observed in hemorrhage. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Valeri, C. Robert] Naval Blood Res Lab Inc, Plymouth, MA 02360 USA.
[Veech, Richard L.] NIAAA, Lab Metab Control, NIH, Rockville, MD 20852 USA.
RP Valeri, CR (reprint author), Naval Blood Res Lab Inc, 195 Bournehurst Dr, Plymouth, MA 02360 USA.
EM navblood@nbrl.org
FU Defense Research Project Administration, DARPA
FX Support for development of the ketone ester from the Defense Research
Project Administration, DARPA, is gratefully acknowledged.
NR 22
TC 3
Z9 3
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1473-0502
J9 TRANSFUS APHER SCI
JI Transfus. Apher. Sci.
PD APR
PY 2012
VL 46
IS 2
BP 121
EP 123
DI 10.1016/j.transci.2012.01.010
PG 3
WC Hematology
SC Hematology
GA 926JI
UT WOS:000302826800002
ER
PT J
AU Liu, Y
Wilson, SH
AF Liu, Yuan
Wilson, Samuel H.
TI DNA base excision repair: a mechanism of trinucleotide repeat expansion
SO TRENDS IN BIOCHEMICAL SCIENCES
LA English
DT Review
ID CELL NUCLEAR ANTIGEN; FLAP ENDONUCLEASE-1; CAG REPEAT;
SACCHAROMYCES-CEREVISIAE; POLYMERASE-BETA; GENETIC INSTABILITY;
SECONDARY STRUCTURE; HUNTINGTON-DISEASE; ESCHERICHIA-COLI; MOUSE MODEL
AB The expansion of trinucleotide repeat (TNR) sequences in human DNA is considered to be a key factor in the pathogenesis of more than 40 neurodegenerative diseases. TNR expansion occurs during DNA replication and also, as suggested by recent studies, during the repair of DNA lesions produced by oxidative stress. In particular, the oxidized guanine base 8-oxoguanine within sequences containing CAG repeats may induce formation of pro-expansion intermediates through strand slippage during DNA base excision repair (BER). In this article, we describe how oxidized DNA lesions are repaired by BER and discuss the importance of the coordinated activities of the key repair enzymes, such as DNA polymerase beta, flap endonuclease 1 (FEN1) and DNA ligase, in preventing strand slippage and TNR expansion.
C1 [Liu, Yuan] Florida Int Univ, Dept Chem & Biochem, Miami, FL 33199 USA.
[Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Liu, Y (reprint author), Florida Int Univ, Dept Chem & Biochem, 11200 SW 8th St, Miami, FL 33199 USA.
EM yualiu@fiu.edu; wilson5@niehs.nih.gov
FU NIH from the National Institute of Environmental Health Sciences (NIEHS)
[Z01-ES050158, Z01-ES050159]; NIH [ES017476]
FX We thank Bonnie Mesmer for editorial assistance and Dr Lawrence Loeb and
students at the University of Washington for discussions. This work was
supported by NIH Projects Z01-ES050158 and Z01-ES050159 from the
National Institute of Environmental Health Sciences (NIEHS) Intramural
Research Program and NIH grant ES017476 (to Y.L.).
NR 75
TC 41
Z9 42
U1 0
U2 24
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0968-0004
J9 TRENDS BIOCHEM SCI
JI Trends Biochem.Sci.
PD APR
PY 2012
VL 37
IS 4
BP 162
EP 172
DI 10.1016/j.tibs.2011.12.002
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 929TC
UT WOS:000303087600005
PM 22285516
ER
PT J
AU Azzam, KM
Fessler, MB
AF Azzam, Kathleen M.
Fessler, Michael B.
TI Crosstalk between reverse cholesterol transport and innate immunity
SO TRENDS IN ENDOCRINOLOGY AND METABOLISM
LA English
DT Review
ID APOLIPOPROTEIN-A-I; PHOSPHOLIPID-TRANSFER PROTEIN;
LIPOPOLYSACCHARIDE-BINDING PROTEIN; TOLL-LIKE RECEPTORS;
NECROSIS-FACTOR-ALPHA; LIVER-X-RECEPTORS; LIPID RAFTS; INFLAMMATORY
RESPONSE; SIGNALING PATHWAYS; MIMETIC PEPTIDE
AB Although lipid metabolism and host defense are widely considered to be very divergent disciplines, compelling evidence suggests that host cell handling of self- and microbe-derived (e.g. lipopolysaccharide, LPS) lipids may have common evolutionary roots, and that they indeed may be inseparable processes. The innate immune response and the homeostatic network controlling cellular sterol levels are now known to regulate each other reciprocally, with important implications for several common diseases, including atherosclerosis. In the present review we discuss recent discoveries that provide new insight into the bidirectional crosstalk between reverse cholesterol transport and innate immunity, and highlight the broader implications of these findings for the development of therapeutics.
C1 [Azzam, Kathleen M.; Fessler, Michael B.] NIEHS, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA.
RP Fessler, MB (reprint author), NIEHS, Lab Resp Biol, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM fesslerm@niehs.nih.gov
FU National Institutes of Health, National Institute of Environmental
Health Sciences [Z01 ES102005]
FX The authors thank Sue Edelstein for figure design. This work was
supported in part by the Intramural Research Program of the National
Institutes of Health, National Institute of Environmental Health
Sciences (Z01 ES102005).
NR 100
TC 25
Z9 25
U1 0
U2 8
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1043-2760
J9 TRENDS ENDOCRIN MET
JI Trends Endocrinol. Metab.
PD APR
PY 2012
VL 23
IS 4
BP 169
EP 178
DI 10.1016/j.tem.2012.02.001
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 927EW
UT WOS:000302890900003
PM 22406271
ER
PT J
AU Sorlie, PD
Bild, DE
Lauer, MS
AF Sorlie, Paul D.
Bild, Diane E.
Lauer, Michael S.
TI Cardiovascular Epidemiology in a Changing World-Challenges to
Investigators and the National Heart, Lung, and Blood Institute
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Editorial Material
DE cardiovascular diseases; epidemiology; National Institutes of Health
(US); research
ID ACUTE MYOCARDIAL-INFARCTION; ELECTRONIC HEALTH RECORDS; RISK PREDICTION;
UNITED-STATES; POPULATION; IMPROVEMENTS; PREVENTION; WORKSHOP; GENOMICS;
PROTEIN
AB Over the past 60 years, revolutionary discoveries made by epidemiologists have contributed to marked declines in cardiovascular disease morbidity and mortality. Now, in an era of increasingly constrained resources, researchers in cardiovascular epidemiology face a number of challenges that call for novel, paradigm-shifting approaches. In this paper, the authors pose to the community 4 critical questions: 1) How can we avoid wasting resources on studies that provide little incremental knowledge? 2) How can we assure that we direct our resources as economically as possible towards innovative science? 3) How can we be nimble, responding quickly to new opportunities? 4) How can we identify prospectively the most meritorious research questions? Senior program staff at the National Heart, Lung, and Blood Institute invite the epidemiology community to join them in an ongoing Web-based blog conversation so that together we might develop novel approaches that will facilitate the next generation of high-impact discoveries.
C1 [Sorlie, Paul D.; Lauer, Michael S.] NHLBI, Div Cardiovasc Sci, Epidemiol Branch, Bethesda, MD 20892 USA.
[Bild, Diane E.] NHLBI, Program Prevent & Populat Sci, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
RP Lauer, MS (reprint author), NHLBI, Div Cardiovasc Sci, Epidemiol Branch, 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 33
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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 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD APR 1
PY 2012
VL 175
IS 7
BP 597
EP 601
DI 10.1093/aje/kws138
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 921NE
UT WOS:000302483500001
PM 22415032
ER
PT J
AU Weinberg, CR
AF Weinberg, Clarice R.
TI Interaction and Exposure Modification: Are We Asking the Right
Questions?
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Editorial Material
DE attributable risk; effect modification; interaction; synergy
ID GENE VARIANTS; RISK; CANCER
AB Most diseases arise not purely through genetic abnormalities nor purely through environmental causes, but as "complex" conditions brought about by the combined effects of genetic susceptibility factors, nongenetic experiences and exposures, and bad luck. Finding simple models capable of both characterizing such joint effects and providing new insight into pathogenesis remains an ongoing challenge in etiologic epidemiology. Additive null models can capture certain pure forms of independent etiologic effects in studies of rare conditions and can be useful for predicting possible effects of interventions. The concept of exposure modification is here proposed as useful, particularly in thinking about biologic interactions between exposures and genetic variants. Openness to parsimonious joint models and the insights they can provide is key to advancing our understanding of etiology.
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
RP Weinberg, CR (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA.
EM weinber2@niehs.nih.gov
FU Intramural NIH HHS; NIEHS NIH HHS [ZO1 ES040007., Z01 ES040007]
NR 13
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Z9 9
U1 2
U2 7
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 APR 1
PY 2012
VL 175
IS 7
BP 602
EP 605
DI 10.1093/aje/kwr495
PG 4
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 921NE
UT WOS:000302483500002
PM 22306562
ER
PT J
AU Pollack, AZ
Schisterman, EF
Goldman, LR
Mumford, SL
Perkins, NJ
Bloom, MS
Rudra, CB
Browne, RW
Wactawski-Wende, J
AF Pollack, Anna Z.
Schisterman, Enrique F.
Goldman, Lynn R.
Mumford, Sunni L.
Perkins, Neil J.
Bloom, Michael S.
Rudra, Carole B.
Browne, Richard W.
Wactawski-Wende, Jean
TI Relation of Blood Cadmium, Lead, and Mercury Levels to Biomarkers of
Lipid Peroxidation in Premenopausal Women
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE cadmium; hydroxyl-octadecadienoic acid; isoprostane; lead; mercury;
oxidative stress; thiobarbituric acid reactive substances; women
ID OXIDATIVE STRESS; MENSTRUAL-CYCLE; FATTY-ACIDS; REPRODUCTIVE HORMONES;
BIOLOGICAL VARIATION; NATIONAL-HEALTH; OXIDANT STRESS; UNITED-STATES;
F-2-ISOPROSTANES; PRODUCTS
AB Exposures to cadmium, lead, and mercury are associated with adverse health effects, including cardiovascular disease, which may be promoted by lipid peroxidation. The authors examined cadmium, lead, and mercury in relation to plasma levels of F-2-8 alpha isoprostanes (isoprostane), 9-hydroperoxy-10,12-octadecadienoic acid (9-HODE), 13-hydroxy-9,11-octadecadienoic acid (13-HODE), and thiobarbituric acid reactive substances (TBARS) in 252 women from western New York State (2005-2007). Healthy premenopausal women were followed for <2 menstrual cycles, with biomarkers of lipid peroxidation being assessed <= 8 times per cycle. Metals were measured at baseline in whole blood. Linear mixed models were used to estimate the association between cadmium, lead, and mercury and lipid peroxidation biomarkers. Median cadmium, lead, and mercury levels were 0.30 mu g/L, 0.86 mu g/dL, and 1.10 mu g/L, respectively. Blood cadmium, lead, and mercury were not associated with increases in isoprostane, TBARS, 9-HODE, or 13-HODE levels. Isoprostane levels decreased 6.80% (95% confidence interval: -10.40, -3.20) per 1% increase in mercury. However, after adjustment for a simulated strong confounding factor, such as precisely measured fish consumption, the observed association was attenuated, suggesting that this unexpected association could be attributable to unmeasured confounding. In this population of healthy premenopausal women with low exposure levels, cadmium, lead, and mercury were not associated with elevated lipid peroxidation biomarkers.
C1 [Pollack, Anna Z.; Schisterman, Enrique F.; Mumford, Sunni L.; Perkins, Neil J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Rockville, MD 20852 USA.
[Pollack, Anna Z.; Goldman, Lynn R.] Johns Hopkins Univ Hosp, Dept Epidemiol, Bloomberg Sch Publ Hlth, Baltimore, MD 21287 USA.
[Bloom, Michael S.] SUNY Albany, Sch Publ Hlth, Dept Environm Hlth Sci, Rensselaer, NY USA.
[Rudra, Carole B.; Browne, Richard W.; Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
RP Schisterman, EF (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, 6100 Execut Blvd,Room 7B03, Rockville, MD 20852 USA.
EM schistee@mail.nih.gov
RI Goldman, Lynn/D-5372-2012;
OI Perkins, Neil/0000-0002-6802-4733; Pollack, Anna/0000-0002-4313-3298;
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 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 52
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U1 0
U2 7
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 APR 1
PY 2012
VL 175
IS 7
BP 645
EP 652
DI 10.1093/aje/kwr375
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 921NE
UT WOS:000302483500009
PM 22302120
ER
PT J
AU Denadai, R
Raposo-Amaral, CE
Bertola, D
Kim, C
Alonso, N
Hart, T
Han, S
Stelini, RF
Buzzo, CL
Raposo-Amaral, CA
Hart, PS
AF Denadai, Rafael
Raposo-Amaral, Cassio E.
Bertola, Debora
Kim, Chong
Alonso, Nivaldo
Hart, Thomas
Han, Sangwoo
Stelini, Rafael F.
Buzzo, Celso L.
Raposo-Amaral, Cesar A.
Hart, P. Suzanne
TI Identification of 2 Novel ANTXR2 Mutations in Patients With Hyaline
Fibromatosis Syndrome and Proposal of a Modified Grading System
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE anthrax toxin receptor 2 protein; capillary morphogenesis protein-2;
hyaline fibromatosis syndrome; infantile systemic hyalinosis; juvenile
hyaline fibromatosis
ID OF-THE-LITERATURE; CAPILLARY MORPHOGENESIS PROTEIN-2; FOLLOW-UP;
JUVENILE; GENE; INFANT
AB Juvenile hyaline fibromatosis (JHF) and infantile systemic hyalinosis (ISH) are rare, autosomal recessive disorders of the connective tissue caused by mutations in the gene encoding the anthrax toxin receptor 2 protein (ANTXR2) located on chromosome 4q21. Characteristically, these conditions present with overlapping clinical features, such as nodules and/or pearly papules, gingival hyperplasia, flexion contractures of the joints, and osteolytic bone defects. The present report describes a pair of sibs and three other JHF/ISH patients whose diagnoses were based on typical clinical manifestations and confirmed by histopathologic analyses and/or molecular analysis. A comparison of ISH and JHF, additional thoughts about new terminology (hyaline fibromatosis syndrome) and a modified grading system are also included. (C) 2012 Wiley Periodicals, Inc.
C1 [Raposo-Amaral, Cassio E.; Buzzo, Celso L.; Raposo-Amaral, Cesar A.] Brazilian Soc Res & Assistance Craniofacial Rehab, Inst Plast & Craniofacial Surg, BR-13094776 Campinas, SP, Brazil.
[Denadai, Rafael] Marilia Univ, Sch Med Sci, Marilia, SP, Brazil.
[Bertola, Debora; Kim, Chong] Univ Sao Paulo, Fac Med, Dept Pediat, Genet Unit,Inst Crianca,Hosp Clin, Sao Paulo, Brazil.
[Alonso, Nivaldo] Univ Sao Paulo, Fac Med, Dept Surg, Div Plast Surg, Sao Paulo, Brazil.
[Hart, Thomas] NIDCR, Human Craniofacial Genet Sect, NIH, Bethesda, MD USA.
[Han, Sangwoo] NIDR, NIH, Bethesda, MD 20892 USA.
[Stelini, Rafael F.] State Univ Campinas UNICAMP, Sch Med Sci, Dept Anat Pathol, Campinas, SP, Brazil.
[Hart, P. Suzanne] NHGRI, Off Clin Director, NIH, Bethesda, MD 20892 USA.
RP Raposo-Amaral, CE (reprint author), Brazilian Soc Res & Assistance Craniofacial Rehab, Inst Plast & Craniofacial Surg, Av Adolpho Lutz 100, BR-13094776 Campinas, SP, Brazil.
EM cassioraposo@hotmail.com
RI Denadai, Rafael/A-8038-2013; Raposo Amaral, Cassio Eduardo/D-1397-2013
OI Denadai, Rafael/0000-0003-0525-3480; Raposo Amaral, Cassio
Eduardo/0000-0001-6201-0827
FU Intramural NIH HHS [Z99 HG999999]
NR 30
TC 15
Z9 16
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD APR
PY 2012
VL 158A
IS 4
BP 732
EP 742
DI 10.1002/ajmg.a.35228
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 922JW
UT WOS:000302544200008
PM 22383261
ER
PT J
AU Shi, M
Murray, JC
Marazita, ML
Munger, RG
Ruczinski, I
Hetmanski, JB
Wu, T
Murray, T
Redett, RJ
Wilcox, AJ
Lie, RT
Jabs, EW
Wu-Chou, YH
Chen, PK
Wang, H
Ye, XQ
Yeow, V
Chong, SS
Shi, B
Christensen, K
Scott, AF
Patel, P
Cheah, F
Beaty, TH
AF Shi, Min
Murray, Jeffrey C.
Marazita, Mary L.
Munger, Ronald G.
Ruczinski, Ingo
Hetmanski, Jacqueline B.
Wu, Tao
Murray, Tanda
Redett, Richard J.
Wilcox, Allen J.
Lie, Rolv T.
Jabs, Ethylin Wang
Wu-Chou, Yah Huei
Chen, Philip K.
Wang, Hong
Ye, Xiaoqian
Yeow, Vincent
Chong, Samuel S.
Shi, Bing
Christensen, Kaare
Scott, Alan F.
Patel, Poorav
Cheah, Felicia
Beaty, Terri H.
TI Genome Wide Study of Maternal and Parent-of-Origin Effects on the
Etiology of Orofacial Clefts
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE GWAS; CL/P; CP; maternal genes; parent-of-origin; family-based study;
association study
ID LINKAGE DISEQUILIBRIUM; 4 POPULATIONS; FLIP-FLOP; PALATE; LIP; GENE;
ASSOCIATION; RISK; TRANSMISSION; REVEALS
AB We performed a genome wide association analysis of maternally-mediated genetic effects and parent-of-origin (POO) effects on risk of orofacial clefting (OC) using over 2,000 case-parent triads collected through an international cleft consortium. We used log-linear regression models to test individual SNPs. For SNPs with a P-value <10(-5) for maternal genotypic effects, we also applied a haplotype-based method, TRIMM, to extract potential information from clusters of correlated SNPs. None of the SNPs were significant at the genome wide level. Our results suggest neither maternal genome nor POO effects play major roles in the etiology of OC in our sample. This finding is consistent with previous genetic studies and recent population-based cohort studies in Norway and Denmark, which showed no apparent difference between mother-to-offspring and father-to-offspring recurrence of clefting. We, however, cannot completely rule out maternal genome or POO effects as risk factors because very small effects might not be detectable with our sample size, they may influence risk through interactions with environmental exposures or may act through a more complex network of interacting genes. Thus, the most promising SNPs identified by this study may still be worth further investigation. Published 2012. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Shi, Min] NIEHS, Biostat Branch, NIH, Durham, NC USA.
[Murray, Jeffrey C.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Marazita, Mary L.] Univ Pittsburgh, Sch Dent Med, Dept Oral Biol, Pittsburgh, PA USA.
[Munger, Ronald G.] Utah State Univ, Dept Nutr & Food Sci, Logan, UT 84322 USA.
[Ruczinski, Ingo] Johns Hopkins Univ, Sch Publ Hlth, Dept Biostat, Baltimore, MD USA.
[Hetmanski, Jacqueline B.; Wu, Tao; Murray, Tanda; Patel, Poorav; Beaty, Terri H.] Johns Hopkins Univ, Sch Med, Dept Epidemiol, Baltimore, MD USA.
[Wu, Tao; Wang, Hong] Peking Univ, Hlth Sci Ctr, Sch Publ Hlth, Dept Epidemiol & Biostat, Beijing 100871, Peoples R China.
[Redett, Richard J.] Johns Hopkins Univ, Dept Plast Surg, Sch Med, Baltimore, MD USA.
[Wilcox, Allen J.] NIEHS, Epidemiol Branch N, NIH, Durham, NC USA.
[Lie, Rolv T.] Univ Bergen, Dept Biostat, Bergen, Norway.
[Jabs, Ethylin Wang; Scott, Alan F.] Johns Hopkins Univ, Inst Med Genet, Baltimore, MD USA.
[Jabs, Ethylin Wang; Ye, Xiaoqian] Mt Sinai Sch Med, Dept Genet & Genom Sci, New York, NY USA.
[Wu-Chou, Yah Huei; Chen, Philip K.] Chang Gung Mem Hosp, Human Mol Genet Lab, Tao Yuan, Taiwan.
[Ye, Xiaoqian] Wuhan Univ, Sch Stomatol, Wuhan 430072, Peoples R China.
[Yeow, Vincent] KK Womens & Childrens Hosp, Dept Plast Reconstruct & Anesthet Surg, Singapore, Singapore.
[Chong, Samuel S.; Cheah, Felicia] Natl Univ Singapore, Natl Univ Hosp, Deparment Pediat, Singapore 117548, Singapore.
[Shi, Bing] Sichuan Univ, W China Sch Stomatol, Chengdu 610064, Peoples R China.
[Christensen, Kaare] Univ So Denmar, Odense, Denmark.
RP Shi, M (reprint author), Natl Inst Environm Hlth Sci, Biostat Branch, Mail Drop A3-03 101-A352, Res Triangle Pk, NC 27709 USA.
EM shi2@niehs.nih.gov
RI Christensen, Kaare/C-2360-2009; Chong, Samuel/D-8098-2015;
OI Christensen, Kaare/0000-0002-5429-5292; Wilcox,
Allen/0000-0002-3376-1311; Jabs, Ethylin/0000-0001-8983-5466
FU National Institute for Dental and Craniofacial Research [U01-DE-018993,
U01-DE-004425]; National Institute of Dental & Craniofacial Research
[R21-DE-013707, R37-DE-08559, R01-DE-014581]; International Consortium
to Identify Genes & Interactions Controlling Oral Clefts; TH Beaty, PI;
NIH [D43 TW06176]; NIH, National Institute of Environmental Health
Sciences
FX Grant sponsor: National Institute for Dental and Craniofacial Research;
Grant number: U01-DE-018993; Grant sponsor: National Institute of Dental
& Craniofacial Research; Grant numbers: R21-DE-013707, R37-DE-08559,
R01-DE-014581.; We sincerely thank all of the families at each
recruitment site for participating in this study, and we gratefully
acknowledge the invaluable assistance of clinical, field, and laboratory
staff who contributed in making this work possible. The International
Cleft Consortium including genotyping and analysis was supported by the
National Institute for Dental and Craniofacial Research through
U01-DE-004425; "International Consortium to Identify Genes &
Interactions Controlling Oral Clefts", 2007-2009; TH Beaty, PI. This
research was supported by R21-DE-013707, R37-DE-08559, R01-DE-014581
from the National Institute of Dental & Craniofacial Research. T. W. is
supported by the International Collaborative Genetics Research Training
Program (ICGRTP), NIH D43 TW06176. This research was also supported by
the Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences. We thank the Smile Train Foundation for
supporting cleft research in China and Operation Smile for research in
the Philippines.
NR 35
TC 10
Z9 11
U1 1
U2 10
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD APR
PY 2012
VL 158A
IS 4
BP 784
EP 794
DI 10.1002/ajmg.a.35257
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 922JW
UT WOS:000302544200014
PM 22419666
ER
PT J
AU Voermans, NC
Kempers, M
Lammens, M
van Alfen, N
Janssen, MC
Bonnemann, C
van Engelen, BG
Hamel, BC
AF Voermans, N. C.
Kempers, M.
Lammens, M.
van Alfen, N.
Janssen, M. C.
Bonnemann, C.
van Engelen, B. G.
Hamel, B. C.
TI Myopathy in a 20-Year-Old Female Patient With D4ST-1 Deficient
Ehlers-Danlos Syndrome Due to a Homozygous CHST14 Mutation
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE Ehlers-Danlos syndrome; myopathy; neuromuscular features; muscle biopsy;
delayed motor development; connective tissue; CHST14;
musculocontractural Ehlers-Danlos syndrome; adducted thumb-clubfoot
syndrome
ID MYOFASCIAL FORCE TRANSMISSION; THUMB-CLUBFOOT SYNDROME; GENITOPATELLAR
SYNDROME; DIFFERENTIAL-DIAGNOSIS; SUPPORT OVERLAP; CONTRACTURES; JOINT;
DYSTROPHY; VALUES; VIB
AB We here report on a 20-year-old female patient with EDS due to a homozygous CHST14 single nucleotide deletion resulting in D4ST-1 deficiency, accompanied by muscle hypoplasia and muscle weakness. Findings of muscle ultrasound, electromyography, and muscle biopsy pointed to a myopathy, similarly as in other EDS types. This myopathy probably contributes to the gross motor developmental delay in this type of EDS. (C) 2012 Wiley Periodicals, Inc.
C1 [Voermans, N. C.] Radboud Univ Nijmegen, Med Ctr, Donders Inst Brain Cognit & Behav, Dept Neurol, NL-6500 HB Nijmegen, Netherlands.
[Kempers, M.; Hamel, B. C.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6500 HB Nijmegen, Netherlands.
[Lammens, M.] Radboud Univ Nijmegen, Med Ctr, Dept Pathol, NL-6500 HB Nijmegen, Netherlands.
[van Alfen, N.] Radboud Univ Nijmegen, Med Ctr, Dept Clin Neurophysiol, NL-6500 HB Nijmegen, Netherlands.
[Janssen, M. C.] Radboud Univ Nijmegen, Med Ctr, Dept Internal Med, NL-6500 HB Nijmegen, Netherlands.
[Bonnemann, C.] NINDS, Neuromuscular & Neurogenet Disorders Childhood Se, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
RP Voermans, NC (reprint author), Radboud Univ Nijmegen, Med Ctr, Donders Inst Brain Cognit & Behav, Dept Neurol, 935,POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM n.voermans@neuro.umcn.nl
RI van Engelen, Baziel/D-3475-2009; van Alfen, Nens/J-6011-2012; Engelen,
B.G.M./H-8027-2014; van Alfen, Nens/L-4172-2015; Voermans,
N.C./L-4724-2015; Janssen, Mirian/D-9777-2016
OI Janssen, Mirian/0000-0003-4668-9977
FU Prinses Beatrix Fonds
FX Grant sponsor: Prinses Beatrix Fonds.
NR 32
TC 11
Z9 11
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD APR
PY 2012
VL 158A
IS 4
BP 850
EP 855
DI 10.1002/ajmg.a.35232
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 922JW
UT WOS:000302544200025
PM 22407744
ER
PT J
AU Gilbert, SA
Grobman, WA
Landon, MB
Spong, CY
Rouse, DJ
Leveno, KJ
Varner, MW
Caritis, SN
Meis, PJ
Sorokin, Y
Carpenter, M
O'Sullivan, MJ
Sibai, BM
Thorp, JM
Ramin, SM
Mercer, BM
AF Gilbert, Sharon A.
Grobman, William A.
Landon, Mark B.
Spong, Catherine Y.
Rouse, Dwight J.
Leveno, Kenneth J.
Varner, Michael W.
Caritis, Steve N.
Meis, Paul J.
Sorokin, Yoram
Carpenter, Marshall
O'Sullivan, Mary J.
Sibai, Baha M.
Thorp, John M.
Ramin, Susan M.
Mercer, Brian M.
CA Eunice Kennedy Shriver Natl Inst C
TI Elective repeat cesarean delivery compared with spontaneous trial of
labor after a prior cesarean delivery: a propensity score analysis
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE elective repeat cesarean delivery; propensity score; trial of labor
ID UTERINE RUPTURE; VAGINAL BIRTH; OUTCOMES; SECTION; NUMBER; WOMEN; RISK
AB OBJECTIVE: The purpose of this study was to determine outcomes, after the use of propensity score techniques, to create balanced groups according to whether a woman undergoes elective repeat cesarean delivery (ERCD) or trial of labor (TOL).
STUDY DESIGN: Women who were eligible for a TOL with 1 previous low transverse incision were categorized according to whether they underwent an ERCD or TOL. A propensity score technique was used to develop ERCD and TOL groups with comparable baseline characteristics. Outcomes were assessed with conditional logistic regression.
RESULTS: The rates of endometritis, operative injury, respiratory distress syndrome, and newborn infant infection were lower and the rates of hysterectomy and wound complication were higher in the ERCD group.
CONCLUSION: Propensity score techniques can be used to generate comparable ERCD and TOL groups. Some types of maternal morbidity (such as hysterectomy) are higher; other types (such as operative injury) are lower in the ERCD group. Although the absolute risk is low, neonatal morbidity appears to be lower in the ERCD group.
C1 [Gilbert, Sharon A.] George Washington Univ, Ctr Biostat, Washington, DC 20052 USA.
[Grobman, William A.] Northwestern Univ, Dept Obstet, Chicago, IL 60611 USA.
[Grobman, William A.] Northwestern Univ, Dept Gynecol, Chicago, IL 60611 USA.
[Landon, Mark B.] Ohio State Univ, Columbus, OH 43210 USA.
[Rouse, Dwight J.] Univ Alabama Birmingham, Birmingham, AL USA.
[Leveno, Kenneth J.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Varner, Michael W.] Univ Utah, Salt Lake City, UT USA.
[Meis, Paul J.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
[Carpenter, Marshall] Brown Univ, Providence, RI 02912 USA.
[O'Sullivan, Mary J.] Univ Miami, Miami, FL USA.
[Sibai, Baha M.] Univ Tennessee, Memphis, TN USA.
[Thorp, John M.] Univ N Carolina, Chapel Hill, NC USA.
[Ramin, Susan M.] Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
[Mercer, Brian M.] Case Western Reserve Univ, Metrohlth Med Ctr, Cleveland, OH USA.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Caritis, Steve N.] Univ Pittsburgh, Pittsburgh, PA USA.
RP Gilbert, SA (reprint author), George Washington Univ, Ctr Biostat, Washington, DC 20052 USA.
RI Varner, Michael/K-9890-2013
OI caritis, steve/0000-0002-2169-0712; Varner, Michael/0000-0001-9455-3973
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) of the National Institutes of Health [HD21410,
HD21414, HD27860, HD27861, HD27869, HD27905, HD27915, HD27917, HD34116,
HD34122, HD34136, HD34208, HD34210, HD40500, HD40485, HD40544, HD40545,
HD40560, HD40512, HD36801]
FX Supported by grants from the Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD) of the National Institutes
of Health (HD21410, HD21414, HD27860, HD27861, HD27869, HD27905,
HD27915, HD27917, HD34116, HD34122, HD34136, HD34208, HD34210, HD40500,
HD40485, HD40544, HD40545, HD40560, HD40512, and HD36801) and its
contents are solely the responsibility of the authors and do not
necessarily represent the official view of National Institute of Child
Health and Human Development or the National Institutes of Health.
NR 29
TC 6
Z9 6
U1 2
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD APR
PY 2012
VL 206
IS 4
AR 311.e1
DI 10.1016/j.ajog.2012.02.002
PG 9
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 918QS
UT WOS:000302266000016
PM 22464069
ER
PT J
AU Kakani, S
Yardeni, T
Poling, J
Ciccone, C
Niethamer, T
Klootwijk, ED
Manoli, I
Darvish, D
Hoogstraten-Miller, S
Zerfas, P
Tian, E
Ten Hagen, KG
Kopp, JB
Gahl, WA
Huizing, M
AF Kakani, Sravan
Yardeni, Tal
Poling, Justin
Ciccone, Carla
Niethamer, Terren
Klootwijk, Enriko D.
Manoli, Irini
Darvish, Daniel
Hoogstraten-Miller, Shelley
Zerfas, Patricia
Tian, E.
Ten Hagen, Kelly G.
Kopp, Jeffrey B.
Gahl, William A.
Huizing, Marjan
TI The Gne M712T Mouse as a Model for Human Glomerulopathy
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID ACETYLGLUCOSAMINE 2-EPIMERASE/N-ACETYLMANNOSAMINE KINASE; SIALIC-ACID
BIOSYNTHESIS; HELIX-POMATIA AGGLUTININ; INCLUSION-BODY MYOPATHY;
N-ACETYLNEURAMINIC ACID; AMINONUCLEOSIDE NEPHROSIS; ACTIN CYTOSKELETON;
EPITHELIAL-CELL; MEMBRANOUS GLOMERULONEPHRITIS; AFFINITY-CHROMATOGRAPHY
AB Pathological glomerular hyposialylation has been implicated in certain unexplained glomerulopathies, including minimal change nephrosis, membranous glomerulonephritis, and IgA nephropathy. We studied our previously established mouse model carrying a homozygous mutation in the key enzyme of sialic acid biosynthesis, N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase. Mutant mice died before postnatal day 3 (P3) from severe glomerulopathy with podocyte effacement and segmental glomerular basement membrane splitting due to hyposialylation. Administration of the sialic acid precursor N-acetylmannosamine (ManNAc) led to improved sialylation and survival of mutant pups beyond P3. We determined the onset of the glomerulopathy in the embryonic stage. A lectin panel, distinguishing normally sialylated from hyposialylated glycans, used WGA, SNA, PNA, Jacalin, HPA, and VVA, indicating glomerular hyposialylation of predominantly O-linked glycoproteins in mutant mice. The glomerular glycoproteins nephrin and podocalyxin were hyposialylated in this unique murine model. ManNAc treatment appeared to ameliorate the hyposialylation status of mutant mice, indicated by a lectin histochemistry pattern similar to that of wild-type mice, with improved sialylation of both nephrin and podocalyxin, as well as reduced albuminuria compared with untreated mutant mice. These findings suggest application of our lectin panel for categorizing human kidney specimens based on glomerular sialylation status. Moreover, the partial restoration of glomerular architecture in ManNAc-treated mice highlights ManNAc as a potential treatment for humans affected with disorders of glomerular hyposialylation. (Am J Pathol 2012, 180:1431-1444; DOI: 10.1016/j.ajpath.2011.12.023)
C1 [Huizing, Marjan] NHGRI, Cell Biol Metab Disorders Unit, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Hoogstraten-Miller, Shelley] NHGRI, Off Lab Anim Med, Bethesda, MD 20892 USA.
[Manoli, Irini; Gahl, William A.] Natl Inst Dent & Craniofacial Res, Off Rare Dis Res, Off Director, Bethesda, MD USA.
[Zerfas, Patricia] Natl Inst Dent & Craniofacial Res, Div Vet Resources, Bethesda, MD USA.
[Tian, E.; Ten Hagen, Kelly G.] Natl Inst Dent & Craniofacial Res, Dev Glycobiol Unit, Off Res Serv, Bethesda, MD USA.
[Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD USA.
[Yardeni, Tal] Tel Aviv Univ, Sackler Sch Med, Grad Partner Program, IL-69978 Tel Aviv, Israel.
[Poling, Justin] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Klootwijk, Enriko D.] UCL, Dept Med, London, England.
[Darvish, Daniel] HIBM Res Grp, Encino, CA USA.
RP Huizing, M (reprint author), NHGRI, Cell Biol Metab Disorders Unit, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
EM mhuizing@mail.nih.gov
OI Manoli, Irini/0000-0003-1543-2941; Kopp, Jeffrey/0000-0001-9052-186X
FU National Human Genome Research Institute; National Dental and
Craniofacial Research Institute; National Institute of Diabetes and
Digestive and Kidney Diseases, NIH, Bethesda, MD
FX Supported by the Intramural Research Programs of the National Human
Genome Research Institute, the National Dental and Craniofacial Research
Institute, and the National Institute of Diabetes and Digestive and
Kidney Diseases, NIH, Bethesda, MD.
NR 82
TC 10
Z9 10
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD APR
PY 2012
VL 180
IS 4
BP 1431
EP 1440
DI 10.1016/j.ajpath.2011.12.023
PG 10
WC Pathology
SC Pathology
GA 919LO
UT WOS:000302329400013
PM 22322304
ER
PT J
AU Howden, R
Cho, HY
Miller-DeGraff, L
Walker, C
Clark, JA
Myers, PH
Rouse, DC
Kleeberger, SR
AF Howden, Reuben
Cho, Hye-Youn
Miller-DeGraff, Laura
Walker, Christopher
Clark, James A.
Myers, Page H.
Rouse, D. Clay
Kleeberger, Steven R.
TI Cardiac Physiologic and Genetic Predictors of Hyperoxia-Induced Acute
Lung Injury in Mice
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE heart rate; hyperoxia; genome-wide mapping
ID HEART-RATE-VARIABILITY; NRF2; RESPONSES; STRESS; OXYGEN; SUSCEPTIBILITY;
INHALATION; INDUCTION; DYSPLASIA; PROTEINS
AB Exposure of mice to hyperoxia produces pulmonary toxicity similar to acute lung injury/acute respiratory distress syndrome, but little is known about the interactions within the cardiopulmonary system. This study was designed to characterize the cardiopulmonary response to hyperoxia, and to identify candidate susceptibility genes in mice. Electrocardiogram and ventilatory data were recorded continuously from 4 inbred and 29 recombinant inbred strains during 96 hours of hyperoxia (100% oxygen). Genome-wide linkage analysis was performed in 27 recombinant inbred strains against response time indices (TIs) calculated from each cardiac phenotype. Reductions in minute ventilation, heart rate (HR), low-frequency(LF) HR variability (HRV), high-frequency HRV, and total power HRV were found in all mice during hyperoxia exposure, but the lag time before these changes began was strain dependent. Significant (chromosome 9) or suggestive (chromosomes 3 and 5) quantitative trait loci were identified for the HRTI and LFTI. Functional polymorphisms in several candidate susceptibility genes were identified within the quantitative trait loci and were associated with hyperoxia susceptibility. This is the first study to report highly significant interstrain variation in hyperoxia-induced changes in minute ventilation, HR, and HRV, and to identify polymorphisms in candidate susceptibility genes that associate with cardiac responses. Results indicate that changes in HR and LF HRV could be important predictors of subsequent adverse outcome during hyperoxia exposure, specifically the pathogenesis of acute lung injury. Understanding the genetic mechanisms of these responses may have significant diagnostic clinical value.
C1 [Howden, Reuben] Univ N Carolina, Dept Kinesiol, Charlotte, NC 28223 USA.
[Cho, Hye-Youn; Miller-DeGraff, Laura; Walker, Christopher; Kleeberger, Steven R.] Natl Inst Environm Hlth Sci, Lab Resp Biol, NIH, Res Triangle Pk, NC USA.
[Clark, James A.; Myers, Page H.] Natl Inst Environm Hlth Sci, Comparat Med Branch, NIH, Res Triangle Pk, NC USA.
[Rouse, D. Clay] Duke Univ, Med Ctr, Div Lab Anim Resources, Durham, NC USA.
RP Howden, R (reprint author), Univ N Carolina, Dept Kinesiol, Charlotte, NC 28223 USA.
EM rhowden@uncc.edu
FU National Institute of Environmental Health Sciences, National Institutes
of Health, Department of Health and Human Services
FX This work was supported by the Intramural Research Program of the
National Institute of Environmental Health Sciences, National Institutes
of Health, Department of Health and Human Services.
NR 30
TC 9
Z9 9
U1 0
U2 0
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1044-1549
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD APR
PY 2012
VL 46
IS 4
BP 470
EP 478
DI 10.1165/rcmb.2011-0204OC
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA 924LC
UT WOS:000302691900008
PM 22052878
ER
PT J
AU Guindo, MA
Shott, JP
Saye, R
Diakite, ML
Sanogo, S
Dembele, MB
Keita, S
Nagel, MC
Ellis, RD
Aebig, JA
Diallo, DA
Doumbo, OK
AF Guindo, Merepen A.
Shott, Joseph P.
Saye, Renion
Diakite, Moussa L.
Sanogo, Sintry
Dembele, Moussa B.
Keita, Sekouba
Nagel, Mary C.
Ellis, Ruth D.
Aebig, Joan A.
Diallo, Dapa A.
Doumbo, Ogobara K.
TI Promoting Good Clinical Laboratory Practices and Laboratory
Accreditation to Support Clinical Trials in Sub-Saharan Africa
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID MALARIA VACCINE; FALCIPARUM-MALARIA; MALI; CHILDREN; PHASE-2; VILLAGE;
ANEMIA
AB Laboratory capacity in the developing world frequently lacks quality management systems (QMS) such as good clinical laboratory practices, proper safety precautions, and adequate facilities; impacting the ability to conduct biomedical research where it is needed most. As the regulatory climate changes globally, higher quality laboratory support is needed to protect study volunteers and to accurately assess biological parameters. The University of Bamako and its partners have undertaken a comprehensive QMS plan to improve quality and productivity using the Clinical and Laboratory Standards Institute standards and guidelines. The clinical laboratory passed the College of American Pathologists inspection in April 2010, and received full accreditation in June 2010. Our efforts to implement high-quality standards have been valuable for evaluating safety and immunogenicity of malaria vaccine candidates in Mali. Other disease-specific research groups in resource-limited settings may benefit by incorporating similar training initiatives, QMS methods, and continual improvement practices to ensure best practices.
C1 [Guindo, Merepen A.; Diakite, Moussa L.; Sanogo, Sintry; Dembele, Moussa B.; Keita, Sekouba; Diallo, Dapa A.; Doumbo, Ogobara K.] Univ Bamako, Malaria Res & Training Ctr, Mali ICER, Bamako, Mali.
[Shott, Joseph P.] NIAID, OD, DIR, Bethesda, MD 20892 USA.
[Saye, Renion] USAID Mali, Bamako, Mali.
[Nagel, Mary C.] Minist Hlth, Lab Natl Sante Publ, Port Au Prince, Haiti.
NIAID, LMIV, DIR, NIH, Rockville, MD USA.
NCI, Clin Monitoring Res Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
GHP, CLSI, Wayne, PA USA.
Univ Bamako, MRTC, FMPOS, Mali Int Ctr Excellence Res ICER, Bamako, Mali.
RP Shott, JP (reprint author), 33 North Dr,MSC 3207, Bethesda, MD 20892 USA.
EM agnes@icermali.org; ShottJ@mail.nih.gov; saye@icermali.org;
mldiakite@icermali.org; ssanogo@icermali.org; moussab@icermali.org;
Sekouba@icermali.org; mcnagel@live.com; ellisru@niaid.nih.gov;
jaebig@niaid.nih.gov; dadiallo@icermali.org; okd@icermali.org
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health; National Cancer
Institute, National Institutes of Health [HHSN261200800001E]; National
Institute of Allergy and Infectious Diseases
FX The clinical laboratory is financially supported by the Division of
Intramural Research, National Institute of Allergy and Infectious
Diseases, National Institutes of Health. This project has been funded in
whole or in part with federal funds from the National Cancer Institute,
National Institutes of Health, under contract no. HHSN261200800001E.
This research was supported (in part) by the National Institute of
Allergy and Infectious Diseases.
NR 15
TC 6
Z9 8
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD APR
PY 2012
VL 86
IS 4
BP 573
EP 579
DI 10.4269/ajtmh.2012.11-0691
PG 7
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 922AR
UT WOS:000302519700005
PM 22492138
ER
PT J
AU Valerio, L
Facchinelli, L
Ramsey, JM
Scott, TW
AF Valerio, Laura
Facchinelli, Luca
Ramsey, Janine M.
Scott, Thomas W.
TI Dispersal of Male Aedes aegypti in a Coastal Village in Southern Mexico
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID DENGUE VECTOR MOSQUITOS; RELEASE-RECAPTURE; SURVIVAL RATES; BORNE
DISEASES; BODY-SIZE; POPULATION; CULICIDAE; DIPTERA; THAILAND;
ALBOPICTUS
AB Most Aedes aegypti dispersal studies have focused on females because of their central role in dengue virus transmission. Only a few mark-release-recapture (MRR) studies provided insights into male Ae. aegypti dispersal. To fill this knowledge gap, we conducted five male Ae. aegypti MRR experiments in a coastal village in southern Mexico. Small and large male cohorts were marked with fluorescent dusts, released outside buildings, and recaptures were carried out by using backpack aspirators. Recapture rates ranged between 0.35% and 6.55% and median distance traveled was 12-166 meters. A statistically significant difference in median distance traveled with large males dispersing farther than small ones was detected only in one experiment (MRR5: U = 3.5, P < 0.01). Male dispersal data will be useful for constructing and estimating parameter values and validating models that will be used to plan the most effective release strategies for genetically modified male Ae. aegypti.
C1 [Valerio, Laura; Facchinelli, Luca; Scott, Thomas W.] Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
[Valerio, Laura] Univ Roma La Sapienza, Inst Pasteur, Cenci Bolognetti Fdn, Rome, Italy.
[Ramsey, Janine M.] INSP, Ctr Reg Invest Salud Publ, Tapachula 30700, Chiapas, Mexico.
[Scott, Thomas W.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Valerio, L (reprint author), Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
EM lvalerio@ucdavis.edu; lfacchinelli@ucdavis.edu; jramsey@insp.mx;
twscott@ucdavis.edu
OI Facchinelli, Luca/0000-0002-8987-1472
FU Pasteur Institute-Cenci Bolognetti Foundation; Foundation for the
National Institutes of Health [316]
FX This study was supported by the Pasteur Institute-Cenci Bolognetti
Foundation and the Foundation for the National Institutes of Health
through the Grand Challenges in Global Health Initiative (GC7 #316).
NR 41
TC 13
Z9 13
U1 0
U2 21
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD APR
PY 2012
VL 86
IS 4
BP 665
EP 676
DI 10.4269/ajtmh.2012.11-0513
PG 12
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 922AR
UT WOS:000302519700019
PM 22492152
ER
PT J
AU Yeh, S
Fahle, G
Flaxel, CJ
Francis, PJ
AF Yeh, Steven
Fahle, Gary
Flaxel, Christina J.
Francis, Peter J.
TI Central Retinal Vascular Occlusion Associated With Acute Retinal
Necrosis
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Editorial Material
C1 [Flaxel, Christina J.; Francis, Peter J.] Oregon Hlth & Sci Univ, Casey Eye Inst, Portland, OR 97239 USA.
[Yeh, Steven] Emory Univ, Sch Med, Emory Eye Ctr, Atlanta, GA USA.
[Fahle, Gary] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
RP Francis, PJ (reprint author), Oregon Hlth & Sci Univ, Casey Eye Inst, 3375 SW Terwilliger Blvd, Portland, OR 97239 USA.
EM francisp@ohsu.edu
NR 7
TC 2
Z9 2
U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD APR
PY 2012
VL 130
IS 4
BP 514
EP 517
PG 4
WC Ophthalmology
SC Ophthalmology
GA 922OK
UT WOS:000302557100016
PM 22491922
ER
PT J
AU Varga, T
Mogyorodi, B
Bago, AG
Cservenak, M
Domokos, D
Renner, E
Gallatz, K
Usdin, TB
Palkovits, M
Dobolyi, A
AF Varga, Tamas
Mogyorodi, Bence
Bago, Attila G.
Cservenak, Melinda
Domokos, Dominika
Renner, Eva
Gallatz, Katalin
Usdin, Ted B.
Palkovits, Miklos
Dobolyi, Arpad
TI Paralemniscal TIP39 is induced in rat dams and may participate in
maternal functions
SO BRAIN STRUCTURE & FUNCTION
LA English
DT Article
DE Tuberoinfundibular peptide of 39 residues; Parathyroid hormone 2
receptor; Medial paralemniscal nucleus; Formalin pain stress; A7
noradrenergic cell group; Pontine tegmentum; Suckling
ID ECHOLOCATING HORSESHOE BATS; CATECHOLAMINE CELL GROUP;
TUBEROINFUNDIBULAR PEPTIDE; 39 RESIDUES; PERIAQUEDUCTAL GRAY;
NERVOUS-SYSTEM; C-FOS; RETICULAR-FORMATION; PROLACTIN-RELEASE;
SQUIRREL-MONKEY
AB The paralemniscal area, situated between the pontine reticular formation and the lateral lemniscus in the pontomesencephalic tegmentum contains some tuberoinfundibular peptide of 39 residues (TIP39)-expressing neurons. In the present study, we measured a 4 times increase in the level of TIP39 mRNA in the paralemniscal area of lactating mothers as opposed to nulliparous females and mothers deprived of pups using real-time RT-PCR. In situ hybridization histochemistry and immunolabeling demonstrated that the induction of TIP39 in mothers takes place within the medial paralemniscal nucleus, a cytoarchitectonically distinct part of the paralemniscal area, and that the increase in TIP39 mRNA levels translates into elevated peptide levels in dams. The paralemniscal area has been implicated in maternal control as well as in pain perception. To establish the function of induced TIP39, we investigated the activation of TIP39 neurons in response to pup exposure as maternal, and formalin injection as noxious stimulus. Both stimuli elicited c-fos expression in the paralemniscal area. Subsequent double labeling demonstrated that 95% of neurons expressing Fos in response to pup exposure also contained TIP39 immunoreactivity and 91% of TIP39 neurons showed c-fos activation by pup exposure. In contrast, formalin-induced Fos does not co-localize with TIP39. Instead, most formalin-activated neurons are situated medial to the TIP39 cell group. Our data indicate that paralemniscal neurons may be involved in the processing of maternal and nociceptive information. However, two different groups of paralemniscal neurons participate in the two functions. In particular, TIP39 neurons may participate in the control of maternal functions.
C1 [Varga, Tamas; Mogyorodi, Bence; Bago, Attila G.; Cservenak, Melinda; Domokos, Dominika; Renner, Eva; Gallatz, Katalin; Palkovits, Miklos; Dobolyi, Arpad] Semmelweis Univ, Neuromorphol & Neuroendocrine Res Lab, Dept Anat Histol & Embryol, H-1094 Budapest, Hungary.
[Bago, Attila G.] Natl Inst Neurosurg, Budapest, Hungary.
[Usdin, Ted B.] NIMH, Sect Fundamental Neurosci, Bethesda, MD 20892 USA.
RP Dobolyi, A (reprint author), Semmelweis Univ, Neuromorphol & Neuroendocrine Res Lab, Dept Anat Histol & Embryol, Tuzolto 58, H-1094 Budapest, Hungary.
EM dobolyi@ana.sote.hu
RI Palkovits, Miklos/F-2707-2013;
OI Palkovits, Miklos/0000-0003-0578-0387
FU Hungarian Academy of Sciences; Hungarian Science Foundation NKTH-OTKA
[K67646]; Hungarian Science Foundation OTKA [CK80180]; NIMH; [OTKA
K100319]; [OTKA NNF85612]
FX Support was provided by the Bolyai Award of the Hungarian Academy of
Sciences, the Hungarian Science Foundation NKTH-OTKA K67646, OTKA
K100319, and OTKA NNF85612 research grants for AD, the Hungarian Science
Foundation OTKA CK80180 research grant for MP, and the NIMH Intramural
Research Program for TBU. We are grateful for the technical assistance
of Szilvia Deak and Nikolett Hanak.
NR 53
TC 4
Z9 4
U1 0
U2 8
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2653
J9 BRAIN STRUCT FUNCT
JI Brain Struct. Funct.
PD APR
PY 2012
VL 217
IS 2
BP 323
EP 335
DI 10.1007/s00429-011-0357-2
PG 13
WC Anatomy & Morphology; Neurosciences
SC Anatomy & Morphology; Neurosciences & Neurology
GA 922UG
UT WOS:000302573200011
PM 22081168
ER
PT J
AU Auner, HW
Pavlu, J
Szydlo, R
Giles, C
Kanfer, E
Macdonald, D
Marin, D
Milojkovic, D
Rezvani, K
Goldman, JM
Apperley, JF
Landgren, O
Rahemtulla, A
AF Auner, Holger W.
Pavlu, Jiri
Szydlo, Richard
Giles, Chrissy
Kanfer, Ed
Macdonald, Donald
Marin, David
Milojkovic, Dragana
Rezvani, Katayoun
Goldman, John M.
Apperley, Jane F.
Landgren, Ola
Rahemtulla, Amin
TI Autologous haematopoietic stem cell transplantation in multiple myeloma
patients from ethnic minority groups in an equal access healthcare
system
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Letter
DE multiple myeloma; stem cell transplantation; ethnicity; race
ID RACE; CHEMOTHERAPY; OUTCOMES
C1 [Auner, Holger W.; Pavlu, Jiri; Szydlo, Richard; Giles, Chrissy; Kanfer, Ed; Macdonald, Donald; Marin, David; Milojkovic, Dragana; Rezvani, Katayoun; Goldman, John M.; Apperley, Jane F.; Rahemtulla, Amin] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Ctr Haematol, London, England.
[Auner, Holger W.] Univ London Imperial Coll Sci Technol & Med, Ctr Clin Sci, MRC, London, England.
[Landgren, Ola] NCI, Multiple Myeloma Sect, Med Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Auner, HW (reprint author), Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, Ctr Haematol, London, England.
EM holger.auner@csc.mrc.ac.uk; a.rahemtulla@imperial.ac.uk
RI Szydlo, Richard/C-6678-2012;
OI Szydlo, Richard/0000-0003-1102-8298; Auner, Holger/0000-0003-4040-0642
FU Medical Research Council [MC_G0802523]
NR 10
TC 3
Z9 3
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD APR
PY 2012
VL 157
IS 1
BP 125
EP 127
DI 10.1111/j.1365-2141.2011.08906.x
PG 3
WC Hematology
SC Hematology
GA 907RZ
UT WOS:000301436700015
PM 22050411
ER
PT J
AU Sherman, ME
Figueroa, JD
Henry, JE
Clare, SE
Rufenbarger, C
Storniolo, AM
AF Sherman, Mark E.
Figueroa, Jonine D.
Henry, Jill E.
Clare, Susan E.
Rufenbarger, Connie
Storniolo, Anna Maria
TI The Susan G. Komen for the Cure Tissue Bank at the IU Simon Cancer
Center: A Unique Resource for Defining the "Molecular Histology" of the
Breast
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID ESTROGEN-RECEPTOR EXPRESSION; RISK-FACTORS; INTERVAL; WOMEN; AGE;
INVOLUTION; PHENOTYPE; MORTALITY; PREGNANCY; THERAPY
AB "Molecular histology" of the breast may be conceptualized as encompassing the normative ranges of histologic structure and marker expression in normal breast tissues in relation to a woman's age and life experiences. Studies of molecular histology can aid our understanding of early events in breast carcinogenesis and provide data for comparison with diseased breast tissues. Until recently, lack of epidemiologically annotated, optimally prepared normal breast tissues obtained from healthy women presented a barrier to breast cancer research. The Komen Tissue Bank at Indiana University (Indianapolis, IN) is a unique biorepository that was developed to overcome this limitation. The Bank enrolls healthy donors who provide questionnaire data, blood, and up to four breast biopsies, which are prepared as both formalin-fixed, paraffin-embedded and frozen tissues. The resource is accessible to researchers worldwide through a proposal submission, review, and approval process. As of November 2010, the Bank had collected specimens and information from 1,174 donors. In this review, we discuss the importance of studying normal breast tissues, assess the strengths and limitations of studying normal tissues obtained from different sources, and summarize the features of the Komen Tissue Bank. As research projects are completed, results will be posted on the Bank's website. Cancer Prev Res; 5(4); 528-35. (C) 2012 AACR.
C1 [Sherman, Mark E.; Figueroa, Jonine D.] NCI, Div Canc Epidemiol & Genet, Hormonal & Reprod Epidemiol Branch, Rockville, MD USA.
[Henry, Jill E.; Clare, Susan E.; Rufenbarger, Connie; Storniolo, Anna Maria] Indiana Univ, Sch Med, IU Simon Canc Ctr, Susan G Komen Cure Tissue Bank, Indianapolis, IN 46202 USA.
[Clare, Susan E.] Indiana Univ, Sch Med, Dept Surg, Div Breast Surg Oncol, Indianapolis, IN 46202 USA.
[Storniolo, Anna Maria] Indiana Univ, Sch Med, Dept Med, Div Hematol Oncol, Indianapolis, IN 46202 USA.
[Rufenbarger, Connie] Catherine Peachey Fund Inc, Warsaw, IN USA.
RP Storniolo, AM (reprint author), Indiana Univ, Sch Med, Melvin & Bren Simon Canc Ctr, 535 Barnhill Dr,Room 473, Indianapolis, IN 46202 USA.
EM astornio@iupui.edu
FU Susan G. Komen for the Cure; Breast Cancer Research Foundation; Oracle
Giving; Catherine Peachey Fund, Inc.; National Cancer Institute
FX This study was supported by Susan G. Komen for the Cure; the Breast
Cancer Research Foundation; Oracle Giving; the Catherine Peachey Fund,
Inc.; and National Cancer Institute, Intramural Research Program.
NR 34
TC 15
Z9 15
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD APR
PY 2012
VL 5
IS 4
BP 528
EP 535
DI 10.1158/1940-6207.CAPR-11-0234
PG 8
WC Oncology
SC Oncology
GA 922TY
UT WOS:000302572400007
PM 22345117
ER
PT J
AU Vitale-Cross, L
Molinolo, AA
Martin, D
Younis, RH
Maruyama, T
Patel, V
Chen, WJ
Schneider, A
Gutkind, JS
AF Vitale-Cross, Lynn
Molinolo, Alfredo A.
Martin, Daniel
Younis, Rania H.
Maruyama, Takashi
Patel, Vyomesh
Chen, Wanjun
Schneider, Abraham
Gutkind, J. Silvio
TI Metformin Prevents the Development of Oral Squamous Cell Carcinomas from
Carcinogen-Induced Premalignant Lesions
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID BREAST-CANCER CELLS; NECK-CANCER; MAMMALIAN TARGET; ANTIDIABETIC DRUG;
MTOR INHIBITION; CYCLE ARREST; IN-VITRO; HEAD; RAPAMYCIN; KINASE
AB Head and neck squamous cell carcinoma (HNSCC) is a major public health concern. The recent identification of the mTOR complex 1 (mTORC1) signaling pathway as a highly prevalent molecular signature underlying HNSCC pathogenesis has provided the foundation to search for novel therapeutic approaches to prevent and treat HNSCC. Here, we asked whether metformin, the most widely used medication for the treatment of type II diabetes, which acts in part by stimulating the AMP-activated protein kinase (AMPK) signaling pathway thereby reducing mTORC1 activity, may lower the risk of HNSCC development. Indeed, we show that metformin reduces the growth of HNSCC cells and diminishes their mTORC1 activity by both AMPK-dependent and -independent mechanisms. We also optimized an oral-specific carcinogenesis mouse model that results in the accumulation of multiple oral premalignant lesions at the end of the carcinogen exposure, some of which then spontaneously progress into HNSCC. Using this mouse model, we observed that metformin specifically inhibits mTORC1 in the basal proliferating epithelial layer of oral premalignant lesions. Remarkably, metformin prevented the development of HNSCC by reducing significantly the size and number of carcinogen-induced oral tumoral lesions and by preventing their spontaneous conversion to squamous cell carcinomas. Collectively, our data underscore the potential clinical benefits of using metformin as a targeted chemopreventive agent in the control of HNSCC development and progression. Cancer Prev Res; 5(4); 562-73. (C) 2012 AACR.
C1 [Vitale-Cross, Lynn; Molinolo, Alfredo A.; Martin, Daniel; Patel, Vyomesh; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Mol Carcinogenesis Sect, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
[Maruyama, Takashi; Chen, Wanjun] Natl Inst Dent & Craniofacial Res, Oral Mucosal Immunol Sect, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA.
[Younis, Rania H.; Schneider, Abraham] Univ Maryland, Sch Dent, Dept Oncol & Diagnost Sci, Baltimore, MD 21201 USA.
[Schneider, Abraham] Univ Maryland, Program Oncol, Greenebaum Canc Ctr, Baltimore, MD 21201 USA.
RP Gutkind, JS (reprint author), Natl Inst Dent & Craniofacial Res, Mol Carcinogenesis Sect, Oral & Pharyngeal Canc Branch, NIH, 30 Convent Dr, Bethesda, MD 20892 USA.
EM aschneider@umaryland.edu; sg39v@nih.gov
FU NIH, National Institute of Dental and Craniofacial Research
[Z01DE00558]; University of Maryland; JSPS at NIH
FX This article was supported by the Intramural Research Program of the
NIH, National Institute of Dental and Craniofacial Research, project
Z01DE00558, and by the University of Maryland (to R.H. Younis and A.
Schneider). T. Maruyama was supported in part by a JSPS Research
Fellowship for Japanese Biomedical and Behavioral Researchers at NIH.
NR 40
TC 46
Z9 49
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD APR
PY 2012
VL 5
IS 4
BP 562
EP 573
DI 10.1158/1940-6207.CAPR-11-0502
PG 12
WC Oncology
SC Oncology
GA 922TY
UT WOS:000302572400011
PM 22467081
ER
PT J
AU Messing, E
Gee, JR
Saltzstein, DR
Kim, K
diSant'Agnese, A
Kolesar, J
Harris, L
Faerber, A
Havighurst, T
Young, JM
Efros, M
Getzenberg, RH
Wheeler, MA
Tangrea, J
Parnes, H
House, M
Busby, JE
Hohl, R
Bailey, H
AF Messing, Edward
Gee, Jason R.
Saltzstein, Daniel R.
Kim, KyungMann
diSant'Agnese, Anthony
Kolesar, Jill
Harris, Linda
Faerber, Adrienne
Havighurst, Thomas
Young, Jay M.
Efros, Mitchell
Getzenberg, Robert H.
Wheeler, Marcia A.
Tangrea, Joseph
Parnes, Howard
House, Margaret
Busby, J. Erik
Hohl, Raymond
Bailey, Howard
TI A Phase 2 Cancer Chemoprevention Biomarker Trial of Isoflavone G-2535
(Genistein) in Presurgical Bladder Cancer Patients
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID TRANSITIONAL-CELL-CARCINOMA; PURIFIED SOY ISOFLAVONES; SINGAPORE CHINESE
HEALTH; AKT SIGNALING PATHWAY; PROSTATE-CANCER; BREAST-CANCER;
PROTEIN-KINASES; INCREASED RISK; DIETARY SOY; KAPPA-B
AB The soy compound genistein has been observed preclinically to inhibit bladder cancer growth with one potential mechanism being the inhibition of epidermal growth factor receptor phosphorylation (p-EGFR). A phase 2 randomized, placebo-controlled trial investigated whether daily, oral genistein (300 or 600 mg/d as the purified soy extract G-2535) for 14 to 21 days before surgery alters molecular pathways in bladder epithelial tissue in 59 subjects diagnosed with urothelial bladder cancer (median age, 71 years). G-2535 treatment was well tolerated; observed toxicities were primarily mild to moderate gastrointestinal or metabolic and usually not attributed to study drug. Genistein was detected in plasma and urine of subjects receiving G-2535 at concentrations greater than placebo subjects' but were not dose-dependent. Reduction in bladder cancer tissue p-EGFR staining between the placebo arm and the combined genistein arms was significant at the protocol-specified significance level of 0.10 (P = 0.07). This difference was most prominent when comparing the 300-mg group with placebo (P = 0.015), but there was no significant reduction in p-EGFR staining between the 600-mg group and placebo. No difference in normal bladder epithelium p-EGFR staining was observed between treatment groups. No significant differences in tumor tissue staining between treatment groups were observed for COX-2, Ki-67, activated caspase-3, Akt, p-Akt, mitogen-activated protein kinase (MAPK), or p-MAPK. No significant differences in urinary survivin or BLCA-4 levels between treatment groups were observed. Genistein displayed a possible bimodal effect (more effective at the lower dose) on bladder cancer tissue EGFR phosphorylation that should be evaluated further, possibly in combination with other agents. Cancer Prev Res; 5(4); 621-30. (C) 2012 AACR.
C1 [Gee, Jason R.; Kim, KyungMann; diSant'Agnese, Anthony; Kolesar, Jill; Harris, Linda; Faerber, Adrienne; Havighurst, Thomas; Bailey, Howard] Univ Wisconsin, Carbone Canc Ctr, Madison, WI 53792 USA.
[Messing, Edward] Univ Rochester, Med Ctr, Rochester, NY 14642 USA.
[Busby, J. Erik] Univ Alabama Birmingham, Birmingham, AL USA.
[Hohl, Raymond] Univ Iowa, Iowa City, IA USA.
[Young, Jay M.] S Orange Cty Med Res Ctr, Tustin, CA USA.
[Saltzstein, Daniel R.] Urol San Antonio Res, San Antonio, TX USA.
[Efros, Mitchell] AccuMed Res Associates LLC, Garden City, NY USA.
[Getzenberg, Robert H.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Tangrea, Joseph; Parnes, Howard; House, Margaret] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Wheeler, Marcia A.] Yale Univ, New Haven, CT USA.
RP Bailey, H (reprint author), Univ Wisconsin, Carbone Canc Ctr, Box 6164 Clin Sci Ctr,600 Highland Ave, Madison, WI 53792 USA.
EM hhb@medicine.wisc.edu
FU NIH [N01 CN35153, P30 CA014520, 1UL1RR025011]
FX The work was supported by NIH contract N01 CN35153 and grants P30
CA014520 and 1UL1RR025011.
NR 55
TC 23
Z9 25
U1 1
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD APR
PY 2012
VL 5
IS 4
BP 621
EP 630
DI 10.1158/1940-6207.CAPR-11-0455
PG 10
WC Oncology
SC Oncology
GA 922TY
UT WOS:000302572400017
PM 22293631
ER
PT J
AU Zaidi, MR
De Fabo, EC
Noonan, FP
Merlino, G
AF Zaidi, M. Raza
De Fabo, Edward C.
Noonan, Frances P.
Merlino, Glenn
TI Shedding Light on Melanocyte Pathobiology In Vivo
SO CANCER RESEARCH
LA English
DT Review
ID INTERFERON-GAMMA; ULTRAVIOLET-RADIATION; HLA-G; CANCER; EXPRESSION;
MICE; MUTATIONS; MECHANISM; CTLA-4; MOUSE
AB Cutaneous malignant melanoma is rapidly increasing in the developed world and continues to be a challenge in the clinic. Although extensive epidemiologic evidence points to solar UV as the major risk factor for melanoma, there is a significant gap in our knowledge about how this most ubiquitous environmental carcinogen interacts with the largest organ of the mammalian body (skin) at the microenvironmental and molecular level. We review some recent advances that have started to close this gap. Cancer Res; 72(7); 1591-5. (C) 2012 AACR.
C1 [Zaidi, M. Raza; Merlino, Glenn] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[De Fabo, Edward C.; Noonan, Frances P.] George Washington Univ, Med Ctr, Lab Photobiol & Photoimmunol, Dept Microbiol Immunol & Trop Med, Washington, DC 20037 USA.
RP Zaidi, MR (reprint author), NCI, Lab Canc Biol & Genet, NIH, 37 Convent Dr,Bldg 37,Room 5002, Bethesda, MD 20892 USA.
EM zaidir@mail.nih.gov
RI Zaidi, M. Raza/H-1386-2016
OI Zaidi, M. Raza/0000-0003-0480-3188
FU Intramural NIH HHS [Z99 CA999999]
NR 29
TC 6
Z9 6
U1 0
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 APR 1
PY 2012
VL 72
IS 7
BP 1591
EP 1595
DI 10.1158/0008-5472.CAN-11-2586
PG 5
WC Oncology
SC Oncology
GA 922MO
UT WOS:000302551800001
PM 22422936
ER
PT J
AU Stevens, KN
Fredericksen, Z
Vachon, CM
Wang, XS
Margolin, S
Lindblom, A
Nevanlinna, H
Greco, D
Aittomaki, K
Blomqvist, C
Chang-Claude, J
Vrieling, A
Flesch-Janys, D
Sinn, HP
Wang-Gohrke, S
Nickels, S
Brauch, H
Ko, YD
Fischer, HP
Schmutzler, RK
Meindl, A
Bartram, CR
Schott, S
Engel, C
Godwin, AK
Weaver, J
Pathak, HB
Sharma, P
Brenner, H
Muller, H
Arndt, V
Stegmaier, C
Miron, P
Yannoukakos, D
Stavropoulou, A
Fountzilas, G
Gogas, HJ
Swann, R
Dwek, M
Perkins, A
Milne, RL
Benitez, J
Zamora, MP
Perez, JIA
Bojesen, SE
Nielsen, SF
Nordestgaard, BG
Flyger, H
Guenel, P
Truong, T
Menegaux, F
Cordina-Duverger, E
Burwinkel, B
Marme, F
Schneeweiss, A
Sohn, C
Sawyer, E
Tomlinson, I
Kerin, MJ
Peto, J
Johnson, N
Fletcher, O
Silva, ID
Fasching, PA
Beckmann, MW
Hartmann, A
Ekici, AB
Lophatananon, A
Muir, K
Puttawibul, P
Wiangnon, S
Schmidt, MK
Broeks, A
Braaf, LM
Rosenberg, EH
Hopper, JL
Apicella, C
Park, DJ
Southey, MC
Swerdlow, AJ
Ashworth, A
Orr, N
Schoemaker, MJ
Anton-Culver, H
Ziogas, A
Bernstein, L
Dur, CC
Shen, CY
Yu, JC
Hsu, HM
Hsiung, CN
Hamann, U
Dunnebier, T
Rudiger, T
Ulmer, HU
Pharoah, PP
Dunning, AM
Humphreys, MK
Wang, Q
Cox, A
Cross, SS
Reed, MW
Hall, P
Czene, K
Ambrosone, CB
Ademuyiwa, F
Hwang, H
Eccles, DM
Garcia-Closas, M
Figueroa, JD
Sherman, ME
Lissowska, J
Devilee, P
Seynaeve, C
Tollenaar, RAEM
Hooning, MJ
Andrulis, IL
Knight, JA
Glendon, G
Mulligan, AM
Winqvist, R
Pylkas, K
Jukkola-Vuorinen, A
Grip, M
John, EM
Miron, A
Alnaes, GG
Kristensen, V
Borresen-Dale, AL
Giles, GG
Baglietto, L
McLean, CA
Severi, G
Kosel, ML
Pankratz, VS
Slager, S
Olson, JE
Radice, P
Peterlongo, P
Manoukian, S
Barile, M
Lambrechts, D
Hatse, S
Dieudonne, AS
Christiaens, MR
Chenevix-Trench, G
Beesley, J
Chen, XQ
Mannermaa, A
Kosma, VM
Hartikainen, JM
Soini, Y
Easton, DF
Couch, FJ
AF Stevens, Kristen N.
Fredericksen, Zachary
Vachon, Celine M.
Wang, Xianshu
Margolin, Sara
Lindblom, Annika
Nevanlinna, Heli
Greco, Dario
Aittomaki, Kristiina
Blomqvist, Carl
Chang-Claude, Jenny
Vrieling, Alina
Flesch-Janys, Dieter
Sinn, Hans-Peter
Wang-Gohrke, Shan
Nickels, Stefan
Brauch, Hiltrud
Ko, Yon-Dschun
Fischer, Hans-Peter
Schmutzler, Rita K.
Meindl, Alfons
Bartram, Claus R.
Schott, Sarah
Engel, Christoph
Godwin, Andrew K.
Weaver, JoEllen
Pathak, Harsh B.
Sharma, Priyanka
Brenner, Hermann
Mueller, Heiko
Arndt, Volker
Stegmaier, Christa
Miron, Penelope
Yannoukakos, Drakoulis
Stavropoulou, Alexandra
Fountzilas, George
Gogas, Helen J.
Swann, Ruth
Dwek, Miriam
Perkins, Annie
Milne, Roger L.
Benitez, Javier
Pilar Zamora, Maria
Arias Perez, Jose Ignacio
Bojesen, Stig E.
Nielsen, Sune F.
Nordestgaard, Borge G.
Flyger, Henrik
Guenel, Pascal
Therese Truong
Menegaux, Florence
Cordina-Duverger, Emilie
Burwinkel, Barbara
Marme, Frederick
Schneeweiss, Andreas
Sohn, Christof
Sawyer, Elinor
Tomlinson, Ian
Kerin, Michael J.
Peto, Julian
Johnson, Nichola
Fletcher, Olivia
dos Santos Silva, Isabel
Fasching, Peter A.
Beckmann, Matthias W.
Hartmann, Arndt
Ekici, Arif B.
Lophatananon, Artitaya
Muir, Kenneth
Puttawibul, Puttisak
Wiangnon, Surapon
Schmidt, Marjanka K.
Broeks, Annegien
Braaf, Linde M.
Rosenberg, Efraim H.
Hopper, John L.
Apicella, Carmel
Park, Daniel J.
Southey, Melissa C.
Swerdlow, Anthony J.
Ashworth, Alan
Orr, Nicholas
Schoemaker, Minouk J.
Anton-Culver, Hoda
Ziogas, Argyrios
Bernstein, Leslie
Dur, Christina Clarke
Shen, Chen-Yang
Yu, Jyh-Cherng
Hsu, Huan-Ming
Hsiung, Chia-Ni
Hamann, Ute
Duennebier, Thomas
Ruediger, Thomas
Ulmer, Hans Ulrich
Pharoah, Paul P.
Dunning, Alison M.
Humphreys, Manjeet K.
Wang, Qin
Cox, Angela
Cross, Simon S.
Reed, Malcom W.
Hall, Per
Czene, Kamila
Ambrosone, Christine B.
Ademuyiwa, Foluso
Hwang, Helena
Eccles, Diana M.
Garcia-Closas, Montserrat
Figueroa, Jonine D.
Sherman, Mark E.
Lissowska, Jolanta
Devilee, Peter
Seynaeve, Caroline
Tollenaar, Rob A. E. M.
Hooning, Maartje J.
Andrulis, Irene L.
Knight, Julia A.
Glendon, Gord
Mulligan, Anna Marie
Winqvist, Robert
Pylkas, Katri
Jukkola-Vuorinen, Arja
Grip, Mervi
John, Esther M.
Miron, Alexander
Alnaes, Grethe Grenaker
Kristensen, Vessela
Borresen-Dale, Anne-Lise
Giles, Graham G.
Baglietto, Laura
McLean, Catriona A.
Severi, Gianluca
Kosel, Matthew L.
Pankratz, V. S.
Slager, Susan
Olson, Janet E.
Radice, Paolo
Peterlongo, Paolo
Manoukian, Siranoush
Barile, Monica
Lambrechts, Diether
Hatse, Sigrid
Dieudonne, Anne-Sophie
Christiaens, Marie-Rose
Chenevix-Trench, Georgia
Beesley, Jonathan
Chen, Xiaoqing
Mannermaa, Arto
Kosma, Veli-Matti
Hartikainen, Jaana M.
Soini, Ylermi
Easton, Douglas F.
Couch, Fergus J.
CA GENICA Network
kConFab Investigators
AOCS Grp
TI 19p13.1 Is a Triple-Negative-Specific Breast Cancer Susceptibility Locus
SO CANCER RESEARCH
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COMMON VARIANTS; RISK-FACTORS; CONFER
SUSCEPTIBILITY; 14Q24.1 RAD51L1; TUMOR SUBTYPES; BRCA1; POPULATION;
CONSORTIUM; COMPLEX
AB The 19p13.1 breast cancer susceptibility locus is a modifier of breast cancer risk in BRCA1 mutation carriers and is also associated with the risk of ovarian cancer. Here, we investigated 19p13.1 variation and risk of breast cancer subtypes, defined by estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) status, using 48,869 breast cancer cases and 49,787 controls from the Breast Cancer Association Consortium (BCAC). Variants from 19p13.1 were not associated with breast cancer overall or with ER-positive breast cancer but were significantly associated with ER-negative breast cancer risk [rs8170 OR, 1.10; 95% confidence interval (CI), 1.05-1.15; P = 3.49 x 10(-5)] and triple-negative (ER-, PR-, and HER2-negative) breast cancer (rs8170: OR, 1.22; 95% CI, 1.13-1.31; P = 2.22 x 10(-7)). However, rs8170 was no longer associated with ER-negative breast cancer risk when triple-negative cases were excluded (OR, 0.98; 95% CI, 0.89-1.07; P = 0.62). In addition, a combined analysis of triple-negative cases from BCAC and the Triple Negative Breast Cancer Consortium (TNBCC; N = 3,566) identified a genome-wide significant association between rs8170 and triple-negative breast cancer risk (OR, 1.25; 95% CI, 1.18-1.33; P = 3.31 x 10-(13)]. Thus, 19p13.1 is the first triple-negativespecific breast cancer risk locus and the first locus specific to a histologic subtype defined by ER, PR, and HER2 to be identified. These findings provide convincing evidence that genetic susceptibility to breast cancer varies by tumor subtype and that triple-negative tumors and other subtypes likely arise through distinct etiologic pathways. Cancer Res; 72(7); 1795-803. (C)2012 AACR.
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[Sinn, Hans-Peter] Univ Heidelberg Hosp, Dept Pathol, Heidelberg, Germany.
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[Bartram, Claus R.] Univ Heidelberg, Inst Human Genet, Heidelberg, Germany.
[Marme, Frederick; Schneeweiss, Andreas] Univ Heidelberg, Natl Ctr Tumor Dis, Heidelberg, Germany.
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[Flesch-Janys, Dieter] Univ Clin Hamburg Eppendorf, Inst Med Biometr & Epidemiol, Hamburg, Germany.
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[Brauch, Hiltrud] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-7000 Stuttgart, Germany.
[Brauch, Hiltrud] Univ Tubingen, Tubingen, Germany.
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[GENICA Network] German Social Accid Insurance IPA, Inst Prevent & Occupat Med, Bochum, Germany.
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[Guenel, Pascal; Therese Truong; Menegaux, Florence; Cordina-Duverger, Emilie] CESP Ctr Res Epidemiol & Populat Hlth, INSERM, U1018, Villejuif, France.
[Guenel, Pascal; Therese Truong; Menegaux, Florence; Cordina-Duverger, Emilie] Univ Paris Sud, UMRS1018, Villejuif, France.
[Tomlinson, Ian] Univ Oxford, Welcome Trust Ctr Human Genet, Oxford, England.
[Tomlinson, Ian] Univ Oxford, Oxford Biomed Res Ctr, Oxford, England.
[Kerin, Michael J.] Univ Hosp Galway, Inst Clin Sci, NUIG Dept Surg, Galway, Ireland.
[Fasching, Peter A.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med, Div Hematol & Oncol, Los Angeles, CA 90095 USA.
[Fasching, Peter A.; Beckmann, Matthias W.] Univ Breast Ctr Franconia, Dept Gynecol & Obstet, Erlangen, Germany.
[Ekici, Arif B.] Univ Erlangen Nurnberg, Inst Human Genet, Erlangen, Germany.
[Hartmann, Arndt] Univ Hosp Erlangen, Inst Pathol, Erlangen, Germany.
[Lophatananon, Artitaya; Muir, Kenneth] Univ Warwick, Warwick Med Sch, Hlth Sci Res Inst, Coventry CV4 7AL, W Midlands, England.
[Puttawibul, Puttisak] Prince Songkla Univ, Sch Med, Dept Surg, Hat Yai, Thailand.
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[Swerdlow, Anthony J.; Schoemaker, Minouk J.] Inst Canc Res, Epidemiol Sect, Sutton, Surrey, England.
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[Cox, Angela; Reed, Malcom W.] Univ Sheffield, Dept Oncol, Fac Med Dent & Hlth, Sheffield, S Yorkshire, England.
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[Chenevix-Trench, Georgia; Beesley, Jonathan; Chen, Xiaoqing; AOCS Grp] Queensland Inst Med Res, Herston, Qld 4006, Australia.
[Mannermaa, Arto; Kosma, Veli-Matti; Hartikainen, Jaana M.; Soini, Ylermi] Univ Eastern Finland, Dept Pathol, Inst Clin Med, Kuopio, Finland.
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RP Couch, FJ (reprint author), Mayo Clin, Dept Lab Med & Pathol, Stabile 2-42,200 1st St SW, Rochester, MN 55905 USA.
EM couch.fergus@mayo.edu
RI manoukian, siranoush/E-7132-2017; Shen, CY/F-6271-2010; Verdrengh,
Evelien/H-4571-2012; truong, therese/A-2837-2013; Kerin,
Michael/D-6748-2013; Ekici, Arif/C-3971-2013; Andrulis,
Irene/E-7267-2013; Radice, Paolo/O-3119-2013; Knight, Julia/A-6843-2012;
Garcia-Closas, Montserrat /F-3871-2015; Hartikainen, Jaana/E-6256-2015;
Vrieling, Alina/A-2725-2016; Bowtell, David/H-1007-2016; Brenner,
Hermann/B-4627-2017
OI ADEMUYIWA, FOLUSO/0000-0002-6766-2258; Giles,
Graham/0000-0003-4946-9099; Arndt, Volker/0000-0001-9320-8684;
Schoemaker, Minouk/0000-0001-8403-2234; Greco,
Dario/0000-0001-9195-9003; Czene, Kamila/0000-0002-3233-5695; Rosenberg,
Efraim/0000-0002-3859-6941; Cross, Simon/0000-0003-2044-1754; Lissowska,
Jolanta/0000-0003-2695-5799; Dunning, Alison
Margaret/0000-0001-6651-7166; Nevanlinna, Heli/0000-0002-0916-2976; dos
Santos Silva, Isabel/0000-0002-6596-8798; Cox,
Angela/0000-0002-5138-1099; Yannoukakos, Drakoulis/0000-0001-7509-3510;
Park, Daniel/0000-0002-6354-0931; manoukian,
siranoush/0000-0002-6034-7562; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Bowtell, David/0000-0001-9089-7525; Brenner,
Hermann/0000-0002-6129-1572
FU NIH [CA122340, RFA-CA-06-503, R01 CA77398, CA58860, CA92044]; SPORE
[CA116201]; Komen Foundation for the Cure; Breast Cancer Research
Foundation (BCRF); Cancer Research UK [C1287/A10118, C1287/A12014];
European Community [223175, HEALTH-F2-2009-223175]; European Union COST
[BM0606]; Institute for Cancer Studies; ABCS; Dutch Cancer Society [NKI
2009-4363, NKI 2007-3839]; Dutch National Genomics Initiative; ACP:
Breast Cancer Research Trust, UK; National Institute for Health Research
(NIHR) Comprehensive Biomedical Research Centre; Guy's & St. Thomas' NHS
Foundation; Oxford Biomedical Research Centre; ABCFS; NC-BCFR; OFBCR;
National Cancer Institute; Cancer Care Ontario [U01 CA69467]; Northern
California Cancer Center [U01 CA69417]; University of Melbourne [U01
CA69638]; ABCFS: National Health and Medical Research Council of
Australia; New South Wales Cancer Council; Victorian Health Promotion
Foundation (Australia); Victorian Breast Cancer Research Consortium;
Asociacion Espanola Contra el Cancer; Fondo de Investigacion Sanitario
[PI081583, PI081120]; The California Teachers Study; California Breast
Cancer Act of 1993; Lon V Smith Foundation [LVS39420]; California Breast
Cancer Research Fund [97-10500]; UCIBCS; ESTHER; Baden Wurttemberg
Ministry of Science; German Cancer Aid (Deutsche Krebshilfe)
FX This work was supported by the NIH grant CA122340, a Specialized Program
of Research Excellence (SPORE) in Breast Cancer (CA116201), the Komen
Foundation for the Cure and the Breast Cancer Research Foundation
(BCRF); the BCAC is funded by Cancer Research UK (C1287/A10118 and
C1287/A12014), by the European Community's Seventh Framework Programme
under grant agreement no. 223175 (HEALTH-F2-2009-223175; COGS), and by
the European Union COST programme (BM0606). D.F. Easton is a Principal
Research Fellow of Cancer Research UK; SBCS: Breast Cancer Campaign
(2004 Nov 49 to A. Cox) and Yorkshire Cancer Research Core Funding
(Institute for Cancer Studies); ABCS: Dutch Cancer Society grant (NKI
2009-4363 and NKI 2007-3839 to M.K. Schmidt) and the Dutch National
Genomics Initiative; ACP: Breast Cancer Research Trust, UK. E. Sawyer is
funded by National Institute for Health Research (NIHR) Comprehensive
Biomedical Research Centre, Guy's & St. Thomas' NHS Foundation Trust in
partnership with King's College London. I. Tomlinson is funded by the
Oxford Biomedical Research Centre; ABCFS, NC-BCFR and OFBCR: National
Cancer Institute, NIH under RFA-CA-06-503, and through cooperative
agreements with members of the Breast Cancer Family Registry (BCFR) and
Principal Investigators, including Cancer Care Ontario (U01 CA69467),
Northern California Cancer Center (U01 CA69417), University of Melbourne
(U01 CA69638); ABCFS: National Health and Medical Research Council of
Australia, the New South Wales Cancer Council, the Victorian Health
Promotion Foundation (Australia), and the Victorian Breast Cancer
Research Consortium. J.L. Hopper is a National Health and Medical
Research Council (NHMRC) Australia Fellow and a Victorian Breast Cancer
Research Consortium Group Leader. M.C. Southey is an NHMRC Senior
Research Fellow and a Victorian Breast Cancer Research Consortium Group
Leader; CNIO-BCS: Genome Spain Foundation, the Red Tematica de
Investigacion Cooperativa en Cancer and grants from the Asociacion
Espanola Contra el Cancer and the Fondo de Investigacion Sanitario
(PI081583 and PI081120); The California Teachers Study: California
Breast Cancer Act of 1993, NIH (R01 CA77398), the Lon V Smith Foundation
[LVS39420]), and the California Breast Cancer Research Fund (contract
97-10500); UCIBCS: NIH (CA58860 and CA92044) and the Lon V Smith
Foundation (LVS39420); ESTHER: Baden Wurttemberg Ministry of Science,
Research and Arts, and the VERDI study supported by a grant from the
German Cancer Aid (Deutsche Krebshilfe); GENICA: Federal Ministry of
Education and Research (BMBF) Germany (01KW9975/5, 01KW9976/8,
01KW9977/0 and 01KW0114), the Robert Bosch Foundation, Stuttgart,
Deutsches Krebsforschungszentrum (DKFZ) Heidelberg, Institute for
Prevention and Occupational Medicine of the German Social Accident
Insurance (IPA), Bochum, and the Department of Internal Medicine,
Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany:
KBCP: Finnish Cancer Society, the Academy of Finland (grant number
127220), the special Government Funding (EVO) of Kuopio University
Hospital (grant number 5654113 and 5501) and by the strategic funding of
the University of Eastern Finland; OBCS: Finnish Cancer Foundation, the
Academy of Finland, the University of Oulu, the Oulu University Hospital
and Biocenter Oulu; RPCI: P30 grant to RPCI (CA016056-32); The
Breakthrough Generations Study: Breakthrough Breast Cancer and the
Institute of Cancer Research (ICR).; ICR acknowledges NHS funding to the
NIHR Biomedical Research Centre; PBCS: Intramural Research Funds of the
National Cancer Institute, Bethesda, MD; HEBCS: Helsinki University
Central Hospital Research Fund, Academy of Finland (132473), the Finnish
Cancer Society, and the Sigrid Juselius Foundation; MARIE: Deutsche
Krebshilfe e.V., grant number 70-2892-BR I, the Hamburg Cancer Society,
the German Cancer Research Center (DKFZ), and the Federal Ministry of
Education and Research (BMBF) Germany grant 01KH0402; GESBC: Deutsche
Krebshilfe e. V. (70492) and the state of Baden-Wurttemberg through the
Medical Faculty of the University of Ulm (P.685); BSUCH: Dietmar Hopp
Foundation, the German Cancer Research Center, DKFZ, and the Helmholtz
association; GC-HBOC: Deutsche Krebshilfe (107054), the Center of
Molecular Medicine, Cologne, the German Cancer Research Center, DKFZ,
and the Helmholtz society; BBCS: Cancer Research UK, Breakthrough Breast
Cancer and the National Cancer Research Network (NCRN); kConFab:
National Breast Cancer Foundation, the National Health and Medical
Research Council (NHMRC) and by the Queensland Cancer Fund, the Cancer
Councils of New South Wales, Victoria, Tasmania, and South Australia,
the Cancer Foundation of Western Australia, and Cancer Australia
#628333; LMBC: 'Stichting tegen Kanker' (232-2008 and 196-2010); MCCS:
Australian National Health and Medical Research Council (grants #209057,
251533, 396414, and 504711), Cancer Council Victoria, and VicHealth;
ORIGO: Dutch Cancer Society; SEARCH: Cancer Research UK (C8197/A10123,
C8197/A10123, and C490/A10124). A.M. Dunning was supported by Cancer
Research UK grant (C8197/A10865) and by the Joseph Mitchell Fund; FCCC:
NIH (U01 CA69631, 5U01 CA113916 to A.K. Godwin), the Eileen Stein Jacoby
Fund, The University of Kansas Cancer Center, and the Kansas Bioscience
Authority Eminent Scholar Program. A.K. Godwin is the Chancellors
Distinguished Chair in Biomedical Sciences endowed Professor.
NR 24
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U1 1
U2 12
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD APR 1
PY 2012
VL 72
IS 7
BP 1795
EP 1803
DI 10.1158/0008-5472.CAN-11-3364
PG 9
WC Oncology
SC Oncology
GA 922MO
UT WOS:000302551800022
PM 22331459
ER
PT J
AU Chen, KG
Sikic, BI
AF Chen, Kevin G.
Sikic, Branimir I.
TI Molecular Pathways: Regulation and Therapeutic Implications of Multidrug
Resistance
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; PHASE-I TRIAL; HUMAN MDR1 GENE; P-GLYCOPROTEIN
EXPRESSION; BREAST-CANCER CELLS; TRANSCRIPTIONAL REGULATION;
LYMPHOCYTIC-LEUKEMIA; EPIGENETIC CHANGES; DRUG-RESISTANCE; PROMOTER
REGION
AB Multidrug transporters constitute major mechanisms of MDR in human cancers. The ABCB1 (MDR1) gene encodes a well-characterized transmembrane transporter, termed P-glycoprotein (P-gp), which is expressed in many normal human tissues and cancers. P-gp plays a major role in the distribution and excretion of drugs and is involved in intrinsic and acquired drug resistance of cancers. The regulation of ABCB1 expression is complex and has not been well studied in a clinical setting. In this review, we elucidate molecular signaling and epigenetic interactions that govern ABCB1 expression and the development of MDR in cancer. We focus on acquired expression of ABCB1 that is associated with genomic instability of cancer cells, including mutational events that alter chromatin structures, gene rearrangements, and mutations in tumor suppressor proteins (e. g., mutant p53), which guard the integrity of genome. In addition, epigenetic modifications of the ABCB1 proximal and far upstream promoters by either demethylation of DNA or acetylation of histone H3 play a pivotal role in inducing ABCB1 expression. We describe a molecular network that coordinates genetic and epigenetic events leading to the activation of ABCB1. These mechanistic insights provide additional translational targets and potential strategies to deal with clinical MDR. Clin Cancer Res; 18(7); 1863-9. (C) 2012 AACR.
C1 [Chen, Kevin G.; Sikic, Branimir I.] Stanford Univ, Dept Med, Div Oncol, Sch Med, Stanford, CA 94305 USA.
[Chen, Kevin G.] Natl Inst Neurol Disorders & Stroke, NIH Stem Cell Unit, NIH, Bethesda, MD USA.
RP Sikic, BI (reprint author), Stanford Univ, Dept Med, Div Oncol, Sch Med, CCSR 1105, Stanford, CA 94305 USA.
EM brandy@stanford.edu
RI Chen, Kevin/D-6769-2011
OI Chen, Kevin/0000-0003-2983-6330
FU National Cancer Institute [CA09302]; NIH [R01 CA52168, R01 CA92474];
General Clinical Research Center, Stanford University [M01 RR0070]
FX This work was supported by National Cancer Institute grant CA09302 (K.G.
Chen), NIH grants R01 CA52168 and R01 CA92474 (B. I. Sikic), and M01
RR0070 (General Clinical Research Center, Stanford University).
NR 68
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U2 22
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 APR 1
PY 2012
VL 18
IS 7
BP 1863
EP 1869
DI 10.1158/1078-0432.CCR-11-1590
PG 7
WC Oncology
SC Oncology
GA 922LX
UT WOS:000302549900008
PM 22344233
ER
PT J
AU Lockwood, WW
Thu, KL
Lin, L
Pikor, LA
Chari, R
Lam, WL
Beer, DG
AF Lockwood, William W.
Thu, Kelsie L.
Lin, Lin
Pikor, Larissa A.
Chari, Raj
Lam, Wan L.
Beer, David G.
TI Integrative Genomics Identified RFC3 As an Amplified Candidate Oncogene
in Esophageal Adenocarcinoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID REPLICATION-FACTOR-C; NUCLEOTIDE POLYMORPHISM ARRAYS; SQUAMOUS-CELL
CARCINOMA; COPY NUMBER ALTERATIONS; BARRETTS-ESOPHAGUS;
CHROMOSOMAL-ABERRATIONS; GASTRIC CARDIA; N-MYC; HYBRIDIZATION; CANCER
AB Purpose: Esophageal adenocarcinoma (EAC) is a lethal malignancy that can develop from the premalignant condition, Barrett's esophagus (BE). Currently, there are no validated simple methods to predict which patients will progress to EAC. A better understanding of the genetic mechanisms driving EAC tumorigenesis is needed to identify new therapeutic targets and develop biomarkers capable of identifying high-risk patients that would benefit from aggressive neoadjuvant therapy. We employed an integrative genomics approach to identify novel genes involved inEAC biology that may serve as useful clinical markers.
Experimental Design: Whole genome tiling-path array comparative genomic hybridization was used to identify significant regions of copy number alteration in 20 EACs and 10 matching BE tissues. Copy number and gene expression data were integrated to identify candidate oncogenes within regions of amplification and multiple additional sample cohorts were assessed to validate candidate genes.
Results: We identified RFC3 as a novel, candidate oncogene activated by amplification in approximately 25% of EAC samples. RFC3 was also amplified in BE from a patient whose EAC harbored amplification and was differentially expressed between nonmalignant and EAC tissues. Copy number gains were detected in other cancer types and RFC3 knockdown inhibited proliferation and anchorage-independent growth of cancer cells with increased copy number but had little effect on those without. Moreover, high RFC3 expression was associated with poor patient outcome in multiple cancer types.
Conclusions: RFC3 is a candidate oncogene amplified in EAC. RFC3 DNA amplification is also prevalent in other epithelial cancer types and RFC3 expression could serve as a prognostic marker. Clin Cancer Res; 18(7); 1936-46. (C) 2012 AACR.
C1 [Lockwood, William W.; Thu, Kelsie L.; Pikor, Larissa A.; Chari, Raj; Lam, Wan L.] British Columbia Canc Res Ctr, Vancouver, BC V5Z 1L3, Canada.
[Lin, Lin; Beer, David G.] Univ Michigan, Dept Surg, Ann Arbor, MI 48109 USA.
RP Lockwood, WW (reprint author), NHGRI, Canc Genet Branch, NIH, 50 South Dr, Bethesda, MD 20892 USA.
EM william.lockwood@nih.gov
FU Canadian Institutes of Health Research; Canadian Cancer Society
FX This work was supported by the Canadian Institutes of Health Research
(W. L. Lam), Canadian Cancer Society (W. L. Lam), and Canadian
Institutes of Health Research Vanier Canada Graduate Scholarships (K. L.
Thu and L. A. Pikor), and CIHR Jean-Francois Saint Denis Fellowship in
Cancer Research (W. W. Lockwood).
NR 47
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U1 1
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD APR 1
PY 2012
VL 18
IS 7
BP 1936
EP 1946
DI 10.1158/1078-0432.CCR-11-1431
PG 11
WC Oncology
SC Oncology
GA 922LX
UT WOS:000302549900015
PM 22328562
ER
PT J
AU Chapman, CM
Sun, XM
Roschewski, M
Aue, G
Farooqui, M
Stennett, L
Gibellini, F
Arthur, D
Perez-Galan, P
Wiestner, A
AF Chapman, Colby M.
Sun, Xiameng
Roschewski, Mark
Aue, Georg
Farooqui, Mohamed
Stennett, Lawrence
Gibellini, Federica
Arthur, Diane
Perez-Galan, Patricia
Wiestner, Adrian
TI ON 01910.Na Is Selectively Cytotoxic for Chronic Lymphocytic Leukemia
Cells through a Dual Mechanism of Action Involving PI3K/AKT Inhibition
and Induction of Oxidative Stress
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID SMALL-MOLECULE INHIBITOR; CLL-B-CELLS; INDUCED APOPTOSIS; THERAPEUTIC
APPROACH; MEDIATED MECHANISM; LYMPHOMA-CELLS; CANCER-CELLS; RECEPTOR;
ROS; PROLIFERATION
AB Purpose: Chronic lymphocytic leukemia (CLL), a malignancy of mature B cells, is incurable with chemotherapy. Signals from the microenvironment support leukemic cell survival and proliferation and may confer chemotherapy resistance. ON 01910.Na (Rigosertib), a multikinase phosphoinositide 3-kinase (PI3K) inhibitor, is entering phase III trials for myelodysplastic syndrome. Our aim was to analyze the efficacy of ON 01910.Na against CLL cells in vitro and investigate the molecular effects of this drug on tumor biology.
Experimental Design: Cytotoxicity of ON 01910.Na against CLL cells from 34 patients was determined in vitro with flow cytometry of cells stained with Annexin V and CD19. Global gene expression profiling on Affymetrix microarrays, flow cytometry, Western blotting, and cocultures with stroma cells were used to delineate ON 01910.Na mechanism of action.
Results: ON 01910.Na induced apoptosis in CLL B cells without significant toxicity against T cells or normal B cells. ON 01910.Na was equally active against leukemic cells associated with a more aggressive disease course [immunoglobulin heavy-chain variable region unmutated, adverse cytogenetics] than against cells without these features. Gene expression profiling revealed two main mechanisms of action: PI3K/AKT inhibition and induction of ROS that resulted in an oxidative stress response through activating protein 1 (AP-1), c-jun-NH2-terminal kinase, and ATF3 culminating in the upregulation of NOXA. ROS scavengers and shRNA mediated knockdown of ATF3- and NOXA-protected cells from drug-induced apoptosis. ON 01910.Na also abrogated the prosurvival effect of follicular dendritic cells on CLL cells and reduced SDF-1-induced migration of leukemic cells.
Conclusions: These data support the clinical development of ON 01910.Na in CLL. Clin Cancer Res; 18(7); 1979-91. (C) 2012 AACR.
C1 [Chapman, Colby M.; Sun, Xiameng; Roschewski, Mark; Aue, Georg; Farooqui, Mohamed; Stennett, Lawrence; Gibellini, Federica; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Arthur, Diane] NCI, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Perez-Galan, Patricia] IDIBAPS, Ctr Esther Koplowitz, Dept Hematooncol, Barcelona 08036, Spain.
RP Wiestner, A (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,CRC 3-5140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM pperez@clinic.ub.es; wiestnea@nhlbi.nih.gov
OI Roschewski, Mark/0000-0003-0278-2635
FU National, Heart, Lung and Blood Institute; National Cancer Institute,
NIH; Spanish Ministry of Science and Innovation [RYC2009-05134]
FX This work was supported by the Intramural Research Program of the
National, Heart, Lung and Blood Institute and the National Cancer
Institute, NIH and the Spanish Ministry of Science and Innovation
(RYC2009-05134).
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U2 9
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 APR 1
PY 2012
VL 18
IS 7
BP 1979
EP 1991
DI 10.1158/1078-0432.CCR-11-2113
PG 13
WC Oncology
SC Oncology
GA 922LX
UT WOS:000302549900019
PM 22351695
ER
PT J
AU Prieto, PA
Yang, JC
Sherry, RM
Hughes, MS
Kammula, US
White, DE
Levy, CL
Rosenberg, SA
Phan, GQ
AF Prieto, Peter A.
Yang, James C.
Sherry, Richard M.
Hughes, Marybeth S.
Kammula, Udai S.
White, Donald E.
Levy, Catherine L.
Rosenberg, Steven A.
Phan, Giao Q.
TI CTLA-4 Blockade with Ipilimumab: Long-term Follow-up of 177 Patients
with Metastatic Melanoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID LYMPHOCYTE-ASSOCIATED ANTIGEN-4; HIGH-DOSE INTERLEUKIN-2; REGULATORY
T-CELLS; RECOMBINANT INTERLEUKIN-2; COMPLETE RESPONSES; CANCER
REGRESSION; TUMOR-REGRESSION; PHASE-I/II; AUTOIMMUNITY; EFFICACY
AB Purpose: Treatment with ipilimumab can cause objective tumor responses in patients with metastatic melanoma. We have treated 177 evaluable patients in three clinical trials and have long-term follow-up to evaluate the durability of responses.
Experimental Design: Patients with metastatic melanoma were treated in three trials from 2002 to 2005. In protocol 1, 56 patients received ipilimumab with gp100 peptides. In protocol 2, 36 patients received ipilimumab with interleukin-2. In protocol 3, 85 patients received ipilimumab with intrapatient dose-escalation and were randomized to receive gp100 peptides. We have analyzed their long-term follow-up and survival data.
Results: With median follow-up for protocols 1, 2, and 3 being 92, 84, and 71 months, median survival was 14, 16, and 13 months with 5-year survival rates being 13%, 25%, and 23%, respectively. Patients in protocol 2 had a 17% complete response (CR) rate, compared with 7% in protocol 1 and 6% in protocol 3. These CR rates are higher than previously reported for the same trials because some patients who eventually became complete responders had continual tumor regression months to years after therapy. All but one of the 15 complete responders are ongoing at 54+ to 99+ months.
Conclusions: This report provides the longest follow-up of patients with melanoma treated with ipilimumab and shows that ipilimumab can induce durable, potentially curative tumor regression in a small percentage of patients with metastatic melanoma. The combination of ipilimumab and interleukin-2 seems to have an increased CR rate, but this needs to be tested in a randomized trial. Clin Cancer Res; 18(7); 2039-47. (C) 2012 AACR.
C1 [Prieto, Peter A.; Yang, James C.; Sherry, Richard M.; Hughes, Marybeth S.; Kammula, Udai S.; White, Donald E.; Levy, Catherine L.; Rosenberg, Steven A.; Phan, Giao Q.] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Phan, GQ (reprint author), NCI, Surg Branch, Ctr Canc Res, NIH, Bldg 10 CRC,Room 3-5760,10 Ctr Dr, Bethesda, MD 20892 USA.
EM Giao.Phan@nih.gov
FU NIH
FX This work was supported by NIH.
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U1 2
U2 15
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 APR 1
PY 2012
VL 18
IS 7
BP 2039
EP 2047
DI 10.1158/1078-0432.CCR-11-1823
PG 9
WC Oncology
SC Oncology
GA 922LX
UT WOS:000302549900025
PM 22271879
ER
PT J
AU Peer, CJ
Sissung, TM
Kim, A
Jain, L
Woo, S
Gardner, ER
Kirkland, CT
Troutman, SM
English, BC
Richardson, ED
Federspiel, J
Venzon, D
Dahut, W
Kohn, E
Kummar, S
Yarchoan, R
Giaccone, G
Widemann, B
Figg, WD
AF Peer, Cody J.
Sissung, Tristan M.
Kim, AeRang
Jain, Lokesh
Woo, Sukyung
Gardner, Erin R.
Kirkland, C. Tyler
Troutman, Sarah M.
English, Bevin C.
Richardson, Emily D.
Federspiel, Joel
Venzon, David
Dahut, William
Kohn, Elise
Kummar, Shivaani
Yarchoan, Robert
Giaccone, Giuseppe
Widemann, Brigitte
Figg, William D.
TI Sorafenib Is an Inhibitor of UGT1A1 but Is Metabolized by UGT1A9:
Implications of Genetic Variants on Pharmacokinetics and
Hyperbilirubinemia
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID CRIGLER-NAJJAR; PHASE-I; UDP-GLUCURONOSYLTRANSFERASE;
ANTITUMOR-ACTIVITY; PROSTATE-CANCER; GLUCURONIDATION; BILIRUBIN;
THERAPY; TRIAL; BEVACIZUMAB
AB Purpose: Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase). We hypothesized that sorafenib inhibits UGT1A1 and individuals carrying UGT1A1*28 and/or UGT1A9 variants experience greater sorafenib exposure and greater increase in sorafenib-induced plasma bilirubin concentration.
Experimental Design: Inhibition of UGT1A1-mediated bilirubin glucuronidation by sorafenib was assessed in vitro. UGT1A1*28 and UGT1A9*3 genotypes were ascertained with fragment analysis or direct sequencing in 120 cancer patients receiving sorafenib on five different clinical trials. Total bilirubin measurements were collected in prostate cancer patients before receiving sorafenib (n=41) and 19 to 30 days following treatment and were compared with UGT1A1*28 genotype.
Results: Sorafenib exhibited mixed-mode inhibition of UGT1A1-mediated bilirubin glucuronidation (IC50 = 18 mu mol/L; K-i = 11.7 mu mol/L) in vitro. Five patients carrying UGT1A1*28/*28 (n = 4) or UGT1A9*3/*3 (n 1) genotypes had first dose, dose-normalized areas under the sorafenib plasma concentration versus time curve (AUC) that were in the 93rd percentile, whereas three patients carrying UGT1A1*28/*28 had AUCs in the bottom quartile of all genotyped patients. The Drug Metabolizing Enzymes and Transporters genotyping platform was applied to DNA obtained from six patients, which revealed the ABCC2-24C>T genotype cosegregated with sorafenib AUC phenotype. Sorafenib exposure was related to plasma bilirubin increases in patients carrying 1 or 2 copies of UGT1A1*28 alleles (n = 12 and n = 5; R-2 = 0.38 and R-2 = 0.77; P = 0.032 and P = 0.051, respectively). UGT1A1*28 carriers showed two distinct phenotypes that could be explained by ABCC2-24C>T genotype and are more likely to experience plasma bilirubin increases following sorafenib if they had high sorafenib exposure.
Conclusions: This pilot study indicates that genotype status of UGT1A1, UGT1A9, and ABCC2 and serum bilirubin concentration increases reflect abnormally highAUCin patients treated with sorafenib. Clin Cancer Res; 18(7); 2099-107. (C) 2012 AACR.
C1 [Figg, William D.] NCI, Med Oncol Branch, CCR, NIH,Clin Pharmacol Program, Bethesda, MD 20892 USA.
[Kim, AeRang; Widemann, Brigitte] NCI, Pharmacol & Expt Therapeut Sect, Bethesda, MD 20892 USA.
[Kirkland, C. Tyler; Troutman, Sarah M.; English, Bevin C.; Richardson, Emily D.; Figg, William D.] NCI, Mol Pharmacol Sect, Bethesda, MD 20892 USA.
[Venzon, David] NCI, Biostat & Data Management Branch, Bethesda, MD 20892 USA.
[Dahut, William; Kohn, Elise; Kummar, Shivaani; Giaccone, Giuseppe] NCI, Med Oncol Branch, Bethesda, MD 20892 USA.
[Yarchoan, Robert] NCI, HIV AIDS Malignancy Branch, Bethesda, MD 20892 USA.
RP Figg, WD (reprint author), NCI, Med Oncol Branch, CCR, NIH,Clin Pharmacol Program, 9000 Rockville Pike,Bldg 10,Room 5A01, Bethesda, MD 20892 USA.
EM wf13e@nih.gov
RI Figg Sr, William/M-2411-2016; Giaccone, Giuseppe/E-8297-2017
OI Giaccone, Giuseppe/0000-0002-5023-7562
NR 32
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U1 2
U2 4
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 APR 1
PY 2012
VL 18
IS 7
BP 2099
EP 2107
DI 10.1158/1078-0432.CCR-11-2484
PG 9
WC Oncology
SC Oncology
GA 922LX
UT WOS:000302549900031
PM 22307138
ER
PT J
AU Narva, AS
AF Narva, Andrew S.
TI Decision Support and CKD: Not There Yet
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Editorial Material
ID PRIMARY-CARE
C1 NIDDKD, Natl Kidney Dis Educ Program, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD 20892 USA.
RP Narva, AS (reprint author), NIDDKD, Natl Kidney Dis Educ Program, Div Kidney Urol & Hematol Dis, NIH, 2 Democracy Pl,Room 645,6707 Democracy Blvd, Bethesda, MD 20892 USA.
EM narvaa@nidclk.nih.gov
NR 9
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Z9 5
U1 0
U2 0
PU AMER SOC NEPHROLOGY
PI WASHINGTON
PA 1725 I ST, NW STE 510, WASHINGTON, DC 20006 USA
SN 1555-9041
J9 CLIN J AM SOC NEPHRO
JI Clin. J. Am. Soc. Nephrol.
PD APR
PY 2012
VL 7
IS 4
BP 525
EP 526
DI 10.2215/CJN.02140212
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 918WK
UT WOS:000302281900001
PM 22422537
ER
EF