FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Sharov, AA
Nishiyama, A
Piao, YL
Correa-Cerro, LS
Amano, T
Thomas, M
Mehta, S
Ko, MSH
AF Sharov, Alexei A.
Nishiyama, Akira
Piao, Yulan
Correa-Cerro, Lina S.
Amano, Tomokazu
Thomas, Marshall
Mehta, Samir
Ko, Minoru S. H.
TI Responsiveness of genes to manipulation of transcription factors in ES
cells is associated with histone modifications and tissue specificity
SO BMC GENOMICS
LA English
DT Article
ID EMBRYONIC STEM-CELLS; RNA-POLYMERASE-II; CPG ISLANDS; MOUSE; GENOME;
METHYLATION; PLURIPOTENT; EXPRESSION; STATE; SET2
AB Background: In addition to determining static states of gene expression (high vs. low), it is important to characterize their dynamic status. For example, genes with H3K27me3 chromatin marks are not only suppressed but also poised for activation. However, the responsiveness of genes to perturbations has never been studied systematically. To distinguish gene responses to specific factors from responsiveness in general, it is necessary to analyze gene expression profiles of cells responding to a large variety of disturbances, and such databases did not exist before.
Results: We estimated the responsiveness of all genes in mouse ES cells using our recently published database on expression change after controlled induction of 53 transcription factors (TFs) and other genes. Responsive genes (N = 4746), which were readily upregulated or downregulated depending on the kind of perturbation, mostly have regulatory functions and a propensity to become tissue-specific upon differentiation. Tissue-specific expression was evaluated on the basis of published (GNF) and our new data for 15 organs and tissues. Non-responsive genes (N = 9562), which did not change their expression much following any perturbation, were enriched in housekeeping functions. We found that TF-responsiveness in ES cells is the best predictor known for tissue-specificity in gene expression. Among genes with CpG islands, high responsiveness is associated with H3K27me3 chromatin marks, and low responsiveness is associated with H3K36me3 chromatin, stronger tri-methylation of H3K4, binding of E2F1, and GABP binding motifs in promoters.
Conclusions: We thus propose the responsiveness of expression to perturbations as a new way to define the dynamic status of genes, which brings new insights into mechanisms of regulation of gene expression and tissue specificity.
C1 [Sharov, Alexei A.; Piao, Yulan; Correa-Cerro, Lina S.; Amano, Tomokazu; Thomas, Marshall; Mehta, Samir; Ko, Minoru S. H.] NIA, Dev Genom & Aging Sect, Genet Lab, NIH, Baltimore, MD 21224 USA.
[Nishiyama, Akira] Yokohama City Univ, Dept Immunol, Grad Sch Med, Kanagawa 2360004, Japan.
[Nishiyama, Akira] Yokohama City Univ, Fac Med, Kanagawa 2360004, Japan.
RP Ko, MSH (reprint author), NIA, Dev Genom & Aging Sect, Genet Lab, NIH, Baltimore, MD 21224 USA.
EM kom@mail.nih.gov
RI Ko, Minoru/B-7969-2009; Amano, Tomokazu/F-9720-2013
OI Ko, Minoru/0000-0002-3530-3015;
FU NIH, National Institute on Aging
FX We thank Bernard Binder for critical reading of the manuscript, Carole
Stagg, Yong Qian, and Dawood Dudekula for providing technical help. This
research was supported entirely by the Intramural Research Program of
the NIH, National Institute on Aging.
NR 42
TC 5
Z9 5
U1 0
U2 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD FEB 9
PY 2011
VL 12
AR 102
DI 10.1186/1471-2164-12-102
PG 13
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 726AM
UT WOS:000287688300001
PM 21306619
ER
PT J
AU Maier, A
Aura, CJ
Leopold, DA
AF Maier, Alexander
Aura, Christopher J.
Leopold, David A.
TI Infragranular Sources of Sustained Local Field Potential Responses in
Macaque Primary Visual Cortex
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID RECORDED FLASH-VEP; EVOKED-POTENTIALS; NEURONAL CIRCUITS; SPIKING
ACTIVITY; CEREBRAL-CORTEX; STRIATE CORTEX; FEEDBACK AXONS; AWAKE
MACAQUE; MONKEY; MECHANISMS
AB A local field potential (LFP) response can be measured throughout the visual cortex in response to the abrupt appearance of a visual stimulus. Averaging LFP responses to many stimulus presentations isolates transient, phase-locked components of the response that are consistent from trial to trial. However, stimulus responses are also composed of sustained components, which differ in their phase from trial to trial and therefore must be evaluated using other methods, such as computing the power of the response of each trial before averaging. Here, we investigate the basis of phase-locked and non-phase-locked LFP responses in the primary visual cortex of the macaque monkey using a novel variant of current source density (CSD) analysis. We applied a linear array of electrode contacts spanning the thickness of the cortex to measure the LFP and compute band-limited CSD power to identify the laminar sites of persistent current exchange that may be the basis of sustained visual LFP responses. In agreement with previous studies, we found a short-latency phase-locked current sink, thought to correspond to thalamocortical input to layer 4C. In addition, we found a prominent non-phase-locked component of the CSD that persisted as long as the stimulus was physically present. The latter was relatively broadband, lasted throughout the stimulus presentation, and was centered similar to 500 mu m deeper than the initial current sink. These findings demonstrate a fundamental difference in the neural mechanisms underlying the initial and sustained processing of simple visual stimuli in the V1 microcircuit.
C1 [Leopold, David A.] NEI, Neurophysiol Imaging Facil, NIMH, NINDS,NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Maier, Alexander; Aura, Christopher J.; Leopold, David A.] NIMH, Unit Cognit Neurophysiol & Imaging, Neuropsychol Lab, Bethesda, MD 20892 USA.
RP Leopold, DA (reprint author), NEI, Neurophysiol Imaging Facil, NIMH, NINDS,NIH,Dept Hlth & Human Serv, 49 Convent Dr,1E21,MSC 4400, Bethesda, MD 20892 USA.
EM leopoldd@mail.nih.gov
RI Maier, Alexander/B-7489-2009;
OI Maier, Alexander/0000-0002-7250-502X; Leopold, David/0000-0002-1345-6360
FU National Institute of Mental Health; National Institute for Neurological
Disorders and Stroke; National Eye Institute
FX This work was supported by the Intramural Research Programs of the
National Institute of Mental Health, National Institute for Neurological
Disorders and Stroke, and the National Eye Institute. We thank Katy
Smith for technical assistance.
NR 47
TC 35
Z9 35
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 FEB 9
PY 2011
VL 31
IS 6
BP 1971
EP 1980
DI 10.1523/JNEUROSCI.5300-09.2011
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 721WV
UT WOS:000287389400006
PM 21307235
ER
PT J
AU Sapieha, P
Stahl, A
Chen, J
Seaward, MR
Willett, KL
Krah, NM
Dennison, RJ
Connor, KM
Aderman, CM
Liclican, E
Carughi, A
Perelman, D
Kanaoka, Y
SanGiovanni, JP
Gronert, K
Smith, LEH
AF Sapieha, Przemyslaw
Stahl, Andreas
Chen, Jing
Seaward, Molly R.
Willett, Keirnan L.
Krah, Nathan M.
Dennison, Roberta J.
Connor, Kip M.
Aderman, Christopher M.
Liclican, Elvira
Carughi, Arianna
Perelman, Dalia
Kanaoka, Yoshihide
SanGiovanni, John Paul
Gronert, Karsten
Smith, Lois E. H.
TI 5-Lipoxygenase Metabolite 4-HDHA Is a Mediator of the Antiangiogenic
Effect of omega-3 Polyunsaturated Fatty Acids
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID OXYGEN-INDUCED RETINOPATHY; ACTIVATED-RECEPTOR-GAMMA; LIPID MEDIATORS;
RETINAL NEOVASCULARIZATION; DOCOSAHEXAENOIC ACID; ANTIINFLAMMATORY
ACTIONS; MYOCARDIAL-INFARCTION; ANTI-INFLAMMATION; PROTECTIN D1;
PPAR-GAMMA
AB Lipid signaling is dysregulated in many diseases with vascular pathology, including cancer, diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration. We have previously demonstrated that diets enriched in omega-3 polyunsaturated fatty acids (PUFAs) effectively reduce pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy, in part through metabolic products that suppress microglialderived tumor necrosis factor-alpha. To better understand the protective effects of omega-3 PUFAs, we examined the relative importance of major lipid metabolic pathways and their products in contributing to this effect. omega-3 PUFA diets were fed to four lines of mice deficient in each key lipid-processing enzyme (cyclooxygenase 1 or 2, or lipoxygenase 5 or 12/15), retinopathy was induced by oxygen exposure; only loss of 5-lipoxygenase (5-LOX) abrogated the protection against retinopathy of dietary omega-3 PUFAs. This protective effect was due to 5-LOX oxidation of the omega-3 PUFA lipid docosahexaenoic acid to 4-hydroxy-docosahexaenoic acid (4-HDHA). 4-HDHA directly inhibited endothelial cell proliferation and sprouting angiogenesis via peroxisome proliferator-activated receptor gamma (PPAR gamma), independent of 4-HDHA's anti-inflammatory effects. Our study suggests that omega-3 PUFAs may be profitably used as an alternative or supplement to current anti-vascular endothelial growth factor (VEGF) treatment for proliferative retinopathy and points to the therapeutic potential of omega-3 PUFAs and metabolites in other diseases of vasoproliferation. It also suggests that cyclooxygenase inhibitors such as aspirin and ibuprofen (but not lipoxygenase inhibitors such as zileuton) might be used without losing the beneficial effect of dietary omega-3 PUFA.
C1 [Sapieha, Przemyslaw; Stahl, Andreas; Chen, Jing; Seaward, Molly R.; Willett, Keirnan L.; Krah, Nathan M.; Dennison, Roberta J.; Connor, Kip M.; Aderman, Christopher M.; Smith, Lois E. H.] Harvard Univ, Sch Med, Childrens Hosp Boston, Dept Ophthalmol, Boston, MA 02115 USA.
[Sapieha, Przemyslaw] Univ Montreal, Maisonneuve Rosemont Hosp Res Ctr, Dept Ophthalmol, Montreal, PQ H1T 2M4, Canada.
[Stahl, Andreas] Univ Eye Hosp Freiburg, D-79106 Freiburg, Germany.
[Liclican, Elvira; Gronert, Karsten] Univ Calif Berkeley, Sch Optometry, Vis Sci Program, Berkeley, CA 94720 USA.
[Carughi, Arianna; Perelman, Dalia] Hlth Res & Studies Ctr, Los Altos, CA 94022 USA.
[Carughi, Arianna; Perelman, Dalia] Palo Alto Med Fdn, Palo Alto, CA 94301 USA.
[Kanaoka, Yoshihide] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Kanaoka, Yoshihide] Brigham & Womens Hosp, Boston, MA 02115 USA.
[SanGiovanni, John Paul] NEI, Div Epidemiol & Clin Res, Bethesda, MD 20892 USA.
RP Smith, LEH (reprint author), Harvard Univ, Sch Med, Childrens Hosp Boston, Dept Ophthalmol, 300 Longwood Ave, Boston, MA 02115 USA.
EM lois.smith@childrens.harvard.edu
FU NIH [EY017017, EY017017-04S1, EY016136]; Children's Hospital Boston
Mental Retardation and Developmental Disabilities Research Center [P01
HD18655]; Research to Prevent Blindness; Alcon Research Institute;
MacTel Foundation; Roche Foundation for Anemia Research; V. Kann
Rasmussen Foundation; Canadian Institutes of Health Research; Charles A.
King Trust; Canadian National Institute for the Blind; Deutsche
Forschungsgemeinschaft; Juvenile Diabetes Research Foundation
International; William Randolph Hearst Award [F32 EY017789]
FX This work was supported by NIH grants EY017017, EY017017-04S1 (L. E. H.
S.), and EY016136 (K. G.); Children's Hospital Boston Mental Retardation
and Developmental Disabilities Research Center grant P01 HD18655 (L. E.
H. S.); Research to Prevent Blindness Senior Investigator Award (L. E.
H. S.); Alcon Research Institute Award (L. E. H. S.); MacTel Foundation
(L. E. H. S.); Roche Foundation for Anemia Research (L. E. H. S.); and
V. Kann Rasmussen Foundation (L. E. H. S.). P. S. holds a Canada
Research Chair in Retinal Cell Biology and is supported by grants from
the Canadian Institutes of Health Research, the Charles A. King Trust
Award, and the Canadian National Institute for the Blind. A. S. is
funded by Deutsche Forschungsgemeinschaft. Additional support was
provided by the Juvenile Diabetes Research Foundation International
(J.C.), the William Randolph Hearst Award F32 EY017789 (K.M.C.).
NR 63
TC 52
Z9 53
U1 1
U2 7
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD FEB 9
PY 2011
VL 3
IS 69
AR 69ra12
DI 10.1126/scitranslmed.3001571
PG 12
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 795JS
UT WOS:000292971100004
PM 21307302
ER
PT J
AU Lau-Kilby, AW
Kretz, CC
Pechhold, S
Price, JD
Dorta, S
Ramos, H
Trinchieri, G
Tarbell, KV
AF Lau-Kilby, Annie W.
Kretz, Cosima C.
Pechhold, Susanne
Price, Jeffrey D.
Dorta, Stephanie
Ramos, Haydee
Trinchieri, Giorgio
Tarbell, Kristin V.
TI Interleukin-2 inhibits FMS-like tyrosine kinase 3 receptor ligand
(flt3L)-dependent development and function of conventional and
plasmacytoid dendritic cells
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
ID COLONY-STIMULATING FACTOR; NONOBESE DIABETIC MICE; INTERFERON-ALPHA;
BONE-MARROW; IN-VIVO; CUTTING EDGE; FLT3 LIGAND; AUTOIMMUNITY;
PRECURSORS; TOLERANCE
AB Steady-state development of plasmacytoid dendritic cells (pDCs) and conventional dendritic cells (cDCs) requires the ligand for FMS-like tyrosine kinase 3 receptor (flt3L), but little is known about how other cytokines may also control this process. In this study, we show that IL-2 inhibits the development of both pDCs and cDCs from bone marrow cells under flt3L stimulation, by acting on lineage(-)flt3(+) precursors. This inhibition of DC development by IL-2 requires IL-2R alpha and IL2R beta. IL-2R alpha is specifically expressed in one stage of the DC precursor: the monocyte and DC progenitors (MDPs). Furthermore, more MDPs are found in flt3L-stimulated bone marrow cultures when IL-2 is present, suggesting that IL-2 may be inhibiting DC development at the MDP stage. Consistent with our in vitro findings, we observe that nonobese diabetic (NOD) mice, which express less IL-2 compared with diabetes-resistant NOD.Idd3/5 mice, have more splenic pDCs. Additionally, DCs developed in vitro in the presence of flt3L and IL-2 display reduced ability to stimulate T-cell proliferation compared with DCs developed in the presence of flt3L alone. Although the addition of IL-2 does not increase the apoptosis of DCs during their development, DCs developed in the presence of IL-2 are more prone to apoptosis upon interaction with T cells. Together our data show that IL-2 can inhibit both the development and the function of DCs. This pathway may have implications for the loss of immune tolerance: Reduced IL-2 signaling may lead to increased DC number and T-cell stimulatory capacity.
C1 [Lau-Kilby, Annie W.; Kretz, Cosima C.; Price, Jeffrey D.; Dorta, Stephanie; Tarbell, Kristin V.] Natl Inst Diabet Digest & Kidney Dis, Immune Tolerance Sect, Diabet Branch, NIH, Bethesda, MD 20892 USA.
[Ramos, Haydee] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
[Trinchieri, Giorgio] NCI, Expt Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Tarbell, KV (reprint author), Natl Inst Diabet Digest & Kidney Dis, Immune Tolerance Sect, Diabet Branch, NIH, Bethesda, MD 20892 USA.
EM tarbellk@niddk.nih.gov
OI Lau-Kilby, Annie/0000-0002-2666-1347; Tarbell,
Kristin/0000-0003-3738-379X
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Cancer Institute; National Institute of Arthritis and
Musculoskeletal and Skin Diseases of the National Institutes of Health
FX We thank Alice Franks, the flow cytometry core facilities at the
National Heart, Lung and Blood Institute and the National Institute of
Allergic and Infectious Disease, and Helen Su and Qian Zhang for
technical support, and Dr. Yasmine Belkaid for critical reading of the
manuscript. This work was supported by the Intramural Research Programs
of the National Institute of Diabetes and Digestive and Kidney Diseases,
the National Cancer Institute, and National Institute of Arthritis and
Musculoskeletal and Skin Diseases of the National Institutes of Health.
NR 40
TC 13
Z9 14
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD FEB 8
PY 2011
VL 108
IS 6
BP 2408
EP 2413
DI 10.1073/pnas.1009738108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717YH
UT WOS:000287084500045
PM 21262836
ER
PT J
AU Shukla, P
Nguyen, HT
Torian, U
Engle, RE
Faulk, K
Dalton, HR
Bendall, RP
Keane, FE
Purcell, RH
Emerson, SU
AF Shukla, Priyanka
Nguyen, Hanh T.
Torian, Udana
Engle, Ronald E.
Faulk, Kristina
Dalton, Harry R.
Bendall, Richard P.
Keane, Frances E.
Purcell, Robert H.
Emerson, Suzanne U.
TI Cross-species infections of cultured cells by hepatitis E virus and
discovery of an infectious virus-host recombinant
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE emerging virus; zoonosis
ID PROTEIN; HEPATOMA; RELEASE; GENOMES; PATIENT
AB The RNA virus, hepatitis E virus (HEV) is the most or second-most important cause of acute clinical hepatitis in adults throughout much of Asia, the Middle East, and Africa. In these regions it is an important cause of acute liver failure, especially in pregnant women who have a mortality rate of 20-30%. Until recently, hepatitis E was rarely identified in industrialized countries, but Hepatitis E now is reported increasingly throughout Western Europe, some Eastern European countries, and Japan. Most of these cases are caused by genotype 3, which is endemic in swine, and these cases are thought to be zoonotically acquired. However, transmission routes are not well understood. HEV that infect humans are divided into nonzoonotic (types 1, 2) and zoonotic (types 3, 4) genotypes. HEV cell culture is inefficient and limited, and thus far HEV has been cultured only in human cell lines. The HEV strain Kernow-C1 (genotype 3) isolated from a chronically infected patient was used to identify human, pig, and deer cell lines permissive for infection. Cross-species infections by genotypes 1 and 3 were studied with this set of cultures. Adaptation of the Kernow-C1 strain to growth in human hepatoma cells selected for a rare virus recombinant that contained an insertion of 174 ribonucleotides (58 amino acids) of a human ribosomal protein gene.
C1 [Engle, Ronald E.; Faulk, Kristina; Purcell, Robert H.] NIAID, Hepatitis Viruses Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Shukla, Priyanka; Nguyen, Hanh T.; Torian, Udana; Emerson, Suzanne U.] NIAID, Sect Mol Hepatitis, NIH, Bethesda, MD 20892 USA.
[Dalton, Harry R.; Bendall, Richard P.; Keane, Frances E.] European Ctr Environm & Human Hlth, Truro TR1 3LJ, Cornwall, England.
[Dalton, Harry R.; Bendall, Richard P.; Keane, Frances E.] Univ Plymouth, Truro TR1 3LJ, Cornwall, England.
[Dalton, Harry R.; Bendall, Richard P.; Keane, Frances E.] Univ Exeter, Truro TR1 3LJ, Cornwall, England.
[Dalton, Harry R.; Bendall, Richard P.; Keane, Frances E.] Royal Cornwall Hosp Trust, Truro TR1 3LJ, Cornwall, England.
RP Purcell, RH (reprint author), NIAID, Hepatitis Viruses Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
EM RPURCELL@niaid.nih.gov; semerson@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX We thank Rebecca DerSimonian and Xiao Liu Biostatistics Research Branch,
National Institute of Allergy and Infectious Diseases, for performing
the statistical analyses. This work was supported by the Intramural
Research Program of the National Institute of Allergy and Infectious
Diseases, National Institutes of Health.
NR 28
TC 93
Z9 94
U1 3
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 FEB 8
PY 2011
VL 108
IS 6
BP 2438
EP 2443
DI 10.1073/pnas.1018878108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717YH
UT WOS:000287084500050
PM 21262830
ER
PT J
AU Song, KM
Bolton, DL
Wei, CJ
Wilson, RL
Camp, JV
Bao, S
Mattapallil, JJ
Herzenberg, LA
Herzenberg, LA
Andrews, CA
Sadoff, JC
Goudsmit, J
Pau, MG
Seder, RA
Kozlowski, PA
Nabel, GJ
Roederer, M
Rao, SS
AF Song, Kaimei
Bolton, Diane L.
Wei, Chih-Jen
Wilson, Robert L.
Camp, Jeremy V.
Bao, Saran
Mattapallil, Joseph J.
Herzenberg, Leonore A.
Herzenberg, Leonard A.
Andrews, Charla A.
Sadoff, Jerald C.
Goudsmit, Jaap
Pau, Maria Grazia
Seder, Robert A.
Kozlowski, Pamela A.
Nabel, Gary J.
Roederer, Mario
Rao, Srinivas S.
TI Genetic immunization in the lung induces potent local and systemic
immune responses (vol 107, pg 22213, 2010)
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Correction
C1 [Song, Kaimei; Bolton, Diane L.; Wei, Chih-Jen; Bao, Saran; Andrews, Charla A.; Seder, Robert A.; Nabel, Gary J.; Roederer, Mario; Rao, Srinivas S.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Wilson, Robert L.; Camp, Jeremy V.; Kozlowski, Pamela A.] Louisiana State Univ, Hlth Sci Ctr, Gene Therapy Program, New Orleans, LA 70803 USA.
[Wilson, Robert L.; Camp, Jeremy V.; Kozlowski, Pamela A.] Louisiana State Univ, Hlth Sci Ctr, Dept Microbiol Immunol & Parasitol, New Orleans, LA 70803 USA.
[Mattapallil, Joseph J.] Uniformed Serv Univ Hlth Sci, Bethesda, MD USA.
[Herzenberg, Leonore A.; Herzenberg, Leonard A.] Stanford Univ, Dept Genet, Stanford, CA 94305 USA.
[Sadoff, Jerald C.] AERAS Global TB Fdn, Rockville, MD 20850 USA.
[Goudsmit, Jaap; Pau, Maria Grazia] Crucell Holland BV, Leiden, Netherlands.
RP Song, KM (reprint author), NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
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 FEB 8
PY 2011
VL 108
IS 6
BP 2629
EP 2629
DI 10.1073/pnas.1100067108
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717YH
UT WOS:000287084500083
ER
PT J
AU Lurie, G
Gaudet, MM
Spurdle, AB
Carney, ME
Wilkens, LR
Yang, HP
Weiss, NS
Webb, PM
Thompson, PJ
Terada, K
Setiawan, VW
Rebbeck, TR
Prescott, J
Orlow, I
O'Mara, T
Olson, SH
Narod, SA
Matsuno, RK
Lissowska, J
Liang, XL
Levine, DA
Le Marchand, L
Kolonel, LN
Henderson, BE
Garcia-Closas, M
Doherty, JA
De Vivo, I
Chen, C
Brinton, LA
Akbari, MR
Goodman, MT
AF Lurie, Galina
Gaudet, Mia M.
Spurdle, Amanda B.
Carney, Michael E.
Wilkens, Lynne R.
Yang, Hannah P.
Weiss, Noel S.
Webb, Penelope M.
Thompson, Pamela J.
Terada, Keith
Setiawan, Veronica Wendy
Rebbeck, Timothy R.
Prescott, Jennifer
Orlow, Irene
O'Mara, Tracy
Olson, Sara H.
Narod, Steven A.
Matsuno, Rayna K.
Lissowska, Jolanta
Liang, Xiaolin
Levine, Douglas A.
Le Marchand, Loic
Kolonel, Laurence N.
Henderson, Brian E.
Garcia-Closas, Montserrat
Doherty, Jennifer Anne
De Vivo, Immaculata
Chen, Chu
Brinton, Louise A.
Akbari, Mohammad R.
Goodman, Marc T.
CA Epidemiology Endometrial Canc
TI The Obesity-Associated Polymorphisms FTO rs9939609 and MC4R rs17782313
and Endometrial Cancer Risk in Non-Hispanic White Women
SO PLOS ONE
LA English
DT Article
ID GENE-EXPRESSION; FAT MASS; ENDOGENOUS HORMONES; ENERGY-EXPENDITURE;
ADULT OBESITY; FOOD-INTAKE; CHILDREN; VARIANT; CHILDHOOD; INSULIN
AB Overweight and obesity are strongly associated with endometrial cancer. Several independent genome-wide association studies recently identified two common polymorphisms, FTO rs9939609 and MC4R rs17782313, that are linked to increased body weight and obesity. We examined the association of FTO rs9939609 and MC4R rs17782313 with endometrial cancer risk in a pooled analysis of nine case-control studies within the Epidemiology of Endometrial Cancer Consortium (E2C2). This analysis included 3601 non-Hispanic white women with histologically-confirmed endometrial carcinoma and 5275 frequency-matched controls. Unconditional logistic regression models were used to assess the relation of FTO rs9939609 and MC4R rs17782313 genotypes to the risk of endometrial cancer. Among control women, both the FTO rs9939609 A and MC4R rs17782313 C alleles were associated with a 16% increased risk of being overweight (p = 0.001 and p = 0.004, respectively). In case-control analyses, carriers of the FTO rs9939609 AA genotype were at increased risk of endometrial carcinoma compared to women with the TT genotype [ odds ratio (OR) = 1.17; 95% confidence interval (CI): 1.03-1.32, p = 0.01]. However, this association was no longer apparent after adjusting for body mass index (BMI), suggesting mediation of the gene-disease effect through body weight. The MC4R rs17782313 polymorphism was not related to endometrial cancer risk (per allele OR = 0.98; 95% CI: 0.91-1.06; p = 0.68). FTO rs9939609 is a susceptibility marker for white non-Hispanic women at higher risk of endometrial cancer. Although FTO rs9939609 alone might have limited clinical or public health significance for identifying women at high risk for endometrial cancer beyond that of excess body weight, further investigation of obesity-related genetic markers might help to identify the pathways that influence endometrial carcinogenesis.
C1 [Lurie, Galina; Wilkens, Lynne R.; Thompson, Pamela J.; Matsuno, Rayna K.; Le Marchand, Loic; Kolonel, Laurence N.; Goodman, Marc T.] Univ Hawaii, Canc Res Ctr Hawaii, Canc Epidemiol Program, Honolulu, HI 96813 USA.
[Gaudet, Mia M.] Amer Canc Soc Inc, Epidemiol Res Program, Atlanta, GA USA.
[Spurdle, Amanda B.; Webb, Penelope M.; O'Mara, Tracy] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Spurdle, Amanda B.; Webb, Penelope M.; O'Mara, Tracy] PO Royal Brisbane Hosp, Brisbane, Qld, Australia.
[Carney, Michael E.; Terada, Keith] Univ Hawaii, Dept Obstet & Gynecol, John A Burns Sch Med, Honolulu, HI 96813 USA.
[Yang, Hannah P.; Garcia-Closas, Montserrat; Brinton, Louise A.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Weiss, Noel S.; Chen, Chu] Univ Washington, Dept Epidemiol, Sch Publ Hlth, Seattle, WA 98195 USA.
[Weiss, Noel S.; Doherty, Jennifer Anne; Chen, Chu] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Setiawan, Veronica Wendy; Henderson, Brian E.] Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90089 USA.
[Rebbeck, Timothy R.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA.
[Rebbeck, Timothy R.] Abramson Canc Ctr, Philadelphia, PA USA.
[Prescott, Jennifer; De Vivo, Immaculata] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Prescott, Jennifer; De Vivo, Immaculata] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab,Dept Med, Boston, MA 02115 USA.
[Orlow, Irene; Olson, Sara H.; Liang, Xiaolin] Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10021 USA.
[O'Mara, Tracy] Queensland Univ Technol, Hormone Dependent Canc Grp, Inst Hlth & Biomed Innovat, Brisbane, Qld 4001, Australia.
[Narod, Steven A.; Akbari, Mohammad R.] Univ Toronto, Womens Coll Res Inst, Toronto, ON, Canada.
[Matsuno, Rayna K.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Levine, Douglas A.] Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10021 USA.
[Chen, Chu] Univ Washington, Dept Otolaryngol Head & Neck Surg, Sch Med, Seattle, WA 98195 USA.
RP Lurie, G (reprint author), Univ Hawaii, Canc Res Ctr Hawaii, Canc Epidemiol Program, Honolulu, HI 96813 USA.
EM glurie@crch.hawaii.edu
RI Beral, Valerie/B-2979-2013; Bandera, Elisa/M-4169-2014; Garcia-Closas,
Montserrat /F-3871-2015; Brinton, Louise/G-7486-2015; Krogh,
Vittorio/K-2628-2016; Weiderpass, Elisabete/M-4029-2016; O'Mara,
Tracy/M-7508-2016; Spurdle, Amanda/A-4978-2011;
OI Bandera, Elisa/0000-0002-8789-2755; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Brinton, Louise/0000-0003-3853-8562; Krogh,
Vittorio/0000-0003-0122-8624; Weiderpass, Elisabete/0000-0003-2237-0128;
O'Mara, Tracy/0000-0002-5436-3232; Webb, Penelope/0000-0003-0733-5930;
Spurdle, Amanda/0000-0003-1337-7897; Lissowska,
Jolanta/0000-0003-2695-5799; La Vecchia, Carlo/0000-0003-1441-897X;
Sacerdote, Carlotta/0000-0002-8008-5096; Orlow,
Irene/0000-0001-6234-6961
FU Australian National Endometrial Cancer Study [339435, 4196615, 403031,
457636]; Estrogen; Diet; Genetics; Endometrial Cancer study, NJ, USA
[NIH R01CA38918]; Fred Hutchinson Cancer Research Center Case-Control
Study, WA, USA [NIH R35 CA 39779, R01 CA 75977, R03 CA 80636, N01 HD
23166, K05 CA 92002, R01 CA 105212, R01 CA87538]; Fred Hutchinson Cancer
Research Center; Hawaii Endometrial Cancer Study, Hawaii, USA [NIH
P01CA33619, R01CA58598, N01CN67001, N01 PC35137]; Nurses' Health Study
[NIH CAO82838, CA134958]; Polish Endometrial Cancer Study of the NCI;
Toronto Case-Control Endometrial Cancer Study (Canadian Institute of
Health Research, CIHR), Multiethnic Cohort Study [NIH CA63464, CA54281];
Women's Insights and Shared Experiences, PA, USA [NIH P01-CA77596];
National Cancer Institute
FX Australian National Endometrial Cancer Study (NHMRC ID #339435, TCCQ ID
#4196615, TCCT IDs #403031 and #457636), Estrogen, Diet, Genetics, and
Endometrial Cancer study, NJ, USA (NIH R01CA38918), Fred Hutchinson
Cancer Research Center Case-Control Study, WA, USA (NIH R35 CA 39779,
R01 CA 75977, R03 CA 80636, N01 HD 23166, K05 CA 92002, R01 CA 105212,
R01 CA87538 and funds from the Fred Hutchinson Cancer Research Center),
Hawaii Endometrial Cancer Study, Hawaii, USA (NIH P01CA33619,
R01CA58598, N01CN67001, N01 PC35137), Nurses' Health Study (NIH
CAO82838, CA134958), Polish Endometrial Cancer Study (Intramural Program
of the NCI), Toronto Case-Control Endometrial Cancer Study (Canadian
Institute of Health Research, CIHR), Multiethnic Cohort Study (NIH
CA63464, CA54281), Women's Insights and Shared Experiences, PA, USA (NIH
P01-CA77596, Dr. Mia Gaudet (American Cancer Society, Atlanta, GA, USA).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.; One of the
authors, Dr. Mia Gaudet is employed by the American Cancer Society
(since October 4th 2010). Dr Gaudet contributed the data for the Polish
Endometrial Cancer Study that was funded by the National Cancer
Institute. Her current employment by the American Cancer Society does
not alter the authors' adherence to all the PLoS ONE policies on sharing
data and materials.
NR 33
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U1 1
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD FEB 8
PY 2011
VL 6
IS 2
AR e16756
DI 10.1371/journal.pone.0016756
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717WH
UT WOS:000287077600021
PM 21347432
ER
PT J
AU McDermott, MM
Ferrucci, L
Liu, KA
Guralnik, JM
Tian, L
Kibbe, M
Liao, YH
Tao, HM
Criqui, MH
AF McDermott, Mary M.
Ferrucci, Luigi
Liu, Kiang
Guralnik, Jack M.
Tian, Lu
Kibbe, Melina
Liao, Yihua
Tao, Huimin
Criqui, Michael H.
TI Women With Peripheral Arterial Disease Experience Faster Functional
Decline Than Men With Peripheral Arterial Disease
SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
LA English
DT Article
DE intermittent claudication; peripheral arterial disease; physical
functioning; sarcopenia
ID SKELETAL-MUSCLE MASS; LOWER-EXTREMITY ISCHEMIA; LEG SYMPTOMS;
ASSOCIATIONS; INDEX; CLASSIFICATION; OSTEOARTHRITIS; IMPAIRMENT;
PREVALENCE; PREDICTORS
AB Objectives We hypothesized that women with lower extremity peripheral arterial disease (PAD) would have greater mobility loss and faster functional decline than men with PAD.
Background Whether rates of mobility loss or functional decline differ between men and women with PAD is currently unknown.
Methods Three hundred eighty men and women with PAD completed the 6-min walk, were assessed for mobility disability, and underwent measures of 4-m walking velocity at baseline and annually for up to 4 years. Computed tomography-assessed calf muscle characteristics were measured biannually. Outcomes included becoming unable to walk for 6 min continuously among participants who walked continuously for 6 min at baseline. Mobility loss was defined as becoming unable to walk for a quarter mile or to walk up and down 1 flight of stairs without assistance among those without baseline mobility disability.
Results were adjusted for age, race, body mass index, physical activity, the ankle brachial index, comorbidities, and other confounders. Results At 4 years of follow-up, women were more likely to become unable to walk for 6 min continuously (hazard ratio: 2.30, 95% confidence interval: 1.30 to 4.06, p = 0.004), more likely to develop mobility disability (hazard ratio: 1.79, 95% confidence interval: 1.30 to 3.03, p = 0.030), and had faster declines in walking velocity (p = 0.022) and the distance achieved in the 6-min walk (p = 0.041) compared with men. Sex differences in functional decline were attenuated after additional adjustment for baseline sex differences in calf muscle area.
Conclusions Women with PAD have faster functional decline and greater mobility loss than men with PAD. These sex differences may be attributable to smaller baseline calf muscle area among women with PAD. (J Am Coll Cardiol 2011;57:707-14) (C) 2011 by the American College of Cardiology Foundation
C1 [McDermott, Mary M.] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Ferrucci, Luigi] NIA, Baltimore, MD 21224 USA.
[Guralnik, Jack M.] NIA, NIH, Bethesda, MD 20892 USA.
[Tian, Lu] Stanford Univ, Dept Hlth Policy & Res, Palo Alto, CA 94304 USA.
[Criqui, Michael H.] Univ Calif San Diego, Dept Family & Prevent Med, La Jolla, CA 92093 USA.
RP McDermott, MM (reprint author), Northwestern Univ, Dept Med, Feinberg Sch Med, 750 N Lake Shore Dr,10th Floor, Chicago, IL 60611 USA.
EM mdm608@northwestern.edu
FU National Heart Lung and Blood Institute [R01-HL58099, R01-HL64739,
R01-HL071223, R01-HL076298]; National Center for Research Resources,
National Institutes of Health [RR-00048]; National Institute on Aging,
National Institutes of Health
FX Department of Family and Preventive Medicine, University of California
at San Diego, La Jolla, California. Supported by grants R01-HL58099,
R01-HL64739, R01-HL071223, and R01-HL076298 from the National Heart Lung
and Blood Institute and by grant RR-00048 from the National Center for
Research Resources, National Institutes of Health. Supported in part by
the Intramural Research Program, National Institute on Aging, National
Institutes of Health. The authors have reported that they have no
relationships to disclose. Healther L. Gornik, MD, served as Guest
Editor for this article.
NR 23
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U1 2
U2 2
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 FEB 8
PY 2011
VL 57
IS 6
BP 707
EP 714
DI 10.1016/j.jacc.2010.09.042
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 715JH
UT WOS:000286880100011
PM 21292130
ER
PT J
AU Hamid, MMA
Remarque, EJ
El Hassan, IM
Hussain, AA
Narum, DL
Thomas, AW
Kocken, CHM
Weiss, WR
Faber, BW
AF Hamid, Muzamil Mahdi Abdel
Remarque, Edmond J.
El Hassan, Ibrahim M.
Hussain, Ayman A.
Narum, David L.
Thomas, Alan W.
Kocken, Clemens H. M.
Weiss, Walter R.
Faber, Bart W.
TI Malaria infection by sporozoite challenge induces high functional
antibody titres against blood stage antigens after a DNA prime, poxvirus
boost vaccination strategy in Rhesus macaques
SO MALARIA JOURNAL
LA English
DT Article
ID APICAL MEMBRANE ANTIGEN-1; PLASMODIUM-FALCIPARUM SPOROZOITES; MEROZOITE
SURFACE-ANTIGENS; IMMUNE-RESPONSES; KNOWLESI MALARIA; IMMUNIZATION;
PROTECTION; PRECURSOR; EFFICACY; BERGHEI
AB Background: A DNA prime, poxvirus (COPAK) boost vaccination regime with four antigens, i. e. a combination of two Plasmodium knowlesi sporozoite (csp/ ssp2) and two blood stage (ama1/ msp142) genes, leads to self- limited parasitaemia in 60% of rhesus monkeys and survival from an otherwise lethal infection with P. knowlesi. In the present study, the role of the blood stage antigens in protection was studied in depth, focusing on antibody formation against the blood stage antigens and the functionality thereof.
Methods: Rhesus macaques were immunized with the four- component vaccine and subsequently challenged i.v. with 100 P. knowlesi sporozoites. During immunization and challenge, antibody titres against the two blood stage antigens were determined, as well as the in vitro growth inhibition capacity of those antibodies. Antigen reversal experiments were performed to determine the relative contribution of antibodies against each of the two blood stage antigens to the inhibition.
Results: After vaccination, PkAMA1 and PkMSP119 antibody titres in vaccinated animals were low, which was reflected in low levels of inhibition by these antibodies as determined by in vitro inhibition assays. Interestingly, after sporozoite challenge antibody titres against blood stage antigens were boosted over 30- fold in both protected and not protected animals. The in vitro inhibition levels increased to high levels (median inhibitions of 59% and 56% at 6 mg/ mL total IgG, respectively). As growth inhibition levels were not significantly different between protected and not protected animals, the ability to control infection appeared cannot be explained by GIA levels. Judged by in vitro antigen reversal growth inhibition assays, over 85% of the inhibitory activity of these antibodies was directed against PkAMA1.
Conclusions: This is the first report that demonstrates that a DNA prime/ poxvirus boost vaccination regimen induces low levels of malaria parasite growth inhibitory antibodies, which are boosted to high levels upon challenge. No association could, however, be established between the levels of inhibitory capacity in vitro and protection, either after vaccination or after challenge.
C1 [Hamid, Muzamil Mahdi Abdel; Remarque, Edmond J.; Thomas, Alan W.; Kocken, Clemens H. M.; Faber, Bart W.] Biomed Primate Res Ctr, Dept Parasitol, Rijswijk, Netherlands.
[Hamid, Muzamil Mahdi Abdel; El Hassan, Ibrahim M.; Hussain, Ayman A.] Univ Khartoum, Inst Endem Dis, Khartoum, Sudan.
[Weiss, Walter R.] Naval Med Res Ctr, Silver Spring, MD USA.
[Narum, David L.] NIAID, Lab Malaria Immunol & Vaccinol, NIH, Bethesda, MD 20892 USA.
[El Hassan, Ibrahim M.] Jazan Univ, Fac Med, Jazan, Saudi Arabia.
RP Faber, BW (reprint author), Biomed Primate Res Ctr, Dept Parasitol, Rijswijk, Netherlands.
EM faber@bprc.nl
OI abdelhamid, muzamil/0000-0002-6157-4388
FU European Malaria Vaccine Initiative (EMVI); Biomedical Primate Research
Centre; NIAID, NIH
FX This work received financial support from the European Malaria Vaccine
Initiative (EMVI) and the Biomedical Primate Research Centre. This
research was supported in part by the Intramural Research Program of
NIAID, NIH. We thank Vanessa Riasat for excellent technical assistance.
NR 37
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U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1475-2875
J9 MALARIA J
JI Malar. J.
PD FEB 8
PY 2011
VL 10
AR 29
DI 10.1186/1475-2875-10-29
PG 11
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 740RR
UT WOS:000288812600003
PM 21303498
ER
PT J
AU Wang, MY
Spinetti, G
Monticone, RE
Zhang, J
Wu, J
Jiang, LQ
Khazan, B
Telljohann, R
Lakatta, EG
AF Wang, Mingyi
Spinetti, Gaia
Monticone, Robert E.
Zhang, Jing
Wu, James
Jiang, Liqun
Khazan, Benjamin
Telljohann, Richard
Lakatta, Edward G.
TI A Local Proinflammatory Signalling Loop Facilitates Adverse
Age-Associated Arterial Remodeling
SO PLOS ONE
LA English
DT Article
ID SMOOTH-MUSCLE-CELLS; GROWTH-FACTOR-BETA; MATRIX-METALLOPROTEINASE;
ANGIOTENSIN-II; TGF-BETA; INVASION; EXPRESSION; DISEASE; MCP-1;
ATHEROSCLEROSIS
AB Background: The coincidence of vascular smooth muscle cells (VSMC) infiltration and collagen deposition within a diffusely thickened intima is a salient feature of central arterial wall inflammation that accompanies advancing age. However, the molecular mechanisms involved remain undefined.
Methodology/Principal Findings: Immunostaining and immunoblotting of rat aortae demonstrate that a triad of proinflammatory molecules, MCP-1, TGF-beta 1, and MMP-2 increases within the aortic wall with aging. Exposure of VSMC isolated from 8-mo-old rats (young) to MCP-1 effects, via CCR-2 signaling, both an increase in TGF-beta 1 activity, up to levels of untreated VSMC from 30-mo-old (old) rats, and a concurrent increase in MMP-2 activation. Furthermore, exposure of young VSMC to TGF-beta 1 increases levels of MCP-1, and MMP-2 activation, to levels of untreated VSMC from old rats. This autocatalytic signaling loop that enhances collagen production and invasiveness of VSMC is effectively suppressed by si-MCP-1, a CCR2 antagonist, or MMP-2 inhibition.
Conclusions/Significance: Threshold levels of MCP-1, MMP-2, or TGF-beta 1 activity trigger a feed-forward signaling mechanism that is implicated in the initiation and progression of adverse age-associated arterial wall remodeling. Intervention that suppressed this signaling loop may potentially retard age-associated adverse arterial remodeling.
C1 [Wang, Mingyi; Spinetti, Gaia; Monticone, Robert E.; Zhang, Jing; Wu, James; Jiang, Liqun; Khazan, Benjamin; Telljohann, Richard; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
[Spinetti, Gaia] MultiMed IRCCS, Milan, Italy.
RP Wang, MY (reprint author), NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA.
EM mingyiw@grc.nia.nih.gov
OI Spinetti, Gaia/0000-0001-7996-6809
FU National Institute on Aging
FX This research was supported by the Intramural Research Program of the
National Institute on Aging. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 30
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Z9 14
U1 1
U2 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD FEB 8
PY 2011
VL 6
IS 2
AR e16653
DI 10.1371/journal.pone.0016653
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717WH
UT WOS:000287077600012
PM 21347430
ER
PT J
AU Dietze, KK
Zelinskyy, G
Gibbert, K
Schimmer, S
Francois, S
Myers, L
Sparwasser, T
Hasenkrug, KJ
Dittmer, U
AF Dietze, Kirsten K.
Zelinskyy, Gennadiy
Gibbert, Kathrin
Schimmer, Simone
Francois, Sandra
Myers, Lara
Sparwasser, Tim
Hasenkrug, Kim J.
Dittmer, Ulf
TI Transient depletion of regulatory T cells in transgenic mice reactivates
virus-specific CD8(+) T cells and reduces chronic retroviral set points
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE cytotoxic T cells; retrovirus; friend virus
ID HUMAN-IMMUNODEFICIENCY-VIRUS; MULTIPLE INHIBITORY RECEPTORS; CHRONIC
VIRAL-INFECTION; FRIEND-VIRUS; CUTTING EDGE; DISEASE PROGRESSION; IMMUNE
ACTIVATION; HIV-INFECTION; IN-VITRO; CD4(+)
AB Although chronic infections with viruses such as HIV and hepatitis C virus have been associated with regulatory T cell (Treg)-mediated suppression of virus-specific CD8(+) T-cell activity, no causal relationship between Tregs and chronic viral set points has been established. Using transgenic mice in which Tregs can be selectively ablated, we now show that transient depletion of Tregs during a chronic retroviral infection allows exhausted CD8(+) T cells to regain antiviral functions, including secretion of cytokines, production of cytotoxic molecules, and virus-specific cytolytic activity. Furthermore, short-term Treg ablation resulted in long-term reductions in chronic virus loads. These results demonstrate that Treg-mediated immunosuppression can be a significant factor in the maintenance of chronic viral infections and that Treg-targeted immunotherapy could be a valuable component in therapeutic strategies to treat chronic infectious diseases.
C1 [Dietze, Kirsten K.; Zelinskyy, Gennadiy; Gibbert, Kathrin; Schimmer, Simone; Francois, Sandra; Dittmer, Ulf] Univ Duisburg Essen, Inst Virol, Univ Clin Essen, D-45122 Essen, Germany.
[Myers, Lara; Hasenkrug, Kim J.] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Sparwasser, Tim] TWINCORE, Inst Infect Immunol, D-30625 Hannover, Germany.
RP Dittmer, U (reprint author), Univ Duisburg Essen, Inst Virol, Univ Clin Essen, D-45122 Essen, Germany.
EM ulf.dittmer@uni-due.de
FU German Research Association (Deutsche Forschungsgemeinschaft) [B4];
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work was supported by the German Research Association (Deutsche
Forschungsgemeinschaft), Transregio 60 project B4, and, in part, by the
Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health.
NR 45
TC 56
Z9 56
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 FEB 8
PY 2011
VL 108
IS 6
BP 2420
EP 2425
DI 10.1073/pnas.1015148108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717YH
UT WOS:000287084500047
PM 21262821
ER
PT J
AU Wang, Q
Chaerkady, R
Wu, JA
Hwang, HJ
Papadopoulos, N
Kopelovich, L
Maitra, A
Matthaei, H
Eshleman, JR
Hruban, RH
Kinzler, KW
Pandey, A
Vogelstein, B
AF Wang, Qing
Chaerkady, Raghothama
Wu, Jian
Hwang, Hee Jung
Papadopoulos, Nick
Kopelovich, Levy
Maitra, Anirban
Matthaei, Hanno
Eshleman, James R.
Hruban, Ralph H.
Kinzler, Kenneth W.
Pandey, Akhilesh
Vogelstein, Bert
TI Mutant proteins as cancer-specific biomarkers
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE genetics; proteomics; pancreatic cancer; genetic diagnosis; companion
diagnostics
ID MASS-SPECTROMETRY; SHOTGUN PROTEOMICS; PLASMA-PROTEINS; TRANSTHYRETIN;
VARIANTS; REPRODUCIBILITY; QUANTIFICATION; CARDIOMYOPATHY; ELECTROSPRAY;
QUANTITATION
AB Cancer biomarkers are currently the subject of intense research because of their potential utility for diagnosis, prognosis, and targeted therapy. In theory, the gene products resulting from somatic mutations are the ultimate protein biomarkers, being not simply associated with tumors but actually responsible for tumorigenesis. We show here that the altered protein products resulting from somatic mutations can be identified directly and quantified by mass spectrometry. The peptides expressed from normal and mutant alleles were detected by selected reaction monitoring (SRM) of their product ions using a triple-quadrupole mass spectrometer. As a prototypical example of this approach, we demonstrated that it is possible to quantify the number and fraction of mutant Ras protein present in cancer cell lines. There were an average of 1.3 million molecules of Ras protein per cell, and the ratio of mutant to normal Ras proteins ranged from 0.49 to 5.6. Similarly, we found that mutant Ras proteins could be detected and quantified in clinical specimens such as colorectal and pancreatic tumor tissues as well as in premalignant pancreatic cyst fluids. In addition to answering basic questions about the relative levels of genetically abnormal proteins in tumors, this approach could prove useful for diagnostic applications.
C1 [Chaerkady, Raghothama; Pandey, Akhilesh] Johns Hopkins Med Inst, McKusick Nathans Inst Genet Med, Baltimore, MD 21205 USA.
[Maitra, Anirban; Matthaei, Hanno; Eshleman, James R.; Hruban, Ralph H.; Pandey, Akhilesh] Johns Hopkins Med Inst, Sol Goldman Pancreat Canc Res Ctr, Baltimore, MD 21205 USA.
[Maitra, Anirban; Matthaei, Hanno; Eshleman, James R.; Hruban, Ralph H.; Pandey, Akhilesh] Johns Hopkins Med Inst, Dept Pathol, Baltimore, MD 21205 USA.
[Pandey, Akhilesh] Johns Hopkins Med Inst, Dept Biol Chem, Baltimore, MD 21205 USA.
[Wang, Qing; Wu, Jian; Hwang, Hee Jung; Papadopoulos, Nick; Kinzler, Kenneth W.; Vogelstein, Bert] Johns Hopkins Kimmel Canc Ctr, Ludwig Ctr Canc Genet & Therapeut, Baltimore, MD 21231 USA.
[Wang, Qing; Wu, Jian; Hwang, Hee Jung; Papadopoulos, Nick; Kinzler, Kenneth W.; Vogelstein, Bert] Johns Hopkins Kimmel Canc Ctr, Howard Hughes Med Inst, Baltimore, MD 21231 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Chaerkady, Raghothama] Inst Bioinformat, Bangalore 560066, Karnataka, India.
RP Pandey, A (reprint author), Johns Hopkins Med Inst, McKusick Nathans Inst Genet Med, Baltimore, MD 21205 USA.
EM pandey@jhmi.edu; bertvog@gmail.com
RI Chaerkady, Raghothama/D-5718-2011; Pandey, Akhilesh/B-4127-2009;
Papadopoulos, Nickolas/K-7272-2012
OI Pandey, Akhilesh/0000-0001-9943-6127;
FU Lustgarten Foundation for Pancreatic Cancer Research, National Cancer
Institute [NO1 CN-43302]; Department of Defense [W81XWH-06-1-0428]; Sol
Goldman Center for Pancreatic Cancer Research; Virginia and D. K. Ludwig
Fund for Cancer Research; Michael Rolfe Foundation; Joseph L. Rabinowitz
Fund for Pancreatic Cancer Research; National Institutes of Health
[CA62924, RR020839, CA130938, CA57345]
FX This work was supported by the Lustgarten Foundation for Pancreatic
Cancer Research, National Cancer Institute Contract NO1 CN-43302,
Department of Defense Award W81XWH-06-1-0428, the Sol Goldman Center for
Pancreatic Cancer Research, the Virginia and D. K. Ludwig Fund for
Cancer Research, the Michael Rolfe Foundation, the Joseph L. Rabinowitz
Fund for Pancreatic Cancer Research, and National Institutes of Health
Grants CA62924, RR020839, CA130938, and CA57345.
NR 37
TC 82
Z9 83
U1 1
U2 27
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 FEB 8
PY 2011
VL 108
IS 6
BP 2444
EP 2449
DI 10.1073/pnas.1019203108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717YH
UT WOS:000287084500051
PM 21248225
ER
PT J
AU Kannan, P
Brimacombe, KR
Kreisl, WC
Liow, JS
Zoghbi, SS
Telu, S
Zhang, Y
Pike, VW
Halldin, C
Gottesman, MM
Innis, RB
Hall, MD
AF Kannan, Pavitra
Brimacombe, Kyle R.
Kreisl, William C.
Liow, Jeih-San
Zoghbi, Sami S.
Telu, Sanjay
Zhang, Yi
Pike, Victor W.
Halldin, Christer
Gottesman, Michael M.
Innis, Robert B.
Hall, Matthew D.
TI Lysosomal trapping of a radiolabeled substrate of P-glycoprotein as a
mechanism for signal amplification in PET
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE ATP-binding cassette; efflux
ID BLOOD-BRAIN-BARRIER; DRUG EFFLUX TRANSPORTERS; MULTIDRUG-RESISTANCE;
CANCER-CELLS; IN-VIVO; RADIOTRACER; AGENTS; INHIBITOR; HUMANS; SPECT
AB The radiotracer [C-11]N-desmethyl-loperamide (dLop) images the in vivo function of P-glycoprotein (P-gp), a transporter that blocks the entry of drugs that are substrates into brain. When P-gp is inhibited, [C-11]dLop, a potent opiate agonist, enters and becomes trapped in the brain. This trapping is beneficial from an imaging perspective, because it amplifies the PET signal, essentially by accumulating radioactivity over time. As we previously demonstrated that this trapping was not caused by binding to opiate receptors, we examined whether [C-11]dLop, a weak base, is ionically trapped in acidic lysosomes. To test this hypothesis, we measured [H-3]dLop accumulation in human cells by using lysosomotropics. Because the in vivo trapping of dLop was seen after P-gp inhibition, we also measured [H-3]dLop uptake in P-gp-expressing cells treated with the P-gp inhibitor tariquidar. All lysosomotropics decreased [H-3]dLop accumulation by at least 50%. In P-gp-expressing cells, tariquidar (and another P-gp inhibitor) surprisingly decreased [H-3]dLop uptake. Consequently, we measured [C-11]dLop uptake before and after tariquidar preadministration in lysosome-rich organs of P-gp KO mice and humans. After tariquidar pretreatment in both species, radioactivity uptake in these organs decreased by 35% to 40%. Our results indicate that dLop is trapped in lysosomes and that tariquidar competes with dLop for lysosomal accumulation in vitro and in vivo. Although tariquidar and dLop compete for lysosomal trapping in the periphery, such competition does not occur in brain because tariquidar has negligible entry into brain. In summary, tariquidar and [C-11]dLop can be used in combination to selectively measure the function of P-gp at the blood-brain barrier.
C1 [Kannan, Pavitra; Kreisl, William C.; Liow, Jeih-San; Zoghbi, Sami S.; Telu, Sanjay; Zhang, Yi; Pike, Victor W.; Innis, Robert B.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Kannan, Pavitra; Halldin, Christer] Karolinska Inst, Dept Clin Neurosci, Psychiat Sect, SE-17176 Stockholm, Sweden.
[Brimacombe, Kyle R.; Gottesman, Michael M.; Hall, Matthew D.] NCI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
EM robert.innis@nih.gov
OI Kannan, Pavitra/0000-0002-9170-6062
FU National Institute of Mental Health [Z01-MH-002795-07,
Z01-MH-002852-07]; National Cancer Institute [Z01-BC-005598]
FX We thank Ms. Wenjie Xiao and Dr. Ellen Sidransky for assistance with
hippocampal neuron cell culture, Eli Lilly and Co. for providing DCPQ,
and Mr. George Leiman for editorial assistance. This research was
supported by the Intramural Research Programs of the National Institute
of Mental Health Projects Z01-MH-002795-07 and Z01-MH-002852-07 and
National Cancer Institute Project Z01-BC-005598.
NR 35
TC 25
Z9 26
U1 0
U2 9
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD FEB 8
PY 2011
VL 108
IS 6
BP 2593
EP 2598
DI 10.1073/pnas.1014641108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717YH
UT WOS:000287084500076
PM 21262843
ER
PT J
AU Mason, CC
Hanson, RL
Ossowski, V
Bian, L
Baier, LJ
Krakoff, J
Bogardus, C
AF Mason, Clinton C.
Hanson, Robert L.
Ossowski, Vicky
Bian, Li
Baier, Leslie J.
Krakoff, Jonathan
Bogardus, Clifton
TI Bimodal distribution of RNA expression levels in human skeletal muscle
tissue
SO BMC GENOMICS
LA English
DT Article
ID DEPENDENT DIABETES-MELLITUS; GLOBAL GENE-EXPRESSION; INSULIN-RESISTANCE;
PIMA-INDIANS; OXIDATIVE-PHOSPHORYLATION; ASSOCIATION; GENOTYPE; DISEASE;
OBESE
AB Background: Many human diseases and phenotypes are related to RNA expression, levels of which are influenced by a wide spectrum of genetic and exposure-related factors. In a large genome-wide study of muscle tissue expression, we found that some genes exhibited a bimodal distribution of RNA expression, in contrast to what is usually assumed in studies of a single healthy tissue. As bimodality has classically been considered a hallmark of genetic control, we assessed the genome-wide prevalence, cause, and association of this phenomenon with diabetes-related phenotypes in skeletal muscle tissue from 225 healthy Pima Indians using exon array expression chips.
Results: Two independent batches of microarrays were used for bimodal assessment and comparison. Of the 17,881 genes analyzed, eight (GSTM1, HLA-DRB1, ERAP2, HLA-DRB5, MAOA, ACTN3, NR4A2, and THNSL2) were found to have bimodal expression replicated in the separate batch groups, while 24 other genes had evidence of bimodality in only one group. Some bimodally expressed genes had modest associations with pre-diabetic phenotypes, of note ACTN3 with insulin resistance. Most of the other bimodal genes have been reported to be involved with various other diseases and characteristics. Association of expression with cis genetic variation in a subset of 149 individuals found all but one of the confirmed bimodal genes and nearly half of all potential ones to be highly significant expression quantitative trait loci (eQTL). The rare prevalence of these bimodally expressed genes found after controlling for batch effects was much lower than the prevalence reported in other studies. Additional validation in data from separate muscle expression studies confirmed the low prevalence of bimodality we observed.
Conclusions: We conclude that the prevalence of bimodal gene expression is quite rare in healthy muscle tissue (<0.2%), and is much lower than limited reports from other studies. The major cause of these clearly bimodal expression patterns in homogeneous tissue appears to be cis-polymorphisms, indicating that such bimodal genes are, for the most part, eQTL. The high frequency of disease associations reported with these genes gives hope that this unique feature may identify or actually be an underlying factor responsible for disease development.
C1 [Mason, Clinton C.; Hanson, Robert L.; Ossowski, Vicky; Bian, Li; Baier, Leslie J.; Krakoff, Jonathan; Bogardus, Clifton] NIDDKD, Phoenix Epidemiol & Clin Res Branch, Phoenix, AZ 85014 USA.
RP Mason, CC (reprint author), NIDDKD, Phoenix Epidemiol & Clin Res Branch, 1550 E Indian Sch Rd, Phoenix, AZ 85014 USA.
EM masonclint@niddk.nih.gov
RI Hanson, Robert/O-3238-2015
OI Hanson, Robert/0000-0002-4252-7068
FU National Institute of Diabetes and Kidney Diseases (NIDDK); American
Diabetes Association [7-04-DCS-02]
FX We gratefully thank the members and participants of the Gila River
Indian Community, whose involvement made these findings possible. We
acknowledge the additional technical help and data handling of Kristine
Friesen and Sayuko Kobes as well as Drs. Paul Franks, Emilio Ortega, and
Helen Looker. This research was supported in part by the Intramural
Research Program of the National Institute of Diabetes and Kidney
Diseases (NIDDK), and by a DCS award to C.B. from the American Diabetes
Association (#7-04-DCS-02).
NR 49
TC 19
Z9 19
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2164
J9 BMC GENOMICS
JI BMC Genomics
PD FEB 7
PY 2011
VL 12
AR 98
DI 10.1186/1471-2164-12-98
PG 15
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 726AL
UT WOS:000287688200001
PM 21299892
ER
PT J
AU Horton, JK
Stefanick, DF
Zeng, JY
Carrozza, MJ
Wilson, SH
AF Horton, Julie K.
Stefanick, Donna F.
Zeng, Jennifer Y.
Carrozza, Michael J.
Wilson, Samuel H.
TI Requirement for NBS1 in the S phase checkpoint response to DNA
methylation combined with PARP inhibition
SO DNA REPAIR
LA English
DT Article
DE PARP inhibitor; Methyl methanesulfonate; NBS1; SMC1; Cell cycle; Chk1;
Chk2
ID NIJMEGEN BREAKAGE SYNDROME; BASE EXCISION-REPAIR; POLY(ADP-RIBOSE)
POLYMERASE-ACTIVITY; DOUBLE-STRAND BREAKS; CELL-CYCLE;
ATAXIA-TELANGIECTASIA; ATM; PROTEIN; DAMAGE; COMPLEX
AB Treatment of PARP-1-expressing cells with the combination of a DNA methylating agent (MMS) and the PARP inhibitor 4-amino-1,8-naphthalimide (4-AN) leads to an ATR/Chk1-dependent S phase checkpoint and cell death by apoptosis. Activation of ATM/Chk2 is involved in sustaining the S phase checkpoint, and double strand break (DSB) accumulation was demonstrated. NBS1, part of the MRN complex that responds to DSBs, is known to modulate ATR- and ATM-dependent checkpoint responses to UV and IR, but a role in the response to PARP inhibition has not been addressed. Here we show that the S phase checkpoint observed 4-8h after MMS+ 4-AN treatment was absent in cells deficient in NBS1, but was present in NBS1-complemented (i.e., functionally wild-type) cells, indicating a critical role for NBS1 in this checkpoint response. NBS1 was phosphorylated in response to MMS +4-AN treatment, and this was partially ATR- and ATM-dependent, suggesting involvement of both upstream kinases. NBS1 expression had little effect on AIR-mediated phosphorylation of Chk1 and ATM-mediated phosphorylation of Chk2 in response to MMS + 4-AN. Phosphorylation of SMC1 was also observed in response to MMS+ 4-AN treatment. In the absence of ATM and NBS1, phosphorylation of SMC1 was weak, especially at early times after MMS + 4-AN treatment. In the absence of AIR activation, reduced SMC1 phosphorylation was seen over a 24h time course. These results suggested that both ATR and ATM phosphorylate SMC1 in response to MMS + 4-AN and that this phosphorylation is enhanced by phospho-NBS1. The loss of the MMS + 4-AN-induced S phase checkpoint in NBS1-deficient cells may be due to a reduced cellular level of the critical downstream effector, phospho-SMC1. Published by Elsevier B.V.
C1 [Horton, Julie K.; Stefanick, Donna F.; Zeng, Jennifer Y.; Carrozza, Michael J.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, NIH, 111 TW Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences [ES050159]
FX We thank Rebecca Childress for technical assistance, Bonnie Mesmer for
editorial assistance, Lois Wyrick and William Beard for help with figure
preparation, and Michelle Heacock for discussion and critical reading of
the manuscript. We thank Dr. Malgorzata Zdzienicka for allowing us to
use the NBS1 and NBS1 comp cells derived in her laboratory, and obtained
by us from the laboratory of Dr. Priscilla Cooper. We thank Carl Bortner
and the Flow Cytometry Center for assistance. This research was
supported by Research Project Number ES050159 in the Intramural Research
Program of the NIH, National Institute of Environmental Health Sciences.
NR 40
TC 7
Z9 7
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD FEB 7
PY 2011
VL 10
IS 2
BP 225
EP 234
DI 10.1016/j.dnarep.2010.11.003
PG 10
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 725VI
UT WOS:000287673900012
PM 21130714
ER
PT J
AU Tatem, AJ
Campiz, N
Gething, PW
Snow, RW
Linard, C
AF Tatem, Andrew J.
Campiz, Nicholas
Gething, Peter W.
Snow, Robert W.
Linard, Catherine
TI The effects of spatial population dataset choice on estimates of
population at risk of disease
SO POPULATION HEALTH METRICS
LA English
DT Article
ID PLASMODIUM-FALCIPARUM MALARIA; GLOBAL DISTRIBUTION; AVIAN INFLUENZA;
BOVINE TUBERCULOSIS; INFECTIOUS-DISEASES; POTENTIAL IMPACT; CONTROL
PROGRAM; GREAT-BRITAIN; LARGE-SCALE; AFRICA
AB Background: The spatial modeling of infectious disease distributions and dynamics is increasingly being undertaken for health services planning and disease control monitoring, implementation, and evaluation. Where risks are heterogeneous in space or dependent on person-to-person transmission, spatial data on human population distributions are required to estimate infectious disease risks, burdens, and dynamics. Several different modeled human population distribution datasets are available and widely used, but the disparities among them and the implications for enumerating disease burdens and populations at risk have not been considered systematically. Here, we quantify some of these effects using global estimates of populations at risk (PAR) of P. falciparum malaria as an example.
Methods: The recent construction of a global map of P. falciparum malaria endemicity enabled the testing of different gridded population datasets for providing estimates of PAR by endemicity class. The estimated population numbers within each class were calculated for each country using four different global gridded human population datasets: GRUMP (similar to 1 km spatial resolution), LandScan (similar to 1 km), UNEP Global Population Databases (similar to 5 km), and GPW3 (similar to 5 km). More detailed assessments of PAR variation and accuracy were conducted for three African countries where census data were available at a higher administrative-unit level than used by any of the four gridded population datasets.
Results: The estimates of PAR based on the datasets varied by more than 10 million people for some countries, even accounting for the fact that estimates of population totals made by different agencies are used to correct national totals in these datasets and can vary by more than 5% for many low-income countries. In many cases, these variations in PAR estimates comprised more than 10% of the total national population. The detailed country-level assessments suggested that none of the datasets was consistently more accurate than the others in estimating PAR. The sizes of such differences among modeled human populations were related to variations in the methods, input resolution, and date of the census data underlying each dataset. Data quality varied from country to country within the spatial population datasets.
Conclusions: Detailed, highly spatially resolved human population data are an essential resource for planning health service delivery for disease control, for the spatial modeling of epidemics, and for decision-making processes related to public health. However, our results highlight that for the low-income regions of the world where disease burden is greatest, existing datasets display substantial variations in estimated population distributions, resulting in uncertainty in disease assessments that utilize them. Increased efforts are required to gather contemporary and spatially detailed demographic data to reduce this uncertainty, particularly in Africa, and to develop population distribution modeling methods that match the rigor, sophistication, and ability to handle uncertainty of contemporary disease mapping and spread modeling. In the meantime, studies that utilize a particular spatial population dataset need to acknowledge the uncertainties inherent within them and consider how the methods and data that comprise each will affect conclusions.
C1 [Tatem, Andrew J.; Campiz, Nicholas] Univ Florida, Dept Geog, Gainesville, FL 32611 USA.
[Tatem, Andrew J.] Univ Florida, Emerging Pathogens Inst, Gainesville, FL USA.
[Tatem, Andrew J.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Gething, Peter W.; Linard, Catherine] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford OX1 3PS, England.
[Snow, Robert W.] Univ Oxford, Wellcome Trust Res Programme, KEMRI, Ctr Geog Med,Malaria Publ Hlth & Epidemiol Grp, Nairobi, Kenya.
[Snow, Robert W.] Univ Oxford, Nuffield Dept Clin Med, Ctr Trop Med, CCVTM, Oxford, England.
[Linard, Catherine] Univ Libre Bruxelles, Brussels, Belgium.
RP Tatem, AJ (reprint author), Univ Florida, Dept Geog, Gainesville, FL 32611 USA.
EM andy.tatem@gmail.com
OI Snow, Robert/0000-0003-3725-6088; Gething, Peter/0000-0001-6759-5449
FU Wellcome Trust [079080]
NR 91
TC 26
Z9 26
U1 0
U2 16
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1478-7954
J9 POPUL HEALTH METR
JI Popul. Health Metr.
PD FEB 7
PY 2011
VL 9
AR 4
DI 10.1186/1478-7954-9-4
PG 14
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 891KP
UT WOS:000300216000001
PM 21299885
ER
PT J
AU Scully, CG
Karaboue, A
Liu, WM
Meyer, J
Innominato, PF
Chon, KH
Gorbach, AM
Levi, F
AF Scully, Christopher G.
Karaboue, Abdoulaye
Liu, Wei-Min
Meyer, Joseph
Innominato, Pasquale F.
Chon, Ki H.
Gorbach, Alexander M.
Levi, Francis
TI Skin surface temperature rhythms as potential circadian biomarkers for
personalized chronotherapeutics in cancer patients
SO INTERFACE FOCUS
LA English
DT Article
DE chronotherapeutics; circadian rhythm; biomarker; body temperature;
cancer; personalized medicine
ID METASTATIC COLORECTAL-CANCER; QUALITY-OF-LIFE; WAVELET ANALYSIS; CLOCKS;
SLEEP; OXALIPLATIN; SURVIVAL; DELIVERY; DISEASE; 5-FLUOROURACIL
AB Chronotherapeutics involve the administration of treatments according to circadian rhythms. Circadian timing of anti-cancer medications has been shown to improve treatment tolerability up to fivefold and double efficacy in experimental and clinical studies. However, the physiological and the molecular components of the circadian timing system (CTS), as well as gender, critically affect the success of a standardized chronotherapeutic schedule. In addition, a wrongly timed therapy or an excessive drug dose disrupts the CTS. Therefore, a non-invasive approach to accurately detect and monitor circadian rhythms is needed for a dynamic assessment of the CTS in order to personalize chronomodulated drug delivery schedule in cancer patients. Since core body temperature is a robust circadian biomarker, we recorded temperature at multiple locations on the skin of the upper chest and back of controls and cancer patients continuously. Variability in the circadian phase existed among patch locations in individual subjects over the course of 2-6 days, demonstrating the need to monitor multiple skin temperature locations to determine the precise circadian phase. Additionally, we observed that locations identified by infrared imaging as relatively cool had the largest 24 h temperature variations. Disruptions in skin temperature rhythms during treatment were found, pointing to the need to continually assess circadian timing and personalize chronotherapeutic schedules.
C1 [Karaboue, Abdoulaye; Innominato, Pasquale F.; Levi, Francis] INSERM, UMRS776, F-94807 Villejuif, France.
[Scully, Christopher G.; Liu, Wei-Min; Meyer, Joseph; Gorbach, Alexander M.] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
[Scully, Christopher G.; Chon, Ki H.] Worcester Polytech Inst, Dept Biomed Engn, Worcester, MA 01609 USA.
[Karaboue, Abdoulaye; Innominato, Pasquale F.; Levi, Francis] Univ Paris 11, UMR S0776, F-91405 Orsay, France.
[Innominato, Pasquale F.; Levi, Francis] Hop Paul Brousse, Dept Cancerol, Unite Chronotherapie, AP HP, F-94807 Villejuif, France.
RP Levi, F (reprint author), INSERM, UMRS776, F-94807 Villejuif, France.
EM francis.levi@inserm.fr
FU European Commission through the Network of Excellence BIOSIM
[LSHBCT-2004-005137]; Association pour la Recherche sur le Temps
Biologique et la Chronotherapie (ARTBC International); Hopital Paul
Brousse, Villejuif (France); National Institute of Biomedical Imaging
and Bioengineering, National Institutes of Health (USA)
FX This research was supported, in part, by the European Commission through
the Network of Excellence BIOSIM (Biosimulation: a new tool for drug
development; contract no. LSHBCT-2004-005137), the Association pour la
Recherche sur le Temps Biologique et la Chronotherapie (ARTBC
International), Hopital Paul Brousse, Villejuif (France) and the
Intramural Research Programme of the National Institute of Biomedical
Imaging and Bioengineering, National Institutes of Health (USA). The
authors thank the subjects who participated in the study, Dr G. Kato, Dr
H. Ackerman and A. Dementyev for insightful discussions and J. Bretes,
FLIR Systems ATS France for the loan of infrared equipment and
assistance for this study.
NR 44
TC 11
Z9 12
U1 1
U2 3
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 2042-8898
J9 INTERFACE FOCUS
JI Interface Focus
PD FEB 6
PY 2011
VL 1
IS 1
BP 48
EP 60
DI 10.1098/rsfs.2010.0012
PG 13
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 851LT
UT WOS:000297272400007
PM 21544221
ER
PT J
AU Meltzer, JA
Braun, AR
AF Meltzer, Jed A.
Braun, Allen R.
TI An EEG-MEG dissociation between online syntactic comprehension and post
hoc reanalysis
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE syntax; Broca's area; semantic; language; complexity; reversibility
ID EVENT-RELATED FMRI; VERBAL WORKING-MEMORY; LANGUAGE COMPREHENSION;
SENTENCE COMPREHENSION; BROCAS AREA; FREQUENCY; RESPONSES; APHASIA;
MAGNETOENCEPHALOGRAPHY; LOCALIZATION
AB Successful comprehension of syntactically complex sentences depends on online language comprehension mechanisms as well as reanalysis in working memory. To differentiate the neural substrates of these processes, we recorded electroencephalography and magnetoencephalography (MEG) during sentence-picture-matching in healthy subjects, assessing the effects of two difficulty factors: syntactic complexity (object-embedded vs. subject-embedded relative clauses) and semantic reversibility on neuronal oscillations during sentence presentation, and during a subsequent memory delay prior to picture onset. Synthetic Aperture magnetometry analysis of MEG showed that semantic reversibility induced left lateralized perisylvian power decreases in a broad frequency range, approximately 8-30 Hz. This effect followed the relative clause presentation and persisted throughout the remainder of the sentence and the subsequent memory delay period, shifting to a more frontal distribution during the delay. In contrast, syntactic complexity induced enhanced power decreases only during the delay period, in bilateral frontal and anterior temporal regions. These results indicate that detailed syntactic parsing of auditory language input may be augmented in the absence of alternative cues for thematic role assignment, as reflected by selective perisylvian engagement for reversible sentences, compared with irreversible sentences in which world knowledge constrains possible thematic roles. Furthermore, comprehension of complex syntax appears to depend on post hoc reanalysis in working memory implemented by frontal regions in both hemispheres.
C1 [Meltzer, Jed A.; Braun, Allen R.] Natl Inst Deafness & Other Commun Disorders, Language Sect, NIH, Bethesda, MD 20892 USA.
RP Meltzer, JA (reprint author), Natl Inst Deafness & Other Commun Disorders, Language Sect, NIH, Bldg 10,Room 5C-410, Bethesda, MD 20892 USA.
EM jed.meltzer@aya.yale.edu
OI Meltzer, Jed/0000-0002-4301-1901
FU NIH, National Institute on Deafness and Other Communication Disorders
FX We gratefully acknowledge technical assistance from Joe McArdle, Suraji
Wagage, Elizabeth Rawson, Judy Mitchell-Francis, Tom Holroyd, and Fred
Carver. This study was funded through the NIH Intramural Research
Program, in the National Institute on Deafness and Other Communication
Disorders.
NR 56
TC 5
Z9 5
U1 3
U2 12
PU FRONTIERS RES FOUND
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD FEB 4
PY 2011
VL 5
AR 10
DI 10.3389/fnhum.2011.00010
PG 15
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 748VK
UT WOS:000289420700001
PM 21331355
ER
PT J
AU Charles, BA
Shriner, D
Doumatey, A
Chen, GJ
Zhou, J
Huang, HX
Herbert, A
Gerry, NP
Christman, MF
Adeyemo, A
Rotimi, CN
AF Charles, Bashira A.
Shriner, Daniel
Doumatey, Ayo
Chen, Guanjie
Zhou, Jie
Huang, Hanxia
Herbert, Alan
Gerry, Norman P.
Christman, Michael F.
Adeyemo, Adebowale
Rotimi, Charles N.
TI A genome-wide association study of serum uric acid in African Americans
SO BMC MEDICAL GENOMICS
LA English
DT Article
ID PROGRESSIVE RENAL-DISEASE; CARDIOVASCULAR-DISEASE;
ESSENTIAL-HYPERTENSION; METABOLIC SYNDROME; RISK-FACTOR; SLC2A9; URATE;
HYPERURICEMIA; INCREASES; EVOLUTION
AB Background: Uric acid is the primary byproduct of purine metabolism. Hyperuricemia is associated with body mass index (BMI), sex, and multiple complex diseases including gout, hypertension (HTN), renal disease, and type 2 diabetes (T2D). Multiple genome-wide association studies (GWAS) in individuals of European ancestry (EA) have reported associations between serum uric acid levels (SUAL) and specific genomic loci. The purposes of this study were: 1) to replicate major signals reported in EA populations; and 2) to use the weak LD pattern in African ancestry population to better localize (fine-map) reported loci and 3) to explore the identification of novel findings cognizant of the moderate sample size.
Methods: African American (AA) participants (n = 1,017) from the Howard University Family Study were included in this study. Genotyping was performed using the Affymetrix (R) Genome-wide Human SNP Array 6.0. Imputation was performed using MACH and the HapMap reference panels for CEU and YRI. A total of 2,400,542 single nucleotide polymorphisms (SNPs) were assessed for association with serum uric acid under the additive genetic model with adjustment for age, sex, BMI, glomerular filtration rate, HTN, T2D, and the top two principal components identified in the assessment of admixture and population stratification.
Results: Four variants in the gene SLC2A9 achieved genome-wide significance for association with SUAL (p-values ranging from 8.88 x 10(-9) to 1.38 x 10(-9)). Fine-mapping of the SLC2A9 signals identified a 263 kb interval of linkage disequilibrium in the HapMap CEU sample. This interval was reduced to 37 kb in our AA and the HapMap YRI samples.
Conclusions: The most strongly associated locus for SUAL in EA populations was also the most strongly associated locus in this AA sample. This finding provides evidence for the role of SLC2A9 in uric acid metabolism across human populations. Additionally, our findings demonstrate the utility of following-up EA populations GWAS signals in African-ancestry populations with weaker linkage disequilibrium.
C1 [Charles, Bashira A.; Shriner, Daniel; Doumatey, Ayo; Chen, Guanjie; Zhou, Jie; Huang, Hanxia; Adeyemo, Adebowale; Rotimi, Charles N.] NHGRI, Ctr Res Genom & Global Hlth, Bethesda, MD 20892 USA.
[Herbert, Alan] Boston Univ, Dept Genet & Genom, Boston, MA 02118 USA.
[Gerry, Norman P.; Christman, Michael F.] Coriell Inst Med Res, Camden, NJ 08103 USA.
RP Rotimi, CN (reprint author), NHGRI, Ctr Res Genom & Global Hlth, Bethesda, MD 20892 USA.
EM rotomic@mail.nih.gov
OI Adeyemo, Adebowale/0000-0002-3105-3231
FU NIGMS/MBRS/SCORE [S06GM008016-320107, S06GM008016-380111]; National
Center for Research Resources (NCRR) a component of the National
Institutes of Health (NIH) [2M01RR010284]; Coriell Institute for
Biomedical Sciences; National Human Genome Research Institute; National
Institutes of Health, in the Center for Research in Genomics and Global
Health [Z01HG200362]
FX The study was supported by grants S06GM008016-320107 to CR and
S06GM008016-380111 to AA, both from the NIGMS/MBRS/SCORE Program.
Participant enrollment was carried out at the Howard University General
Clinical Research Center (GCRC), which is supported by grant number
2M01RR010284 from the National Center for Research Resources (NCRR), a
component of the National Institutes of Health (NIH). Additional support
was provided by the Coriell Institute for Biomedical Sciences. This
research was supported in part by the Intramural Research Program of the
National Human Genome Research Institute, National Institutes of Health,
in the Center for Research in Genomics and Global Health (Z01HG200362).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 45
TC 44
Z9 51
U1 0
U2 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1755-8794
J9 BMC MED GENOMICS
JI BMC Med. Genomics
PD FEB 4
PY 2011
VL 4
AR 17
DI 10.1186/1755-8794-4-17
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 726WT
UT WOS:000287758200001
PM 21294900
ER
PT J
AU Hanover, JA
AF Hanover, John A.
TI A Versatile Sugar Transferase Makes the Cut
SO CELL
LA English
DT Editorial Material
ID CELL-PROLIFERATION; HCF-1
AB The nutrient sensor O-GlcNAc transferase modifies proteins with the O-GlcNAc moiety. In this issue, Capotosti et al. (2011) reveal that O-GlcNAc transferase not only glycosylates the cell-cycle regulator host cell factor 1 but activates it through proteolytic cleavage, providing a surprising link between metabolism and epigenetic regulation of the cell cycle.
C1 NIDDK, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Hanover, JA (reprint author), NIDDK, Cellular & Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
EM jah@helix.nih.gov
NR 10
TC 5
Z9 5
U1 1
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD FEB 4
PY 2011
VL 144
IS 3
BP 321
EP 323
DI 10.1016/j.cell.2011.01.025
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 716MK
UT WOS:000286973100003
PM 21295693
ER
PT J
AU Wong, YF
Kopp, JB
Roberts, C
Scambler, PJ
Abe, Y
Rankin, AC
Dutt, N
Hendry, BM
Xu, QH
AF Wong, Yuen Fei
Kopp, Jeffrey B.
Roberts, Catherine
Scambler, Peter J.
Abe, Yoshifusa
Rankin, Alexandra C.
Dutt, Neelanjana
Hendry, Bruce M.
Xu, Qihe
TI Endogenous Retinoic Acid Activity in Principal Cells and Intercalated
Cells of Mouse Collecting Duct System
SO PLOS ONE
LA English
DT Article
ID VITAMIN-A-DEFICIENCY; VACUOLAR H+-ATPASE; DEPENDENT ACTIVATION; NEPHRON
DEVELOPMENT; MOLECULAR-CLONING; GENE-EXPRESSION; KIDNEY; RECEPTORS;
RATS; ORGANOGENESIS
AB Background: Retinoic acid is the bioactive derivative of vitamin A, which plays an indispensible role in kidney development by activating retinoic acid receptors. Although the location, concentration and roles of endogenous retinoic acid in postnatal kidneys are poorly defined, there is accumulating evidence linking post-natal vitamin A deficiency to impaired renal concentrating and acidifying capacity associated with increased susceptibility to urolithiasis, renal inflammation and scarring. The aim of this study is to examine the presence and the detailed localization of endogenous retinoic acid activity in neonatal, young and adult mouse kidneys, to establish a fundamental ground for further research into potential target genes, as well as physiological and pathophysiological roles of endogenous retinoic acid in the post-natal kidneys.
Methodology/Principal Findings: RARE-hsp68-lacZ transgenic mice were employed as a reporter for endogenous retinoic acid activity that was determined by X-gal assay and immunostaining of the reporter gene product, beta-galactosidase. Double immunostaining was performed for beta-galactosidase and markers of kidney tubules to localize retinoic acid activity. Distinct pattern of retinoic acid activity was observed in kidneys, which is higher in neonatal and 1- to 3-week-old mice than that in 5- and 8-week-old mice. The activity was present specifically in the principal cells and the intercalated cells of the collecting duct system in all age groups, but was absent from the glomeruli, proximal tubules, thin limbs of Henle's loop and distal tubules.
Conclusions/Significance: Endogenous retinoic acid activity exists in principal cells and intercalated cells of the mouse collecting duct system after birth and persists into adulthood. This observation provides novel insights into potential roles for endogenous retinoic acid beyond nephrogenesis and warrants further studies to investigate target genes and functions of endogenous retinoic acid in the kidney after birth, particularly in the collecting duct system.
C1 [Wong, Yuen Fei; Rankin, Alexandra C.; Hendry, Bruce M.; Xu, Qihe] Kings Coll London, Dept Renal Med, London WC2R 2LS, England.
[Dutt, Neelanjana] Kings Coll Hosp London, Dept Histopathol, London, England.
[Kopp, Jeffrey B.; Abe, Yoshifusa] NIDDKD, Kidney Dis Sect, NIH, Bethesda, MD 20892 USA.
[Roberts, Catherine; Scambler, Peter J.] Inst Child Hlth, Mol Med Unit, London, England.
RP Wong, YF (reprint author), Kings Coll London, Dept Renal Med, London WC2R 2LS, England.
EM qihe.xu@kcl.ac.uk
RI Scambler, Peter/C-4998-2008;
OI Scambler, Peter/0000-0002-1487-4628; Kopp, Jeffrey/0000-0001-9052-186X
FU Kidney Research United Kingdom project [RP29/2/06]; National Institutes
of Health [Z01 DK043308]
FX This work was supported by a Kidney Research United Kingdom project
grant (RP29/2/06) awarded to QX and BMH and a National Institutes of
Health Intramural Program grant (Z01 DK043308) to JBK. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 37
TC 7
Z9 7
U1 0
U2 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD FEB 4
PY 2011
VL 6
IS 2
AR e16770
DI 10.1371/journal.pone.0016770
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717IN
UT WOS:000287037000020
PM 21326615
ER
PT J
AU Oakley, RH
Cidlowski, JA
AF Oakley, Robert H.
Cidlowski, John A.
TI Cellular Processing of the Glucocorticoid Receptor Gene and Protein: New
Mechanisms for Generating Tissue-specific Actions of Glucocorticoids
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Review
ID PRE-MESSENGER-RNA; BETA-ISOFORM; TRANSCRIPTIONAL ACTIVITY; BINDING
DOMAIN; EXPRESSION; CELLS; PHOSPHORYLATION; ALPHA; TRANSACTIVATION;
REPRESSION
AB Glucocorticoids regulate numerous physiological processes and are mainstays in the treatment of inflammation, autoimmune disease, and cancer. The traditional view that glucocorticoids act through a single glucocorticoid receptor (GR) protein has changed in recent years with the discovery of a large cohort of receptor subtypes arising from alternative processing of the GR gene. These isoforms differ in their expression, gene regulatory, and functional profiles. Post-translational modification of these proteins further expands GR diversity. Here, we discuss the origin and molecular properties of the GR isoforms and their contribution to the sensitivity and specificity of the glucocorticoid response.
C1 [Oakley, Robert H.; Cidlowski, John A.] NIEHS, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Cidlowski, JA (reprint author), NIEHS, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, POB 12233, Res Triangle Pk, NC 27709 USA.
EM cidlows1@niehs.nih.gov
FU NIEHS, National Institutes of Health
FX This work was supported, in whole or in part, by the NIEHS Intramural
Research Program of the National Institutes of Health. This is the
fourth article in the Thematic Minireview Series on Nuclear Receptors in
Biology and Diseases. This minireview will be reprinted in the 2011
Minireview Compendium, which will be available in January, 2012.
NR 98
TC 129
Z9 135
U1 1
U2 18
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 FEB 4
PY 2011
VL 286
IS 5
BP 3177
EP 3184
DI 10.1074/jbc.R110.179325
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 712GE
UT WOS:000286653200001
PM 21149445
ER
PT J
AU Van Itallie, CM
Mitic, LL
Anderson, JM
AF Van Itallie, Christina M.
Mitic, Laura L.
Anderson, James M.
TI Claudin-2 Forms Homodimers and Is a Component of a High Molecular Weight
Protein Complex
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID BLUE NATIVE ELECTROPHORESIS; TIGHT-JUNCTION LOCALIZATION;
BIOCHEMICAL-CHARACTERIZATION; PLASMA-MEMBRANE; OCCLUDIN; BARRIER;
PALMITOYLATION; SOLUBILIZATION; PERMEABILITY; TRICELLULIN
AB Tight junctions are multiprotein complexes that form the fundamental physiologic and anatomic barrier between epithelial and endothelial cells, yet little information is available about their molecular organization. To begin to understand how the transmembrane proteins of the tight junction are organized into multiprotein complexes, we used blue native-PAGE (BN-PAGE) and cross-linking techniques to identify complexes extracted from MDCK II cells and mouse liver. In nonionic detergent extracts from MDCK II cells, the tight junction integral membrane protein claudin-2 was preferentially isolated as a homodimer, whereas claudin-4 was monomeric. Analysis of the interactions between chimeras of claudin-2 and -4 are consistent with the transmembrane domains of claudin-2 being responsible for dimerization, and mutational analysis followed by cross-linking indicated that the second transmembrane domains were arranged in close proximity in homodimers. BN-PAGE of mouse liver membrane identified a relatively discrete high molecular weight complex containing at least claudin-1, claudin-2, and occludin; the difference in the protein complex sizes between cultured cells and tissues may reflect differences in tight junction protein or lipid composition or post-translational modifications. Our results suggest that BN-PAGE may be a useful tool in understanding tight junction structure.
C1 Univ N Carolina, Dept Med, Chapel Hill, NC 27599 USA.
[Mitic, Laura L.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94158 USA.
[Anderson, James M.] Univ N Carolina, Dept Cell & Mol Physiol, Chapel Hill, NC 27599 USA.
RP Van Itallie, CM (reprint author), NHLBI, NIH, Bldg 50,Rm 4530, Bethesda, MD 20892 USA.
EM Christina.VanItallie@nih.gov
FU National Institutes of Health [RO1 DK45134]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant RO1 DK45134.
NR 44
TC 30
Z9 31
U1 0
U2 3
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD FEB 4
PY 2011
VL 286
IS 5
BP 3442
EP 3450
DI 10.1074/jbc.M110.195578
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 712GE
UT WOS:000286653200030
PM 21098027
ER
PT J
AU Kodama, S
Negishi, M
AF Kodama, Susumu
Negishi, Masahiko
TI Pregnane X Receptor PXR Activates the GADD45 beta Gene, Eliciting the
p38 MAPK Signal and Cell Migration
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NF-KAPPA-B; NUCLEAR RECEPTORS; CROSS-TALK; TGF-BETA;
HEPATOCELLULAR-CARCINOMA; LIVER-REGENERATION; KINASE ACTIVATION;
PROTEIN-KINASE; EXPRESSION; CAR
AB Pregnane X receptor (PXR) was originally characterized as a transcription factor that induces hepatic drug metabolism by activating cytochrome P450 genes. Here we have now demonstrated a novel function of PXR, that of eliciting p38 mitogen-activated protein kinase (MAPK) phosphorylation for cell migration. Upon xenobiotic activation of ectopic human PXR, human hepatocellular carcinoma HepG2 cells were found to exhibit increased phosphorylation of p38 MAPK and to subsequently change morphology and migrate. p38 MAPK was responsible for the regulation of these morphological changes and cell migration because the p38 MAPK inhibitor SB239063 repressed both. Prior to this phosphorylation, PXR directly activated the early response GADD45 beta gene by binding to a distal direct repeat 4 site of the GADD45 beta promoter. Ectopic expression of GADD45 beta increased p38 MAPK phosphorylation, whereas siRNA knockdown of GADD45 beta decreased the PXR-induced p38 MAPK phosphorylation, confirming that GADD45 beta can regulate PXR-induced p38 MAPK phosphorylation in HepG2 cells. These results indicate that PXR activates the GADD45 beta gene, increasing p38 MAPK phosphorylation, and leading HepG2 cells to change morphology and migrate. The GADD45 beta gene is a direct target for PXR, eliciting cell signals to regulate various cellular functions.
C1 [Kodama, Susumu; Negishi, Masahiko] NIEHS, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Negishi, M (reprint author), NIEHS, Pharmacogenet Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
EM negishi@niehs.nih.gov
FU National Institutes of Health through NIEHS [Z01ES1005-01]
FX This work was supported, in whole or in part, by National Institutes of
Health Intramural Research Program Grant Z01ES1005-01 through the NIEHS.
NR 37
TC 25
Z9 25
U1 0
U2 1
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 FEB 4
PY 2011
VL 286
IS 5
BP 3570
EP 3578
DI 10.1074/jbc.M110.179812
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 712GE
UT WOS:000286653200041
PM 21127053
ER
PT J
AU Ammosova, T
Yedavalli, VRK
Niu, XM
Jerebtsova, M
Van Eynde, A
Beullens, M
Bollen, M
Jeang, KT
Nekhai, S
AF Ammosova, Tatiana
Yedavalli, Venkat R. K.
Niu, Xiaomei
Jerebtsova, Marina
Van Eynde, Aleyde
Beullens, Monique
Bollen, Mathieu
Jeang, Kuan-Teh
Nekhai, Sergei
TI Expression of a Protein Phosphatase 1 Inhibitor, cdNIPP1, Increases CDK9
Threonine 186 Phosphorylation and Inhibits HIV-1 Transcription
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RNA-POLYMERASE-II; LONG-TERMINAL REPEAT; P-TEFB; TAT TRANSACTIVATION;
CYCLIN T1; 7SK SNRNA; KINASE; VIRUS; ACETYLATION; ELONGATION
AB CDK9/cyclin T1, a key enzyme in HIV-1 transcription, is negatively regulated by 7SK RNA and the HEXIM1 protein. Dephosphorylation of CDK9 on Thr(186) by protein phosphatase 1 (PP1) in stress-induced cells or by protein phosphatase M1A in normally growing cells activates CDK9. Our previous studies showed that HIV-1 Tat protein binds to PP1 through the Tat Q(35)VCF(38) sequence, which is similar to the PP1-binding RVXF motif and that this interaction facilitates HIV-1 transcription. In the present study, we analyzed the effect of expression of the central domain of nuclear inhibitor of PP1 (cdNIPP1) in an engineered cell line and also when cdNIPP1 was expressed as part of HIV-1 pNL4-3 in place of nef. Stable expression of cdNIPP1 increased CDK9 phosphorylation on Thr(186) and the association of CDK9 with 7SK RNA. The stable expression of cdNIPP1 disrupted the interaction of Tat and PP1 and inhibited HIV-1 transcription. Expression of cdNIPP1 as a part of the HIV-1 genome inhibited HIV-1 replication. Our study provides a proof-of-concept for the future development of PP1-targeting compounds as inhibitors of HIV-1 replication.
C1 [Ammosova, Tatiana; Niu, Xiaomei; Nekhai, Sergei] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20001 USA.
[Yedavalli, Venkat R. K.; Jeang, Kuan-Teh] NIAID, Natl Inst Hlth, Mol Virol Sect, Mol Microbiol Lab, Bethesda, MD 20817 USA.
[Jerebtsova, Marina] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Van Eynde, Aleyde; Beullens, Monique; Bollen, Mathieu] Catholic Univ Louvain, Dept Mol Cell Biol, B-3000 Louvain, Belgium.
RP Nekhai, S (reprint author), Howard Univ, Ctr Sickle Cell Dis, 1840 7th St NW,HURB1,Suite 202, Washington, DC 20001 USA.
EM snekhai@howard.edu
RI Jeang, Kuan-Teh/A-2424-2008
FU National Institutes of Health Research by NHLBI [2 R25 HL003679-12];
Office of Research on Minority by National Institute for General Medical
Sciences [1SC1GM082325-03]; Howard University; Research Centers in
Minority Institutions Program, Division of Research Infrastructure,
National Center for Research Resources, National Institutes of Health
[RCMI-NIH 2G12RR003048-22]
FX This work was supported by National Institutes of Health Research Grant
2 R25 HL003679-12 funded by the NHLBI. This work was also supported by
the Office of Research on Minority, Grant 1SC1GM082325-03, funded by the
National Institute for General Medical Sciences; by a Howard University
Seed Grant (to S. N.); and by Grant RCMI-NIH 2G12RR003048-22 from the
Research Centers in Minority Institutions Program, Division of Research
Infrastructure, National Center for Research Resources, National
Institutes of Health.
NR 41
TC 22
Z9 22
U1 0
U2 5
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD FEB 4
PY 2011
VL 286
IS 5
BP 3798
EP 3804
DI 10.1074/jbc.M110.196493
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 712GE
UT WOS:000286653200061
PM 21098020
ER
PT J
AU Beisel, CL
Storz, G
AF Beisel, Chase L.
Storz, Gisela
TI The Base-Pairing RNA Spot 42 Participates in a Multioutput Feedforward
Loop to Help Enact Catabolite Repression in Escherichia coli
SO MOLECULAR CELL
LA English
DT Article
ID REGULATING GENE-EXPRESSION; NETWORK MOTIFS; NONCODING RNA; PROTEIN; CRP;
IDENTIFICATION; TRANSCRIPTION; SPOT-42-RNA; METABOLISM; MOLECULE
AB Bacteria selectively consume some carbon sources over others through a regulatory mechanism termed catabolite repression. Here, we show that the base-pairing RNA Spot 42 plays a broad role in catabolite repression in Escherichia coli by directly repressing genes involved in central and secondary metabolism, redox balancing, and the consumption of diverse non-preferred carbon sources. Many of the genes repressed by Spot 42 are transcriptionally activated by the global regulator CRP. Since CRP represses Spot 42, these regulators participate in a specific regulatory circuit called a multioutput feedforward loop. We found that this loop can reduce leaky expression of target genes in the presence of glucose and can maintain repression of target genes under changing nutrient conditions. Our results suggest that base-pairing RNAs in feedforward loops can help shape the steady-state levels and dynamics of gene expression.
C1 [Beisel, Chase L.; Storz, Gisela] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, Bethesda, MD 20892 USA.
RP Beisel, CL (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, Bethesda, MD 20892 USA.
EM beiselcl@mail.nih.gov; storz@helix.nih.gov
RI Beisel, Chase/D-4823-2015;
OI Beisel, Chase/0000-0003-0650-9943; Storz, Gisela/0000-0001-6698-1241
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development
FX We thank E. Fozo, R. Fuchs, S. Gottesman, M. Goulian, E. Hobbs, B.
Janson, M. Thomason, and L. Waters for their comments on this manuscript
and S. Durand for technical assistance. P. Mandin kindly provided the E.
coli strain PM1205 and the plasmid pSpot42, and N. Majdalani kindly
provided the E. coli strain NM525. Work carried out in the laboratory of
G.S. is supported by the Intramural Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development. C.L.B.
is a Gordon and Betty Moore Foundation Fellow of the Life Sciences
Research Foundation.
NR 41
TC 89
Z9 90
U1 1
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1097-2765
EI 1097-4164
J9 MOL CELL
JI Mol. Cell
PD FEB 4
PY 2011
VL 41
IS 3
BP 286
EP 297
DI 10.1016/j.molcel.2010.12.027
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 722UM
UT WOS:000287460500007
PM 21292161
ER
PT J
AU Lee, J
Romero, R
Xu, Y
Kim, JS
Topping, V
Yoo, W
Kusanovic, JP
Chaiworapongsa, T
Hassan, SS
Yoon, BH
Kim, CJ
AF Lee, JoonHo
Romero, Roberto
Xu, Yi
Kim, Jung-Sun
Topping, Vanessa
Yoo, Wonsuk
Pedro Kusanovic, Juan
Chaiworapongsa, Tinnakorn
Hassan, Sonia S.
Yoon, Bo Hyun
Kim, Chong Jai
TI A Signature of Maternal Anti-Fetal Rejection in Spontaneous Preterm
Birth: Chronic Chorioamnionitis, Anti-Human Leukocyte Antigen
Antibodies, and C4d
SO PLOS ONE
LA English
DT Article
ID NEONATAL ALLOIMMUNE THROMBOCYTOPENIA; SOLID-ORGAN TRANSPLANTATION;
RENAL-ALLOGRAFT REJECTION; CLINICAL-SIGNIFICANCE; HLA ANTIBODIES;
RECURRENT ABORTION; MEDIATED REJECTION; HUMORAL IMMUNITY; UNKNOWN
ETIOLOGY; HUMAN-PREGNANCY
AB Background: Chronic chorioamnionitis is found in more than one-third of spontaneous preterm births. Chronic chorioamnionitis and villitis of unknown etiology represent maternal anti-fetal cellular rejection. Antibody-mediated rejection is another type of transplantation rejection. We investigated whether there was evidence for antibody-mediated rejection against the fetus in spontaneous preterm birth.
Methods and Findings: This cross-sectional study included women with (1) normal pregnancy and term delivery (n = 140) and (2) spontaneous preterm delivery (n = 140). We analyzed maternal and fetal sera for panel-reactive anti-HLA class I and class II antibodies, and determined C4d deposition on umbilical vein endothelium by immunohistochemistry. Maternal anti-HLA class I seropositivity in spontaneous preterm births was higher than in normal term births (48.6% vs. 32.1%, p = 0.005). Chronic chorioamnionitis was associated with a higher maternal anti-HLA class I seropositivity (p<0.01), significant in preterm and term birth. Villitis of unknown etiology was associated with increased maternal and fetal anti-HLA class I and II seropositivity (p<0.05, for each). Fetal anti-HLA seropositivity was closely related to maternal anti-HLA seropositivity in both groups (p<0.01, for each). C4d deposition on umbilical vein endothelium was more frequent in preterm labor than term labor (77.1% vs. 11.4%, p<0.001). Logistic regression analysis revealed that chronic chorioamnionitis (OR = 6.10, 95% CI 1.29-28.83), maternal anti-HLA class I seropositivity (OR = 5.90, 95% CI 1.60-21.83), and C4d deposition on umbilical vein endothelium (OR = 36.19, 95% CI 11.42-114.66) were associated with preterm labor and delivery.
Conclusions: A major subset of spontaneous preterm births has a signature of maternal anti-fetal cellular and antibody-mediated rejections with links to fetal graft-versus-host disease and alloimmune reactions.
C1 [Lee, JoonHo; Romero, Roberto; Xu, Yi; Topping, Vanessa; Pedro Kusanovic, Juan; Chaiworapongsa, Tinnakorn; Hassan, Sonia S.; Kim, Chong Jai] NICHHD, Perinatol Res Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Lee, JoonHo; Romero, Roberto; Xu, Yi; Topping, Vanessa; Pedro Kusanovic, Juan; Chaiworapongsa, Tinnakorn; Hassan, Sonia S.; Kim, Chong Jai] NICHHD, Perinatol Res Branch, NIH, US Dept HHS, Detroit, MI USA.
[Romero, Roberto; Chaiworapongsa, Tinnakorn; Hassan, Sonia S.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
[Kim, Jung-Sun] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul, South Korea.
[Yoo, Wonsuk] Wayne State Univ, Sch Med, Dept Internal Med, Detroit, MI 48201 USA.
[Pedro Kusanovic, Juan] Hosp Dr Sotero del Rio, Dept Obstet & Gynecol, Santiago, Chile.
[Pedro Kusanovic, Juan] Pontificia Univ Catolica Chile, Sch Med, Dept Obstet & Gynecol, Santiago, Chile.
[Yoon, Bo Hyun] Seoul Natl Univ, Coll Med, Dept Obstet & Gynecol, Seoul, South Korea.
[Kim, Chong Jai] Wayne State Univ, Sch Med, Dept Pathol, Detroit, MI 48201 USA.
RP Lee, J (reprint author), NICHHD, Perinatol Res Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
EM prbchiefstaff@med.wayne.edu; cjkim@med.wayne.edu
RI Yoon, Bo Hyun/H-6344-2011
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, USA
FX This work was supported by the Perinatology Research Branch, Division of
Intramural Research, Eunice Kennedy Shriver National Institute of Child
Health and Human Development, USA. No additional external funding was
received for this study. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 58
TC 40
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U1 0
U2 10
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD FEB 4
PY 2011
VL 6
IS 2
AR e16806
DI 10.1371/journal.pone.0016806
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 717IN
UT WOS:000287037000022
PM 21326865
ER
PT J
AU Collins, FS
AF Collins, Francis S.
TI Faces of the Genome
SO SCIENCE
LA English
DT Editorial Material
C1 NIH, Bethesda, MD 20892 USA.
RP Collins, FS (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
NR 0
TC 14
Z9 15
U1 0
U2 2
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD FEB 4
PY 2011
VL 331
IS 6017
BP 546
EP 546
DI 10.1126/science.1202894
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 715ZE
UT WOS:000286933600037
PM 21292963
ER
PT J
AU Colbourne, JK
Pfrender, ME
Gilbert, D
Thomas, WK
Tucker, A
Oakley, TH
Tokishita, S
Aerts, A
Arnold, GJ
Basu, MK
Bauer, DJ
Caceres, CE
Carmel, L
Casola, C
Choi, JH
Detter, JC
Dong, QF
Dusheyko, S
Eads, BD
Frohlich, T
Geiler-Samerotte, KA
Gerlach, D
Hatcher, P
Jogdeo, S
Krijgsveld, J
Kriventseva, EV
Kultz, D
Laforsch, C
Lindquist, E
Lopez, J
Manak, JR
Muller, J
Pangilinan, J
Patwardhan, RP
Pitluck, S
Pritham, EJ
Rechtsteiner, A
Rho, M
Rogozin, IB
Sakarya, O
Salamov, A
Schaack, S
Shapiro, H
Shiga, Y
Skalitzky, C
Smith, Z
Souvorov, A
Sung, W
Tang, ZJ
Tsuchiya, D
Tu, H
Vos, H
Wang, M
Wolf, YI
Yamagata, H
Yamada, T
Ye, YZ
Shaw, JR
Andrews, J
Crease, TJ
Tang, HX
Lucas, SM
Robertson, HM
Bork, P
Koonin, EV
Zdobnov, EM
Grigoriev, IV
Lynch, M
Boore, JL
AF Colbourne, John K.
Pfrender, Michael E.
Gilbert, Donald
Thomas, W. Kelley
Tucker, Abraham
Oakley, Todd H.
Tokishita, Shinichi
Aerts, Andrea
Arnold, Georg J.
Basu, Malay Kumar
Bauer, Darren J.
Caceres, Carla E.
Carmel, Liran
Casola, Claudio
Choi, Jeong-Hyeon
Detter, John C.
Dong, Qunfeng
Dusheyko, Serge
Eads, Brian D.
Froehlich, Thomas
Geiler-Samerotte, Kerry A.
Gerlach, Daniel
Hatcher, Phil
Jogdeo, Sanjuro
Krijgsveld, Jeroen
Kriventseva, Evgenia V.
Kueltz, Dietmar
Laforsch, Christian
Lindquist, Erika
Lopez, Jacqueline
Manak, J. Robert
Muller, Jean
Pangilinan, Jasmyn
Patwardhan, Rupali P.
Pitluck, Samuel
Pritham, Ellen J.
Rechtsteiner, Andreas
Rho, Mina
Rogozin, Igor B.
Sakarya, Onur
Salamov, Asaf
Schaack, Sarah
Shapiro, Harris
Shiga, Yasuhiro
Skalitzky, Courtney
Smith, Zachary
Souvorov, Alexander
Sung, Way
Tang, Zuojian
Tsuchiya, Dai
Tu, Hank
Vos, Harmjan
Wang, Mei
Wolf, Yuri I.
Yamagata, Hideo
Yamada, Takuji
Ye, Yuzhen
Shaw, Joseph R.
Andrews, Justen
Crease, Teresa J.
Tang, Haixu
Lucas, Susan M.
Robertson, Hugh M.
Bork, Peer
Koonin, Eugene V.
Zdobnov, Evgeny M.
Grigoriev, Igor V.
Lynch, Michael
Boore, Jeffrey L.
TI The Ecoresponsive Genome of Daphnia pulex
SO SCIENCE
LA English
DT Article
ID CAENORHABDITIS-ELEGANS; DUPLICATE GENES; EXPRESSION; MAGNA; EVOLUTION
AB We describe the draft genome of the microcrustacean Daphnia pulex, which is only 200 megabases and contains at least 30,907 genes. The high gene count is a consequence of an elevated rate of gene duplication resulting in tandem gene clusters. More than a third of Daphnia's genes have no detectable homologs in any other available proteome, and the most amplified gene families are specific to the Daphnia lineage. The coexpansion of gene families interacting within metabolic pathways suggests that the maintenance of duplicated genes is not random, and the analysis of gene expression under different environmental conditions reveals that numerous paralogs acquire divergent expression patterns soon after duplication. Daphnia-specific genes, including many additional loci within sequenced regions that are otherwise devoid of annotations, are the most responsive genes to ecological challenges.
C1 [Colbourne, John K.; Gilbert, Donald; Choi, Jeong-Hyeon; Dong, Qunfeng; Eads, Brian D.; Lopez, Jacqueline; Patwardhan, Rupali P.; Rechtsteiner, Andreas; Smith, Zachary; Tang, Zuojian; Tsuchiya, Dai; Shaw, Joseph R.; Andrews, Justen; Tang, Haixu] Indiana Univ, Ctr Genom & Bioinformat, Bloomington, IN 47405 USA.
[Pfrender, Michael E.] Utah State Univ, Dept Biol, Logan, UT 84322 USA.
[Gilbert, Donald; Tucker, Abraham; Casola, Claudio; Eads, Brian D.; Schaack, Sarah; Andrews, Justen; Lynch, Michael] Indiana Univ, Dept Biol, Bloomington, IN 47405 USA.
[Thomas, W. Kelley; Tucker, Abraham; Bauer, Darren J.; Hatcher, Phil; Jogdeo, Sanjuro; Sung, Way] Univ New Hampshire, Hubbard Ctr Genome Studies, Durham, NH 03824 USA.
[Oakley, Todd H.; Geiler-Samerotte, Kerry A.; Sakarya, Onur] Univ Calif Santa Barbara, Dept Ecol Evolut & Marine Biol, Santa Barbara, CA 93106 USA.
[Tokishita, Shinichi; Shiga, Yasuhiro; Yamagata, Hideo] Tokyo Univ Pharm & Life Sci, Sch Life Sci, Div Environm Sci, Lab Environm & Mol Biol, Tokyo 1920392, Japan.
[Aerts, Andrea; Detter, John C.; Dusheyko, Serge; Lindquist, Erika; Pangilinan, Jasmyn; Pitluck, Samuel; Salamov, Asaf; Shapiro, Harris; Tu, Hank; Wang, Mei; Lucas, Susan M.; Grigoriev, Igor V.; Boore, Jeffrey L.] JGI, Dept Energy, Walnut Creek, CA 94598 USA.
[Arnold, Georg J.; Froehlich, Thomas] Univ Munich, Gene Ctr, Lab Funct Genome Anal LAFUGA, D-82152 Planegg Martinsried, Germany.
[Basu, Malay Kumar; Carmel, Liran; Rogozin, Igor B.; Souvorov, Alexander; Wolf, Yuri I.; Koonin, Eugene V.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
[Caceres, Carla E.] Univ Illinois, Sch Integrat Biol, Urbana, IL 61801 USA.
[Gerlach, Daniel; Kriventseva, Evgenia V.; Zdobnov, Evgeny M.] Univ Geneva, Sch Med, CH-1211 Geneva, Switzerland.
[Gerlach, Daniel; Kriventseva, Evgenia V.; Zdobnov, Evgeny M.] Swiss Inst Bioinformat, CH-1211 Geneva, Switzerland.
[Krijgsveld, Jeroen; Vos, Harmjan] Univ Utrecht, Bijvoet Ctr Biomol Res, Biomol Mass Spectrometry & Prote Grp, NL-3584 CA Utrecht, Netherlands.
[Krijgsveld, Jeroen; Vos, Harmjan] Univ Utrecht, Utrecht Inst Pharmaceut Sci, NL-3584 CA Utrecht, Netherlands.
[Krijgsveld, Jeroen; Vos, Harmjan] Univ Utrecht, Netherlands Prote Ctr, NL-3584 CA Utrecht, Netherlands.
[Kueltz, Dietmar] Univ Calif Davis, Dept Anim Sci, Davis, CA 95616 USA.
[Laforsch, Christian] Univ Munich, Dept Biol 2, D-82152 Planegg Martinsried, Germany.
[Laforsch, Christian] Univ Munich, GeoBio Ctr Munich, D-82152 Planegg Martinsried, Germany.
[Manak, J. Robert; Skalitzky, Courtney] Roche NimbleGen Inc, Gene Express, Madison, WI 53719 USA.
[Muller, Jean; Yamada, Takuji; Bork, Peer] European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany.
[Pritham, Ellen J.; Schaack, Sarah] Univ Texas Arlington, Dept Biol, Arlington, TX 76019 USA.
[Rho, Mina; Ye, Yuzhen; Tang, Haixu] Indiana Univ, Sch Informat & Comp, Bloomington, IN 47408 USA.
[Shaw, Joseph R.] Indiana Univ, Sch Publ & Environm Affairs, Bloomington, IN 47405 USA.
[Crease, Teresa J.] Univ Guelph, Dept Integrat Biol, Guelph, ON N1G 2W1, Canada.
[Robertson, Hugh M.] Univ Illinois, Dept Entomol, Urbana, IL 61801 USA.
[Zdobnov, Evgeny M.] Univ London Imperial Coll Sci Technol & Med, London SW7 2AZ, England.
[Boore, Jeffrey L.] Genome Project Solut, Hercules, CA 94547 USA.
[Boore, Jeffrey L.] Univ Calif Berkeley, Dept Integrat Biol, Berkeley, CA 94720 USA.
RP Colbourne, JK (reprint author), Indiana Univ, Ctr Genom & Bioinformat, 915 E 3rd St, Bloomington, IN 47405 USA.
EM jcolbour@indiana.edu
RI Choi, Jeong-Hyeon/E-3084-2010; Krijgsveld, Jeroen/F-5974-2011; Zdobnov,
Evgeny/K-1133-2012; Bork, Peer/F-1813-2013; Choi, Justin/F-8792-2014;
Colbourne, John/L-7748-2014; Crease, Teresa/E-2932-2015; Frohlich,
Thomas/C-6735-2011;
OI Bork, Peer/0000-0002-2627-833X; Colbourne, John/0000-0002-6966-2972;
Crease, Teresa/0000-0001-8074-8024; Oakley, Todd/0000-0002-4478-915X;
Gerlach, Daniel/0000-0001-9338-3765; Muller, Jean/0000-0002-7682-559X
FU Office of Science of the U.S. Department of Energy [DE-AC02-05CH11231];
Daphnia Genomics Consortium (DGC); NSF [0221837, 0328516]; NIH
[R24GM07827401]; METACyt Initiative of Indiana University; Lilly
Endowment, Inc.
FX We thank M. Frazer (JGI), P. Cherbas (CGB), R. Green, and T. Takova
(Roche NimbleGen, Inc.). The work conducted by the U.S. Department of
Energy Joint Genome Institute (JGI) was supported by the Office of
Science of the U.S. Department of Energy under contract
DE-AC02-05CH11231 and in collaboration with the Daphnia Genomics
Consortium (DGC). This project was also supported by NSF grants 0221837
and 0328516 and NIH grant R24GM07827401. Coordination infrastructure for
the DGC is provided by the Center for Genomics and Bioinformatics (CGB)
at Indiana University, which is supported in part by the METACyt
Initiative of Indiana University, funded in part through a major grant
from the Lilly Endowment, Inc. Additional contributions and
acknowledgments are provided in the SOM. Our work benefits from and
contributes to the Daphnia Genomics Consortium. Daphnia pulex genome
assembly version 1.1 and annotations are deposited at DNA Data Bank of
Japan, European Molecular Biology Laboratory, and GenBank databases
under accession ACJG00000000. ESTs (FE274839 to FE425949) are in
GenBank. Microarray platforms GPL11200 to GPL11201 and data GSE25823 are
deposited at National Center for Biotechnology Information Gene
Expression Omnibus database.
NR 24
TC 515
Z9 535
U1 31
U2 244
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD FEB 4
PY 2011
VL 331
IS 6017
BP 555
EP 561
DI 10.1126/science.1197761
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 715ZE
UT WOS:000286933600046
PM 21292972
ER
PT J
AU Chakrabarty, S
Snyder, JT
Shen, JJ
Azmi, H
Hu, PQ
Chen, QA
Ragheb, JA
AF Chakrabarty, Sagarika
Snyder, James T.
Shen, Jijia
Azmi, Hooman
Hu, Paul Q.
Chen, Qian
Ragheb, Jack A.
TI Human CD14(hi) monocytes and myeloid dendritic cells provide a cell
contact-dependent costimulatory signal for early CD40 ligand expression
SO BLOOD
LA English
DT Article
ID ACTIVATED T-CELLS; GERMINAL CENTER FORMATION; IL-2 MESSENGER-RNA;
RESTING B-CELLS; CD40-CD40 LIGAND; ANTIGEN PRESENTATION; HUMORAL
IMMUNITY; CD154 EXPRESSION; GAMMA PRODUCTION; IGM SYNDROME
AB CD40L on CD4(+) T cells plays a vital role in the activation of antigen-presenting cells, thus catalyzing a positive feedback loop for T-cell activation. Despite the pivotal juxtaposition of CD40L between antigen-presenting cells and T-cell activation, only a T-cell receptor stimulus is thought to be required for early CD40L surface expression. We show, for the first time, that CD40L expression on peripheral blood CD4(+) T cells is highly dependent on a cell-cell interaction with CD14(hi)CD16(-) monocytes. Interactions with ICAM-1, LFA-3, and to a lesser extent CD80/CD86 contribute to this enhancement of CD40L expression but are not themselves sufficient. The contact-mediated increase in CD40L expression is dependent on new mRNA and protein synthesis. Circulating myeloid dendritic cells also possess this costimulatory activity. By contrast, CD14(lo)CD16(+) monocytes, plasmacytoid dendritic cells, B-cell lymphoma lines, and resting, activated, and Epstein-Barr virus-immortalized primary B cells all lack the capacity to up-regulate early CD40L. The latter indicates that a human B cell cannot activate its cognate T cell to deliver CD40L-mediated help. This finding has functional implications for the role of biphasic CD40L expression, suggesting that the early phase is associated with antigen-presenting cell activation, whereas the late phase is related to B-cell activation. (Blood. 2011; 117(5): 1585-1594)
C1 [Chakrabarty, Sagarika; Snyder, James T.; Shen, Jijia; Azmi, Hooman; Hu, Paul Q.; Chen, Qian; Ragheb, Jack A.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Ragheb, Jack A.] US FDA, Immunol Lab, Div Therapeut Prot, Off Biol Prod,Ctr Drug Evaluat & Res,Dept Hlth &, Bethesda, MD 20014 USA.
RP Ragheb, JA (reprint author), 29 Lincoln Dr,Bldg 29B,Rm 4G13,HFD 122, Bethesda, MD 20892 USA.
EM jr50b@nih.gov
FU Department of Health and Human Services
FX This work was supported by the Department of Health and Human Services
(intramural funding).
NR 68
TC 3
Z9 3
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD FEB 3
PY 2011
VL 117
IS 5
BP 1585
EP 1594
DI 10.1182/blood-2008-01-130252
PG 10
WC Hematology
SC Hematology
GA 715WV
UT WOS:000286925500025
PM 20634374
ER
PT J
AU Roberts, DD
AF Roberts, David D.
TI Activate Rac to rescue new vessels
SO BLOOD
LA English
DT Editorial Material
ID NITRIC-OXIDE SYNTHASE; ANGIOGENESIS
C1 Natl Canc Inst, Bethesda, MD 20892 USA.
RP Roberts, DD (reprint author), Natl Canc Inst, Bethesda, MD 20892 USA.
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
NR 10
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U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD FEB 3
PY 2011
VL 117
IS 5
BP 1444
EP 1445
DI 10.1182/blood-2010-11-317198
PG 2
WC Hematology
SC Hematology
GA 715WV
UT WOS:000286925500007
PM 21292786
ER
PT J
AU Mansoor, A
Pittaluga, S
Beck, PL
Wilson, WH
Ferry, JA
Jaffe, ES
AF Mansoor, Adnan
Pittaluga, Stefania
Beck, Paul L.
Wilson, Wyndham H.
Ferry, Judith A.
Jaffe, Elaine S.
TI NK-cell enteropathy: a benign NK-cell lymphoproliferative disease
mimicking intestinal lymphoma: clinicopathologic features and follow-up
in a unique case series
SO BLOOD
LA English
DT Article
ID NATURAL-KILLER-CELLS; DELTA T-CELL; CELIAC-DISEASE; ADAPTIVE IMMUNITY;
MUCOSAL; PROLIFERATION; SKIN; LYMPHOCYTES; DISORDER; INNATE
AB Intestinal T-cell and natural killer (NK)-cell lymphomas are clinically aggressive and can be challenging to diagnose in small endoscopic biopsies. We describe 8 patients in whom atypical NK-cell lymphoproliferative lesions mimicked NK-or T-cell lymphoma. The patients (2 men; 6 women; ages 27-68 years) presented with vague gastrointestinal symptoms with lesions involving stomach, duodenum, small intestine, and colon. At endoscopy, the lesions exhibited superficial ulceration, edema, and hemorrhage. Biopsies revealed a mucosal infiltrate of atypical cells with an NK-cell phenotype (CD56(+)/TIA-1(+)/Granzyme B(+)/cCD3(+)), which displaced but did not invade the glandular epithelium. Epstein-Barr virus-encoded RNA in situ hybridization was negative, and T-cell receptor-gamma gene rearrangement showed no evidence of a clonal process. Based on an original diagnosis of lymphoma, 3 patients received aggressive chemotherapy followed by autologous bone marrow transplantation in 2. Five patients were followed without treatment. However, no patient developed progressive disease or died of lymphoma (median follow-up, 30 months). Repeat endoscopies in 6 of 8 patients showed persistence or recurrence of superficial gastrointestinal lesions. This unique entity mimics intestinal and NK-/T-cell lymphomas on endoscopic biopsies and can result in erroneous diagnosis, leading to aggressive chemotherapy. We propose the term "NK-cell enteropathy" for this syndrome of as yet unknown etiology. (Blood. 2011; 117(5): 1447-1452)
C1 [Mansoor, Adnan] Calgary Lab Serv, Dept Pathol & Lab Med, Calgary, AB, Canada.
[Pittaluga, Stefania; Jaffe, Elaine S.] NCI, Hematopathol Sect, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Beck, Paul L.] Univ Calgary, Div Gastroenterol, Calgary, AB, Canada.
[Wilson, Wyndham H.] NCI, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Ferry, Judith A.] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02114 USA.
RP Jaffe, ES (reprint author), NIH, Hematopathol Sect, Pathol Lab, 10 Ctr Dr,Bldg 10,Rm 2B42, Bethesda, MD 20892 USA.
EM elainejaffe@nih.gov
OI Jaffe, Elaine/0000-0003-4632-0301
FU Center for Cancer Research, National Cancer Institute
FX This work was supported by the intramural research budget of the Center
for Cancer Research, National Cancer Institute.
NR 39
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U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD FEB 3
PY 2011
VL 117
IS 5
BP 1447
EP 1452
DI 10.1182/blood-2010-08-302737
PG 6
WC Hematology
SC Hematology
GA 715WV
UT WOS:000286925500009
PM 20966166
ER
PT J
AU Larochelle, A
Savona, M
Wiggins, M
Anderson, S
Ichwan, B
Keyvanfar, K
Morrison, SJ
Dunbar, CE
AF Larochelle, Andre
Savona, Michael
Wiggins, Michael
Anderson, Stephanie
Ichwan, Brian
Keyvanfar, Keyvan
Morrison, Sean J.
Dunbar, Cynthia E.
TI Human and rhesus macaque hematopoietic stem cells cannot be purified
based only on SLAM family markers
SO BLOOD
LA English
DT Article
ID CORD BLOOD-CELLS; LONG-TERM; BONE-MARROW; MULTIPOTENT PROGENITORS;
CD34(+)CD38(-) CELLS; EXPRESSION; MICE; RECEPTORS; CD34; TRANSPLANTATION
AB Various combinations of antibodies directed to cell surface markers have been used to isolate human and rhesus macaque hematopoietic stem cells (HSCs). These protocols result in poor enrichment or require multiple complex steps. Recently, a simple phenotype for HSCs based on cell surface markers from the signaling lymphocyte activation molecule (SLAM) family of receptors has been reported in the mouse. We examined the possibility of using the SLAM markers to facilitate the isolation of highly enriched populations of HSCs in humans and rhesus macaques. We isolated SLAM (CD150(+)CD48(-)) and nonSLAM (not CD150(+)CD48(-)) cells from human umbilical cord blood CD34(+) cells as well as from human and rhesus macaque mobilized peripheral blood CD34(+) cells and compared their ability to form colonies in vitro and reconstitute immune-deficient (nonobese diabetic/severe combined immunodeficiency/interleukin-2 gamma c receptor(null), NSG) mice. We found that the CD34(+) SLAM population contributed equally or less to colony formation in vitro and to long-term reconstitution in NSG mice compared with the CD34(+) non-SLAM population. Thus, SLAM family markers do not permit the same degree of HSC enrichment in humans and rhesus macaques as in mice. (Blood. 2011; 117(5): 1550-1554)
C1 [Larochelle, Andre; Ichwan, Brian; Keyvanfar, Keyvan; Dunbar, Cynthia E.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Savona, Michael; Morrison, Sean J.] Univ Michigan, Howard Hughes Med Inst, Dept Internal Med, Ctr Stem Cell Biol, Ann Arbor, MI 48109 USA.
[Savona, Michael; Morrison, Sean J.] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
[Savona, Michael; Wiggins, Michael; Anderson, Stephanie] San Antonio Mil Med Ctr, Dept Hematol & Oncol, San Antonio, TX USA.
RP Dunbar, CE (reprint author), NHLBI, NIH, Bldg 10 CRC,Rm 4-5132,10 Ctr Dr,MSC 1202, Bethesda, MD 20892 USA.
EM dunbarc@nhlbi.nih.gov
FU University of Michigan Flow Cytometry Core Facility; National Heart,
Lung and Blood Institute of the National Institutes of Health; Howard
Hughes Medical Institute; Michigan Institute for Clinical and Health
Research Pilot
FX The authors thank D. Stroncek, J. Procter, M. Sabatino, and S. Leitman
for providing human CD34+ cells; Sue Ellen Frodigh and Quyen
Chau for processing UCB samples; R. Donahue, M. Metzger, and A. Krouse
for mobilization and apheresis of rhesus macaques; D. Adams, M. White,
and the University of Michigan Flow Cytometry Core Facility for support;
and the animal core facility staff at the National Institutes of Health
and the University of Michigan for excellent animal care.; This work was
supported in part by the intramural research program of the National
Heart, Lung and Blood Institute of the National Institutes of Health and
in part by the Howard Hughes Medical Institute and by a Michigan
Institute for Clinical and Health Research Pilot Grant.
NR 26
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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 FEB 3
PY 2011
VL 117
IS 5
BP 1550
EP 1554
DI 10.1182/blood-2009-03-212803
PG 5
WC Hematology
SC Hematology
GA 715WV
UT WOS:000286925500021
PM 21163926
ER
PT J
AU Goldin, LR
Landgren, O
Kristinsson, SY
Bjorkholm, M
Paltiel, O
AF Goldin, Lynn R.
Landgren, Ola
Kristinsson, Sigurdur Y.
Bjorkholm, Magnus
Paltiel, Ora
TI Infection in infancy and subsequent risk of developing lymphoma in
children and young adults
SO BLOOD
LA English
DT Article
ID NON-HODGKINS-LYMPHOMA; CANCER; AGENTS
AB There is evidence that certain infections and autoimmunity predispose to the development of non-Hodgkin lymphomas (NHLs). A previous study reported that hospitalization for infections in infancy led to an increased risk of NHL. By using population-based registries in Sweden, we compared the rate of hospitalization for infections in infancy between lymphoma cases and matched controls for patients born since 1964. A history of infection was associated with a significantly increased risk of aggressive B-cell lymphomas (odds ratio 2.1, 95% confidence interval 1.11-4.04, P = .02). The specific infections involved were respiratory and intestinal. No effects were observed among cases of Hodgkin lymphoma. This association could result from the infection, its treatment, or could be a surrogate marker for underlying immune defects. Further studies are needed to determine whether this association is present among NHL occurring in older adults and if improved survival of patients with immune defects has contributed to the secular increases in incidence of NHLs. (Blood. 2011; 117(5): 1670-1672)
C1 [Goldin, Lynn R.] NCI, Genet Epidemiol Branch, DCEG, Bethesda, MD 20892 USA.
[Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Univ Hosp Solna, Div Hematol, Dept Med, Stockholm, Sweden.
[Kristinsson, Sigurdur Y.; Bjorkholm, Magnus] Karolinska Inst, Stockholm, Sweden.
[Paltiel, Ora] Hadassah Hebrew Univ Hosp, Dept Hematol, Jerusalem, Israel.
[Paltiel, Ora] Hadassah Hebrew Univ Hosp, Sch Publ Hlth, Jerusalem, Israel.
RP Goldin, LR (reprint author), NCI, Genet Epidemiol Branch, DCEG, 6120 Execut Blvd,Rm 7008,MSC 7236, Bethesda, MD 20892 USA.
EM goldinl@mail.nih.gov
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
FU National Cancer Institute, National Institutes of Health; Swedish Cancer
Society; Stockholm County Council; Karolinska Institutet Foundations
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, National Institutes of Health and by grants
from the Swedish Cancer Society, Stockholm County Council, and the
Karolinska Institutet Foundations.
NR 16
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U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD FEB 3
PY 2011
VL 117
IS 5
BP 1670
EP 1672
DI 10.1182/blood-2010-09-306274
PG 3
WC Hematology
SC Hematology
GA 715WV
UT WOS:000286925500034
PM 21127175
ER
PT J
AU Koh, KK
Quon, MJ
Han, SH
Lee, Y
Park, JB
Kim, SJ
Koh, Y
Shin, EK
AF Koh, Kwang Kon
Quon, Michael J.
Han, Seung Hwan
Lee, Yonghee
Park, Jeong Beom
Kim, Soo Jin
Koh, Yesl
Shin, Eak Kyun
TI Additive beneficial effects of atorvastatin combined with amlodipine in
patients with mild-to-moderate hypertension
SO INTERNATIONAL JOURNAL OF CARDIOLOGY
LA English
DT Article
DE HMG-CoA reductase inhibitor; Calcium channel blocker; Endothelial
function; Adiponectin; Insulin resistance; Hypertension
ID ASSESSING INSULIN SENSITIVITY; RANDOMIZED CONTROLLED-TRIAL; ENDOTHELIAL
FUNCTION; METABOLIC PARAMETERS; THERAPEUTIC INTERVENTIONS; RECIPROCAL
RELATIONSHIPS; CARDIOVASCULAR-DISEASE; GLUCOSE-METABOLISM; ADIPONECTIN
LEVELS; OXIDATIVE STRESS
AB Background: We hypothesized that atorvastatin combined with amlodipine has additive beneficial vascular and metabolic effects that are superior to monotherapy in patients with hypertension.
Methods: Forty-two patients were given atorvastatin 20 mg/day and placebo, atorvastatin 20 mg/day and amlodipine 10 mg/day, or amlodipine 10 mg/day and placebo during each 2-month treatment period of a randomized, single-blind, placebo-controlled cross-over trial with two 2-month washout periods.
Results: Atorvastatin combined with amlodipine or amlodipine alone significantly reduced blood pressure to a greater extent than atorvastatin alone (all P<0.001 by ANOVA). Atorvastatin combined with amlodipine significantly reduced plasma malondialdehyde and improved flow-mediated dilation to a greater extent than atorvastatin or amlodipine alone (all P<0.001 by ANOVA). Atorvastatin therapy significantly increased insulin levels (P=0.004) and decreased plasma adiponectin levels (P=0.016) and insulin sensitivity (determined by QUICKI; P=0.026) relative to baseline measurements. Amlodipine therapy significantly decreased insulin levels (P=0.001) and increased adiponectin levels (P<0.001) and insulin sensitivity (P=0.003) relative to baseline measurements. Atorvastatin combined with amlodipine therapy significantly increased adiponectin levels (P<0.001) and insulin sensitivity (P=0.034) relative to baseline measurements. Effects of all three therapeutic arms on adiponectin levels and insulin sensitivity were statistically significant (P<0.001 by ANOVA).
Conclusions: Atorvastatin combined with amlodipine therapy improves endothelial function and increases adiponectin levels and insulin sensitivity to a greater extent than monotherapy with either drug in hypertensive patients. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [Koh, Kwang Kon; Han, Seung Hwan; Park, Jeong Beom; Kim, Soo Jin; Shin, Eak Kyun] Gachon Univ, Gil Med Ctr, Vasc Med & Atherosclerosis Unit Cardiol, Inchon 405760, South Korea.
[Quon, Michael J.] NIH, Diabet Unit, NCCAM, Bethesda, MD 20892 USA.
[Koh, Yesl] Northwestern Univ, Weinberg Coll Arts & Sci, Evanston, IL USA.
[Lee, Yonghee] Univ Seoul, Dept Stat, Seoul, South Korea.
RP Koh, KK (reprint author), Gachon Univ, Gil Med Ctr, Vasc Med & Atherosclerosis Unit Cardiol, 1198 Kuwol Dong, Inchon 405760, South Korea.
EM kwangk@gilhospital.com
OI Quon, Michael/0000-0002-9601-9915; Quon , Michael /0000-0002-5289-3707
FU Gachon University Gil Medical Center [2005-1, 2006-1]
FX This study was partly supported by grants from established investigator
award (2005-1, 2006-1), Gachon University Gil Medical Center and not
supported by any pharmaceutical companies.
NR 42
TC 18
Z9 18
U1 1
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0167-5273
J9 INT J CARDIOL
JI Int. J. Cardiol.
PD FEB 3
PY 2011
VL 146
IS 3
BP 319
EP 325
DI 10.1016/j.ijcard.2009.07.002
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 709SA
UT WOS:000286460500011
PM 19651449
ER
PT J
AU Koh, KK
Quon, MJ
Sakuma, I
Lee, Y
Lim, S
Han, SH
Shin, EK
AF Koh, Kwang Kon
Quon, Michael J.
Sakuma, Ichiro
Lee, Yonghee
Lim, Soo
Han, Seung Hwan
Shin, Eak Kyun
TI Effects of simvastatin therapy on circulating adipocytokines in patients
with hypercholesterolemia
SO INTERNATIONAL JOURNAL OF CARDIOLOGY
LA English
DT Letter
DE Statins; Adipocytokines; Insulin resistance; Metabolic syndrome
ID CAUSES INSULIN-RESISTANCE; CARDIOVASCULAR-DISEASE; HYPERTENSIVE
PATIENTS; METABOLIC PARAMETERS; ADIPONECTIN LEVELS; PRAVASTATIN;
INTERVENTIONS; ATORVASTATIN; SENSITIVITY; INHIBITION
C1 [Koh, Kwang Kon] Gachon Univ, Gil Med Ctr, Vasc Med & Atherosclerosis Unit, Inchon 405760, South Korea.
[Quon, Michael J.] NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Sakuma, Ichiro] Hokko Mem Clin, Sapporo, Hokkaido, Japan.
[Lee, Yonghee] Univ Seoul, Dept Stat, Seoul, South Korea.
[Lim, Soo] Seoul Natl Univ, Coll Med, Seoul Natl Univ Bundang Hosp, Div Endocrinol, Songnam, South Korea.
RP Koh, KK (reprint author), Gachon Univ, Gil Med Ctr, Vasc Med & Atherosclerosis Unit, 1198 Kuwol Dong, Inchon 405760, South Korea.
EM kwangk@gilhospital.com
OI Quon, Michael/0000-0002-9601-9915; Quon , Michael /0000-0002-5289-3707
NR 19
TC 15
Z9 15
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0167-5273
J9 INT J CARDIOL
JI Int. J. Cardiol.
PD FEB 3
PY 2011
VL 146
IS 3
BP 434
EP 437
DI 10.1016/j.ijcard.2010.10.103
PG 4
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 709SA
UT WOS:000286460500039
PM 21095021
ER
PT J
AU Wang, W
Petralia, RS
Takamiya, K
Xia, J
Li, YQ
Huganir, RL
Tao, YX
Yaster, M
AF Wang, Wei
Petralia, Ronald S.
Takamiya, Kogo
Xia, Jun
Li, Yun-Qing
Huganir, Richard L.
Tao, Yuan-Xiang
Yaster, Myron
TI Preserved acute pain and impaired neuropathic pain in mice lacking
protein interacting with C Kinase 1
SO MOLECULAR PAIN
LA English
DT Article
ID METABOTROPIC GLUTAMATE RECEPTORS; PERIPHERAL-NERVE INJURY; CORD
DORSAL-HORN; SPINAL-CORD; PDZ DOMAIN; PERSISTENT PAIN; EXCITATORY
SYNAPSES; INFLAMMATORY PAIN; GANGLION NEURONS; PICK1 INTERACTS
AB Protein interacting with C Kinase 1 (PICK1), a PDZ domain-containing scaffolding protein, interacts with multiple different proteins in the mammalian nervous system and is believed to play important roles in diverse physiological and pathological conditions. In this study, we report that PICK1 is expressed in neurons of the dorsal root ganglion (DRG) and spinal cord dorsal horn, two major pain-related regions. PICK1 was present in approximately 29.7% of DRG neurons, most of which were small-less than 750 mu m(2) in cross-sectional area. Some of these PICK1-positive cells co-labeled with isolectin B4 or calcitonin-gene-related peptide. In the dorsal horn, PICK1 immunoreactivity was concentrated in the superficial dorsal horn, where it was prominent in the postsynaptic density, axons, and dendrites. Targeted disruption of PICK1 gene did not affect basal paw withdrawal responses to acute noxious thermal and mechanical stimuli or locomotor reflex activity, but it completely blocked the induction of peripheral nerve injury-induced mechanical and thermal pain hypersensitivities. PICK1 appears to be required for peripheral nerve injury-induced neuropathic pain development and to be a potential biochemical target for treating this disorder.
C1 [Wang, Wei; Li, Yun-Qing; Tao, Yuan-Xiang; Yaster, Myron] Johns Hopkins Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21205 USA.
[Wang, Wei; Li, Yun-Qing] Fourth Mil Med Univ, Dept Anat Histol & Embryol, KK Leung Brain Res Ctr, Xian 710032, Peoples R China.
[Petralia, Ronald S.] Natl Inst Deafness & Other Commun Disorders, Neurochem Lab, NIH, Bethesda, MD 20892 USA.
[Takamiya, Kogo; Xia, Jun; Huganir, Richard L.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21287 USA.
[Xia, Jun] Hong Kong Univ Sci & Technol, Dept Biochem, Kowloon, Hong Kong, Peoples R China.
RP Tao, YX (reprint author), Johns Hopkins Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21205 USA.
EM ytau@jhmi.edu; myaster1@jhmi.edu
RI Xia, Jun/C-7234-2009;
OI Xia, Jun/0000-0001-9308-2188
FU National Institutes of Health [NS058886]; Blaustein Pain Research Fund;
Mr. David Koch and the Patrick C. Walsh Prostate Cancer Research Fund;
Brain Science Institute at the Johns Hopkins University; Department of
Anesthesiology; NIDCD
FX This work was supported by National Institutes of Health (NS058886), the
Blaustein Pain Research Fund, Mr. David Koch and the Patrick C. Walsh
Prostate Cancer Research Fund, and Brain Science Institute at the Johns
Hopkins University (Y.X.T.), Department of Anesthesiology (M.Y.), and
the Intramural Research Program of NIDCD (R.S.P.). We thank Mrs. Ya-Xian
Wang for help with the immunogold experiments. The authors thank Claire
Levine, MS, for editorial assistance.
NR 39
TC 19
Z9 20
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1744-8069
J9 MOL PAIN
JI Mol. Pain
PD FEB 3
PY 2011
VL 7
AR 11
DI 10.1186/1744-8069-7-11
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 720SJ
UT WOS:000287300500001
PM 21291534
ER
PT J
AU Kosti, O
Goldman, L
Saha, DT
Orden, RA
Pollock, AJ
Madej, HL
Hsing, AW
Chu, LW
Lynch, JH
Goldman, R
AF Kosti, O.
Goldman, L.
Saha, D. T.
Orden, R. A.
Pollock, A. J.
Madej, H. L.
Hsing, A. W.
Chu, L. W.
Lynch, J. H.
Goldman, R.
TI DNA damage phenotype and prostate cancer risk
SO MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS
LA English
DT Article
DE Prostate cancer; Benign prostatic hyperplasia; Comet assay; DNA repair;
Case-control study
ID DOUBLE-STRAND BREAKS; EXCISION-REPAIR CAPACITY; COMET ASSAY; MUTAGEN
SENSITIVITY; IONIZING-RADIATION; LUNG-CANCER; BLOOD CELLS; WHOLE-BLOOD;
BODY-MASS; INSTABILITY
AB The capacity of an individual to process DNA damage is considered a crucial factor in carcinogenesis. The comet assay is a phenotypic measure of the combined effects of sensitivity to a mutagen exposure and repair capacity. In this paper, we evaluate the association of the DNA repair kinetics, as measured by the comet assay, with prostate cancer risk. In a pilot study of 55 men with prostate cancer, 53 men without the disease, and 71 men free of cancer at biopsy, we investigated the association of DNA damage with prostate cancer risk at early (0-15 min) and later (15-45 min) stages following gamma-radiation exposure. Although residual damage within 45 min was the same for all groups (65% of DNA in comet tail disappeared), prostate cancer cases had a slower first phase (38% vs. 41%) and faster second phase (27% vs. 22%) of the repair response compared to controls. When subjects were categorized into quartiles, according to efficiency of repairing DNA damage, high repair-efficiency within the first 15 min after exposure was not associated with prostate cancer risk while higher at the 15-45 min period was associated with increased risk (OR for highest-to-lowest quartiles = 3.24, 95% CI = 0.98-10.66, p-trend = 0.04). Despite limited sample size, our data suggest that DNA repair kinetics marginally differ between prostate cancer cases and controls. This small difference could be associated with differential responses to DNA damage among susceptible individuals. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Goldman, R.] Georgetown Univ, Dept Oncol, LCC, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
[Hsing, A. W.; Chu, L. W.] NCI, Div Canc Epidembl & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Lynch, J. H.] Georgetown Univ, Dept Urol, Lombardi Comprehens Canc Ctr, Washington, DC 20057 USA.
RP Goldman, R (reprint author), Georgetown Univ, Dept Oncol, LCC, Lombardi Comprehens Canc Ctr, S183,3800 Reservoir Rd NW, Washington, DC 20057 USA.
EM rg26@georgetown.edu
RI Pollock, Allison/E-5367-2016
OI Pollock, Allison/0000-0003-2361-4390
FU National Institutes of Health National Center for Research Resources
[M01RR-023942]; Department of Defense [PC081609]; NCI [R01 CA115625];
National Institute of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics, USA
FX We wish to thank Dr Borges, Department of Urology, Veterans
Administration Medical Center, for facilitating recruitment at the VA
hospital and Dr Dritschilo, Radiation Medicine, for recruitment at the
Georgetown University Hospital. The Clinical Molecular Epidemiology
Shared Resources at the Lombardi Comprehensive Cancer Center provided
services for questionnaire data entry. This project was conducted
through the General Clinical Research Center at Georgetown University
and supported by the National Institutes of Health National Center for
Research Resources, grant M01RR-023942. This study was supported in part
by the Department of Defense Prostate Cancer Research Program grant
PC081609 and NCI grant R01 CA115625 awarded to RG and Intramural
Research Program of the National Institute of Health, National Cancer
Institute, Division of Cancer Epidemiology and Genetics, USA (AWH and
LWC).
NR 41
TC 3
Z9 3
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1383-5718
J9 MUTAT RES-GEN TOX EN
JI Mutat. Res. Genet. Toxicol. Environ. Mutagen.
PD FEB 3
PY 2011
VL 719
IS 1-2
BP 41
EP 46
DI 10.1016/j.mrgentox.2010.11.005
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 717NY
UT WOS:000287055900007
PM 21095241
ER
PT J
AU Gupta, N
Stopfer, M
AF Gupta, Nitin
Stopfer, Mark
TI Negative results need airing too
SO NATURE
LA English
DT Letter
C1 [Gupta, Nitin; Stopfer, Mark] NICHD, NIH, Bethesda, MD 20892 USA.
RP Gupta, N (reprint author), NICHD, NIH, Bethesda, MD 20892 USA.
EM nitin.gupta2@nih.gov
NR 0
TC 9
Z9 9
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD FEB 3
PY 2011
VL 470
IS 7332
BP 39
EP 39
DI 10.1038/470039a
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 715LQ
UT WOS:000286886400018
PM 21293361
ER
PT J
AU Diep, CQ
Ma, DD
Deo, RC
Holm, TM
Naylor, RW
Arora, N
Wingert, RA
Bollig, F
Djordjevic, G
Lichman, B
Zhu, H
Ikenaga, T
Ono, F
Englert, C
Cowan, CA
Hukriede, NA
Handin, RI
Davidson, AJ
AF Diep, Cuong Q.
Ma, Dongdong
Deo, Rahul C.
Holm, Teresa M.
Naylor, Richard W.
Arora, Natasha
Wingert, Rebecca A.
Bollig, Frank
Djordjevic, Gordana
Lichman, Benjamin
Zhu, Hao
Ikenaga, Takanori
Ono, Fumihito
Englert, Christoph
Cowan, Chad A.
Hukriede, Neil A.
Handin, Robert I.
Davidson, Alan J.
TI Identification of adult nephron progenitors capable of kidney
regeneration in zebrafish
SO NATURE
LA English
DT Article
ID TRANSGENIC ZEBRAFISH; GENES; MORPHOGENESIS; PRONEPHROS; REPORTER
AB Loss of kidney function underlies many renal diseases(1). Mammals can partly repair their nephrons (the functional units of the kidney), but cannot form new ones(2,3). By contrast, fish add nephrons throughout their lifespan and regenerate nephrons de novo after injury(4,5), providing a model for understanding how mammalian renal regeneration may be therapeutically activated. Here we trace the source of new nephrons in the adult zebrafish to small cellular aggregates containing nephron progenitors. Transplantation of single aggregates comprising 10-30 cells is sufficient to engraft adults and generate multiple nephrons. Serial transplantation experiments to test self-renewal revealed that nephron progenitors are long-lived and possess significant replicative potential, consistent with stem-cell activity. Transplantation of mixed nephron progenitors tagged with either green or red fluorescent proteins yielded some mosaic nephrons, indicating that multiple nephron progenitors contribute to a single nephron. Consistent with this, live imaging of nephron formation in transparent larvae showed that nephrogenic aggregates form by the coalescence of multiple cells and then differentiate into nephrons. Taken together, these data demonstrate that the zebrafish kidney probably contains self-renewing nephron stem/progenitor cells. The identification of these cells paves the way to isolating or engineering the equivalent cells in mammals and developing novel renal regenerative therapies.
C1 [Diep, Cuong Q.; Ma, Dongdong; Deo, Rahul C.; Holm, Teresa M.; Naylor, Richard W.; Wingert, Rebecca A.; Cowan, Chad A.; Handin, Robert I.; Davidson, Alan J.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Ma, Dongdong; Handin, Robert I.] Brigham & Womens Hosp, Div Hematol, Boston, MA 02115 USA.
[Wingert, Rebecca A.; Cowan, Chad A.; Handin, Robert I.; Davidson, Alan J.] Harvard Stem Cell Inst, Cambridge, MA 02138 USA.
[Bollig, Frank; Englert, Christoph] Fritz Lipmann Inst, Leibniz Inst Age Res, D-07745 Jena, Germany.
[Zhu, Hao] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Ikenaga, Takanori; Ono, Fumihito] NIAAA, Sect Model Synapt Syst, Lab Mol Physiol, NIH, Bethesda, MD 20892 USA.
[Englert, Christoph] Friedrich Schiller Univ, D-07743 Jena, Germany.
[Cowan, Chad A.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
[Hukriede, Neil A.] Univ Pittsburgh, Sch Med, Dept Dev Biol, Pittsburgh, PA 15260 USA.
[Diep, Cuong Q.; Deo, Rahul C.; Holm, Teresa M.; Naylor, Richard W.; Arora, Natasha; Wingert, Rebecca A.; Djordjevic, Gordana; Lichman, Benjamin; Cowan, Chad A.; Davidson, Alan J.] Massachusetts Gen Hosp, Ctr Regenerat Med, Boston, MA 02114 USA.
RP Davidson, AJ (reprint author), Univ Auckland, Sch Med Sci, Dept Mol Med & Pathol, Auckland 1142, New Zealand.
EM a.davidson@auckland.ac.nz
OI Ikenaga, Takanori/0000-0002-7321-9703; Zhu, Hao/0000-0002-8417-9698;
Lichman, Benjamin/0000-0002-0033-1120
FU Harvard Stem Cell Institute; American Society of Nephrology; National
Institutes of Health/National Institute of Diabetes and Digestive and
Kidney Diseases [P50DK074030]
FX We thank E. C. Liao for help with suturing, and R. Ethier and L. Gyr for
zebrafish care. A.J.D. was supported by the Harvard Stem Cell Institute,
the American Society of Nephrology and the National Institutes of
Health/National Institute of Diabetes and Digestive and Kidney Diseases
(P50DK074030).
NR 23
TC 105
Z9 108
U1 2
U2 22
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD FEB 3
PY 2011
VL 470
IS 7332
BP 95
EP U108
DI 10.1038/nature09669
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 715LQ
UT WOS:000286886400041
PM 21270795
ER
PT J
AU Ngo, VN
Young, RM
Schmitz, R
Jhavar, S
Xiao, WM
Lim, KH
Kohlhammer, H
Xu, WH
Yang, YD
Zhao, H
Shaffer, AL
Romesser, P
Wright, G
Powell, J
Rosenwald, A
Muller-Hermelink, HK
Ott, G
Gascoyne, RD
Connors, JM
Rimsza, LM
Campo, E
Jaffe, ES
Delabie, J
Smeland, EB
Fisher, RI
Braziel, RM
Tubbs, RR
Cook, JR
Weisenburger, DD
Chan, WC
Staudt, LM
AF Ngo, Vu N.
Young, Ryan M.
Schmitz, Roland
Jhavar, Sameer
Xiao, Wenming
Lim, Kian-Huat
Kohlhammer, Holger
Xu, Weihong
Yang, Yandan
Zhao, Hong
Shaffer, Arthur L.
Romesser, Paul
Wright, George
Powell, John
Rosenwald, Andreas
Muller-Hermelink, Hans Konrad
Ott, German
Gascoyne, Randy D.
Connors, Joseph M.
Rimsza, Lisa M.
Campo, Elias
Jaffe, Elaine S.
Delabie, Jan
Smeland, Erlend B.
Fisher, Richard I.
Braziel, Rita M.
Tubbs, Raymond R.
Cook, J. R.
Weisenburger, Denny D.
Chan, Wing C.
Staudt, Louis M.
TI Oncogenically active MYD88 mutations in human lymphoma
SO NATURE
LA English
DT Article
ID B-CELL LYMPHOMA; NF-KAPPA-B; TNFAIP3 A20; GENE; INHIBITORS; SIGNATURES;
PATHWAYS; SURVIVAL; SUBTYPES; KINASE
AB The activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) remains the least curable form of this malignancy despite recent advances in therapy(1). Constitutive nuclear factor (NF)-kappa B and JAK kinase signalling promotes malignant cell survival in these lymphomas, but the genetic basis for this signalling is incompletely understood. Here we describe the dependence of ABC DLBCLs on MYD88, an adaptor protein that mediates toll and interleukin (IL)-1 receptor signalling(2,3), and the discovery of highly recurrent oncogenic mutations affecting MYD88 in ABC DLBCL tumours. RNA interference screening revealed that MYD88 and the associated kinases IRAK1 and IRAK4 are essential for ABC DLBCL survival. High-throughput RNA resequencing uncovered MYD88 mutations in ABC DLBCL lines. Notably, 29% of ABC DLBCL tumours harboured the same amino acid substitution, L265P, in the MYD88 Toll/IL-1 receptor (TIR) domain at an evolutionarily invariant residue in its hydrophobic core. This mutation was rare or absent in other DLBCL subtypes and Burkitt's lymphoma, but was observed in 9% of mucosa-associated lymphoid tissue lymphomas. At a lower frequency, additional mutations were observed in the MYD88 TIR domain, occurring in both the ABC and germinal centre B-cell-like (GCB) DLBCL subtypes. Survival of ABC DLBCL cells bearing the L265P mutation was sustained by the mutant but not the wild-type MYD88 isoform, demonstrating that L265P is a gain-of-function driver mutation. The L265P mutant promoted cell survival by spontaneously assembling a protein complex containing IRAK1 and IRAK4, leading to IRAK4 kinase activity, IRAK1 phosphorylation, NF-kappa B signalling, JAK kinase activation of STAT3, and secretion of IL-6, IL-10 and interferon-beta. Hence, the MYD88 signalling pathway is integral to the pathogenesis of ABC DLBCL, supporting the development of inhibitors of IRAK4 kinase and other components of this pathway for the treatment of tumours bearing oncogenic MYD88 mutations.
C1 [Ngo, Vu N.; Young, Ryan M.; Schmitz, Roland; Jhavar, Sameer; Lim, Kian-Huat; Kohlhammer, Holger; Xu, Weihong; Yang, Yandan; Zhao, Hong; Shaffer, Arthur L.; Romesser, Paul; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Xiao, Wenming; Powell, John] NIH, Bioinformat & Mol Anal Sect, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Romesser, Paul] NIH, Howard Hughes Med Inst, Res Scholars Program, Bethesda, MD 20892 USA.
[Wright, George] NCI, Biometr Res Branch, DCTD, NIH, Bethesda, MD 20892 USA.
[Rosenwald, Andreas; Muller-Hermelink, Hans Konrad] Univ Wurzburg, Dept Pathol, D-97080 Wurzburg, Germany.
[Ott, German] Robert Bosch Krankenhaus, Dept Clin Pathol, D-70376 Stuttgart, Germany.
[Ott, German] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-70376 Stuttgart, Germany.
[Gascoyne, Randy D.; Connors, Joseph M.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Rimsza, Lisa M.] Univ Arizona, Dept Pathol, Tucson, AZ 85724 USA.
[Rimsza, Lisa M.; Fisher, Richard I.; Braziel, Rita M.; Tubbs, Raymond R.; Cook, J. R.] SW Oncol Grp, Ann Arbor, MI 48106 USA.
[Campo, Elias] Univ Barcelona, Hosp Clin, E-08036 Barcelona, Spain.
[Jaffe, Elaine S.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Delabie, Jan] Univ Hosp, Rikshosp, Pathol Clin, N-0310 Oslo, Norway.
[Smeland, Erlend B.] Univ Hosp, Rikshosp, Inst Canc Res, N-0310 Oslo, Norway.
[Smeland, Erlend B.] Univ Oslo, Norwegian Radium Hosp, Fac Div, Ctr Canc Biomed, N-0310 Oslo, Norway.
[Fisher, Richard I.] Univ Rochester, Sch Med, James P Wilmot Canc Ctr, Rochester, NY 14642 USA.
[Braziel, Rita M.] Oregon Hlth & Sci Univ, Portland, OR 97239 USA.
[Tubbs, Raymond R.; Cook, J. R.] Cleveland Clin, Pathol & Lab Med Inst, Cleveland, OH 44195 USA.
[Weisenburger, Denny D.; Chan, Wing C.] Univ Nebraska Med Ctr, Dept Pathol, Omaha, NE 68198 USA.
[Weisenburger, Denny D.; Chan, Wing C.] Univ Nebraska Med Ctr, Dept Microbiol, Omaha, NE 68198 USA.
RP Staudt, LM (reprint author), NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM lstaudt@mail.nih.gov
OI Romesser, Paul/0000-0001-8268-2903; Delabie, Jan/0000-0001-5023-0689;
Jaffe, Elaine/0000-0003-4632-0301; Lim, Kian-Huat/0000-0002-2766-200X;
Campo, elias/0000-0001-9850-9793
FU NIH, National Cancer Institute, Center for Cancer Research; NCI SPECS
[UO1-CA 114778]; Foundation for NIH; Lymphoma/Leukemia Molecular
Profiling Project (LLMPP); Dr Mildred Scheel Stiftung fur Krebsforschung
(Deutsche Krebshilfe)
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research, an NCI SPECS
grant (UO1-CA 114778), and by the Foundation for NIH, through a gift
from the Richard A. Lauderbaugh Memorial Fund. This study was conducted
under the auspices of the Lymphoma/Leukemia Molecular Profiling Project
(LLMPP). R.S. is supported by the Dr Mildred Scheel Stiftung fur
Krebsforschung (Deutsche Krebshilfe). P.R. was an HHMI-NIH Research
Scholar. This study used the high-performance computational capabilities
of the Biowulf Linux cluster at the National Institutes of Health,
Bethesda, Maryland (http://biowulf.nih.gov). We thank D. Staudt for
discussions, K. Meyer for help with the GEO submission, and X. Li for
IRAK1 plasmids. We are grateful to B. Tran and the Center for Cancer
Research Sequencing Facility for implementation of next generation RNA
sequencing.
NR 27
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Z9 509
U1 10
U2 81
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD FEB 3
PY 2011
VL 470
IS 7332
BP 115
EP U133
DI 10.1038/nature09671
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 715LQ
UT WOS:000286886400045
PM 21179087
ER
PT J
AU Christian, KM
Miracle, AD
Wellman, CL
Nakazawa, K
AF Christian, K. M.
Miracle, A. D.
Wellman, C. L.
Nakazawa, K.
TI CHRONIC STRESS-INDUCED HIPPOCAMPAL DENDRITIC RETRACTION REQUIRES CA3
NMDA RECEPTORS
SO NEUROSCIENCE
LA English
DT Article
DE HPA axis; CA3; NMDA receptor; chronic stress; dendritic retraction;
Golgi staining
ID CHRONIC PSYCHOSOCIAL STRESS; MEDIAL PREFRONTAL CORTEX; PYRAMIDAL
NEURONS; APICAL DENDRITES; RAT HIPPOCAMPUS; INDUCED ATROPHY; SPATIAL
MEMORY; PLASTICITY; MORPHOLOGY; BRAIN
AB Chronic stress induces dendritic retraction in the hippocampal CA3 subregion, but the mechanisms responsible for this retraction and its impact on neural circuitry are not well understood. To determine the role of NMDA (N-methyl-D-aspartic acid) receptor (NMDAR)-mediated signaling in this process, we compared the effects of chronic immobilization stress (CIS) on hippocampal dendritic morphology, hypothalamic-pituitary-adrenal (HPA) axis activation, and anxiety-related and hippocampus-dependent behaviors, in transgenic male mice in which the NMDAR had been selectively deleted in CA3 pyramidal cells and in non-mutant littermates. We found that CIS exposure for 10 consecutive days in non-mutant mice effectively induces HPA axis activation and dendritic retraction of CA3 short-shaft pyramidal neurons, but not CA3 long-shaft pyramidal neurons, suggesting a differential cellular stress response in this region. Dendritic reorganization of short-shaft neurons occurred throughout the longitudinal axis of the hippocampus and, in particular, in the ventral pole of this structure. We also observed a robust retraction of dendrites in dorsal CA1 pyramidal neurons in the non-mutant C57BL/6 mouse strain. Strikingly, chronic stress-induced dendritic retraction was not evident in any of the neurons in either CA3 or CA1 in the mutant mice that had a functional lack of NMDARs restricted to CA3 pyramidal neurons. Interestingly, the prevention of dendritic retraction in the mutant mice had a minimal effect on HPA axis activation and behavioral alterations that were induced by chronic stress. These data support a role for NMDAR-dependent glutamatergic signaling in CA3 in the cell-type specific induction of dendritic retraction in two hippocampal subregions following chronic stress. Published by Elsevier Ltd on behalf of IBRO.
C1 [Christian, K. M.; Miracle, A. D.; Nakazawa, K.] NIMH, Unit Genet Cognit & Behav, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Wellman, C. L.] Indiana Univ, Dept Psychologol & Brain Sci, Bloomington, IN 47405 USA.
[Wellman, C. L.] Indiana Univ, Program Neurosci, Bloomington, IN 47405 USA.
RP Nakazawa, K (reprint author), NIMH, Unit Genet Cognit & Behav, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM nakazawk@mail.nih.gov
RI Nakazawa, Kazutoshi/J-6195-2015
OI Nakazawa, Kazutoshi/0000-0001-5699-9093
FU National Institute of Mental Health
FX This work was supported by the Intramural Research Programs of the
National Institute of Mental Health. We thank Drs. Cameron HA, Chen G,
Young WS, and Holmes A for critical reading of the earlier version of
the manuscript.
NR 42
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U1 2
U2 8
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 FEB 3
PY 2011
VL 174
BP 26
EP 36
DI 10.1016/j.neuroscience.2010.11.033
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 711AL
UT WOS:000286558000003
PM 21108993
ER
PT J
AU St Hilaire, C
Ziegler, SG
Markello, TC
Brusco, A
Groden, C
Gill, F
Carlson-Donohoe, H
Lederman, RJ
Chen, MY
Yang, D
Siegenthaler, MP
Arduino, C
Mancini, C
Freudenthal, B
Stanescu, HC
Zdebik, AA
Chaganti, RK
Nussbaum, RL
Kleta, R
Gahl, WA
Boehm, M
AF St Hilaire, Cynthia
Ziegler, Shira G.
Markello, Thomas C.
Brusco, Alfredo
Groden, Catherine
Gill, Fred
Carlson-Donohoe, Hannah
Lederman, Robert J.
Chen, Marcus Y.
Yang, Dan
Siegenthaler, Michael P.
Arduino, Carlo
Mancini, Cecilia
Freudenthal, Bernard
Stanescu, Horia C.
Zdebik, Anselm A.
Chaganti, R. Krishna
Nussbaum, Robert L.
Kleta, Robert
Gahl, William A.
Boehm, Manfred
TI NT5E Mutations and Arterial Calcifications
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID NONSPECIFIC ALKALINE-PHOSPHATASE; VASCULAR CALCIFICATION;
MINERALIZATION; ADENOSINE; INFANCY; ENPP1; CELLS
AB BACKGROUND
Arterial calcifications are associated with increased cardiovascular risk, but the genetic basis of this association is unclear.
METHODS
We performed clinical, radiographic, and genetic studies in three families with symptomatic arterial calcifications. Single-nucleotide-polymorphism analysis, targeted gene sequencing, quantitative polymerase-chain-reaction assays, Western blotting, enzyme measurements, transduction rescue experiments, and in vitro calcification assays were performed.
RESULTS
We identified nine persons with calcifications of the lower-extremity arteries and hand and foot joint capsules: all five siblings in one family, three siblings in another, and one patient in a third family. Serum calcium, phosphate, and vitamin D levels were normal. Affected members of Family 1 shared a single 22.4-Mb region of homozygosity on chromosome 6 and had a homozygous nonsense mutation (c.662C -> A, p.S221X) in NT5E, encoding CD73, which converts AMP to adenosine. Affected members of Family 2 had a homozygous missense mutation (c.1073G -> A, p.C358Y) in NT5E. The proband of Family 3 was a compound heterozygote for c.662C -> A and c.1609dupA (p.V537fsX7). All mutations found in the three families result in nonfunctional CD73. Cultured fibroblasts from affected members of Family 1 showed markedly reduced expression of NT5E messenger RNA, CD73 protein, and enzyme activity, as well as increased alkaline phosphatase levels and accumulated calcium phosphate crystals. Genetic rescue experiments normalized the CD73 and alkaline phosphatase activity in patients' cells, and adenosine treatment reduced the levels of alkaline phosphatase and calcification.
CONCLUSIONS
We identified mutations in NT5E in members of three families with symptomatic arterial and joint calcifications. This gene encodes CD73, which converts AMP to adenosine, supporting a role for this metabolic pathway in inhibiting ectopic tissue calcification.
C1 [Markello, Thomas C.; Groden, Catherine; Gahl, William A.] NHGRI, NIH Undiagnosed Dis Program, NIH, Bethesda, MD 20892 USA.
[St Hilaire, Cynthia; Lederman, Robert J.; Chen, Marcus Y.; Yang, Dan; Siegenthaler, Michael P.; Boehm, Manfred] NHLBI, NIH, Bethesda, MD 20892 USA.
[Gill, Fred] NIH, Off Rare Dis Res, Ctr Clin, Bethesda, MD 20892 USA.
[Brusco, Alfredo; Arduino, Carlo; Mancini, Cecilia] Direz Univ Med Genet, Azienda Osped Univ San Giovanni Battista, Turin, Italy.
[Brusco, Alfredo; Arduino, Carlo; Mancini, Cecilia] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy.
[Freudenthal, Bernard; Stanescu, Horia C.; Zdebik, Anselm A.; Kleta, Robert] UCL, Dept Med, London WC1E 6BT, England.
[Freudenthal, Bernard; Stanescu, Horia C.; Zdebik, Anselm A.; Kleta, Robert] UCL, Dept Physiol, London WC1E 6BT, England.
[Chaganti, R. Krishna] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Nussbaum, Robert L.] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA.
RP Gahl, WA (reprint author), NHGRI, NIH Undiagnosed Dis Program, NIH, 10 Ctr Dr,Bldg 10,Rm 10C-103, Bethesda, MD 20892 USA.
EM bgahl@helix.nih.gov
RI St. Hilaire, Cynthia/I-4713-2014; Brusco, Alfredo/A-1811-2013;
OI Brusco, Alfredo/0000-0002-8318-7231; St. Hilaire,
Cynthia/0000-0003-1871-6915
FU National Human Genome Research Institute (NHGRI); National Heart, Lung,
and Blood Institute (NHLBI) of the National Institutes of Health
FX Supported by the Intramural Research Programs of the National Human
Genome Research Institute (NHGRI) and the National Heart, Lung, and
Blood Institute (NHLBI) of the National Institutes of Health.
NR 29
TC 143
Z9 147
U1 1
U2 25
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 FEB 3
PY 2011
VL 364
IS 5
BP 432
EP 442
DI 10.1056/NEJMoa0912923
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 715LL
UT WOS:000286885900008
PM 21288095
ER
PT J
AU Miller, FG
Joffe, S
AF Miller, Franklin G.
Joffe, Steven
TI Equipoise and the Dilemma of Randomized Clinical Trials
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID METASTATIC COLORECTAL-CANCER; ESTROGEN PLUS PROGESTIN; THERAPEUTIC
MISCONCEPTION; 1ST-LINE CHEMOTHERAPY; RESPONSE RATES; BREAST-CANCER;
SURVIVAL; BENEFIT; MELANOMA; ETHICS
C1 [Miller, Franklin G.] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
[Joffe, Steven] Dana Farber Canc Inst, Dept Pediat Oncol, Boston, MA 02115 USA.
[Joffe, Steven] Childrens Hosp, Dept Med, Boston, MA 02115 USA.
RP Miller, FG (reprint author), NIH, Dept Bioeth, Ctr Clin, Bldg 10, Bethesda, MD 20892 USA.
OI Joffe, Steven/0000-0002-0667-7384
NR 35
TC 78
Z9 78
U1 0
U2 8
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 FEB 3
PY 2011
VL 364
IS 5
BP 476
EP 480
DI 10.1056/NEJMsb1011301
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 715LL
UT WOS:000286885900016
PM 21288100
ER
PT J
AU Shad, MU
Bidesi, AS
Chen, LA
Thomas, BP
Ernst, M
Rao, U
AF Shad, Mujeeb U.
Bidesi, Anup S.
Chen, Li-Ann
Thomas, Binu P.
Ernst, Monique
Rao, Uma
TI Neurobiology of decision-making in adolescents
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Neurobiology; Choice; Selection; Adolescents; Decision-making; Rewards
ID MEDIAL PREFRONTAL CORTEX; ANTERIOR CINGULATE CORTEX; FAMILY HISTORY
METHOD; ORBITOFRONTAL CORTEX; NUCLEUS-ACCUMBENS; NEURAL RESPONSES;
CHOICE SELECTION; PUBERTAL CHANGES; MONETARY REWARD; DORSAL STRIATUM
AB The study examined the relationship between risk-taking behavior during selection of monetary rewards and activations in the anterior cingulate cortex (ACC), orbitofrontal cortex (OFC) and medial prefrontal cortex (mPFC), brain regions that are associated with decision-making. Thirty-three adolescents with no personal or family history of any psychiatric illness were administered the Wheel of Fortune (WOF) task using a functional magnetic resonance imaging protocol. The WOF is a computerized two-choice, probabilistic monetary reward task. Selection of a reward, particularly a low-probability/high-magnitude reward choice, induced greater activations in dorsal ACC, ventrolateral OFC and mPFC than the control condition. Although similar findings have been reported by earlier studies, the results from this study were not impacted by reaction times and expected values and persisted even after controlling for sociodemographic factors. Post hoc analysis revealed greater activation of ACC and mPFC in response to selection of rewards of larger magnitude than those of smaller magnitude when the probability of reward was maintained constant. Adolescents with greater frequency of high-risk behavior (defined as low-probability/high-magnitude reward choice) had lower activation of ACC, OFC and mPFC than those who engaged in this behavior less frequently. These findings suggest individual differences in prefrontal cortical function with regards to decision-making process in adolescents. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Shad, Mujeeb U.] Univ Texas Hlth Sci Ctr, Houston, TX 77054 USA.
[Bidesi, Anup S.; Chen, Li-Ann; Thomas, Binu P.; Rao, Uma] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Ernst, Monique] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
RP Shad, MU (reprint author), Univ Texas Hlth Sci Ctr, 1941 East Rd,BBSB 3118, Houston, TX 77054 USA.
EM mujeeb.u.shad@uth.tmc.edu
FU Eli Lilly; National Institutes of Health [DA14037, DA15131, DA17804,
DA17805, MH62464, MH68391]
FX The primary author has received funding from Eli Lilly for other
research. The other authors have no conflicts of interest.; This work
was supported, in part, by grants from the National Institutes of Health
(DA14037, DA15131, DA17804, DA17805, MH62464 and MH68391), and the Sarah
M. and Charles.
NR 83
TC 10
Z9 11
U1 4
U2 20
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD FEB 2
PY 2011
VL 217
IS 1
BP 67
EP 76
DI 10.1016/j.bbr.2010.09.033
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 710TK
UT WOS:000286539700010
PM 20933020
ER
PT J
AU Barakat, M
Doyon, J
Debas, K
Vandewalle, G
Morin, A
Poirier, G
Martin, N
Lafortune, M
Karni, A
Ungerleider, LG
Benali, H
Carrier, J
AF Barakat, M.
Doyon, J.
Debas, K.
Vandewalle, G.
Morin, A.
Poirier, G.
Martin, N.
Lafortune, M.
Karni, A.
Ungerleider, L. G.
Benali, H.
Carrier, J.
TI Fast and slow spindle involvement in the consolidation of a new motor
sequence
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Motor sequence learning; Memory consolidation; Sleep; Fast sleep
spindles; Slow sleep spindles
ID LEARNING-DEPENDENT CHANGES; EYE-MOVEMENT SLEEP; MEMORY CONSOLIDATION;
STAGE-2 SLEEP; REM-SLEEP; TIME-COURSE; PLASTICITY; BRAIN; OSCILLATIONS;
PERFORMANCE
AB This study aimed to determine the distinct contribution of slow (11-13 Hz) and fast (13-15 Hz) spindles in the consolidation process of a motor sequence learning task (MSL). Young subjects (n = 12) were trained on both a finger MSL task and a control (CTRL) condition, which were administered one week apart in a counterbalanced order. Subjects were asked to practice the MSL or CTRL task in the evening (approximately 9:00 p.m.) and their performance was retested on the same task 12 h later (approximately 9:00 a.m.). Polysomnographic (PSG) recordings were performed during the night following training on either task, and an automatic algorithm was used to detect fast and slow spindles and to quantify their characteristics (i.e., density, amplitude, and duration). Statistical analyses revealed higher fast (but not slow) spindle density after training on the MSL than after practice of the CTRL task. The increase in fast spindle density on the MSL task correlated positively with overnight performance gains on the MSL task and with difference in performance gain between the MSL and CTRL tasks. Together, these results suggest that fast sleep spindles help activate the cerebral network involved in overnight MSL consolidation, while slow spindles do not appear to play a role in this mnemonic process. (C) 2010 Elsevier B.V. All rights reserved.
C1 [Barakat, M.; Vandewalle, G.; Morin, A.; Poirier, G.; Martin, N.; Lafortune, M.; Carrier, J.] Hop Sacre Coeur, Ctr Adv Res Sleep Med, Montreal, PQ H4J 1C5, Canada.
[Barakat, M.; Doyon, J.; Debas, K.; Vandewalle, G.; Morin, A.; Martin, N.; Lafortune, M.; Carrier, J.] Inst Univ Geriatrie Montreal, Ctr Rech, Unite Neuroimagerie Fonct, Montreal, PQ, Canada.
[Karni, A.] Univ Haifa, Brain Behav Ctr, Lab Funct Brain Imaging & Learning Res, IL-31999 Haifa, Israel.
[Ungerleider, L. G.] NIMH, NIH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Benali, H.] Univ Paris 06, Ctr Hosp Univ Pitie Salpetriere, Inst Natl Sante & Rech Med, Unite Mixte Rech S 678, Paris, France.
RP Carrier, J (reprint author), Hop Sacre Coeur, Ctr Adv Res Sleep Med, 5400 Gouin Blvd W, Montreal, PQ H4J 1C5, Canada.
EM julie.carrier.1@umontreal.ca
OI Martin, Nicholas/0000-0003-4069-8020
FU Canadian Institutes of Health Research (CIHR); FRSQ
FX Support for this research was provided by a grant from the Canadian
Institutes of Health Research (CIHR) to JD, JC, AHT, AK, HB, and LGU,
and by an FRSQ scholarship awarded to JC. The authors are grateful to
Sonia Frenette and Jean Paquet for their technical assistance.
NR 35
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U1 1
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD FEB 2
PY 2011
VL 217
IS 1
BP 117
EP 121
DI 10.1016/j.bbr.2010.10.019
PG 5
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 710TK
UT WOS:000286539700017
PM 20974183
ER
PT J
AU Thanos, PK
Cho, J
Kim, R
Michaelides, M
Primeaux, S
Bray, G
Wang, GJ
Volkow, ND
AF Thanos, Panayotis K.
Cho, Jacob
Kim, Ronald
Michaelides, Michael
Primeaux, Stefany
Bray, George
Wang, Gene-Jack
Volkow, Nora D.
TI Bromocriptine increased operant responding for high fat food but
decreased chow intake in both obesity-prone and resistant rats
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Hyperphagia; Addiction; Dopamine; D2; Diet
ID DOPAMINE D2 RECEPTOR; ORBITOFRONTAL CORTEX; DEFICIENT MICE; WEIGHT-GAIN;
BODY-WEIGHT; IMPULSIVITY; ADDICTION; INHIBITION; BEHAVIOR
AB Dopamine (DA) and DA D(2) receptors (D2R) have been implicated in obesity and are thought to be involved in the rewarding properties of food. Osborne-Mendel (OM) rats are susceptible to diet induced obesity (DIO) while S5B/P (S5B) rats are resistant when given a high-fat diet. Here we hypothesized that the two strains would differ in high-fat food self-administration (FSA) and that the D2R agonist bromocriptine (BC) would differently affect their behavior. Ad-libitum fed OM and S5B/P rats were tested in a FSA operant chamber and were trained to lever press for high-fat food pellets under a fixed-ratio (FR1) and a progressive ratio (PR) schedule. After sixteen days of PR sessions, rats were treated with three different doses of BC (1, 10 and 20 mg/kg). No significant differences were found between the two strains in the number of active lever presses. BC treatment (10 mg/kg and 20 mg/kg) increased the number of active lever presses (10 mg/kg having the strongest effect) whereas it decreased rat chow intake in the home cage with equivalent effects in both strains. These effects were not observed on the day of BC administration but on the day following its administration. Our results suggest that these two strains have similar motivation for procuring high fat food using this paradigm. BC increased operant responding for high-fat pellets but decreased chow intake in both strains, suggesting that D2R stimulation may have enhanced the motivational drive to procure the fatty food while correspondingly decreasing the intake of regular food. These findings suggest that susceptibility to dietary obesity (prior to the onset of obesity) may not affect operant motivation for a palatable high fat food and that differential susceptibility to obesity may be related to differential sensitivity to D2R stimulation. Published by Elsevier B.V.
C1 [Thanos, Panayotis K.; Volkow, Nora D.] NIAAA, NIH, Dept Hlth & Human Serv, Lab Neuroimaging, Bethesda, MD USA.
[Thanos, Panayotis K.; Cho, Jacob; Kim, Ronald; Michaelides, Michael; Wang, Gene-Jack; Volkow, Nora D.] Brookhaven Natl Lab, Behav Neuropharmacol & Neuroimaging Lab, Upton, NY 11973 USA.
[Thanos, Panayotis K.; Kim, Ronald; Michaelides, Michael] SUNY Stony Brook, Stony Brook, NY 11794 USA.
[Primeaux, Stefany; Bray, George] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
RP Thanos, PK (reprint author), NIAAA, NIH, Dept Hlth & Human Serv, Lab Neuroimaging, Bethesda, MD USA.
EM thanos@bnl.gov
RI Michaelides, Michael/K-4736-2013
OI Michaelides, Michael/0000-0003-0398-4917
FU NIAAA [AA11034, AA07574, AA07611]
FX Support for the study has been contributed by NIAAA Intramural Research
Program: (AA11034 and AA07574, AA07611).
NR 27
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U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD FEB 2
PY 2011
VL 217
IS 1
BP 165
EP 170
DI 10.1016/j.bbr.2010.10.027
PG 6
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 710TK
UT WOS:000286539700024
PM 21034777
ER
PT J
AU Eddy, MT
Hermida, OT
Andreas, L
Wagner, G
Rostovtseva, TK
Griffin, RG
AF Eddy, Matthew T.
Hermida, Oscar T.
Andreas, Loren
Wagner, Gerhard
Rostovtseva, Tatiana K.
Griffin, Robert G.
TI Investigating VDAC Gating via Magic Angle Spinning NMR and
Electrophysiological Measurements Under Extreme pH Conditions:
Implications for the Voltage-Gating Mechanism
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Eddy, Matthew T.; Andreas, Loren; Griffin, Robert G.] MIT, Francis Bitter Natl Magnet Lab, Cambridge, MA 02139 USA.
[Hermida, Oscar T.; Rostovtseva, Tatiana K.] NICHD, Lab Phys & Struct Biol, PPB, NIH, Bethesda, MD USA.
[Wagner, Gerhard] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 8
EP 9
PG 2
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600045
ER
PT J
AU Forbes, JG
Wittebort, RJ
Wang, K
AF Forbes, Jeffrey G.
Wittebort, Richard J.
Wang, Kuan
TI Transient Alpha and Pi Helical Conversion of BLUE Octads in the Elastic
and Disordered Region of C. elegans TTN-1
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Forbes, Jeffrey G.] NIAMS, NIH, DHHS, Bethesda, MD USA.
[Wittebort, Richard J.] Univ Louisville, Louisville, KY 40292 USA.
[Wang, Kuan] Acad Sinica, Taipei 115, Taiwan.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 13
EP 14
PG 2
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600071
ER
PT J
AU Tjandra, N
Ma, JH
Edlich, F
Youle, R
AF Tjandra, Nico
Ma, Junhe
Edlich, Frank
Youle, Richard
TI Structural Insights into Cytomegalovirus Resistance to Apoptosis
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Tjandra, Nico; Ma, Junhe] NHLBI, NIH, Bethesda, MD 20892 USA.
[Edlich, Frank; Youle, Richard] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 17
EP 17
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600088
ER
PT J
AU Kraft, ML
Frisz, JF
Lou, K
Hanafin, W
Weber, PK
Carpenter, KJ
Zimmerberg, J
Hutcheon, ID
AF Kraft, Mary L.
Frisz, Jessica F.
Lou, Kaiyan
Hanafin, William
Weber, Peter K.
Carpenter, Kevin J.
Zimmerberg, Joshua
Hutcheon, Ian D.
TI Chemical Imaging of Lipid Organization in the Plasma Membranes of Intact
Cells with High Lateral Resolution
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Kraft, Mary L.; Frisz, Jessica F.; Lou, Kaiyan; Hanafin, William] Univ Illinois, Urbana, IL 61801 USA.
[Weber, Peter K.; Carpenter, Kevin J.; Hutcheon, Ian D.] Lawrence Livermore Natl Lab, Livermore, CA USA.
[Zimmerberg, Joshua] NIH, Bethesda, MD 20892 USA.
RI Lou, Kaiyan/D-4199-2012
OI Lou, Kaiyan/0000-0003-3443-0343
NR 0
TC 0
Z9 0
U1 1
U2 6
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 19
EP 20
PG 2
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600102
ER
PT J
AU Kumar, J
Schuck, P
Mayer, ML
AF Kumar, Janesh
Schuck, Peter
Mayer, Mark L.
TI Structure & Mechanisms Underlying Heteromeric Glutamate Receptor
Assembly
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Kumar, Janesh; Mayer, Mark L.] NICHD, Lab Cellular & Mol Neurophysiol, Porter Neurosci Res Ctr, NIH,DHHS, Bethesda, MD USA.
[Schuck, Peter] NIBIB, Lab Bioengn & Phys Sci, NIH, DHHS, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 24
EP 24
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600123
ER
PT J
AU Kawate, T
Robertson, JL
Li, MF
Silberberg, SD
Swartz, KJ
AF Kawate, Toshimitsu
Robertson, Janice L.
Li, Mufeng
Silberberg, Shai D.
Swartz, Kenton J.
TI Ion Access Pathway to the Transmembrane Pore in P2X Receptors
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Kawate, Toshimitsu; Li, Mufeng; Silberberg, Shai D.; Swartz, Kenton J.] NIH, Bethesda, MD 20892 USA.
[Robertson, Janice L.] Brandeis Univ, Waltham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 25
EP 25
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600127
ER
PT J
AU Balla, T
AF Balla, Tamas
TI Mapping the Phosphoinositide Landscape in Mammalian Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Balla, Tamas] NICHD, Sect Mol Signal Transduct, Program Dev Neurosci, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 26
EP 26
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600131
ER
PT J
AU Johnson, ME
Hummer, G
AF Johnson, Margaret E.
Hummer, Gerhard
TI Nonspecific Binding Limits the Number of Proteins in a Cell and Shapes
their Interaction Networks
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Johnson, Margaret E.; Hummer, Gerhard] NIH, Bethesda, MD 20892 USA.
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
NR 0
TC 0
Z9 0
U1 0
U2 2
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 32
EP 32
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600164
ER
PT J
AU Xu, Y
Nussionv, R
Ma, BY
AF Xu, Yu
Nussionv, Ruth
Ma, Buyong
TI Construct and Simulate Virtual Cell with Minimum Genome at the Nanoscale
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Xu, Yu] Minzu Univ China, Inst Chinese Minor Tradit Med, Beijing, Peoples R China.
[Nussionv, Ruth; Ma, Buyong] NCI Frederick, SAIC Frederick, NIH, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 32
EP 32
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288600162
ER
PT J
AU Smyth, JT
Wu, SL
Putney, JW
AF Smyth, Jeremy T.
Wu, Shilan
Putney, James W.
TI Definition of STIM1 Phosphorylation Sites that Contribute to Suppression
of Store-Operated Calcium Entry During Mitosis
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Smyth, Jeremy T.; Wu, Shilan; Putney, James W.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 181
EP 181
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288601372
ER
PT J
AU Rouzina, I
Qualley, DF
Wu, TY
Iwatani, Y
Chan, DSB
Hertz, A
Chaurasiya, K
Levin, JG
Williams, MC
Musier-Forsyth, K
AF Rouzina, Ioulia
Qualley, Dominic F.
Wu, Tiyun
Iwatani, Yasumasa
Chan, Denise S. B.
Hertz, Amber
Chaurasiya, Kathy
Levin, Judith G.
Williams, Mark C.
Musier-Forsyth, Karin
TI Complex Kinetics of Apobec3g Interaction with Single-Stranded Nucleic
Acids
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Rouzina, Ioulia] Univ Minnesota, Minneapolis, MN USA.
[Qualley, Dominic F.; Musier-Forsyth, Karin] Ohio State Univ, Columbus, OH 43210 USA.
[Wu, Tiyun; Hertz, Amber; Levin, Judith G.] NIH, Bethesda, MD 20892 USA.
[Iwatani, Yasumasa] Natl Hosp Org, Clin Res Ctr, Nagoya Med Ctr, Nagoya, Aichi, Japan.
[Chan, Denise S. B.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Chaurasiya, Kathy; Williams, Mark C.] Northeastern Univ, Dept Phys, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 192
EP 192
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288601427
ER
PT J
AU Jin, AJ
Li, EJ
Pang, LJ
Kotova, S
Sackett, DL
Smith, PD
Lafer, EM
Nossal, RJ
AF Jin, Albert J.
Li, Eileen J.
Pang, Lisa J.
Kotova, Svetlana
Sackett, Dan L.
Smith, Paul D.
Lafer, Eileen M.
Nossal, Ralph J.
TI Nanomechanics of Clathrin Protein Shells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Jin, Albert J.; Li, Eileen J.; Pang, Lisa J.; Kotova, Svetlana; Smith, Paul D.] NIBIB, NIH, Bethesda, MD USA.
[Sackett, Dan L.; Nossal, Ralph J.] NICHD, NIH, Bethesda, MD USA.
[Lafer, Eileen M.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
OI Jin, Albert/0000-0003-3826-1081
NR 0
TC 0
Z9 0
U1 0
U2 3
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 198
EP 199
PG 2
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288601460
ER
PT J
AU Hummer, G
AF Hummer, Gerhard
TI Proton Pumping and Energy Transduction in Cytochrome C Oxidase
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Hummer, Gerhard] NIH, Bethesda, MD 20892 USA.
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
NR 0
TC 0
Z9 0
U1 0
U2 3
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 343
EP 343
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603008
ER
PT J
AU Chung, HS
Gopich, IV
McHale, K
Louis, JM
Eaton, WA
AF Chung, Hoi Sung
Gopich, Irina V.
McHale, Kevin
Louis, John M.
Eaton, William A.
TI Photon-By-Photon Analysis of Single Molecule Fluorescence Trajectories
Determines an Upper Bound for the Transition Path Time in Protein
Folding
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Chung, Hoi Sung; Gopich, Irina V.; McHale, Kevin; Louis, John M.; Eaton, William A.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 7
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 349
EP 349
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603036
ER
PT J
AU Capone, R
Kotler, SA
Jang, H
Connelly, LS
Nussinov, R
Lal, R
AF Capone, Ricardo
Kotler, Samuel A.
Jang, Hyunbum
Connelly, Laura S.
Nussinov, Ruth
Lal, Ratnesh
TI Probing Structural Features of Alzheimer's beta-Amyloid Ion Channels in
Membranes Using A beta Mutants
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Capone, Ricardo; Kotler, Samuel A.; Connelly, Laura S.; Lal, Ratnesh] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Jang, Hyunbum; Nussinov, Ruth] NCI, SAIC Frederick, Ctr Canc Res, Nanobiol Program, Frederick, MD 21701 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Tel Aviv, Israel.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 350
EP 350
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603041
ER
PT J
AU Renz, M
Lippincott-Schwartz, J
AF Renz, Malte
Lippincott-Schwartz, Jennifer
TI Single-Molecule Counting with Palm
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Renz, Malte; Lippincott-Schwartz, Jennifer] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 350
EP 350
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603038
ER
PT J
AU Sengupta, P
Talisman, T
Veatch, S
Lippincott-Schwartz, J
AF Sengupta, Prabuddha
Talisman, Tijana
Veatch, Sarah
Lippincott-Schwartz, Jennifer
TI Nano-Scale Spatial Organization of Plasma Membrane Revealed by
Pair-Correlation Analysis
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Sengupta, Prabuddha; Talisman, Tijana; Lippincott-Schwartz, Jennifer] NIH, Bethesda, MD 20892 USA.
[Veatch, Sarah] Univ Michigan, Ann Arbor, MI 48109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 350
EP 350
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603040
ER
PT J
AU Brochet, DXP
Yang, DM
Cheng, HP
Lederer, WJ
AF Brochet, Didier X. P.
Yang, Dongmei
Cheng, Heping
Lederer, W. Jonathan
TI Small Ca2+ Release Events in Rabbit Ventricular Myocytes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Brochet, Didier X. P.; Lederer, W. Jonathan] BioMET, Baltimore, MD USA.
[Yang, Dongmei] NIA, NIH, Baltimore, MD 21224 USA.
[Cheng, Heping] Peking Univ, Beijing 100871, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 352
EP 353
PG 2
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603053
ER
PT J
AU Ma, XF
Adelstein, RS
AF Ma, Xuefei
Adelstein, Robert S.
TI The Enzymatic Motor Activity of Nonmuscle Myosin II-B is not Critical
for Cardiac Myocyte Cytokinesis
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Ma, Xuefei; Adelstein, Robert S.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 354
EP 354
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603060
ER
PT J
AU Castronovo, M
Lucesoli, A
Choi, D
Inverso, V
Parisse, P
Kurnikova, A
Malhotra, A
Grassi, M
Grassi, G
Scaggiante, B
Casalis, L
Scoles, G
AF Castronovo, Matteo
Lucesoli, Agnese
Choi, Dianne
Inverso, Vincent
Parisse, Pietro
Kurnikova, Anastasia
Malhotra, Aseem
Grassi, Mario
Grassi, Gabriele
Scaggiante, Bruna
Casalis, Loredana
Scoles, Giacinto
TI The Effect of Confinement on Enzyme Diffusion and Reactions Inside DNA
Nanostructures
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Castronovo, Matteo; Choi, Dianne; Inverso, Vincent; Kurnikova, Anastasia; Malhotra, Aseem; Scoles, Giacinto] Temple Univ, Philadelphia, PA 19122 USA.
[Castronovo, Matteo] CBM, Trieste, Italy.
[Lucesoli, Agnese] Hosp San Salvatore, Pesaro, Italy.
[Lucesoli, Agnese; Scoles, Giacinto] SISSA, I-34014 Trieste, Italy.
[Inverso, Vincent] Univ Penn, Philadelphia, PA 19104 USA.
[Parisse, Pietro; Casalis, Loredana] Sincrotrone Trieste Scrl, Trieste, Italy.
[Kurnikova, Anastasia] NIH, Bethesda, MD 20892 USA.
[Grassi, Mario; Grassi, Gabriele; Scaggiante, Bruna] Univ Trieste, Trieste, Italy.
[Grassi, Mario] Univ Hosp Cattinara, Trieste, Italy.
[Casalis, Loredana] IIT, Trieste, Italy.
NR 0
TC 0
Z9 0
U1 1
U2 7
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 357
EP 357
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603075
ER
PT J
AU Fodeke, AA
Minton, AP
AF Fodeke, Adedayo A.
Minton, Allen P.
TI Quantitative Characterization of Protein-Protein and Protein-Polymer
Interaction via Nonideal Tracer Sedimentation Equilibrium
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Fodeke, Adedayo A.; Minton, Allen P.] NIH, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 357
EP 357
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603076
ER
PT J
AU Zhao, HY
Brown, PH
Schuck, P
AF Zhao, Huaying
Brown, Patrick H.
Schuck, Peter
TI Studying Rapidly Reversible Protein-Protein Interactions by
Sedimentation Velocity Analytical Ultracentrifugation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
DE protein interactions; transport; sedimentation; signal transduction
C1 [Zhao, Huaying; Brown, Patrick H.; Schuck, Peter] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 387
EP 387
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288603228
ER
PT J
AU Losert, W
Driscoll, M
McCann, C
Fourkas, J
Parent, C
AF Losert, Wolfgang
Driscoll, Meghan
McCann, Colin
Fourkas, John
Parent, Carole
TI Cell Shape Dynamics: from Waves to Motion
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Losert, Wolfgang; Driscoll, Meghan; McCann, Colin; Fourkas, John] Univ Maryland, College Pk, MD 20742 USA.
[Parent, Carole] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 513
EP 514
PG 2
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288604310
ER
PT J
AU Vinogradova, TM
Lakatta, EG
AF Vinogradova, Tatiana M.
Lakatta, Edward G.
TI Basal Phospholipase C (PLC) Activation is Obligatory for Cardiac
Pacemaker Activity
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Vinogradova, Tatiana M.; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 1
Z9 1
U1 2
U2 4
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 517
EP 517
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288604327
ER
PT J
AU Ma, BY
Nussinov, R
AF Ma, Buyong
Nussinov, Ruth
TI The Evolution of the Natively Disordered Region in P53 Family Proteins
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Ma, Buyong; Nussinov, Ruth] NCI Frederick, SAIC Frederick, NIH, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 518
EP 518
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288604333
ER
PT J
AU Soubias, O
Teague, WE
Hines, KG
Gawrisch, K
AF Soubias, Olivier
Teague, Walter E.
Hines, Kirk G.
Gawrisch, Klaus
TI Rhodopsin - Rhodopsin Oligomerization in Model Lipid Bilayers -
Functional Implications
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Soubias, Olivier; Teague, Walter E.; Hines, Kirk G.; Gawrisch, Klaus] NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 525
EP 526
PG 2
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288604374
ER
PT J
AU Fawzi, NL
Ying, JF
Torchia, DA
Clore, GM
AF Fawzi, Nicolas L.
Ying, Jinfa
Torchia, Dennis A.
Clore, G. Marius
TI Kinetics of Amyloid-Beta Monomer to Oligomer Exchange by NMR Relaxation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Fawzi, Nicolas L.; Ying, Jinfa; Torchia, Dennis A.; Clore, G. Marius] NIDDK, NIH, Bethesda, MD USA.
RI Clore, G. Marius/A-3511-2008
OI Clore, G. Marius/0000-0003-3809-1027
NR 0
TC 0
Z9 0
U1 0
U2 2
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 531
EP 531
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288604403
ER
PT J
AU Miller, Y
Ma, BY
Nussinov, R
AF Miller, Yifat
Ma, Buyong
Nussinov, Ruth
TI Alzheimer A beta Amyloid Annular Fibrils: Insight Into Polymorphism
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 55th Annual Meeting of the Biophysical-Society
CY MAR 05-09, 2011
CL Baltimore, MD
SP Biophys Soc
C1 [Ma, Buyong; Nussinov, Ruth] NCI, SAIC Frederick Inc, NIH, Frederick, MD 21701 USA.
NR 0
TC 1
Z9 1
U1 0
U2 4
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 FEB 2
PY 2011
VL 100
IS 3
SU 1
BP 531
EP 531
PG 1
WC Biophysics
SC Biophysics
GA 972PF
UT WOS:000306288604401
ER
PT J
AU Rui, HA
Lee, KI
Pastor, RW
Im, W
AF Rui, Huan
Lee, Kyu Il
Pastor, Richard W.
Im, Wonpil
TI Molecular Dynamics Studies of Ion Permeation in VDAC
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID DEPENDENT ANION CHANNEL; RAT-LIVER MITOCHONDRIA; PEPTIDE-SPECIFIC
ANTIBODIES; OUTER-MEMBRANE; OMPF PORIN; VOLTAGE; SIMULATION; PROTEIN;
SELECTIVITY; CHARMM
AB The voltage-dependent anion channel (VDAC) in the outer membrane of mitochondria serves an essential role in the transport of metabolites and electrolytes between the cell matrix and mitochondria. To examine its structure, dynamics, and the mechanisms underlying its electrophysiological properties, we performed a total of 1.77 mu s molecular dynamics simulations of human VDAC isoform 1 in DOPE/DOPC mixed bilayers in 1 M KCl solution with transmembrane potentials of 0, +/- 25, +/- 50, +/- 75, and +/- 100 mV. The calculated conductance and ion selectivity are in good agreement with the experimental measurements. In addition, ion density distributions inside the channel reveal possible pathways for different ion species. Based on these observations, a mechanism underlying the anion selectivity is proposed; both ion species are transported across the channel, but the rate for K(+) is smaller than that for Cl(-) because of the attractive interactions between K(+) and residues on the channel wall. This difference leads to the anion selectivity of VDAC.
C1 [Rui, Huan; Lee, Kyu Il; Im, Wonpil] Univ Kansas, Dept Mol Biosci, Lawrence, KS 66045 USA.
[Rui, Huan; Lee, Kyu Il; Im, Wonpil] Univ Kansas, Ctr Bioinformat, Lawrence, KS 66045 USA.
[Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Im, W (reprint author), Univ Kansas, Dept Mol Biosci, Lawrence, KS 66045 USA.
EM wonpil@ku.edu
FU University of Kansas; National Institutes of Health [R01-GM092950];
National Science Foundation [NSF OCI-0503992]; National Institutes of
Health, National Heart, Lung, and Blood Institute
FX This work was supported in part by institutional funding from the
University of Kansas, including J. R. and Inez Jay funds, the National
Institutes of Health (R01-GM092950), the National Science Foundation
(NSF OCI-0503992) through TeraGrid resources provided by Purdue
University (to W.I.), and the Intramural Research Program of the
National Institutes of Health, National Heart, Lung, and Blood Institute
(to R.W.P.).
NR 46
TC 41
Z9 41
U1 1
U2 5
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 FEB 2
PY 2011
VL 100
IS 3
BP 602
EP 610
DI 10.1016/j.bpj.2010.12.3711
PG 9
WC Biophysics
SC Biophysics
GA 716GN
UT WOS:000286957200010
PM 21281574
ER
PT J
AU Lee, KI
Rui, HA
Pastor, RW
Im, W
AF Lee, Kyu Il
Rui, Huan
Pastor, Richard W.
Im, Wonpil
TI Brownian Dynamics Simulations of Ion Transport through the VDAC
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID DEPENDENT ANION CHANNEL; ALPHA-HEMOLYSIN; ELECTRODIFFUSION THEORY;
MITOCHONDRIAL CHANNEL; MOLECULAR-DYNAMICS; SELECTIVITY; PERMEATION;
PROTEIN; MEMBRANE; MODELS
AB It is important to gain a physical understanding of ion transport through the voltage-dependent anion channel (VDAC) because this channel provides primary permeation pathways for metabolites and electrolytes between the cytosol and mitochondria. We performed grand canonical Monte Carlo/Brownian dynamics (GCMC/BD) simulations to explore the ion transport properties of human VDAC isoform 1 (hVDAC1; PDB:2K4T) embedded in an implicit membrane. When the MD-derived, space-dependent diffusion constant was used in the GCMC/BD simulations, the current-voltage characteristics and ion number profiles inside the pore showed excellent agreement with those calculated from all-atom molecular-dynamics (MD) simulations, thereby validating the GCMC/BD approach. Of the 20 NMR models of hVDAC1 currently available, the third one (NMR03) best reproduces both experimental single-channel conductance and ion selectivity (i.e., the reversal potential). In addition, detailed analyses of the ion trajectories, one-dimensional multi-ion potential of mean force, and protein charge distribution reveal that electrostatic interactions play an important role in the channel structure and ion transport relationship. Finally, the GCMC/BD simulations of various mutants based on NMR03 show good agreement with experimental ion selectivity. The difference in ion selectivity between the wild-type and the mutants is the result of altered potential of mean force profiles that are dominated by the electrostatic interactions.
C1 [Lee, Kyu Il; Rui, Huan; Im, Wonpil] Univ Kansas, Ctr Bioinformat, Lawrence, KS 66045 USA.
[Lee, Kyu Il; Rui, Huan; Im, Wonpil] Univ Kansas, Dept Mol Biosci, Lawrence, KS 66045 USA.
[Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Im, W (reprint author), Univ Kansas, Ctr Bioinformat, Lawrence, KS 66045 USA.
EM wonpil@ku.edu
FU University of Kansas; J. R. and Inez Jay Fund; National Institutes of
Health [R01-GM092950]; National Science Foundation [NSF OCI-0503992];
National Heart, Lung, and Blood Institute; Korean Government
[KRF-2006-352-D00132]
FX This work was supported in part by institutional funding from the
University of Kansas, the J. R. and Inez Jay Fund, the National
Institutes of Health (R01-GM092950), the National Science Foundation
(NSF OCI-0503992) through TeraGrid resources provided by Purdue
University (to W.I.), and the Intramural Research Program of the
National Heart, Lung, and Blood Institute (to R.W.P.). K.I.L. was
supported by a Korea Research Foundation Grant funded by the Korean
Government (KRF-2006-352-D00132).
NR 34
TC 28
Z9 28
U1 2
U2 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD FEB 2
PY 2011
VL 100
IS 3
BP 611
EP 619
DI 10.1016/j.bpj.2010.12.3708
PG 9
WC Biophysics
SC Biophysics
GA 716GN
UT WOS:000286957200011
PM 21281575
ER
PT J
AU Lu, JX
Yau, WM
Tycko, R
AF Lu, Jun-Xia
Yau, Wai-Ming
Tycko, Robert
TI Evidence from Solid-State NMR for Nonhelical Conformations in the
Transmembrane Domain of the Amyloid Precursor Protein
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID NUCLEAR-MAGNETIC-RESONANCE; ANGLE-SPINNING NMR; C-TERMINAL DOMAIN;
ALZHEIMERS-DISEASE; GAMMA-SECRETASE; CHEMICAL-SHIFTS; LIPID RAFTS;
PHOSPHOLIPID-BILAYERS; SECONDARY-STRUCTURE; C-13 NMR
AB The amyloid precursor protein (APP) is subject to proteolytic processing by gamma-secretase within neuronal membranes, leading to Alzheimer's disease-associated beta-amyloid peptide production by cleavage near the midpoint of the single transmembrane (TM) segment of APP. Conformational properties of the TM segment may affect its susceptibility to gamma-secretase cleavage, but these properties have not been established definitively, especially in bilayer membranes with physiologically relevant lipid compositions. In this article, we report an investigation of the APP-TM conformation, using C-13 chemical shifts obtained with two-dimensional solid-state NMR spectroscopy as site-specific conformational probes. We find that the APP-TM conformation is not a simple alpha-helix, particularly at 37 degrees C in multilamellar vesicles with compositions that mimic the composition of neuronal cell membranes. Instead, we observe a mixture of helical and nonhelical conformations at the N- and C-termini and in the vicinity of the gamma-cleavage site. Conformational plasticity of the TM segment of APP may be an important factor in the gamma-secretase cleavage mechanism.
C1 [Lu, Jun-Xia; Yau, Wai-Ming; Tycko, Robert] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Tycko, R (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM robertty@mail.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases of the
National Institutes of Health.
NR 54
TC 19
Z9 19
U1 1
U2 19
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 FEB 2
PY 2011
VL 100
IS 3
BP 711
EP 719
DI 10.1016/j.bpj.2010.12.3696
PG 9
WC Biophysics
SC Biophysics
GA 716GN
UT WOS:000286957200022
PM 21281586
ER
PT J
AU Mishra, SK
Tisel, SM
Orestes, P
Bhangoo, SK
Hoon, MA
AF Mishra, Santosh K.
Tisel, Sarah M.
Orestes, Peihan
Bhangoo, Sonia K.
Hoon, Mark A.
TI TRPV1-lineage neurons are required for thermal sensation
SO EMBO JOURNAL
LA English
DT Article
DE itch; pain; thermal; TRPM8; TRPV1
ID MAMMALIAN TASTE RECEPTORS; CAPSAICIN-RECEPTOR; MICE LACKING; IN-VIVO;
BEHAVIORAL-RESPONSES; NEUROPATHIC PAIN; TRP CHANNEL; COLD;
THERMOSENSATION; ACTIVATION
AB The ion-channel TRPV1 is believed to be a major sensor of noxious heat, but surprisingly animals lacking TRPV1 still display marked responses to elevated temperature. In this study, we explored the role of TRPV1-expressing neurons in somatosensation by generating mice wherein this lineage of cells was selectively labelled or ablated. Our data show that TRPV1 is an embryonic marker of many nociceptors including all TRPV1- and TRPM8-neurons as well as many Mrg-expressing neurons. Mutant mice lacking these cells are completely insensitive to hot or cold but in marked contrast retain normal touch and mechanical pain sensation. These animals also exhibit defective body temperature control and lose both itch and pain reactions to potent chemical mediators. Together with previous cell ablation studies, our results define and delimit the roles of TRPV1- and TRPM8-neurons in thermosensation, thermoregulation and nociception, thus significantly extending the concept of labelled lines in somatosensory coding. The EMBO Journal (2011) 30, 582-593. doi:10.1038/emboj.2010.325; Published online 7 December 2010
C1 [Mishra, Santosh K.; Tisel, Sarah M.; Orestes, Peihan; Bhangoo, Sonia K.; Hoon, Mark A.] NIDCR, Mol Genet Unit, Lab Sensory Biol, NIH, Bethesda, MD 20892 USA.
RP Hoon, MA (reprint author), NIDCR, Mol Genet Unit, Lab Sensory Biol, NIH, Bldg 49,Room 1A16,49 Convent Dr, Bethesda, MD 20892 USA.
EM mark.hoon@nih.gov
FU NIH, NIDCR
FX We thank Dr Lars von Buchholtz for the taste data and review of the
manuscript. We are also very grateful to Nick Ryba for encouragement and
helpful advice and Drs Nguyen, Usdin, Gutkind and Siraganian for
valuable suggestions. Transgenic mice were generated by Andrew Cho in
the NIDCR-core. This research was supported by the intramural research
programme of the NIH, NIDCR (MAH).
NR 48
TC 76
Z9 77
U1 1
U2 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0261-4189
J9 EMBO J
JI Embo J.
PD FEB 2
PY 2011
VL 30
IS 3
BP 582
EP 593
DI 10.1038/emboj.2010.325
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 721YN
UT WOS:000287394200013
PM 21139565
ER
PT J
AU Lantos, J
Matlock, AM
Wendler, D
AF Lantos, John
Matlock, Ann Marie
Wendler, David
TI Clinician Integrity and Limits to Patient Autonomy
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Article
ID EMERGENCY CONTRACEPTION; DECISION-MAKING; HEALTH-CARE; CONSCIENCE;
VALUES
AB A 28-year-old man with chronic granulomatous disease developed worsening respiratory status in the setting of chronic bacterial and fungal infections. The attending physician recommended transfer to the intensive care unit (ICU), but the patient declined. The patient understood that the nurses in the ICU have expertise in caring for patients with poor respiratory function. He also understood that he faced an increased risk of dying if he remained on the medical ward. At the same time, the patient was familiar with the nurses on the medical ward and felt comfortable there. Unsure of whether it was appropriate for clinicians to agree to provide less than optimal care for a critically ill patient, the clinicians on the medical ward requested a bioethics consultation. This article reviews the ethical issues that arise when patients ask clinicians to provide less than optimal care. Although it is well established that clinicians ought to respect patient autonomy, that obligation conflicted, in the present case, with the clinicians' sense of professional integrity. Future research on this vital but underexplored topic is needed to determine the extent to which clinicians' professional integrity places limits on the types of patient requests to which they should agree. JAMA. 2011;305(5):495-499 www.jama.com
C1 [Lantos, John] Childrens Mercy Hosp, Childrens Mercy Bioeth Ctr, Kansas City, MO 64108 USA.
[Matlock, Ann Marie; Wendler, David] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Lantos, J (reprint author), Childrens Mercy Hosp, Childrens Mercy Bioeth Ctr, 2401 Gilham Rd, Kansas City, MO 64108 USA.
EM jlantos@cmh.edu
FU Department of Bioethics at the National Institutes of Health Clinical
Center; National Institutes of Health Clinical Center
FX This work was funded by the Department of Bioethics at the National
Institutes of Health Clinical Center.; The National Institutes of Health
Clinical Center had no role in the design and conduct of the study, in
the collection, management, analysis, and interpretation of the data, or
in the preparation, review, or approval of the manuscript.
NR 17
TC 23
Z9 23
U1 1
U2 6
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD FEB 2
PY 2011
VL 305
IS 5
BP 495
EP 499
DI 10.1001/jama.2011.32
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 714LI
UT WOS:000286810700023
PM 21285427
ER
PT J
AU Dobi, A
Seabold, GK
Christensen, CH
Bock, R
Alvarez, VA
AF Dobi, Alice
Seabold, Gail K.
Christensen, Christine H.
Bock, Roland
Alvarez, Veronica A.
TI Cocaine-Induced Plasticity in the Nucleus Accumbens Is Cell Specific and
Develops without Prolonged Withdrawal
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID MEDIUM SPINY NEURONS; VENTRAL TEGMENTAL AREA; LONG-TERM DEPRESSION;
DENDRITIC SPINES; BEHAVIORAL SENSITIZATION; DOPAMINE-RECEPTORS;
GENE-EXPRESSION; TOPOGRAPHICAL ORGANIZATION; TYROSINE-HYDROXYLASE;
SYNAPTIC PLASTICITY
AB Cocaine induces plasticity at glutamatergic synapses in the nucleus accumbens (NAc). Withdrawal was suggested to play an important role in the development of this plasticity by studies showing that some changes only appear several weeks after the final cocaine exposure. In this study, the requirement for prolonged withdrawal was evaluated by comparing the changes in glutamatergic transmission induced by two different noncontingent cocaine treatments: a short treatment followed by prolonged withdrawal, and a longer treatment without prolonged withdrawal. Recordings were performed from mouse medium spiny neurons (MSNs) in the NAc at the same time after the first cocaine injection under both treatments. A similar increase in the frequency of glutamate-mediated miniature EPSCs was observed in D(1)-expressing MSNs after both cocaine treatments, demonstrating that prolonged withdrawal was not required. Furthermore, larger AMPA receptor-to-NMDA receptor ratios, higher spine density, and enlarged spine heads were observed in the absence of withdrawal after a long cocaine treatment. These synaptic adaptations expressed in D(1)-containing MSNs of the NAc core were not further enhanced by protracted withdrawal. In conclusion, a few repeated cocaine injections are enough to trigger adaptations at glutamatergic synapses in D(1)-expressing MSNs, which, although they take time to develop, do not require prolonged cocaine withdrawal.
C1 [Dobi, Alice; Seabold, Gail K.; Christensen, Christine H.; Bock, Roland; Alvarez, Veronica A.] NIAAA, NIH, Bethesda, MD 20892 USA.
RP Alvarez, VA (reprint author), NIAAA, NIH, 5625 Fishers Lane, Bethesda, MD 20892 USA.
EM alvarezva@mail.nih.gov
RI Alvarez, Veronica /E-9745-2015; Bock, Roland/G-2982-2016
OI Alvarez, Veronica /0000-0003-2611-8675; Bock, Roland/0000-0002-8654-1080
FU National Institute on Alcohol Abuse and Alcoholism; National Institute
of Neurological Disorders and Stroke at the National Institutes of
Health
FX This work was funded by the intramural programs of National Institute on
Alcohol Abuse and Alcoholism and National Institute of Neurological
Disorders and Stroke at the National Institutes of Health. We are
grateful to Dr. Fumi Ono for sharing his confocal microscope. We thank
John T. Williams, Christina Gremel, Christopher Ford, and the members of
the Alvarez Laboratory for the helpful comments and discussions of this
manuscript.
NR 54
TC 42
Z9 42
U1 1
U2 4
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD FEB 2
PY 2011
VL 31
IS 5
BP 1895
EP 1904
DI 10.1523/JNEUROSCI.5375-10.2011
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 715WE
UT WOS:000286922100038
PM 21289199
ER
PT J
AU Langhorne, J
Buffet, P
Galinski, M
Good, M
Harty, J
Leroy, D
Mota, MM
Pasini, E
Renia, L
Riley, E
Stins, M
Duffy, P
AF Langhorne, Jean
Buffet, Pierre
Galinski, Mary
Good, Michael
Harty, John
Leroy, Didier
Mota, Maria M.
Pasini, Erica
Renia, Laurent
Riley, Eleanor
Stins, Monique
Duffy, Patrick
TI The relevance of non-human primate and rodent malaria models for humans
SO MALARIA JOURNAL
LA English
DT Editorial Material
AB At the 2010 Keystone Symposium on "Malaria: new approaches to understanding Host-Parasite interactions", an extra scientific session to discuss animal models in malaria research was convened at the request of participants. This was prompted by the concern of investigators that skepticism in the malaria community about the use and relevance of animal models, particularly rodent models of severe malaria, has impacted on funding decisions and publication of research using animal models. Several speakers took the opportunity to demonstrate the similarities between findings in rodent models and human severe disease, as well as points of difference. The variety of malaria presentations in the different experimental models parallels the wide diversity of human malaria disease and, therefore, might be viewed as a strength. Many of the key features of human malaria can be replicated in a variety of nonhuman primate models, which are very under-utilized. The importance of animal models in the discovery of new anti-malarial drugs was emphasized. The major conclusions of the session were that experimental and human studies should be more closely linked so that they inform each other, and that there should be wider access to relevant clinical material.
C1 [Langhorne, Jean] MRC Natl Inst Med Res, Div Parasitol, London NW7 1AA, England.
[Buffet, Pierre] Grp Hosp Pitie Salpetriere, F-75651 Paris, France.
[Galinski, Mary] Emory Univ, Sch Med, Int Ctr Malaria Res Educ & Dev, Yerkes Natl Primate Res Ctr, Atlanta, GA 30329 USA.
[Good, Michael] Griffith Univ, Inst Glyc, Griffith, Qld 4222, Australia.
[Harty, John] Univ Iowa, Carver Coll Med, Dept Microbiol, Iowa City, IA 52242 USA.
[Harty, John] Univ Iowa, Carver Coll Med, Dept Pathol, Iowa City, IA 52242 USA.
[Harty, John] Univ Iowa, Carver Coll Med, Interdisciplinary Program Immunol, Iowa City, IA 52242 USA.
[Leroy, Didier] Med Malaria Venture, CH-15 Geneva 15, Switzerland.
[Mota, Maria M.] Inst Mol Med, Unidade Malaria, P-1649028 Lisbon, Portugal.
[Pasini, Erica] BPRC, NL-2288 GJ Rijswijk, Netherlands.
[Renia, Laurent] ASTAR, Singapore Immunol Network, Lab Malaria Immunobiol, Singapore 138648, Singapore.
[Riley, Eleanor] London Sch Hyg & Trop Med, Fac Infect & Trop Dis, Dept Immunol & Infect, London WC1, England.
[Stins, Monique] Johns Hopkins Sch Med, RT Johnson Div NeuroImmunol, Baltimore, MD 21231 USA.
[Duffy, Patrick] NIAID, Lab Malaria Immunol & Vaccinol, NIH, Rockville, MD 20852 USA.
RP Langhorne, J (reprint author), MRC Natl Inst Med Res, Div Parasitol, London NW7 1AA, England.
EM jlangho@nimr.mrc.ac.uk
RI Renia, Laurent/E-2117-2011; Riley, Eleanor/C-8960-2013;
OI Renia, Laurent/0000-0003-0349-1557; Riley, Eleanor/0000-0003-3447-3570;
Mota, Maria Manuel/0000-0002-2858-1041
NR 15
TC 55
Z9 57
U1 0
U2 15
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1475-2875
J9 MALARIA J
JI Malar. J.
PD FEB 2
PY 2011
VL 10
AR 23
DI 10.1186/1475-2875-10-23
PG 4
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA 740RK
UT WOS:000288811900004
PM 21288352
ER
PT J
AU Hancock, DB
Haberg, SE
Furu, K
Whitworth, KW
Nafstad, P
Nystad, W
London, SJ
AF Hancock, D. B.
Haberg, S. E.
Furu, K.
Whitworth, K. W.
Nafstad, P.
Nystad, W.
London, S. J.
TI Oral Contraceptive Use Before Pregnancy and Respiratory Outcomes in the
Offspring: Comparison of Estrogen-Progestin Combined Pills and
Progestin-Only Pills
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT American-Academy-of-Allergy-Asthma-and-Immunology Annual Meeting
CY MAR 18-22, 2011
CL San Francisco, CA
SP Amer Acad Allergy Asthma & Immunol
C1 [Hancock, D. B.; Whitworth, K. W.; London, S. J.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Haberg, S. E.; Furu, K.; Nafstad, P.; Nystad, W.] Norwegian Inst Publ Hlth, Oslo, Norway.
[Nafstad, P.] Univ Oslo, Oslo, Norway.
[Furu, K.] Univ Tromso, Tromso, Norway.
RI Hancock, Dana/D-8577-2012
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD FEB
PY 2011
VL 127
IS 2
SU S
BP AB173
EP AB173
DI 10.1016/j.jaci.2010.12.689
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA 832YI
UT WOS:000295846400671
ER
PT J
AU Heimall, J
Siegel, AM
Shaw, PA
Hsu, A
Holland, SM
Freeman, AF
Milner, JD
AF Heimall, J.
Siegel, A. M.
Shaw, P. A.
Hsu, A.
Holland, S. M.
Freeman, A. F.
Milner, J. D.
TI Early onset of Varicella Zoster Virus Reactivation (VZV, Shingles) in
Patients with Autosomal Dominant Hyper IgE Syndrome (AD-HIES)
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT American-Academy-of-Allergy-Asthma-and-Immunology Annual Meeting
CY MAR 18-22, 2011
CL San Francisco, CA
SP Amer Acad Allergy Asthma & Immunol
C1 [Heimall, J.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Siegel, A. M.; Shaw, P. A.; Hsu, A.; Holland, S. M.; Freeman, A. F.; Milner, J. D.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD FEB
PY 2011
VL 127
IS 2
SU S
BP AB88
EP AB88
DI 10.1016/j.jaci.2010.12.356
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA 832YI
UT WOS:000295846400339
ER
PT J
AU Leiding, JW
Heimall, J
Song, Y
Holland, SM
Siegel, RM
Freeman, AF
AF Leiding, J. W.
Heimall, J.
Song, Y.
Holland, S. M.
Siegel, R. M.
Freeman, A. F.
TI Idiopathic CD4+ Lymphocytopenia: Clinical and Autoimmune Phenotype
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the American-Academy-of-Allergy-Asthma-and-Immunology
(AAAAI)
CY MAR 18-22, 2011
CL San Francisco, CA
SP Amer Acad Allergy Asthma & Immunol (AAAAI)
C1 [Leiding, J. W.; Holland, S. M.; Freeman, A. F.] Natl Inst Allerg & Infect Dis, Bethesda, MD USA.
[Heimall, J.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Song, Y.; Siegel, R. M.] NIAMSD, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 1
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD FEB
PY 2011
VL 127
IS 2
SU S
BP AB89
EP AB89
DI 10.1016/j.jaci.2010.12.358
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA 832YI
UT WOS:000295846400341
ER
PT J
AU Price, CC
Rao, VK
Danielian, S
Meffre, E
AF Price, C. C.
Rao, V. K.
Danielian, S.
Meffre, E.
TI Defective Peripheral B Cell Tolerance In Alps Patients With Fas
Mutations
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT American-Academy-of-Allergy-Asthma-and-Immunology Annual Meeting
CY MAR 18-22, 2011
CL San Francisco, CA
SP Amer Acad Allergy Asthma & Immunol
C1 [Price, C. C.; Meffre, E.] Yale Univ, New Haven, CT USA.
[Rao, V. K.] NIH, Bethesda, MD 20892 USA.
[Danielian, S.] Hosp Pediat Juan P Garrahan, Buenos Aires, DF, Argentina.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD FEB
PY 2011
VL 127
IS 2
SU S
BP AB226
EP AB226
DI 10.1016/j.jaci.2010.12.900
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA 832YI
UT WOS:000295846401015
ER
PT J
AU Scurlock, AM
Leung, DYM
Sampson, HA
Lindblad, R
Liu, AH
Wood, RA
Jones, SM
Plaut, M
Burks, W
Stablein, D
Sicherer, SH
AF Scurlock, A. M.
Leung, D. Y. M.
Sampson, H. A.
Lindblad, R.
Liu, A. H.
Wood, R. A.
Jones, S. M.
Plaut, M.
Burks, W.
Stablein, D.
Sicherer, S. H.
TI Association of Atopic Dermatitis (AD) Severity to Milk and Egg Allergy
Outcomes in a Cohort of Atopic, Food-allergic Children (COFAR)
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT American-Academy-of-Allergy-Asthma-and-Immunology Annual Meeting
CY MAR 18-22, 2011
CL San Francisco, CA
SP Amer Acad Allergy Asthma & Immunol
C1 [Scurlock, A. M.; Jones, S. M.] UAMS AR Childrens Hosp, Little Rock, AR USA.
[Leung, D. Y. M.; Liu, A. H.] Natl Jewish Hlth Ctr, Denver, CO USA.
[Sampson, H. A.; Sicherer, S. H.] Mt Sinai Sch Med, New York, NY USA.
[Lindblad, R.; Stablein, D.] EMMES Corp, Rockville, MD USA.
[Wood, R. A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Plaut, M.] NIAID, NIH, Bethesda, MD 20892 USA.
[Burks, W.] Duke Univ, Med Ctr, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD FEB
PY 2011
VL 127
IS 2
SU S
BP AB36
EP AB36
DI 10.1016/j.jaci.2010.12.153
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA 832YI
UT WOS:000295846400137
ER
PT J
AU Sharma, HP
Mansoor, DK
Sprunger, AC
Zalos, K
Taylor, H
Martin, X
Mikhail, IJ
AF Sharma, H. P.
Mansoor, D. K.
Sprunger, A. C.
Zalos, K.
Taylor, H.
Martin, X.
Mikhail, I. J.
TI Racial Disparities in the Presentation of Pediatric Eosinophilic
Esophagitis
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT American-Academy-of-Allergy-Asthma-and-Immunology Annual Meeting
CY MAR 18-22, 2011
CL San Francisco, CA
SP Amer Acad Allergy Asthma & Immunol
C1 [Sharma, H. P.; Mansoor, D. K.; Sprunger, A. C.; Zalos, K.; Taylor, H.; Martin, X.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Mikhail, I. J.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 8
Z9 8
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD FEB
PY 2011
VL 127
IS 2
SU S
BP AB110
EP AB110
DI 10.1016/j.jaci.2010.12.440
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA 832YI
UT WOS:000295846400422
ER
PT J
AU Stellato, C
Fang, X
Abdelmohsen, K
Gorospe, M
Ishmael, FT
AF Stellato, C.
Fang, X.
Abdelmohsen, K.
Gorospe, M.
Ishmael, F. T.
TI Glucocorticoid (GC) Modulation of Global miRNA Profile in Human Airway
Epithelial Cells
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Meeting Abstract
CT American-Academy-of-Allergy-Asthma-and-Immunology Annual Meeting
CY MAR 18-22, 2011
CL San Francisco, CA
SP Amer Acad Allergy Asthma & Immunol
C1 [Stellato, C.; Fang, X.] Johns Hopkins Univ, Baltimore, MD USA.
[Abdelmohsen, K.; Gorospe, M.] NIA, NIH, Baltimore, MD 21224 USA.
[Ishmael, F. T.] Penn State Univ, Coll Med, Hershey, PA USA.
RI Stellato, Cristiana/P-3001-2015
OI Stellato, Cristiana/0000-0002-1294-8355
NR 0
TC 0
Z9 0
U1 0
U2 4
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD FEB
PY 2011
VL 127
IS 2
SU S
BP AB64
EP AB64
DI 10.1016/j.jaci.2010.12.267
PG 1
WC Allergy; Immunology
SC Allergy; Immunology
GA 832YI
UT WOS:000295846400250
ER
PT J
AU Payne, AR
Kellman, P
Anderson, R
Chen, MY
McPhaden, AR
Watkins, S
Schenke, W
Wright, V
Lederman, RJ
Aletras, AH
Arai, AE
Berry, C
AF Payne, A. R.
Kellman, P.
Anderson, R.
Chen, M. Y.
McPhaden, A. R.
Watkins, S.
Schenke, W.
Wright, V.
Lederman, R. J.
Aletras, A. H.
Arai, A. E.
Berry, C.
TI T2-weighted magnetic resonance imaging has high diagnostic accuracy for
myocardial haemorrhage in myocardial infarction: a preclinical
validation study in swine
SO SCOTTISH MEDICAL JOURNAL
LA English
DT Meeting Abstract
C1 [Payne, A. R.; Kellman, P.; Anderson, R.; Chen, M. Y.; Schenke, W.; Wright, V.; Lederman, R. J.; Aletras, A. H.; Arai, A. E.; Berry, C.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Payne, A. R.; McPhaden, A. R.; Watkins, S.; Berry, C.] Univ Glasgow, BHF Glasgow Cardiovasc Res Ctr, Glasgow, Lanark, Scotland.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SCOTTISH MEDICAL JOURNAL
PI GLASGOW
PA MR K BURNSIDE, 12 BUCCLEUCH DRIVE, BEARSDEN, GLASGOW, G61 3LW, SCOTLAND
SN 0036-9330
J9 SCOT MED J
JI Scott. Med. J.
PD FEB
PY 2011
VL 56
IS 1
BP 51
EP 51
DI 10.1258/smj.2011.011040
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 824KC
UT WOS:000295199800030
ER
PT J
AU Trimble, EL
Fujiwara, K
Marth, C
Abrams, J
AF Trimble, Edward L.
Fujiwara, Keiichi
Marth, Christian
Abrams, Jeffrey
TI Use of IP Chemotherapy in Ovarian Cancer: The Critical Questions THE
GONZALEZ/GREEN/MUGGIA ARTICLE REVIEWED
SO ONCOLOGY-NEW YORK
LA English
DT Editorial Material
ID INTRAPERITONEAL CHEMOTHERAPY; SURVIVAL; SURGERY; METAANALYSIS
C1 [Trimble, Edward L.; Abrams, Jeffrey] NCI, Bethesda, MD 20892 USA.
[Fujiwara, Keiichi] Saitama Med Univ, Int Med Ctr, Saitama, Japan.
[Marth, Christian] Innsbruck Med Univ Hosp, Innsbruck, Austria.
RP Trimble, EL (reprint author), NCI, Bethesda, MD 20892 USA.
NR 12
TC 1
Z9 1
U1 0
U2 0
PU UBM MEDICA
PI NORWALK
PA 535 CONNECTICUT AVE, STE 300, NORWALK, CT 06854 USA
SN 0890-9091
J9 ONCOLOGY-NY
JI Oncology-NY
PD FEB
PY 2011
VL 25
IS 2
BP 170
EP 174
PG 3
WC Oncology
SC Oncology
GA 800EM
UT WOS:000293342600008
PM 21456388
ER
PT J
AU Travlos, GS
Hard, GC
Betz, LJ
Kissling, GE
AF Travlos, Greg S.
Hard, Gordon C.
Betz, Laura J.
Kissling, Grace E.
TI Chronic Progressive Nephropathy in Male F344 Rats in 90-Day Toxicity
Studies: Its Occurrence and Association with Renal Tubule Tumors in
Subsequent 2-Year Bioassays
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE chronic progressive nephropathy; CPN; NIH-07 and NTP-2000 diets;
toxicity and carcinogenicity studies; CPN exacerbation; renal tubule
neoplasia
ID NATIONAL TOXICOLOGY PROGRAM; HUMAN RISK-ASSESSMENT; LABORATORY RAT;
KIDNEY TUMORS; CARCINOGENICITY; ALPHA-2U-GLOBULIN; LESIONS; RODENT
AB The occurrence and severity of spontaneous chronic progressive nephropathy (CPN) in control male F344 rats as well as the frequency of treatment-related CPN exacerbation were histopathologically reevaluated. A series of 43 National Toxicology Program (NTP) 90-day toxicity studies comparing the influence of NIH-07 or NTP-2000 diets was examined. Relationships between the histopathologic findings at 90 days and renal tubule proliferative lesions recorded in subsequent 2-year bioassays for 24 chemicals were statistically analyzed. CPN lesions were observed in 100% of the control male rats regardless of diet, but CPN was more severe in control rats fed NIH-07. Approximately one-third of the 90-day studies demonstrated a treatment-related exacerbation of CPN severity, which was independent of diet. For chemicals that proceeded to 2-year bioassays, all studies with a statistically significant increase in renal tubule tumors (RTT) at 2 years had treatment-related exacerbation of CPN in the 90-day and 2-year studies. These findings indicate that CPN occurs ubiquitously in young male F344 rats and that treatment-related exacerbation of CPN in 90-day studies is a relatively common occurrence, having the potential to be predictive of an increased incidence of RTT in subsequent 2-year bioassays.
C1 [Travlos, Greg S.; Kissling, Grace E.] NIEHS, NIH, Res Triangle Pk, NC 27709 USA.
[Betz, Laura J.] SRA Int Inc, Durham, NC USA.
RP Travlos, GS (reprint author), NIEHS, NIH, POB 12233,MD B3-06, Res Triangle Pk, NC 27709 USA.
EM travlos@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences; NIH
[N01ES55547]
FX This research was supported, in part, by the Intramural Research Program
of the NIH, National Institute of Environmental Health Sciences, and by
NIH contract N01ES55547. The authors wish to thank Drs. Kim Weber and
Louise Fitzgerald for their assistance in the preliminary organization
of Table 1.
NR 37
TC 12
Z9 12
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 FEB
PY 2011
VL 39
IS 2
BP 381
EP 389
DI 10.1177/0192623310388432
PG 9
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 800QW
UT WOS:000293380000007
PM 21422264
ER
PT J
AU Reagan, WJ
Irizarry-Rovira, A
Poitout-Belissent, F
Bolliger, AP
Ramaiah, SK
Travlos, G
Walker, D
Bounous, D
Walter, G
AF Reagan, William J.
Irizarry-Rovira, Armando
Poitout-Belissent, Florence
Bolliger, Anne Provencher
Ramaiah, Shashi K.
Travlos, Greg
Walker, Dana
Bounous, Denise
Walter, Gail
CA Bone Marrow Working Grp ASVCP STP
TI Best Practices for Evaluation of Bone Marrow in Nonclinical Toxicity
Studies
SO TOXICOLOGIC PATHOLOGY
LA English
DT Article
DE bone marrow; best practice; cytology; histopathology; flow cytometry
ID FLOW-CYTOMETRIC EVALUATION; CYNOMOLGUS MONKEYS; CELL COUNTS; WISTAR
RATS; ULTRASTRUCTURAL TECHNIQUES; MYELODYSPLASTIC SYNDROMES;
PERIPHERAL-BLOOD; FEED RESTRICTION; BIOPSY SPECIMENS; IN-VITRO
AB This manuscript is intended to provide a best practice approach to accurately and consistently assess toxicant-induced bone marrow effects of test articles. In nonclinical toxicity studies, complete blood count data in conjunction with the histological examination of the bone marrow are recommended as the foundation for assessing the effect of test articles on the hematopoietic system. This approach alone can be used successfully in many studies. However, in some situations it may be necessary to further characterize effects on the different hematopoietic lineages, either by cytological or flow cytometric evaluation of the bone marrow. Both modalities can be used successfully, and which one is selected will depend on the expertise, preference of the facility, and the nature of the change in the bone marrow. Other specialized techniques such as clonogenic assays or electron microscopy are used rarely to further characterize hematotoxicity. The indications and techniques to successfully employ histological, cytological, or flow cytometric evaluation as well as clonogenic assays and electron microscopy are reviewed.
C1 [Reagan, William J.] Pfizer Inc, Groton, CT 06340 USA.
[Irizarry-Rovira, Armando] Eli Lilly & Co Inc, Indianapolis, IN USA.
[Poitout-Belissent, Florence] Charles River Labs, Senneville, PQ, Canada.
[Bolliger, Anne Provencher] Charles River Labs, Sherbrooke, PQ, Canada.
[Ramaiah, Shashi K.] Pfizer Inc, Cambridge, MA USA.
[Travlos, Greg] NIEHS, Res Triangle Pk, NC 27709 USA.
[Walker, Dana] Bristol Myers Squibb Co, Wallingford, CT 06492 USA.
[Bounous, Denise] Bristol Myers Squibb Co, Princeton, NJ USA.
[Walter, Gail] DVM PLC, Gail Walter, Kalamazoo, MI USA.
RP Reagan, WJ (reprint author), Pfizer Global Res & Dev, Drug Safety Res & Dev, 8274-1203 Eastern Point Rd, Groton, CT 06340 USA.
EM william.j.reagan@pfizer.com
NR 88
TC 15
Z9 15
U1 1
U2 3
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 FEB
PY 2011
VL 39
IS 2
BP 435
EP 448
DI 10.1177/0192623310396907
PG 14
WC Pathology; Toxicology
SC Pathology; Toxicology
GA 800QW
UT WOS:000293380000015
PM 21300792
ER
PT J
AU Ratain, MJ
Collins, JM
Doroshow, JH
AF Ratain, M. J.
Collins, J. M.
Doroshow, J. H.
TI Merrill Jon Egorin, MD, 1948-2010 OBITUARY
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Biographical-Item
AB Merrill Egorin was born in Baltimore, Maryland, where he completed his undergraduate and graduate education. He was a pioneer in understanding the relationship of pharmacokinetic variability to the pharmacodynamics of anticancer agents. He is remembered as a compassionate physician, an outstanding scientist, an entertaining lecturer, a superb mentor, and a friend to many.
C1 [Ratain, M. J.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Collins, J. M.; Doroshow, J. H.] NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
RP Ratain, MJ (reprint author), Univ Chicago, Dept Med, 5841 S Maryland Ave, Chicago, IL 60637 USA.
EM mratain@medicine.bsd.uchicago.edu
NR 1
TC 0
Z9 0
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD FEB
PY 2011
VL 89
IS 2
BP 163
EP 165
DI 10.1038/clpt.2010.294
PG 3
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 711JA
UT WOS:000286585500007
PM 21252931
ER
PT J
AU Bornstein, MH
Mash, C
Arterberry, ME
AF Bornstein, Marc H.
Mash, Clay
Arterberry, Martha E.
TI Young infants' eye movements over "natural" scenes and "experimental"
scenes
SO INFANT BEHAVIOR & DEVELOPMENT
LA English
DT Article
DE Infants; Eye movements; Natural scenes; Object perception; Context
ID MEMORY RETRIEVAL; STIMULUS CONTEXT; PERCEPTION; RECOGNITION; ATTENTION;
OBJECT
AB Eye movements of 30 4-month-olds were tracked as infants viewed animals and vehicles in "natural" scenes and, for comparison, in homogeneous "experimental" scenes. Infants showed equivalent looking time preferences for natural and experimental scenes overall, but fixated natural scenes and objects in natural scenes more than experimental scenes and objects in experimental scenes and shifted fixations between objects and contexts more in natural than in experimental scenes. The findings show how infants treat objects and contexts in natural scenes and suggest that they treat more commonly used experimental scenes differently. Published by Elsevier Inc.
C1 [Bornstein, Marc H.; Mash, Clay; Arterberry, Martha E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, US Dept HHS, Bethesda, MD 20892 USA.
[Arterberry, Martha E.] Colby Coll, Waterville, ME 04901 USA.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, US Dept HHS, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
FU Intramural NIH HHS [Z01 HD001119-20]
NR 26
TC 2
Z9 2
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0163-6383
J9 INFANT BEHAV DEV
JI Infant Behav. Dev.
PD FEB
PY 2011
VL 34
IS 1
BP 206
EP 210
DI 10.1016/j.infbeh.2010.12.010
PG 5
WC Psychology, Developmental
SC Psychology
GA 728RI
UT WOS:000287891800021
PM 21195480
ER
PT J
AU Dinse, GE
Peddada, SD
AF Dinse, Gregg E.
Peddada, Shyamal D.
TI Comparing Tumor Rates in Current and Historical Control Groups in Rodent
Cancer Bioassays
SO STATISTICS IN BIOPHARMACEUTICAL RESEARCH
LA English
DT Article
DE Bootstrap; Carcinogenicity study; Extra variation; Historical range;
National Toxicology Program (NTP); Poly-3 survival adjustment; Quantal
response
ID TESTS; CARCINOGENICITY; LESIONS
AB When evaluating carcinogenicity, tumor rates from the current study are informally assessed within the context of relevant historical control tumor rates. Current rates outside the range of historical rates raise concerns. We propose a statistical procedure that formally compares tumor rates in current and historical control groups. We use a normal approximation for the null distribution of the proposed test when there are at least five historical control groups and the average tumor rate is above 0.5%; otherwise, we apply standard bootstrap techniques. For comparison purposes, we show that formally basing decisions on the range of historical control rates would yield unusually high false positive rates. That is, a range-based decision rule would not maintain the nominal 5% significance level and could produce Type I error rates as high as 67%. In other cases, the power could go to zero. The proposed test, however, controls Type I errors while adjusting for survival and extra variability among the historical studies. We illustrate the methods with data from a study of benzophenone. Compared to a range-based decision rule, the proposed test has several important advantages, including operating at the specified level and being applicable with as few as one historical study.
C1 [Dinse, Gregg E.; Peddada, Shyamal D.] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
RP Peddada, SD (reprint author), NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
EM peddada@niehs.nih.gov
RI Peddada, Shyamal/D-1278-2012
FU NIH, National Institute of Environmental Health Sciences [Z01-ES045007,
Z01-ES101744]
FX This research was supported by the Intramural Research Program of the
NIH, National Institute of Environmental Health Sciences (Z01-ES045007
and Z01-ES101744). The authors thank Grace Kissling, Joseph Haseman, and
the reviewers for their helpful comments.
NR 13
TC 5
Z9 5
U1 0
U2 5
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 732 N WASHINGTON ST, ALEXANDRIA, VA 22314-1943 USA
SN 1946-6315
J9 STAT BIOPHARM RES
JI Stat. Biopharm. Res.
PD FEB
PY 2011
VL 3
IS 1
BP 97
EP 105
DI 10.1198/sbr.2010.09044
PG 9
WC Mathematical & Computational Biology; Statistics & Probability
SC Mathematical & Computational Biology; Mathematics
GA 791HS
UT WOS:000292656400009
PM 21566728
ER
PT J
AU Powers, JF
Fliedner, SM
Leav, I
Altieri, DC
Pacak, K
Tischler, AS
AF Powers, J. F.
Fliedner, S. M.
Leav, I.
Altieri, D. C.
Pacak, K.
Tischler, A. S.
TI TRAP-1 Is a New Surrogate Marker for SDH Mutation in
Pheochromocytoma/Paraganglioma and a Potential Target for Chemotherapy
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Tufts Med Ctr, Boston, MA USA.
NICHD, NIH, Bethesda, MD USA.
Univ Massachusetts, Med Ctr, Worcester, MA USA.
Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA.
RI Fliedner, Stephanie/D-3406-2012
NR 0
TC 0
Z9 0
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 590
BP 141A
EP 141A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000030
ER
PT J
AU Aung, PP
Russell, L
Weinstein, D
Heller, T
Kleiner, D
Kammula, U
Rudloff, U
Avital, I
Quezado, M
AF Aung, P. P.
Russell, L.
Weinstein, D.
Heller, T.
Kleiner, D.
Kammula, U.
Rudloff, U.
Avital, I.
Quezado, M.
TI Morphologic Findings in a Novel Familial Polyposis Syndrome
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
NIDDK, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 597
BP 143A
EP 143A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000037
ER
PT J
AU Aly, FZ
Hanson, JC
Yang, W
Kreitman, MS
Merino, MJ
Linehan, MW
Pinto, PA
Adams, LG
Stevenson, HS
Edelman, DC
Emmert-Buck, MR
Rodriguez-Canales, J
AF Aly, F. Z.
Hanson, J. C.
Yang, W.
Kreitman, M. S.
Merino, M. J.
Linehan, M. W.
Pinto, P. A.
Adams, L. G.
Stevenson, H. S.
Edelman, D. C.
Emmert-Buck, M. R.
Rodriguez-Canales, J.
TI Regional Variation in Epigenetic Patterns in Prostate Cancer
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Aly, F. Z.; Hanson, J. C.; Yang, W.; Kreitman, M. S.; Merino, M. J.; Linehan, M. W.; Pinto, P. A.; Adams, L. G.; Stevenson, H. S.; Edelman, D. C.; Emmert-Buck, M. R.; Rodriguez-Canales, J.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 739
BP 176A
EP 176A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000179
ER
PT J
AU Aung, PP
Walter, BA
Garcia, C
Bratslavsky, G
Merino, MJ
AF Aung, P. P.
Walter, B. A.
Garcia, C.
Bratslavsky, G.
Merino, M. J.
TI Potential Role of HER2/Neu as a Molecular Target in the Treatment of
High Grade Urothelial Cancer. Determination of Gene Amplification by
FISH, CISH and IHC
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Univ Salamanca, E-37008 Salamanca, Spain.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 748
BP 179A
EP 179A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000189
ER
PT J
AU Cannata-Ortiz, P
Rodriguez, BW
Bratslavsky, G
Linehan, WM
Merino, MJ
AF Cannata-Ortiz, P.
Rodriguez, B. Walter
Bratslavsky, G.
Linehan, W. M.
Merino, M. J.
TI Hybrid Tumors: All You Need To Know and More
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Cannata-Ortiz, P.; Rodriguez, B. Walter; Bratslavsky, G.; Linehan, W. M.; Merino, M. J.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 766
BP 182A
EP 183A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000206
ER
PT J
AU Cubilla, AL
Chaux, A
Rodriguez, IM
Barreto, JE
Netto, GJ
Bosch, FX
de Sanjose, S
Munoz, N
Hildesheim, A
AF Cubilla, A. L.
Chaux, A.
Rodriguez, I. M.
Barreto, J. E.
Netto, G. J.
Bosch, F. X.
de Sanjose, S.
Munoz, N.
Hildesheim, A.
TI Phimosis, Lichen Sclerosus, Smoking, Poverty, Sexually Related
Epidemiological Factors and Late Diagnosis Are Prevalent among Patients
with Penile Cancer in Paraguay
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Inst Patol & Invest, Asuncion, Paraguay.
Johns Hopkins Univ, Baltimore, MD USA.
Inst Catalan Oncol, Barcelona, Spain.
CIBER Epidemiol & Salud Publ, Barcelona, Spain.
NCI, Bethesda, MD 20892 USA.
RI de Sanjose Llongueras, Silvia/H-6339-2014; Hildesheim,
Allan/B-9760-2015; BOSCH JOSE, FRANCESC XAVIER/J-6339-2012
OI Hildesheim, Allan/0000-0003-0257-2363; BOSCH JOSE, FRANCESC
XAVIER/0000-0002-7172-3412
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 784
BP 186A
EP 187A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000224
ER
PT J
AU Cubilla, AL
Chaux, A
Rodriguez, IM
Barreto, JE
Netto, GJ
Bosch, FX
de Sanjose, S
Munoz, N
Hildesheim, A
AF Cubilla, A. L.
Chaux, A.
Rodriguez, I. M.
Barreto, J. E.
Netto, G. J.
Bosch, F. X.
de Sanjose, S.
Munoz, N.
Hildesheim, A.
TI Sexual History and Distinctive Pathological Features in HPV-Related
Penile Carcinomas
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Inst Patol & Invest, Asuncion, Paraguay.
Johns Hopkins Univ, Baltimore, MD USA.
Inst Catalan Oncol, Barcelona, Spain.
CIBER Epidemiol & Salud Publ, Barcelona, Spain.
NCI, Bethesda, MD 20892 USA.
RI de Sanjose Llongueras, Silvia/H-6339-2014; Hildesheim,
Allan/B-9760-2015; BOSCH JOSE, FRANCESC XAVIER/J-6339-2012
OI Hildesheim, Allan/0000-0003-0257-2363; BOSCH JOSE, FRANCESC
XAVIER/0000-0002-7172-3412
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 785
BP 187A
EP 187A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000225
ER
PT J
AU Sorbellini, M
McNeal, B
Athauda, G
Cohen, B
Giubellino, A
Simpson, H
Coleman, J
Getzenberg, RH
Netto, GJ
Linehan, MW
Pinto, PA
Bottaro, DP
AF Sorbellini, M.
McNeal, B.
Athauda, G.
Cohen, B.
Giubellino, A.
Simpson, H.
Coleman, J.
Getzenberg, R. H.
Netto, G. J.
Linehan, M. W.
Pinto, P. A.
Bottaro, D. P.
TI Urinary Met Level as a Novel Biomarker for Urothelial Carcinoma of the
Bladder
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Johns Hopkins Univ, Baltimore, MD USA.
RI Bottaro, Donald/F-8550-2010
OI Bottaro, Donald/0000-0002-5057-5334
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 951
BP 225A
EP 225A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000391
ER
PT J
AU Romero, VAV
Rodriguez, BAW
Sobel, M
Linehan, WM
Merino, MJ
AF Romero, V. A. Valera
Rodriguez, B. A. Walter
Sobel, M.
Linehan, W. M.
Merino, M. J.
TI miR-210 (Hypoxia-Responsive) a Marker of Poor Prognosis in Clear Cell
Renal Cell Carcinoma.
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Romero, V. A. Valera; Rodriguez, B. A. Walter; Sobel, M.; Linehan, W. M.; Merino, M. J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 965
BP 228A
EP 229A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000405
ER
PT J
AU Rodriguez, BAW
Vargas, MP
Romero, VAV
Sobel, M
Pinto, P
Merino, MJ
AF Rodriguez, B. A. Walter
Vargas, M. P.
Romero, V. A. Valera
Sobel, M.
Pinto, P.
Merino, M. J.
TI microRNA Expression Profiling in Prostate Cancer: Possible Role as a
Biomarkers and/or Molecular Therapy.
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
NCI NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 968
BP 229A
EP 229A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000408
ER
PT J
AU Parrilla-Castellar, ER
Merino, MJ
AF Parrilla-Castellar, E. R.
Merino, M. J.
TI Cross-Sectional Study of Cervical Cancer among Hispanic Versus
Non-Hispanic White Women Living in the United States.
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Parrilla-Castellar, E. R.; Merino, M. J.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1113
BP 262A
EP 262A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000553
ER
PT J
AU Carvajal, A
Sua, L
Silva, N
Pittaluga, S
Royo, C
Sargent, RL
Climent, F
Jacobs, SA
Delabie, J
Naresh, K
Bagg, A
Harris, NL
Swerdlow, SH
Jaffe, ES
Campo, E
AF Carvajal, A.
Sua, L.
Silva, N.
Pittaluga, S.
Royo, C.
Sargent, R. L.
Climent, F.
Jacobs, S. A.
Delabie, J.
Naresh, K.
Bagg, A.
Harris, N. L.
Swerdlow, S. H.
Jaffe, E. S.
Campo, E.
TI "In Situ" Mantle Cell Lymphoma (MCL), an Incidental Finding with an
Indolent Clinical Course
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Hosp Clin Barcelona, Barcelona, Spain.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Univ Pittsburgh, Pittsburgh, PA 15260 USA.
Oslo Univ Hosp, Oslo, Norway.
Hammersmith Hosp, London, England.
Hosp Univ Penn, Philadelphia, PA 19104 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NCI, Bethesda, MD 20892 USA.
RI Royo, Cristina/H-3193-2015
OI Royo, Cristina/0000-0002-1214-4656
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1228
BP 289A
EP 289A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000668
ER
PT J
AU Huppmann, AR
Leung, AA
Jaffe, ES
Raffeld, M
Pittaluga, S
AF Huppmann, A. R.
Leung, A. A.
Jaffe, E. S.
Raffeld, M.
Pittaluga, S.
TI SOX11 Is a Marker of Follicular Dendritic Cell Neoplasms
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Huppmann, A. R.; Leung, A. A.; Jaffe, E. S.; Raffeld, M.; Pittaluga, S.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1284
BP 302A
EP 302A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000724
ER
PT J
AU Liu, Q
Jegalian, A
Raffeld, M
Pittaluga, S
Jaffe, ES
AF Liu, Q.
Jegalian, A.
Raffeld, M.
Pittaluga, S.
Jaffe, E. S.
TI Pediatric Follicular Lymphoma: A Comparison with Follicular Lymphoma in
Young Adults
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Liu, Q.; Jegalian, A.; Raffeld, M.; Pittaluga, S.; Jaffe, E. S.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1308
BP 307A
EP 307A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000748
ER
PT J
AU Maric, I
Simakova, O
Olivares, N
Chew, S
Metcalfe, DD
Wilson, TM
AF Maric, I.
Simakova, O.
Olivares, N.
Chew, S.
Metcalfe, D. D.
Wilson, T. M.
TI Monocytosis in Systemic Mastocytosis: Clinico-Pathological and
Prognostic Correlates
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NIH, CC, Bethesda, MD 20892 USA.
NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1310
BP 308A
EP 308A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285000750
ER
PT J
AU Shao, H
Gronborg, M
Yuan, CM
Kreitman, RJ
Stetler-Stevenson, M
AF Shao, H.
Gronborg, M.
Yuan, C. M.
Kreitman, R. J.
Stetler-Stevenson, M.
TI Hairy Cell Leukemia and Variant: Immunophenotypic Comparison and
Variations
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, NIH, Bethesda, MD 20892 USA.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1362
BP 320A
EP 321A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001018
ER
PT J
AU Song, JY
Dunleavy, K
Grant, N
Davies-Hill, T
Raffeld, M
Wilson, WH
Jaffe, ES
Pittaluga, S
AF Song, J. Y.
Dunleavy, K.
Grant, N.
Davies-Hill, T.
Raffeld, M.
Wilson, W. H.
Jaffe, E. S.
Pittaluga, S.
TI Clinicopathologic Features of Lymphomatoid Granulomatosis, a Single
Institute Experience
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Song, J. Y.; Dunleavy, K.; Grant, N.; Davies-Hill, T.; Raffeld, M.; Wilson, W. H.; Jaffe, E. S.; Pittaluga, S.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1369
BP 322A
EP 323A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001025
ER
PT J
AU Spencer, DV
Foulks, CL
Geigerman, CM
Akl, PS
Lai, AY
Wade, PA
Jaye, DL
Hill, CE
AF Spencer, D. V.
Foulks, C. L.
Geigerman, C. M.
Akl, P. S.
Lai, A. Y.
Wade, P. A.
Jaye, D. L.
Hill, C. E.
TI Gene and Protein Isoform Expression Analysis of the BCL-6 Associated
Transcriptional Corepressor MTA3 in B- lineage Cells
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Emory Univ, Atlanta, GA 30322 USA.
NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1371
BP 323A
EP 323A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001027
ER
PT J
AU Summers, TA
Eberle, FC
Pittaluga, S
Wilson, WH
Dunleavy, K
Raffeld, M
Hewitt, SM
Jaffe, ES
AF Summers, T. A.
Eberle, F. C.
Pittaluga, S.
Wilson, W. H.
Dunleavy, K.
Raffeld, M.
Hewitt, S. M.
Jaffe, E. S.
TI Gray Zone Lymphomas: Becoming More Black and White?
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Summers, T. A.; Eberle, F. C.; Pittaluga, S.; Wilson, W. H.; Dunleavy, K.; Raffeld, M.; Hewitt, S. M.; Jaffe, E. S.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1375
BP 324A
EP 324A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001031
ER
PT J
AU Tembhare, PR
Yuan, CM
Xi, L
Janik, J
Morris, J
Raffeld, M
Stetler-Stevenson, M
AF Tembhare, P. R.
Yuan, C. M.
Xi, L.
Janik, J.
Morris, J.
Raffeld, M.
Stetler-Stevenson, M.
TI Detection of T Cell Clonality at Diagnosis, in Small Samples and
Monitoring of Minimal Residual Disaease (MRD) Using TCR-V Beta
Repertoire Analysis
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, Ctr Canc Res, Mark O Hatfield Clin Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1381
BP 326A
EP 326A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001037
ER
PT J
AU Venkataraman, G
Traverse-Glehen, A
Song, JY
Eberle, FC
Hanson, JC
Dirnhofer, S
Tzankov, A
Heinze, G
Raffeld, MA
Pittaluga, S
Jaffe, ES
AF Venkataraman, G.
Traverse-Glehen, A.
Song, J. Y.
Eberle, F. C.
Hanson, J. C.
Dirnhofer, S.
Tzankov, A.
Heinze, G.
Raffeld, M. A.
Pittaluga, S.
Jaffe, E. S.
TI Aberrant T-Cell Antigen Expression in Classical Hodgkin Lymphoma Is
Associated with Decreased Event-Free Survival (EFS) and Overall Survival
(OS)
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Ctr Hosp Lyon Sud, Hosp Civils Lyon, F-69310 Pierre Benite, France.
Univ Basel Hosp, CH-4031 Basel, Switzerland.
Med Univ Vienna, Vienna, Austria.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1385
BP 326A
EP 327A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001041
ER
PT J
AU Wang, W
Plyler, R
Janik, JE
Jaffe, ES
Calvo, KR
AF Wang, W.
Plyler, R.
Janik, J. E.
Jaffe, E. S.
Calvo, K. R.
TI microRNA Profiling of Follicular Lymphoma and Tumor Infiltrating T-Cells
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NIH, Ctr Clin, Bethesda, MD 20892 USA.
NCI, Bethesda, MD 20892 USA.
RI Calvo, Katherine/A-8109-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1391
BP 328A
EP 328A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001047
ER
PT J
AU Hodgin, JB
Nair, V
Zhang, H
Randolph, A
Harris, RC
Nelson, RG
Brosius, FC
Kretzler, M
AF Hodgin, J. B.
Nair, V.
Zhang, H.
Randolph, A.
Harris, R. C.
Nelson, R. G.
Brosius, F. C.
Kretzler, M.
TI Cross-Species Identification of Conserved Glomerular Transcriptional
Networks of Progressive Diabetic Nephropathy in Mouse and Man
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Univ Michigan, Ann Arbor, MI 48109 USA.
Vanderbilt Univ, Nashville, TN USA.
NIDDK, Phoenix, AZ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1466
BP 345A
EP 345A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001122
ER
PT J
AU Yang, HC
Wang, SW
Pastan, I
Matsusaka, T
Ichikawa, I
Fogo, AB
AF Yang, H-C
Wang, S-W
Pastan, I.
Matsusaka, T.
Ichikawa, I.
Fogo, A. B.
TI Angiotensin II Type I Receptor Blocker Is Limited in Protection Against
Severe Podocyte Injury-Induced FSGS
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA.
NCI, NIH, Bethesda, MD 20892 USA.
Tokai Univ, Sch Med, Kanagawa 2591100, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1503
BP 354A
EP 355A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001159
ER
PT J
AU Brunt, EM
Kleiner, DE
Wilson, LA
Belt, PH
Neuschwander-Tetri, BA
AF Brunt, E. M.
Kleiner, D. E.
Wilson, L. A.
Belt, P. H.
Neuschwander-Tetri, B. A.
TI The Nonalcoholic Fatty Liver Disease Activity Score (NAS) and the
Histopathologic Diagnosis in Nonalcoholic Fatty Liver Disease: Distinct
Clinicopathologic Meanings
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Washington Univ, Sch Med, St Louis, MO USA.
NCI, Washington, DC USA.
Johns Hopkins Univ, Baltimore, MD USA.
St Louis Univ, Sch Med, St Louis, MO 63103 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1516
BP 357A
EP 358A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001172
ER
PT J
AU Doherty, AR
Ferrell, LD
Morse, CG
Kleiner, DE
AF Doherty, A. R.
Ferrell, L. D.
Morse, C. G.
Kleiner, D. E.
TI Hepatic Pigment Accumulation in HIV Patients on HAART Therapy
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Univ Calif San Francisco, San Francisco, CA 94143 USA.
NIAID, Bethesda, MD 20892 USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1522
BP 359A
EP 359A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001178
ER
PT J
AU Martin, SE
Badve, SS
Steeg, P
Hattab, EM
AF Martin, S. E.
Badve, S. S.
Steeg, P.
Hattab, E. M.
TI Luminal A Subtype Predicts Improved Survival in Patients with Metastatic
Breast Carcinoma to the Brain
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Indiana Univ Sch Med, Indianapolis, IN USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1625
BP 383A
EP 383A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001281
ER
PT J
AU Parrilla-Castellar, E
Zhou, W
Liu, J
Tessarollo, L
Levens, D
AF Parrilla-Castellar, E.
Zhou, W.
Liu, J.
Tessarollo, L.
Levens, D.
TI FBP Knock-Out Leads to a Hematopoietic Maturation Defect
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NIH, Bethesda, MD 20892 USA.
NIH, Frederick, MD USA.
RI Levens, David/C-9216-2009
OI Levens, David/0000-0002-7616-922X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1686
BP 396A
EP 396A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001342
ER
PT J
AU Liu, C
Galli, S
Tsokos, M
AF Liu, C.
Galli, S.
Tsokos, M.
TI miR-17-5b Inhibition Decreases Rhabdomyosarcoma Cell Growth In Vitro
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Liu, C.; Galli, S.; Tsokos, M.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1712
BP 402A
EP 402A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001368
ER
PT J
AU Vargas, MP
Carter, D
Merino, MJ
AF Vargas, M. P.
Carter, D.
Merino, M. J.
TI Pulmonary Lesions Associated with BHD Syndrome
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Vargas, M. P.; Carter, D.; Merino, M. J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1813
BP 426A
EP 427A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001469
ER
PT J
AU Killian, K
Wang, L
Walker, B
Glatfelter, A
Smith, WI
Meltzer, PS
AF Killian, K.
Wang, L.
Walker, B.
Glatfelter, A.
Smith, W. I.
Meltzer, P. S.
TI Rapid and Reliable Method To Isolate Nuclei from FFPE Specimens for
Genomic-Scale Molecular Profiling.
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Suburban Hosp, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1887
BP 443A
EP 444A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001542
ER
PT J
AU Hipp, J
Cheng, J
Hanson, J
Yan, W
Rodriguez-Canales, J
Hipp, J
Tangrea, M
Emmert-Buck, MR
Han, S
Hewitt, S
Monaco, J
Madabhushi, A
Balis, U
AF Hipp, J.
Cheng, J.
Hanson, J.
Yan, W.
Rodriguez-Canales, J.
Hipp, J.
Tangrea, M.
Emmert-Buck, M. R.
Han, S.
Hewitt, S.
Monaco, J.
Madabhushi, A.
Balis, U.
TI SIVQ Image Analysis: A High-Throughput Morphology Discovery Tool for
Surgical Pathologists
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Univ Michigan, Ann Arbor, MI 48109 USA.
NCI, NIH, Bethesda, MD 20892 USA.
Rutgers State Univ, Piscataway, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1913
BP 449A
EP 449A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 773CQ
UT WOS:000291285001568
ER
PT J
AU Driscoll, JJ
Minter, A
Driscoll, DA
Burris, JK
AF Driscoll, James J.
Minter, Alex
Driscoll, Daniel A.
Burris, Jason K.
TI The Ubiquitin plus Proteasome Protein Degradation Pathway as a
Therapeutic Strategy in the Treatment of Solid Tumor Malignancies
SO ANTI-CANCER AGENTS IN MEDICINAL CHEMISTRY
LA English
DT Article
DE Ubiquitin; Proteasome; Bortezomib; Solid Tumors
ID KINASE INHIBITOR P27; MULTIPLE-MYELOMA CELLS; CANCER-THERAPY;
PI3K/AKT/MTOR PATHWAY; MOLECULAR-BASIS; LUNG-CANCER; KAPPA-B;
BORTEZOMIB; RESISTANCE; TARGET
AB A concept that currently steers the development of cancer therapies has been that agents directed against specific proteins that facilitate tumorigenesis or maintain a malignant phenotype will have greater efficacy, less toxicity and a more sustained response relative to traditional cytotoxic chemotherapeutic agents. The clinical success of the targeted agent Imatinib mesylate as an inhibitor of the tyrosine kinase associated with the breakpoint cluster region-Abelson oncogene locus (BCR-ABL) in the treatment of Philadelphia-positive chronic myelogenous leukemia (CML) has served as a paradigm. While intellectually gratifying, the selective targeting of a single driver event by a small molecule, e. g., kinase inhibitor, to dampen a tumor-promoting pathway in the treatment of solid tumors is limited by many factors. Focus can alternatively be placed on targeting fundamental cellular processes that regulate multiple events, e. g., protein degradation, through the Ubiquitin (Ub)+Proteasome System (UPS). The UPS plays a critical role in modulating numerous cellular proteins to regulate cellular processes such as signal transduction, growth, proliferation, differentiation and apoptosis. Clinical success with the proteasome inhibitor bortezomib revolutionized treatment of B-cell lineage malignancies such as Multiple Myeloma (MM). However, many patients harbor primary resistance and do not respond to bortezomib and those that do respond inevitably develop resistance (secondary resistance). The lack of clinical efficacy of proteasome inhibitors in the treatment of solid tumors may be linked mechanistically to the resistance detected during treatment of hematologic malignancies. Potential mechanisms of resistance and means to improve the response to proteasome inhibitors in solid tumors are discussed.
C1 [Driscoll, James J.; Minter, Alex; Burris, Jason K.] NCI, Med Oncol Branch, Magnuson Canc Ctr, NIH, Bethesda, MD 20892 USA.
[Minter, Alex; Burris, Jason K.] Walter Reed Army Med Ctr, Dept Med, Hematol Oncol Serv, Washington, DC 20307 USA.
[Driscoll, Daniel A.] Harvard Univ, Cambridge, MA 02138 USA.
RP Driscoll, JJ (reprint author), NCI, Med Oncol Branch, Magnuson Canc Ctr, NIH, 10 Ctr Dr,12N-226, Bethesda, MD 20892 USA.
EM driscollj@mail.nih.gov
NR 61
TC 13
Z9 15
U1 0
U2 6
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1871-5206
J9 ANTI-CANCER AGENT ME
JI Anti-Cancer Agents Med. Chem.
PD FEB
PY 2011
VL 11
IS 2
BP 242
EP 246
PG 5
WC Oncology; Chemistry, Medicinal
SC Oncology; Pharmacology & Pharmacy
GA 764EY
UT WOS:000290613000010
PM 21355840
ER
PT J
AU Weaver, DL
Ashikaga, T
Krag, DN
Skelly, JM
Anderson, SJ
Harlow, SP
Julian, TB
Mamounas, EP
Wolmark, N
AF Weaver, D. L.
Ashikaga, T.
Krag, D. N.
Skelly, J. M.
Anderson, S. J.
Harlow, S. P.
Julian, T. B.
Mamounas, E. P.
Wolmark, N.
TI Survival Impact of Occult Metastases in NSABP B-32: Sentinel Lymph Node
Biopsy Versus Axillary Dissection in Node-Negative Breast Cancer.
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Univ Vermont, Coll Med, Burlington, VT 05405 USA.
Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA.
Allegheny Gen Hosp, Pittsburgh, PA 15212 USA.
Aultman Caner Ctr, Canton, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 280
BP 69A
EP 69A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282300281
ER
PT J
AU Powers, JF
Fliedner, SM
Leav, I
Altieri, DC
Pacak, K
Tischler, AS
AF Powers, J. F.
Fliedner, S. M.
Leav, I.
Altieri, D. C.
Pacak, K.
Tischler, A. S.
TI TRAP-1 Is a New Surrogate Marker for SDH Mutation in
Pheochromocytoma/Paraganglioma and a Potential Target for Chemotherapy
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Tufts Med Ctr, Boston, MA USA.
NICHD, NIH, Bethesda, MD USA.
Univ Massachusetts, Med Ctr, Worcester, MA USA.
Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 590
BP 141A
EP 141A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282300592
ER
PT J
AU Aung, PP
Walter, BA
Garcia, C
Bratslavsky, G
Merino, MJ
AF Aung, P. P.
Walter, B. A.
Garcia, C.
Bratslavsky, G.
Merino, M. J.
TI Potential Role of HER2/Neu as a Molecular Target in the Treatment of
High Grade Urothelial Cancer. Determination of Gene Amplification by
FISH, CISH and IHC
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Univ Salamanca, E-37008 Salamanca, Spain.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 749
BP 179A
EP 179A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282300751
ER
PT J
AU Cubilla, AL
Chaux, A
Rodriguez, IM
Barreto, JE
Netto, GJ
Bosch, FX
de Sanjose, S
Munoz, N
Hildesheim, A
AF Cubilla, A. L.
Chaux, A.
Rodriguez, I. M.
Barreto, J. E.
Netto, G. J.
Bosch, F. X.
de Sanjose, S.
Munoz, N.
Hildesheim, A.
TI Phimosis, Lichen Sclerosus, Smoking, Poverty, Sexually Related
Epidemiological Factors and Late Diagnosis Are Prevalent among Patients
with Penile Cancer in Paraguay.
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Inst Patol & Invest, Asuncion, Paraguay.
Johns Hopkins Univ, Baltimore, MD USA.
Inst Catalan Oncol, Barcelona, Spain.
CIBER Epidemiol & Salud Publ, Barcelona, Spain.
NCI, Bethesda, MD 20892 USA.
RI de Sanjose Llongueras, Silvia/H-6339-2014; Hildesheim,
Allan/B-9760-2015; BOSCH JOSE, FRANCESC XAVIER/J-6339-2012
OI Hildesheim, Allan/0000-0003-0257-2363; BOSCH JOSE, FRANCESC
XAVIER/0000-0002-7172-3412
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 784
BP 186A
EP 187A
PG 2
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282300786
ER
PT J
AU Cubilla, AL
Chaux, A
Rodriguez, IM
Barreto, JE
Netto, GJ
Bosch, FX
de Sanjose, S
Munoz, N
Hildesheim, A
AF Cubilla, A. L.
Chaux, A.
Rodriguez, I. M.
Barreto, J. E.
Netto, G. J.
Bosch, F. X.
de Sanjose, S.
Munoz, N.
Hildesheim, A.
TI Sexual History and Distinctive Pathological Features in HPV-Related
Penile Carcinomas.
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Inst Patol & Invest, Asuncion, Paraguay.
Johns Hopkins Univ, Baltimore, MD USA.
Inst Catalan Oncol, Barcelona, Spain.
CIBER Epidemiol & Salud Publ, Barcelona, Spain.
NCI, Bethesda, MD 20892 USA.
RI de Sanjose Llongueras, Silvia/H-6339-2014; Hildesheim,
Allan/B-9760-2015; BOSCH JOSE, FRANCESC XAVIER/J-6339-2012
OI Hildesheim, Allan/0000-0003-0257-2363; BOSCH JOSE, FRANCESC
XAVIER/0000-0002-7172-3412
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 785
BP 187A
EP 187A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282300787
ER
PT J
AU Sorbellini, M
McNeal, B
Athauda, G
Cohen, B
Giubellino, A
Simpson, H
Coleman, J
Getzenberg, RH
Netto, GJ
Linehan, MW
Pinto, PA
Bottaro, DP
AF Sorbellini, M.
McNeal, B.
Athauda, G.
Cohen, B.
Giubellino, A.
Simpson, H.
Coleman, J.
Getzenberg, R. H.
Netto, G. J.
Linehan, M. W.
Pinto, P. A.
Bottaro, D. P.
TI Urinary Met Level as a Novel Biomarker for Urothelial Carcinoma of the
Bladder
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 951
BP 225A
EP 225A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301106
ER
PT J
AU Carvajal, A
Sua, L
Silva, N
Pittaluga, S
Royo, C
Sargent, RL
Climent, F
Jacobs, SA
Delabie, J
Naresh, K
Bagg, A
Harris, NL
Swerdlow, SH
Jaffe, ES
Campo, E
AF Carvajal, A.
Sua, L.
Silva, N.
Pittaluga, S.
Royo, C.
Sargent, R. L.
Climent, F.
Jacobs, S. A.
Delabie, J.
Naresh, K.
Bagg, A.
Harris, N. L.
Swerdlow, S. H.
Jaffe, E. S.
Campo, E.
TI "In Situ" Mantle Cell Lymphoma (MCL), an Incidental Finding with an
Indolent Clinical Course.
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Hosp Clin Barcelona, Barcelona, Spain.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Univ Pittsburgh, Pittsburgh, PA 15260 USA.
Oslo Univ Hosp, Oslo, Norway.
Hammersmith Hosp, London, England.
Hosp Univ Penn, Philadelphia, PA 19104 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NCI, Bethesda, MD 20892 USA.
RI Royo, Cristina/H-3193-2015
OI Royo, Cristina/0000-0002-1214-4656
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1228
BP 289A
EP 289A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301383
ER
PT J
AU Shao, H
Gronborg, M
Yuan, CM
Kreitman, RJ
Stetler-Stevenson, M
AF Shao, H.
Gronborg, M.
Yuan, C. M.
Kreitman, R. J.
Stetler-Stevenson, M.
TI Hairy Cell Leukemia and Variant: Immunophenotypic Comparison and
Variations
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 NCI, NIH, Bethesda, MD 20892 USA.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1362
BP 320A
EP 321A
PG 2
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301517
ER
PT J
AU Shao, H
Xi, L
Raffeld, M
Feldman, AL
Ketterling, RP
Knudson, R
Rodriguez-Canales, J
Hanson, J
Pittaluga, S
Jaffe, ES
AF Shao, H.
Xi, L.
Raffeld, M.
Feldman, A. L.
Ketterling, R. P.
Knudson, R.
Rodriguez-Canales, J.
Hanson, J.
Pittaluga, S.
Jaffe, E. S.
TI Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma with
Transformation to Histiocytic/Dendritic Cell Sarcoma: Alterations of 17p
as a Potential Risk Factor
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
Mayo Clin, Rochester, MN USA.
RI Feldman, Andrew/D-5028-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1363
BP 321A
EP 321A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301518
ER
PT J
AU Spencer, DV
Foulks, CL
Geigerman, CM
Akl, PS
Lai, AY
Wade, PA
Jaye, DL
Hill, CE
AF Spencer, D. V.
Foulks, C. L.
Geigerman, C. M.
Akl, P. S.
Lai, A. Y.
Wade, P. A.
Jaye, D. L.
Hill, C. E.
TI Gene and Protein Isoform Expression Analysis of the BCL-6 Associated
Transcriptional Corepressor MTA3 in B- lineage Cells
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Emory Univ, Atlanta, GA 30322 USA.
NIEHS, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1371
BP 323A
EP 323A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301526
ER
PT J
AU Venkataraman, G
Traverse-Glehen, A
Song, JY
Eberle, FC
Hanson, JC
Dirnhofer, S
Tzankov, A
Heinze, G
Raffeld, MA
Pittaluga, S
Jaffe, ES
AF Venkataraman, G.
Traverse-Glehen, A.
Song, J. Y.
Eberle, F. C.
Hanson, J. C.
Dirnhofer, S.
Tzankov, A.
Heinze, G.
Raffeld, M. A.
Pittaluga, S.
Jaffe, E. S.
TI Aberrant T-Cell Antigen Expression in Classical Hodgkin Lymphoma Is
Associated with Decreased Event-Free Survival (EFS) and Overall Survival
(OS)
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Ctr Hosp Lyon Sud, Hosp Civils Lyon, F-69310 Pierre Benite, France.
Univ Basel Hosp, CH-4031 Basel, Switzerland.
Med Univ Vienna, Vienna, Austria.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1385
BP 326A
EP 327A
PG 2
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301540
ER
PT J
AU Hodgin, JB
Nair, V
Zhang, H
Randolph, A
Harris, RC
Nelson, RG
Brosius, FC
Kretzler, M
AF Hodgin, J. B.
Nair, V.
Zhang, H.
Randolph, A.
Harris, R. C.
Nelson, R. G.
Brosius, F. C.
Kretzler, M.
TI Cross-Species Identification of Conserved Glomerular Transcriptional
Networks of Progressive Diabetic Nephropathy in Mouse and Man.
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Univ Michigan, Ann Arbor, MI 48109 USA.
Vanderbilt Univ, Nashville, TN USA.
NIDDK, Phoenix, AZ USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1466
BP 345A
EP 345A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301621
ER
PT J
AU Yang, HC
Wang, SW
Pastan, I
Matsusaka, T
Ichikawa, I
Fogo, AB
AF Yang, H-C
Wang, S-W
Pastan, I.
Matsusaka, T.
Ichikawa, I.
Fogo, A. B.
TI Angiotensin II Type I Receptor Blocker Is Limited in Protection Against
Severe Podocyte Injury-Induced FSGS
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA.
NCI, NIH, Bethesda, MD 20892 USA.
Tokai Univ, Sch Med, Kanagawa 2591100, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1503
BP 354A
EP 355A
PG 2
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301658
ER
PT J
AU Brunt, EM
Kleiner, DE
Wilson, LA
Belt, PH
Neuschwander-Tetri, BA
AF Brunt, E. M.
Kleiner, D. E.
Wilson, L. A.
Belt, P. H.
Neuschwander-Tetri, B. A.
TI The Nonalcoholic Fatty Liver Disease Activity Score (NAS) and the
Histopathologic Diagnosis in Nonalcoholic Fatty Liver Disease: Distinct
Clinicopathologic Meanings
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Washington Univ, Sch Med, St Louis, MO USA.
NCI, Washington, DC USA.
Johns Hopkins Univ, Baltimore, MD USA.
St Louis Univ, Sch Med, St Louis, MO 63103 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1516
BP 357A
EP 358A
PG 2
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301671
ER
PT J
AU Doherty, AR
Ferrell, LD
Morse, CG
Kleiner, DE
AF Doherty, A. R.
Ferrell, L. D.
Morse, C. G.
Kleiner, D. E.
TI Hepatic Pigment Accumulation in HIV Patients on HAART Therapy
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Univ Calif San Francisco, San Francisco, CA 94143 USA.
NIAID, Bethesda, MD 20892 USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1522
BP 359A
EP 359A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282301677
ER
PT J
AU Martin, SE
Badve, SS
Steeg, P
Hattab, EM
AF Martin, S. E.
Badve, S. S.
Steeg, P.
Hattab, E. M.
TI Luminal A Subtype Predicts Improved Survival in Patients with Metastatic
Breast Carcinoma to the Brain.
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Indiana Univ, Sch Med, Indianapolis, IN USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1625
BP 383A
EP 383A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282302071
ER
PT J
AU Hipp, J
Cheng, J
Hanson, J
Yan, W
Rodriguez-Canales, J
Tangrea, M
Emmert-Buck, MR
Han, S
Hewitt, S
Monaco, J
Madabhushi, A
Balis, U
AF Hipp, J.
Cheng, J.
Hanson, J.
Yan, W.
Rodriguez-Canales, J.
Tangrea, M.
Emmert-Buck, M. R.
Han, S.
Hewitt, S.
Monaco, J.
Madabhushi, A.
Balis, U.
TI SIVQ Image Analysis: A High-Throughput Morphology Discovery Tool for
Surgical Pathologists
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 100th Annual Meeting United States-and-Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP United States Canadian Acad Pathol
C1 Univ Michigan, Ann Arbor, MI 48109 USA.
NCI, NIH, Bethesda, MD 20892 USA.
Rutgers State Univ, Piscataway, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2011
VL 24
SU 1
MA 1913
BP 449A
EP 449A
PG 1
WC Pathology
SC Pathology
GA 720LN
UT WOS:000287282302358
ER
PT J
AU Barkan, D
El Touny, LH
Michalowski, AM
Smith, JA
Chu, I
Davis, AS
Webster, JD
Hoover, S
Simpson, MR
Gauldie, J
Green, JE
AF Barkan, Dalit
El Touny, Lara H.
Michalowski, Aleksandra M.
Smith, Jane Ann
Chu, Isabel
Davis, Anne Sally
Webster, Joshua D.
Hoover, Shelley
Simpson, Mark R.
Gauldie, Jack
Green, Jeffrey E.
TI Type I collagen enrichment at the metastatic site: The 'soil' triggering
the transition from tumor dormancy to metastatic growth
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Barkan, Dalit] Univ Haifa, IL-31999 Haifa, Israel.
[El Touny, Lara H.; Michalowski, Aleksandra M.; Chu, Isabel; Webster, Joshua D.; Hoover, Shelley; Simpson, Mark R.; Green, Jeffrey E.] NCI, Bethesda, MD 20892 USA.
[Smith, Jane Ann; Gauldie, Jack] McMaster Univ, Hamilton, ON, Canada.
[Davis, Anne Sally] NIAID, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 174
EP 174
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200057
ER
PT J
AU Balamurugan, K
Sarkar, TR
Wang, JM
Sharan, S
Anver, MM
Sterneck, E
Leighty, R
AF Balamurugan, Kuppusamy
Sarkar, Tapasree Roy
Wang, Ju M.
Sharan, Shikha
Anver, Miriam M.
Sterneck, Esta
Leighty, Robert
TI The tumor suppressor C/EBP delta (CEBPD) promotes metastasis of MMTV-Neu
mouse mammary tumors and augments mTOR/AKT/HIF-1 activity through
inhibition of FBXW7 expression
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Balamurugan, Kuppusamy; Sarkar, Tapasree Roy; Sharan, Shikha; Sterneck, Esta; Leighty, Robert] NCI, Frederick, MD 21701 USA.
[Wang, Ju M.] Natl Cheng Kung Univ, Tainan 70101, Taiwan.
[Anver, Miriam M.] SAIC, Frederick, MD USA.
NR 6
TC 0
Z9 0
U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 185
EP 185
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200093
ER
PT J
AU Gril, B
Palmieri, D
Qian, Y
Liewehr, DJ
Steinberg, SM
Ileva, L
Steeg, PS
AF Gril, Brunilde
Palmieri, Diane
Qian, Yong
Liewehr, David J.
Steinberg, Seth M.
Ileva, Lilia
Steeg, Patricia S.
TI Pazopanib reveals a role for B-Raf in tumorigenesis, angiogenesis and
prevention of brain metastatic colonization of HER2+breast cancer cells
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Gril, Brunilde; Palmieri, Diane; Qian, Yong; Liewehr, David J.; Steinberg, Seth M.; Steeg, Patricia S.] NCI, Bethesda, MD 20892 USA.
[Ileva, Lilia] NCI, Frederick, MD 21701 USA.
RI Palmieri, Diane/B-4258-2015
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 193
EP 194
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200117
ER
PT J
AU Evans, LM
Palmieri, D
Steeg, PS
AF Evans, Lynda M.
Palmieri, Diane
Steeg, Patricia S.
TI Full-length L1CAM is overexpressed on brain-seeking MDA-MB-231 breast
cancer cells and may play a role in binding Tenascin C and colony
formation in vitro
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Evans, Lynda M.; Palmieri, Diane; Steeg, Patricia S.] NIH, Bethesda, MD 20892 USA.
RI Palmieri, Diane/B-4258-2015
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 194
EP 194
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200119
ER
PT J
AU Fitzgerald, DP
Palmieri, D
Qian, YZ
Vega-Valle, E
Davis, S
Meltzer, P
Steeg, PS
AF Fitzgerald, Daniel Patrick
Palmieri, Diane
Qian, Yongzhen
Vega-Valle, Eleazar
Davis, Sean
Meltzer, Paul
Steeg, Patricia S.
TI Genetic studies in murine/xenograft models of breast cancer brain
metastasis
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Palmieri, Diane; Davis, Sean; Meltzer, Paul; Steeg, Patricia S.] NCI, Bethesda, MD 20892 USA.
[Qian, Yongzhen; Vega-Valle, Eleazar] SAIC, NIH, Frederick, MD USA.
RI Palmieri, Diane/B-4258-2015
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 194
EP 195
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200120
ER
PT J
AU Mailer, O
Lyons, TR
Green, JE
Schedin, PJ
AF Mailer, Ori
Lyons, Traci R.
Green, Jeffrey E.
Schedin, Pepper J.
TI The function of extracellular matrix in breast cancer dormancy
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
ID CELLS
C1 [Mailer, Ori; Lyons, Traci R.; Schedin, Pepper J.] Univ Colorado Denver, Aurora, CO USA.
[Green, Jeffrey E.] NIH, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 210
EP 210
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200165
ER
PT J
AU Liu, H
Yukinari, K
Erzinger, SA
Kiriakova, GM
Palmieri, D
Steeg, PS
Price, JE
AF Liu, Hui
Yukinari, Kato
Erzinger, Stephanie A.
Kiriakova, Galina M.
Palmieri, Diane
Steeg, Patricia S.
Price, Janet E.
TI shRNA mediated inhibition of MMP-1 attenuates breast cancer growth and
metastasis to brain
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Liu, Hui; Yukinari, Kato; Erzinger, Stephanie A.; Kiriakova, Galina M.; Price, Janet E.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Palmieri, Diane; Steeg, Patricia S.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 220
EP 220
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200192
ER
PT J
AU Alsarraj, J
Walker, RC
Webster, JD
Simpson, RM
Ozato, K
Hunter, KW
AF Alsarraj, Jude
Walker, Renard C.
Webster, Joshua D.
Simpson, R. Mark
Ozato, Keiko
Hunter, Kent W.
TI A mutant of the metastasis susceptibility gene Brd4 promotes EMT, stem
cell-like conversion and metastatic progression in a mouse mammary tumor
model
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Alsarraj, Jude; Walker, Renard C.; Webster, Joshua D.; Simpson, R. Mark; Hunter, Kent W.] NCI, NIH, Bethesda, MD 20892 USA.
[Ozato, Keiko] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 226
EP 226
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200212
ER
PT J
AU Clark, RJ
Marasa, B
Otto, K
Gorospe, M
Rinker-Schaeffer, C
AF Clark, Robert J.
Marasa, Bernard
Otto, Kristen
Gorospe, Myriam
Rinker-Schaeffer, Carrie
TI The regulation of mitogen-activated kinase kinase 4 by microRNA-24 in
prostate cancer cell lines
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Clark, Robert J.; Otto, Kristen; Rinker-Schaeffer, Carrie] Univ Chicago, Chicago, IL 60637 USA.
[Marasa, Bernard; Gorospe, Myriam] NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 227
EP 228
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200218
ER
PT J
AU Mkrtichyan, M
Naiiar, YG
Raulfs, EC
Khleif, SN
AF Mkrtichyan, Mikayel
Naiiar, Yana G.
Raulfs, Estella C.
Khleif, Samir N.
TI Defining a novel mechanism of a-PD1 synergy with vaccine to induce
potent anti-tumor effects
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Mkrtichyan, Mikayel; Naiiar, Yana G.; Raulfs, Estella C.; Khleif, Samir N.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 247
EP 248
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200279
ER
PT J
AU Murthv, SRK
Lee, T
Cawley, N
Loh, P
AF Murthv, Saravana Radha Krishna
Lee, Terence
Cawley, Niamh
Loh, Peng
TI A spliced isoform of carboxypeptidase E drives tumor metastasis
epigenetically and predicts future malignancy for different cancers
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Murthv, Saravana Radha Krishna; Cawley, Niamh; Loh, Peng] NICHD, NIH, Bethesda, MD USA.
[Lee, Terence] Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 249
EP 249
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200282
ER
PT J
AU Flores, NM
Sledge, GW
Badve, S
Palmieri, D
Steeg, P
AF Flores, Natasha M.
Sledge, George W., Jr.
Badve, Sunil
Palmieri, Diane
Steeg, Patricia
TI A structural and functional analysis of BARD1 and RAD51 overexpression
in the MCF10A cell line
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Flores, Natasha M.; Palmieri, Diane; Steeg, Patricia] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Sledge, George W., Jr.; Badve, Sunil] Indiana Univ Sch Med, Indianapolis, IN USA.
RI Palmieri, Diane/B-4258-2015
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 259
EP 259
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200309
ER
PT J
AU Li, M
Kapoor, A
Mazilu, D
Horvath, KA
AF Li, Ming
Kapoor, Ankur
Mazilu, Dumitru
Horvath, Keith A.
TI Pneumatic Actuated Robotic Assistant System for Aortic Valve Replacement
Under MRI Guidance
SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING
LA English
DT Article
DE MRI robot; real-time MRI (rtMRI)-guided intervention; transapical aortic
valve replacement
ID PROSTATE INTERVENTIONS; COMPATIBLE MANIPULATOR; INTERACTIVE MRI; DESIGN;
INSTRUMENTS; TRACKING; DEVICES; BREAST
AB We present a pneumatic actuated robotic assistant system for transapical aortic valve replacement under MRI guidance in a beating heart. This is a minimally invasive procedure that is currently performed manually inside the MRI bore. A robotic assistance system that integrates an interactive real-time MRI system, a robotic arm with a newly developed robotic valve delivery module, as well as user interfaces for the physician to plan the procedure and manipulate the robot, would be advantageous for the procedure. An Innomotion arm with hands-on cooperative interface was used as a device holder. A compact MRI compatible robotic delivery module was developed for delivering both balloon-expandable and self-expanding prostheses. A compact fiducial that can be placed close to the volume of interest and requires a single image plane was used for image-based robot registration. The system provides different user interfaces at various stages of the procedure. We present the development and evaluation of the components and the system in ex-vivo experiments.
C1 [Li, Ming; Kapoor, Ankur; Mazilu, Dumitru; Horvath, Keith A.] NIH, Bethesda, MD 20892 USA.
RP Li, M (reprint author), NIH, Bldg 10, Bethesda, MD 20892 USA.
EM lim2@mail.nih.gov; kapooran@mail.nih.gov; mazilud@mail.nih.gov;
horvathka@mail.nih.gov
FU National Heart Lung and Blood Institute and Clinical Center, National
Institutes of Health, Department of Health and Human Services, USA
FX This work was supported through the Intramural Research Program of the
National Heart Lung and Blood Institute and Clinical Center, National
Institutes of Health, Department of Health and Human Services, USA.
NR 27
TC 15
Z9 16
U1 1
U2 4
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0018-9294
J9 IEEE T BIO-MED ENG
JI IEEE Trans. Biomed. Eng.
PD FEB
PY 2011
VL 58
IS 2
BP 443
EP 451
DI 10.1109/TBME.2010.2089983
PG 9
WC Engineering, Biomedical
SC Engineering
GA 710LZ
UT WOS:000286514500027
PM 21041156
ER
PT J
AU Kristinsson, SY
Landgren, O
AF Kristinsson, Sigurdur Y.
Landgren, Ola
TI What Causes Waldenstrom's Macroglobulinemia: Genetic or Immune-Related
Factors, or a Combination?
SO CLINICAL LYMPHOMA MYELOMA & LEUKEMIA
LA English
DT Article; Proceedings Paper
CT 6th International Workshop on Waldenstroms Macroglobulinemia
CY OCT 06-10, 2010
CL Venice, ITALY
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; NON-HODGKIN-LYMPHOMA; FAMILIAL
AGGREGATION; RHEUMATOID-ARTHRITIS; RISK; PATTERNS; SUSCEPTIBILITY;
CANCER; TUMORS
AB Population-based studies suggest a role for chronic immune stimulation and genetic factors in the causation of lymphoplasmacytic lymphoma (LPL)/Waldenstrom's macroglobulinemia (WM). In this review we summarize and discuss our current understanding on etiology and pathogenesis of LPL/WM. We also highlight on gaps in the literature and propose Enure directions for population-based and molecular studies designed to expand our knowledge and uncover biological underpinnings of identified associations. Further, we address clinical implications and provide perspective on the relevance of these data for patient counseling and clinical follow-up.
C1 [Kristinsson, Sigurdur Y.] Karolinska Univ Hosp Solna, Dept Med, Div Hematol, SE-17176 Stockholm, Sweden.
[Kristinsson, Sigurdur Y.] Karolinska Inst, Stockholm, Sweden.
[Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Kristinsson, SY (reprint author), Karolinska Univ Hosp Solna, Dept Med, Div Hematol, SE-17176 Stockholm, Sweden.
EM sigurdur.kristinsson@karolinska.se
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
FU Intramural NIH HHS
NR 23
TC 4
Z9 4
U1 0
U2 2
PU CIG MEDIA GROUP, LP
PI DALLAS
PA 3500 MAPLE AVENUE, STE 750, DALLAS, TX 75219-3931 USA
SN 2152-2650
EI 2152-2669
J9 CL LYMPH MYELOM LEUK
JI Clin. Lymphoma Myeloma Leuk.
PD FEB
PY 2011
VL 11
IS 1
BP 85
EP 87
DI 10.3816/CLML.2011.n.015
PG 3
WC Oncology; Hematology
SC Oncology; Hematology
GA 748IF
UT WOS:000289383600016
PM 21454199
ER
PT J
AU Murphy, DL
Moya, PR
AF Murphy, Dennis L.
Moya, Pablo R.
TI Human serotonin transporter gene (SLC6A4) variants: their contributions
to understanding pharmacogenomic and other functional G x G and G x E
differences in health and disease
SO CURRENT OPINION IN PHARMACOLOGY
LA English
DT Article
ID OBSESSIVE-COMPULSIVE DISORDER; DEPRESSIVE SYMPTOMS; POLYMORPHISMS;
ASSOCIATION; METAANALYSIS; GENOTYPE; ANXIETY; MICE; ACTIVATION;
MODERATION
AB Recent major findings from studies of SLC6A4 and its corresponding protein, the serotonin (5-HT) transporter (SERT) in humans, rodents and non-human primates indicate that combinations of SLC6A4 non-coding 5', 3' UTRs and intronic regions plus coding variants acting together can change 5HT transport as much as 40-fold in vitro. In vivo, SLC6A4 variants in humans and other species lead to marked physiological changes, despite mitigating neurodevelopmental adaptations in 5-HT receptors plus compensatory alterations in 5-HT synthesis and metabolism. Polymorphisms in SLC6A4 are associated with differences in emotional, endocrine, and personality characteristics as well as many diseases. This gene, in combinations with gene x gene (G x G) and gene x environment (G x E) interactions nonetheless remains incompletely understood, with some association findings remaining controversial. Considering its primary importance in the regulation and function of the entire serotonergic system (as evidenced by the consequences of SERT-mediated reuptake inhibition by SRIs like fluoxetine in humans and of genetically engineered changes in mice and rats), it seems likely that SLC6A4 and SERT will remain areas of high interest in our field's attempts to better understand and treat 5-HT-related disorders.
C1 [Murphy, Dennis L.; Moya, Pablo R.] NIMH, Clin Sci Lab, Intramural Res Program, Bethesda, MD 20892 USA.
RP Murphy, DL (reprint author), NIMH, Clin Sci Lab, Intramural Res Program, Bethesda, MD 20892 USA.
EM dm30h@nih.gov
FU NIMH; NIH
FX This research was supported by the Intramural Research Program of the
NIMH, NIH. The authors are also grateful to Theresa B. DeGuzman for her
editorial and graphical assistance.
NR 48
TC 33
Z9 34
U1 1
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4892
J9 CURR OPIN PHARMACOL
JI Curr. Opin. Pharmacol.
PD FEB
PY 2011
VL 11
IS 1
BP 3
EP 10
DI 10.1016/j.coph.2011.02.008
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 752NL
UT WOS:000289698700002
PM 21439906
ER
PT J
AU Pinheiro, RO
Salles, JD
Sarno, EN
Sampaio, EP
AF Pinheiro, Roberta Olmo
Salles, Jorgenilce de Souza
Sarno, Euzenir Nunes
Sampaio, Elizabeth Pereira
TI Mycobacterium leprae-host-cell interactions and genetic determinants in
leprosy: an overview
SO FUTURE MICROBIOLOGY
LA English
DT Review
DE leprosy; Mycobacterium leprae; Schwann cells; thalidomide; TNF-alpha
ID NECROSIS-FACTOR-ALPHA; ERYTHEMA-NODOSUM LEPROSUM; HUMAN SCHWANN-CELLS;
TOLL-LIKE RECEPTOR-2; TYPE-1 REVERSAL REACTIONS; PHENOLIC GLYCOLIPID-I;
LEPROMATOUS LEPROSY; DC-SIGN; TNF-ALPHA; DENDRITIC CELLS
AB Leprosy, also known as Hansen's disease, is a chronic infectious disease caused by Mycobacterium leprae in which susceptibility to the mycobacteria and its clinical manifestations are attributed to the host immune response. Even though leprosy prevalence has decreased dramatically, the high number of new cases indicates active transmission. Owing to its singular features, M. leprae infection is an attractive model for investigating the regulation of human immune responses to pathogen-induced disease. Leprosy is one of the most common causes of nontraumatic peripheral neuropathy worldwide. The proportion of patients with disabilities is affected by the type of leprosy and delay in diagnosis. This article briefly reviews the clinical features as well as the immunopathological mechanisms related to the establishment of the different polar forms of leprosy, the mechanisms related to M. leprae-host cell interactions and prophylaxis and diagnosis of this complex disease. Host genetic factors are summarized and the impact of the development of interventions that prevent, reverse or limit leprosy-related nerve impairments are discussed.
C1 [Pinheiro, Roberta Olmo; Salles, Jorgenilce de Souza; Sarno, Euzenir Nunes; Sampaio, Elizabeth Pereira] Fiocruz MS, Leprosy Lab, Inst Oswaldo Cruz, BR-21040213 Rio De Janeiro, Brazil.
[Sampaio, Elizabeth Pereira] NIH, Immunopathogenesis Sect, Lab Clin Infect Dis, LCID, Bethesda, MD 20892 USA.
RP Sampaio, EP (reprint author), Fiocruz MS, Leprosy Lab, Inst Oswaldo Cruz, Av Brasil 4365, BR-21040213 Rio De Janeiro, Brazil.
EM esampaio@ioc.fiocruz.br
FU IOC/FIOCRUZ; CNPq, Brazil; NIH/NIAID
FX This work was supported by IOC/FIOCRUZ, CNPq, Brazil, and in part by the
Intramural Research Program of NIH/NIAID. The authors' group at the
Rockefeller University, NY, USA, had a patent received for the work on
thalidomide action developed in 1990/1991. 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 152
TC 14
Z9 14
U1 0
U2 15
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1746-0913
J9 FUTURE MICROBIOL
JI Future Microbiol.
PD FEB
PY 2011
VL 6
IS 2
BP 217
EP 230
DI 10.2217/FMB.10.173
PG 14
WC Microbiology
SC Microbiology
GA 737SP
UT WOS:000288588800015
PM 21366421
ER
PT J
AU Hall, RH
AF Hall, Robert H.
TI A De in the life of cholera
SO INDIAN JOURNAL OF MEDICAL RESEARCH
LA English
DT Review
DE Cholera toxin; De; EL Tor; Vibrio cholerae
ID VIBRIO-CHOLERAE; VACCINE; DE,S.N.; SCIENCE
AB The 50-year commemoration of S.N. De's seminal 1959 publication in Nature provides an opportunity to reflect on scientific discovery, recognition, and public health. De's paper marked the first major conceptual advance in cholera research since 1884, when Robert Koch definitively identified Der Konunabazillus as the aetiological agent of cholera. Unfortunately, Koch reported that systemic toxinosis and multi-organ failure led to severe dehydrating diarrhoea, thereby mistaking cause for effect. As a consequence, while work on other microbial pathogens advanced into the development of vaccines and therapeutics, cholera research languished as scientists injected animals parenterally in decades of futile effort to develop an animal model of diarrhoea. This fundamental misconception in cholera pathogenesis was swept away when S.N. De used ligated loops of rabbit ileum to demonstrate lumenal fluid accumulation in the presence of Vibrio cholerae culture filtrates. After some delay, De's observation of a diarrhoeagenic exotoxin became the founding principle of modern cholera research, vaccination, and treatment; and a burst of discovery saw V. cholerae transformed into the enteric pathogen best understood at the molecular level. The scientific basis for orally administering vaccines to induce mucosal immunity was established, and the success of oral rehydration, what has been described as one of the 20(th) century's most important medical advances, was explained.
Nobel laureate Joshua Lederberg wrote of De's iconoclastic creativity, experimental skill, and observational mastery, and many other leaders in the field concurred. De was nominated for the Nobel Prize in Physiology or Medicine more than once. But despite the passage of half a century from De's work, cholera remains a frustrating problem: we are clearly missing something. In reviewing the scientific and programmatic impact of S.N. De on cholera, it is clear that a defining victory against the disease is achievable, but only if basic scientific discoveries are relentlessly driven towards progress in public health.
C1 NIAID, NIH, Bethesda, MD 20892 USA.
RP Hall, RH (reprint author), NIAID, NIH, 6610 Rockledge Dr,Rm 5106, Bethesda, MD 20892 USA.
EM rhall@niaid.nih.gov
NR 33
TC 0
Z9 0
U1 0
U2 7
PU INDIAN COUNCIL MEDICAL RES
PI NEW DELHI
PA PO BOX 4911 ANSARI NAGAR, NEW DELHI 110029, INDIA
SN 0971-5916
J9 INDIAN J MED RES
JI Indian J. Med. Res.
PD FEB
PY 2011
VL 133
IS 2
BP 146
EP 152
PG 7
WC Immunology; Medicine, General & Internal; Medicine, Research &
Experimental
SC Immunology; General & Internal Medicine; Research & Experimental
Medicine
GA 747LW
UT WOS:000289322300005
PM 21415488
ER
PT J
AU Britton, KA
Fox, CS
AF Britton, Kathryn A.
Fox, Caroline S.
TI Perivascular adipose tissue and vascular disease
SO CLINICAL LIPIDOLOGY
LA English
DT Review
DE cardiovascular; epidemiology; imaging; mechanisms; perivascular adipose
tissue
ID NECROSIS-FACTOR-ALPHA; CARDIOVASCULAR MAGNETIC-RESONANCE; CORONARY
ENDOTHELIAL FUNCTION; MUSCLE RESISTANCE ARTERIES; II-INDUCED
HYPERTENSION; VISCERAL ABDOMINAL FAT; NITRIC-OXIDE SYNTHASE; PERICARDIAL
FAT; INSULIN-RESISTANCE; EPICARDIAL FAT
AB Perivascular adipose tissue is a local deposit of adipose tissue surrounding the vasculature. Perivascular adipose tissue is present throughout the body and has been shown to have a local effect on blood vessels. The influence of perivascular adipose tissue on the vasculature changes with increasing adiposity. This article describes the anatomy and pathophysiology of perivascular adipose tissue and the experimental evidence supporting its local adverse effect on the vasculature. Methods for quantifying perivascular adipose tissue in free-living populations will be described. Finally, the epidemiological literature demonstrating an association between perivascular adipose tissue and cardiometabolic disease will be explored.
C1 [Britton, Kathryn A.] NHLBI, Farmingham Heart Study, Framingham, MA USA.
[Britton, Kathryn A.; Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Britton, Kathryn A.] Brigham & Womens Hosp, Div Cardiovasc Med, Boston, MA 02115 USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Div Endocrinol Metab & Hypertens, Boston, MA 02115 USA.
[Fox, Caroline S.] Ctr Populat Studies, Framingham, MA USA.
RP Fox, CS (reprint author), 73 mt Wayne Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
FU Intramural NIH HHS [Z99 HL999999, ZIA HL006094-01]
NR 85
TC 23
Z9 23
U1 3
U2 9
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1758-4299
J9 CLIN LIPIDOL
JI Clin. Lipidol.
PD FEB
PY 2011
VL 6
IS 1
BP 79
EP 91
DI 10.2217/CLP.10.89
PG 13
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 741DX
UT WOS:000288844400013
PM 21686058
ER
PT J
AU Brooks, BP
AF Brooks, Brian P.
TI Making progress in albinism
SO JOURNAL OF AAPOS
LA English
DT Editorial Material
ID EFFICACY
C1 NEI, Ophthalm Genet Branch, Bethesda, MD 20892 USA.
RP Brooks, BP (reprint author), NEI, Ophthalm Genet Branch, 10 Ctr Dr,MSC 1860,Bldg 10,Room 10N226, Bethesda, MD 20892 USA.
EM brooksb@mail.nih.gov
NR 9
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1091-8531
J9 J AAPOS
JI J. AAPOS
PD FEB
PY 2011
VL 15
IS 1
BP 1
EP 2
DI 10.1016/j.jaapos.2011.01.002
PG 2
WC Ophthalmology; Pediatrics
SC Ophthalmology; Pediatrics
GA 740VI
UT WOS:000288822100001
PM 21397796
ER
PT J
AU Saporito, RA
Norton, RA
Andriamaharavo, NR
Garraffo, HM
Spande, TF
AF Saporito, Ralph A.
Norton, Roy A.
Andriamaharavo, Nirina R.
Garraffo, Hugo Martin
Spande, Thomas F.
TI Alkaloids in the Mite Scheloribates laevigatus: Further Alkaloids Common
to Oribatid Mites and Poison Frogs
SO JOURNAL OF CHEMICAL ECOLOGY
LA English
DT Article
DE Chemical defense; Dendrobatids; Indolizidines; Oil glands; Opisthonotal
glands; Pumiliotoxins; Scheloribatidae; Tricyclic alkaloids; Poison frog
ID FEEDING PREFERENCES; ACARI; ANTS; PUMILIOTOXIN; SYMBIONT; PATTERNS;
ANATOMY; FOREST; DIET; SKIN
AB Poison frogs are chemically defended from predators by diverse alkaloids, almost all of which are sequestered unchanged from alkaloid-containing arthropods in the frog diet. Oribatid mites recently have been proposed as a major dietary source of poison frog alkaloids. Here, we report on alkaloids common to an oribatid mite and poison frogs. Gas chromatographic-mass spectrometric analysis of methanol extracts of adult Scheloribates laevigatus (Oribatida: Scheloribatidae) revealed nine alkaloids. Five of these have been detected previously in the skin glands of poison frogs: two isomers of the pumiliotoxin 291G, two isomers of the 5,6,8-trisubstituted indolizidine 209C, and the 5,6,8-trisubstituted indolizidine 195G. The other four alkaloids, a pumiliotoxin, a tricyclic (coccinelline-like), and two isomers of an izidine, were not previously known, but are similar in structure to alkaloids found in poison frogs. Alkaloids were not detected in immature S. laevigatus, suggesting that they are adult-specific and possibly the result of mite biosynthesis. Although most of the alkaloids detected in S. laevigatus are common to poison frogs, the geographic distributions of these organisms are not sympatric. The findings of this study indicate that oribatid mites, and in particular, members of the genus Scheloribates, represent a relatively unexplored arthropod repository for alkaloids and a significant dietary source of alkaloids in poison frogs.
C1 [Saporito, Ralph A.] John Carroll Univ, Dept Biol, University Hts, OH 44118 USA.
[Norton, Roy A.] SUNY Syracuse, Coll Environm Sci & Forestry, Syracuse, NY 13210 USA.
[Andriamaharavo, Nirina R.; Garraffo, Hugo Martin; Spande, Thomas F.] NIDDK, Bioorgan Chem Lab, NIH, DHHS, Bethesda, MD 20892 USA.
RP Saporito, RA (reprint author), John Carroll Univ, Dept Biol, University Hts, OH 44118 USA.
EM ralph.saporito@gmail.com
FU NIDDK; National Science Foundation; NIH
FX J.M. Snyder provided comments that improved the quality of this
manuscript. An NIH Courtesy Appointment and a National Science
Foundation Postdoctoral Research Fellowship supported R.A.S. The
research at NIH was funded by intramural funds of NIDDK.
NR 33
TC 17
Z9 17
U1 2
U2 21
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0098-0331
J9 J CHEM ECOL
JI J. Chem. Ecol.
PD FEB
PY 2011
VL 37
IS 2
BP 213
EP 218
DI 10.1007/s10886-011-9914-7
PG 6
WC Biochemistry & Molecular Biology; Ecology
SC Biochemistry & Molecular Biology; Environmental Sciences & Ecology
GA 741NI
UT WOS:000288870000011
PM 21318398
ER
PT J
AU Feng, JX
Wang, HS
Shin, DM
Masiuk, M
Qi, CF
Morse, HC
AF Feng, Jianxun
Wang, Hongsheng
Shin, Dong-Mi
Masiuk, Marek
Qi, Chen-Feng
Morse, Herbert C., III
TI IFN Regulatory Factor 8 Restricts the Size of the Marginal Zone and
Follicular B Cell Pools
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID LEUKEMIA-LIKE SYNDROME; POSITIVE SELECTION; GERMINAL CENTER; IN-VIVO;
LYMPHOCYTE DEVELOPMENT; ANTIGEN RECEPTOR; DENDRITIC CELLS; FATE
DECISION; LINEAGE; MICE
AB Transcriptional control of marginal zone (MZ) and follicular (FO) B cell development remains incompletely understood. The transcription factor, IFN regulatory factor (IRF)8, is known to play important roles in the differentiation of early B cells. In this article, we demonstrate that IRF8 is also required for normal development of MZ and FO B cells. Mice with a conventional knockout of Irf8 (IRF8(-/-)) or a point mutation in the IRF association domain of IRF8 had increased numbers of MZ B cells. To determine the B cell-intrinsic effects of IRF8 deficiency, we generated mice with a conditional allele of Irf8 crossed with CD19-Cre mice (designated IRF8-conditional knockout [CKO]). These mice had enlarged MZ and increased numbers of MZ and FO B cells compared with controls. The FO B cells of CKO mice exhibited reduced expression of CD23 and moderately increased expression of CD21. Gene-expression profiling showed that increased B cell production in IRF8-CKO mice was associated with changes in expression of genes involved in regulation of transcription, signaling, and inflammation. Functional studies showed that IRF8-CKO mice generated normal Ab responses to T-independent and T-dependent Ags. Thus, IRF8 controls the expansion and maturation of MZ and FO B cells but has little effect on B cell function. The Journal of Immunology, 2011, 186: 1458-1466.
C1 [Feng, Jianxun; Wang, Hongsheng; Shin, Dong-Mi; Masiuk, Marek; Qi, Chen-Feng; Morse, Herbert C., III] NIAID, Immunopathol Lab, NIH, Rockville, MD 20852 USA.
[Masiuk, Marek] Pomeranian Med Univ, Dept Pathol, PL-70252 Szczecin, Poland.
RP Morse, HC (reprint author), NIAID, Immunopathol Lab, NIH, 5640 Fishers Lane, Rockville, MD 20852 USA.
EM wanghongs@niaid.nih.gov; hmorse@niaid.nih.gov
RI Masiuk, Marek/M-8485-2014;
OI Morse, Herbert/0000-0002-9331-3705
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases.
NR 48
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U1 1
U2 3
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD FEB 1
PY 2011
VL 186
IS 3
BP 1458
EP 1466
DI 10.4049/jimmunol.1001950
PG 9
WC Immunology
SC Immunology
GA 708RE
UT WOS:000286381200024
PM 21178004
ER
PT J
AU Schenekar, T
Winkler, KA
Troyer, JL
Weiss, S
AF Schenekar, Tamara
Winkler, Kathrin A.
Troyer, Jennifer L.
Weiss, Steven
TI Isolation and Characterization of the CYP2D6 Gene in Felidae with
Comparison to Other Mammals
SO JOURNAL OF MOLECULAR EVOLUTION
LA English
DT Article
DE Cytochrome P450; Cats; Selection; dN/dS; Slightly deleterious mutations
ID NONSYNONYMOUS NUCLEOTIDE SUBSTITUTIONS; DETECTING POSITIVE SELECTION;
HUMAN CYTOCHROME-P450 2D6; ADVERSE DRUG-REACTIONS; AMINO-ACID; MOLECULAR
ADAPTATION; MAXIMUM-LIKELIHOOD; EVOLUTION; METABOLISM; POLYMORPHISMS
AB The highly polymorphic CYP2D6 protein metabolizes about 25% of commonly used drugs and underlies a broad spectrum of drug responses among individuals. In contrast to extensive knowledge on the human CYP2D6 gene, little is known about the gene in non-human mammals. CYP2D6 mRNA from 23 cats (Felidae) spanning seven species were compared to available CYPD6 sequences in ten additional mammals and multiple allelic variants in humans. A relatively high mean dN/dS ratio (0.565) was observed, especially within Felidae. Pairwise dN/dS ratios were non-monotonically distributed with respect to evolutionary distance suggesting either positive selection or retention of slightly deleterious mutations. Positive selection on specific codons, most notably in regions involved in substrate recognition and membrane anchoring is supported and the possible influence of diet on specific amino acid changes in substrate binding sites is discussed.
C1 [Schenekar, Tamara; Winkler, Kathrin A.; Weiss, Steven] Karl Franzens Univ Graz, Inst Zool, A-8010 Graz, Austria.
[Troyer, Jennifer L.] NCI, SAIC Frederic Inc, Lab Genom Div, Frederick, MD 21702 USA.
RP Weiss, S (reprint author), Karl Franzens Univ Graz, Inst Zool, Univ Pl 2, A-8010 Graz, Austria.
EM steven.weiss@uni-graz.at
RI Troyer, Jennifer/B-8415-2012; Weiss, Steven/L-6016-2015
OI Weiss, Steven/0000-0002-4734-5984
FU Faculty of Natural Sciences of the Karl-Franzens University Graz; NIH,
National Cancer Institute, Center for Cancer Research; National
Institutes of Health [HHSN26120080001E]; National Cancer Institute
FX We thank Stephen O'Brien for his generous support, provision of tissue
samples and access to facilities. We also thank Natalie Baggett for cDNA
preparation. The work was partially funded by the Faculty of Natural
Sciences of the Karl-Franzens University Graz. This research was
supported in part by the Intramural Research Program of the NIH,
National Cancer Institute, Center for Cancer Research and has also been
funded in part with federal funds from the National Cancer Institute and
National Institutes of Health, under contract HHSN26120080001E. The
content of this publication does not necessarily reflect the views or
policies of the Department of Health and Human Services, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the US Government.
NR 57
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U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0022-2844
J9 J MOL EVOL
JI J. Mol. Evol.
PD FEB
PY 2011
VL 72
IS 2
BP 222
EP 231
DI 10.1007/s00239-010-9424-1
PG 10
WC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Evolutionary Biology; Genetics &
Heredity
GA 740QB
UT WOS:000288808400010
PM 21188366
ER
PT J
AU Prentice, RL
Rossouw, JE
AF Prentice, Ross L.
Rossouw, Jacques E.
TI "Preventing breast cancer in postmenopausal women by achievable diet
modification: A missed opportunity in public health policy" (Dayal HH
and Kalia A, The Breast 2010; 19: 309-311)
SO BREAST
LA English
DT Letter
ID MODIFICATION TRIAL; FAT; PATTERN; RISK
C1 [Prentice, Ross L.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Rossouw, Jacques E.] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Prentice, RL (reprint author), Fred Hutchinson Canc Res Ctr, 1100 Fairview Ave N,M3-A410,POB 19024, Seattle, WA 98109 USA.
EM rprentic@fhcrc.org; rossouwj@nhlbi.nih.gov
NR 10
TC 0
Z9 0
U1 1
U2 1
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0960-9776
J9 BREAST
JI Breast
PD FEB
PY 2011
VL 20
IS 1
BP 99
EP 99
DI 10.1016/j.breast.2010.11.001
PG 1
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 736GL
UT WOS:000288478900019
PM 21112212
ER
PT J
AU Caron, WP
Clewell, H
Dedrick, R
Ramanathan, R
Yu, N
Tonda, M
Schellens, JH
Beijnen, JH
Zamboni, WC
AF Caron, Whitney P.
Clewell, Harvey
Dedrick, Robert
Ramanathan, Ramesh
Yu, Ning
Tonda, Margaret
Schellens, Jan H.
Beijnen, Jos H.
Zamboni, William C.
TI Symp IXb Preclinical and Translational Pharmacology of Nanoparticle
Therapeutics
SO INTERNATIONAL JOURNAL OF TOXICOLOGY
LA English
DT Meeting Abstract
CT 31st Annual Meeting of the American-College-of-Toxicology
CY NOV 07-10, 2010
CL Baltimore, MD
SP Amer Coll Toxicol
DE nanoparticles; pharmacology/pharmacokinetics; allometric scaling
C1 [Caron, Whitney P.; Zamboni, William C.] Univ N Carolina, Div Pharmacotherapy & Expt Therapeut, Eshelman Sch Pharm, Res Triangle Pk, NC USA.
[Clewell, Harvey] Hamner Inst Hlth Sci, Res Triangle Pk, NC USA.
[Dedrick, Robert] NIH, Biomed Engn & Instrumentat Branch, Div Res Serv, Publ Hlth Serv,US Dept Hlth Educ & Welf, Bethesda, MD 20892 USA.
[Ramanathan, Ramesh] Univ Pittsburgh, Pittsburgh Canc Inst, Mol Therapeut & Drug Discovery Program, Pittsburgh, PA USA.
[Yu, Ning; Tonda, Margaret] ALZA Coporat, Mountain View, CA USA.
[Schellens, Jan H.; Beijnen, Jos H.] Netherlands Canc Inst, Slotervaart Hosp, Dept Pharm & Pharmacol, Amsterdam, Netherlands.
[Zamboni, William C.] UNC Lineberger Comprehens Canc Ctr, Chapel Hill, NC USA.
[Zamboni, William C.] UNC Inst Pharmacogenom & Individualized Therapy, Chapel Hill, NC USA.
[Zamboni, William C.] Carolina Ctr Canc Nanotechnol Excellence, Chapel Hill, NC USA.
[Zamboni, William C.] N Carolina Bioanalyt Innovat Network, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 10
U2 10
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1091-5818
J9 INT J TOXICOL
JI Int. J. Toxicol.
PD FEB
PY 2011
VL 30
IS 1
BP 125
EP 126
PG 2
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 733RJ
UT WOS:000288280200108
ER
PT J
AU Miller, FG
Brody, H
AF Miller, Franklin G.
Brody, Howard
TI Understanding and Harnessing Placebo Effects: Clearing Away the
Underbrush
SO JOURNAL OF MEDICINE AND PHILOSOPHY
LA English
DT Article
DE clinical medicine; placebo effect
ID CONTEXT
AB Despite strong growth in scientific investigation of the placebo effect, understanding of this phenomenon remains deeply confused. We investigate critically seven common conceptual distinctions that impede clear understanding of the placebo effect: (1) verum/placebo, (2) active/inactive, (3) signal/noise, (4) specific/nonspecific, (5) objective/subjective, (6) disease/illness, and (7) intervention/context. We argue that some of these should be eliminated entirely, whereas others must be used with caution to avoid bias. Clearing away the conceptual underbrush is needed to lay down a path to understanding and harnessing placebo effects in clinical medicine.
C1 [Miller, Franklin G.] NIH, Dept Bioeth, Ctr Clin, Bethesda, MD 20892 USA.
[Brody, Howard] Univ Texas Med Branch, Galveston, TX USA.
RP Miller, FG (reprint author), NIH, Dept Bioeth, Ctr Clin, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM fmiller@nih.gov
NR 18
TC 10
Z9 11
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0360-5310
J9 J MED PHILOS
JI J. Med. Philos.
PD FEB
PY 2011
VL 36
IS 1
BP 69
EP 78
DI 10.1093/jmp/jhq061
PG 10
WC Ethics; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Biomedical Social Sciences
GA 720BW
UT WOS:000287256200005
PM 21220523
ER
PT J
AU Miller, B
Molfese, V
Berninger, V
AF Miller, Brett
Molfese, Victoria
Berninger, Virginia
TI Introduction to special issue on writing
SO READING AND WRITING
LA English
DT Editorial Material
C1 [Miller, Brett] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Molfese, Victoria] Univ Nebraska, Dept Child Youth & Family Studies, Lincoln, NE USA.
[Berninger, Virginia] Univ Washington Educ Psychol, Seattle, WA USA.
RP Miller, B (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
EM millerbre@mail.nih.gov
NR 0
TC 1
Z9 1
U1 1
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0922-4777
J9 READ WRIT
JI Read. Writ.
PD FEB
PY 2011
VL 24
IS 2
BP 117
EP 119
DI 10.1007/s11145-010-9268-5
PG 3
WC Education & Educational Research; Psychology, Educational
SC Education & Educational Research; Psychology
GA 721MZ
UT WOS:000287360300001
ER
PT J
AU Miller, B
McCardle, P
AF Miller, Brett
McCardle, Peggy
TI Reflections on the need for continued research on writing
SO READING AND WRITING
LA English
DT Article
DE Writing; Literacy; Research directions; NIH; NICHD
ID WRITTEN LANGUAGE; INTERVENTION; METAANALYSIS; STUDENTS
AB A focused scientific research effort on writing research and its relationship to language development and reading is needed to address the writing and broader literacy needs of today's and tomorrow's learners and workers. In the United States, as well as in many other nations, research on writing has been neglected in relation to the emphasis on reading and oral language more generally. The authors argue first for why there is a need for this refocused effort, what should be focused on, and how as a field we should consider moving forward and addressing this imperative. In addressing the why, the authors argue that need is not limited to a particular age or developmental range but rather is broad-based, beginning with our youngest learners and continuing through those transitioning into post-secondary and the workplace. The clear message is that the picture is surprisingly similar across age ranges with a demonstrated need beginning with those coming from less advantaged backgrounds into formal education to the majority of students transitioning from twelfth grade into the workplace or post secondary settings. The authors suggest next steps for research addressing both what and how: what areas of science are areas of high need and how the field may consider moving forward to address these needs. Interdisciplinary research on writing is needed that addresses and integrates cognitive, biological, and social-cultural traditions, contributions, and methods.
C1 [Miller, Brett; McCardle, Peggy] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, US Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RP Miller, B (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, US Dept Hlth & Human Serv, NIH, 6100 Execut Blvd,Suite 4B05,MSC 7510, Bethesda, MD 20892 USA.
EM millerbre@mail.nih.gov; mccardlp@mail.nih.gov
NR 41
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U1 0
U2 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0922-4777
J9 READ WRIT
JI Read. Writ.
PD FEB
PY 2011
VL 24
IS 2
BP 121
EP 132
DI 10.1007/s11145-010-9267-6
PG 12
WC Education & Educational Research; Psychology, Educational
SC Education & Educational Research; Psychology
GA 721MZ
UT WOS:000287360300002
ER
PT J
AU Simoni, JM
Safren, SA
Manhart, LE
Lyda, K
Grossman, CI
Rao, D
Mimiaga, MJ
Wong, FY
Catz, SL
Blank, MB
DiClemente, R
Wilson, IB
AF Simoni, Jane M.
Safren, Steven A.
Manhart, Lisa E.
Lyda, Karen
Grossman, Cynthia I.
Rao, Deepa
Mimiaga, Matthew J.
Wong, Frank Y.
Catz, Sheryl L.
Blank, Michael B.
DiClemente, Ralph
Wilson, Ira B.
TI Challenges in Addressing Depression in HIV Research: Assessment,
Cultural Context, and Methods
SO AIDS AND BEHAVIOR
LA English
DT Article
DE HIV/AIDS; Depression; Research methods; Measurement
ID HUMAN-IMMUNODEFICIENCY-VIRUS; QUALITY-OF-LIFE; SUBSTANCE USE DISORDERS;
INTERNATIONAL NEUROPSYCHIATRIC INTERVIEW; RANDOMIZED CONTROLLED-TRIAL;
POSITIVE PREGNANT-WOMEN; MAJOR DEPRESSION; INFECTED INDIVIDUALS;
PRIMARY-CARE; GAY MEN
AB Depression is one of the most common co-morbidities of HIV infection. It negatively impacts self-care, quality of life, and biomedical outcomes among people living with HIV (PLWH) and may interfere with their ability to benefit from health promotion interventions. State-of-the-science research among PLWH, therefore, must address depression. To guide researchers, we describe the main diagnostic, screening, and symptom-rating measures of depression, offering suggestions for selecting the most appropriate instrument. We also address cultural considerations in the assessment of depression among PLWH, emphasizing the need to consider measurement equivalence and offering strategies for developing measures that are valid cross-culturally. Finally, acknowledging the high prevalence of depression among PLWH, we provide guidance to researchers on incorporating depression into the theoretical framework of their studies and employing procedures that account for participants with depression.
C1 [Simoni, Jane M.] Univ Washington, Dept Psychol, Seattle, WA 98195 USA.
[Safren, Steven A.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Manhart, Lisa E.] UW Ctr AIDS & STD, Dept Epidemiol, Seattle, WA USA.
[Lyda, Karen] Univ Colorado Denver, Univ Colorado Hosp, Sch Med, Div Infect Dis, Aurora, CO USA.
[Grossman, Cynthia I.] NIMH, Ctr Mental Hlth Res AIDS, Bethesda, MD 20892 USA.
[Rao, Deepa] Univ Washington, Dept Global Hlth, Seattle, WA 98195 USA.
[Mimiaga, Matthew J.] Fenway Community Hlth, Boston, MA USA.
[Wong, Frank Y.; DiClemente, Ralph] Emory Univ, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.
[Catz, Sheryl L.] Grp Hlth Res Inst, Seattle, WA USA.
[Blank, Michael B.] Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
[Wilson, Ira B.] Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Boston, MA USA.
RP Simoni, JM (reprint author), Univ Washington, Dept Psychol, Box 351525, Seattle, WA 98195 USA.
EM jsimoni@uw.edu
RI Wilson, Ira/F-9190-2016;
OI Wilson, Ira/0000-0002-0246-738X; Simoni, Jane/0000-0002-8711-1576
FU NIAID NIH HHS [P30 AI027757, P30 AI027757-18]; NIMH NIH HHS [K23
MH084551, K23 MH084551-05, K23 MH084551-06, K24 MH092242]
NR 142
TC 31
Z9 31
U1 9
U2 15
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1090-7165
J9 AIDS BEHAV
JI AIDS behav.
PD FEB
PY 2011
VL 15
IS 2
BP 376
EP 388
DI 10.1007/s10461-010-9836-3
PG 13
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 715YX
UT WOS:000286932800014
PM 21046221
ER
PT J
AU Prosser, LA
Stanley, CJ
Norman, TL
Park, HS
Damiano, DL
AF Prosser, Laura A.
Stanley, Christopher J.
Norman, Tracy L.
Park, Hyung S.
Damiano, Diane L.
TI Comparison of elliptical training, stationary cycling, treadmill walking
and overground walking. Electromyographic patterns
SO GAIT & POSTURE
LA English
DT Article
DE Gait; EMG; Muscle activity; Lower extremity; Elliptical; Cycling
ID MUSCLE-ACTIVITY; CEREBRAL-PALSY; KINEMATICS; BIOMECHANICS; ADOLESCENTS;
ONSET; SEMG
AB The most common functional motor goal of lower extremity rehabilitation is to improve walking ability. For reasons of feasibility, safety or intensity, devices are frequently used to facilitate or augment gait training. The objective of this study was to compare the muscle activity patterns of the rectus femoris and semitendinosus muscles during four conditions: overground walking, treadmill walking, stationary cycling, and elliptical training. Ten healthy adults (six male, four female; mean age 22.7 +/- 2.9 years, range 20-29) participated and surface electromyographic data were recorded. Linear envelope curves were generated and time normalized from 0 to 100% cycle. The mean plus three standard deviations from a static trial was used as the threshold for muscle activity. Repeated measures analysis of variance procedures were used to detect differences between conditions. Elliptical training demonstrated greater rectus femoris activity and greater rectus femoris/semitendinosus coactivation than all other conditions. Consistent with previous work, treadmill walking demonstrated greater rectus femoris activity than overground walking. Minimal differences in semitendinosus activation were observed between conditions, limited to lower peak activity during cycling compared to treadmill walking. These results provide normative values for rectus femoris and semitendinosus activation for different locomotor training methods and may assist in selecting the most appropriate training device for specific patients. Clinicians and researchers should also consider the kinematic and kinetic differences between tasks, which cannot necessarily be inferred from muscle activation patterns. 2010 Published by Elsevier B.V.
C1 [Prosser, Laura A.; Stanley, Christopher J.; Norman, Tracy L.; Park, Hyung S.; Damiano, Diane L.] NIH, Funct & Appl Biomech Sect, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Damiano, DL (reprint author), NIH, Funct & Appl Biomech Sect, Dept Rehabil Med, Ctr Clin, Bldg 10,Room 1-1469, Bethesda, MD 20892 USA.
EM damianod@cc.nih.gov
RI Park, Hyung-Soon/B-3334-2010; Prosser, Laura/C-1242-2009; Van Mulders,
Benjamin/P-1241-2014; Damiano, Diane/B-3338-2010
OI Park, Hyung-Soon/0000-0003-4274-7420; Damiano, Diane/0000-0002-2770-5356
FU NIH Clinical Center
FX This work was funded by the Intramural Research Program at the NIH
Clinical Center.
NR 18
TC 15
Z9 15
U1 0
U2 7
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0966-6362
J9 GAIT POSTURE
JI Gait Posture
PD FEB
PY 2011
VL 33
IS 2
BP 244
EP 250
DI 10.1016/j.gaitpost.2010.11.013
PG 7
WC Neurosciences; Orthopedics; Sport Sciences
SC Neurosciences & Neurology; Orthopedics; Sport Sciences
GA 737LF
UT WOS:000288569600018
PM 21215636
ER
PT J
AU Boykin, S
Diez-Roux, AV
Carnethon, M
Shrager, S
Ni, HY
Whitt-Glover, M
AF Boykin, Shawn
Diez-Roux, Ana V.
Carnethon, Mercedes
Shrager, Sandi
Ni, Hanyu
Whitt-Glover, Melicia
TI Racial/ethnic Heterogeneity in the Socioeconomic Patterning of CVD Risk
Factors: in the United States: The Multi-Ethnic Study of Atherosclerosis
SO JOURNAL OF HEALTH CARE FOR THE POOR AND UNDERSERVED
LA English
DT Article
DE Cardiovascular disease; risk factors; socioeconomic status; race;
ethnicity
ID CORONARY-HEART-DISEASE; BODY-MASS INDEX; NUTRITION EXAMINATION SURVEY;
3RD NATIONAL-HEALTH; CARDIOVASCULAR-DISEASE; BLOOD-PRESSURE;
SERUM-LIPIDS; MORTALITY; EDUCATION; RACE
AB Many studies document racial variation, gender differences, and socioeconomic status (SES) patterning in cardiovascular disease (CVD) risk factors but few studies have investigated heterogeneity in SES differences by race/ethnicity or gender. Using data from the Multi-Ethnic Study of Atherosclerosis (N=6,814) and stratified regression models, we investigated race/ethnic differences in the SES patterning of diabetes, hypertension, smoking, and body mass index (BMI). Inverse socioeconomic gradients in hypertension, diabetes, smoking, and BMI were observed in White and Black women but associations were weaker or absent in Hispanic and Chinese women (except in the case of diabetes for Hispanic women). Even greater heterogeneity in social patterning of risk factors was observed in men. In White men all four risk factors were inversely associated with socioeconomic position, although often associations were only present or were stronger for education than for income. The inverse socioeconomic patterning was much less consistent in men of other races/ethnic groups, and higher SES was associated with higher BMI in non-White men. These findings have implications for understanding the causes of social patterning, for the analysis of SES adjusted race/ethnic differences, and for the targeting of interventions.
C1 [Boykin, Shawn] Univ Michigan, Sch Publ Hlth, Ctr Integrat Approaches Hlth Dispar, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Diez-Roux, Ana V.] Univ Michigan, Ctr Social Epidemiol Populat Hlth, Dept Epidemiol, Ann Arbor, MI 48109 USA.
[Carnethon, Mercedes] Northeastern Univ, Feinberg Sch Med, Dept Preventat Med, Boston, MA USA.
[Shrager, Sandi] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Ni, Hanyu] NHLBI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD USA.
[Whitt-Glover, Melicia] Gramercy Res Grp, Winston Salem, NC USA.
RP Boykin, S (reprint author), Univ Michigan, Sch Publ Hlth, Ctr Integrat Approaches Hlth Dispar, Dept Epidemiol, 1415 Washington Hts,3645 SPH Tower 1, Ann Arbor, MI 48109 USA.
EM sdhb@umich.edu
FU NHLBI NIH HHS [N01HC95169, N01HC95165, N01-HC-95159, N01-HC-95165,
N01-HC-95169, N01HC95159]; NIMHD NIH HHS [P60 MD002249-03, P60 MD002249]
NR 41
TC 28
Z9 28
U1 0
U2 6
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
21218-4363 USA
SN 1049-2089
J9 J HEALTH CARE POOR U
JI J. Health Care Poor Underserved
PD FEB
PY 2011
VL 22
IS 1
BP 111
EP 127
PG 17
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 718ZK
UT WOS:000287165100010
PM 21317510
ER
PT J
AU Dunton, GF
Atienza, AA
Tscherne, J
Rodriguez, D
AF Dunton, Genevieve Fridlund
Atienza, Audie A.
Tscherne, James
Rodriguez, Daniel
TI Identifying Combinations of Risk and Protective Factors Predicting
Physical Activity Change in High School Students
SO PEDIATRIC EXERCISE SCIENCE
LA English
DT Article
ID DEPRESSIVE SYMPTOMS; ADOLESCENT GIRLS; UNITED-STATES; BEHAVIOR
SURVEILLANCE; LOGISTIC-REGRESSION; MIDDLE SCHOOL; SMOKING; YOUTH;
QUESTIONNAIRE; VALIDATION
AB Research sought to identify combinations of risk and protective factors predicting change in physical activity (PA) over one year in high school students. Adolescents (N = 344; M = 15.7 years) participated in a longitudinal study with assessment of demographics, substance use/smoking exposure, height and weight, psychological factors, and PA in 10th and 11th grade. PA participation in 11th grade was greatest for adolescents who engaged in PA and had high sports competence (78%), and least for adolescents who did not engage in or enjoy PA (13%) in 10th grade. Identifying adolescent subgroups at risk for decreasing PA can inform the development of tailored interventions.
C1 [Dunton, Genevieve Fridlund] Univ So Calif, Dept Prevent Med, Alhambra, CA USA.
[Atienza, Audie A.] NCI, Hlth Promot Res Branch, Rockville, MD USA.
[Tscherne, James; Rodriguez, Daniel] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
RP Dunton, GF (reprint author), Univ So Calif, Dept Prevent Med, Alhambra, CA USA.
FU Prevent Cancer Foundation (Rodriguez, PI)
FX This work was supported by the Prevent Cancer Foundation (Rodriguez,
PI).
NR 42
TC 2
Z9 2
U1 0
U2 0
PU HUMAN KINETICS PUBL INC
PI CHAMPAIGN
PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA
SN 0899-8493
J9 PEDIATR EXERC SCI
JI Pediatr. Exerc. Sci.
PD FEB
PY 2011
VL 23
IS 1
BP 106
EP 121
PG 16
WC Pediatrics; Physiology; Sport Sciences
SC Pediatrics; Physiology; Sport Sciences
GA 737UC
UT WOS:000288592700012
PM 21467595
ER
PT J
AU Major, EO
Ryschkewitsch, CF
Jensen, PN
Monaco, MC
AF Major, Eugene O.
Ryschkewitsch, Caroline F.
Jensen, Peter N.
Monaco, Maria Chiara
TI Assay Design and Sample Collection Can Affect Anti-John Cunningham Virus
Antibody Detection Reply
SO ANNALS OF NEUROLOGY
LA English
DT Letter
C1 [Major, Eugene O.; Ryschkewitsch, Caroline F.; Jensen, Peter N.; Monaco, Maria Chiara] NINDS, Lab Mol Med & Neurosci, NIH, Bethesda, MD 20892 USA.
RP Major, EO (reprint author), NINDS, Lab Mol Med & Neurosci, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z01 NS003049-02]
NR 4
TC 2
Z9 2
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0364-5134
J9 ANN NEUROL
JI Ann. Neurol.
PD FEB
PY 2011
VL 69
IS 2
BP 430
EP 431
DI 10.1002/ana.22364
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 733TD
UT WOS:000288284900035
PM 21387394
ER
PT J
AU Hirankarn, S
Hammer, GB
Schulman, SR
Drover, DR
Dombrowsky, E
Zajicek, A
Cohane, C
Barrett, JS
AF Hirankarn, S.
Hammer, G. B.
Schulman, S. R.
Drover, D. R.
Dombrowsky, E.
Zajicek, A.
Cohane, C.
Barrett, J. S.
TI POPULATION K-PD MODEL OF SODIUM NITROPRUSSIDE IN CHILDREN
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Meeting Abstract
CT 112th Annual Meeting of the
American-Society-for-Clinical-Pharmacology-and-Therapeutics
CY MAR 02-05, 2011
CL Dallas, TX
SP Amer Soc Clin Pharmacol & Therapeut
C1 [Hirankarn, S.; Dombrowsky, E.; Barrett, J. S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Hammer, G. B.; Drover, D. R.; Cohane, C.] Stanford Univ, Palo Alto, CA 94304 USA.
[Schulman, S. R.] Duke Univ, Durham, NC USA.
[Zajicek, A.] NICHD, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD FEB
PY 2011
VL 89
SU 1
BP S55
EP S55
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 712DE
UT WOS:000286644100176
ER
PT J
AU Peer, CJ
Sissung, TM
Jain, L
Woo, S
Gardner, ER
Kirkland, CT
English, BC
Federspiel, J
Figg, WD
AF Peer, C. J.
Sissung, T. M.
Jain, L.
Woo, S.
Gardner, E. R.
Kirkland, C. T.
English, B. C.
Federspiel, J.
Figg, W. D.
TI SORAFENIB IS AN INHIBITOR OF UGT1A1 BUT IS METABOLIZED BY UGT1A9:
IMPLICATIONS OF UGT1A GENETIC VARIANTS ON SORAFENIB EXPOSURE AND
SORAFENIB-INDUCED HYPERBILIRUBINEMIA
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Meeting Abstract
CT 112th Annual Meeting of the
American-Society-for-Clinical-Pharmacology-and-Therapeutics
CY MAR 02-05, 2011
CL Dallas, TX
SP Amer Soc Clin Pharmacol & Therapeut
C1 [Peer, C. J.; Sissung, T. M.; Jain, L.; Woo, S.; Gardner, E. R.; English, B. C.; Figg, W. D.] NCI, Clin Pharmacol Program, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Kirkland, C. T.] NCI, Mol Pharmacol Sect, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Federspiel, J.] Georgetown Coll, Dept Chem, Georgetown, KY USA.
RI Figg Sr, William/M-2411-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD FEB
PY 2011
VL 89
SU 1
BP S46
EP S47
PG 2
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 712DE
UT WOS:000286644100147
ER
PT J
AU Sissung, T
Fernandez, E
Kirkland, CT
Gardner, ER
Venzon, D
Kelly, R
Bates, SE
Figg, WD
AF Sissung, T.
Fernandez, E.
Kirkland, C. T.
Gardner, E. R.
Venzon, D.
Kelly, R.
Bates, S. E.
Figg, W. D.
TI ABCB1 POLYMORPHISMS ARE ASSOCIATED WITH TARIQUIDAR-INDUCED INCREASES IN
DOCETAXEL HALF-LIFE.
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Meeting Abstract
CT 112th Annual Meeting of the
American-Society-for-Clinical-Pharmacology-and-Therapeutics
CY MAR 02-05, 2011
CL Dallas, TX
SP Amer Soc Clin Pharmacol & Therapeut
C1 [Sissung, T.; Fernandez, E.; Kirkland, C. T.; Gardner, E. R.; Venzon, D.; Kelly, R.; Bates, S. E.; Figg, W. D.] NCI, Bethesda, MD 20892 USA.
RI Figg Sr, William/M-2411-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0009-9236
J9 CLIN PHARMACOL THER
JI Clin. Pharmacol. Ther.
PD FEB
PY 2011
VL 89
SU 1
BP S75
EP S75
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 712DE
UT WOS:000286644100242
ER
PT J
AU Vyas, NS
Patel, NH
Puri, BK
AF Vyas, Nora S.
Patel, Neva H.
Puri, Basant K.
TI Neurobiology and phenotypic expression in early onset schizophrenia
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Review
DE adolescence; cognition; imaging; intelligence; prognosis; schizophrenia
ID CARDIO-FACIAL SYNDROME; FIRST-EPISODE SCHIZOPHRENIA; 22Q11 DELETION
SYNDROME; COPY-NUMBER VARIATION; LONG-TERM COURSE; GRAY-MATTER LOSS;
CHILDHOOD-ONSET; ADOLESCENT-ONSET; FOLLOW-UP; PREMORBID ADJUSTMENT
AB Aim:
Early-onset schizophrenia (onset before adulthood) is a rare and severe form of the disorder that shows phenotypic and neurobiological continuity with adult-onset schizophrenia. Here, we provide a synthesis of keynote findings in this enriched population to understand better the neurobiology and pathophysiology of early-onset schizophrenia.
Methods:
A synthetic and integrative approach is applied to review studies stemming from epidemiology, phenomenology, cognition, genetics and neuroimaging data. We provide conclusions and future directions of research on early-onset schizophrenia.
Results:
Childhood and adolescent-onset schizophrenia is associated with severe clinical course, greater rates of premorbid abnormalities, poor psychosocial functioning and increased severity of brain abnormalities. Early-onset cases show similar neurobiological correlates and phenotypic deficits to adult-onset schizophrenia, but show worse long-term psychopathological outcome. Emerging technological advances have provided important insights into the genomic architecture of early-onset schizophrenia, suggesting that some genetic variations may occur more frequently and at a higher rate in young-onset than adult-onset cases.
Conclusions:
Clinical, cognitive, genetic and imaging data suggest increased severity in early-onset schizophrenia. Studying younger-onset cases can provide useful insights into the neurobiological mechanisms of schizophrenia and the complexity of gene-environment interactions leading to the emergence of this debilitating disorder.
C1 [Vyas, Nora S.] Kings Coll London, Inst Psychiat, SGDP Ctr, London SE5 8AF, England.
[Vyas, Nora S.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Vyas, Nora S.] Imperial Coll Healthcare NHS Trust, Hammersmith Hosp, Dept Nucl Med, London, England.
[Patel, Neva H.] Imperial Coll Healthcare NHS Trust, Hammersmith Hosp, Radiol Sci Unit, London, England.
[Puri, Basant K.] Imperial Coll Healthcare NHS Trust, Hammersmith Hosp, Dept Imaging, London, England.
[Puri, Basant K.] Univ Limerick, Fac Educ & Hlth Sci, Limerick, Ireland.
RP Vyas, NS (reprint author), Kings Coll London, Inst Psychiat, SGDP Ctr, POB 66,Crespigny Pk, London SE5 8AF, England.
EM drnoravyas@gmail.com
RI Vyas, Nora/C-3570-2011
FU US-UK Fulbright Commission
FX Dr Nora S Vyas is supported by the Distinguished Scholar Award by the
US-UK Fulbright Commission. The US-UK Fulbright Commission had no
further role in writing this review; and in the decision to submit the
paper for publication.
NR 151
TC 28
Z9 29
U1 9
U2 20
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1751-7885
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD FEB
PY 2011
VL 5
IS 1
BP 3
EP 14
DI 10.1111/j.1751-7893.2010.00253.x
PG 12
WC Psychiatry
SC Psychiatry
GA 712LZ
UT WOS:000286669600002
PM 21272270
ER
PT J
AU Madan, RA
Gulley, JL
AF Madan, Ravi A.
Gulley, James L.
TI Sipuleucel-T: harbinger of a new age of therapeutics for prostate cancer
SO EXPERT REVIEW OF VACCINES
LA English
DT Article
DE cancer treatment; cancer vaccine; immunotherapy; prostate cancer
ID ANDROGEN-DEPRIVATION THERAPY; COMBINATION THERAPY; PHASE-II; ABIRATERONE
ACETATE; ANTITUMOR-ACTIVITY; IMMUNE-RESPONSES; ACID-PHOSPHATASE;
DENDRITIC CELLS; PLUS PREDNISONE; END-POINTS
AB Sipuleucel-T (Provenge (R)) is the first therapeutic cancer vaccine approved by the US FDA. The approval heralds the long-awaited promise of improved patient survival with minimal toxicity by therapies designed to generate an active, specific anticancer immune response. The development of this first-in-class agent as well as other therapeutic vaccines in clinical evaluation has also led to a better understanding of relevant patient populations and end points for clinical trials. This article discusses the development and approval of sipuleucel-T in the context of other approved therapies for prostate cancer, as well as controversies and novel paradigms brought about by this new agent.
C1 [Madan, Ravi A.; Gulley, James L.] NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Madan, Ravi A.; Gulley, James L.] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Gulley, JL (reprint author), NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, 10 Ctr Dr,8B09 MSC 1750, Bethesda, MD 20892 USA.
EM gulleyj@mail.nih.gov
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
FU Intramural NIH HHS [Z01 BC010666-03]
NR 77
TC 9
Z9 12
U1 1
U2 3
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1476-0584
EI 1744-8395
J9 EXPERT REV VACCINES
JI Expert Rev. Vaccines
PD FEB
PY 2011
VL 10
IS 2
BP 141
EP 150
DI 10.1586/ERV.10.173
PG 10
WC Immunology
SC Immunology
GA 732NM
UT WOS:000288192200006
PM 21332262
ER
PT J
AU Landgren, O
Polliack, A
Tadmor, T
AF Landgren, Ola
Polliack, Aaron
Tadmor, Tamar
TI Associations between multiple myeloma and other malignancies
SO LEUKEMIA & LYMPHOMA
LA English
DT Editorial Material
C1 [Landgren, Ola] NCI, Multiple Myeloma Sect, NIH, Ctr Canc Res,Med Oncol Branch, Bethesda, MD 20892 USA.
[Polliack, Aaron] Hebrew Univ Jerusalem, Sch Med, Hadassah Univ Hosp, Dept Hematol, IL-91010 Jerusalem, Israel.
[Tadmor, Tamar] Bnai Zion Med Ctr, Hematol Oncol Unit, Haifa, Israel.
RP Landgren, O (reprint author), NCI, Multiple Myeloma Sect, NIH, Ctr Canc Res,Med Oncol Branch, 9000 Rockville Pike,Bldg 10,Room 13N240, Bethesda, MD 20892 USA.
EM landgreo@mail.nih.gov
NR 9
TC 3
Z9 3
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1042-8194
J9 LEUKEMIA LYMPHOMA
JI Leuk. Lymphoma
PD FEB
PY 2011
VL 52
IS 2
BP 161
EP 162
DI 10.3109/10428194.2010.538942
PG 2
WC Oncology; Hematology
SC Oncology; Hematology
GA 717ZV
UT WOS:000287089100003
PM 21261502
ER
PT J
AU Maddali, K
Kumar, V
Marchand, C
Pommier, Y
Malhotra, SV
AF Maddali, Kasthuraiah
Kumar, Vineet
Marchand, Christophe
Pommier, Yves
Malhotra, Sanjay V.
TI Biological evaluation of imidazolium- and ammonium-based salts as HIV-1
integrase inhibitors
SO MEDCHEMCOMM
LA English
DT Article
ID BETA-DIKETO ACIDS; CELL-LINE HELA; IONIC LIQUIDS; ANTI-HIV; STRAND
TRANSFER; NUCLEOBASE SCAFFOLDS; CATIONIC SURFACTANTS; VIRAL REPLICATION;
CATALYTIC DOMAIN; DNA
AB Ammonium- and imidazolium-based ionic salts were studied for their application as inhibitors of HIV-1 integrase (IN). These compounds were active in the inhibition of both the 3'-processing (3'-P) and strand transfer (ST) steps of the integration reaction. A correlation of activity with chain length of the alkyl substituent in both classes of ionic salts was observed.
C1 [Maddali, Kasthuraiah; Marchand, Christophe; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kumar, Vineet; Malhotra, Sanjay V.] NCI, Lab Synthet Chem, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Pommier, Y (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM pommier@nih.gov; malhotrasa@mail.nih.gov
FU National Cancer Institute (NCI); NCI, National Institutes of Health
[HSN261200800001E]; Center for Cancer Research
FX The authors would like to thank the National Cancer Institute (NCI)
Developmental Therapeutics Program. This project has been funded in
whole or in part with federal funds from the NCI, National Institutes of
Health, under Contract No. HSN261200800001E. KM and YP are supported by
the Center for Cancer Research, NIH Intramural Program of the National
Cancer institute. 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 60
TC 6
Z9 6
U1 0
U2 3
PU ROYAL SOC CHEMISTRY
PI CAMBRIDGE
PA THOMAS GRAHAM HOUSE, SCIENCE PARK, MILTON RD, CAMBRIDGE CB4 0WF, CAMBS,
ENGLAND
SN 2040-2503
J9 MEDCHEMCOMM
JI MedChemComm
PD FEB
PY 2011
VL 2
IS 2
BP 143
EP 150
DI 10.1039/c0md00201a
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 733XF
UT WOS:000288297100008
ER
PT J
AU Charizopoulou, N
Lelli, A
Schraders, M
Ray, K
Hildebrand, MS
Ramesh, A
Srisailapathy, CRS
Oostrik, J
Admiraal, RJC
Neely, HR
Latoche, JR
Smith, RJH
Northup, JK
Kremer, H
Holt, JR
Noben-Trauth, K
AF Charizopoulou, Nikoletta
Lelli, Andrea
Schraders, Margit
Ray, Kausik
Hildebrand, Michael S.
Ramesh, Arabandi
Srisailapathy, C. R. Srikumari
Oostrik, Jaap
Admiraal, Ronald J. C.
Neely, Harold R.
Latoche, Joseph R.
Smith, Richard J. H.
Northup, John K.
Kremer, Hannie
Holt, Jeffrey R.
Noben-Trauth, Konrad
TI Gipc3 mutations associated with audiogenic seizures and sensorineural
hearing loss in mouse and human
SO NATURE COMMUNICATIONS
LA English
DT Article
ID BLACK-SWISS MICE; INNER HAIR CELL; MYOSIN-VI; PDZ DOMAIN; G-PROTEIN;
RGS-GAIP; GENE; IMPAIRMENT; RECEPTOR; DEAFNESS
AB Sensorineural hearing loss affects the quality of life and communication of millions of people, but the underlying molecular mechanisms remain elusive. Here, we identify mutations in Gipc3 underlying progressive sensorineural hearing loss (age-related hearing loss 5, ahl5) and audiogenic seizures (juvenile audiogenic monogenic seizure 1, jams1) in mice and autosomal recessive deafness DFNB15 and DFNB95 in humans. Gipc3 localizes to inner ear sensory hair cells and spiral ganglion. A missense mutation in the PDZ domain has an attenuating effect on mechanotransduction and the acquisition of mature inner hair cell potassium currents. Magnitude and temporal progression of wave I amplitude of afferent neurons correlate with susceptibility and resistance to audiogenic seizures. The Gipc3(343A) allele disrupts the structure of the stereocilia bundle and affects long-term function of auditory hair cells and spiral ganglion neurons. Our study suggests a pivotal role of Gipc3 in acoustic signal acquisition and propagation in cochlear hair cells.
C1 [Charizopoulou, Nikoletta; Neely, Harold R.; Latoche, Joseph R.; Noben-Trauth, Konrad] Natl Inst Deafness & Other Commun Disorders, Neurogenet Sect, Mol Biol Lab, NIH, Rockville, MD 20850 USA.
[Lelli, Andrea; Holt, Jeffrey R.] Univ Virginia, Dept Neurosci & Otolaryngol, Sch Med, Charlottesville, VA 22908 USA.
[Schraders, Margit; Oostrik, Jaap; Admiraal, Ronald J. C.; Kremer, Hannie] Radboud Univ Nijmegen, Dept Otorhinolaryngol, Donders Inst Brain Cognit & Behav, Med Ctr, NL-6525 GA Nijmegen, Netherlands.
[Schraders, Margit; Oostrik, Jaap; Kremer, Hannie] Radboud Univ Nijmegen, Nijmegen Ctr Mol Life Sci, NL-6525 GA Nijmegen, Netherlands.
[Ray, Kausik; Northup, John K.] Natl Inst Deafness & Other Commun Disorders, Sect Signal Transduct, Lab Cellular Biol, NIH, Rockville, MD 20850 USA.
[Hildebrand, Michael S.; Smith, Richard J. H.] Univ Iowa, Dept Otolaryngol, Iowa City, IA 52242 USA.
[Ramesh, Arabandi; Srisailapathy, C. R. Srikumari] Univ Madras, Dept Genet, Madras, Tamil Nadu, India.
RP Noben-Trauth, K (reprint author), Natl Inst Deafness & Other Commun Disorders, Neurogenet Sect, Mol Biol Lab, NIH, Rockville, MD 20850 USA.
EM nobentk@nidcd.nih.gov
RI Kremer, Hannie/F-5126-2010; Admiraal, R.J.C./L-4171-2015; Schraders,
Margit/A-1607-2016; Oostrik, Jaap/A-1703-2016;
OI Kremer, Hannie/0000-0002-0841-8693; Hildebrand,
Michael/0000-0003-2739-0515
FU Division of Intramural Research at NIH/NIDCD; NIH/NIDCD [DC05439,
DC002842]; RNID [GR36]; Fonds NutsOhra [SNO-T-0702-102]; EU
[LSHG-CT-2004-512063]; Oticon Foundation; University Grants Commission
Research Scientist Scheme in New Delhi, India
FX We thank Feng Qian, Katerina Vorvolakos and Dennis Drayna for comments
on the manuscript. We also thank Charles Askew for assistance with
cochlear dissections, M'Hamed Grati and Leonardo De Andrade for SEM
imaging, Glen Martin for help with the DPOAEs and Eric Wawrousek of the
NEI transgenic core facility. This work was supported by the Division of
Intramural Research at NIH/NIDCD (K.N.-T. and J.K.N.), NIH/NIDCD grants
DC05439 (J.R.H.) and DC002842 (R.J.H.S.). M.S. was supported by RNID
GR36 and H.K. received funds from Fonds NutsOhra (SNO-T-0702-102), the
EU (LSHG-CT-2004-512063), and the Oticon Foundation. C.R.S.S. was
supported by the University Grants Commission Research Scientist Scheme
in New Delhi, India. M.S.H. was supported by an Australian NHMRC
Overseas Biomedical Postdoctoral Training Fellowship.
NR 46
TC 37
Z9 39
U1 1
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 FEB
PY 2011
VL 2
AR 201
DI 10.1038/ncomms1200
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 732YP
UT WOS:000288225900030
PM 21326233
ER
PT J
AU Kim, JH
Wu, TH
Budde, MD
Lee, JM
Song, SK
AF Kim, Joong Hee
Wu, Tzy-Haw
Budde, Matthew D.
Lee, Jin-Moo
Song, Sheng-Kwei
TI Noninvasive detection of brainstem and spinal cord axonal degeneration
in an amyotrophic lateral sclerosis mouse model
SO NMR IN BIOMEDICINE
LA English
DT Article
DE diffusion tensor imaging; mice; cervical spinal cord; axial and radial
diffusivity; diffusion anisotropy; G93A-SOD1; amyotrophic lateral
sclerosis
ID MOTOR-NEURON DEGENERATION; MULTIPLE-SCLEROSIS; TRANSGENIC MICE;
DIFFUSION; ALS; INJURY; MRI; DISEASE; NEURODEGENERATION; MARKERS
AB Degeneration of motor neurons and their associated axons is a hallmark of amyotrophic lateral sclerosis, but reliable noninvasive lesion detection is lacking. In vivo diffusion tensor imaging was performed to evaluate neurodegeneration in the brainstem and cervical spinal cord of wild-type and G93A-SOD1 transgenic mice, an animal model of amyotrophic lateral sclerosis. A statistically significant reduction in the apparent diffusion coefficient was observed in the motor nuclei VII and XII of G93A-SOD1 transgenic mice relative to wild-type mice. No significant difference in diffusion anisotropy was observed in dorsal white or gray matter in cervical and lumbar segments of the spinal cord. In contrast, statistically significant decreases in axial diffusivity (diffusivity parallel to the axis of the spinal cord) and apparent diffusion coefficient were found in the ventrolateral white matter of G93A-SOD1 mice in both the cervical and lumbar spinal cord. The reduction in axial diffusivity, suggestive of axonal injury, in the white matter of the spinal cord of G93A-SOD1 mice was verified by immunostaining with nonphosphorylated neurofilament. The present study demonstrates that in vivo diffusion tensor imaging-derived axial diffusivity may be used to accurately evaluate axonal degeneration in an animal model of amyotrophic lateral sclerosis. Copyright (C) 2010 John Wiley & Sons, Ltd.
C1 [Kim, Joong Hee] Washington Univ, Sch Med, Biomed MR Lab, Dept Radiol, St Louis, MO 63110 USA.
[Wu, Tzy-Haw] Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan.
[Budde, Matthew D.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Lee, Jin-Moo] Washington Univ, Sch Med, Hope Ctr Neurol Disorders, St Louis, MO 63110 USA.
[Lee, Jin-Moo] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
RP Kim, JH (reprint author), Washington Univ, Sch Med, Biomed MR Lab, Dept Radiol, Campus Box 8227,Room 2313,4525 Scott Ave, St Louis, MO 63110 USA.
EM jhkim@bmr.wustl.edu
FU National Multiple Sclerosis Society [RG 3376-A-2/1, CA 1012-A-13];
National Institutes of Health [R01 NS047592, R01 NS048283, P01 NS032636,
R01 NS48283, R01 NS67905, P01NS32636]; University of Missouri;
Washington University Small Animal Imaging Resource (WUSAIR) [NIH: R24
CA83060]; Animal Models Core of the Hope Center for Neurological
Disorders
FX This study was supported in part by the National Multiple Sclerosis
Society (RG 3376-A-2/1 and CA 1012-A-13), National Institutes of Health
(R01 NS047592, R01 NS048283, P01 NS032636, R01 NS48283, R01 NS67905,
P01NS32636), University of Missouri Spinal Cord Injuries Program, and
the Washington University Small Animal Imaging Resource (WUSAIR) (NIH:
R24 CA83060) and the Animal Models Core of the Hope Center for
Neurological Disorders.
NR 46
TC 11
Z9 12
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0952-3480
J9 NMR BIOMED
JI NMR Biomed.
PD FEB
PY 2011
VL 24
IS 2
BP 163
EP 169
DI 10.1002/nbm.1567
PG 7
WC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
SC Biophysics; Radiology, Nuclear Medicine & Medical Imaging; Spectroscopy
GA 732SG
UT WOS:000288209300006
PM 21344532
ER
PT J
AU Yang, ZW
Li, DJ
Liu, C
Han, P
Yang, YL
Su, DF
Shen, FM
AF Yang, Zhong-wei
Li, Dong-jie
Liu, Chong
Han, Ping
Yang, Yi-li
Su, Ding-feng
Shen, Fu-ming
TI Role of vascular K-ATP channels in blood pressure variability after
sinoaortic denervation in rats
SO ACTA PHARMACOLOGICA SINICA
LA English
DT Article
DE ATP-sensitive potassium channels; blood pressure variability; sinoaotic
denervation
ID SENSITIVE POTASSIUM CHANNELS; LEFT-VENTRICULAR HYPERTROPHY;
SMOOTH-MUSCLE-CELLS; PROTEIN-KINASE-C; ARTERIAL-PRESSURE; CONSCIOUS RAT;
ORGAN DAMAGE; LABILITY; HYPERTENSION; KIR6.1
AB Aim: To investigate the role of ATP-sensitive potassium (K-ATP) channels on blood pressure variability (BPV) in sinoaortic denervated (SAD) rats.
Methods: SAD was performed on male Sprague-Dawley rats 4 weeks before the study. mRNA expression of Kir6.1, Kir6.2 and SUR2 in aorta and mesenteric artery was determined using real-time quantitative polymerase chain reaction, and confirmed at the protein level using Western blotting and laser confocal immunofluorescence assays. Concentration-response curves of isolated aortic and mesenteric arterial rings to adenosine and pinacidil were established. Effects of K-ATP channel openers and blocker on BPV were examined in conscious SAD rats.
Results: Aortic SUR2 expression was significantly greater, while Kir6.1 was lower, in SAD rats than in sham-operated controls. In contrast, in the mesenteric artery both SUR2 and Kir6.1 expression were markedly lower in SAD rats than controls. For both arteries, Kir6.2 expression was indistinguishable between sham-operated and SAD rats. These findings were confirmed at the protein level. Responses of the aorta to both adenosine and pinacidil were enhanced after SAD, while the mesenteric response to adenosine was attenuated. Pinacidil, diazoxide, nicorandil, and glibenclamide significantly decreased BPV.
Conclusion: These findings indicate that expression of vascular K-ATP channels is altered by chronic SAD. These alterations influence vascular reactivity, and may play a role in the increased BPV in chronic SAD rats.
C1 [Yang, Zhong-wei; Li, Dong-jie; Liu, Chong; Han, Ping; Su, Ding-feng; Shen, Fu-ming] Second Mil Med Univ, Sch Pharm, Dept Pharmacol, Shanghai 200433, Peoples R China.
[Yang, Yi-li] NCI, Canc & Dev Biol Lab, NIH, Frederick, MD 21702 USA.
RP Shen, FM (reprint author), Second Mil Med Univ, Sch Pharm, Dept Pharmacol, Shanghai 200433, Peoples R China.
EM fumingshen@126.com
FU National Natural Science Foundation of China [81070118]; Shanghai
Municipal Education Commission [10ZZ52]; National Basic Research Program
of China [2009CB521900]
FX This work was supported in part by the grants from National Natural
Science Foundation of China (81070118), Shanghai Municipal Education
Commission (10ZZ52), and the National Basic Research Program of China
(2009CB521900).
NR 36
TC 5
Z9 5
U1 0
U2 6
PU ACTA PHARMACOLOGICA SINICA
PI SHANGHAI
PA 294 TAI-YUAN RD, SHANGHAI, 200031, PEOPLES R CHINA
SN 1671-4083
EI 1745-7254
J9 ACTA PHARMACOL SIN
JI Acta Pharmacol. Sin.
PD FEB
PY 2011
VL 32
IS 2
BP 194
EP 200
DI 10.1038/aps.2010.195
PG 7
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA 716KT
UT WOS:000286968200009
PM 21293472
ER
PT J
AU Flatz, L
Roychoudhuri, R
Honda, M
Filali, A
Goulet, JP
Kettaf, N
Roederer, M
Haddad, E
Sekaly, RP
Nabel, GJ
AF Flatz, L.
Roychoudhuri, R.
Honda, M.
Filali, A.
Goulet, J. P.
Kettaf, N.
Roederer, M.
Haddad, E.
Sekaly, R. P.
Nabel, G. J.
TI Single cell gene expression profiling reveals qualitatively distinct CD8
T cells elicited by different gene-based vaccines
SO ALLERGOLOGIE
LA English
DT Meeting Abstract
C1 [Flatz, L.] CHUV, Inst Dermatol, Lausanne, Switzerland.
[Roychoudhuri, R.; Honda, M.; Roederer, M.; Nabel, G. J.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Filali, A.; Goulet, J. P.; Kettaf, N.; Haddad, E.; Sekaly, R. P.] Vaccine & Gene Therapy Inst, Port St Lucie, FL USA.
RI Roychoudhuri, Rahul/A-7442-2010
OI Roychoudhuri, Rahul/0000-0002-5392-1853
NR 0
TC 0
Z9 0
U1 0
U2 1
PU DUSTRI-VERLAG DR KARL FEISTLE
PI DEISENHOFEN-MUENCHEN
PA BAHNHOFSTRASSE 9 POSTFACH 49, D-82032 DEISENHOFEN-MUENCHEN, GERMANY
SN 0344-5062
J9 ALLERGOLOGIE
JI Allergologie
PD FEB
PY 2011
VL 34
IS 2
BP 81
EP 81
PG 1
WC Allergy
SC Allergy
GA 727XM
UT WOS:000287836500016
ER
PT J
AU O'Brien, PMS
Backstrom, T
Brown, C
Dennerstein, L
Endicott, J
Epperson, CN
Eriksson, E
Freeman, E
Halbreich, U
Ismail, KMK
Panay, N
Pearlstein, T
Rapkin, A
Reid, R
Schmidt, P
Steiner, M
Studd, J
Yonkers, K
AF O'Brien, Patrick Michael Shaughn
Backstrom, Torbjorn
Brown, Candace
Dennerstein, Lorraine
Endicott, Jean
Epperson, C. Neill
Eriksson, Elias
Freeman, Ellen
Halbreich, Uriel
Ismail, Khaled M. K.
Panay, Nicholas
Pearlstein, Teri
Rapkin, Andrea
Reid, Robert
Schmidt, Peter
Steiner, Meir
Studd, John
Yonkers, Kimberley
TI Towards a consensus on diagnostic criteria, measurement and trial design
of the premenstrual disorders: the ISPMD Montreal consensus
SO ARCHIVES OF WOMENS MENTAL HEALTH
LA English
DT Review
DE PMS; PMDD; Premenstrual disorder; Diagnostic criteria; Quantification;
Trial design; International consensus
ID MENSTRUAL-CYCLE; DYSPHORIC DISORDER; HORMONES; WOMEN; MOOD; CYCLICITY
AB Premenstrual disorders (PMD) are characterised by a cluster of somatic and psychological symptoms of varying severity that occur during the luteal phase of the menstrual cycle and resolve during menses (Freeman and Sondheimer, Prim Care Companion J Clin Psychiatry 5:30-39, 2003; Halbreich, Gynecol Endocrinol 19:320-334, 2004). Although PMD have been widely recognised for many decades, their precise cause is still unknown and there are no definitive, universally accepted diagnostic criteria. To consider this issue, an international multidisciplinary group of experts met at a face-to-face consensus meeting to review current definitions and diagnostic criteria for PMD. This was followed by extensive correspondence. The consensus group formally became established as the International Society for Premenstrual Disorders (ISPMD). The inaugural meeting of the ISPMD was held in Montreal in September 2008. The primary aim was to provide a unified approach for the diagnostic criteria of PMD, their quantification and guidelines on clinical trial design. This report summarises their recommendations. It is hoped that the criteria proposed here will inform discussions of the next edition of the World Health Organisation's International Classification of Diseases (ICD-11), and the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-V) criteria that are currently under consideration. It is also hoped that the proposed definitions and guidelines could be used by all clinicians and investigators to provide a consistent approach to the diagnosis and treatment of PMD and to aid scientific and clinical research in this field.
C1 [O'Brien, Patrick Michael Shaughn] Keele Univ, Acad Unit Obstet & Gynaecol, Sch Med, Univ Hosp N Staffordshire, Stoke On Trent, Staffs, England.
[Backstrom, Torbjorn] Norrland Univ Hosp, Umea Neurosteroid Res Ctr, Dept Clin Sci, Umea, Sweden.
[Brown, Candace] Univ Tennessee, Ctr Hlth Sci, Dept Psychiat, Memphis, TN 38163 USA.
[Brown, Candace] Univ Tennessee, Ctr Hlth Sci, Dept Obstet, Memphis, TN 38163 USA.
[Brown, Candace] Univ Tennessee, Ctr Hlth Sci, Dept Gynaecol, Memphis, TN 38163 USA.
[Dennerstein, Lorraine] Univ Melbourne, Dept Psychiat, Melbourne, Vic, Australia.
[Dennerstein, Lorraine] Natl Ageing Res Inst, Melbourne, Vic, Australia.
[Reid, Robert] Queens Univ, Kingston, ON, Canada.
[Schmidt, Peter] NIMH, Sect Behav Endocrinol, Bethesda, MD 20892 USA.
[Steiner, Meir] McMaster Univ, Dept Psychiat, Hamilton, ON L8P3B6, Canada.
[Steiner, Meir] McMaster Univ, Dept Behav Neurosci, Hamilton, ON L8P3B6, Canada.
[Steiner, Meir] McMaster Univ, Dept Obstet, Hamilton, ON L8P3B6, Canada.
[Steiner, Meir] McMaster Univ, Dept Gynaecol, Hamilton, ON L8P3B6, Canada.
[Studd, John] Chelsea & Westminster Hosp, Dept Gynaecol, London, England.
[Epperson, C. Neill] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Yonkers, Kimberley] Dept Obstet, New Haven, CT USA.
[Yonkers, Kimberley] Dept Gynaecol, New Haven, CT USA.
[Halbreich, Uriel] SUNY Buffalo, Buffalo, NY 14260 USA.
[Halbreich, Uriel] WPA, New York, NY USA.
[Panay, Nicholas] Chelsea & Westminster Hosp, Dept Obstet & Gynaecol, London, England.
[Pearlstein, Teri] Brown Univ, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Rapkin, Andrea] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Endicott, Jean] Columbia Univ, Dept Psychiat, New York, NY USA.
[Epperson, C. Neill] Yale Univ, Sch Med, Dept Obstet & Gynaecol, New Haven, CT USA.
[Epperson, C. Neill] Yale Univ, Sch Med, Dept Reprod Sci, New Haven, CT USA.
[Eriksson, Elias] Univ Gothenburg, Inst Neurosci & Physiol, Gothenburg, Sweden.
[Freeman, Ellen] Univ Penn, Dept Psychiat, Philadelphia, PA 19104 USA.
[Freeman, Ellen] Univ Penn, Dept Obstet, Philadelphia, PA 19104 USA.
[Freeman, Ellen] Univ Penn, Dept Gynaecol, Philadelphia, PA 19104 USA.
RP O'Brien, PMS (reprint author), Keele Univ, Acad Unit Obstet & Gynaecol, Sch Med, Univ Hosp N Staffordshire, Stoke On Trent, Staffs, England.
EM pmsob@hotmail.co.uk
RI Steiner, Meir /B-2121-2016;
OI Steiner, Meir/0000-0001-7838-2246
FU NIDA NIH HHS [K24 DA030301, R01 DA018359]; NIMH NIH HHS [R01 MH064845]
NR 34
TC 50
Z9 51
U1 4
U2 10
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 1434-1816
J9 ARCH WOMEN MENT HLTH
JI Arch. Womens Ment. Health
PD FEB
PY 2011
VL 14
IS 1
BP 13
EP 21
DI 10.1007/s00737-010-0201-3
PG 9
WC Psychiatry
SC Psychiatry
GA 716BM
UT WOS:000286939900003
PM 21225438
ER
PT J
AU Zhang, LP
Ten Hagen, KG
AF Zhang, Liping
Ten Hagen, Kelly G.
TI The cellular microenvironment and cell adhesion: a role for
O-glycosylation
SO BIOCHEMICAL SOCIETY TRANSACTIONS
LA English
DT Article
DE cancer; cell adhesion; double-stranded RNA (dsRNA); Drosophila;
extracellular matrix (ECM); O-glycosylation; tumour
ID POLYPEPTIDE N-ACETYLGALACTOSAMINYLTRANSFERASE; PS2 INTEGRIN;
DROSOPHILA-MELANOGASTER; PROTEIN; TIGGRIN; LIGAND; REQUIREMENTS;
MUTATIONS; VIABILITY; BIOLOGY
AB Glycosylation is one of the most abundant protein modifications in Nature, having roles in protein stability, secretion and function. Alterations in mucin-type O-glycosylation are responsible for a number of human diseases and developmental defects, as well as associated with certain types of cancer. However, the mechanistic role of this form of glycosylation in many of these instances is unclear. Here we describe how one glycosyltransferase responsible for initiating mucin-type O-glycosylation (PGANT3), specifically modulates integrin-mediated cell adhesion by influencing the secretion and localization of an integrin ligand. The integrin ligand Tiggrin, is normally O-glycosylated and localized to the basal matrix, where adhesion of two opposing cell layers takes place. In pgant3 mutants, Tiggrin is no longer O-glycosylated and fails to be properly secreted to the basal cell layer interface, resulting in disruption of proper cell adhesion. pgant3-mediated effects are dependent on the enzymatic activity of PGANT3 and cannot be rescued by another pgant family member, indicating a unique role for this glycosyltransferase. These results provide in vivo evidence for the role of O-glycosylation in the secretion of specific extracellular matrix proteins, which thereby influences the composition of the cellular 'microenvironment' and modulates cell adhesion events. The studies described in this review provide insight into the long-standing association between aberrant O-glycosylation and tumorigenesis, as changes in tumour environment and cell adhesion are hallmarks of cancer progression.
C1 [Zhang, Liping; Ten Hagen, Kelly G.] NIDCR, Dev Glycobiol Unit, NIH, Bethesda, MD 20892 USA.
RP Ten Hagen, KG (reprint author), NIDCR, Dev Glycobiol Unit, NIH, Bethesda, MD 20892 USA.
EM Kelly.Tenhagen@nih.gov
FU National Institute of Dental and Craniofacial Research of the National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Dental and Craniofacial Research of the National
Institutes of Health.
NR 26
TC 11
Z9 11
U1 0
U2 14
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0300-5127
J9 BIOCHEM SOC T
JI Biochem. Soc. Trans.
PD FEB
PY 2011
VL 39
BP 378
EP 382
DI 10.1042/BST0390378
PN 1
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 722NC
UT WOS:000287438000070
PM 21265808
ER
PT J
AU Archer, TK
AF Archer, Trevor K.
TI The 26S proteasome: When degradation is just not enough!
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
LA English
DT Editorial Material
ID UBIQUITIN SYSTEM; DESTRUCTION; PROTEINS
C1 NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Archer, TK (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, 111 Alexander Dr,POB 12233,MD D4-01, Res Triangle Pk, NC 27709 USA.
EM archer1@niehs.nih.gov
NR 11
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-9399
J9 BBA-GENE REGUL MECH
JI Biochim. Biophys. Acta-Gene Regul. Mech.
PD FEB
PY 2011
VL 1809
IS 2
SI SI
BP 65
EP 66
DI 10.1016/j.bbagrm.2010.11.005
PG 2
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 722LR
UT WOS:000287434200001
PM 21130191
ER
PT J
AU Amarnath, S
Laurence, AD
Mariotti, J
Foley, JE
O'Shea, JJ
Fowler, DH
AF Amarnath, S.
Laurence, A. D.
Mariotti, J.
Foley, J. E.
O'Shea, J. J.
Fowler, D. H.
TI STAT3 PROMOTES BOTH NATURAL AND INDUCIBLE T REGULATORY CELL PLASTICITY
DURING MURINE ACUTE GVHD
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Amarnath, S.; Mariotti, J.; Foley, J. E.; Fowler, D. H.] NCI, CCR, Bethesda, MD 20892 USA.
[Laurence, A. D.; O'Shea, J. J.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 372
BP S288
EP S288
DI 10.1016/j.bbmt.2010.12.408
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500372
ER
PT J
AU Baird, K
Steinberg, SM
Grkovic, L
Pulanic, D
Cowen, EW
Mitchell, SA
Williams, KM
Datiles, M
Fall-Dickson, JM
Carpenter, A
Avila, DN
Taylor, T
Urban, A
Joe, G
Comis, L
Berger, A
Stratton, P
Shelhamer, J
Gea-Banacloche, J
Sportes, C
Fowler, DH
Bishop, MR
Gress, RE
Pavletic, SZ
AF Baird, K.
Steinberg, S. M.
Grkovic, L.
Pulanic, D.
Cowen, E. W.
Mitchell, S. A.
Williams, K. M.
Datiles, M.
Fall-Dickson, J. M.
Carpenter, A.
Avila, D. N.
Taylor, T.
Urban, A.
Joe, G.
Comis, L.
Berger, A.
Stratton, P.
Shelhamer, J.
Gea-Banacloche, J.
Sportes, C.
Fowler, D. H.
Bishop, M. R.
Gress, R. E.
Pavletic, S. Z.
TI VALIDATION OF THE NATIONAL INSTITUTES OF HEALTH (NIH) CONSENSUS CRITERIA
FOR CHRONIC GVHD (cGVHD) STAGING CORRELATED WITH ESTABLISHED INDICATORS
OF DISEASE SEVERITY AND PROGNOSIS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Baird, K.; Steinberg, S. M.; Grkovic, L.; Pulanic, D.; Cowen, E. W.; Mitchell, S. A.; Williams, K. M.; Datiles, M.; Fall-Dickson, J. M.; Carpenter, A.; Avila, D. N.; Taylor, T.; Urban, A.; Joe, G.; Comis, L.; Berger, A.; Stratton, P.; Shelhamer, J.; Gea-Banacloche, J.; Sportes, C.; Fowler, D. H.; Bishop, M. R.; Gress, R. E.; Pavletic, S. Z.] NIH, Bethesda, MD 20892 USA.
[Grkovic, L.; Pulanic, D.] Univ Hosp Ctr Zagreb, Zagreb, Croatia.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 27
BP S160
EP S161
DI 10.1016/j.bbmt.2010.12.033
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500028
ER
PT J
AU Battiwalla, M
McIver, Z
Draper, D
Haggerty, J
Koklanaris, E
Chawla, K
Superata, J
Childs, R
Kurlander, R
Stroncek, D
Khuu, H
Citrin, D
Sabatino, M
Leitman, S
Barrett, J
AF Battiwalla, M.
McIver, Z.
Draper, D.
Haggerty, J.
Koklanaris, E.
Chawla, K.
Superata, J.
Childs, R.
Kurlander, R.
Stroncek, D.
Khuu, H.
Citrin, D.
Sabatino, M.
Leitman, S.
Barrett, J.
TI 4-LOG EX-VIVO T-LYMPHOCYTE DEPLETED MYELOABLATIVE HLA-MATCHED SIBLING
TRANSPLANTS; A PLATFORM FOR ADOPTIVE IMMUNOTHERAPY INFLUENCED BY
CONDITIONING INTENSITY
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Battiwalla, M.; McIver, Z.; Draper, D.; Haggerty, J.; Koklanaris, E.; Chawla, K.; Superata, J.; Childs, R.; Barrett, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Kurlander, R.; Stroncek, D.; Khuu, H.; Sabatino, M.; Leitman, S.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Citrin, D.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 368
BP S287
EP S287
DI 10.1016/j.bbmt.2010.12.404
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500368
ER
PT J
AU Battiwalla, M
Le, RQ
Melenhorst, J
McIver, Z
Hill, B
Memon, S
Hensel, NF
Koklanaris, E
Keyvanfar, K
Hakim, FT
Douek, DC
Bevans, M
Mitchell, S
Barrett, J
AF Battiwalla, M.
Le, R. Q.
Melenhorst, J.
McIver, Z.
Hill, B.
Memon, S.
Hensel, N. F.
Koklanaris, E.
Keyvanfar, K.
Hakim, F. T.
Douek, D. C.
Bevans, M.
Mitchell, S.
Barrett, J.
TI SURVIVOR HEALTH AND IMMUNE RECONSTITUTION IN THE SECOND DECADE AFTER
ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Battiwalla, M.; Le, R. Q.; Melenhorst, J.; McIver, Z.; Hensel, N. F.; Koklanaris, E.; Keyvanfar, K.; Barrett, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Hill, B.; Douek, D. C.] NIAID, NIH, Bethesda, MD 20892 USA.
[Memon, S.; Hakim, F. T.] NCI, NIH, Bethesda, MD 20892 USA.
RI Memon, Sarfraz/E-1198-2013
NR 0
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 228
BP S238
EP S238
DI 10.1016/j.bbmt.2010.12.256
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500228
ER
PT J
AU Buxbaum, NP
Williams, KM
Treadwell, S
Amarnath, S
Eckhans, M
Gress, RE
AF Buxbaum, N. P.
Williams, K. M.
Treadwell, S.
Amarnath, S.
Eckhans, M.
Gress, R. E.
TI IMPAIRED THYMOPOIESIS WITH NORMAL T REGULATORY CELL NUMBERS IS
ASSOCIATED WITH SEVERE CHRONIC GRAFT-VERSUS-HOST DISEASE
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Buxbaum, N. P.; Williams, K. M.; Treadwell, S.; Amarnath, S.; Eckhans, M.; Gress, R. E.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 526
BP S341
EP S342
DI 10.1016/j.bbmt.2010.12.563
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500526
ER
PT J
AU Foley, JE
Amarnath, S
Felizardo, TC
He, A
Fowler, DH
AF Foley, J. E.
Amarnath, S.
Felizardo, T. C.
He, A.
Fowler, D. H.
TI STATI DEFICIENCY FAILS TO PROTECT AGAINST MURINE CHRONIC GVHD
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Foley, J. E.; Amarnath, S.; Felizardo, T. C.; He, A.; Fowler, D. H.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 499
BP S332
EP S333
DI 10.1016/j.bbmt.2010.12.536
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500499
ER
PT J
AU Fowler, DH
Mossoba, ME
Hakim, FT
Kurlander, R
Gea-Banacloche, J
Sportes, C
Hardy, NM
Pavletic, SZ
Steinberg, SM
Khuu, HM
Sabatino, M
Stroncek, DF
Leitman, SF
Rowley, SD
Donato, M
Goy, A
Friedman, TM
Korngold, R
Pecora, AL
Levine, BL
June, CH
Gress, RE
Bishop, MR
AF Fowler, D. H.
Mossoba, M. E.
Hakim, F. T.
Kurlander, R.
Gea-Banacloche, J.
Sportes, C.
Hardy, N. M.
Pavletic, S. Z.
Steinberg, S. M.
Khuu, H. M.
Sabatino, M.
Stroncek, D. F.
Leitman, S. F.
Rowley, S. D.
Donato, M.
Goy, A.
Friedman, T. M.
Korngold, R.
Pecora, A. L.
Levine, B. L.
June, C. H.
Gress, R. E.
Bishop, M. R.
TI T-RAPA CELL DLI SAFELY BALANCES Th1/Th2 CYTOKINE ACTIVATION AFTER
LOW-INTENSITY ALLOGENEIC HEMATOPOIETIC CELL TRANSPLANTATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Fowler, D. H.; Mossoba, M. E.; Hakim, F. T.; Gea-Banacloche, J.; Sportes, C.; Hardy, N. M.; Pavletic, S. Z.; Steinberg, S. M.; Gress, R. E.; Bishop, M. R.] NCI, Bethesda, MD 20892 USA.
[Kurlander, R.; Khuu, H. M.; Sabatino, M.; Stroncek, D. F.; Leitman, S. F.] NIH, Bethesda, MD 20892 USA.
[Rowley, S. D.; Donato, M.; Goy, A.; Friedman, T. M.; Korngold, R.; Pecora, A. L.] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
[Levine, B. L.; June, C. H.] Univ Penn, Ctr Canc, Philadelphia, PA 19104 USA.
RI Levine, Bruce/D-1688-2009
NR 0
TC 1
Z9 1
U1 1
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 19
BP S157
EP S157
DI 10.1016/j.bbmt.2010.12.023
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500020
ER
PT J
AU Grkovic, L
Baird, K
Steinberg, SM
Pulanic, D
Cowen, EW
Mitchell, SA
Williams, KM
Carpenter, AE
Wroblewski, SG
Hakim, FT
Avila, DN
Taylor, TN
Rowley, SD
Zhang, D
Gea-Banachloche, JC
Sportes, C
Fowler, DH
Bishop, MR
Gress, RE
Pavletic, SZ
AF Grkovic, L.
Baird, K.
Steinberg, S. M.
Pulanic, D.
Cowen, E. W.
Mitchell, S. A.
Williams, K. M.
Carpenter, A. E.
Wroblewski, S. G.
Hakim, F. T.
Avila, D. N.
Taylor, T. N.
Rowley, S. D.
Zhang, D.
Gea-Banachloche, J. C.
Sportes, C.
Fowler, D. H.
Bishop, M. R.
Gress, R. E.
Pavletic, S. Z.
TI ROLE OF CLINICAL LABORATORY MARKERS OF INFLAMMATION IN ASSESSING CHRONIC
GRAFT VERSUS HOST DISEASE (CGVHD) ACTIVITY AND SEVERITY
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Grkovic, L.; Baird, K.; Steinberg, S. M.; Cowen, E. W.; Mitchell, S. A.; Williams, K. M.; Carpenter, A. E.; Wroblewski, S. G.; Hakim, F. T.; Avila, D. N.; Taylor, T. N.; Zhang, D.; Gea-Banachloche, J. C.; Sportes, C.; Fowler, D. H.; Bishop, M. R.; Gress, R. E.; Pavletic, S. Z.] NCI, NIH, Bethesda, MD 20892 USA.
[Pulanic, D.] Univ Hosp Ctr Zagreb, Zagreb, Croatia.
[Rowley, S. D.] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 524
BP S340
EP S341
DI 10.1016/j.bbmt.2010.12.561
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500524
ER
PT J
AU Hanash, AM
Kappel, LW
Yim, NL
Nejat, RA
Goldberg, GL
Smith, OM
Rao, UK
Dykstra, L
Na, IK
Holland, AM
Liu, C
Murphy, GF
Leonard, WJ
Heller, G
van den Brink, MRM
AF Hanash, A. M.
Kappel, L. W.
Yim, N. L.
Nejat, R. A.
Goldberg, G. L.
Smith, O. M.
Rao, U. K.
Dykstra, L.
Na, I-K
Holland, A. M.
Liu, C.
Murphy, G. F.
Leonard, W. J.
Heller, G.
van den Brink, M. R. M.
TI ABROGATION OF DONOR T CELL IL-21 SIGNALING LEADS TO TISSUE-SPECIFIC
MODULATION OF IMMUNITY AND SEPARATION OF GVHD FROM GVL
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Hanash, A. M.; Kappel, L. W.; Yim, N. L.; Nejat, R. A.; Goldberg, G. L.; Smith, O. M.; Rao, U. K.; Dykstra, L.; Holland, A. M.; Heller, G.; van den Brink, M. R. M.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Na, I-K] Charite CBF Univ Med Berlin, Berlin, Germany.
[Liu, C.] Univ Florida, Coll Med, Gainesville, FL USA.
[Murphy, G. F.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Leonard, W. J.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 32
BP S163
EP S163
DI 10.1016/j.bbmt.2010.12.038
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500033
ER
PT J
AU Hardy, NM
Hakim, FT
Fellowes, VS
Rose, JJ
Gress, RE
Bishop, MR
AF Hardy, N. M.
Hakim, F. T.
Fellowes, V. S.
Rose, J. J.
Gress, R. E.
Bishop, M. R.
TI TUMOR-INFILTRATING LYMPHOCYTES ARE PRESENT IN CANCER RELAPSE AFTER
ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION (ALLOHSCT), OF DONOR
ORIGIN, DISTINCT FROM PERIPHERAL BLOOD DONOR LYMPHOCYTES AND EXHIBIT
EFFECTOR FUNCTION WITH CD3/CD28 COSTIMULATION EX-VIVO
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Hardy, N. M.; Hakim, F. T.; Fellowes, V. S.; Rose, J. J.; Gress, R. E.; Bishop, M. R.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 151
BP S209
EP S209
DI 10.1016/j.bbmt.2010.12.174
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500152
ER
PT J
AU Inamoto, Y
Kurland, BF
Chai, S
Heffernan, MJ
Martin, PJ
Flowers, MED
Carpenter, PA
Cutler, C
Jacobsohn, D
Jagasia, M
Johnston, L
Vogelsang, GB
Pavletic, SZ
Lee, SJ
AF Inamoto, Y.
Kurland, B. F.
Chai, S.
Heffernan, M. J.
Martin, P. J.
Flowers, M. E. D.
Carpenter, P. A.
Cutler, C.
Jacobsohn, D.
Jagasia, M.
Johnston, L.
Vogelsang, G. B.
Pavletic, S. Z.
Lee, S. J.
TI EVALUATION OF SCALES CORRELATED WITH CLINICIAN AND PATIENT-PERCEIVED
SYMPTOM CHANGE IN OCULAR GRAFT-VERSUS-HOST DISEASE: RESULTS FROM THE
CHRONIC GVHD CONSORTIUM
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Inamoto, Y.; Kurland, B. F.; Chai, S.; Heffernan, M. J.; Martin, P. J.; Flowers, M. E. D.; Carpenter, P. A.; Lee, S. J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Cutler, C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Jacobsohn, D.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Jagasia, M.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Johnston, L.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Vogelsang, G. B.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Pavletic, S. Z.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 63
BP S175
EP S176
DI 10.1016/j.bbmt.2010.12.073
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500064
ER
PT J
AU Kang, EM
Kelly, C
Hilligoss, DM
Marquesen, MM
DeCastro, R
Wilder, J
Kwatemaa, AN
Khuu, H
Stroncek, D
Malech, HL
AF Kang, E. M.
Kelly, C.
Hilligoss, D. M.
Marquesen, M. M.
DeCastro, R.
Wilder, J.
Kwatemaa, A. N.
Khuu, H.
Stroncek, D.
Malech, H. L.
TI A NOVEL NON MYELOABLATIVE REGIMEN FOR RELATED AND UNRELATED ALLOGENEIC
TRANSPLANTATION OF HIGH RISK PATIENTS WITH CHRONIC GRANULOMATOUS DISEASE
(CGD)
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Kang, E. M.; Kelly, C.; Hilligoss, D. M.; Marquesen, M. M.; DeCastro, R.; Wilder, J.; Kwatemaa, A. N.; Khuu, H.; Stroncek, D.; Malech, H. L.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 390
BP S295
EP S295
DI 10.1016/j.bbmt.2010.12.426
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500390
ER
PT J
AU Kang, EM
Yau, YY
Maxwell, S
DeRavin, SS
Borge, PD
Malech, HL
Leitman, SF
AF Kang, E. M.
Yau, Y. Y.
Maxwell, S.
DeRavin, S. S.
Borge, P. D.
Malech, H. L.
Leitman, S. F.
TI MOBILIZATION OF CD34+CELLS WITH GRANULOCYTE COLONY STIMULATING FACTOR
(GCSF) VERSUS GCSF PLUS PLERIXAFOR IN PATIENTS WITH PRIMARY
IMMUNODEFICIENCY DISORDERS (PIDS) UNDERGOING AUTOLOGOUS PERIPHERAL BLOOD
STEM CELL (PBSC) COLLECTION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Kang, E. M.; Yau, Y. Y.; Maxwell, S.; DeRavin, S. S.; Borge, P. D.; Malech, H. L.; Leitman, S. F.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 181
BP S220
EP S220
DI 10.1016/j.bbmt.2010.12.205
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500182
ER
PT J
AU Kochenderfer, JN
Dudley, ME
Maric, I
Feldman, SA
Salit, R
Hardy, NM
Layton, P
Blacklock-Schuver, B
Wilder, J
Devillier, L
Gress, RE
Morgan, RA
Rosenberg, SA
Bishop, MR
AF Kochenderfer, J. N.
Dudley, M. E.
Maric, I
Feldman, S. A.
Salit, R.
Hardy, N. M.
Layton, P.
Blacklock-Schuver, B.
Wilder, J.
Devillier, L.
Gress, R. E.
Morgan, R. A.
Rosenberg, S. A.
Bishop, M. R.
TI DRAMATIC REGRESSION OF CHRONIC LYMPHOCYTIC LEUKEMIA IN THE FIRST PATIENT
TREATED WITH DONOR-DERIVED GENETICALLY-ENGINEERED ANTI-CD
19-CHIMERIC-ANTIGEN-RECEPTOR-EXPRESSING T CELLS AFTER ALLOGENEIC
HEMATOPOIETIC STEM CELL TRANSPLANTATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Kochenderfer, J. N.; Dudley, M. E.; Feldman, S. A.; Salit, R.; Hardy, N. M.; Layton, P.; Blacklock-Schuver, B.; Wilder, J.; Devillier, L.; Gress, R. E.; Morgan, R. A.; Rosenberg, S. A.; Bishop, M. R.] NCI, Bethesda, MD 20892 USA.
[Maric, I] NIH, Bethesda, MD 20892 USA.
NR 0
TC 8
Z9 8
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 21
BP S158
EP S158
DI 10.1016/j.bbmt.2010.12.025
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500022
ER
PT J
AU Lafond, S
Pulanic, TK
Turner, M
Bishop, M
Fowler, D
Mackall, C
Stratton, P
AF Lafond, S.
Pulanic, Klepac T.
Turner, M.
Bishop, M.
Fowler, D.
Mackall, C.
Stratton, P.
TI GENITAL GRAFT VERSUS HOST DISEASE: ACUTE VERSUS EARLY ONSET CHRONIC
DISEASE
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Lafond, S.; Turner, M.; Bishop, M.; Fowler, D.] NCI, NIH, Bethesda, MD 20892 USA.
[Lafond, S.] George Washington Univ, Sch Med, Washington, DC USA.
[Pulanic, Klepac T.] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 532
BP S344
EP S344
DI 10.1016/j.bbmt.2010.12.569
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500532
ER
PT J
AU Lucas, PJ
Sivarapatna, A
Wang, J
Gress, RE
AF Lucas, P. J.
Sivarapatna, A.
Wang, J.
Gress, R. E.
TI RAPID PRECLINICAL SCREENING OF CHEMOTHERAPEUTIC AGENTS EFFECTIVE IN
COMBINATION WITH IMMUNOTHERAPY
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Lucas, P. J.; Sivarapatna, A.; Wang, J.; Gress, R. E.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 512
BP S337
EP S337
DI 10.1016/j.bbmt.2010.12.549
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500512
ER
PT J
AU McIver, ZA
Mielke, S
Shenoy, A
Fellows, V
Stroncek, D
Leitman, S
Childs, R
Batiwalla, M
Koklanaris, EK
Haggerty, J
Savani, BN
Rezvani, K
Barrett, AJ
AF McIver, Z. A.
Mielke, S.
Shenoy, A.
Fellows, V
Stroncek, D.
Leitman, S.
Childs, R.
Batiwalla, M.
Koklanaris, E. K.
Haggerty, J.
Savani, B. N.
Rezvani, K.
Barrett, A. J.
TI SELECTIVELY T CELL DEPLETED ALLOGRAFTS FROM HLA-MATCHED SIBLING DONORS
FOLLOWED BY LOW-DOSE POST TRANSPLANT IMMUNOSUPPRESSION TO LIMIT DISEASE
RELAPSE IN PATIENTS WITH HEMATOLOGICAL MALIGNANCIES
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [McIver, Z. A.; Fellows, V; Stroncek, D.; Leitman, S.; Childs, R.; Batiwalla, M.; Koklanaris, E. K.; Haggerty, J.; Barrett, A. J.] NIH, Bethesda, MD 20892 USA.
[Mielke, S.] Univ Wurzburg, Wurzburg, Germany.
[Shenoy, A.] Washington Hosp Ctr, Washington, DC 20010 USA.
[Savani, B. N.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Rezvani, K.] Univ London Imperial Coll Sci Technol & Med, Hammersmith Hosp, London, England.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 366
BP S286
EP S286
DI 10.1016/j.bbmt.2010.12.402
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500366
ER
PT J
AU Melenhorst, JJ
Leen, AM
Bollard, CM
Quigley, MF
Price, DA
Rooney, CM
Brenner, MK
Barrett, AJ
Heslop, HE
AF Melenhorst, J. J.
Leen, A. M.
Bollard, C. M.
Quigley, M. F.
Price, D. A.
Rooney, C. M.
Brenner, M. K.
Barrett, A. J.
Heslop, H. E.
TI ALLOGENEIC VIRUS-SPECIFIC T CELLS WITH HLA ALLOREACTIVITY DO NOT PRODUCE
GRAFT-VERSUS-HOST DISEASE IN HUMAN SUBJECTS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Melenhorst, J. J.; Barrett, A. J.] NHLBI, Bethesda, MD 20892 USA.
[Leen, A. M.; Bollard, C. M.; Rooney, C. M.; Brenner, M. K.; Heslop, H. E.] Baylor Coll Med, Houston, TX 77030 USA.
[Quigley, M. F.; Price, D. A.] NIAID, Bethesda, MD 20892 USA.
RI Price, David/C-7876-2013
OI Price, David/0000-0001-9416-2737
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 22
BP S158
EP S158
DI 10.1016/j.bbmt.2010.12.026
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500023
ER
PT J
AU Melver, ZA
Battiwalla, M
Barrett, AJ
AF Melver, Z. A.
Battiwalla, M.
Barrett, A. J.
TI MISMATCHED DONOR LYMPHOCYTE INFUSIONS FOR RELAPSED ACUTE LEUKEMIA
FOLLOWING HLA IDENTICAL ALLOGENEIC STEM CELL TRANSPLANT
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Melver, Z. A.; Battiwalla, M.; Barrett, A. J.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 167
BP S215
EP S215
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500168
ER
PT J
AU Pantin, JM
Robert, HF
Chen, MY
Timothy, H
Randall, CR
Childs, RW
AF Pantin, J. M.
Robert, H. F.
Chen, M. Y.
Timothy, H.
Randall, C. R.
Childs, R. W.
TI IMPACT OF INJECTION VOLUME AND INFUSION RATE IN A LARGE ANIMAL MODEL
DESIGNED TO OPTIMIZE INTRABONE TRANSPLANTATION OF HEMATOPOIETIC STEM
CELLS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Pantin, J. M.; Robert, H. F.; Chen, M. Y.; Timothy, H.; Randall, C. R.; Childs, R. W.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 401
BP S299
EP S299
DI 10.1016/j.bbmt.2010.12.437
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500401
ER
PT J
AU Papanicolau, G
Kurtzberg, J
Westervelt, P
Gea-Banacloche, J
Warlick, E
Lanier, R
Anderson, M
Painter, W
AF Papanicolau, G.
Kurtzberg, J.
Westervelt, P.
Gea-Banacloche, J.
Warlick, E.
Lanier, R.
Anderson, M.
Painter, W.
TI EXPERIENCE WITH CMX001, A NOVEL ANTIVIRAL DRUG, FOR CYTOMEGALOVIRUS
INFECTIONS IN STEM TRANSPLANT PATIENTS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Papanicolau, G.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Kurtzberg, J.] Duke Univ, Med Ctr, Durham, NC USA.
[Westervelt, P.] Washington Univ, Sch Med, St Louis, MO USA.
[Gea-Banacloche, J.] NCI, Bethesda, MD 20892 USA.
[Warlick, E.] Univ Minnesota, Minneapolis, MN USA.
[Lanier, R.; Anderson, M.; Painter, W.] Chimerix Inc, Durham, NC USA.
NR 0
TC 3
Z9 3
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 330
BP S273
EP S274
DI 10.1016/j.bbmt.2010.12.364
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500330
ER
PT J
AU Pidala, J
Kurland, B
Chai, X
Majhail, N
Weisdorf, D
Pavletic, S
Cutler, C
Arai, S
Jagasia, M
Palmer, J
Lee, SJ
AF Pidala, J.
Kurland, B.
Chai, X.
Majhail, N.
Weisdorf, D.
Pavletic, S.
Cutler, C.
Arai, S.
Jagasia, M.
Palmer, J.
Lee, S. J.
TI CHRONIC GVHD SEVERITY AND SENSITIVITY TO CHANGE IN PATIENT-REPORTED
QUALITY OF LIFE: RESULTS FROM THE CHRONIC GVHD CONSORTIUM
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Pidala, J.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Kurland, B.; Chai, X.; Lee, S. J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Majhail, N.; Weisdorf, D.] Univ Minnesota, Minneapolis, MN 55455 USA.
[Pavletic, S.] NCI, Bethesda, MD 20892 USA.
[Cutler, C.] Dana Farber Canc Inst, Boston, MA USA.
[Arai, S.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Jagasia, M.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Palmer, J.] Med Coll Wisconsin, Milwaukee, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 229
BP S238
EP S238
DI 10.1016/j.bbmt.2010.12.257
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500229
ER
PT J
AU Ren, J
Stroncek, D
Jin, P
Castiello, L
Tran, K
Balakumaran, A
Robey, P
Sabatino, M
AF Ren, J.
Stroncek, D.
Jin, P.
Castiello, L.
Tran, K.
Balakumaran, A.
Robey, P.
Sabatino, M.
TI SENESCENCE OF CULTURED BONE MARROW STROMAL CELLS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Ren, J.; Stroncek, D.; Jin, P.; Castiello, L.; Tran, K.; Balakumaran, A.; Robey, P.; Sabatino, M.] NIH, Bethesda, MD 20892 USA.
RI Robey, Pamela/H-1429-2011
OI Robey, Pamela/0000-0002-5316-5576
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 171
BP S216
EP S217
DI 10.1016/j.bbmt.2010.12.194
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500172
ER
PT J
AU Sullivan, KM
Froshaug, DB
Furst, DE
Nash, RA
Mayes, MD
Crofford, LJ
McSweeney, PA
Goldmuntz, EA
Keyes-Elstein, L
Khanna, D
AF Sullivan, K. M.
Froshaug, D. B.
Furst, D. E.
Nash, R. A.
Mayes, M. D.
Crofford, L. J.
McSweeney, P. A.
Goldmuntz, E. A.
Keyes-Elstein, L.
Khanna, D.
TI ORGAN FUNCTION AND QUALITY OF LIFE CORRELATES AT RANDOMIZATION ON THE
SCOT (SCLERODERMA: CYCLOPHOSPHAMIDE OR TRANSPLANTATION) TRIAL
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Sullivan, K. M.] Duke Univ, Med Ctr, Durham, NC USA.
[Froshaug, D. B.; Keyes-Elstein, L.] Rho Fed Syst, Chapel Hill, NC USA.
[Furst, D. E.; Khanna, D.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Nash, R. A.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Mayes, M. D.] Univ Texas Houston, Houston, TX USA.
[Crofford, L. J.] Univ Kentucky, Lexington, KY USA.
[McSweeney, P. A.] Rocky Mt Canc Ctr, Denver, CO USA.
[Goldmuntz, E. A.] NIH, Bethesda, MD 20892 USA.
RI Crofford, Leslie/J-8010-2013
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 113
BP S195
EP S195
DI 10.1016/j.bbmt.2010.12.134
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500114
ER
PT J
AU Watson, TM
Fry, TJ
Jacobsohn, DA
Sande, J
Yates, B
Stevenson, A
AF Watson, T. M.
Fry, T. J.
Jacobsohn, D. A.
Sande, J.
Yates, B.
Stevenson, A.
TI PROCALCITONIN IN PEDIATRIC ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANT
(AHSCT) RECIPIENTS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Watson, T. M.; Jacobsohn, D. A.; Sande, J.; Yates, B.; Stevenson, A.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Fry, T. J.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Sande, J.] George Washington Univ, Sch Med, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 314
BP S268
EP S268
DI 10.1016/j.bbmt.2010.12.345
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500314
ER
PT J
AU Wehrlen, LD
Prachenko, O
Prince, P
Foruraghi, L
Shelburne, N
Wallen, GR
Bevans, MF
AF Wehrlen, L. D.
Prachenko, O.
Prince, P.
Foruraghi, L.
Shelburne, N.
Wallen, G. R.
Bevans, M. F.
TI THE QUALITY OF THE ADULT CAREGIVER-RECIPIENT RELATIONSHIP MAY BUFFER
CAREGIVER BURDEN DURING ALLOGENEIC TRANSPLANTATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Wehrlen, L. D.; Prachenko, O.; Prince, P.; Shelburne, N.; Wallen, G. R.; Bevans, M. F.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Foruraghi, L.] NIDDKD, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 109
BP S193
EP S194
DI 10.1016/j.bbmt.2010.12.128
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500110
ER
PT J
AU Williams, KM
Hnatiuk, O
Steinberg, SM
Mitchell, S
Baird, K
Gadalla, SM
Carpenter, A
Avila, D
Taylor, T
Urban, A
Comis, LE
Blacklock-Schuver, B
Gress, RE
Pavletic, SZ
AF Williams, K. M.
Hnatiuk, O.
Steinberg, S. M.
Mitchell, S.
Baird, K.
Gadalla, S. M.
Carpenter, A.
Avila, D.
Taylor, T.
Urban, A.
Comis, L. E.
Blacklock-Schuver, B.
Gress, R. E.
Pavletic, S. Z.
TI NHANES III EQUATIONS FOR PFT INTERPRETATION SIGNIFICANTLY ALTERS BOS
DIAGNOSES, SEVERITY, AND PROGNOSIS AFTER HEMATOPOIETIC STEM CELL
TRANSPLANTATION (HSCT)
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Williams, K. M.; Hnatiuk, O.; Steinberg, S. M.; Mitchell, S.; Baird, K.; Gadalla, S. M.; Carpenter, A.; Avila, D.; Taylor, T.; Urban, A.; Comis, L. E.; Blacklock-Schuver, B.; Gress, R. E.; Pavletic, S. Z.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 494
BP S331
EP S331
DI 10.1016/j.bbmt.2010.12.531
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500494
ER
PT J
AU Williams, KM
Moore, AR
Gress, RE
AF Williams, K. M.
Moore, A. R.
Gress, R. E.
TI FLT-3 LIGAND ENHANCES THYMOPOIESIS IN HEMATOPOIETIC STEM CELL
TRANSPLANTS (HSCT) INVOLVING AGED DONOR AND RECIPIENT MICE BY INCREASING
SURVIVAL AND TRAFFICKING OF EARLY THYMOCYTE PROGENITORS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood Marrow Transplantat, Ctr Int Blood Marrow Transplant Res
C1 [Williams, K. M.; Moore, A. R.; Gress, R. E.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 223
BP S236
EP S236
DI 10.1016/j.bbmt.2010.12.250
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500223
ER
PT J
AU Carter, TC
Olney, RS
Mitchell, AA
Romitti, PA
Bell, EM
Druschel, CM
AF Carter, Tonia C.
Olney, Richard S.
Mitchell, Allen A.
Romitti, Paul A.
Bell, Erin M.
Druschel, Charlotte M.
CA Natl Birth Defects Prevention Stud
TI Maternal Self-Reported Genital Tract Infections During Pregnancy and the
Risk of Selected Birth Defects
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Article; Proceedings Paper
CT 50th Annual Meeting of the Teratology-Society
CY JUN 26-30, 2010
CL Louisville, KY
SP Teratol Soc
DE Chlamydia; congenital abnormalities; female genital diseases; gonorrhea;
herpes genitalis
ID HERPES-SIMPLEX-VIRUS; CHLAMYDIA-TRACHOMATIS INFECTION;
PELVIC-INFLAMMATORY-DISEASE; NEURAL-TUBE DEFECTS;
CONGENITAL-ABNORMALITIES; BACTERIAL VAGINOSIS; PRETERM DELIVERY;
HUMAN-PAPILLOMAVIRUS; NO ASSOCIATION; WOMEN
AB BACKGROUND: Genital tract infections are common during pregnancy and can result in adverse outcomes including preterm birth and neonatal infection. This hypothesis-generating study examined whether these infections are associated with selected birth defects. METHODS: We conducted a case-control study of 5913 children identified as controls and 12,158 cases with birth defects from the National Birth Defects Prevention Study (1997-2004). Maternal interviews provided data on genital tract infections that occurred from one month before pregnancy through the end of the first trimester. Infections were either grouped together as a single overall exposure or were considered as a subgroup that included chlamydia/gonorrhea/pelvic inflammatory disease. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression with adjustment for potential confounders. RESULTS: Genital tract infections were associated with bilateral renal agenesis/hypoplasia (OR, 2.89; 95% CI, 1.11-7.50), cleft lip with or without cleft palate (OR, 1.46; 95% CI, 1.03-2.06), and transverse limb deficiency (OR, 1.84; 95% CI, 1.04-3.26). Chlamydia/gonorrhea/pelvic inflammatory disease was associated with cleft lip only (OR, 2.81; 95% CI, 1.39-5.69). These findings were not statistically significant after adjustment for multiple comparisons. CONCLUSIONS: Caution is needed in interpreting these findings due to the possible misclassification of infection, the limited sample size that constrained consideration of the effects of treatment, and the possibility of chance associations. Although these data do not provide strong evidence for an association between genital tract infections and birth defects, additional research on the possible effects of these relatively common infections is needed. Birth Defects Research (Part A) 91:108-116, 2011. (C) 2010 Wiley-Liss, Inc.
C1 [Carter, Tonia C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Natl Inst Hlth, Dept Hlth & Human Serv, Bethesda, MD USA.
[Olney, Richard S.] Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA USA.
[Mitchell, Allen A.] Boston Univ, Slone Epidemiol Ctr, Boston, MA 02215 USA.
[Romitti, Paul A.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
[Bell, Erin M.; Druschel, Charlotte M.] SUNY Albany, Sch Publ Hlth, Dept Epidemiol & Biostat, Albany, NY USA.
[Druschel, Charlotte M.] New York State Dept Hlth, Congenital Malformat Registry, Troy, NY USA.
RP Carter, TC (reprint author), 6100 Execut Blvd,Room 7B03, Bethesda, MD 20892 USA.
EM carterto@mail.nih.gov
RI Publications, NBDPS/B-7692-2013;
OI Mitchell, Allen/0000-0003-0950-6799
FU Intramural NIH HHS; NCBDD CDC HHS [U01 DD000492]; PHS HHS
[U50/CCU223184]
NR 53
TC 7
Z9 9
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD FEB
PY 2011
VL 91
IS 2
BP 108
EP 116
DI 10.1002/bdra.20749
PG 9
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 730LU
UT WOS:000288035600006
PM 21319278
ER
PT J
AU Patel, V
Collins, PY
Copeland, J
Kakuma, R
Katontoka, S
Lamichhane, J
Naik, S
Skeen, S
AF Patel, Vikram
Collins, Pamela Y.
Copeland, John
Kakuma, Ritsuko
Katontoka, Sylvester
Lamichhane, Jagannath
Naik, Smita
Skeen, Sarah
TI The Movement for Global Mental Health
SO BRITISH JOURNAL OF PSYCHIATRY
LA English
DT Editorial Material
AB The Movement for Global Mental Health is a coalition of individuals and institutions committed to collective actions that aim to close the treatment gap for people living with mental disorders worldwide, based on two fundamental principles: evidence on effective treatments and the human rights of people with mental disorders.
C1 [Patel, Vikram; Naik, Smita] Sangath Ctr, Alto Porvorim 403521, Goa, India.
[Patel, Vikram] London Sch Hyg & Trop Med, Ctr Global Mental Hlth, London, England.
[Collins, Pamela Y.] NIMH, NIH, Bethesda, MD 20892 USA.
[Copeland, John] Univ Liverpool, Div Psychiat, Liverpool L69 3BX, Merseyside, England.
[Kakuma, Ritsuko] Ctr Addict & Mental Hlth, Hlth Syst Res & Consulting Unit, Toronto, ON, Canada.
[Kakuma, Ritsuko] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON M5S 1A1, Canada.
[Kakuma, Ritsuko; Skeen, Sarah] Univ Cape Town, Dept Psychiat & Mental Hlth, Mental Hlth & Poverty Project, ZA-7700 Rondebosch, South Africa.
[Katontoka, Sylvester] Mental Hlth Users Network Zambia, Lusaka, Zambia.
[Lamichhane, Jagannath] NMHF, Kathmandu, Nepal.
RP Patel, V (reprint author), Sangath Ctr, Alto Porvorim 403521, Goa, India.
EM vikram.patel@lshtm.ac.uk
OI Patel, Vikram/0000-0003-1066-8584
FU Wellcome Trust [091834]
NR 8
TC 21
Z9 21
U1 0
U2 7
PU ROYAL COLLEGE OF PSYCHIATRISTS
PI LONDON
PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON SW1X 8PG,
ENGLAND
SN 0007-1250
J9 BRIT J PSYCHIAT
JI Br. J. Psychiatry
PD FEB
PY 2011
VL 198
IS 2
BP 88
EP 90
DI 10.1192/bjp.bp.109.074518
PG 3
WC Psychiatry
SC Psychiatry
GA 719BE
UT WOS:000287173400003
PM 21282777
ER
PT J
AU Selby, P
Sitzia, J
AF Selby, Peter
Sitzia, John
TI NHS research governance procedures (December, pg 637, 2010)
SO CLINICAL MEDICINE
LA English
DT Correction
C1 [Selby, Peter; Sitzia, John] NIH, Res Clin Res Network, Bethesda, MD 20892 USA.
RP Selby, P (reprint author), NIH, Res Clin Res Network, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 1
U2 4
PU ROY COLL PHYS LONDON EDITORIAL OFFICE
PI LONDON
PA 11 ST ANDREWS PLACE REGENTS PARK, LONDON NW1 4LE, ENGLAND
SN 1470-2118
J9 CLIN MED
JI Clin. Med.
PD FEB
PY 2011
VL 11
IS 1
BP 99
EP 99
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 730SI
UT WOS:000288054200037
ER
PT J
AU Schindler, CW
Gilman, JP
Panlilio, LV
McCann, DJ
Goldberg, SR
AF Schindler, Charles W.
Gilman, Joanne P.
Panlilio, Leigh V.
McCann, David J.
Goldberg, Steven R.
TI Comparison of the Effects of Methamphetamine, Bupropion, and
Methylphenidate on the Self-Administration of Methamphetamine by Rhesus
Monkeys
SO EXPERIMENTAL AND CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE methamphetamine; self-administration; bupropion; methylphenidate; rhesus
monkeys
ID D-AMPHETAMINE TREATMENT; PROGRESSIVE-RATIO SCHEDULE; PLACEBO-CONTROLLED
TRIAL; COCAINE-DEPENDENCE; AGONIST-LIKE; FOOD; ABUSE; PHARMACOTHERAPY;
DEXAMPHETAMINE; METHADONE
AB The effectiveness of methadone as a treatment for opioid abuse and nicotine preparations as treatments for tobacco smoking has led to an interest in developing a similar strategy for treating psychostimulant abuse. The current study investigated the effects of three such potential therapies on intravenous methamphetamine self-administration (1 30 mu g/kg/injection) in rhesus monkeys. When given as a presession intramuscular injection, a high dose of methamphetamine (1.0 mg/kg) decreased intravenous methamphetamine self-administration but did not affect responding for a food reinforcer during the same sessions. However, the dose of intramuscular methamphetamine required to reduce intravenous methamphetamine self-administration exceeded the cumulative amount taken during a typical self-administration session, and pretreatment with a low dose of methamphetamine (0.3 mg/kg) actually increased self-administration in some monkeys at the lower self-administration dose. Like pretreatment with methamphetamine, pretreatment with bupropion (3.2 mg/kg) decreased methamphetamine self-administration but did not affect responding for food. Pretreatment with methylphenidate (0.56 mg/kg) did not significantly alter methamphetamine self-administration. These results suggest that some agonist-like agents can decrease methamphetamine self-administration. Although the most robust effects occurred with a high dose of methamphetamine, safety and abuse liability considerations suggest that bupropion should also be considered for further evaluation as a methamphetamine addiction treatment.
C1 [Schindler, Charles W.; Gilman, Joanne P.; Panlilio, Leigh V.; Goldberg, Steven R.] NIDA, Preclin Pharmacol Sect, NIH,Behav Neurosci Branch, Intramural Res Program,US Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
[McCann, David J.] NIDA, Div Pharmacotherapies & Med Consequences Drug Abu, DHHS, NIH, Baltimore, MD 21224 USA.
RP Schindler, CW (reprint author), NIDA, Preclin Pharmacol Sect, NIH,Behav Neurosci Branch, Intramural Res Program,US Dept Hlth & Human Serv, 251 Bayview Blvd,Suite 200, Baltimore, MD 21224 USA.
EM cschindl@helix.nih.gov
FU NIH, NIDA; NIDA Division of Pharmacotherapies and Medical Consequences
of Drug Abuse
FX This research was supported by the Intramural Research Program of the
NIH, NIDA, and by the NIDA Division of Pharmacotherapies and Medical
Consequences of Drug Abuse.
NR 47
TC 14
Z9 15
U1 0
U2 1
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1064-1297
J9 EXP CLIN PSYCHOPHARM
JI Exp. Clin. Psychopharmacol.
PD FEB
PY 2011
VL 19
IS 1
BP 1
EP 10
DI 10.1037/a0022432
PG 10
WC Psychology, Biological; Psychology, Clinical; Pharmacology & Pharmacy;
Psychiatry
SC Psychology; Pharmacology & Pharmacy; Psychiatry
GA 722WM
UT WOS:000287466000001
PM 21341918
ER
PT J
AU Gualco, G
Weiss, LM
Barber, GN
Bacchi, CE
AF Gualco, Gabriela
Weiss, Lawrence M.
Barber, Glen N.
Bacchi, Carlos E.
TI Diffuse Large B-Cell Lymphoma Involving the Central Nervous System
SO INTERNATIONAL JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE primary central nervous system lymphoma; central nervous system
lymphoma; diffuse large B-cell lymphoma; WHO classification; human
immunodeficiency virus; immunocompromised; immunocompetent;
immunohistochemistry; EBV
ID PRIMARY CNS LYMPHOMA; EPSTEIN-BARR-VIRUS; GENE-EXPRESSION;
IMMUNOCOMPETENT PATIENTS; PATTERN; CXCR4
AB Lymphomas involving the central nervous system are recognized increasingly in immunocompetent as well as immunosuppressed individuals, and the majority of the cases are diffuse large B-cell lymphoma (DLBCL). The aim of this study was to compare the immunophenotype, clinicopathological features, and association with Epstein-Barr virus (EBV) of DLBCL of the central nervous system (CNS) in 3 different clinical situations: primary, in immunocompetent patients; "primary," in immunosuppressed patients; and in patients with secondary involvement by systemic lymphoma. The authors reviewed the clinicopathological features, morphology, immunophenotype (according to germinal-center B-cell like and nongerminal B-cell like subtypes), and association with EBV in 36 cases of DLBCL of the CNS, including 25 primary cases, 5 associated with immunosuppression, and 6 cases with secondary involvement. Survival was evaluated in 15 cases of primary CNS lymphomas. Of the 36 patients, 19 were male and 18 female. Only 2 cases of lymphomas were EBV-positive; both occurred in immunosuppressed patients. Separation into germinal-center and non-germinal center subtypes by an immunohistochemistry panel showed that 68% of primary, 80% of secondary, and 83% of the cases associated with immunosuppression were of non-germinal-center subtype, respectively. Patients with non-germinal-center immunophenotype showed significantly worse survival than those with CNS lymphomas of the germinal-center subtype.
C1 [Gualco, Gabriela; Bacchi, Carlos E.] Consultoria Patol, BR-18602010 Botucatu, SP, Brazil.
[Weiss, Lawrence M.] City Hope Natl Med Ctr, Div Pathol, Duarte, CA 91010 USA.
[Barber, Glen N.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Barber, Glen N.] Fogarty Int Ctr, Sylvester Canc Ctr, Miami, FL USA.
RP Bacchi, CE (reprint author), Consultoria Patol, Rua Major Leonidas Cardoso 739, BR-18602010 Botucatu, SP, Brazil.
EM bacchi@conspat.com.br
NR 31
TC 5
Z9 5
U1 0
U2 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1066-8969
J9 INT J SURG PATHOL
JI Int. J. Surg. Pathol.
PD FEB
PY 2011
VL 19
IS 1
BP 44
EP 50
DI 10.1177/1066896910386476
PG 7
WC Pathology; Surgery
SC Pathology; Surgery
GA 709OY
UT WOS:000286451200007
PM 21087986
ER
PT J
AU Meleth, AD
Mettu, P
Agron, E
Chew, EY
Sadda, SR
Ferris, FL
Wong, WT
AF Meleth, Annal D.
Mettu, Pradeep
Agron, Elvira
Chew, Emily Y.
Sadda, Srinivas R.
Ferris, Frederick L.
Wong, Wai T.
TI Changes in Retinal Sensitivity in Geographic Atrophy Progression as
Measured by Microperimetry
SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
LA English
DT Article
ID OPTICAL COHERENCE TOMOGRAPHY; IDIOPATHIC MACULAR TELANGIECTASIA;
AGE-RELATED MACULOPATHY; VISUAL-ACUITY LOSS; FUNDUS AUTOFLUORESCENCE;
MP-1 MICROPERIMETER; FIXATION PATTERNS; CENTRAL SCOTOMAS; RISK-FACTORS;
DEGENERATION
AB PURPOSE. To characterize changes in macular sensitivity during geographic atrophy (GA) progression using microperimetry.
METHODS. Retinal sensitivity in the macular area was evaluated by microperimetry in 10 patients with bilateral GA, with adequate data obtained in 9 of 10 patients (n = 18 eyes). Patients had been enrolled in an interventional trial in which one eye had been randomized to treatment and the other eye observed. No treatment effect with regard to GA growth and microperimetric measurements was detected, and all eyes were analyzed. Microperimetric assessments of the central 20 of the macula were performed every 6 months over 24 months. Parameters analyzed included number of scotomatous points, mean retinal sensitivity of responding points, and fixation stability. Autofluorescence imaging and fundus photography were also obtained.
RESULTS. Microperimetric parameters demonstrated statistically significant changes as a function of time. Mean number of scotomatous points increased significantly with time (P = 0.004) at a rate of 4.4 points/year. Mean retinal sensitivities of all points, all responding points, and all perilesional points all decreased significantly with time (P < 0.003), as did fixation quality within the 2 and 4 circles (P < 0.002). The growth of GA lesion area was associated with the changes in the number of scotomatous points (P = 0.01) but not with changes in the other microperimetric parameters.
CONCLUSIONS. Macular sensitivity and fixation quality undergo progressive change during the GA progression, reflecting alterations in macular function extending beyond the GA lesion proper. Microperimetric measurements may provide useful functional outcome measures for the clinical study of GA. (Invest Ophthalmol Vis Sci. 2011; 52:1119-1126) DOI:10.1167/iovs.10-6075
C1 [Mettu, Pradeep; Wong, Wai T.] NIH, Unit Neuron Glia Interact Retinal Dis, Bethesda, MD 20892 USA.
[Meleth, Annal D.; Mettu, Pradeep; Agron, Elvira; Chew, Emily Y.; Ferris, Frederick L.; Wong, Wai T.] NIH, Div Epidemiol & Clin Applicat, Bethesda, MD 20892 USA.
[Sadda, Srinivas R.] Univ So Calif, Keck Sch Med, Doheny Image Reading Ctr, Doheny Eye Inst, Los Angeles, CA 90033 USA.
RP Wong, WT (reprint author), NIH, Unit Neuron Glia Interact Retinal Dis, 7 Mem Dr,Bldg 7,Room 217, Bethesda, MD 20892 USA.
EM wongw@nih.gov
RI Wong, Wai/B-6118-2017
OI Wong, Wai/0000-0003-0681-4016
FU National Eye Institute
FX Supported by funding from the National Eye Institute Intramural Research
Program.
NR 42
TC 31
Z9 32
U1 0
U2 5
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 FEB
PY 2011
VL 52
IS 2
BP 1119
EP 1126
DI 10.1167/iovs.10-6075
PG 8
WC Ophthalmology
SC Ophthalmology
GA 728AQ
UT WOS:000287846300066
PM 20926818
ER
PT J
AU Arancibia, S
Benitez, D
Nunez, LE
Jewell, CM
Langjahr, P
Candia, E
Zapata-Torres, G
Cidlowski, JA
Gonzalez, MJ
Hermoso, MA
AF Arancibia, Sergio
Benitez, Dixan
Nunez, Lucia E.
Jewell, Christine M.
Langjahr, Patricia
Candia, Enzo
Zapata-Torres, Gerald
Cidlowski, John A.
Gonzalez, Maria-Julieta
Hermoso, Marcela A.
TI Phosphatidylinositol 3-kinase interacts with the glucocorticoid receptor
upon TLR2 activation
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE lung mucosa inflammation; TLR2; glucocorticoid receptor;
phosphatidylinositol-3-kinase
ID NF-KAPPA-B; TOLL-LIKE RECEPTOR-2; GENE-EXPRESSION; SIGNAL-TRANSDUCTION;
P65 SUBUNIT; PHOSPHOINOSITIDE 3-KINASE; INNATE IMMUNITY; CELLS; PATHWAY;
LIPOPOLYSACCHARIDE
AB Airway inflammation is a common condition where glucocorticoids (GC) are a well-established therapy. It has been demonstrated that GC stimulate components of innate immunity. Specifically, GC up-regulate TLR2 expression and activation upon inflammatory stimuli; however, little is known about the signalling involved in this process. To determine the mechanism by which dexamethasone modulates TLR2-induced cytokine production this signalling pathway was monitored in a lung epithelial cell line exposed to the TLR2 synthetic agonist, Pam3-Cys-Ser-Lys4. These experiments demonstrate that phosphatidylinositol 3-kinase (PI3K) is critical for the TLR2 downstream effects of GC. Cells expressing a PI3K mutant (p85-dominant negative, DN; p85 Delta 478-511) and exposed to Pam3-Cys-Ser-Lys4 in the presence or absence of dexamethasone, showed enhanced tumour necrosis factor (TNF)alpha expression while AP-1 and NF-kappa B transcriptional activity were repressed. We provide experimental evidence that PI3K physically interacts with the glucocorticoid receptor (GR) through two putative PI3K recruitment consensus YxxM binding motifs in the GR, suggesting that some functions regulated by this receptor might occur through kinase interaction. Mutations of two tyrosine residues in the GR, 598 and 663, to phenylalanine significantly reduced interaction with PI3K and the GC effects on TLR2-induced TNF-alpha expression. However, these mutations did not alter GR transcriptional activity nor affect cellular localization of the expressed mutant GR in COS-1 cells. Therefore, the PI3K-GR interaction may contribute to the effects of GC on the TLR2 pro-inflammatory signalling cascade, thus defining a novel signalling mechanism with a profound impact on innate immune responses.
C1 [Hermoso, Marcela A.] Univ Chile, Fac Med, Inst Ciencias Biomed, Programa Disciplinario Inmunol,Sch Med, Santiago 7, Chile.
[Jewell, Christine M.; Cidlowski, John A.] NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Zapata-Torres, Gerald] Univ Chile, Fac Chem & Pharm, Dept Inorgan & Analyt Chem, Santiago 7, Chile.
[Gonzalez, Maria-Julieta] Univ Chile, Sch Med, Inst Biomed Sci, Cell & Mol Biol Program, Santiago 7, Chile.
RP Hermoso, MA (reprint author), Univ Chile, Fac Med, Inst Ciencias Biomed, Programa Disciplinario Inmunol,Sch Med, Independencia 1027, Santiago 7, Chile.
EM mhermoso@med.uchile.cl
FU FONDECYT [1080290, 1050451]; NIEHS/NIH
FX Funding support from FONDECYT 1080290, 1050451 and NIEHS/NIH, and to P.
Silva and C. Beltran for technical support and to Dr. F. Salazar for
providing cytokines and cell line supplies.
NR 45
TC 7
Z9 8
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1582-1838
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD FEB
PY 2011
VL 15
IS 2
BP 339
EP 349
DI 10.1111/j.1582-4934.2009.00958.x
PG 11
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 726TL
UT WOS:000287749000015
PM 19874421
ER
PT J
AU Muller-Hocker, J
Horvath, R
Schafer, S
Hessel, H
Muller-Felber, W
Kuhr, J
Copeland, WC
Seibel, P
AF Mueller-Hoecker, J.
Horvath, R.
Schaefer, S.
Hessel, H.
Mueller-Felber, W.
Kuehr, J.
Copeland, W. C.
Seibel, P.
TI Mitochondrial DNA depletion and fatal infantile hepatic failure due to
mutations in the mitochondrial polymerase gamma (POLG) gene: a combined
morphological/enzyme histochemical and immunocytochemical/biochemical
and molecular genetic study
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE depletion of mtDNA; polymerase gamma; mitochondrial single stranded
binding protein(mtSSB); mitochondrial transcription factor A (mtTFA);
liver failure; in situ hybridization
ID PROGRESSIVE EXTERNAL OPHTHALMOPLEGIA; DEOXYGUANOSINE KINASE GENE; MTDNA
DEPLETION; ALPERS-SYNDROME; RESPIRATORY-CHAIN; TRANSCRIPTION FACTOR;
INSITU HYBRIDIZATION; TK2 DEFICIENCY; LIVER-DISEASE; COPY NUMBER
AB Combined morphological, immunocytochemical, biochemical and molecular genetic studies were performed on skeletal muscle, heart muscle and liver tissue of a 16-months boy with fatal liver failure. The pathological characterization of the tissues revealed a severe depletion of mtDNA (mitochondrial DNA) that was most pronounced in liver, followed by a less severe, but still significant depletion in skeletal muscle and the heart. The primary cause of the disease was linked to compound heterozygous mutations in the polymerase gamma (POLG) gene (DNA polymerase gamma; A467T, K1191N). We present evidence, that compound heterozygous POLG mutations lead to tissue selective impairment of mtDNA replication and thus to a mosaic defect pattern even in the severely affected liver. A variable defect pattern was found in liver, muscle and heart tissue as revealed by biochemical, cytochemical, immunocytochemical and in situ hybridization analysis. Functionally, a severe deficiency of cytochrome-c-oxidase (cox) activity was seen in the liver. Although mtDNA depletion was detected in heart and skeletal muscle, there was no cox deficiency in these tissues. Depletion of mtDNA and microdissection of cox-positive or negative areas correlated with the histological pattern in the liver. Interestingly, the mosaic pattern detected for cox-activity and mtDNA copy number fully aligned with the immunohistologically revealed defect pattern using Pol gamma, mtSSB-and mtTFA-antibodies, thus substantiating the hypothesis that nuclear encoded proteins located within mitochondria become unstable and are degraded when they are not actively bound to mtDNA. Their disappearance could also aggravate the mtDNA depletion and contribute to the non-homogenous defect pattern.
C1 [Mueller-Hoecker, J.; Schaefer, S.; Hessel, H.] Univ Munich, Inst Pathol, D-80337 Munich, Germany.
[Horvath, R.] Univ Munich, Dept Neurol, Friedrich Baur Inst, D-80337 Munich, Germany.
[Horvath, R.] Newcastle Univ, Inst Ageing & Hlth, Mitochondrial Res Grp, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Mueller-Felber, W.] Univ Munich, Neurol Klin & Poliklin, Friedrich Baur Inst, D-80337 Munich, Germany.
[Kuehr, J.] Municipal Hosp Karlsruhe, Clin Pediat & Adolescent Med, Karlsruhe, Germany.
[Copeland, W. C.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Seibel, P.] Univ Leipzig, Biotechnol Biomed Zentrum, Leipzig, Germany.
RP Muller-Hocker, J (reprint author), Univ Munich, Inst Pathol, Thalkirchnerstr 36, D-80337 Munich, Germany.
EM josef.mueller-hoecker@med.uni-muenchen.de
FU National Institutes of Health, NIEHS; Sachsische Ministerium fur
Wissenschaft und Kunst; Deutsche Forschungsgemeinschaft [HO 2505/2-1]
FX The authors are indebted to Mrs. Diane Raabe and Mrs. Monika
Attmanspacher for invaluable help in preparing the manuscript. Funding
information: W. C. C. is funded by intramural funds from the National
Institutes of Health, NIEHS. This work was in part (P. S.) supported by
the Sachsische Ministerium fur Wissenschaft und Kunst. RH is supported
by the Deutsche Forschungsgemeinschaft HO 2505/2-1.
NR 63
TC 5
Z9 5
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1582-1838
J9 J CELL MOL MED
JI J. Cell. Mol. Med.
PD FEB
PY 2011
VL 15
IS 2
BP 445
EP 456
DI 10.1111/j.1582-4934.2009.00819.x
PG 12
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 726TL
UT WOS:000287749000023
PM 19538466
ER
PT J
AU Versiani, MA
Diyabalanage, T
Ratnayake, R
Henrich, CJ
Bates, SE
McMahon, JB
Gustafson, KR
AF Versiani, Muhammad Ali
Diyabalanage, Thushara
Ratnayake, Ranjala
Henrich, Curtis J.
Bates, Susan E.
McMahon, James B.
Gustafson, Kirk R.
TI Flavonoids from Eight Tropical Plant Species That Inhibit the Multidrug
Resistance Transporter ABCG2
SO JOURNAL OF NATURAL PRODUCTS
LA English
DT Article
ID PROTEIN; CANCER; LEAVES; FLAVANONES; AGLYCONES; ASSAY
AB Overexpression of ABCG2, a membrane-bound multidrug transporter, can make tumor cells resistant to treatment with conventional chemotherapeutic agents. A high-throughput screening effort with the NCI repository of natural product extracts revealed that eight tropical plant extracts significantly inhibited the function of ABCG2. This activity was tracked throughout the extract fractionation process to a series of ABCG2 inhibitory flavonoids (1-13). Their structures were identified by a combination of NMR, mass spectrometry, and circular dichroism studies, and this resulted in the elucidation of (2S)-5,7,3'-trihydroxy-4'-methoxy-8-(3 ''-methylbut-2 ''-enyl)-flavonone (1), (2S)-5,7,3',5'-tetrahydroxy-8-[3 '',8 ''-dimethylocta-2 ''(E),7 ''-dienyl]flavonone (3), and 5,7,3'-trihydroxy-3,5'-dimethoxy-2'-(3'-methylbut-2-enyl)flavone (12,) as new compounds.
C1 [Versiani, Muhammad Ali; Diyabalanage, Thushara; Ratnayake, Ranjala; Henrich, Curtis J.; McMahon, James B.; Gustafson, Kirk R.] NCI Frederick, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21702 USA.
[Henrich, Curtis J.] NCI Frederick, SAIC Frederick, Frederick, MD 21702 USA.
[Bates, Susan E.] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Gustafson, KR (reprint author), NCI Frederick, Mol Targets Lab, Ctr Canc Res, Frederick, MD 21702 USA.
EM gustafki@mail.nih.gov
OI Versiani, Muhammad Ali/0000-0002-9587-5891
FU Higher Education Commission (HEC), Government of Pakistan; NIH, National
Cancer Institute, Center for Cancer Research; National Cancer Institute,
National Institutes of Health [HHSN261200800001E]
FX We thank D. Newman (NCI) and T. McCloud (SAIC-Frederick) for the plant
extracts and M. Dyba and S. Terasova (Biophysics Resource, SBL,
NCI-Frederick) for assistance with the HRLCMS studies, M.A.V. gratefully
acknowledges the Higher Education Commission (HEC), Government of
Pakistan, for providing a Post Doctoral scholarship. This research was
supported in part by the Intramural Research Program of NIH, National
Cancer Institute, Center for Cancer Research. This project was also
funded in part with Federal funds from the National Cancer Institute,
National Institutes of Health, under contract HHSN261200800001E. The
content of this publication does not necessarily reflect the views or
policies of the Department of Health and Human Services, nor does
mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government.
NR 29
TC 10
Z9 11
U1 0
U2 9
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 FEB
PY 2011
VL 74
IS 2
BP 262
EP 266
DI 10.1021/np100797y
PG 5
WC Plant Sciences; Chemistry, Medicinal; Pharmacology & Pharmacy
SC Plant Sciences; Pharmacology & Pharmacy
GA 725IB
UT WOS:000287637300022
PM 21275386
ER
PT J
AU Le, K
Coelho, C
Mozeiko, J
Grafman, J
AF Le, Karen
Coelho, Carl
Mozeiko, Jennifer
Grafman, Jordan
TI Measuring Goodness of Story Narratives
SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH
LA English
DT Article
DE discourse analysis; content analysis; story grammar; narrative discourse
ID TRAUMATIC BRAIN-INJURY; CLOSED-HEAD-INJURY; DISCOURSE PRODUCTION;
ADULTS; ADOLESCENTS; KNOWLEDGE; CHILDREN; ABILITY; SKILLS; MILD
AB Purpose: The purpose of this article was to evaluate a new measure of story narrative performance: story completeness. It was hypothesized that by combining organizational (story grammar) and completeness measures, story "goodness" could be quantified.
Method: Discourse samples from 46 typically developing adults were compared with those from 24 adults with acquired brain injuries. Story retellings were elicited and analyzed for episode structure (story grammar). Each story was also evaluated for the presence of 5 key components, yielding the story completeness score. Story goodness was quantified by combining the story grammar and completeness measures using a 2-coordinate grid system. A multivariate analysis of variance was performed as well as correlational analyses between the story grammar and story completeness scores.
Results: There were significant group differences on both story grammar and story completeness. Moderate correlations were noted between the 2 measures, suggesting that the indices were not entirely measuring the same abilities. Plotting the 2 sets of scores into quadrants discriminated the comparison group and the group with brain injury into 4 distinct categories of story "goodness."
Conclusion: The combination of measures provided a more accurate depiction of discourse performance than either measure alone. Results suggest the measure is sensitive, is reliable, and has potential utility for investigating discourse deficits in clinical populations.
C1 [Le, Karen; Coelho, Carl; Mozeiko, Jennifer] Univ Connecticut, Storrs, CT USA.
[Grafman, Jordan] NIH, Bethesda, MD 20892 USA.
RP Grafman, J (reprint author), NINDS, Cognit Neurosci Sect, Bldg 10,7D43,MSC 1440, Bethesda, MD 20892 USA.
EM grafmanj@ninds.nih.gov
OI Grafman, Jordan H./0000-0001-8645-4457
NR 30
TC 12
Z9 12
U1 0
U2 3
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1092-4388
J9 J SPEECH LANG HEAR R
JI J. Speech Lang. Hear. Res.
PD FEB 1
PY 2011
VL 54
IS 1
BP 118
EP 126
DI 10.1044/1092-4388(2010/09-0022)
PG 9
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 714IY
UT WOS:000286804500015
PM 20719868
ER
PT J
AU Baccarelli, A
Benjamin, EJ
AF Baccarelli, Andrea
Benjamin, Emelia J.
TI Triggers of MI for the individual and in the community
SO LANCET
LA English
DT Editorial Material
ID AMERICAN-HEART-ASSOCIATION; AIR-POLLUTION; DISEASE; UPDATE
C1 [Baccarelli, Andrea] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Exposure Epidemiol & Risk Program, Boston, MA 02115 USA.
[Benjamin, Emelia J.] NHLBI, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Cardiol Sect, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Prevent Med Sect, Boston, MA 02118 USA.
RP Baccarelli, A (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Exposure Epidemiol & Risk Program, Boston, MA 02115 USA.
EM abaccare@hsph.harvard.edu
OI Baccarelli, Andrea/0000-0002-3436-0640; Benjamin,
Emelia/0000-0003-4076-2336
FU NIEHS NIH HHS [P30 ES000002, P30 ES000002-46]
NR 10
TC 6
Z9 6
U1 0
U2 0
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 FEB-MAR
PY 2011
VL 377
IS 9767
BP 694
EP 696
DI 10.1016/S0140-6736(10)62348-3
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 729JQ
UT WOS:000287946000005
PM 21353302
ER
PT J
AU Kutlesic, V
AF Kutlesic, Vesna
TI Empowering schools to serve as safety nets for children with behavior
problems in Serbia
SO LEARNING AND INDIVIDUAL DIFFERENCES
LA English
DT Article
DE Special education; Behavior problems; Serbia; Eastern Europe
AB Children with special needs have been a focus of institutional reforms in Serbia for nearly two decades. Historically, as in other Eastern European countries, children with severe developmental, emotional, and/or behavior disorders in Serbia were often placed in institutions far from their families for much of their lives. Since the fall of communism, extensive government reforms in Serbia, guided by Western development agencies, have focused on deinstitutionalizing youth, but only with modest results. Underdeveloped special education programs within the Serbian public school system, have also contributed to children with special needs being at increased risk for leaving school and having legal problems. However, newly passed legislation is empowering Serbian schools and communities to serve as safety nets for vulnerable youth. Published by Elsevier Inc.
C1 [Kutlesic, Vesna] US NIH, UNICEF, Belgrade 11000, Serbia.
RP Kutlesic, V (reprint author), US NIH, Off Director, 1 Ctr Dr,Room 114, Bethesda, MD 20892 USA.
EM vkutlesic@aol.com
NR 25
TC 0
Z9 0
U1 1
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1041-6080
J9 LEARN INDIVID DIFFER
JI Learn. Individ. Differ.
PD FEB
PY 2011
VL 21
IS 1
BP 41
EP 48
DI 10.1016/j.lindif.2010.10.007
PG 8
WC Psychology, Educational
SC Psychology
GA 713EZ
UT WOS:000286719100006
ER
PT J
AU Liu, ZF
Jia, B
Zhao, HY
Chen, XY
Wang, F
AF Liu, Zhaofei
Jia, Bing
Zhao, Huiyun
Chen, Xiaoyuan
Wang, Fan
TI Specific Targeting of Human Integrin alpha(v)beta(3) with In-111-Labeled
Abegrin (TM) in Nude Mouse Models
SO MOLECULAR IMAGING AND BIOLOGY
LA English
DT Article
DE Tumor; Integrin alpha(v)beta(3); In-111; Abegrin (TM); Imaging
ID POSITRON-EMISSION-TOMOGRAPHY; RGD-BOMBESIN HETERODIMER;
MONOCLONAL-ANTIBODY LA22; IN-VITRO; CANCER-THERAPY; TUMOR; RECEPTOR;
ALPHA-V-BETA-3; EXPRESSION; ANGIOGENESIS
AB The cell adhesion molecule integrin alpha(v)beta(3) is an important player in the process of tumor angiogenesis and metastasis. Abegrin (TM), a fully humanized anti-integrin alpha(v)beta(3) monoclonal antibody, was currently in clinical trials for cancer therapy. Herein, we labeled Abegrin (TM) with In-111, evaluated the in vitro and in vivo characteristics, and investigated whether the expression of integrin alpha(v)beta(3) in tumors could be imaged with In-111-labeled Abegrin (TM).
The binding affinity and specificity of Abegrin (TM) was analyzed using U87MG glioblastoma cells. Abegrin (TM) was coupled with 1,4,7,10-tetraazadodecane-N,N',NaEuro(3),N'aEuro(3)-tetraacetic acid (DOTA) for In-111 radiolabeling. gamma Imaging of In-111-DOTA-Abegrin (TM) was carried out in nude mice bearing both integrin alpha(v)beta(3)-positive U87MG and integrin alpha(v)beta(3)-negative HT-29 tumors. Biodistribution and blocking studies of In-111-DOTA-Abegrin (TM) were investigated in U87MG tumor-bearing nude mice.
Abegrin (TM) exhibited high-binding affinity to human integrin alpha(v)beta(3) expressed on U87MG cells (K (d) of 0.35 +/- 0.06 nM). The antibody retained antigen-binding affinity/specificity after DOTA conjugation. gamma Imaging showed that the tumor uptake of In-111-DOTA-Abegrin (TM) in integrin alpha(v)beta(3)-positive U87MG tumors was much higher than that in integrin alpha(v)beta(3)-negative HT-29 tumors. In the HT-29 tumors, Abegrin (TM) was mainly nonspecifically accumulated around the blood vessels, while in the U87MG tumors, besides the nonspecific tumor retention, Abegrin (TM) also specifically bound the human integrin alpha(v)beta(3) expressed on the tumor cells. Biodistribution and blocking studies exhibited that the U87MG tumor uptake of In-111-DOTA-Abegrin (TM) decreased from 14.12 +/- 0.44 to 6.93 +/- 0.94 percentage of injected dose per gram of tissue after coinjection of excess dose of cold Abegrin (TM), which confirmed the in vivo integrin alpha(v)beta(3) binding specificity of In-111-DOTA-Abegrin (TM).
Abegrin (TM) showed specific binding to human integrin alpha(v)beta(3) expressed on the tumor cells. In-111-DOTA-Abegrin (TM) can specifically target the human integrin alpha(v)beta(3) expression in the nude mouse model. In-111-DOTA-Abegrin (TM) has a potential for clinical translation as an agent for integrin alpha(v)beta(3)-positive tumor imaging, evaluating tumor angiogenic status and monitoring the therapeutic efficacy of Abegrin (TM)-based cancer therapy.
C1 [Liu, Zhaofei; Jia, Bing; Zhao, Huiyun; Wang, Fan] Peking Univ, Sch Basic Med Sci, Med Isotopes Res Ctr, Beijing 100191, Peoples R China.
[Liu, Zhaofei; Jia, Bing; Zhao, Huiyun; Wang, Fan] Peking Univ, Sch Basic Med Sci, Dept Radiat Med, Beijing 100191, Peoples R China.
[Chen, Xiaoyuan] Stanford Univ, Sch Med, MIPS, Dept Radiol,Biophys & Biox Program, Stanford, CA 94305 USA.
[Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
RP Wang, F (reprint author), Peking Univ, Sch Basic Med Sci, Med Isotopes Res Ctr, 38 Xueyuan Rd, Beijing 100191, Peoples R China.
EM wangfan@bjmu.edu.cn
RI Jia, Bing/C-3796-2008
FU NSFC [30930030, 30870728, 30900373, 20820102035]; 863 project
[2007AA02Z467]; Ministry of Science and Technology of China
[2009ZX09103-733, 2009ZX09301-010, 2009ZX09103-746]
FX We thank Mr. Zhi Yang and Mr. Cunjing Jin for their excellent technical
assistance with gamma-imaging and biodistribution studies. This work is
jointly supported by NSFC projects (30930030, 30870728, 30900373, and
20820102035), an 863 project (2007AA02Z467), and grants from the
Ministry of Science and Technology of China (2009ZX09103-733,
2009ZX09301-010, and 2009ZX09103-746).
NR 39
TC 12
Z9 12
U1 2
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1536-1632
EI 1860-2002
J9 MOL IMAGING BIOL
JI Mol. Imaging. Biol.
PD FEB
PY 2011
VL 13
IS 1
BP 112
EP 120
DI 10.1007/s11307-010-0302-4
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 708WS
UT WOS:000286395600015
PM 20383594
ER
PT J
AU Riddle, LR
Kumar, R
Griffin, SA
Grundt, P
Newman, AH
Luedtke, RR
AF Riddle, Lindsay R.
Kumar, Rakesh
Griffin, Suzy A.
Grundt, Peter
Newman, Amy Hauck
Luedtke, Robert R.
TI Evaluation of the D3 dopamine receptor selective agonist/partial agonist
PG01042 on L-dopa dependent animal involuntary movements in rats
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Parkinson's Disease; Dyskinesia; L-dopa; Dopamine receptors; D3 dopamine
receptors
ID FUNCTIONALIZED LINKING CHAINS; ABUSE THERAPEUTIC AGENTS; MESSENGER-RNA;
IN-VIVO; PREFRONTAL CORTEX; PHOSPHOLIPASE-D; D-3 RECEPTOR; INDUCED
DYSKINESIAS; PARKINSONS-DISEASE; NUCLEUS-ACCUMBENS
AB The substituted 4-phenylpiperazine D3 dopamine receptor selective antagonist PG01037 ((E)-N-(4-(4-(2,3-dichlorophenyl)piperazin-1-yl)but-2-enyl)-4-(pyridin-2-yl)benzamide) was reported to attenuate L-dopa-associated abnormal involuntary movements (AIMS) in unilaterally lesioned rats, a model of L-dopa-dependent dyskinesia in patients with Parkinson's Disease (Kumar et al., 2009a). We now report that PG01042 (N-(4-(4-(2,3-dichlorophenyl)piperazin-1-yl)butyl)-4-(pyridin-3-yl)benzamide), which is a D3 dopamine receptor selective agonist for adenylyl cyclase inhibition and a partial agonist for mitogenesis, is also capable of attenuating AIMs scores. The intrinsic activity of PG01037 and PG01042 were determined using a) a forskolin-dependent adenylyl cyclase inhibition assay and b) an assay for agonist-associated mitogenesis. It was observed that the in vivo efficacy of PG01042 increased when administered by intraperitoneal (i.p.) injection simultaneously with L-dopa/benserazide (8 mg/kg each), as compared to a 60 min or 30 min pretreatment. PG01042 was found to attenuate AIM scores in these animals in a dose dependent manner. While PG01042 did not effectively inhibit SKF 81297-dependent AIMs, it inhibited apomorphine-dependent AIM scores. Rotarod studies indicate that PG01042 at a dose of 10 mg/kg did not adversely affect motor coordination of the unilaterally lesioned rats. Evaluation of lesioned rats using a cylinder test behavioral paradigm indicated that PG01042 did not dramatically attenuate the beneficial effects of L-dopa. These studies and previously published studies suggest that both D3 dopamine receptor selective antagonists, partial agonists and agonists, as defined by an adenylyl cyclase inhibition assay and a mitogenic assay, are pharmacotherapeutic candidates for the treatment of L-dopa-associated dyskinesia in patients with Parkinson's Disease. (C) 2010 Published by Elsevier Ltd.
C1 [Riddle, Lindsay R.; Kumar, Rakesh; Griffin, Suzy A.; Luedtke, Robert R.] Univ N Texas Hlth Sci Ctr, Dept Pharmacol & Neurosci, Ft Worth, TX 76107 USA.
[Grundt, Peter; Newman, Amy Hauck] Natl Inst Drug Abuse, Med Chem Sect, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Luedtke, RR (reprint author), Univ N Texas Hlth Sci Ctr, Dept Pharmacol & Neurosci, 3500 Camp Bowie, Ft Worth, TX 76107 USA.
EM robert.luedke@unthsc.edu
FU Michael J. Fox Foundation for Parkinson's Research; NIDA-IRP;
[N01DA-1-8816]; [R-01 DA13584-0351]
FX This research was supported by a Community Fast Track 2006 from the
Michael J. Fox Foundation for Parkinson's Research and R-01 DA13584-0351
(RRL) and the NIDA-IRP (AHN and PG). The authors would like to thank
Drs. Eunson Jung and Nathalie Sumien for their assistance with the
statistical analysis and helpful discussions. The authors also thank the
NIDA Addiction Treatment Discovery Program for contract resources used
to conduct the D2 and D3 receptor based mitogenic assays. These were
contract N01DA-1-8816 to SRI International (PI Larry Toll) and
interagency agreement IAGY1 DA 5007-05 to the Portland VA Medical Center
(PI Aaron Janowsky).
NR 79
TC 7
Z9 7
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD FEB-MAR
PY 2011
VL 60
IS 2-3
BP 284
EP 294
DI 10.1016/j.neuropharm.2010.09.011
PG 11
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 717NL
UT WOS:000287054600011
PM 20850462
ER
PT J
AU Dlamini, JN
Hu, ZH
Somaroo, H
Highbarger, HC
Follmann, DA
Dewar, RL
Pau, AK
AF Dlamini, Judith N.
Hu, Zonghui
Somaroo, Harsha
Highbarger, Helene C.
Follmann, Dean A.
Dewar, Robin L.
Pau, Alice K.
TI Lack of Effect from a Previous Single Dose of Nevirapine on Virologic
and Immunologic Responses After 6 Months of Antiretroviral Regimens
Containing Either Efavirenz or Lopinavir-Ritonavir
SO PHARMACOTHERAPY
LA English
DT Article; Proceedings Paper
CT 16th Conference on Retroviruses and Opportunistic Infections (CROI)
CY FEB 08-11, 2009
CL Montreal, CANADA
DE single-dose nevirapine; efavirenz; human immunodeficiency virus; HIV;
response; antiretroviral; South Africa; women
ID OPEN-LABEL TRIAL; THERAPY; HIV-1; TRANSMISSION; EXPOSURE; WOMEN;
RESISTANCE; MOTHERS; AFRICA
AB Study Objective. To evaluate the effect of a previous single dose of nevirapine given to prevent mother-to-child transmission of human immunodeficiency virus (HIV) on virologic and immunologic measures after 6 months of an antiretroviral regimen containing either efavirenz or lopinavir-ritonavir.
Design. Retrospective subgroup analysis of data from the Phidisa II trial.
Setting. Six South African research clinics.
Patients. A total of 394 women with HIV who completed 6 months of combination antiretroviral regimen containing either efavirenz or lopinavir-ritonavir as part of the Phidisa II trial.
Measurements and Main Results. During the screening process for the Phidisa II study, 478 women were asked about previous nevirapine use: 392 women (82%) were nevirapine naive, and 86 (18%) had received nevirapine. During the study, patients received either an efavirenz-based or lopinavir-ritonavir based antiretroviral regimen. After 6 months of treatment, virologic (HIV RNA levels) and immunologic (CD4(+) cell count) responses were measured. These data were compared between women with or without previous nevirapine exposure, and between women who received efavirenz versus lopinavir-ritonavir. After 6 months of treatment, 394 women (324 nevirapine naive, 70 exposed to nevirapine) had follow-up HIV RNA results. Two hundred twenty-seven (70.1%) of the nevirapine-naive patients and 48 (68.6%) of the nevirapine-exposed patients achieved HIV RNA levels lower than 400 copies/ml (p=0.89), with CD4(+) cell count increases of 115.5 and 120.4 cells/mm(3), respectively (p=0.67). Among the nevirapine-exposed women, 27 (75%) of 36 efavirenz-treated and 21 (61.8%) of 34 lopinavir-ritonavir-treated patients had HIV RNA levels lower than 400 copies/ml at 6 months (p=0.31).
Conclusion. In this retrospective analysis of a small cohort, previous exposure to a single dose of nevirapine did not affect virologic outcomes after 6 months of either an efavirenz-based or lopinavir-ritonavir-based antiretroviral regimen. As efavirenz is one of the first-line combination antiretroviral therapies administered in Africa, it remains an option for women who received single-dose nevirapine.
C1 [Hu, Zonghui; Follmann, Dean A.; Pau, Alice K.] NIAID, Div Clin Res, NIH, Bethesda, MD 20892 USA.
[Dlamini, Judith N.; Somaroo, Harsha] S African Mil Hlth Serv, Project Phidisa, Centurion, South Africa.
[Highbarger, Helene C.; Dewar, Robin L.] NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Pau, AK (reprint author), NIAID, Div Clin Res, NIH, Bldg 10,Room 11C103,MSC 1880, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z99 AI999999]
NR 15
TC 0
Z9 0
U1 0
U2 1
PU PHARMACOTHERAPY PUBLICATIONS INC
PI BOSTON
PA NEW ENGLAND MEDICAL CENTER, 806, 750 WASHINGTON ST, BOSTON, MA 02111 USA
SN 0277-0008
J9 PHARMACOTHERAPY
JI Pharmacotherapy
PD FEB
PY 2011
VL 31
IS 2
BP 158
EP 163
DI 10.1592/phco.31.2.158
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 716IX
UT WOS:000286963400005
PM 21275494
ER
PT J
AU Abe, K
Puertollano, R
AF Abe, Ken
Puertollano, Rosa
TI Role of TRP Channels in the Regulation of the Endosomal Pathway
SO PHYSIOLOGY
LA English
DT Review
ID MUCOLIPIDOSIS TYPE-IV; RECEPTOR POTENTIAL CHANNEL; ADENINE-DINUCLEOTIDE
PHOSPHATE; VARITINT-WADDLER PHENOTYPE; CYCLIC ADP-RIBOSE;
PLASMA-MEMBRANE; CATION CHANNEL; CA2+-PERMEABLE CHANNEL; ENDOCYTIC
PATHWAY; CELL DEGENERATION
AB Some members of the transient receptor potential (TRP) channel superfamily have proved to be essential in maintaining adequate ion homeostasis, signaling, and membrane trafficking in the endosomal pathway. The unique properties of the TRP channels confer cells the ability to integrate cytosolic and intraluminal stimuli and allow maintained and regulated release of Ca2+ from endosomes and lysosomes.
C1 [Abe, Ken; Puertollano, Rosa] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Abe, K (reprint author), NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
EM puertolr@mail.nih.gov
FU National Heart, Lung, and Blood Institute
FX This project was supported by the Intramural Research Program of the
National Heart, Lung, and Blood Institute.
NR 101
TC 26
Z9 28
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1548-9213
J9 PHYSIOLOGY
JI Physiology
PD FEB
PY 2011
VL 26
IS 1
BP 14
EP 22
DI 10.1152/physiol.00048.2010
PG 9
WC Physiology
SC Physiology
GA 728GC
UT WOS:000287861600003
PM 21357899
ER
PT J
AU Migueles, SA
Rood, JE
Berkley, AM
Guo, T
Mendoza, D
Patamawenu, A
Hallahan, CW
Cogliano, NA
Frahm, N
Duerr, A
McElrath, MJ
Connors, M
AF Migueles, Stephen A.
Rood, Julia E.
Berkley, Amy M.
Guo, Tiffany
Mendoza, Daniel
Patamawenu, Andy
Hallahan, Claire W.
Cogliano, Nancy A.
Frahm, Nicole
Duerr, Ann
McElrath, M. Juliana
Connors, Mark
TI Trivalent Adenovirus Type 5 HIV Recombinant Vaccine Primes for Modest
Cytotoxic Capacity That Is Greatest in Humans with Protective HLA Class
I Alleles
SO PLOS PATHOGENS
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; T-CELL RESPONSES; LONG-TERM
NONPROGRESSORS; IMMUNE CONTROL; ELITE SUPPRESSORS; VIRAL LOAD;
INFECTION; REPLICATION; PROLIFERATION; IMMUNOGENICITY
AB If future HIV vaccine design strategies are to succeed, improved understanding of the mechanisms underlying protection from infection or immune control over HIV replication remains essential. Increased cytotoxic capacity of HIV-specific CD8(+) T-cells associated with efficient elimination of HIV-infected CD4(+) T-cell targets has been shown to distinguish long-term nonprogressors (LTNP), patients with durable control over HIV replication, from those experiencing progressive disease. Here, measurements of granzyme B target cell activity and HIV-1-infected CD4(+) T-cell elimination were applied for the first time to identify antiviral activities in recipients of a replication incompetent adenovirus serotype 5 (Ad5) HIV-1 recombinant vaccine and were compared with HIV-negative individuals and chronically infected patients, including a group of LTNP. We observed readily detectable HIV-specific CD8(+) T-cell recall cytotoxic responses in vaccinees at a median of 331 days following the last immunization. The magnitude of these responses was not related to the number of vaccinations, nor did it correlate with the percentages of cytokine-secreting T-cells determined by ICS assays. Although the recall cytotoxic capacity of the CD8(+) T-cells of the vaccinee group was significantly less than that of LTNP and overlapped with that of progressors, we observed significantly higher cytotoxic responses in vaccine recipients carrying the HLA class I alleles B*27, B*57 or B*58, which have been associated with immune control over HIV replication in chronic infection. These findings suggest protective HLA class I alleles might lead to better outcomes in both chronic infection and following immunization due to more efficient priming of HIV-specific CD8(+) T-cell cytotoxic responses.
C1 [Migueles, Stephen A.; Rood, Julia E.; Berkley, Amy M.; Guo, Tiffany; Mendoza, Daniel; Patamawenu, Andy; Cogliano, Nancy A.; Connors, Mark] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Frahm, Nicole; Duerr, Ann; McElrath, M. Juliana] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Div, Seattle, WA 98104 USA.
[Frahm, Nicole; Duerr, Ann; McElrath, M. Juliana] Fred Hutchinson Canc Res Ctr, HIV Vaccine Trials Network, Seattle, WA 98104 USA.
[Hallahan, Claire W.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
RP Migueles, SA (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM mconnors@niaid.nih.gov
OI Mendoza, Daniel/0000-0002-6362-0771
FU NIH, National Institute of Allergy and Infectious Diseases; HVTN
Laboratory (NIH) [U01 AI068618]; Seattle Vaccine Unit (NIH) [U01
AI069481]; HVTN Core Leadership [U01 AI068614]
FX This research was supported in part by the Intramural Research Program
of the NIH, National Institute of Allergy and Infectious Diseases. The
HVTN Laboratory Program (NIH U01 AI068618), the Seattle Vaccine Unit
(NIH U01 AI069481) and HVTN Core Leadership (U01 AI068614) provided
additional support. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 39
TC 18
Z9 18
U1 0
U2 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD FEB
PY 2011
VL 7
IS 2
AR e1002002
DI 10.1371/journal.ppat.1002002
PG 10
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 726DE
UT WOS:000287698200046
PM 21383976
ER
PT J
AU Whitney, JB
Hraber, PT
Luedemann, C
Giorgi, EE
Daniels, MG
Bhattacharya, T
Rao, SS
Mascola, JR
Nabel, GJ
Korber, BT
Letvin, NL
AF Whitney, James B.
Hraber, Peter T.
Luedemann, Corinne
Giorgi, Elena E.
Daniels, Marcus G.
Bhattacharya, Tanmoy
Rao, Srinivas S.
Mascola, John R.
Nabel, Gary J.
Korber, Bette T.
Letvin, Norman L.
TI Genital Tract Sequestration of SIV following Acute Infection
SO PLOS PATHOGENS
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; DRUG-RESISTANCE MUTATIONS; PRIMARY HIV-1
INFECTION; CD4(+) T-CELLS; SEXUAL TRANSMISSION; SEMINAL PLASMA; VIRAL
LOAD; HETEROSEXUAL TRANSMISSION; HIV-1-INFECTED MEN; GENETIC ALGORITHM
AB We characterized the evolution of simian immunodeficiency virus (SIV) in the male genital tract by examining blood-and semen-associated virus from experimentally and sham vaccinated rhesus monkeys during primary infection. At the time of peak virus replication, SIV sequences were intermixed between the blood and semen supporting a scenario of high-level virus "spillover" into the male genital tract. However, at the time of virus set point, compartmentalization was apparent in 4 of 7 evaluated monkeys, likely as a consequence of restricted virus gene flow between anatomic compartments after the resolution of primary viremia. These findings suggest that SIV replication in the male genital tract evolves to compartmentalization after peak viremia resolves.
C1 [Whitney, James B.; Luedemann, Corinne; Letvin, Norman L.] Beth Israel Deaconess Med Ctr, Dept Med, Div Viral Pathogenesis, Boston, MA 02215 USA.
[Whitney, James B.; Letvin, Norman L.] Harvard Univ, Sch Med, Boston, MA USA.
[Hraber, Peter T.; Giorgi, Elena E.; Daniels, Marcus G.; Bhattacharya, Tanmoy; Korber, Bette T.] Los Alamos Natl Lab, Los Alamos, NM USA.
[Rao, Srinivas S.; Mascola, John R.; Nabel, Gary J.; Letvin, Norman L.] NIAID, Vaccine Res Ctr, Bethesda, MD 20892 USA.
RP Whitney, JB (reprint author), Beth Israel Deaconess Med Ctr, Dept Med, Div Viral Pathogenesis, Boston, MA 02215 USA.
EM jwhitne2@bidmc.harvard.edu
RI Bhattacharya, Tanmoy/J-8956-2013;
OI Bhattacharya, Tanmoy/0000-0002-1060-652X; Korber,
Bette/0000-0002-2026-5757; Hraber, Peter/0000-0002-2920-4897
FU Vaccine Research Center (VRC); National Institute of Allergy and
Infectious Diseases (NIAID); Center for HIV/AIDS Vaccine Immunology
(CHAVI) [AI067854]
FX This work was supported by the Intramural Research Program of the
Vaccine Research Center (VRC), and the National Institute of Allergy and
Infectious Diseases (NIAID), and the Center for HIV/AIDS Vaccine
Immunology (CHAVI) AI067854. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
NR 77
TC 12
Z9 12
U1 0
U2 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1553-7366
J9 PLOS PATHOG
JI PLoS Pathog.
PD FEB
PY 2011
VL 7
IS 2
AR e1001293
DI 10.1371/journal.ppat.1001293
PG 13
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 726DE
UT WOS:000287698200031
PM 21379569
ER
PT J
AU Berger, VW
AF Berger, Vance W.
TI Intent-to-Treat: Further Insight
SO RESEARCH IN NURSING & HEALTH
LA English
DT Letter
ID CLINICAL-TRIALS
C1 NCI, Biometry Res Grp, Bethesda, MD 20892 USA.
RP Berger, VW (reprint author), NCI, Biometry Res Grp, Execut Plaza N,Suite 3131,6130 Execut Blvd,MSC 73, Bethesda, MD 20892 USA.
NR 4
TC 2
Z9 2
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0160-6891
J9 RES NURS HEALTH
JI Res. Nurs. Health
PD FEB
PY 2011
VL 34
IS 1
BP 4
EP 4
DI 10.1002/nur.20405
PG 1
WC Nursing
SC Nursing
GA 710WH
UT WOS:000286547200002
PM 20957665
ER
PT J
AU Brzezinski, K
Dauter, Z
Baj, A
Walejko, P
Witkowski, S
AF Brzezinski, Krzysztof
Dauter, Zbigniew
Baj, Aneta
Walejko, Piotr
Witkowski, Stanislaw
TI rac-6-Hydroxy-2,5,7,8-tetramethylchroman-2-carboxamide from synchrotron
data
SO ACTA CRYSTALLOGRAPHICA SECTION E-STRUCTURE REPORTS ONLINE
LA English
DT Article
ID (2R,4'R,8'R)-ALPHA-TOCOPHEROL VITAMIN-E; ANTIOXIDANT ACTIVITY;
INTERMEDIATE; DERIVATIVES; ENANTIOMERS; PRECURSOR; CHROMANS; ACID
AB The crystal structure of the title water-soluble analogue of vitamin E, trolox amide, C14H19NO3, solved and refined against synchrotron diffraction data, contains two molecules in the asymmetric unit. In both molecules, the heterocyclic ring is in a half-chair conformation. The crystal packing features a herring-bone pattern generated by N-H center dot center dot center dot O hydrogen bonds between the hydroxy and amide groups. O-H center dot center dot center dot O hydrogen bonds also occur.
C1 [Brzezinski, Krzysztof; Dauter, Zbigniew] Argonne Natl Lab, Synchrotron Radiat Res Sect, MCL, Natl Canc Inst,Biosci Div, Argonne, IL 60439 USA.
[Baj, Aneta; Walejko, Piotr; Witkowski, Stanislaw] Univ Bialystok, Inst Chem, PL-15443 Bialystok, Poland.
RP Brzezinski, K (reprint author), Argonne Natl Lab, Synchrotron Radiat Res Sect, MCL, Natl Canc Inst,Biosci Div, Bldg 202, Argonne, IL 60439 USA.
EM kbrzezinski@anl.gov
FU Polish Ministry of Science and Higher Education [N N204 177639]; NIH,
National Cancer Institute, Center for Cancer Research; US Department of
Energy [W-31-109-Eng-38]
FX Financial support from the Polish Ministry of Science and Higher
Education (grant No. N N204 177639) is gratefully acknowledged. This
work was in part supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research. X-ray data
were collected at the NECAT 24ID-C beamline of the Advanced Photon
Source, Argonne National Laboratory. Use of the APS was supported by the
US Department of Energy under contract No. W-31-109-Eng-38.
NR 20
TC 1
Z9 1
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1600-5368
J9 ACTA CRYSTALLOGR E
JI Acta Crystallogr. Sect. E.-Struct Rep. Online
PD FEB
PY 2011
VL 67
BP O503
EP U1854
DI 10.1107/S1600536811002807
PN 2
PG 14
WC Crystallography
SC Crystallography
GA 719PF
UT WOS:000287216300159
PM 21523156
ER
PT J
AU Khan, A
Nasir, K
Khosa, F
Saghir, A
Sarwar, S
Clouse, ME
AF Khan, Atif
Nasir, Khurram
Khosa, Faisal
Saghir, Amina
Sarwar, Sheryar
Clouse, Melvin E.
TI Prospective Gating With 320-MDCT Angiography: Effect of Volume Scan
Length on Radiation Dose
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article
DE 320-MDCT; cardiac imaging; coronary artery disease; radiation dose
reduction; volume scan length
ID MULTISLICE COMPUTED-TOMOGRAPHY; CORONARY CT ANGIOGRAPHY; DIAGNOSTIC
PERFORMANCE; IMAGE QUALITY; PEDIATRIC-PATIENTS; EXPOSURE; HEART; CHEST;
REDUCTION; ARTERIES
AB OBJECTIVE. The purpose of this study was to evaluate the relation between radiation dose reduction and volume scan length for prospectively ECG-gated 320-MDCT angiography in the diagnosis of coronary artery disease.
MATERIALS AND METHODS. MDCT with prospective ECG gating was performed at one of the three volume scan lengths depending on heart length. Of 175 patients, 95 (55%; body mass index, 29 +/- 5.9; mean heart rate, 59 +/- 7 beats/min) underwent scanning at 160 mm; 46 (26%; body mass index, 30 +/- 4.1; mean heart rate, 56 +/- 5.74 beats/min) at 140 mm; and 34 (19%; body mass index, 30 +/- 3.71; mean heart rate, 58 +/- 3.96 beats/min) at 120 mm.
RESULTS. The median radiation doses were 6.5 mSv (95% CI, 6.03-7.2 mSv) for the 95 patients who underwent scanning at a volume scan length of 160 mm, 4.33 mSv (95% CI, 4.06-6.62 mSv) for the 46 patients who underwent scanning at 140 mm, and 3.47 mSv (95% CI, 3.15-3.62 mSv) for the 34 patients who underwent scanning at 120 mm. The reduction in scan length from 160 to 140 mm represented a reduction in scan length of 12.5% and the reduction to 120 mm a reduction of 25%. The median radiation dose was reduced 33% when volume scan length was changed to 140 mm and 47% when the length was changed to 120 mm.
CONCLUSION. Dose optimization remains an important concern in cardiac CT, and for 320-MDCT angiography, substantial dose reduction can be achieved by reducing volume scan length so that it is in concert with the patient's heart length.
C1 [Khan, Atif; Khosa, Faisal; Saghir, Amina; Sarwar, Sheryar; Clouse, Melvin E.] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Radiol, Boston, MA 02215 USA.
[Nasir, Khurram] Boston Univ, Dept Med, Boston Med Ctr, Boston, MA USA.
[Khan, Atif] NCI, Bethesda, MD 20892 USA.
[Sarwar, Sheryar] NHLBI, Bethesda, MD USA.
RP Clouse, ME (reprint author), Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Radiol, 1 Deaconess Rd,WCC 308A, Boston, MA 02215 USA.
EM mclouse@bidmc.harvard.edu
OI Khosa, Faisal/0000-0001-5681-7683
FU NCI [T32 CA059367-14]; NHLBI [P50-HL083813]
FX Supported by grants NCI T32 CA059367-14 and NHLBI P50-HL083813.
NR 38
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U1 0
U2 5
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
EI 1546-3141
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD FEB
PY 2011
VL 196
IS 2
BP 407
EP 411
DI 10.2214/AJR.10.4903
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 718OZ
UT WOS:000287135600026
PM 21257894
ER
PT J
AU Biagi, JJ
Oza, AM
ChalChal, HI
Grimshaw, R
Ellard, SL
Lee, U
Hirte, H
Sederias, J
Ivy, SP
Eisenhauer, EA
AF Biagi, J. J.
Oza, A. M.
ChalChal, H. I.
Grimshaw, R.
Ellard, S. L.
Lee, U.
Hirte, H.
Sederias, J.
Ivy, S. P.
Eisenhauer, E. A.
TI A phase II study of sunitinib in patients with recurrent epithelial
ovarian and primary peritoneal carcinoma: an NCIC Clinical Trials Group
Study
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE clinical trial; recurrent ovarian cancer; sunitinib; targeted therapy
ID TYROSINE KINASE INHIBITOR; ENDOTHELIAL GROWTH-FACTOR; METASTATIC
BREAST-CANCER; CELL LUNG-CANCER; ANTITUMOR-ACTIVITY; FACTOR RECEPTOR;
SOLID TUMORS; BEVACIZUMAB; SU11248; VEGF
AB Purpose: Sunitinib is a multitargeted receptor tyrosine kinase inhibitor. We conducted a two-stage phase II study to evaluate the objective response rate of oral sunitinib in recurrent epithelial ovarian cancer.
Patients and methods: Eligibility required measurable disease and one or two prior chemotherapies, at least one platinum based. Platinum-sensitive or -resistant disease was allowed. Initial dose schedule was sunitinib 50 mg daily, 4 of 6 weeks. Observation of fluid accumulations during off-treatment periods resulted in adoption of continuous 37.5 mg daily dosing in the second stage of accrual.
Results: Of 30 eligible patients, most had serous histology (67%), were platinum sensitive (73%) and had two prior chemotherapies (60%). One partial response (3.3%) and three CA125 responses (10%) were observed, all in platinum-sensitive patients using intermittent dosing. Sixteen (53%) had stable disease. Five had >30% decrease in measurable disease. Overall median progression-free survival was 4.1 months. Common adverse events included fatigue, gastrointestinal symptoms, hand-foot syndrome and hypertension. No gastrointestinal perforation occurred.
Conclusions: Single-agent sunitinib has modest activity in recurrent platinum-sensitive ovarian cancer, but only at the 50 mg intermittent dose schedule, suggesting that dose and schedule may be vital considerations in further evaluation of sunitinib in this cancer setting.
C1 [Biagi, J. J.] Canc Ctr S Eastern Ontario, Dept Oncol, Kingston, ON K7L 5P9, Canada.
[Oza, A. M.] Princess Margaret Hosp, Dept Med, Univ Hlth Network, Toronto, ON M4X 1K9, Canada.
[ChalChal, H. I.] Allan Blair Canc Ctr, Dept Med, Regina, SK, Canada.
[Grimshaw, R.] Queen Elizabeth 2 Hlth Sci Ctr, Dept Obstet & Gynecol, Halifax, NS, Canada.
[Ellard, S. L.] So Interior Ctr, BC Canc Agcy, Dept Med, Kelowna, BC, Canada.
[Lee, U.] Fraser Valley Ctr, Dept Med, Surrey, BC, Canada.
[Lee, U.] Fraser Valley Ctr, BC Canc Agcy, Surrey, BC, Canada.
[Hirte, H.] Juravinski Canc Ctr, Dept Med, Hamilton, ON, Canada.
[Sederias, J.] Queens Univ, Dept Oncol, Kingston, ON, Canada.
[Sederias, J.; Eisenhauer, E. A.] Queens Univ, NCIC Clin Trials Grp, Kingston, ON, Canada.
[Ivy, S. P.] NCI, Div Canc Treatment & Diag, Canc Therapy Evaluat Program, Invest Drug Branch, Bethesda, MD 20892 USA.
RP Biagi, JJ (reprint author), Canc Ctr S Eastern Ontario, Dept Oncol, 25 King St W, Kingston, ON K7L 5P9, Canada.
EM jim.biagi@krcc.on.ca
FU Canadian Cancer Society
FX Canadian Cancer Society to NCIC Clinical Trials Group.
NR 28
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U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0923-7534
J9 ANN ONCOL
JI Ann. Oncol.
PD FEB
PY 2011
VL 22
IS 2
BP 335
EP 340
DI 10.1093/annonc/mdq357
PG 6
WC Oncology
SC Oncology
GA 712NL
UT WOS:000286673400014
PM 20705911
ER
PT J
AU Berger, VW
AF Berger, Vance W.
TI Assessing the Quality of Surgical Trials Further Insight
SO ANNALS OF SURGERY
LA English
DT Letter
C1 NCI, Biometry Res Grp, Bethesda, MD 20892 USA.
RP Berger, VW (reprint author), NCI, Biometry Res Grp, Execut Plaza N,Ste 3131,6130 Execut Blvd,MSC 7354, Bethesda, MD 20892 USA.
EM vb78c@nih.gov
NR 5
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-4932
J9 ANN SURG
JI Ann. Surg.
PD FEB
PY 2011
VL 253
IS 2
BP 420
EP 421
DI 10.1097/SLA.0b013e318208043a
PG 2
WC Surgery
SC Surgery
GA 708OV
UT WOS:000286374400036
PM 21173689
ER
PT J
AU Piram, M
Frenkel, J
Gattorno, M
Ozen, S
Lachmann, HJ
Goldbach-Mansky, R
Hentgen, V
Neven, B
Stojanovic, KS
Simon, A
Kuemmerle-Deschner, J
Hoffman, H
Stojanov, S
Duquesne, A
Pillet, P
Martini, A
Pouchot, J
Kone-Paut, I
AF Piram, Maryam
Frenkel, Joost
Gattorno, Marco
Ozen, Seza
Lachmann, Helen J.
Goldbach-Mansky, Raphaela
Hentgen, Veronique
Neven, Benedicte
Stojanovic, Katia Stankovic
Simon, Anna
Kuemmerle-Deschner, Jasmin
Hoffman, Hal
Stojanov, Silvia
Duquesne, Agnes
Pillet, Pascal
Martini, Alberto
Pouchot, Jacques
Kone-Paut, Isabelle
CA EUROFEVER Network
EUROTRAPS Network
TI A preliminary score for the assessment of disease activity in hereditary
recurrent fevers: results from the AIDAI (Auto-Inflammatory Diseases
Activity Index) Consensus Conference
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Article
ID FAMILIAL-MEDITERRANEAN-FEVER; JUVENILE IDIOPATHIC ARTHRITIS; PERIODIC
SYNDROME; CRITERIA; CHILDREN; CLASSIFICATION; ADOLESCENTS; DIAGNOSIS;
SEVERITY; PATIENT
AB Background The systemic autoinflammatory disorders (SAID) share many clinical manifestations, albeit with variable patterns, intensity and frequency. A common definition of disease activity would be rational and useful in the management of these lifelong diseases. Moreover, standardised disease activity scores are required for the assessment of new therapies in constant development. The aim of this study was to develop preliminary activity scores for familial Mediterranean fever, mevalonate kinase deficiency, tumour necrosis factor receptor-1-associated periodic syndrome and cryopyrin-associated periodic syndromes (CAPS).
Methods The study was conducted using two well-recognised consensus formation methods: the Delphi technique and the nominal group technique. The results from a two-step survey and data from parent/patient interviews were used as preliminary data to develop the agenda for a consensus conference to build a provisional scoring system.
Results 24 of 65 experts in SAID from 20 countries answered the web questionnaire and 16 attended the consensus conference. There was consensus agreement to develop separate activity scores for each disease but with a common format based on patient diaries. Fever and disease-specific clinical variables were scored according to their severity. A final score was generated by summing the score of all the variables divided by the number of days over which the diary was completed. Scores varied from 0 to 16 (0-13 in CAPS). These scores were developed for the purpose of clinical studies but could be used in clinical practice.
Conclusion Using widely recognised consensus formation techniques, preliminary scores were obtained to measure disease activity in four main SAID. Further prospective validation study of this instrument will follow.
C1 [Piram, Maryam; Kone-Paut, Isabelle] Univ Paris 11, Bicetre Univ Hosp, Natl Reference Ctr Autoinflammatory Disorders, Dept Pediat & Pediat Rheumatol, F-94270 Le Kremlin Bicetre, France.
[Frenkel, Joost] Univ Med Ctr, Dept Pediat, Utrtecht, Netherlands.
[Gattorno, Marco; Martini, Alberto] Univ Genoa, I-16126 Genoa, Italy.
[Gattorno, Marco; Martini, Alberto] G Gaslini Inst Children, UO Pediat 2, Genoa, Italy.
[Gattorno, Marco; Martini, Alberto] G Gaslini Inst Children, Dept Pediat, Genoa, Italy.
[Ozen, Seza] Hacettepe Univ, Fac Med, Dept Pediat, TR-06100 Ankara, Turkey.
[Lachmann, Helen J.] UCL, Sch Med, Natl Amyloidosis Ctr, London W1N 8AA, England.
[Goldbach-Mansky, Raphaela] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Hentgen, Veronique] A Mignot Hosp, Natl Reference Ctr Autoinflammatory Disorders, Dept Pediat, Versailles, France.
[Neven, Benedicte] Necker Enfants Malades Hosp, Dept Pediat Immunohematol & Pediat Rheumatol, Paris, France.
[Stojanovic, Katia Stankovic] Univ Paris 06, Tenon Univ Hosp, Natl Reference Ctr Inflammatory Amyloidosis & Fam, Dept Internal Med, Paris, France.
[Simon, Anna] Radboud Univ Nijmegen, Med Ctr, Dept Gen Internal Med, NL-6525 ED Nijmegen, Netherlands.
[Kuemmerle-Deschner, Jasmin] Univ Tubingen Hosp, Dept Pediat, Div Pediat Rheumatol, Tubingen, Germany.
[Hoffman, Hal] Univ Calif San Diego, Rady Childrens Hosp San Diego, Dept Pediat & Med, San Diego, CA 92103 USA.
[Stojanov, Silvia] Univ Childrens Hosp, Dept Immunol & Infect Dis, Munich, Germany.
[Duquesne, Agnes] Hosp Civils Lyon, Hop Femme Mere Enfant, Dept Nephrol & Pediat Rheumatol, Lyon, France.
[Pillet, Pascal] Childrens Hosp Bordeaux, Dept Pediat, Bordeaux, France.
[Pouchot, Jacques] Paris Descartes Univ, European Georges Pompidou Hosp, Dept Internal Med, Paris, France.
RP Kone-Paut, I (reprint author), Univ Paris 11, Bicetre Univ Hosp, Natl Reference Ctr Autoinflammatory Disorders, Dept Pediat & Pediat Rheumatol, 78 Rue Gen Leclerc, F-94270 Le Kremlin Bicetre, France.
EM isabelle.kone-paut@bct.aphp.fr
RI Simon, Anna/D-3757-2009;
OI Simon, Anna/0000-0002-6141-7921; Lachmann, Helen/0000-0001-8378-2498
FU French Ministry of Health; Assistance Publique-Hopitaux de Paris (APHP)
FX This study was supported by grants from the French Ministry of Health
(PHRC 2008) and Assistance Publique-Hopitaux de Paris (APHP).
NR 25
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U1 0
U2 2
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD FEB
PY 2011
VL 70
IS 2
BP 309
EP 314
DI 10.1136/ard.2010.132613
PG 6
WC Rheumatology
SC Rheumatology
GA 705ZG
UT WOS:000286179000014
PM 21081528
ER
PT J
AU Chen, CZ
Kulakova, L
Southall, N
Marugan, JJ
Galkin, A
Austin, CP
Herzberg, O
Zheng, W
AF Chen, Catherine Z.
Kulakova, Liudmila
Southall, Noel
Marugan, Juan J.
Galkin, Andrey
Austin, Christopher P.
Herzberg, Osnat
Zheng, Wei
TI High-Throughput Giardia lamblia Viability Assay Using Bioluminescent ATP
Content Measurements
SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
LA English
DT Article
ID IN-VITRO; DRUG SUSCEPTIBILITY; ANTIGENIC VARIATION; ANAEROBIC PROTOZOA;
IDENTIFICATION; INHIBITION; INVITRO; INTESTINALIS; INFECTIONS;
DUODENALIS
AB The human pathogen Giardia lamblia is an anaerobic protozoan parasite that causes giardiasis, one of the most common diarrheal diseases worldwide. Although several drugs are available for the treatment of giardiasis, drug resistance has been reported and is likely to increase, and recurrent infections are common. The search for new drugs that can overcome the drug-resistant strains of Giardia is an unmet medical need. New drug screen methods can facilitate the drug discovery process and aid with the identification of new drug targets. Using a bioluminescent ATP content assay, we have developed a phenotypic drug screen method to identify compounds that act against the actively growing trophozoite stage of the parasite. This assay is homogeneous, robust, and suitable for high-throughput screening of large compound collections. A screen of 4,096 pharmacologically active small molecules and approved drugs revealed 43 compounds with selective anti-Giardia properties, including 32 previously reported and 11 novel anti-Giardia agents. The most potent novel compound was fumagillin, which showed 50% inhibitory concentrations of 10 nM against the WB isolate and 2 nM against the GS isolate.
C1 [Kulakova, Liudmila; Galkin, Andrey; Herzberg, Osnat] Univ Maryland, Inst Biotechnol, Ctr Adv Res Biotechnol, Rockville, MD 20850 USA.
[Chen, Catherine Z.; Southall, Noel; Marugan, Juan J.; Austin, Christopher P.; Zheng, Wei] NHGRI, NIH Chem Genom Ctr, NIH, Bethesda, MD 20892 USA.
RP Herzberg, O (reprint author), Univ Maryland, Inst Biotechnol, Ctr Adv Res Biotechnol, 9600 Gudelsky Dr, Rockville, MD 20850 USA.
EM osnat@umd.edu; wzheng@mail.nih.gov
RI Southall, Noel/H-8991-2012; Zheng, Wei/J-8889-2014
OI Southall, Noel/0000-0003-4500-880X; Zheng, Wei/0000-0003-1034-0757
FU National Institutes of Health [R01 AI059733]; Molecular Libraries
Initiative of the NIH Roadmap for Medical Research
FX This study was supported by National Institutes of Health grant R01
AI059733 (to O.H.) and the Molecular Libraries Initiative of the NIH
Roadmap for Medical Research.
NR 53
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U1 0
U2 5
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 FEB
PY 2011
VL 55
IS 2
BP 667
EP 675
DI 10.1128/AAC.00618-10
PG 9
WC Microbiology; Pharmacology & Pharmacy
SC Microbiology; Pharmacology & Pharmacy
GA 709FE
UT WOS:000286422500028
PM 21078930
ER
PT J
AU Nybo, K
Green, E
AF Nybo, Kristie
Green, Eric
TI Influencing the Field
SO BIOTECHNIQUES
LA English
DT Editorial Material
C1 [Green, Eric] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU BIOTECHNIQUES OFFICE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 0736-6205
J9 BIOTECHNIQUES
JI Biotechniques
PD FEB
PY 2011
VL 50
IS 2
BP 83
EP 83
DI 10.2144/000113606
PG 1
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 726KF
UT WOS:000287719700002
ER
PT J
AU Smith, HE
AF Smith, Harold E.
TI Identifying insertion mutations by whole-genome sequencing
SO BIOTECHNIQUES
LA English
DT Article
DE Next-generation sequencing; whole-genome resequencing; mutation
identification; insertion mapping
ID ESCHERICHIA-COLI
AB Insertion mutagenesis via mobile genetic element is a common technique for the analysis of gene function in model organisms. Next-generation sequencing offers an attractive approach for localizing the site of insertion, but alignment-based mapping of mobile genetic elements is challenging. A computational method for identifying insertion sites is reported herein. The technique was validated by mapping transposons in both bacterial and nematode species. The approach should be extensible to other systems that employ mobile genetic elements to generate mutations.
C1 NIDDKD, NIH, Bethesda, MD 20892 USA.
RP Smith, HE (reprint author), NIDDKD, NIH, 8 Ctr Dr,Room 1A11, Bethesda, MD 20892 USA.
EM smith-he2@niddk.nih.gov
FU National Institutes of Health (NIH), National Institute of Diabetes and
Digestive and Kidney Diseases
FX Thanks to Lee Rosner, Bob Martin, and Kevin O'Connell for providing DNA
samples, and to Michael Krause for comments on the manuscript and
fruitful discussions. This research was supported by the Intramural
Research Program of the National Institutes of Health (NIH), National
Institute of Diabetes and Digestive and Kidney Diseases. This paper is
subject to the NIH Public Access Policy.
NR 10
TC 10
Z9 10
U1 0
U2 2
PU BIOTECHNIQUES OFFICE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 0736-6205
J9 BIOTECHNIQUES
JI Biotechniques
PD FEB
PY 2011
VL 50
IS 2
BP 96
EP 97
DI 10.2144/000113600
PG 2
WC Biochemical Research Methods; Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 726KF
UT WOS:000287719700006
PM 21486250
ER
PT J
AU Trabert, B
Peters, U
De Roos, AJ
Scholes, D
Holt, VL
AF Trabert, Britton
Peters, Ulrike
De Roos, Anneclaire J.
Scholes, Delia
Holt, Victoria L.
TI Diet and risk of endometriosis in a population-based case-control study
SO BRITISH JOURNAL OF NUTRITION
LA English
DT Article
DE Case-control studies; Population-based studies; Diet; Endometriosis
ID ESTROGEN; CONSUMPTION; FAT; EPIDEMIOLOGY; CARBENDAZIM; DATABASE;
DISEASE; WOMEN; SERUM
AB Diet plausibly has a role in the aetiology of endometriosis through effects on steroid hormone levels; however, few published studies have examined the diet and endometriosis risk. We evaluated dietary risk factors for endometriosis in a population-based case-control study. Cases were 284 Group Health (GH) enrollees aged 18-49 years with newly diagnosed, surgically confirmed endometriosis between 1996 and 2001. Controls were 660 randomly selected age-matched female GH enrollees without a history of endometriosis. Nutrients and selected food groups were assessed using the Women's Health Initiative FFQ. OR of endometriosis risk associated with dietary exposures were estimated using unconditional logistic regression and adjusted for identified covariates. Increased total fat consumption was associated with decreased endometriosis risk (fourth quartile v. lowest: OR 0.5, 95% CI 0.2, 1.0, P-trend = 0.12). Increased beta-carotene consumption and servings/d of fruit were associated with increased risk (beta-carotene third quartile v. lowest: OR 1.7, 95% CI 1.1, 2.6; fourth quartile v. lowest: OR 1.6, 95% CI 1.0, 2.5, P-trend 0.16; fruit >2 servings/d v. <1: OR 1.5, 95% CI 1.0, 2.3, P-trend = 0.04). We also found a suggestion of decreased endometriosis risk associated with the consumption of dairy products (2 servings/d v. <= 1: OR 0.6, >2 servings/d v. <= 1: OR 0.7), but this association was not statistically significant for the highest tertile. The present study suggests that specific dietary components may be associated with endometriosis risk.
C1 [Trabert, Britton; Peters, Ulrike; De Roos, Anneclaire J.; Holt, Victoria L.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Trabert, Britton; De Roos, Anneclaire J.; Holt, Victoria L.] Fred Hutchinson Canc Res Ctr, Epidemiol Res Unit, Seattle, WA 98109 USA.
[Trabert, Britton] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Peters, Ulrike] Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA 98109 USA.
[Scholes, Delia] Grp Hlth Cooperat Puget Sound, Ctr Hlth Studies, Seattle, WA 98101 USA.
RP Trabert, B (reprint author), Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
EM trabertbl@mail.nih.gov
RI Trabert, Britton/F-8051-2015
FU National Institute of Child Health and Human Services, National
Institute of Health [R01 HD33792, T32 HD052462]; Center for Ecogenetics
and Environmental Health; University of Washington
FX None of the authors has any conflicts of interest. The present research
was supported by grants numbered R01 HD33792 and T32 HD052462 from the
National Institute of Child Health and Human Services, National
Institute of Health. Pilot grant funding from the Center for Ecogenetics
and Environmental Health and the Royalty Research Fund at the University
of Washington also supported this research. The authors and their
contributions are as follows: B. T. was involved with the interpretation
and analysis of the data and drafting the manuscript. U. P. was involved
with the analysis and interpretation of data and revision of the
manuscript. A. J. D. was involved with interpretation of the data and
revision of the manuscript. D. S. was involved with study design, data
acquisition and revision of the manuscript. V. L. H. was the principal
investigator; she was involved with study design, data acquisition, data
analysis, interpretation of the data and drafting and revision of the
manuscript.
NR 29
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U1 1
U2 9
PU CAMBRIDGE UNIV PRESS
PI CAMBRIDGE
PA EDINBURGH BLDG, SHAFTESBURY RD, CB2 8RU CAMBRIDGE, ENGLAND
SN 0007-1145
EI 1475-2662
J9 BRIT J NUTR
JI Br. J. Nutr.
PD FEB
PY 2011
VL 105
IS 3
BP 459
EP 467
DI 10.1017/S0007114510003661
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 724VX
UT WOS:000287605400015
PM 20875189
ER
PT J
AU He, JA
Zhang, YM
Ito, Y
Sun, WJ
AF He, Jiao
Zhang, Yongmin
Ito, Yoichiro
Sun, Wenji
TI Semi-Preparative Isolation and Purification of Three Tauro-Conjugated
Cholic Acids from Pulvis Fellis Suis by HSCCC Coupled with ELSD
Detection
SO CHROMATOGRAPHIA
LA English
DT Article
DE High-speed countercurrent chromatography; Tauro-conjugated cholic acids;
Pulvis Fellis Suis; Sus scrofa domestica Brisson
ID COUNTER-CURRENT CHROMATOGRAPHY; PREPARATIVE ISOLATION; BILE-ACIDS;
SEPARATION
AB Coupled with evaporative light scattering detection, a high-speed countercurrent chromatography method was successfully applied to the separation and purification of three tauro-conjugated cholic acids from the traditional Chinese medicine Pulvis Fellis Suis. With a two-phase solvent system composed of chloroform-methanol-water-acetic acid (4:4:2:0.3, v/v), taurochenodeoxycholic acid (10.2 mg), taurohyodeoxycholic acid (11.8 mg) and taurohyocholic acid (5.3 mg), were obtained from 100 mg of the crude extract with purities of 94.6, 96.5 and 95.4%, respectively, in one-step separation. The structures of the three tauro-conjugated cholic acids were identified by ESI-MS, (1)H NMR and (13)C NMR.
C1 [He, Jiao; Sun, Wenji] NW Univ Xian, Biomed Key Lab Shaanxi Prov, Xian 710069, Peoples R China.
[Zhang, Yongmin] Univ Paris 06, Inst Parisien Chim Mol, CNRS, UMR 7201, F-75005 Paris, France.
[Ito, Yoichiro] NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Sun, WJ (reprint author), NW Univ Xian, Biomed Key Lab Shaanxi Prov, 229 Taibai N Rd, Xian 710069, Peoples R China.
EM cxbml@nwu.edu.cn
FU Northwest University of the People's Republic of China [09YZZ61];
Education Department of Shaanxi Provincial Government of the People's
Republic of China [2010JS096]
FX The authors thank Prof. Zhongfu Wang and Sha Xu of the Key Laboratory of
Resource Biology and Biotechnology in western China for assistance in
ESI-MS experiments. This work was financially supported in part by the
Project of Graduate Innovation and Creativity Funds of Northwest
University of the People's Republic of China (09YZZ61) and Project of
Scientific Research Plan of Education Department of Shaanxi Provincial
Government of the People's Republic of China (2010JS096).
NR 29
TC 4
Z9 5
U1 0
U2 14
PU VIEWEG
PI WIESBADEN
PA ABRAHAM-LINCOLN-STRABE 46, POSTFACH 15 47, D-65005 WIESBADEN, GERMANY
SN 0009-5893
J9 CHROMATOGRAPHIA
JI Chromatographia
PD FEB
PY 2011
VL 73
IS 3-4
BP 361
EP 365
DI 10.1007/s10337-010-1893-2
PG 5
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 719KQ
UT WOS:000287204000020
PM 21442029
ER
PT J
AU Johnson, AD
Prakash, S
AF Johnson, Andrew D.
Prakash, Siddharth
TI Top Advances in Functional Genomics and Translational Biology for 2010
SO CIRCULATION-CARDIOVASCULAR GENETICS
LA English
DT Article
DE function; genomic studies; metabolomics; pharmacogenetics; proteomics
ID CORONARY-ARTERY-DISEASE; CHOLESTEROL HOMEOSTASIS; CYP2C19 GENOTYPE;
RISK; ASSOCIATION; DELETIONS; OUTCOMES; OBESITY
RP Johnson, AD (reprint author), NHLBI, Framingham Heart Study, 73 Mt Wayte Ave, Framingham, MA 01702 USA.
EM Johnsonad2@nhlbi.nih.gov
RI Johnson, Andrew/G-6520-2013
NR 15
TC 0
Z9 0
U1 0
U2 1
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 FEB
PY 2011
VL 4
IS 1
BP 94
EP 97
DI 10.1161/CIRCGENETICS.111.959502
PG 4
WC Cardiac & Cardiovascular Systems; Genetics & Heredity
SC Cardiovascular System & Cardiology; Genetics & Heredity
GA 721KS
UT WOS:000287353200023
PM 21325166
ER
PT J
AU Rouphael, NG
Satola, S
Farley, MM
Rudolph, K
Schmidt, DS
Gomez-de-Leon, P
Robbins, JB
Schneerson, R
Carlone, GM
Romero-Steiner, S
AF Rouphael, Nadine G.
Satola, Sarah
Farley, Monica M.
Rudolph, Karen
Schmidt, Daniel S.
Gomez-de-Leon, Patricia
Robbins, John B.
Schneerson, Rachel
Carlone, George M.
Romero-Steiner, Sandra
TI Evaluation of Serum Bactericidal Antibody Assays for Haemophilus
influenzae Serotype a
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Article
ID CAPSULAR POLYSACCHARIDE; INVASIVE INFECTIONS; A DISEASE; VIRULENCE;
EPIDEMIOLOGY; CHILDREN; VACCINE
AB Haemophilus influenzae type a (Hia) is an important pathogen for some American Indian, Alaskan native, and Northern Canada aboriginal populations. Assays to measure serum bactericidal activity (SBA) to Hia have not been developed or validated. Here, we describe two methods for the measurement of SBA: SBA with a viability endpoint (CFU counts) and SBA with a fluorometric endpoint using alamarBlue as the metabolic indicator. Both SBA assays measure Hia-specific functional antibody and correlate with anti-Hia IgG enzyme-linked immunosorbent assay (ELISA) concentration of naturally acquired antibodies.
C1 [Romero-Steiner, Sandra] Ctr Dis Control & Prevent, Vaccinol Lab, Div Bacterial Dis, Atlanta, GA 30333 USA.
[Rouphael, Nadine G.; Satola, Sarah; Farley, Monica M.] Emory Univ, Sch Med, Div Infect Dis, Atlanta, GA 30303 USA.
[Rudolph, Karen] Ctr Dis Control & Prevent, Arctic Invest Program, Anchorage, AK 99508 USA.
[Satola, Sarah; Farley, Monica M.] Atlanta Vet Affairs Med Ctr, Decatur, GA 30033 USA.
[Gomez-de-Leon, Patricia] Univ Nacl Autonoma Mexico, Fac Med, Dept Salud Publ, Mexico City 04510, DF, Mexico.
[Robbins, John B.; Schneerson, Rachel] NICHHD, NIH, Bethesda, MD 20892 USA.
RP Romero-Steiner, S (reprint author), Ctr Dis Control & Prevent, Vaccinol Lab, Div Bacterial Dis, Bldg 18,Room B-105,Mailstop A-36,CDC,1600 Clifton, Atlanta, GA 30333 USA.
EM SSteiner@cdc.gov
OI Romero-Steiner, Sandra/0000-0003-4128-7768
NR 19
TC 5
Z9 5
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1556-6811
J9 CLIN VACCINE IMMUNOL
JI Clin. Vaccine Immunol.
PD FEB
PY 2011
VL 18
IS 2
BP 243
EP 247
DI 10.1128/CVI.00219-10
PG 5
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 712GJ
UT WOS:000286653900008
PM 21177919
ER
PT J
AU Bai, O
Rathi, V
Lin, P
Huang, DD
Battapady, H
Fei, DY
Schneider, L
Houdayer, E
Chen, XD
Hallett, M
AF Bai, Ou
Rathi, Varun
Lin, Peter
Huang, Dandan
Battapady, Harsha
Fei, Ding-Yu
Schneider, Logan
Houdayer, Elise
Chen, Xuedong
Hallett, Mark
TI Prediction of human voluntary movement before it occurs
SO CLINICAL NEUROPHYSIOLOGY
LA English
DT Article
DE Human intention; Voluntary movement; Prediction; Movement-related
cortical potentials (MRCP); Event-related desynchronization (ERD);
Electroencephalography (EEG); Brain-computer interface (BCI);
Consciousness
ID BRAIN-COMPUTER-INTERFACE; EVENT-RELATED DESYNCHRONIZATION; SINGLE-TRIAL
EEG; CORTICAL POTENTIALS; FINGER MOVEMENTS; BETA-RHYTHM; CLASSIFICATION;
HAND; PROSTHESIS; INITIATION
AB Objective: Human voluntary movement is associated with two changes in electroencephalography ( EEG) that can be observed as early as 1.5 s prior to movement: slow DC potentials and frequency power shifts in the alpha and beta bands. Our goal was to determine whether and when we can reliably predict human natural movement BEFORE it occurs from EEG signals ONLINE IN REAL-TIME.
Methods: We developed a computational algorithm to support online prediction. Seven healthy volunteers participated in this study and performed wrist extensions at their own pace.
Results: The average online prediction time was 0.62 +/- 0.25 s before actual movement monitored by EMG signals. There were also predictions that occurred without subsequent actual movements, where subjects often reported that they were thinking about making a movement.
Conclusion: Human voluntary movement can be predicted before movement occurs.
Significance: The successful prediction of human movement intention will provide further insight into how the brain prepares for movement, as well as the potential for direct cortical control of a device which may be faster than normal physical control. (C) 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
C1 [Bai, Ou; Rathi, Varun; Huang, Dandan; Battapady, Harsha; Fei, Ding-Yu] Virginia Commonwealth Univ, Dept Biomed Engn, EEG & BCI Lab, Richmond, VA 23284 USA.
[Lin, Peter; Schneider, Logan; Houdayer, Elise; Hallett, Mark] Natl Inst Neurol Disorders, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Chen, Xuedong] Huazhong Univ Sci & Technol, State Key Lab Digital Mfg Equipment & Technol, Wuhan 430074, Hubei, Peoples R China.
RP Bai, O (reprint author), Virginia Commonwealth Univ, Dept Biomed Engn, EEG & BCI Lab, 401 W Main St,Room 1252,POB 843067, Richmond, VA 23284 USA.
EM obai@vcu.edu
RI Huang, Dandan/I-3108-2013
FU NIH, National Institute of Neurological Disorders and Stroke; State Key
Laboratory of Digital Manufacturing, Equipment & Technology, Huazhong
University of Science and Technology
FX This research was partly supported by the Intramural Research Program of
the NIH, National Institute of Neurological Disorders and Stroke. O. Bai
received partial support from State Key Laboratory of Digital
Manufacturing, Equipment & Technology, Huazhong University of Science
and Technology.
NR 49
TC 56
Z9 59
U1 0
U2 21
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 1388-2457
J9 CLIN NEUROPHYSIOL
JI Clin. Neurophysiol.
PD FEB
PY 2011
VL 122
IS 2
BP 364
EP 372
DI 10.1016/j.clinph.2010.07.010
PG 9
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 703QP
UT WOS:000285995400019
PM 20675187
ER
PT J
AU White, R
Chileshe, M
Dawson, L
Donnell, D
Hillier, S
Morar, N
Noguchi, L
Dixon, D
AF White, Rhonda
Chileshe, Modesta
Dawson, Liza
Donnell, Deborah
Hillier, Sharon
Morar, Neetha
Noguchi, Lisa
Dixon, Dennis
TI Fostering community understanding of sufficient benefit and early
stopping for a phase 2B HIV prevention clinical trial in Africa
SO CLINICAL TRIALS
LA English
DT Article
AB Background Most trials of interventions are designed to address the traditional null hypothesis of no benefit. VOICE, a phase 2B HIV prevention trial funded by NIH and conducted in Africa, is designed to assess if the intervention will prevent a substantial fraction of infections. Planned interim analysis may provide conclusive evidence against the traditional null hypothesis without establishing substantial benefit. At this interim point, the Data and Safety Monitoring Board would then face the dilemma of knowing the product has some positive effect, but perhaps not as great an effect as the protocol has declared necessary.
Purpose In March 2008, NIH program staff recommended that the VOICE protocol team discuss the stopping rules with stakeholders prior to initiating the protocol. The goals of the workshop were to inform community representatives about the potential ethical dilemma associated with stopping rules and engage in dialogue about these issues. We describe the resulting community consultation and summarize the outcomes.
Methods A 2-day workshop was convened with the goal of having a clear and transparent consultation with the stakeholders around the question, 'Given emerging evidence that a product could prevent some infections, would the community support a decision to continue accruing to the trial?' Participants included research staff and community stakeholders. Lectures with visual aids, discussions, and exercises using interactive learning tasks were used, with a focus on statistics and interpreting data from trials, particularly interim data.
Results Results of oral and written evaluations by participants were reviewed. The feedback was mostly positive, with some residual confusion regarding statistical concepts. However, discussions with attendees later revealed that not all felt prepared to engage fully in the workshop.
Limitations This was the presenters' first experience facilitating a formal discussion with an audience that had no advanced science, research, or mathematics training. Community representatives' concern regarding speaking for their communities without consulting them also created a challenge for the workshop.
Conclusions Open discussion around trial stopping rules requires that all discussants have an understanding of trial design concepts and feel a sense of empowerment to ask and answer questions. The VOICE CWG workshop was a first step toward the goal of open discussion regarding trial stopping rules and interim results for the study; however, ongoing education and dialogue must occur to ensure that all stakeholders fully participate in the process. Clinical Trials 2011; 8: 103-111. http://ctj.sagepub.
C1 [White, Rhonda] FHI, Res Triangle Pk, NC 27709 USA.
[Chileshe, Modesta] Ctr Infect Dis Res Zambia, Lusaka, Zambia.
[Dawson, Liza; Dixon, Dennis] NIAID, NIH, Dept Hlth & Human Serv, Washington, DC USA.
[Donnell, Deborah] Fred Hutchinson Canc Res Ctr, Vaccine & Infect Dis Inst, Seattle, WA 98104 USA.
[Hillier, Sharon] Univ Pittsburgh, Magee Womens Hosp, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA 15213 USA.
[Morar, Neetha] S African MRC, Durban, South Africa.
[Noguchi, Lisa] Microbicide Trials Network, Pittsburgh, PA USA.
RP White, R (reprint author), FHI, POB 13950, Res Triangle Pk, NC 27709 USA.
EM rwhite@fhi.org
OI Donnell, Deborah/0000-0002-0587-7480
FU NIAID, US National Institutes of Health [5U01AI068633]; NICHD, US
National Institutes of Health; NIMH, US National Institutes of Health
FX This effort was supported by the Microbicide Trials Network (MTN), which
is funded by NIAID (5U01AI068633), NICHD, and NIMH, all of which are
institutes of the US National Institutes of Health.
NR 3
TC 5
Z9 6
U1 0
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
J9 CLIN TRIALS
JI Clin. Trials
PD FEB
PY 2011
VL 8
IS 1
BP 103
EP 111
DI 10.1177/1740774510387170
PG 9
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 723LX
UT WOS:000287509200011
PM 21335592
ER
PT J
AU Ingraham, RH
Gless, RD
Lo, HY
AF Ingraham, R. H.
Gless, R. D.
Lo, H. Y.
TI Soluble Epoxide Hydrolase Inhibitors and their Potential for Treatment
of Multiple Pathologic Conditions
SO CURRENT MEDICINAL CHEMISTRY
LA English
DT Review
DE AR9281; BTP2; EPHX2; epoxyeicosatrienoic acid; eicosanoids; sEH; soluble
epoxide hydrolase
ID ISCHEMIA-REPERFUSION INJURY; EPOXYEICOSATRIENOIC ACIDS; THERAPEUTIC
TARGET; BLOOD-PRESSURE; GENE DELETION; CEREBRAL-ISCHEMIA;
HYPERTENSIVE-RATS; WATER SOLUBILITY; HIGHLY POTENT; HUMAN BRONCHI
AB Epoxyeicosanoids, including the epoxyeicosatrienoic acids, are signaling molecules which appear to help ameliorate the effects of a wide variety of pathological conditions. The enzyme soluble epoxide hydrolase (sEH) metabolizes these molecules by converting them to their corresponding vicinal diols. Inhibition of sEH either by knockout or chemical inhibitors increases epoxyeicosanoid levels in vivo and provides significant organ protection in models of brain, cardiac, and renal injury. sEH also appears to be involved in modulating inflammation, pain pathways, pulmonary function, hypertension, and diabetes. Potent sEH inhibitors have been developed in academic, pharmaceutical, and biotech laboratories and described in the patent and scientific literature. Most of the inhibitor scaffolds employ a urea or amide which functions as an active-site transition state mimic. Arete Therapeutics compound AR9281 successfully completed phase Ia and Ib studies. A phase IIa proof of concept trial for treatment of impaired glucose tolerance has been completed, but the results are not yet reported.
C1 [Ingraham, R. H.] NIH, Ctr Sci Review, Bethesda, MD USA.
[Lo, H. Y.] Boehringer Ingelheim Pharmaceut Inc, Ingelheim, Germany.
RP Ingraham, RH (reprint author), 913 Beacon Sq Court, Gaithersburg, MD USA.
EM rhingraham@gmail.com
NR 118
TC 16
Z9 16
U1 1
U2 4
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 0929-8673
J9 CURR MED CHEM
JI Curr. Med. Chem.
PD FEB
PY 2011
VL 18
IS 4
BP 587
EP 603
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology &
Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 720SN
UT WOS:000287301000008
PM 21143109
ER
PT J
AU David, IA
Volchan, E
Vila, J
Keil, A
de Oliveira, L
Faria, AJP
Perakakis, P
Dias, EC
Mocaiber, I
Pereira, MG
Machado-Pinheiro, W
AF David, Isabel A.
Volchan, Eliane
Vila, Jaime
Keil, Andreas
de Oliveira, Leticia
Faria-Junior, Aydamari J. P.
Perakakis, Pandelis
Dias, Elisa C.
Mocaiber, Izabela
Pereira, Mirtes G.
Machado-Pinheiro, Walter
TI Stroop matching task: role of feature selection and temporal modulation
SO EXPERIMENTAL BRAIN RESEARCH
LA English
DT Article
DE Stroop; ERP; Feature attention; Matching task
ID ANTERIOR CINGULATE CORTEX; EVENT-RELATED POTENTIALS; FEATURE-BASED
ATTENTION; TIME-COURSE; IRRELEVANT INFORMATION; RELEVANT INFORMATION;
INTERFERENCE; COLOR; WORD; CONFLICT
AB We conducted an event-related potential (ERP) study to investigate the electrocortical dynamics of attentional feature-based processing in the Stroop matching task. Participants in the study (n = 37) compared the ink color of a colored word with the meaning of a color-word in white ink. The two task stimuli were presented simultaneously or with SOAs (Stimulus Onset Asynchrony) of 400 and 1,200 ms. The Stroop matching effect was maximal during SOA-0, was reduced at SOA-400, and was inverted at SOA-1200. We focused the ERP analysis on the N1 component. Paralleling the behavioral results, the N1 amplitude was greater for congruent stimuli than incongruent stimuli during SOA-0. This difference was attenuated at SOA-400, and at SOA-1200, an inverse pattern was observed. The results provide evidence that early selection processing participated in the Stroop matching task phenomenon and also suggest that the temporal modulation of early attention is a function of task characteristics such as SOA.
C1 [David, Isabel A.; de Oliveira, Leticia; Pereira, Mirtes G.] Univ Fed Fluminense, Dept Fisiol & Farmacol, Inst Biomed, BR-24210130 Niteroi, RJ, Brazil.
[Mocaiber, Izabela; Machado-Pinheiro, Walter] Univ Fed Fluminense, Dept Interdisciplinar, Rio Das Ostras, RJ, Brazil.
[Volchan, Eliane] Univ Fed Rio de Janeiro, Inst Biofis Carlos Chagas Filho, Programa Neurobiol, BR-21941 Rio De Janeiro, Brazil.
[Vila, Jaime; Perakakis, Pandelis] Univ Granada, Fac Psicol, Dept Personalidad Evaluac & Tratamiento Psicol, Granada, Spain.
[Keil, Andreas] Univ Florida, Dept Psychol, NIMH, Ctr Study Emot & Attent, Gainesville, FL 32611 USA.
[Faria-Junior, Aydamari J. P.] Univ Fed Amapa, Dept Pesquisa, Macapa, AP, Brazil.
[Dias, Elisa C.] Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA.
RP David, IA (reprint author), Univ Fed Fluminense, Dept Fisiol & Farmacol, Inst Biomed, Prof Ernani de Melo 101, BR-24210130 Niteroi, RJ, Brazil.
EM isabeldavid@vm.uff.br
RI Vila, Jaime/F-9719-2010; Fisiologia, Ciencias Biologicas/C-2407-2012;
David, Isabel/I-6090-2012; Keil, Andreas/F-9427-2011; Pereira,
Mirtes/J-6222-2016;
OI Vila, Jaime/0000-0002-1767-8606; Keil, Andreas/0000-0002-4064-1924;
Pereira, Mirtes/0000-0003-4682-223X; Perakakis,
Pandelis/0000-0002-9130-3247
FU Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de
Janeiro; Conselho Nacional de Desenvolvimento Cientifico e Tecnologico
(CNPq); Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior
(CAPES); IBNNet/FINEP; PROPP-UFF; Society for Psychophysiological
Research (SPR)
FX This research was supported by Fundacao Carlos Chagas Filho de Amparo a
Pesquisa do Estado do Rio de Janeiro, Conselho Nacional de
Desenvolvimento Cientifico e Tecnologico (CNPq), and Coordenacao de
Aperfeicoamento de Pessoal de Nivel Superior (CAPES). Partial support
was also provided by grants from IBNNet/FINEP and PROPP-UFF. We extend
special thanks to the Society for Psychophysiological Research (SPR) for
the fellowship training program to the first author (IAD).
NR 52
TC 10
Z9 11
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0014-4819
EI 1432-1106
J9 EXP BRAIN RES
JI Exp. Brain Res.
PD FEB
PY 2011
VL 208
IS 4
BP 595
EP 605
DI 10.1007/s00221-010-2507-9
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 711QV
UT WOS:000286607400011
PM 21161193
ER
PT J
AU Dubrac, S
Elentner, A
Gonzalez, FJ
Schmuth, M
AF Dubrac, S.
Elentner, A.
Gonzalez, F. J.
Schmuth, M.
TI Pregnane X Receptor (PXR) links xenobiotic metabolism to the cutaneous
immune response
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
Arbeitsgemeinschaft-Dermatologishche-Forschung
CY FEB 17-19, 2011
CL Tuebingen, GERMANY
SP Arbeitsgemeinsch Dermatol Forsch
C1 [Dubrac, S.; Elentner, A.; Schmuth, M.] Innsbruck Med Univ, Dept Dermatol, A-6020 Innsbruck, Austria.
[Gonzalez, F. J.] NIH, Lab Metab, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0906-6705
J9 EXP DERMATOL
JI Exp. Dermatol.
PD FEB
PY 2011
VL 20
IS 2
MA P029
BP 167
EP 167
PG 1
WC Dermatology
SC Dermatology
GA 709UZ
UT WOS:000286468200048
ER
PT J
AU Wolf, R
Mascia, F
Dharamsi, A
Howard, ZO
Cattaisson, C
Bliskovski, V
Winston, J
Feigenbaum, L
Lichti, U
Ruzicka, T
Chavakis, T
Yuspa, SH
AF Wolf, R.
Mascia, F.
Dharamsi, A.
Howard, Z. O.
Cattaisson, C.
Bliskovski, V.
Winston, J.
Feigenbaum, L.
Lichti, U.
Ruzicka, T.
Chavakis, T.
Yuspa, S. H.
TI Small S100 molecules with cutaneous antimicrobial activity prime skin
for inflammation: a mouse model for psoriasis susceptibility
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
Arbeitsgemeinschaft-Dermatologishche-Forschung
CY FEB 17-19, 2011
CL Tuebingen, GERMANY
SP Arbeitsgemeinsch Dermatol Forsch
C1 [Wolf, R.; Mascia, F.; Dharamsi, A.; Cattaisson, C.; Bliskovski, V.; Winston, J.; Lichti, U.; Yuspa, S. H.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Wolf, R.; Ruzicka, T.] Univ Munich, Dept Dermatol & Allergol, Munich, Germany.
[Howard, Z. O.] NCI, Mol Immunoregulat Lab, NIH, Frederick, MD 21701 USA.
[Feigenbaum, L.] SAIC, Lab Anim Serv Program, Frederick, MD USA.
[Chavakis, T.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Chavakis, T.] Tech Univ Dresden, Dept Med, D-8027 Dresden, Germany.
[Chavakis, T.] Tech Univ Dresden, Inst Physiol, D-8027 Dresden, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0906-6705
J9 EXP DERMATOL
JI Exp. Dermatol.
PD FEB
PY 2011
VL 20
IS 2
MA P031
BP 167
EP 167
PG 1
WC Dermatology
SC Dermatology
GA 709UZ
UT WOS:000286468200050
ER
PT J
AU Jalili, A
Pashenkov, M
Kriehuber, E
Wagner, C
Nakano, H
Stingl, G
Wagner, SN
AF Jalili, A.
Pashenkov, M.
Kriehuber, E.
Wagner, C.
Nakano, H.
Stingl, G.
Wagner, S. N.
TI Induction of targeted cell migration by cutaneous administration of a
DNA vector encoding a biologically active chemokine CCL21
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
Arbeitsgemeinschaft-Dermatologishche-Forschung
CY FEB 17-19, 2011
CL Tuebingen, GERMANY
SP Arbeitsgemeinsch Dermatol Forsch
C1 [Jalili, A.; Pashenkov, M.; Kriehuber, E.; Wagner, C.; Stingl, G.; Wagner, S. N.] Med Univ Vienna, Div Immunol, Dept Dermatol, Vienna, Austria.
[Nakano, H.] NIEHS, NIH, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0906-6705
J9 EXP DERMATOL
JI Exp. Dermatol.
PD FEB
PY 2011
VL 20
IS 2
MA P086
BP 176
EP 176
PG 1
WC Dermatology
SC Dermatology
GA 709UZ
UT WOS:000286468200105
ER
PT J
AU Ghoreschi, K
Laurence, A
Yang, X
Tato, C
McGeachy, M
Konkel, J
Ramos, H
Wei, L
Davidson, T
Bouladoux, N
Grainger, J
Chen, Q
Kanno, Y
Watford, W
Sun, H
Eberl, G
Shevach, E
Belkaid, Y
Cua, D
Chen, W
O'Shea, JJ
AF Ghoreschi, K.
Laurence, A.
Yang, X.
Tato, C.
McGeachy, M.
Konkel, J.
Ramos, H.
Wei, L.
Davidson, T.
Bouladoux, N.
Grainger, J.
Chen, Q.
Kanno, Y.
Watford, W.
Sun, H.
Eberl, G.
Shevach, E.
Belkaid, Y.
Cua, D.
Chen, W.
O'Shea, J. J.
TI Pathogenic T-bet+Th17 cells develop in the absence of TGF-beta signaling
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
Arbeitsgemeinschaft-Dermatologishche-Forschung
CY FEB 17-19, 2011
CL Tuebingen, GERMANY
SP Arbeitsgemeinsch Dermatol Forsch
C1 [Ghoreschi, K.; Laurence, A.; Yang, X.; Konkel, J.; Ramos, H.; Wei, L.; Davidson, T.; Bouladoux, N.; Grainger, J.; Chen, Q.; Kanno, Y.; Watford, W.; Sun, H.; Shevach, E.; Belkaid, Y.; Chen, W.; O'Shea, J. J.] NIH, Bethesda, MD 20892 USA.
[Tato, C.; McGeachy, M.; Cua, D.] Merck Res Labs, Palo Alto, CA 94304 USA.
[Eberl, G.] Inst Pasteur, F-75724 Paris, France.
RI Laurence, Arian/A-8770-2009; Eberl, Gerard/A-1160-2013; Wei,
Lai/D-1088-2014
OI Laurence, Arian/0000-0003-0942-8292;
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0906-6705
J9 EXP DERMATOL
JI Exp. Dermatol.
PD FEB
PY 2011
VL 20
IS 2
MA P150
BP 186
EP 186
PG 1
WC Dermatology
SC Dermatology
GA 709UZ
UT WOS:000286468200168
ER
PT J
AU Wolf, R
Voscopolous, C
Winston, J
Cattaisson, C
Darwiche, N
Glick, A
Weinberg, WC
Vogel, JC
Goldsmith, P
Hennings, H
Yuspa, SH
AF Wolf, R.
Voscopolous, C.
Winston, J.
Cattaisson, C.
Darwiche, N.
Glick, A.
Weinberg, W. C.
Vogel, J. C.
Goldsmith, P.
Hennings, H.
Yuspa, S. H.
TI S100A7 (psoriasin) and S100A15 (koebnerisin) marks tumor progression
during skin carcinogenesis
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
Arbeitsgemeinschaft-Dermatologishche-Forschung
CY FEB 17-19, 2011
CL Tuebingen, GERMANY
SP Arbeitsgemeinsch Dermatol Forsch
C1 [Wolf, R.; Voscopolous, C.; Winston, J.; Cattaisson, C.; Darwiche, N.; Glick, A.; Hennings, H.; Yuspa, S. H.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Wolf, R.] Univ Munich, Dept Dermatol & Allergol, Munich, Germany.
[Weinberg, W. C.] US FDA, Bethesda, MD 20014 USA.
[Vogel, J. C.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Goldsmith, P.] NCI, Antibody & Prot Purificat Unit, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0906-6705
J9 EXP DERMATOL
JI Exp. Dermatol.
PD FEB
PY 2011
VL 20
IS 2
MA P222
BP 197
EP 197
PG 1
WC Dermatology
SC Dermatology
GA 709UZ
UT WOS:000286468200240
ER
PT J
AU Eberle, F
Rodriguez-Canales, J
Wei, L
Hanson, J
Killian, J
Sun, H
Adams, L
Hewitt, S
Wilson, W
Pittaluga, S
Meltzer, P
Staudt, L
Emmert-Buck, M
Jaffe, E
AF Eberle, F.
Rodriguez-Canales, J.
Wei, L.
Hanson, J.
Killian, J.
Sun, H.
Adams, L.
Hewitt, S.
Wilson, W.
Pittaluga, S.
Meltzer, P.
Staudt, L.
Emmert-Buck, M.
Jaffe, E.
TI Epigenetic profiling of lymphoma reveals a distinctive signature for
mediastinalgray zone lymphoma
SO EXPERIMENTAL DERMATOLOGY
LA English
DT Meeting Abstract
CT 38th Annual Meeting of the
Arbeitsgemeinschaft-Dermatologishche-Forschung
CY FEB 17-19, 2011
CL Tuebingen, GERMANY
SP Arbeitsgemeinsch Dermatol Forsch
C1 [Eberle, F.; Rodriguez-Canales, J.; Wei, L.; Hanson, J.; Killian, J.; Sun, H.; Adams, L.; Hewitt, S.; Wilson, W.; Pittaluga, S.; Meltzer, P.; Staudt, L.; Emmert-Buck, M.; Jaffe, E.] NIH, Bethesda, MD 20892 USA.
RI Wei, Lai/D-1088-2014
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0906-6705
J9 EXP DERMATOL
JI Exp. Dermatol.
PD FEB
PY 2011
VL 20
IS 2
MA P255
BP 202
EP 202
PG 1
WC Dermatology
SC Dermatology
GA 709UZ
UT WOS:000286468200273
ER
PT J
AU Conjeevaram, HS
Wahed, AS
Afdhal, N
Howell, CD
Everhart, JE
Hoofnagle, JH
AF Conjeevaram, Hari S.
Wahed, Abdus S.
Afdhal, Nezam
Howell, Charles D.
Everhart, James E.
Hoofnagle, Jay H.
CA Virahep-C Study Grp
TI Changes in Insulin Sensitivity and Body Weight During and After
Peginterferon and Ribavirin Therapy for Hepatitis C
SO GASTROENTEROLOGY
LA English
DT Article
DE Obesity; Metabolic Response; Liver Disease; Clinical Trial
ID BETA-CELL FUNCTION; HOMEOSTASIS MODEL ASSESSMENT; VIRUS-INFECTION;
DIABETES-MELLITUS; FIBROSIS PROGRESSION; RESISTANCE; STEATOSIS; GLUCOSE
AB BACKGROUND & AIMS: Chronic hepatitis C is associated with an increased prevalence of insulin resistance, which might result from liver disease, metabolic factors, or the hepatitis C virus (HCV) itself. The effect of antiviral treatment on insulin sensitivity is not well-known. We evaluated changes in insulin resistance and weight in patients with hepatitis C during and after peginterferon and ribavirin therapy. METHODS: Virahep-C was a prospective, multicenter study of a 48-week course of combination antiviral therapy in patients infected with HCV genotype 1. Insulin resistance (IR) was estimated by the homeostasis model assessment index (HOMA2-IR) based on fasting glucose and insulin levels. RESULTS: Among 341 patients, 40% had insulin resistance (HOMA2-IR > 2.0). The presence of insulin resistance was associated with increasing age, body mass index (BMI), and fibrosis stage. Among patients with insulin resistance at the start of the trial, median decreases in HOMA2-IR values during treatment were 0.74 at 24 weeks and 0.89 at 48 weeks, whereas BMI decreased by 1.2 and 2.2 at the same time points (P < .001 for all). At follow-up, HOMA2-IR and BMI levels returned toward baseline values in patients who did not respond or relapsed, but HOMA2-IR values remained significantly lower in patients with sustained virologic response (SVR) (P < .001), despite increases in BMI. CONCLUSIONS: In patients with HCV genotype 1 infections, therapy with peginterferon and ribavirin is associated with decreases in body weight and insulin resistance. Among patients with insulin resistance before treatment, resolution of HCV infection results in sustained improvements in the HOMA-IR index, suggesting that HCV could have a direct role in the pathogenesis of insulin resistance.
C1 [Conjeevaram, Hari S.] Univ Michigan, Div Gastroenterol, Ann Arbor, MI 48109 USA.
[Wahed, Abdus S.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15261 USA.
[Afdhal, Nezam] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA.
[Howell, Charles D.] Univ Maryland, Baltimore, MD 21201 USA.
[Everhart, James E.; Hoofnagle, Jay H.] NIDDK, NIH, Bethesda, MD USA.
RP Conjeevaram, HS (reprint author), Univ Michigan, Div Gastroenterol, 3912 Taubman Ctr,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM omsairam@med.umich.edu
OI Wahed, Abdus/0000-0001-6911-7221
FU National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK); National Center on Minority Health and Health Disparities
(NCMHD); National Cancer Institute (NCI); Roche Laboratories, Inc.;
National Center for Research Resources (NCRR) [M01 RR00645, M02
RR000079, M01 RR16500, M01 RR000042, M01 RR00046]; [U01 DK60329]; [U01
DK60340]; [U01 DK60324]; [U01 DK60344]; [U01 DK60327]; [U01
DK60335]; [U01 DK60352]; [U01 DK60342]; [U01 DK60345]; [U01
DK60309]; [U01 DK60346]; [U01 DK60349]; [U01 DK60341]
FX Supported by a cooperative agreement by the National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK) with cosupport from
the National Center on Minority Health and Health Disparities (NCMHD)
and the Intramural Research Program of the National Cancer Institute
(NCI) with further support under a Cooperative Research and Development
Agreement (CRADA) with Roche Laboratories, Inc. Clinical trial number:
NCT00038974 (URL: http://www.virahepc.org). Grant numbers: U01 DK60329,
U01 DK60340, U01 DK60324, U01 DK60344, U01 DK60327, U01 DK60335, U01
DK60352, U01 DK60342, U01 DK60345, U01 DK60309, U01 DK60346, U01
DK60349, U01 DK60341. Other support includes the National Center for
Research Resources (NCRR) General Clinical Research Centers Program
grants: M01 RR00645 (New York Presbyterian), M02 RR000079 (University of
California, San Francisco), M01 RR16500 (University of Maryland), M01
RR000042 (University of Michigan), M01 RR00046 (University of North
Carolina).
NR 26
TC 33
Z9 33
U1 1
U2 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD FEB
PY 2011
VL 140
IS 2
BP 469
EP 477
DI 10.1053/j.gastro.2010.11.002
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 711LR
UT WOS:000286593600026
PM 21070775
ER
PT J
AU Landry, JW
Banerjee, S
Taylor, B
Aplan, PD
Singer, A
Wu, C
AF Landry, Joseph W.
Banerjee, Subhadra
Taylor, Barbara
Aplan, Peter D.
Singer, Alfred
Wu, Carl
TI Chromatin remodeling complex NURF regulates thymocyte maturation
SO GENES & DEVELOPMENT
LA English
DT Article
DE NURF; SRF; AP-1; Bptf; chromatin remodeling; positive selection
ID T-CELL DEVELOPMENT; POSITIVE SELECTION; INTERLEUKIN-2 GENE;
MOLECULAR-BASIS; LYMPHOCYTE DEVELOPMENT; FUNCTIONAL ELEMENTS; IN-VIVO;
NUCLEOSOME; EXPRESSION; TRANSCRIPTION
AB The maturation of T cells requires signaling from both cytokine and T-cell receptors to gene targets in chromatin, but how chromatin architecture influences this process is largely unknown. Here we show that thymocyte maturation post-positive selection is dependent on the nucleosome remodeling factor (NURF). Depletion of Bptf (bromodomain PHD finger transcription factor), the largest NURF subunit, in conditional mouse mutants results in developmental arrest beyond the CD4(+) CD8(int) stage without affecting cellular proliferation, cellular apoptosis, or coreceptor gene expression. In the Bptf mutant, specific subsets of genes important for thymocyte development show aberrant expression. We also observed defects in DNase I-hypersensitive chromatin structures at Egr1, a prototypical Bptf-dependent gene that is required for efficient thymocyte development. Moreover, chromatin binding of the sequence-specific factor Srf (serum response factor) to Egr1 regulatory sites is dependent on Bptf function. Physical interactions between NURF and Srf suggest a model in which Srf recruits NURF to facilitate transcription factor binding at Bptf-dependent genes. These findings provide evidence for causal connections between NURF, transcription factor occupancy, and gene regulation during thymocyte development.
C1 [Landry, Joseph W.; Wu, Carl] NCI, Lab Biochem & Mol Cell Biol, NIH, Bethesda, MD 20892 USA.
[Banerjee, Subhadra; Taylor, Barbara] NCI, FACS Core Lab, NIH, Bethesda, MD 20892 USA.
[Aplan, Peter D.] NCI, Genet Branch, NIH, Bethesda, MD 20889 USA.
[Singer, Alfred] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Landry, JW (reprint author), Virginia Commonwealth Univ, Dept Human & Mol Genet, Sch Med, Bldg 37,Room 6068, Richmond, VA 23298 USA.
EM jwlandry2@vcu.edu
RI Aplan, Peter/K-9064-2016
FU American Cancer Society [PF-05-122-01-DDC]; National Cancer Institute
and Mammalian Genome Society; National Institutes of Health
FX We thank members of the Wu, Singer, and Aplan laboratories for
critically reading the manuscript, discussions, and technical
assistance. We thank Ron Schwartz, Remy Bousselut, Paul Love, and John
Ashwell for helpful discussions. We thank John Stamatoyannopoulos and
his laboratory for help with the quantitative chromatin profiling. We
thank Paul Meltzer's laboratory for technical help with microarray
experiments. We acknowledge the Frederick Histopathology Laboratory for
providing sections of thymus tissue. This research was supported through
fellowship #PF-05-122-01-DDC from the American Cancer Society and travel
awards from the National Cancer Institute and Mammalian Genome Society
to J.L., and National Institutes of Health intramural research grants to
A.S., P.A., and C.W. J.L. designed and performed experiments with input
from P.A., A.S., and C.W. S.B. and B.T. performed electronic cell
sorting. J.L. and C.W. wrote the manuscript and correspondence with
contributions from P.A. and A.S.
NR 61
TC 29
Z9 29
U1 1
U2 3
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 0890-9369
J9 GENE DEV
JI Genes Dev.
PD FEB 1
PY 2011
VL 25
IS 3
BP 275
EP 286
DI 10.1101/gad.2007311
PG 12
WC Cell Biology; Developmental Biology; Genetics & Heredity
SC Cell Biology; Developmental Biology; Genetics & Heredity
GA 715JL
UT WOS:000286880600009
PM 21289071
ER
PT J
AU Marenne, G
Rodriguez-Santiago, B
Closas, MG
Perez-Jurado, L
Rothman, N
Rico, D
Pita, G
Pisano, DG
Kogevinas, M
Silverman, DT
Valencia, A
Real, FX
Chanock, SJ
Genin, E
Malats, N
AF Marenne, Gaelle
Rodriguez-Santiago, Benjamin
Garcia Closas, Montserrat
Perez-Jurado, Luis
Rothman, Nathaniel
Rico, Daniel
Pita, Guillermo
Pisano, David G.
Kogevinas, Manolis
Silverman, Debra T.
Valencia, Alfonso
Real, Francisco X.
Chanock, Stephen J.
Genin, Emmanuelle
Malats, Nuria
TI Assessment of Copy Number Variation Using the Illumina Infinium 1M
SNP-Array: A Comparison of Methodological Approaches in the Spanish
Bladder Cancer/EPICURO Study
SO HUMAN MUTATION
LA English
DT Article
DE copy number variation; genome-wide association study; specificity;
sensitivity; reliability; accuracy; CNVpartition; PennCNV; QuantiSNP
ID GENOME-WIDE ASSOCIATION; HIDDEN-MARKOV MODEL; STRUCTURAL VARIATION;
GENOTYPING DATA; HUMAN-DISEASE; SCHIZOPHRENIA; VARIANTS; RISK; GENES;
AUTISM
AB High-throughput single nucleotide polymorphism (SNP)-array technologies allow to investigate copy number variants (CNVs) in genome-wide scans and specific calling algorithms have been developed to determine CNV location and copy number. We report the results of a reliability analysis comparing data from 96 pairs of samples processed with CNVpartition, PennCNV, and QuantiSNP for Infinium Illumina Human 1Million probe chip data. We also performed a validity assessment with multiplex ligation-dependent probe amplification (MLPA) as a reference standard. The number of CNVs per individual varied according to the calling algorithm. Higher numbers of CNVs were detected in saliva than in blood DNA samples regardless of the algorithm used. All algorithms presented low agreement with mean Kappa Index (KI) < 66. PennCNV was the most reliable algorithm (KI(w)=98.96) when assessing the number of copies. The agreement observed in detecting CNV was higher in blood than in saliva samples. When comparing to MLPA, all algorithms identified poorly known copy aberrations (sensitivity=0.19-0.28). In contrast, specificity was very high (0.97-0.99). Once a CNV was detected, the number of copies was truly assessed (sensitivity > 0.62). Our results indicate that the current calling algorithms should be improved for high performance CNV analysis in genome-wide scans. Further refinement is required to assess CNVs as risk factors in complex diseases. Hum Mutat 32:240-248, 2011. (C) 2011 Wiley-Liss, Inc.
C1 [Marenne, Gaelle; Rico, Daniel; Pita, Guillermo; Pisano, David G.; Valencia, Alfonso; Real, Francisco X.; Malats, Nuria] CNIO, Madrid, Spain.
[Marenne, Gaelle; Genin, Emmanuelle] Univ Paris Diderot, Inst Univ Hematol, INSERM, UMR S946, Paris, France.
[Rodriguez-Santiago, Benjamin; Perez-Jurado, Luis] Univ Pompeu Fabra, Dept Ciencies Expt & Salut, Barcelona, Spain.
[Rodriguez-Santiago, Benjamin; Perez-Jurado, Luis] CIBERER, E-08003 Barcelona, Spain.
[Garcia Closas, Montserrat; Rothman, Nathaniel; Silverman, Debra T.; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, US Dept HHS, Bethesda, MD 20892 USA.
[Perez-Jurado, Luis] Hosp Univ Vall Hebron, Programa Med Mol & Genet, E-08035 Barcelona, Spain.
[Perez-Jurado, Luis] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
[Kogevinas, Manolis] Hosp Mar, IMIM, Barcelona, Spain.
[Kogevinas, Manolis] Ctr Res Environm Epidemiol CREAL, Barcelona, Spain.
RP Malats, N (reprint author), CNIO, Madrid, Spain.
EM nmalats@cnio.es
RI Pisano, David/N-5817-2014; Genin, Emmanuelle/C-4974-2013; Garcia-Closas,
Montserrat /F-3871-2015; Malats, Nuria/H-7041-2015; Valencia,
Alfonso/I-3127-2015; Perez Jurado, Luis Alberto/M-7706-2015; Real
Arribas, Francisco/H-5275-2015; Kogevinas, Manolis/C-3918-2017;
OI Rico, Daniel/0000-0002-6561-2310; Pisano, David/0000-0002-4895-4124;
Genin, Emmanuelle/0000-0003-4117-2813; Garcia-Closas, Montserrat
/0000-0003-1033-2650; Malats, Nuria/0000-0003-2538-3784; Valencia,
Alfonso/0000-0002-8937-6789; Real Arribas,
Francisco/0000-0001-9501-498X; Rodriguez-Santiago,
Benjamin/0000-0003-1167-3852
FU Fondo de Investigacion Sanitaria, Spain [G03/174, PI061614, FI09/00205];
Asociacion Espanola Contra el Cancer (AECC); Fundacio Marato de TV3; Red
Tematica de Investigacion Cooperativa en Cancer (RTICC), Spain; Division
of Cancer Epidemiology and Genetics, National Cancer Institute;
Egide-PHRC Picasso
FX Contract grant sponsor: The Fondo de Investigacion Sanitaria, Spain;
Contract grant numbers: G03/174; PI061614; FI09/00205; Contract grant
sponsors: Asociacion Espanola Contra el Cancer (AECC), Fundacio Marato
de TV3, Red Tematica de Investigacion Cooperativa en Cancer (RTICC),
Spain; The Intramural Research Program of the Division of Cancer
Epidemiology and Genetics, National Cancer Institute; Egide-PHRC Picasso
Travel Grant.
NR 51
TC 25
Z9 26
U1 0
U2 7
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1059-7794
J9 HUM MUTAT
JI Hum. Mutat.
PD FEB
PY 2011
VL 32
IS 2
BP 240
EP 248
DI 10.1002/humu.21398
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 721SU
UT WOS:000287376300012
PM 21089066
ER
PT J
AU Zhou, D
Cheung, KF
Chen, Y
Lau, ST
Zhou, QF
Shung, KK
Luo, HS
Dai, JY
Chan, HLW
AF Zhou, Dan
Cheung, Kwok Fung
Chen, Yan
Lau, Sien Ting
Zhou, Qifa
Shung, K. Kirk
Luo, Hao Su
Dai, Jiyan
Chan, Helen Lai Wa
TI Fabrication and Performance of Endoscopic Ultrasound Radial Arrays Based
on PMN-PT Single Crystal/Epoxy 1-3 Composite
SO IEEE TRANSACTIONS ON ULTRASONICS FERROELECTRICS AND FREQUENCY CONTROL
LA English
DT Article
ID PIEZOELECTRIC TRANSDUCERS; EUS; DESIGN; PZT; FNA
AB In this paper, 0.7Pb(Mg(1/3)Nb(2/3))O(3)-0.3PbTiO(3) (PMN-PT) single crystal/epoxy 1-3 composite was used as the active material of the endoscopic ultrasonic radial array transducer, because this composite exhibited ultrahigh electromechanical coupling coefficient (k(t) = 0.81%), very low mechanical quality factor (Q(m) = 11) and relatively low acoustic impedance (Z(t) = 12 MRayls). A 6.91 MHz PMN-PT/epoxy 1-3 composite radial array transducer with 64 elements was tested in a pulse-echo response measurement. The -6-dB bandwidth of the composite array transducer was 102%, which was similar to 30% larger than that of traditional lead zirconate titanate array transducer. The two-way insertion loss was found to be -32.3 dB. The obtained results show that this broadband array transducer is promising for acquiring high-resolution endoscopic ultrasonic images in many clinical applications.
C1 [Zhou, Dan; Cheung, Kwok Fung; Chen, Yan; Shung, K. Kirk; Dai, Jiyan; Chan, Helen Lai Wa] Hong Kong Polytech Univ, Dept Appl Phys, Hong Kong, Hong Kong, Peoples R China.
[Zhou, Dan; Cheung, Kwok Fung; Chen, Yan; Shung, K. Kirk; Dai, Jiyan; Chan, Helen Lai Wa] Hong Kong Polytech Univ, Mat Res Ctr, Hong Kong, Hong Kong, Peoples R China.
[Lau, Sien Ting; Zhou, Qifa; Shung, K. Kirk] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
[Lau, Sien Ting; Zhou, Qifa; Shung, K. Kirk] Univ So Calif, NIH Transducer Resource Ctr, Los Angeles, CA USA.
[Luo, Hao Su] Chinese Acad Sci, Shanghai Inst Ceram, Informat Mat & Devices Res Ctr, Shanghai 200050, Peoples R China.
[Lau, Sien Ting] Univ So Calif, NIH Resource Ctr Med Ultrason Transducer Technol, Los Angeles, CA USA.
RP Zhou, D (reprint author), Hong Kong Polytech Univ, Dept Appl Phys, Hong Kong, Hong Kong, Peoples R China.
EM apdaijy@inet.polyu.edu.hk
RI Lau, Sien-Ting/B-6091-2013; Dai, Jiyan/I-7098-2013; CHAN, Helen Lai
Wa/B-5633-2014
OI Dai, Jiyan/0000-0002-7720-8032; CHAN, Helen Lai Wa/0000-0002-8508-3049
FU Hong Kong Innovative Technology Council [ZP-1H]; Department of Applied
Physics of the Hong Kong Polytechnic University; NIH [P41-EB2182]
FX This work was supported by the Hong Kong Innovative Technology Council
(Project No. ZP-1H), the Department of Applied Physics of the Hong Kong
Polytechnic University and NIH Grant #P41-EB2182.
NR 29
TC 20
Z9 21
U1 3
U2 27
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0885-3010
J9 IEEE T ULTRASON FERR
JI IEEE Trans. Ultrason. Ferroelectr. Freq. Control
PD FEB
PY 2011
VL 58
IS 2
BP 477
EP 484
DI 10.1109/TUFFC.2011.1825
PG 8
WC Acoustics; Engineering, Electrical & Electronic
SC Acoustics; Engineering
GA 725TY
UT WOS:000287670200022
PM 21342833
ER
PT J
AU Averdam, A
Kuschal, C
Otto, N
Westphal, N
Roos, C
Reinhardt, R
Walter, L
AF Averdam, Anne
Kuschal, Christiane
Otto, Nicole
Westphal, Nico
Roos, Christian
Reinhardt, Richard
Walter, Lutz
TI Sequence analysis of the grey mouse lemur (Microcebus murinus) MHC class
II DQ and DR region
SO IMMUNOGENETICS
LA English
DT Article
DE MHC class II; Evolution; Polymorphism; Mouse lemur; BAC sequencing
ID MAJOR HISTOCOMPATIBILITY COMPLEX; RHESUS MACAQUES; COMPARATIVE GENETICS;
CYNOMOLGUS MACAQUES; DRB GENES; POLYMORPHISMS; HAPLOTYPES;
MICROSATELLITE; VARIABILITY
AB We here report the genomic organisation of the grey mouse lemur (Microcebus murinus) MHC class II DQ and DR region based on BAC clone analysis. The sequenced Mimu-MHC haplotype spans 343 kb and encompasses the genes TAP2, DOB, DQB, DQA, DRB, DRA, BTNL2 and a further BTNL gene. The DQ and DR genes of this haplotype are not duplicated. Mimu-DOB is not transcribed and represents a pseudogene due to deletions and premature stop codons. Analysis of BAC clone DNA, a cDNA sample and eight genomic DNA samples suggests that Mimu-DRB, Mimu-DQA and Mimu-DQB are highly polymorphic with the majority of peptide-binding residues being affected by polymorphisms. In contrast, Mimu-DRA is moderately polymorphic, and the variable amino acid positions are not part of the peptide-binding region. Phylogenetic analysis of Mimu-DQA and Mimu-DQB and other primate DQA and DQB genes indicates that duplication of DQA and DQB loci occurred in Anthropoidea after the split from Strepsirrhini.
C1 [Walter, Lutz] Deutsch Primatenzentrum GmbH, Abt Primatengenet, D-37077 Gottingen, Germany.
[Reinhardt, Richard] Max Planck Inst Plant Breeding Res, Genome Ctr Cologne, Cologne, Germany.
[Roos, Christian; Walter, Lutz] German Primate Ctr, Gene Bank Primates, Gottingen, Germany.
[Kuschal, Christiane] NCI, DNA Repair Sect, DB, CCR,NIH, Bethesda, MD 20892 USA.
[Averdam, Anne] Univ Munich, Klinikum Grosshadern, Dept Neurol, Munich, Germany.
[Averdam, Anne; Kuschal, Christiane; Otto, Nicole; Westphal, Nico; Roos, Christian; Walter, Lutz] German Primate Ctr, Primate Genet Lab, Gottingen, Germany.
RP Walter, L (reprint author), Deutsch Primatenzentrum GmbH, Abt Primatengenet, Kellnerweg 4, D-37077 Gottingen, Germany.
EM lwalter@gwdg.de
OI Kuschal, Christiane/0000-0001-6113-3585; Walter,
Lutz/0000-0001-9408-3131
FU Pakt fur Forschung und Innovation of the Leibniz-Gemeinschaft
'Biodiversitat der Primaten: Erfassung, Ursachen und Erhalt'; Nationales
Genomforschungsnetz (NGFN)
FX The authors thank Manfred Eberle for providing DNA samples and Fabienne
Aujard for the liver sample of M. murinus. This study was supported by
the Pakt fur Forschung und Innovation of the Leibniz-Gemeinschaft
'Biodiversitat der Primaten: Erfassung, Ursachen und Erhalt' and by the
Nationales Genomforschungsnetz (NGFN).
NR 27
TC 7
Z9 7
U1 0
U2 11
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0093-7711
J9 IMMUNOGENETICS
JI Immunogenetics
PD FEB
PY 2011
VL 63
IS 2
BP 85
EP 93
DI 10.1007/s00251-010-0487-3
PG 9
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 718QL
UT WOS:000287140500003
PM 20938657
ER
PT J
AU Nock, CJ
Brell, JM
Bokar, JA
Cooney, MM
Cooper, B
Gibbons, J
Krishnamurthi, S
Manda, S
Savvides, P
Remick, SC
Ivy, P
Dowlati, A
AF Nock, Charles J.
Brell, Joanna M.
Bokar, Joseph A.
Cooney, Matthew M.
Cooper, Brenda
Gibbons, Joseph
Krishnamurthi, Smitha
Manda, Sudhir
Savvides, Panayiotis
Remick, Scot C.
Ivy, Percy
Dowlati, Afshin
TI A phase I study of rebeccamycin analog in combination with oxaliplatin
in patients with refractory solid tumors
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Phase I; Rebeccamycin; Oxaliplatin; Solid tumors; Rebeccamycin analog;
Becatecarin
ID NSC-655649; TOPOTECAN; CANCER; MALIGNANCIES; DERIVATIVES
AB Rebeccamycin analog (RA) is an antitumor antibiotic with both topoisomerase I and II inhibiting activity. Topoisomerase inhibitors have demonstrated synergy with platinum agents. We performed a phase I trial of combination RA with oxaliplatin in patients with refractory solid tumors. RA was administered as a 1-hour infusion daily on days 1-5 with oxaliplatin administered on day 5. Cycles were repeated every 21 days. A total of 17 patients were enrolled. The MTD for RA was 80 mg/m(2)/d for five days along with oxaliplatin 130 mg/m(2) on day 5. Myelosuppression was a common occurrence but was mild except in one instance. Dose limiting toxicities included atrial fibrillation and hypophosphatemia. There was evidence of antitumor activity including 3 partial responses in patients with esophageal, gallbladder and hepato-cellular carcinoma; 5 additional patients had stable disease. Thus, the combination of RA and oxaliplatin is both tolerable and has evidence of clinical activity, but given the lack of significant activity for single agent RA across a variety of disease sites, it is unlikely to proceed to phase II development.
C1 [Nock, Charles J.; Brell, Joanna M.; Bokar, Joseph A.; Cooney, Matthew M.; Cooper, Brenda; Gibbons, Joseph; Krishnamurthi, Smitha; Manda, Sudhir; Savvides, Panayiotis; Remick, Scot C.; Ivy, Percy; Dowlati, Afshin] Univ Hosp Cleveland, Case Med Ctr, Cleveland, OH 44106 USA.
[Nock, Charles J.; Brell, Joanna M.; Bokar, Joseph A.; Cooney, Matthew M.; Cooper, Brenda; Gibbons, Joseph; Krishnamurthi, Smitha; Manda, Sudhir; Savvides, Panayiotis; Remick, Scot C.; Ivy, Percy; Dowlati, Afshin] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Ivy, Percy] NCI, Bethesda, MD 20892 USA.
RP Dowlati, A (reprint author), Univ Hosp Cleveland, Case Med Ctr, 11100 Euclid Ave, Cleveland, OH 44106 USA.
EM afshin.dowlati@case.edu
FU [U01 CA62502]; [MO1 RR00080]; [K23 CA109348]
FX Supported in part by grants U01 CA62502, MO1 RR00080 and K23 CA109348.
NR 17
TC 8
Z9 9
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD FEB
PY 2011
VL 29
IS 1
BP 126
EP 130
DI 10.1007/s10637-009-9322-9
PG 5
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 702GK
UT WOS:000285882400013
PM 19774342
ER
PT J
AU Burnett, JC
Tam, LN
AF Burnett, James C.
Tam Luong Nguyen
TI Is Stoichiometry a New Metric for Evaluating Folded Proteins?
SO JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS
LA English
DT Editorial Material
C1 [Burnett, James C.; Tam Luong Nguyen] NCI Frederick, Target Struct Based Drug Discovery Grp, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Tam, LN (reprint author), NCI Frederick, Target Struct Based Drug Discovery Grp, SAIC Frederick Inc, Frederick, MD 21702 USA.
EM nguyent5@mail.nih.gov
NR 5
TC 1
Z9 1
U1 0
U2 1
PU ADENINE PRESS
PI SCHENECTADY
PA 2066 CENTRAL AVE, SCHENECTADY, NY 12304 USA
SN 0739-1102
J9 J BIOMOL STRUCT DYN
JI J. Biomol. Struct. Dyn.
PD FEB
PY 2011
VL 28
IS 4
BP 641
EP 642
PG 2
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 710AI
UT WOS:000286482400031
PM 21142245
ER
PT J
AU Gai, ND
Talagala, SL
Butman, JA
AF Gai, Neville D.
Talagala, S. Lalith
Butman, John A.
TI Whole-Brain Cerebral Blood Flow Mapping Using 3D Echo Planar Imaging and
Pulsed Arterial Tagging
SO JOURNAL OF MAGNETIC RESONANCE IMAGING
LA English
DT Article
DE arterial spin labeling; 3D PULSAR; blurring reduction; whole brain
perfusion imaging
ID LABELING PERFUSION MEASUREMENTS; MRI; SIGNAL; INVERSION
AB Purpose: To quantitate cerebral blood flow (CBF) in the entire brain using the 3D echo planar imaging (EPI) PULSAR (pulsed star labeling) technique.
Materials and Methods: The PULSAR technique was modified to 1) incorporate a nonselective inversion pulse to suppress background signal; 2) to use 3D EPI acquisition; and 3) to modulate flip angle in such a manner as to minimize the blurring resulting from T1 modulation along the slice encoding direction. Computation of CBF was performed using the general kinetic model (GKM). In a series of healthy volunteers (n = 12), we first investigated the effects of introducing an inversion pulse on the measured value of CBF and on the temporal stability of the perfusion signal. Next we investigated the effect of flip angle modulation on the spatial blurring of the perfusion signal. Finally, we evaluated the repeatability of the CBF measurements, including the influence of the measurement of arterial blood magnetization (a calibration factor for the GKM).
Results: The sequence provides sufficient perfusion signal to achieve whole brain coverage in approximate to 5 minutes. Introduction of the inversion pulse for background suppression did not significantly affect computed CBF values, but did reduce the fluctuation in the perfusion signal. Flip angle modulation reduced blurring, resulting in higher estimates of gray matter (GM) CBF and lower estimates of white matter (WM) CBF. The repeatability study showed that measurement of arterial blood signal did not result in significantly higher error in the perfusion measurement.
Conclusion: Improvements in acquisition and sequence preparation presented here allow for better quantification and localization of perfusion signal, allowing for accurate whole-brain CBF measurements in 5 minutes.
C1 [Gai, Neville D.; Butman, John A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Talagala, S. Lalith] NINDS, NIH MRI Res Facil, NIH, Bethesda, MD 20892 USA.
RP Gai, ND (reprint author), NIH, Radiol & Imaging Sci RAD&IS, Ctr Clin, 9000 Rockville Pike,Bldg 10,Rm 10502X, Bethesda, MD 20892 USA.
EM gaind@cc.nih.gov
RI Butman, John/J-2780-2013
OI Butman, John/0000-0002-1547-9195
FU National Institutes of Health (NIH)
FX Contract grant sponsor: Intramural Research Program of the National
Institutes of Health (NIH).
NR 25
TC 8
Z9 8
U1 0
U2 0
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1053-1807
J9 J MAGN RESON IMAGING
JI J. Magn. Reson. Imaging
PD FEB
PY 2011
VL 33
IS 2
BP 287
EP 295
DI 10.1002/jmri.22437
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 716FA
UT WOS:000286953300003
PM 21274969
ER
PT J
AU Akilov, O
Grant, C
Geskin, L
Piekarz, R
Bates, S
AF Akilov, Oleg
Grant, Cliona
Geskin, Larisa
Piekarz, Richard
Bates, Susan
TI Low dose electron beam radiation to localized symptomatic CTCL lesions
further improves clinical responses to romidepsin
SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
LA English
DT Meeting Abstract
CT 69th Annual Meeting of the American-Academy-of-Dermatology
CY FEB 04-08, 2011
CL New Orleans, LA
SP Amer Acad Dermatol
C1 [Akilov, Oleg; Geskin, Larisa] Univ Pittsburgh, Pittsburgh, PA USA.
[Grant, Cliona; Piekarz, Richard; Bates, Susan] NIH, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0190-9622
J9 J AM ACAD DERMATOL
JI J. Am. Acad. Dermatol.
PD FEB
PY 2011
VL 64
IS 2
SU 1
BP AB114
EP AB114
PG 1
WC Dermatology
SC Dermatology
GA 714AY
UT WOS:000286780500449
ER
PT J
AU Baddour, LM
Epstein, AE
Erickson, CC
Knight, BP
Levison, ME
Lockhart, PB
Masoudi, FA
Okum, EJ
Wilson, WR
Beerman, LB
Bolger, AF
Estes, NAM
Gewitz, M
Newburger, JW
Schron, EB
Taubert, KA
AF Baddour, Larry M.
Epstein, Andrew E.
Erickson, Christopher C.
Knight, Bradley P.
Levison, Matthew E.
Lockhart, Peter B.
Masoudi, Frederick A.
Okum, Eric J.
Wilson, Walter R.
Beerman, Lee B.
Bolger, Ann F.
Estes, N. A. Mark, III
Gewitz, Michael
Newburger, Jane W.
Schron, Eleanor B.
Taubert, Kathryn A.
CA Council Cardiovasc Disease Young
Council Cardiovasc Surg & Anesthe
Council Cardiovasc Nursing
Council Clinical Cardiology
Interdisciplinary Council Quality
TI A summary of the update on cardiovascular implantable electronic device
infections and their management A scientific statement from the American
Heart Association
SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION
LA English
DT Article
DE American Heart Association scientific statements; infection; device;
cardiovascular implantable electronic device; pacemaker; defibrillator;
endocarditis; bacteremia; antibiotic prophylaxis
ID COAGULASE-NEGATIVE STAPHYLOCOCCI; PERMANENT PACEMAKER IMPLANTATION;
ANTIBIOTIC-PROPHYLAXIS; CARDIOVERTER-DEFIBRILLATORS; ANTIMICROBIAL
PROPHYLAXIS; ENDOCARDIAL PACEMAKER; SUSTAINED BACTEREMIA; AUREUS
BACTEREMIA; DENTAL PROCEDURES; LEAD EXTRACTION
AB Background. The purpose of this statement is to update the recommendations by the American Heart Association (AHA) for cardiovascular implantable electronic device (CIED) infections and their management, which were last published in 2003.
Methods and Results. The AHA commissioned this scientific statement to educate clinicians about CIED infections, provide explicit recommendations for the care of patients with suspected or established CIED infections and highlight areas of needed research. The recommendations in this statement reflect analyses of relevant literature, to include recent advances in our understanding of the epidemiology, risk factors, microbiology, management and prevention of CIED infections.
Conclusion. There are no scientific data to support the use of antimicrobial prophylaxis for dental or other invasive procedures.
Clinical Implications. The concerns about life-threatening drug reactions, the development of resistant strains of bacterial pathogens, medicolegal issues and cost to the health care system are, thus, avoided.
C1 [Baddour, Larry M.] Carolinas Med Ctr, Dept Oral Med, Charlotte, NC 28232 USA.
[Baddour, Larry M.; Wilson, Walter R.] Mayo Clin, Div Infect Dis, Coll Med, Rochester, MN USA.
[Epstein, Andrew E.] Univ Penn, Philadelphia VA Med Ctr, Philadelphia, PA 19104 USA.
[Epstein, Andrew E.] Univ Penn, Div Cardiovasc, Philadelphia, PA 19104 USA.
[Erickson, Christopher C.] Univ Nebraska, Med Ctr, Dept Pediat, Omaha, NE USA.
[Erickson, Christopher C.] Univ Nebraska, Med Ctr, Dept Internal Med, Omaha, NE USA.
[Erickson, Christopher C.] Creighton Univ, Sch Med, Dept Pediat, Omaha, NE 68178 USA.
[Erickson, Christopher C.] Childrens Hosp & Med Ctr, Omaha, NE USA.
[Knight, Bradley P.] NW Med Ctr, Div Cardiol, Chicago, IL USA.
[Levison, Matthew E.] Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19104 USA.
[Levison, Matthew E.] Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
[Masoudi, Frederick A.] Denver Hlth Med Ctr, Div Cardiol, Denver, CO USA.
[Okum, Eric J.] Cardiac Vasc & Thorac Surg, Cincinnati, OH USA.
[Beerman, Lee B.] Univ Pittsburgh, Div Pediat Cardiol, Childrens Hosp Pittsburgh, Ctr Med, Pittsburgh, PA 15260 USA.
[Bolger, Ann F.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Bolger, Ann F.] San Francisco Gen Hosp, Div Cardiol, San Francisco, CA USA.
[Estes, N. A. Mark, III] Tufts Med Ctr, Cardiac Arrhythmia Serv, Boston, MA USA.
[Gewitz, Michael] Maria Fareri Childrens Hosp, Westchester Med Ctr, Valhalla, NY USA.
[Gewitz, Michael] New York Med Coll, Valhalla, NY 10595 USA.
[Newburger, Jane W.] Childrens Hosp, Dept Cardiol, Boston, MA 02115 USA.
[Schron, Eleanor B.] NEI, Vis Res Program, Natl Inst Hlth, Rockville, MD USA.
[Taubert, Kathryn A.] World Heart Federat, Geneva, NY USA.
RP Lockhart, PB (reprint author), Carolinas Med Ctr, Dept Oral Med, POB 32861, Charlotte, NC 28232 USA.
EM Peter.Lockhart@carolinashealthcare.org
FU St. Jude Medical, St. Paul, Minn; Boston Scientific, Natick, Mass
FX Dr. Erickson has received a research grant from St. Jude Medical, St.
Paul, Minn. Dr. Estes has received research support from Boston
Scientific, Natick, Mass.; is a consultant to Boston Scientific; and has
received honoraria from Boston Scientific and St. Jude Medical. None of
the other authors reported any disclosures.
NR 69
TC 15
Z9 16
U1 0
U2 1
PU AMER DENTAL ASSOC
PI CHICAGO
PA 211 E CHICAGO AVE, CHICAGO, IL 60611 USA
SN 0002-8177
J9 J AM DENT ASSOC
JI J. Am. Dent. Assoc.
PD FEB
PY 2011
VL 142
IS 2
BP 159
EP 165
PG 7
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 716UU
UT WOS:000286999800017
PM 21282681
ER
PT J
AU Reedy, J
Krebs-Smith, SM
AF Reedy, Jill
Krebs-Smith, Susan M.
TI Labeling Solid Fats and Added Sugars As Empty Calories Response
SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION
LA English
DT Letter
C1 [Reedy, Jill] NCI, Risk Factor Monitoring & Methods Appl Res Program, Div Canc Control & Populat Serv, Bethesda, MD 20892 USA.
RP Reedy, J (reprint author), NCI, Risk Factor Monitoring & Methods Appl Res Program, Div Canc Control & Populat Serv, Bethesda, MD 20892 USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU AMER DIETETIC ASSOC
PI CHICAGO
PA 120 S RIVERSIDE PLZ, STE 2000, CHICAGO, IL 60606-6995 USA
SN 0002-8223
J9 J AM DIET ASSOC
JI J. Am. Diet. Assoc.
PD FEB
PY 2011
VL 111
IS 2
BP 223
EP 224
DI 10.1016/j.jada.2010.12.004
PG 2
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 717UV
UT WOS:000287073800008
ER
PT J
AU Wright, JD
Wang, CY
AF Wright, Jacqueline D.
Wang, Chia-Yih
TI Awareness of Federal Dietary Guidance in Persons Aged 16 Years and
Older: Results from the National Health and Nutrition Examination Survey
2005-2006
SO JOURNAL OF THE AMERICAN DIETETIC ASSOCIATION
LA English
DT Article
ID USDA FOOD GUIDE; EATING PLAN; TRIAL; RISK; BEHAVIOR
AB The National Health and Nutrition Examination Survey 2005-2006 included questions on awareness of the Dietary Guidelines for Americans (DGA), the Food Guide Pyramid, and the 5 A Day for Better Health Program. Prevalence of awareness of federal dietary guidance was estimated and differences were tested across demographic traits, health characteristics, and diet-related attitudes and behavior. The continuous National Health and Nutrition Examination Survey uses a nationally representative cross-sectional sample design. The analytic sample consisted of 5,499 persons aged 16 years and older with complete data. Among persons aged 16 years and older, 83.8% had heard of at least one of the initiatives: 49.2% had heard of the DGA, 80.6% had heard of the Food Guide Pyramid, and 51.2% had heard of the 5 A Day program. There was a linear trend of decreasing awareness of at least one of the guidance efforts with increasing age. Differences by sex, race/ethnicity, education, and income were also observed. Differences by body mass index were not statistically significant; however, significant differences were seen with fatalistic beliefs about body weight. Differences by smoking, self-assessed diet quality, and eating out frequency were not statistically significant after adjustment for sex, age, race/ethnicity, education, and income. These results may be useful in promotion of the upcoming edition of the DGA and to suggest population groups that may benefit from strengthened and more innovative education efforts at the public health program level and at the clinic level. J Am Diet Assoc. 2011;111:295-300.
C1 [Wright, Jacqueline D.] NHLBI, Epidemiol Branch, Div Cardiovasc Sci, NIH,Rockledge Ctr 2, Bethesda, MD 20892 USA.
[Wright, Jacqueline D.; Wang, Chia-Yih] Ctr Dis Control & Prevent, Div Natl Hlth & Nutr Examinat Surveys, Natl Ctr Hlth Stat, Hyattsville, MD USA.
RP Wright, JD (reprint author), NHLBI, Epidemiol Branch, Div Cardiovasc Sci, NIH,Rockledge Ctr 2, Suite 10018,6701 Rockledge Dr MSC 7936, Bethesda, MD 20892 USA.
EM jacqueline.wright@nih.gov
NR 23
TC 11
Z9 11
U1 0
U2 3
PU AMER DIETETIC ASSOC
PI CHICAGO
PA 120 S RIVERSIDE PLZ, STE 2000, CHICAGO, IL 60606-6995 USA
SN 0002-8223
J9 J AM DIET ASSOC
JI J. Am. Diet. Assoc.
PD FEB
PY 2011
VL 111
IS 2
BP 295
EP 300
DI 10.1016/j.jada.2010.10.049
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 717UV
UT WOS:000287073800019
PM 21272706
ER
PT J
AU Arnold, MA
Shandilya, S
Galli, S
Killian, JK
Raffeld, M
Tsokos, M
Meltzer, PS
Warren, KE
Quezado, MM
AF Arnold, M. A.
Shandilya, S.
Galli, S.
Killian, J. K.
Raffeld, M.
Tsokos, M.
Meltzer, P. S.
Warren, K. E.
Quezado, M. M.
TI Morphological and Molecular Profiling of Pediatric Brain Stem Gliomas
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Arnold, M. A.; Shandilya, S.; Galli, S.; Killian, J. K.; Raffeld, M.; Tsokos, M.; Meltzer, P. S.; Warren, K. E.; Quezado, M. M.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 1
BP 4A
EP 4A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 716ZG
UT WOS:000287011400002
ER
PT J
AU Weaver, DL
Ashikaga, T
Krag, DN
Skelly, JM
Anderson, SJ
Harlow, SP
Julian, TB
Mamounas, EP
Wolmark, N
AF Weaver, D. L.
Ashikaga, T.
Krag, D. N.
Skelly, J. M.
Anderson, S. J.
Harlow, S. P.
Julian, T. B.
Mamounas, E. P.
Wolmark, N.
TI Survival Impact of Occult Metastases in NSABP B-32: Sentinel Lymph Node
Biopsy Versus Axillary Dissection in Node-Negative Breast Cancer
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 Univ Vermont, Coll Med, Burlington, VT 05405 USA.
Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA.
Allegheny Gen Hosp, Pittsburgh, PA 15212 USA.
Aultman Caner Ctr, Canton, OH USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 280
BP 69A
EP 69A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 716ZG
UT WOS:000287011400281
ER
PT J
AU Aung, PP
Pathak, A
Xi, L
Filie, AC
Raffeld, M
AF Aung, P. P.
Pathak, A.
Xi, L.
Filie, A. C.
Raffeld, M.
TI Identification of a DNA Methylation Marker That Differentiates Malignant
Mesothelioma from Reactive Mesothelial Cells on Effusion Samples
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Aung, P. P.; Pathak, A.; Xi, L.; Filie, A. C.; Raffeld, M.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 339
BP 83A
EP 83A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 716ZG
UT WOS:000287011400341
ER
PT J
AU Chowdhuri, SR
Fetsch, P
Hughes, MS
Filie, AC
AF Chowdhuri, S. Roy
Fetsch, P.
Hughes, M. S.
Filie, A. C.
TI KBA.62 and KIT Expression Patterns in Fine-Needle Aspirates of Malignant
Melanoma Metastatic to the Liver
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Chowdhuri, S. Roy; Fetsch, P.; Hughes, M. S.; Filie, A. C.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 427
BP 103A
EP 104A
PG 2
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 716ZG
UT WOS:000287011400429
ER
PT J
AU Chowdhuri, SR
Xi, L
Pham, T
Hanson, J
Giaccone, G
Emmerert-Buck, M
Raffeld, M
Filie, AC
AF Chowdhuri, S. Roy
Xi, L.
Pham, T.
Hanson, J.
Giaccone, G.
Emmerert-Buck, M.
Raffeld, M.
Filie, A. C.
TI High Sensitivity EGFR Mutation Detection in Cytologic Preparations
Enabled by Laser Capture Microdissection (LCM)
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Chowdhuri, S. Roy; Xi, L.; Pham, T.; Hanson, J.; Giaccone, G.; Emmerert-Buck, M.; Raffeld, M.; Filie, A. C.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 428
BP 104A
EP 104A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 716ZG
UT WOS:000287011400430
ER
PT J
AU Liu, YC
Rosenberg, SA
Lee, CCR
AF Liu, Y-C
Rosenberg, S. A.
Lee, C-C R.
TI Target Marker for Immunotherapy in Metastatic Melanomas of Rare
Morphology Subtypes
SO LABORATORY INVESTIGATION
LA English
DT Meeting Abstract
CT 100th Annual Meeting of the United States and
Canadian-Academy-of-Pathology
CY FEB 26-MAR 04, 2011
CL San Antonio, TX
SP Canadian Acad Pathol
C1 [Liu, Y-C; Rosenberg, S. A.; Lee, C-C R.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0023-6837
J9 LAB INVEST
JI Lab. Invest.
PD FEB
PY 2011
VL 91
SU 1
MA 499
BP 120A
EP 120A
PG 1
WC Medicine, Research & Experimental; Pathology
SC Research & Experimental Medicine; Pathology
GA 716ZG
UT WOS:000287011400501
ER
PT J
AU Gulley, SP
Rasch, EK
Chan, L
AF Gulley, Stephen P.
Rasch, Elizabeth K.
Chan, Leighton
TI If We Build It, Who Will Come? Working-Age Adults With Chronic Health
Care Needs and the Medical Home
SO MEDICAL CARE
LA English
DT Article
DE patient-centered care; chronic illness; people with disabilities; health
care reform
ID CHILDREN; POLICY
AB Background: Currently, there is a call to implement and test the patient-centered medical home in adult populations, particularly among those with chronic conditions. However, the size, composition, and service use of the population who might require this coordinated care model need to be assessed, as does the way they are defined and identified.
Objectives: Using nationally representative data from the 2002 to 2004 Medical Expenditure Panel Survey, we provide a preliminary profile of the population of working-age adults with chronic health care needs (ACHCN), including those with chronic health conditions and disabilities.
Results: ACHCN comprised the majority (52%) of the working-aged population. Relative to persons without chronic health care needs, they had significantly more service use, access problems, and 4 times more health care expenditures. Of the 2 disability groups within the larger population of ACHCN, those reporting need for help or supervision with activities of daily livings (ADLs) or instrumental ADLs (IADLs) had the highest rates/percentages of the following: mean chronic (3.5) and acute (4.4) conditions during the year, service use (all services), and access problems. The ADL/IADL-limited group reported annual medical expenditures totaling 100 billion dollars, more than what was spent on the entire working-age population without chronic health care needs.
Conclusions: These data reveal the drawbacks of selecting the potential population targeted for a medical home on the basis of diagnosis alone. New measurement approaches on the basis of shared need for ongoing health and related services are required to bridge the division between disability and chronic health conditions.
C1 [Gulley, Stephen P.] Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA USA.
[Gulley, Stephen P.; Rasch, Elizabeth K.; Chan, Leighton] NIH, Dept Rehabil Med, Clin Res Ctr, Bethesda, MD 20892 USA.
RP Gulley, SP (reprint author), NIH, Dept Rehabil Med, Mark O Hatfield Clin Res Ctr, Bldg 10-CRC,Room 1-1469,10 Ctr Dr,MSC 1604, Bethesda, MD 20892 USA.
EM gulley@brandeis.edu
FU NIH
FX Supported by NIH Intramural Research Program.
NR 23
TC 17
Z9 17
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0025-7079
J9 MED CARE
JI Med. Care
PD FEB
PY 2011
VL 49
IS 2
BP 149
EP 155
DI 10.1097/MLR.0b013e3182028380
PG 7
WC Health Care Sciences & Services; Health Policy & Services; Public,
Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA 706BR
UT WOS:000286191000006
PM 21206295
ER
PT J
AU Melo, VH
Pinto, JA
Freimanis-Hance, L
Gutierrez, C
Peixoto, M
Santos, B
Machado, DM
Joao, EC
Robergeau, K
Read, JS
AF Melo, Victor H.
Pinto, Jorge A.
Freimanis-Hance, Laura
Gutierrez, Cesar
Peixoto, Mario
Santos, Breno
Machado, Daisy M.
Joao, Esau C.
Robergeau, Kathleen
Read, Jennifer S.
TI Postpartum changes in plasma viral load and CD4 percentage among
HIV-infected women from Latin American and Caribbean countries: the
NISDI Perinatal Study
SO MEMORIAS DO INSTITUTO OSWALDO CRUZ
LA English
DT Article
DE HIV; pregnancy; postpartum period; viral load; CD4 counts
ID PREGNANT-WOMEN; ANTIRETROVIRAL TREATMENT; RANDOMIZED-TRIAL; THERAPY;
INTERRUPTION; DELIVERY
AB The goal of this study was to evaluate changes in plasma human immunodeficiency virus (HIV) RNA concentration [viral load (VL)] and CD4(+) percentage (CD4%) during 6-12 weeks postpartum (PP) among HIV-infected women and to assess differences according to the reason for receipt of antiretrovirals (ARVs) during pregnancy [prophylaxis (PR) vs. treatment (TR)]. Data from a prospective cohort of HIV-infected pregnant women (National Institute of Child Health and Human Development International Site Development Initiative Perinatal Study) were analyzed. Women experiencing their first pregnancy who received ARVs for PR (started during pregnancy, stopped PP) or for TR (initiated prior to pregnancy and/or continued PP) were included and were followed PP. Increases in plasma VL (>= 0.5 log(10)) and decreases in CD4% (>= 20% relative decrease in CD4%) between hospital discharge (HD) and PP were assessed. Of the 1,229 women enrolled, 1,119 met the inclusion criteria (PR: 601; TR: 518). At enrollment, 87% were asymptomatic. The median CD4% values were: HD [34% (PR); 25% (TR)] and PP [29% (PR); 24% (TR)]. The VL increases were 60% (PR) and 19% (TR) (p < 0.0001). The CD4% decreases were 36% (PR) and 18% (TR) (p < 0.0001). Women receiving PR were more likely to exhibit an increase in VL [adjusted odds ratio (AOR) 7.7 (95% CI: 5.5-10.9) and a CD4% decrease (AOR 2.3; 95% CI: 1.6-3.2). Women receiving PR are more likely to have VL increases and CD4% decreases compared to those receiving TR. The clinical implications of these VL and CD4% changes remain to be explored.
C1 [Melo, Victor H.; Pinto, Jorge A.] Univ Fed Minas Gerais, Fac Med, BR-30130100 Belo Horizonte, MG, Brazil.
[Freimanis-Hance, Laura; Robergeau, Kathleen] Westat Corp, Rockville, MD USA.
[Gutierrez, Cesar] Univ Nacl Mayor San Marcos, Lima 14, Peru.
[Peixoto, Mario] Hosp Femina, Porto Alegre, RS, Brazil.
[Santos, Breno] Hosp Conceicao, Porto Alegre, RS, Brazil.
[Machado, Daisy M.] Univ Fed Sao Paulo, Sao Paulo, Brazil.
[Joao, Esau C.] Hosp Servidores Estado, Rio De Janeiro, Brazil.
[Read, Jennifer S.] Natl Inst Child Hlth, Pediat Adolescent & Maternal AIDS Branch, NIH, Bethesda, MD USA.
[Read, Jennifer S.] NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Melo, VH (reprint author), Univ Fed Minas Gerais, Fac Med, Av Alfredo Balena 190 4 Andar, BR-30130100 Belo Horizonte, MG, Brazil.
EM victormelo@terra.com.br
FU NICHD [HHSN267200800001C/N01-DK-8-0001]
FX Financial support: NICHD (HHSN267200800001C/N01-DK-8-0001)
NR 17
TC 6
Z9 6
U1 1
U2 3
PU FUNDACO OSWALDO CRUZ
PI RIO DE JANEIRO, RJ
PA AV BRASIL 4365, 21045-900 RIO DE JANEIRO, RJ, BRAZIL
SN 0074-0276
J9 MEM I OSWALDO CRUZ
JI Mem. Inst. Oswaldo Cruz
PD FEB
PY 2011
VL 106
IS 1
BP 97
EP 104
PG 8
WC Parasitology; Tropical Medicine
SC Parasitology; Tropical Medicine
GA 726HW
UT WOS:000287712000016
PM 21340363
ER
PT J
AU Yang, RQ
Gaidamakov, SA
Xie, JW
Lee, J
Martino, L
Kozlov, G
Crawford, AK
Russo, AN
Conte, MR
Gehring, K
Maraia, RJ
AF Yang, Ruiqing
Gaidamakov, Sergei A.
Xie, Jingwei
Lee, Joowon
Martino, Luigi
Kozlov, Guennadi
Crawford, Amanda K.
Russo, Amy N.
Conte, Maria R.
Gehring, Kalle
Maraia, Richard J.
TI La-Related Protein 4 Binds Poly(A), Interacts with the Poly(A)-Binding
Protein MLLE Domain via a Variant PAM2w Motif, and Can Promote mRNA
Stability
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID POLYMERASE-III TRANSCRIPTS; C-TERMINAL DOMAIN; SACCHAROMYCES-CEREVISIAE;
EUKARYOTIC TRANSLATION; STRUCTURAL BASIS; DEPENDENT TRANSLATION;
INITIATION-FACTOR; STRESS GRANULES; RECOGNITION; RIBONUCLEOPROTEIN
AB The conserved RNA binding protein La recognizes UUU-3`OH on its small nuclear RNA ligands and stabilizes them against 3`-end-mediated decay. We report that newly described La-related protein 4 (LARP4) is a factor that can bind poly(A) RNA and interact with poly(A) binding protein (PABP). Yeast two-hybrid analysis and reciprocal immunoprecipitations (IPs) from HeLa cells revealed that LARP4 interacts with RACK1, a 40S ribosome-and mRNA-associated protein. LARP4 cosediments with 40S ribosome subunits and polyribosomes, and its knockdown decreases translation. Mutagenesis of the RNA binding or PABP interaction motifs decrease LARP4 association with polysomes. Several translation and mRNA metabolism-related proteins use a PAM2 sequence containing a critical invariant phenylalanine to make direct contact with the MLLE domain of PABP, and their competition for the MLLE is thought to regulate mRNA homeostasis. Unlike all similar to 150 previously analyzed PAM2 sequences, LARP4 contains a variant PAM2 (PAM2w) with tryptophan in place of the phenylalanine. Binding and nuclear magnetic resonance (NMR) studies have shown that a peptide representing LARP4 PAM2w interacts with the MLLE of PABP within the affinity range measured for other PAM2 motif peptides. A cocrystal of PABC bound to LARP4 PAM2w shows tryptophan in the pocket in PABC-MLLE otherwise occupied by phenylalanine. We present evidence that LARP4 expression stimulates luciferase reporter activity by promoting mRNA stability, as shown by mRNA decay analysis of luciferase and cellular mRNAs. We propose that LARP4 activity is integrated with other PAM2 protein activities by PABP as part of mRNA homeostasis.
C1 [Yang, Ruiqing; Gaidamakov, Sergei A.; Lee, Joowon; Crawford, Amanda K.; Russo, Amy N.; Maraia, Richard J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
[Martino, Luigi; Conte, Maria R.] Kings Coll London, Randall Div Cell & Mol Biophys, London WC2R 2LS, England.
[Xie, Jingwei; Kozlov, Guennadi; Gehring, Kalle] McGill Univ, Dept Biochem, Montreal, PQ, Canada.
[Maraia, Richard J.] US PHS, Commissioned Corps, Washington, DC USA.
RP Maraia, RJ (reprint author), 31 Ctr Dr,Bldg 31,Room 2A25, Bethesda, MD 20892 USA.
EM maraiar@mail.nih.gov
RI Conte, Maria/C-4102-2008; Martino, Luigi/B-3491-2009; Gehring,
Kalle/I-4403-2013;
OI Conte, Maria/0000-0001-8558-2051; Gehring, Kalle/0000-0001-6500-1184;
Martino, Luigi/0000-0001-5871-3124
FU NICHD, NIH; Canadian Institutes of Health [MOP-14219]
FX This work was supported by Intramural Research Program of the NICHD,
NIH, grants to CHESS and Canadian Institutes of Health grant MOP-14219.
L.M. is a fellow of the European Molecular Biology Organization (EMBO).
M.R.C. acknowledges the Wellcome Trust for the Centre of Biomolecular
Spectroscopy.
NR 72
TC 18
Z9 18
U1 0
U2 6
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD FEB
PY 2011
VL 31
IS 3
BP 542
EP 556
DI 10.1128/MCB.01162-10
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 706AV
UT WOS:000286185900015
PM 21098120
ER
PT J
AU Bley, A
Tifft, C
Kahn, S
Eichler, F
AF Bley, Annette
Tifft, Cynthia
Kahn, Susan
Eichler, Florian
TI Natural history of infantile GM2 gangliosidosis - Survey of 97 patients
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Meeting Abstract
CT 7th Annual World Symposium of the Lysosomal-Disease-Network
CY FEB 16-18, 2011
CL Las Vegas, NV
SP Lysosomal Dis Network
C1 [Bley, Annette; Eichler, Florian] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Tifft, Cynthia] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD FEB
PY 2011
VL 102
IS 2
BP S9
EP S9
DI 10.1016/j.ymgme.2010.11.028
PG 1
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 715CW
UT WOS:000286859000047
ER
PT J
AU Choi, J
Motabar, O
Zheng, W
Marugan, J
Sidransky, E
Goldin, E
AF Choi, Jae
Motabar, Omid
Zheng, Wei
Marugan, Juan
Sidransky, Ellen
Goldin, Ehud
TI The use of saposin C and phosphatidylserine in functional studies of
glucocerebrosidase
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Meeting Abstract
CT 7th Annual World Symposium of the Lysosomal-Disease-Network
CY FEB 16-18, 2011
CL Las Vegas, NV
SP Lysosomal Dis Network
C1 [Choi, Jae; Sidransky, Ellen; Goldin, Ehud] NHGRI, NIH, Bethesda, MD 20892 USA.
[Motabar, Omid; Zheng, Wei; Marugan, Juan] NIH Chem Genom Ctr, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD FEB
PY 2011
VL 102
IS 2
BP S11
EP S11
DI 10.1016/j.ymgme.2010.11.037
PG 1
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 715CW
UT WOS:000286859000055
ER
PT J
AU Gustafson, AM
Velayati, A
Blech-Hermoni, Y
Choi, J
Westbroek, W
Landazabal, C
Goldin, E
Stubblefield, B
Sidransky, E
Tayebi, N
AF Gustafson, Ann Marie
Velayati, Arash
Blech-Hermoni, Yotam
Choi, Jae
Westbroek, Wendy
Landazabal, Claudia
Goldin, Ehud
Stubblefield, Barbara
Sidransky, Ellen
Tayebi, Nahid
TI The evaluation of a loss-of-function GBA variant found in Gaucher
patients with Parkinson disease
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Meeting Abstract
CT 7th Annual World Symposium of the Lysosomal-Disease-Network
CY FEB 16-18, 2011
CL Las Vegas, NV
SP Lysosomal Dis Network
C1 [Gustafson, Ann Marie; Velayati, Arash; Blech-Hermoni, Yotam; Choi, Jae; Westbroek, Wendy; Landazabal, Claudia; Goldin, Ehud; Stubblefield, Barbara; Sidransky, Ellen; Tayebi, Nahid] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD FEB
PY 2011
VL 102
IS 2
BP S19
EP S20
DI 10.1016/j.ymgme.2010.11.066
PG 2
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 715CW
UT WOS:000286859000084
ER
PT J
AU Sidransky, E
Ozlem, GA
Masdeu, J
Kohn, P
Lopez, G
Eisenberg, D
Groden, C
Chaflin, M
Ianni, A
Berman, K
Sidransky, E
AF Sidransky, Ellen
Ozlem, Goker-Alpan
Masdeu, Joseph
Kohn, Phillip
Lopez, Grisel
Eisenberg, Daniel
Groden, Catherine
Chaflin, M.
Ianni, Angela
Berman, Karen
Sidransky, Ellen
TI The neurobiology of glucocerebrosidase associated PD: studies of
dopamine synthesis and rCBF in GBA mutation carriers with and without
parkinsonism
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Meeting Abstract
CT 7th Annual World Symposium of the Lysosomal-Disease-Network
CY FEB 16-18, 2011
CL Las Vegas, NV
SP Lysosomal Dis Network
C1 [Sidransky, Ellen; Ozlem, Goker-Alpan; Masdeu, Joseph; Kohn, Phillip; Lopez, Grisel; Eisenberg, Daniel; Groden, Catherine; Chaflin, M.; Ianni, Angela; Berman, Karen; Sidransky, Ellen] NHGRI, NIH, Bethesda, MD 20892 USA.
RI Eisenberg, Daniel/C-7432-2014; Eisenberg, Daniel/S-4342-2016
NR 0
TC 0
Z9 0
U1 1
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD FEB
PY 2011
VL 102
IS 2
BP S41
EP S42
DI 10.1016/j.ymgme.2010.11.139
PG 2
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 715CW
UT WOS:000286859000156
ER
PT J
AU Velayati, A
Moaven, N
Saranjam, H
Westbroek, W
Goldin, E
Tayebi, N
Stubblefield, B
Sidransky, E
AF Velayati, Arash
Moaven, Nima
Saranjam, Hamid
Westbroek, Wendy
Goldin, Ehud
Tayebi, Nahid
Stubblefield, Barbara
Sidransky, Ellen
TI Exploring the interaction between glucocerebrosidase and alpha-synuclein
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Meeting Abstract
CT 7th Annual World Symposium of the Lysosomal-Disease-Network
CY FEB 16-18, 2011
CL Las Vegas, NV
SP Lysosomal Dis Network
C1 [Velayati, Arash; Moaven, Nima; Saranjam, Hamid; Westbroek, Wendy; Goldin, Ehud; Tayebi, Nahid; Stubblefield, Barbara; Sidransky, Ellen] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 1096-7192
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD FEB
PY 2011
VL 102
IS 2
BP S43
EP S43
DI 10.1016/j.ymgme.2010.11.145
PG 1
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA 715CW
UT WOS:000286859000162
ER
PT J
AU Renaud, S
Loukinov, D
Alberti, L
Vostrov, A
Kwon, YW
Bosman, FT
Lobanenkov, V
Benhattar, J
AF Renaud, Stephanie
Loukinov, Dmitri
Alberti, Loredana
Vostrov, Alexander
Kwon, Yoo-Wook
Bosman, Fred T.
Lobanenkov, Victor
Benhattar, Jean
TI BORIS/CTCFL-mediated transcriptional regulation of the hTERT telomerase
gene in testicular and ovarian tumor cells
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID CATALYTIC SUBUNIT HTERT; REVERSE-TRANSCRIPTASE; DNA METHYLATION;
CANCER-CELLS; CPG ISLAND; PROMOTER REGION; RNA COMPONENT; CTCF-BINDING;
FACTOR BORIS; EXPRESSION
AB Telomerase activity, not detectable in somatic cells but frequently activated during carcinogenesis, confers immortality to tumors. Mechanisms governing expression of the catalytic subunit hTERT, the limiting factor for telomerase activity, still remain unclear. We previously proposed a model in which the binding of the transcription factor CTCF to the two first exons of hTERT results in transcriptional inhibition in normal cells. This inhibition is abrogated, however, by methylation of CTCF binding sites in 85% of tumors. Here, we showed that hTERT was unmethylated in testicular and ovarian tumors and in derivative cell lines. We demonstrated that CTCF and its paralogue, BORIS/CTCFL, were both present in the nucleus of the same cancer cells and bound to the first exon of hTERT in vivo. Moreover, exogenous BORIS expression in normal BORIS-negative cells was sufficient to activate hTERT transcription with an increasing number of cell passages. Thus, expression of BORIS was sufficient to allow hTERT transcription in normal cells and to counteract the inhibitory effect of CTCF in testicular and ovarian tumor cells. These results define an important contribution of BORIS to immortalization during tumorigenesis.
C1 [Renaud, Stephanie; Alberti, Loredana; Bosman, Fred T.; Benhattar, Jean] CHU Vaudois, Inst Pathol, CH-1011 Lausanne, Switzerland.
[Renaud, Stephanie; Loukinov, Dmitri; Vostrov, Alexander; Kwon, Yoo-Wook; Lobanenkov, Victor] NIAID, Immunopathol Lab, NIH, Rockville, MD 20892 USA.
RP Benhattar, J (reprint author), CHU Vaudois, Inst Pathol, CH-1011 Lausanne, Switzerland.
EM jean.benhattar@chuv.ch
OI Lobanenkov, Victor/0000-0001-6665-3635
FU Swiss National Science Foundation [3100AO-101732, 3100A0-113505];
National Institutes of Health, National Institute of Allergy and
Infectious Diseases
FX Swiss National Science Foundation (3100AO-101732 and 3100A0-113505, in
part); Intramural Research Program of the National Institutes of Health,
National Institute of Allergy and Infectious Diseases. Funding for open
access charge: Swiss National Science Foundation.
NR 54
TC 25
Z9 28
U1 0
U2 1
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 FEB
PY 2011
VL 39
IS 3
BP 862
EP 873
DI 10.1093/nar/gkq827
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 720CJ
UT WOS:000287257500014
PM 20876690
ER
PT J
AU Bebenek, K
Pedersen, LC
Kunkel, TA
AF Bebenek, Katarzyna
Pedersen, Lars C.
Kunkel, Thomas A.
TI Replication infidelity via a mismatch with Watson-Crick geometry
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE mutagenesis; replication fidelity; nascent base pair; mispair
ID DNA-POLYMERASE-LAMBDA; ACTIVE-SITE; DEOXYRIBONUCLEIC-ACID; STRAND
MISALIGNMENT; POL LAMBDA; FIDELITY; INTERMEDIATE; ERRORS; METAL; BETA
AB In describing the DNA double helix, Watson and Crick suggested that "spontaneous mutation may be due to a base occasionally occurring in one of its less likely tautomeric forms." Indeed, among many mispairing possibilities, either tautomerization or ionization of bases might allow a DNA polymerase to insert a mismatch with correct Watson-Crick geometry. However, despite substantial progress in understanding the structural basis of error prevention during polymerization, no DNA polymerase has yet been shown to form a natural base-base mismatch with Watson-Crick-like geometry. Here we provide such evidence, in the form of a crystal structure of a human DNA polymerase lambda variant poised to misinsert dGTP opposite a template T. All atoms needed for catalysis are present at the active site and in positions that overlay with those for a correct base pair. The mismatch has Watson-Crick geometry consistent with a tautomeric or ionized base pair, with the pH dependence of misinsertion consistent with the latter. The results support the original idea that a base substitution can originate from a mismatch having Watson-Crick geometry, and they suggest a common catalytic mechanism for inserting a correct and an incorrect nucleotide. A second structure indicates that after misinsertion, the now primer-terminal G.T mismatch is also poised for catalysis but in the wobble conformation seen in other studies, indicating the dynamic nature of the pathway required to create a mismatch in fully duplex DNA.
C1 [Bebenek, Katarzyna; Pedersen, Lars C.; Kunkel, Thomas A.] NIEHS, Struct Biol Lab, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
[Bebenek, Katarzyna; Kunkel, Thomas A.] NIEHS, Mol Genet Lab, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
RP Kunkel, TA (reprint author), NIEHS, Mol Genet Lab, NIH, US Dept HHS, Res Triangle Pk, NC 27709 USA.
EM kunkel@niehs.nih.gov
FU US Department of Energy, Office of Science, Office of Basic Energy
Sciences [W-31-109-Eng-38]; Division of Intramural Research of the
National Institutes of Health, National Institute of Environmental
Health Sciences [Z01 ES065070]
FX We thank Lee Pedersen and William Beard for helpful discussions and
critical reading of the manuscript. Data were collected at Southeast
Regional Collaborative Access Team (SER-CAT) 22-ID (or 22-BM) beamline
at the Advanced Photon Source, Argonne National Laboratory. Supporting
institutions may be found at www.ser-cat.org/members.html. Use of the
Advanced Photon Source was supported by the US Department of Energy,
Office of Science, Office of Basic Energy Sciences, under Contract
W-31-109-Eng-38. This work was supported by the Division of Intramural
Research of the National Institutes of Health, National Institute of
Environmental Health Sciences (Project Z01 ES065070 to T.A.K.).
NR 34
TC 65
Z9 66
U1 1
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 FEB 1
PY 2011
VL 108
IS 5
BP 1862
EP 1867
DI 10.1073/pnas.1012825108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 714JA
UT WOS:000286804700024
PM 21233421
ER
PT J
AU Gapud, EJ
Dorsett, Y
Yin, B
Callen, E
Bredemeyer, A
Mahowald, GK
Omi, KQ
Walker, LM
Bednarski, JJ
McKinnon, PJ
Bassing, CH
Nussenzweig, A
Sleckman, BP
AF Gapud, Eric J.
Dorsett, Yair
Yin, Bu
Callen, Elsa
Bredemeyer, Andrea
Mahowald, Grace K.
Omi, Kazuo Q.
Walker, Laura M.
Bednarski, Jeffrey J.
McKinnon, Peter J.
Bassing, Craig H.
Nussenzweig, Andre
Sleckman, Barry P.
TI Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have
overlapping activities during chromosomal signal joint formation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE DNA repair; lymphoid tumors; lymphocyte development
ID DEPENDENT PROTEIN-KINASE; DOUBLE-STRAND-BREAK; T-CELL DEVELOPMENT; V(D)J
RECOMBINATION; PHOSPHORYLATION SITES; CATALYTIC SUBUNIT; DEFICIENT
LYMPHOCYTES; RAG PROTEINS; RSS ENDS; IN-VIVO
AB Lymphocyte antigen receptor gene assembly occurs through the process of V(D)J recombination, which is initiated when the RAG endonuclease introduces DNA DSBs at two recombining gene segments to form broken DNA coding end pairs and signal end pairs. These paired DNA ends are joined by proteins of the nonhomologous end-joining (NHEJ) pathway of DSB repair to form a coding joint and signal joint, respectively. RAG DSBs are generated in G1-phase developing lymphocytes, where they activate the ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases to orchestrate diverse cellular DNA damage responses including DSB repair. Paradoxically, although Atm and DNA-PKcs both function during coding joint formation, Atm appears to be dispensible for signal joint formation; and although some studies have revealed an activity for DNA-PKcs during signal joint formation, others have not. Here we show that Atm and DNA-PKcs have overlapping catalytic activities that are required for chromosomal signal joint formation and for preventing the aberrant resolution of signal ends as potentially oncogenic chromosomal translocations.
C1 [Gapud, Eric J.; Dorsett, Yair; Bredemeyer, Andrea; Mahowald, Grace K.; Omi, Kazuo Q.; Walker, Laura M.; Sleckman, Barry P.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
[Bednarski, Jeffrey J.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
[Callen, Elsa; Nussenzweig, Andre] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Yin, Bu; Bassing, Craig H.] Univ Penn, Childrens Hosp Philadelphia, Dept Pathol & Lab Med, Abramson Family Canc Res Inst,Sch Med,Ctr Childho, Philadelphia, PA 19104 USA.
[McKinnon, Peter J.] St Jude Childrens Hosp, Dept Genet & Tumor Cell Biol, Memphis, TN 38105 USA.
RP Sleckman, BP (reprint author), Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
EM sleckman@wustl.edu
OI Bredemeyer, Andrea/0000-0003-2970-5998
FU National Institutes of Health [AI074953, AI47829, CA136470, CA125195,
CA096832]; Cancer Research Institute; Washington University; National
Institutes of Health Ruth L. Kirschstein National Research Service Award
[T32 HD007499]; Children's Discovery Institute
FX We thank Dr. Eugene Oltz for critical review of the manuscript and Drs.
Greg Longmore and Yunfeng Feng for pFLRU, pHR'Delta 8.2R, and pCMV-VSVg.
This work is supported by National Institutes of Health Grants AI074953
(to B. P. S.), AI47829 (to B. P. S.), CA136470 (to B. P. S and C. H. B),
CA125195 (to C. H. B.), and CA096832 (to P.J.M.). B.Y. and E.J.G. are
supported by the Cancer Research Institute Pre-doctoral Emphasis Pathway
in Tumor Immunology Training grant awarded to the University of
Pennsylvania (to B.Y.) and Washington University (to E.J.G.). J.J.B. is
supported by a National Institutes of Health Ruth L. Kirschstein
National Research Service Award (T32 HD007499) and a Children's
Discovery Institute Fellows Award. C. H. B. is a Pew Scholar in the
Biomedical Sciences program.
NR 46
TC 29
Z9 29
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 FEB 1
PY 2011
VL 108
IS 5
BP 2022
EP 2027
DI 10.1073/pnas.1013295108
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 714JA
UT WOS:000286804700052
PM 21245316
ER
PT J
AU Chew, EY
Glassman, AR
Beck, RW
Bressler, NM
Fish, GE
Ferris, FL
Kinyoun, JL
AF Chew, Emily Y.
Glassman, Adam R.
Beck, Roy W.
Bressler, Neil M.
Fish, Gary E.
Ferris, Fredrick L.
Kinyoun, James L.
CA Diabet Retinopathy Clinical Res
TI OCULAR SIDE EFFECTS ASSOCIATED WITH PERIBULBAR INJECTIONS OF
TRIAMCINOLONE ACETONIDE FOR DIABETIC MACULAR EDEMA
SO RETINA-THE JOURNAL OF RETINAL AND VITREOUS DISEASES
LA English
DT Article
DE triamcinolone acetonide; diabetic macular edema; peribulbar injections
ID INTRAVITREAL; PHOTOCOAGULATION; INFUSION; TRIAL
AB Purpose: To evaluate long-term effects of anterior and posterior peribulbar injections of triamcinolone acetonide on intraocular pressure (IOP) elevation and cataract development.
Methods: This study reports on IOP and cataract progression through 2 years in 96 eyes with diabetic macular edema randomized to focal/grid photocoagulation, 20 mg triamcinolone acetonide anterior injection, anterior injection followed by laser, 40 mg triamcinolone acetonide posterior injection, or posterior injection followed by laser.
Results: Intraocular pressure increased from baseline by >= 10 mmHg at >= 1 visit through 2 years in 2 eyes (8%) in the laser group, 11 eyes (31%) in the anterior groups, and 6 eyes (17%) in the posterior groups. Among phakic eyes at baseline, 0, 5 (17%), and 1 (3%) in the 3 groups, respectively, underwent cataract surgery before the 2-year visit.
Conclusion: Based on this small randomized trial, it appears that over 2 years, anterior peribulbar triamcinolone acetonide injections are associated with an increased incidence of IOP elevation and an increased risk of cataract development compared with laser or posterior peribulbar injections. The association of posterior injections with IOP elevation is less certain. Although the study involved eyes with diabetic macular edema, the results should be relevant to other conditions treated with peribulbar corticosteroids.
RETINA 31: 284-289, 2011
C1 [Glassman, Adam R.; Beck, Roy W.] Jaeb Ctr Hlth Res, Tampa, FL 33647 USA.
[Chew, Emily Y.; Ferris, Fredrick L.] NIH, NEI, Bethesda, MD 20892 USA.
[Bressler, Neil M.] Wilmer Eye Inst, Baltimore, MD 21287 USA.
[Fish, Gary E.] Texas Retina Associates, Dallas, TX USA.
[Kinyoun, James L.] Univ Washington, Dept Ophthalmol, Seattle, WA 98195 USA.
RP Glassman, AR (reprint author), Jaeb Ctr Hlth Res, 15310 Amberly Dr,Suite 350, Tampa, FL 33647 USA.
EM drcrstat2@jaeb.org
FU NEI NIH HHS [EY14231, EY14229, EY018817, U10 EY014229, U10 EY014231, U10
EY018817, U10 EY023207]
NR 17
TC 10
Z9 13
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0275-004X
J9 RETINA-J RET VIT DIS
JI Retin.-J. Retin. Vitr. Dis.
PD FEB
PY 2011
VL 31
IS 2
BP 284
EP 289
DI 10.1097/IAE.0b013e3181f049a8
PG 6
WC Ophthalmology
SC Ophthalmology
GA 711JG
UT WOS:000286586500011
PM 20948459
ER
PT J
AU Misteli, T
AF Misteli, Tom
TI The Inner Life of the Genome
SO SCIENTIFIC AMERICAN
LA English
DT Article
C1 NCI, Bethesda, MD 20892 USA.
RP Misteli, T (reprint author), NCI, Bethesda, MD 20892 USA.
NR 0
TC 7
Z9 8
U1 1
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0036-8733
J9 SCI AM
JI Sci.Am.
PD FEB
PY 2011
VL 304
IS 2
BP 66
EP 73
DI 10.1038/scientificamerican0211-66
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 707VR
UT WOS:000286318300033
PM 21319544
ER
PT J
AU Harrison, A
Lemey, P
Hurles, M
Moyes, C
Horn, S
Pryor, J
Malani, J
Supuri, M
Masta, A
Teriboriki, B
Toatu, T
Penny, D
Rambaut, A
Shapiro, B
AF Harrison, Abby
Lemey, Philippe
Hurles, Matthew
Moyes, Chris
Horn, Susanne
Pryor, Jan
Malani, Joji
Supuri, Mathias
Masta, Andrew
Teriboriki, Burentau
Toatu, Tebuka
Penny, David
Rambaut, Andrew
Shapiro, Beth
TI Genomic Analysis of Hepatitis B Virus Reveals Antigen State and Genotype
as Sources of Evolutionary Rate Variation
SO VIRUSES-BASEL
LA English
DT Article
DE hepatitis B virus; molecular clock; Bayesian phylogenetics
ID CORE PROMOTER; VERTICAL TRANSMISSION; MOLECULAR EVOLUTION; SEQUENCE
VARIATION; C VIRUS; INFECTION; HISTORY; POPULATIONS; MUTATIONS; HBV
AB Hepatitis B virus (HBV) genomes are small, semi-double-stranded DNA circular genomes that contain alternating overlapping reading frames and replicate through an RNA intermediary phase. This complex biology has presented a challenge to estimating an evolutionary rate for HBV, leading to difficulties resolving the evolutionary and epidemiological history of the virus. Here, we re-examine rates of HBV evolution using a novel data set of 112 within-host, transmission history (pedigree) and among-host genomes isolated over 20 years from the indigenous peoples of the South Pacific, combined with 313 previously published HBV genomes. We employ Bayesian phylogenetic approaches to examine several potential causes and consequences of evolutionary rate variation in HBV. Our results reveal rate variation both between genotypes and across the genome, as well as strikingly slower rates when genomes are sampled in the Hepatitis B e antigen positive state, compared to the e antigen negative state. This Hepatitis B e antigen rate variation was found to be largely attributable to changes during the course of infection in the preCore and Core genes and their regulatory elements.
C1 [Harrison, Abby] Univ Oxford, Nuffield Dept Med, Oxford OX1 3SY, England.
[Harrison, Abby; Pryor, Jan; Malani, Joji] Fiji Sch Med, Suva, Fiji.
[Lemey, Philippe] Katholieke Univ Leuven, Rega Inst, Dept Microbiol & Immunol, B-3000 Louvain, Belgium.
[Hurles, Matthew] Wellcome Trust Sanger Inst, Hinxton CB10 1SA, England.
[Moyes, Chris] Hepatitis Fdn New Zealand, Ohope 3121, Whakatane, New Zealand.
[Horn, Susanne] Max Planck Inst Evolutionary Anthropol, D-04103 Leipzig, Germany.
[Supuri, Mathias; Masta, Andrew] Univ Papua New Guinea, Sch Med & Hlth Sci, Port Moresby, Ncd, Papua N Guinea.
[Teriboriki, Burentau; Toatu, Tebuka] Nawerwere Hosp, Kiribati Minist Hlth, Tawara, Kiribati.
[Penny, David] Massey Univ, Allan Wilson Ctr Mol Ecol & Evolut, Palmerston North 4442, New Zealand.
[Rambaut, Andrew] Inst Evolutionary Biol, Ashworth Labs, Edinburgh EH8 3JT, Midlothian, Scotland.
[Rambaut, Andrew] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Shapiro, Beth] Penn State Univ, Dept Biol, University Pk, PA 16802 USA.
RP Harrison, A (reprint author), Univ Oxford, Nuffield Dept Med, Peter Medawar Bldg Pathogen Res,S Parks Rd, Oxford OX1 3SY, England.
EM a.g.l.harrison@gmail.com; philippe.lemey@rega.kuleuven.be;
meh@sanger.ac.uk; chris.moyes@bopdhb.govt.nz; horn@eva.mpg.de;
pryor.jan@gmail.com; joji.malani@fnu.ac.fj; sapuri@daltron.com.pg;
masta@daltron.com.pg; dhsmhms@yahoo.com; tebtoatu@yahoo.com;
d.penny@massey.ac.nz; a.rambaut@ed.ac.uk; beth.shapiro@psu.edu
RI Penny, David/E-9410-2011;
OI Rambaut, Andrew/0000-0003-4337-3707; Shapiro, Beth/0000-0002-2733-7776
FU NIH [R01 GM083983-01]; Wellcome Trust; New Zealand Health Research
Council
FX Thanks to the following for provision of or assistance with the
collection of HBV samples: Nakapi Teferani, John Vince, and Mark Paul
from the University of Papua New Guinea School of Medicine and Health
Sciences Papua New Guinea (UPNG-SMHS); Peta Siba from the Papua New
Guinea Institute of Medical Research (PNG-IMR); Gilbert Hiawaly from the
Papua New Guinea Ministry of Health (PNG-MOH); Elenoa Areito, Bale
Maleli Naiguilevu from the Fiji School of Medicine (FSM) Fiji; Kabwea
Tiban, Airam Metai, Tekaibeti Tarataake, Artin Ruatu and Rosemary
Tekoaua from the Kiribati Ministry of Health (KMOH) Kiribati; J. Clegg
From the Oxford University England (retired); A. Berlioz-Arthaud from
the Institut Pasteur de Nouvelle Caledonie; W. Schienfenhovel of the Max
Planck-Institute of Behavioural Physiology, Andechs, Germany. This work
was partially supported by NIH R01 GM083983-01, the Wellcome Trust and
the New Zealand Health Research Council.
NR 54
TC 14
Z9 14
U1 0
U2 3
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD FEB
PY 2011
VL 3
IS 2
BP 83
EP 101
DI 10.3390/v3020083
PG 19
WC Virology
SC Virology
GA 726NC
UT WOS:000287728600002
PM 21765983
ER
PT J
AU Higgins, RD
AF Higgins, Rosemary D.
TI Untitled
SO AMERICAN JOURNAL OF PERINATOLOGY
LA English
DT Editorial Material
ID PATENT DUCTUS-ARTERIOSUS; PREMATURE-INFANTS; ORAL IBUPROFEN; CLOSURE
C1 NICHD, Ctr Dev Biol & Perinatal Med, NIH, Bethesda, MD 20892 USA.
RP Higgins, RD (reprint author), NICHD, Ctr Dev Biol & Perinatal Med, NIH, Bethesda, MD 20892 USA.
NR 7
TC 0
Z9 0
U1 1
U2 1
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0735-1631
J9 AM J PERINAT
JI Am. J. Perinatol.
PD FEB
PY 2011
VL 28
IS 2
BP 89
EP 90
DI 10.1055/s-0031-1272553
PG 2
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 716KJ
UT WOS:000286967200001
ER
PT J
AU Jiang, FX
Lin, DC
Horkay, F
Langrana, NA
AF Jiang, Frank Xue
Lin, David C.
Horkay, Ferenc
Langrana, Noshir A.
TI Probing Mechanical Adaptation of Neurite Outgrowth on a Hydrogel
Material Using Atomic Force Microscopy
SO ANNALS OF BIOMEDICAL ENGINEERING
LA English
DT Article
DE Spinal cord neuron; Stiffness; Topography; Mechanical stiffness;
Elasticity map
ID EXTRACELLULAR-MATRIX; ROBUST STRATEGIES; CURVE ANALYSIS; NEURONS; CELLS;
SOFT; NANOMECHANICS; INDENTATION; ADHESION; GROWTH
AB In this study, we describe the design and initial results of probing mechanical adaptation of neurite growth of lightly fixed neurons on a hydrogel substrate by using atomic force microscopy (AFM). It has been shown previously that cells are responsive to the physical conditions of their micro-environment, and that certain cells can adjust their own stiffness as part of the adaptation to the substrate. AFM, a powerful tool to probe micro- and nano-scale structures, has been utilized in assessing topography, morphology, and structural change of neuronal cells. We used AFM with a robust force analysis approach in this study to probe the mechanical properties of both neurites and the substrate at close proximity. We first confirmed the robustness and consistency of the approach specific to soft materials by comparing measurements made on the same reference material using different methods. Subsequently, it was found that the primary spinal cord neurons that were lightly fixed exhibited different stiffnesses between the cell body and neurites. Furthermore, in comparison to the rigidity of the substrate, the stiffness of the neurites was lower, whereas that of the neuronal cell body was higher.
C1 [Jiang, Frank Xue; Langrana, Noshir A.] Rutgers State Univ, Dept Biomed Engn, Piscataway, NJ 08854 USA.
[Langrana, Noshir A.] Rutgers State Univ, Dept Mech & Aerosp Engn, Piscataway, NJ 08854 USA.
[Lin, David C.; Horkay, Ferenc] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Tissue Biophys & Biomimet, Program Pediat Imaging & Tissue Sci, NIH, Bethesda, MD 20892 USA.
RP Langrana, NA (reprint author), Rutgers State Univ, Dept Biomed Engn, Piscataway, NJ 08854 USA.
EM langrana@rutgers.edu
FU NIH; New Jersey Commission on Spinal Cord Research; NIH, NICHD
FX F.X.J. and N.A.L. acknowledge the support from NIH and New Jersey
Commission on Spinal Cord Research, and D. C. L. and F. H. acknowledge
the support of the Intramural Research Program of the NIH, NICHD. We
would like to thank Dr. Emillios K. Dimitriadis (NIBIB, NIH) for his
assistance with the AFM measurements and data analysis, Dr. Bonnie
Firestein's laboratory for assistance with neuronal culture, and Dr.
Michelle L. Previtera for constructive comments.
NR 26
TC 9
Z9 9
U1 2
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0090-6964
J9 ANN BIOMED ENG
JI Ann. Biomed. Eng.
PD FEB
PY 2011
VL 39
IS 2
BP 706
EP 713
DI 10.1007/s10439-010-0194-0
PG 8
WC Engineering, Biomedical
SC Engineering
GA 719OD
UT WOS:000287213300009
PM 21063777
ER
PT J
AU Shukla, S
Fujita, KI
Xiao, Q
Liao, ZY
Garfield, S
Srinivasula, SM
AF Shukla, Sudhanshu
Fujita, Ken-ichi
Xiao, Qi
Liao, Zhiyong
Garfield, Susan
Srinivasula, Srinivasa M.
TI A shear stress responsive gene product PP1201 protects against
Fas-mediated apoptosis by reducing Fas expression on the cell surface
SO APOPTOSIS
LA English
DT Article
DE Apoptosis; Fas; PP1201; Golgi; Trafficking; Cystic medial degeneration
ID HUMAN ENDOTHELIAL-CELLS; NITRIC-OXIDE SYNTHASE; SMOOTH-MUSCLE-CELLS;
FAS/FAS-L PATHWAY; LIFEGUARD/NEURONAL MEMBRANE-PROTEIN-35; DEATH;
TRAFFICKING; MECHANISM; RECEPTOR; SIGNALS
AB Cells that form vascular system employ different mechanisms to offset deleterious consequences of exposure to cytokines and cells present in blood. Vascular homeostasis is sustained in part by genes, whose expression increases in response to hemodynamic forces in these cells. PP1201 (also known as RECS1) is one such gene whose expression level increases in response to laminar shear stress. Aged mice deficient in PP1201 are prone to develop cystic medial degeneration (CMD), a form of aortic aneurism manifested with loss of smooth muscle cells and accumulation of basophilic substances. Here we found that higher levels of PP1201 can protect against Fas ligand (FasL)-induced apoptosis. PP1201 interacted with the Fas receptor (CD95/Apo1) and colocalized with it in the Golgi compartment. Unlike its homolog lifeguard (LFG), PP1201 overexpression in several types of cells including primary human aortic smooth muscle cells (AoSMC) decreased the expression of Fas on the plasma membrane without changing the total Fas levels. Only high but not constitutive level of PP1201 controls Fas signaling. Our data suggest that PP1201 functions as an anti-apoptotic protein and its increased expression in vascular cells can contribute to homeostasis by reducing Fas trafficking to the cell membrane.
C1 [Shukla, Sudhanshu; Fujita, Ken-ichi; Xiao, Qi; Liao, Zhiyong; Srinivasula, Srinivasa M.] NCI, Lab Immune Cell Biol, NIH, Bethesda, MD 20892 USA.
[Garfield, Susan] NCI, Confocal Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
RP Srinivasula, SM (reprint author), 9000 Rockville Pike,Bldg 37,Room 3016A, Bethesda, MD 20892 USA.
EM srinivsr@mail.nih.gov
OI Shukla, Sudhanshu/0000-0002-7091-7215
FU National Institutes of Health, Center for Cancer research, National
Cancer Institute
FX This work was supported by the intramural Research Program of the
National Institutes of Health, Center for Cancer research, National
Cancer Institute. We thank Richard Siegel for CFP-Fas plasmid, Stanley
Lipkowitz for GST-TRAIL and Hiroshi Nojima for human PP1201 cDNA
containing plasmids.
NR 38
TC 8
Z9 9
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1360-8185
J9 APOPTOSIS
JI Apoptosis
PD FEB
PY 2011
VL 16
IS 2
BP 162
EP 173
DI 10.1007/s10495-010-0556-y
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 718RE
UT WOS:000287142800006
PM 21107705
ER
PT J
AU Kuntsche, E
Kuntsche, S
Knibbe, R
Simons-Morton, B
Farhat, T
Hublet, A
Bendtsen, P
Godeau, E
Demetrovics, Z
AF Kuntsche, Emmanuel
Kuntsche, Sandra
Knibbe, Ronald
Simons-Morton, Bruce
Farhat, Tilda
Hublet, Anne
Bendtsen, Pernille
Godeau, Emmanuelle
Demetrovics, Zsolt
TI Cultural and Gender Convergence in Adolescent Drunkenness Evidence From
23 European and North American Countries
SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE
LA English
DT Article
ID DRINKING; BEHAVIOR; TRENDS
AB Objective: To investigate time-trend changes in the frequency of drunkenness among European and North American adolescents.
Design: Cross-sectional surveys in the 1997/1998 and 2005/2006 Health Behaviour in School-Aged Children Study (HBSC).
Setting: High schools in 23 countries.
Participants: A sample of 77 586 adolescents aged 15 years was analyzed by means of hierarchical linear modeling.
Main Outcome Measure: The frequency of drunkenness.
Results: We observed a significant increase of about 40% in the mean frequency of drunkenness in all 7 participating Eastern European countries. This increase was evident among both genders, but most consistently among girls. Meanwhile, it declined in 13 of 16 Western countries, about 25% on average. Declines in Western countries were particularly notable among boys and in North America, Scandinavia, the United Kingdom, and Ireland. Despite this gender convergence, with few exceptions (Greenland, Norway, United Kingdom) boys continued to have a higher frequency of drunkenness in 2005/2006 than girls.
Conclusions: The confirmed cultural convergence implies that adoption and implementation of evidence-based measures to mitigate the frequency of adolescent drunkenness such as tax increases and restricting alcohol access and advertisement should get the same priority in Eastern European countries as in Western countries. Policy measures that might facilitate decreases in drunkenness such as server training and the promotion of alcohol-free leisure-time activities should be reinforced in Western countries. The gender convergence implies that prevention policy should be less exclusively focused on male adolescents.
C1 [Kuntsche, Emmanuel; Kuntsche, Sandra] Addict Info Switzerland, Res Inst, CH-1001 Lausanne, Switzerland.
[Kuntsche, Emmanuel] Univ Lausanne, Inst Social & Prevent Med, Res Grp Adolescent Hlth, Lausanne, Switzerland.
[Kuntsche, Emmanuel] Radboud Univ Nijmegen, Inst Behav Sci, NL-6525 ED Nijmegen, Netherlands.
[Knibbe, Ronald] Univ Maastricht, Dept Hlth Promot, Maastricht, Netherlands.
[Simons-Morton, Bruce; Farhat, Tilda] NICHHD, Prevent Res Branch, NIH, Bethesda, MD 20892 USA.
[Hublet, Anne] Univ Ghent, Dept Publ Hlth, B-9000 Ghent, Belgium.
[Bendtsen, Pernille] Univ So Denmark, Natl Inst Publ Hlth, Copenhagen, Denmark.
[Godeau, Emmanuelle] Univ Toulouse 3, Unite Mixte Rech, Inst Natl Sante, F-31062 Toulouse, France.
[Godeau, Emmanuelle] Univ Toulouse 3, Rech Med Unit 558, F-31062 Toulouse, France.
[Godeau, Emmanuelle] Serv Med Rectorat, Toulouse, France.
[Demetrovics, Zsolt] Eotvos Lorand Univ, Inst Grp Addict Res, Budapest, Hungary.
[Demetrovics, Zsolt] Natl Inst Drug Prevent, Budapest, Hungary.
RP Kuntsche, E (reprint author), Addict Info Switzerland, Res Inst, POB 870, CH-1001 Lausanne, Switzerland.
EM ekuntsche@addiction-info.ch
OI Simons-Morton, Bruce/0000-0003-1099-6617
FU Swiss Federal Office of Public Health [09.000925/204.0001/-573]; Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health [N01-HD-53401]
FX Data collection was funded by each of the participating countries and
regions separately. Elaboration of the manuscript was mainly funded by
grant 09.000925/204.0001/-573 from the Swiss Federal Office of Public
Health and in part by grant N01-HD-53401 from the intramural research
program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development, National Institutes of Health. Additional
Information: Data from the following countries were included in the
present study (principal investigators are listed in parentheses):
Austria (Wolfgang Dur), Belgium (Flemish-speaking: Lea Maes [1997/ 1998]
and Carine Vereecken [2005/2006]; French-speaking: Danielle Piette),
Canada (William Boyce), Czech Republic (Ladislav Csemy), Denmark (Bjorn
Hostein [1997/1998] and Pernille Due [2005/2006]), Estonia (Mai Maser
[1997/1998] and Katrin Aasvee [2005/2006]), Finland (Jorma Tynj l),
France (Emmanuelle Godeau), Germany (Klaus Hurrelmann [1997/1998] and
Ulrike Ravens-Sieberer [2005/2006]), Greece (Anna Kokkevi), Hungary
(Anna Aszmann [1997/1998] and Agnes Nemeth [2005/2006]), Ireland
(Saoirse Nic Gabhainn), Latvia (Ieva Ranka [1997/1998] and Iveta Pudule
[2005/2006]), Lithuania (Apolinaras Zaborskis), Norway (Oddrun Samdal),
Poland (Barbara Woynarowska [1997/1998] and Joanna Mazur [2005/2006]),
Portugal (Margarida Gaspar De Matos), Russian Federation (Alexander
Komkov), Sweden (Ulla Marklund [1997/1998] and Lilly Eriksson
[2005/2006]), Switzerland (Beatrice Janin Jacquat [1997/1998] and
Emmanuel Kuntsche [2005/2006]), Ukraine (Olga Balakireva), United
Kingdom (England: Antony Morgan; Scotland: Candace Currie; Wales: Chris
Roberts), and United States (Mary Overpeck [1997/1998] and Ronald
Iannotti [2005/2006]).
NR 29
TC 54
Z9 54
U1 1
U2 14
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 1072-4710
J9 ARCH PEDIAT ADOL MED
JI Arch. Pediatr. Adolesc. Med.
PD FEB
PY 2011
VL 165
IS 2
BP 152
EP 158
DI 10.1001/archpediatrics.2010.191
PG 7
WC Pediatrics
SC Pediatrics
GA 717KH
UT WOS:000287042100009
PM 20921343
ER
PT J
AU Greinix, HT
Loddenkemper, C
Pavletic, SZ
Holler, E
Socie, G
Lawitschka, A
Halter, J
Wolff, D
AF Greinix, Hildegard T.
Loddenkemper, Christoph
Pavletic, Steven Z.
Holler, Ernst
Socie, Gerard
Lawitschka, Anita
Halter, Joerg
Wolff, Daniel
TI Diagnosis and Staging of Chronic Graft-versus-Host Disease in the
Clinical Practice
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Article
DE Chronic GVHD; Staging; Severity scoring
ID CONSENSUS DEVELOPMENT PROJECT; STEM-CELL TRANSPLANTATION; WORKING
GROUP-REPORT; BONE-MARROW-TRANSPLANTATION; CHRONIC GVHD; BRONCHIOLITIS
OBLITERANS; CRITERIA; TRIALS; MULTICENTER; SURVIVAL
AB Based on expert opinion and retrospective data the National Institutes of Health (NIH) Consensus Development Project proposed criteria for diagnosis and staging of both overall severity as well as organ severity of chronic graft-versus-host disease (cGVHD) for use in clinical trials. In 2008, representatives of German and Austrian allogeneic hematopoietic stem cell transplant (HSCT) centers established a study group on cGVHD during the annual meeting of the German Working Group on Bone Marrow and Blood Stem Cell Transplantation (DAG-KBT) to intensify a dialog among HSCT physicians, pathologists, and medical consultants focusing on the usefulness of the NIH consensus criteria for patient care in clinical practice and to promote collaborations between HSCT centers as well as different medical specialities involved in HSCT. We first conducted a survey of current practices of diagnosis, staging, and overall grading of cGVHD in daily clinical routine by sending an electronic questionnaire to the heads of the HSCT centers. During 3 meetings in 2009, more representatives of allogeneic HSCT centers were included into the discussion process, resulting in 81% participation representing 88% of all allogeneic HSCT activities in Germany, Austria, and Switzerland. During the third consensus meeting held in Regensburg, Germany, from November 6 to November 7, 2009, important agreements were achieved among participant having a strong impact on care of patients with cGVHD. Areas of disagreement such as distinction between classical NIH cGVHD and overlap syndrome or assignment of liver GVHD after day 100 to acute or chronic category will be further assessed in prospective observational studies among participants in the near future. Bioi Blood Marrow Transplant 17: 167-175 (2011) (C) 2011 American Society for Blood and Marrow Transplantation
C1 [Greinix, Hildegard T.] Med Univ Vienna, Dept Internal Med 1, Vienna, Austria.
[Loddenkemper, Christoph] Charite, Inst Pathol, Res Ctr ImmunoSci RCIS, D-13353 Berlin, Germany.
[Loddenkemper, Christoph] Tech Univ Muenchen, Inst Pathol, Munich, Germany.
[Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Holler, Ernst; Wolff, Daniel] Univ Regensburg, Dept Hematol & Oncol, D-8400 Regensburg, Germany.
[Socie, Gerard] Hop St Louis, Serv Hematol Greffe, Paris, France.
[Socie, Gerard] Hop St Louis, INSERM, Paris, France.
[Lawitschka, Anita] St Anna Childrens Hosp, Dept Stem Cell Transplantat, A-1090 Vienna, Austria.
[Halter, Joerg] Univ Basel Hosp, Dept Hematol, CH-4031 Basel, Switzerland.
RP Greinix, HT (reprint author), Med Univ Wien, Innere Med Klin 1, Knochenmarktransplanta Waehringer Guertel 18-20, A-1090 Vienna, Austria.
EM hildegard.greinix@meduniwien.ac.at
RI Halter, Joerg/C-9487-2012
FU Jose Carreras Foundation; European Commission [037703]
FX The authors are grateful to Stephanie Lee, Mohamad Mohty, and Sharon
Elad for their contributions and would like to thank all participants of
the consensus meetings for their valuable input. The conference in
Regensburg was supported by the Jose Carreras Foundation project
"Competence centre Regensburg." The authors are grateful to the German
Registry of Stem Cell Transplantation (DRST), the Austrian Registry of
Stem Cell Transplantation (ASCT), and die Swiss National Stem Cell
Transplant Registry for providing the information on annual HSCT numbers
in these countries.; H.T. was supported by European Commission Grant
037703 STEMDIAGNOSTICS.
NR 35
TC 25
Z9 26
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
BP 167
EP 175
DI 10.1016/j.bbmt.2010.07.017
PG 9
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JW
UT WOS:000287350400002
PM 20691801
ER
PT J
AU Garantziotis, S
AF Garantziotis, S.
TI Modulation of plasma complement by the initial dose of
epirubicin/docetaxel therapy in breast cancer and its predictive value
SO BRITISH JOURNAL OF CANCER
LA English
DT Letter
ID ALPHA-TRYPSIN INHIBITOR; PROTEINS
C1 [Garantziotis, S.] Natl Inst Environm Hlth Sci, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
[Garantziotis, S.] Univ N Carolina, Dept Med, Chapel Hill, NC USA.
RP Garantziotis, S (reprint author), Natl Inst Environm Hlth Sci, Lab Resp Biol, POB 12233,MD-CU01,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM garantziotis@niehs.nih.gov
RI Garantziotis, Stavros/A-6903-2009
OI Garantziotis, Stavros/0000-0003-4007-375X
NR 8
TC 1
Z9 1
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
J9 BRIT J CANCER
JI Br. J. Cancer
PD FEB 1
PY 2011
VL 104
IS 3
BP 542
EP 542
DI 10.1038/sj.bjc.6606068
PG 1
WC Oncology
SC Oncology
GA 722IY
UT WOS:000287427100025
PM 21224852
ER
PT J
AU Schiffman, M
AF Schiffman, Mark
TI The Need for Forward-Looking Decision Analyses to Guide Cervical Cancer
Prevention
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Editorial Material
ID HUMAN-PAPILLOMAVIRUS; WOMEN; COLPOSCOPY; RISK
C1 NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
RP Schiffman, M (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 7012, Rockville, MD 20852 USA.
EM schiffmm@mail.nih.gov
NR 6
TC 1
Z9 1
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD FEB
PY 2011
VL 20
IS 2
BP 219
EP 220
DI 10.1158/1055-9965.EPI-10-1130
PG 2
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 717CU
UT WOS:000287021400001
PM 21300615
ER
PT J
AU Zhou, J
Enewold, L
Zahm, SH
Devesa, SS
Anderson, WF
Potter, JF
McGlynn, KA
Zhu, KM
AF Zhou, Jing
Enewold, Lindsey
Zahm, Shelia H.
Devesa, Susan S.
Anderson, William F.
Potter, John F.
McGlynn, Katherine A.
Zhu, Kangmin
TI Melanoma Incidence Rates among Whites in the U.S. Military
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID NONMELANOMA SKIN-CANCER; VITAMIN-D; CUTANEOUS MELANOMA;
MALIGNANT-MELANOMA; SUN PROTECTION; UNITED-STATES; TANNING BEDS;
RISK-FACTORS; EPIDEMIOLOGY; PREVENTION
AB Background: The U. S. Military and general populations may differ in the exposure to sunlight and other risk factors for melanoma and therefore the incidence rates of melanoma may be different in these two populations. However, few studies have compared melanoma incidence rates and trends over time between the military and the general population.
Methods: Melanoma incidence rates from 1990 to 2004 among white active-duty military personnel and the general U. S. population were compared using data from the Department of Defense Automated Central Tumor Registry and the National Cancer Institute Surveillance, Epidemiology, and End Results program.
Results: Age-adjusted melanoma rates overall were significantly lower in the military than in the general population; the incidence rate ratio was 0.75 for men and 0.56 for women. Age-specific rates, however, were significantly lower among individuals younger than 45 years, but significantly higher among those 45 years or older (P < 0.05). Melanoma incidence increased from 1990-1994 to 2000-2004 in both populations, with the most rapid increase (40%) among younger men in the military. Melanoma incidence rates also varied by branch of military service; rates were highest in the air force.
Conclusion: These results suggest that melanoma incidence rate patterns differ between the military and the general population.
Impact: Further studies of risk factors for melanoma in the military are needed to explain these findings. Cancer Epidemiol Biomarkers Prev; 20(2); 318-23. (C)2010 AACR.
C1 [Zhou, Jing; Enewold, Lindsey; Potter, John F.; Zhu, Kangmin] Walter Reed Army Med Ctr, US Mil Canc Inst, Washington, DC 20307 USA.
[Zahm, Shelia H.; Devesa, Susan S.; Anderson, William F.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Potter, John F.; Zhu, Kangmin] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
RP Zhu, KM (reprint author), Walter Reed Army Med Ctr, US Mil Canc Inst, Bldg 1,Suite A-109,6900 Georgia Ave NW, Washington, DC 20307 USA.
EM Kangmin.zhu@amedd.army.mil
RI Zahm, Shelia/B-5025-2015
FU United States Military Cancer Institute via the Uniformed Services
University of the Health Sciences under the auspices of the Henry M.
Jackson Foundation for the Advancement of Military Medicine; Division of
Cancer Epidemiology and Genetics (DCEG), National Cancer Institute
FX This research was supported by the United States Military Cancer
Institute via the Uniformed Services University of the Health Sciences
under the auspices of the Henry M. Jackson Foundation for the
Advancement of Military Medicine and by the Division of Cancer
Epidemiology and Genetics (DCEG), National Cancer Institute.
NR 44
TC 4
Z9 5
U1 0
U2 8
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD FEB
PY 2011
VL 20
IS 2
BP 318
EP 323
DI 10.1158/1055-9965.EPI-10-0869
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 717CU
UT WOS:000287021400014
PM 21148122
ER
PT J
AU Douglas, JB
Silverman, DT
Weinstein, SJ
Graubard, BI
Pollak, MN
Tao, YZ
Virtamo, J
Albanes, D
Stolzenberg-Solomon, RZ
AF Douglas, Jason B.
Silverman, Debra T.
Weinstein, Stephanie J.
Graubard, Barry I.
Pollak, Michael N.
Tao, Yuzhen
Virtamo, Jarmo
Albanes, Demetrius
Stolzenberg-Solomon, Rachael Z.
TI Serum C-Reactive Protein and Risk of Pancreatic Cancer in Two Nested,
Case-Control Studies
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID DUCTAL ADENOCARCINOMA; COLORECTAL-CANCER; INFLAMMATORY RESPONSE;
SCREENING TRIAL; MALE SMOKERS; VITAMIN-D; REPRODUCIBILITY;
QUESTIONNAIRE; PROSTATE; PLASMA
AB Background: Many epidemiologic studies have examined the association between C-reactive protein (CRP) and risk of cancer with inconsistent results.
Methods: We conducted two nested, case-control studies in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) and Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) to test whether prediagnostic circulating CRP concentrations were associated with pancreatic adenocarcinoma. Between 1985 and 2004, 311 cases occurred in ATBC and between 1994 and 2006, 182 cases occurred in PLCO. Controls (n = 510 in ATBC, n = 374 in PLCO) were alive at the time the case was diagnosed and were matched by age, date of blood draw, sex, and race. We used conditional logistic regression adjusted for smoking to calculate OR and 95% CI for pancreatic cancer.
Results: CRP concentrations (ng/mL) tended to be inversely or not associated with pancreatic cancer risk in ATBC, PLCO, and combined analyses [per standardized quintile increase in CRP, continuous OR = 0.94 (95% CI, 0.89-0.99), OR = 0.99 (95% CI, 0.95-1.04), OR = 0.98 (95% CI, 0.95-1.01), respectively]. In combined analyses, we observed a significant interaction (P(interaction) = 0.02) such that inverse associations were suggestive in younger (OR = 0.95; 95% CI, 0.90-1.01), but not older, participants.
Conclusion: Our results do not support the hypothesis that higher CRP concentrations are associated with incident pancreatic cancer.
Impact: Our results highlight the importance of investigating more specific biomarkers for inflammation that may reflect the biological mechanisms underlying pancreatic cancer in prospective cohort studies. Cancer Epidemiol Biomarkers Prev; 20(2); 359-69. (C)2010 AACR.
C1 [Douglas, Jason B.; Weinstein, Stephanie J.; Albanes, Demetrius; Stolzenberg-Solomon, Rachael Z.] NCI, Nutr Epidemiol Branch, Dept Hlth & Human Serv, Rockville, MD USA.
[Silverman, Debra T.] NCI, Occupat Epidemiol Branch, Dept Hlth & Human Serv, Rockville, MD USA.
[Graubard, Barry I.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Rockville, MD USA.
[Pollak, Michael N.; Tao, Yuzhen] McGill Univ, Jewish Gen Hosp, Cancer Prevent Program, Montreal, PQ H3T 1E2, Canada.
[Virtamo, Jarmo] Natl Inst Hlth & Welfare, Dept Chron Dis Prevent, Helsinki, Finland.
RP Stolzenberg-Solomon, RZ (reprint author), 6120 Execut Blvd,Suite 320, Rockville, MD 20852 USA.
EM rs221z@nih.gov
RI Pollak, Michael/G-9094-2011; Albanes, Demetrius/B-9749-2015
OI Pollak, Michael/0000-0003-3047-0604;
FU National Institutes of Health, Division of Cancer Epidemiology and
Genetics; National Cancer Institute, Department of Health and Human
Services
FX This study was supported by the Intramural Research Program of the
National Institutes of Health, Division of Cancer Epidemiology and
Genetics, National Cancer Institute, Department of Health and Human
Services.
NR 31
TC 10
Z9 11
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD FEB
PY 2011
VL 20
IS 2
BP 359
EP 369
DI 10.1158/1055-9965.EPI-10-1024
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 717CU
UT WOS:000287021400018
PM 21173171
ER
PT J
AU Liu, AM
Yang, JL
Gonzalez, FJ
Cheng, GQ
Dai, RK
AF Liu, Aiming
Yang, Julin
Gonzalez, Frank J.
Cheng, Gary Q.
Dai, Renke
TI Biphasic Regulation of Intracellular Calcium by Gemfibrozil Contributes
to Inhibiting L6 Myoblast Differentiation: Implications for Clinical
Myotoxicity
SO CHEMICAL RESEARCH IN TOXICOLOGY
LA English
DT Article
ID LIPID-LOWERING DRUGS; SKELETAL-MUSCLE; MITOCHONDRIAL-FUNCTION;
GLUCURONIDE INHIBIT; HEPATIC-UPTAKE; STATINS; RAT; RHABDOMYOLYSIS;
CERIVASTATIN; APOPTOSIS
AB Gemfibrozil is the most myotoxic fibrate drug commonly used for dyslipidemia, but the mechanism is poorly understood. The current study revealed that gemfibrozil inhibits myoblast differentiation through the regulation of intracellular calcium ([Ca(2+)]i) as revealed in L6 myoblasts by use of laser scan confocal microscopy and flow cytometry using Fluo-4 AM as a probe. Gemfibrozil at 20-400 mu M, could regulate [Ca(2+)]i in L6 cells in a biphasic manner, and sustained reduction was observed when the concentration reached 200 mu M. Inhibition of L6 differentiation by gemfibrozil was concentration-dependent with maximal effect noted between 200 and 400 mu M, as indicated by creatine kinase activities and the differentiation index, respectively. In differentiating L6 myoblasts, gemfibrozil at concentrations below 400 mu M led to no significant signs of apoptosis or cytotoxicity, whereas differentiation, inhibited by 200 mu M gemfibrozil, was only partially recovered. A good correlation was noted between gemfibrozil concentrations that regulate [Ca(2+)]i and inhibit L6 myoblasts differentiation, and both are within the range of total serum concentrations found in the clinic. These data suggest a potential pharmacodynamic effect of gemfibrozil on myogenesis as a warning sign, in addition to the complex pharmacokinetic interactions. It is also noteworthy that mobilization of [Ca(2+)]i by gemfibrozil may trigger complex biological responses besides myocyte differentiation. Information revealed in this study explores the mechanism of gemfibrozil-induced myotoxicity through the regulation of intracellular calcium.
C1 [Dai, Renke] S China Univ Technol, Sch Biosci & Bioengn, Guangzhou 510641, Guangdong, Peoples R China.
[Liu, Aiming] Ningbo Univ, Sch Med, Ningbo 315211, Zhejiang, Peoples R China.
[Yang, Julin] Ningbo Coll Hlth Sci, Ningbo 315100, Zhejiang, Peoples R China.
[Gonzalez, Frank J.] NCI, NIH, Bethesda, MD 20892 USA.
[Cheng, Gary Q.] S China Ctr Innovat Pharmaceut, Guangzhou 510006, Guangdong, Peoples R China.
RP Dai, RK (reprint author), S China Univ Technol, Sch Biosci & Bioengn, Guangzhou 510641, Guangdong, Peoples R China.
EM renke_dai@yahoo.com
FU Zhejiang Provincial Education Department [Y200906207]; Ningbo Natural
Science Foundation [2010A610069]; Chinese government [2008AA02Z314,
2009DFA31530, 2009ZX09301-015]
FX This study was supported by Scientific Research Fund of Zhejiang
Provincial Education Department [grant Y200906207], Ningbo Natural
Science Foundation [grant 2010A610069], and Chinese government grants
[2008AA02Z314, 2009DFA31530 and 2009ZX09301-015].
NR 39
TC 4
Z9 6
U1 2
U2 7
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 FEB
PY 2011
VL 24
IS 2
BP 229
EP 237
DI 10.1021/tx100312h
PG 9
WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology
SC Pharmacology & Pharmacy; Chemistry; Toxicology
GA 721XP
UT WOS:000287391400011
PM 21175127
ER
PT J
AU Huang, MC
Greig, NH
Luo, WN
Tweedie, D
Schwartz, JB
Longo, DL
Ferrucci, L
Ershler, WB
Goetzl, EJ
AF Huang, Mei-Chuan
Greig, Nigel H.
Luo, Weinning
Tweedie, David
Schwartz, Janice B.
Longo, Dan L.
Ferrucci, Luigi
Ershler, William B.
Goetzl, Edward J.
TI Preferential enhancement of older human T cell cytokine generation,
chemotaxis, proliferation and survival by lenalidomide
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE Human; T lymphocytes; Cytokines; Proliferation; Apoptosis; Chemotaxis
ID ALPHA INHIBITORY-ACTIVITY; IMMUNOMODULATORY DRUGS; TNF-ALPHA; DENDRITIC
CELLS; AGED HUMANS; THALIDOMIDE; CD4(+); NAIVE; MEMORY; INTERLEUKIN-2
AB Lenalidomide, an analog of thalidomide, modified responses of stimulated T cells from healthy young (ages 21-40 years) and (>= old age 65 years) subjects. At 0.03 mu M to 1 mu M, lenalidomide enhanced generation of IL-2 and IFN-gamma by T cell receptor-stimulated T cells of young subjects up to respective maximum increases of 17-fold and three-fold, but at 0.3 mu M and 1 mu M suppressed IL-17 generation. The same concentrations of lenalidomide enhanced IL-2 and IFN-gamma generation by stimulated T cells of old subjects more, with greater respective maximal increases of up to 120-fold and six-fold, without suppressing IL-17 generation. Lenalidomide enhanced proliferation and suppressed apoptosis of stimulated T cells from old subjects, by IL-2-dependent mechanisms, and restored diminished T cell chemotactic responses to CCL21 and sphingosine 1-phosphate. The reversal of T cell abnormalities of immunosenescence by low concentrations of lenalidomide suggest a potential for improvement of immunity in the elderly. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Goetzl, Edward J.] Univ Calif San Francisco, Med Ctr, Dept Med, San Francisco, CA 94143 USA.
[Greig, Nigel H.; Luo, Weinning; Tweedie, David; Longo, Dan L.; Ferrucci, Luigi; Ershler, William B.] NIA, NIH, Baltimore, MD 21224 USA.
[Goetzl, Edward J.] Univ Calif San Francisco, Dept Microbiol Immunol, San Francisco, CA 94143 USA.
RP Goetzl, EJ (reprint author), Univ Calif San Francisco, Med Ctr, Dept Med, Room UB8B UC,Box 0711,533 Parnassus & 4th Ave, San Francisco, CA 94143 USA.
EM edward.goetzl@ucsf.edu
FU Kenneth Rainin Foundation; National Institute on Aging
FX This research was supported by a grant from the Kenneth Rainin
Foundation and by the Intramural Research Program of the National
Institute on Aging. The authors are grateful to Judith H. Goetzl for
preparation of graphics and for textual editing. The authors declare no
conflicts of interest. Authors' contributions: N.H.G., D.L.L., J.B.S.
and E.J.G. designed research; L.F., W.B.E.,. J.B.S. and E.J.G.
identified and evaluated subjects; D.T., W.L. and N.H.G. synthesized and
analyzed compounds: M.-C. H. and E.J.G. performed research and analyzed
data; E.J.G., L.F. and J.B.S. wrote the paper.
NR 49
TC 8
Z9 9
U1 0
U2 2
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD FEB
PY 2011
VL 138
IS 2
BP 201
EP 211
DI 10.1016/j.clim.2010.11.002
PG 11
WC Immunology
SC Immunology
GA 719QP
UT WOS:000287223800009
PM 21130040
ER
PT J
AU Schecter, A
Smith, S
Colacino, J
Malik, N
Opel, M
Paepke, O
Birnbaum, L
AF Schecter, Arnold
Smith, Sarah
Colacino, Justin
Malik, Noor
Opel, Matthias
Paepke, Olaf
Birnbaum, Linda
TI Contamination of U.S. Butter with Polybrominated Diphenyl Ethers from
Wrapping Paper
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE butter; dietary intake; food; PBDEs; United States
ID DIETARY-INTAKE; HUMAN EXPOSURE; UNITED-STATES; MARKET BASKET;
HOUSE-DUST; POLYCHLORINATED DIOXINS; AGENT-ORANGE; INDOOR DUST; PBDE
LEVELS; FOOD
AB OBJECTIVES: Our aim was to report the first known incidence of U.S. butter contamination with extremely high levels of polybrominated diphenyl ethers (PBDEs).
METHODS: Ten butter samples were individually analyzed for PBDEs. One of the samples and its paper wrapper contained very high levels of higher-brominated PBDEs. Dietary estimates were calculated using the 2007 U.S. Department of Agriculture Loss-Adjusted Food Availability data, excluding the elevated sample.
RESULTS: The highly contaminated butter sample had a total upper bound PBDE level of 42,252 pg/g wet weight (ww). Levels of brominated diphenyl ether (BDE)-206, -207, and -209 were 2,000, 2,290, and 37,600 pg/g ww, respectively. Its wrapping paper contained a total upper-bound PBDE concentration of 804,751 pg/g ww, with levels of BDE-206, -207, and -209 of 51,000, 11,700, and 614,000 pg/g, respectively. Total PBDE levels in the remaining nine butter samples ranged from 180 to 1,212 pg/g, with geometric mean of 483 and median of 284 pg/g. Excluding the outlier, total PBDE daily intake from all food was 22,764 pg/day, lower than some previous U.S. dietary intake estimates.
CONCLUSION: Higher-brominated PBDE congeners were likely transferred from contaminated wrapping paper to butter. A larger representative survey may help determine how frequently PBDE contamination occurs. Sampling at various stages in food production may identify contamination sources and reduce risk.
C1 [Schecter, Arnold; Smith, Sarah; Malik, Noor] Univ Texas Sch Publ Hlth Dallas, Dallas, TX 75390 USA.
[Colacino, Justin] Univ Michigan Sch Publ Hlth, Ann Arbor, MI USA.
[Opel, Matthias; Paepke, Olaf] Eurofins GfA GmbH, Hamburg, Germany.
[Birnbaum, Linda] NCI, Natl Inst Environm Sci, NIH, Dept Hlth & Human Resources, Res Triangle Pk, NC USA.
RP Schecter, A (reprint author), Univ Texas Sch Publ Hlth Dallas, 5323 Harry Hines,V8-112, Dallas, TX 75390 USA.
EM arnold.schecter@utsouthwestern.edu
FU Gustavus and Louise Pfeiffer Research Foundation
FX The authors acknowledge the Gustavus and Louise Pfeiffer Research
Foundation for their generous grant, which funded this research.
NR 38
TC 14
Z9 14
U1 1
U2 8
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD FEB
PY 2011
VL 119
IS 2
BP 151
EP 154
DI 10.1289/ehp.1002604
PG 4
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 714IP
UT WOS:000286803400014
PM 21138809
ER
PT J
AU Purdue, MP
Bakke, B
Stewart, P
De Roos, AJ
Schenk, M
Lynch, CF
Bernstein, L
Morton, LM
Cerhan, JR
Severson, RK
Cozen, W
Davis, S
Rothman, N
Hartge, P
Colt, JS
AF Purdue, Mark P.
Bakke, Berit
Stewart, Patricia
De Roos, Anneclaire J.
Schenk, Maryjean
Lynch, Charles F.
Bernstein, Leslie
Morton, Lindsay M.
Cerhan, James R.
Severson, Richard K.
Cozen, Wendy
Davis, Scott
Rothman, Nathaniel
Hartge, Patricia
Colt, Joanne S.
TI A Case-Control Study of Occupational Exposure to Trichloroethylene and
Non-Hodgkin Lymphoma
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Article
DE cancer; non-Hodgkin lymphoma; occupational; solvents; trichloroethylene
ID CANCER INCIDENCE; ORGANIC-SOLVENTS; NONDIFFERENTIAL MISCLASSIFICATION;
AEROSPACE WORKERS; RISK; MORTALITY; COHORT; CHLOROPHENOLS; EPIDEMIOLOGY;
CHEMICALS
AB BACKGROUND: Previous epidemiologic findings suggest an association between exposure to trichloro-ethylene (TCE), a chlorinated solvent primarily used for vapor degreasing of metal parts, and non-Hodgkin lymphoma (NHL).
OBJECTIVES: We investigated the association between occupational TCE exposure and NHL within a population-based case-control study using detailed exposure assessment methods.
METHODS: Cases (n = 1,189; 76% participation rate) and controls (n = 982; 52% participation rate) provided information on their occupational histories and, for selected occupations, on possible workplace exposure to TCE using job-specific interview modules. An industrial hygienist assessed potential TCE exposure based on this information and a review of the TCE industrial hygiene literature. We computed odds ratios (ORs) and 95% confidence intervals (CIs) relating NHL and different metrics of estimated TCE exposure, categorized using tertiles among exposed controls, with unexposed subjects as the reference group.
RESULTS: We observed associations with NHL for the highest tertiles of estimated average weekly exposure (23 exposed cases; OR = 2.5; 95% CI, 1.1-6.1) and cumulative exposure (24 exposed cases; OR = 2.3; 95% CI, 1.0-5.0) to TCE. Tests for trend with these metrics surpassed or approached statistical significance (p-value for trend = 0.02 and 0.08, respectively); however, we did not observe dose-response relationships across the exposure levels. Overall, neither duration nor intensity of exposure was associated with NHL, although we observed an association with the lowest tertile of exposure duration (OR = 2.1; 95% CI, 1.0-4.7).
CONCLUSIONS: Our findings offer additional support for an association between high levels of exposure to TCE and increased risk of NHL. However, we cannot rule out the possibility of confounding from other chlorinated solvents used for vapor degreasing and note that our exposure assessment methods have not been validated.
C1 [Purdue, Mark P.; Bakke, Berit; Stewart, Patricia; Morton, Lindsay M.; Rothman, Nathaniel; Hartge, Patricia; Colt, Joanne S.] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20892 USA.
[Bakke, Berit] Natl Inst Occupat Hlth, Oslo, Norway.
[Stewart, Patricia] Stewart Exposure Assessments LLC, Arlington, VA USA.
[De Roos, Anneclaire J.; Davis, Scott] Univ Washington, Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98195 USA.
[De Roos, Anneclaire J.; Davis, Scott] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Schenk, Maryjean; Severson, Richard K.] Wayne State Univ, Dept Family Med & Publ Hlth Sci, Detroit, MI USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Iowa City, IA USA.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, Duarte, CA 91010 USA.
[Cerhan, James R.] Mayo Clin Coll Med, Dept Hlth Sci Res, Rochester, MN USA.
[Cozen, Wendy] Univ So Calif, Dept Prevent Med, Los Angeles, CA 90089 USA.
RP Purdue, MP (reprint author), NCI, Div Canc Epidemiol & Genet, EPS 8114,6120 Execut Blvd, Rockville, MD 20892 USA.
EM purduem@mail.nih.gov
RI Morton, Lindsay/B-5234-2015; Purdue, Mark/C-9228-2016;
OI Morton, Lindsay/0000-0001-9767-2310; Purdue, Mark/0000-0003-1177-3108;
Cerhan, James/0000-0002-7482-178X
FU NIH, National Cancer Institute; Public Health Service [N01-PC-65064,
N01-PC-67008, N01-PC-67009, N01-PC-67010, N02-PC-71105]
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, with Public Health Service contracts
N01-PC-65064, N01-PC-67008, N01-PC-67009, N01-PC-67010, and
N02-PC-71105.
NR 44
TC 22
Z9 24
U1 2
U2 14
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD FEB
PY 2011
VL 119
IS 2
BP 232
EP 238
DI 10.1289/ehp.1002106
PG 7
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 714IP
UT WOS:000286803400026
PM 21370516
ER
PT J
AU Jung, P
AF Jung, Paul
TI Product Biomonitoring and Responsible Reporting
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Editorial Material
ID ETHICS
C1 NIEHS, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Jung, P (reprint author), NIEHS, NIH, Dept Hlth & Human Serv, POB 12233, Res Triangle Pk, NC 27709 USA.
EM jungp@niehs.nih.gov
NR 17
TC 0
Z9 0
U1 0
U2 1
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD FEB
PY 2011
VL 119
IS 2
BP A58
EP A59
DI 10.1289/ehp.1003355
PG 2
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 714IP
UT WOS:000286803400004
PM 21288807
ER
PT J
AU Koonin, EV
AF Koonin, Eugene V.
TI The virus world, horizontal gene transfer vehicles and the perennial
arms race
SO ENVIRONMENTAL MICROBIOLOGY REPORTS
LA English
DT Editorial Material
ID TRANSFER AGENT; CRISPR; PROKARYOTES; BACTERIA; DEFENSE; ARCHAEA
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM koonin@ncbi.nlm.nih.gov
NR 16
TC 0
Z9 0
U1 1
U2 14
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1758-2229
J9 ENV MICROBIOL REP
JI Environ. Microbiol. Rep.
PD FEB
PY 2011
VL 3
IS 1
BP 10
EP 12
PG 3
WC Environmental Sciences; Microbiology
SC Environmental Sciences & Ecology; Microbiology
GA 718RS
UT WOS:000287144400006
ER
PT J
AU Manalo, KB
Choong, PFM
Becerra, SP
Dass, CR
AF Manalo, Katrina B.
Choong, Peter F. M.
Becerra, S. Patricia
Dass, Crispin R.
TI Pigment epithelium-derived factor as an anticancer drug and new
treatment methods following the discovery of its receptors: a patent
perspective
SO EXPERT OPINION ON THERAPEUTIC PATENTS
LA English
DT Article
DE angiogenesis; cancer; drug; patent; PEDF; PEDF receptor; therapy
ID FACTOR PEDF; RETINOBLASTOMA CELLS; OSTEOSARCOMA; GROWTH; BINDING;
ANGIOGENESIS; SERPIN; PHOTORECEPTORS; FIBROBLASTS; EXPRESSION
AB Traditional forms of cancer therapy, which include chemotherapy, have largely been overhauled due to the significant degree of toxicity they pose to normal, otherwise healthy tissue. It is hoped that the use of biological agents, most of which are endogenously present in the body, will lead to safer treatment outcomes, without sacrificing efficacy. The finding that pigment epithelium-derived factor (PEDF), a naturally-occurring protein, is a potent angiogenesis inhibitor has become the basis for studying the role of PEDF in tumours that are highly resistant to chemotherapy. The determination of the direct role of PEDF against cancer paves the way for understanding and developing PEDF as a novel drug. This review focuses on the patent applications behind testing the anticancer therapeutic effect of PEDF via its receptors as an antiangiogenic agent and as a direct anticancer agent. The majority of the PEDF patents describe the antiangiogenic ability and usage of recombinant vectors as the mode of treatment delivery. PEDF's therapeutic potential against different diseases and the discovery of its receptors open possibilities for improving PEDF-based peptide design and drug delivery modes.
C1 [Dass, Crispin R.] Victoria Univ, Sch Biomed & Hlth Sci, St Albans, Vic, Australia.
[Manalo, Katrina B.] St Vincents Hosp, Dept Orthopaed, Sydney, NSW, Australia.
[Manalo, Katrina B.] Univ Melbourne, Dept Med, St Vincents Hosp, Melbourne, Vic 3010, Australia.
[Choong, Peter F. M.] Univ Melbourne, Dept Surg, Melbourne, Vic 3010, Australia.
[Choong, Peter F. M.] Peter MacCallum Canc Inst, Sarcoma Serv, Melbourne, Vic, Australia.
[Becerra, S. Patricia] NEI, Sect Prot Struct & Funct, NIH, Bethesda, MD 20892 USA.
RP Dass, CR (reprint author), Victoria Univ, Sch Biomed & Hlth Sci, St Albans, Vic, Australia.
EM crispin.dass@vu.edu.au
FU Intramural NIH HHS [ZIA EY000306-16, ZIA EY000306-18]
NR 49
TC 18
Z9 18
U1 1
U2 1
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 FEB
PY 2011
VL 21
IS 2
BP 121
EP 130
DI 10.1517/13543776.2011.545347
PG 10
WC Chemistry, Medicinal; Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 720PB
UT WOS:000287291500001
PM 21204726
ER
PT J
AU Park, JK
AF Park, John K.
TI Recurrent Glioblastoma: Not Only Surgery Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
C1 Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20889 USA.
RP Park, JK (reprint author), Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20889 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD FEB 1
PY 2011
VL 29
IS 4
BP R103
EP R103
DI 10.1200/JCO.2010.32.7676
PG 1
WC Oncology
SC Oncology
GA 717XR
UT WOS:000287081800015
ER
PT J
AU Sugaya, M
Reed, S
Rose, PP
de la Motte, S
Raggo, CM
Kurtz, SE
Moses, AV
Fruh, K
Blauvelt, A
AF Sugaya, Makoto
Reed, Stacy
Rose, Patrick P.
de la Motte, Stacy
Raggo, Camilo M.
Kurtz, Stephen E.
Moses, Ashlee V.
Frueh, Klaus
Blauvelt, Andrew
TI Kaposi's sarcoma and human dermal microvascular endothelial cells
infected with Kaposi's sarcoma-associated herpesvirus express CCL21
SO JOURNAL OF DERMATOLOGICAL SCIENCE
LA English
DT Letter
ID CHEMOKINE RECEPTOR CCR7; ONCOSTATIN-M
C1 [Sugaya, Makoto] Univ Tokyo, Dept Dermatol, Fac Med, Bunkyo Ku, Tokyo 1138655, Japan.
[Sugaya, Makoto; Blauvelt, Andrew] NCI, Dermatol Branch, Bethesda, MD 20892 USA.
[Reed, Stacy; de la Motte, Stacy; Kurtz, Stephen E.; Blauvelt, Andrew] VA Med Ctr, Dermatol Serv, Portland, OR USA.
[Rose, Patrick P.; Raggo, Camilo M.; Moses, Ashlee V.; Frueh, Klaus] Oregon Hlth & Sci Univ, Vaccine & Gene Therapy Inst, Portland, OR 97201 USA.
[Rose, Patrick P.; Raggo, Camilo M.; Moses, Ashlee V.; Frueh, Klaus; Blauvelt, Andrew] Oregon Hlth & Sci Univ, Dept Mol Microbiol & Immunol, Portland, OR 97201 USA.
[Blauvelt, Andrew] Oregon Hlth & Sci Univ, Dept Dermatol, Portland, OR 97201 USA.
RP Sugaya, M (reprint author), Univ Tokyo, Dept Dermatol, Fac Med, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM sugayam-der@h.u-tokyo.ac.jp
FU NCI NIH HHS [R01 CA099906, R01CA99906]; NIAID NIH HHS [R01CA/AI94011];
NIAMS NIH HHS [R21 AR054495]
NR 10
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 0923-1811
J9 J DERMATOL SCI
JI J. Dermatol. Sci.
PD FEB
PY 2011
VL 61
IS 2
BP 139
EP 142
DI 10.1016/j.jdermsci.2010.11.017
PG 4
WC Dermatology
SC Dermatology
GA 724BG
UT WOS:000287550500011
PM 21176872
ER
PT J
AU Edwards, DRV
Romero, R
Kusanovic, JP
Hassan, SS
Mazaki-Tovi, S
Vaisbuch, E
Kim, CJ
Erez, O
Chaiworapongsa, T
Pearce, BD
Bartlett, J
Friel, LA
Salisbury, BA
Anant, MK
Vovis, GF
Lee, MS
Gomez, R
Behnke, E
Oyarzun, E
Tromp, G
Menon, R
Williams, SM
AF Edwards, Digna R. Velez
Romero, Roberto
Kusanovic, Juan Pedro
Hassan, Sonia S.
Mazaki-Tovi, Shali
Vaisbuch, Edi
Kim, Chong Jai
Erez, Offer
Chaiworapongsa, Tinnakorn
Pearce, Brad D.
Bartlett, Jacquelaine
Friel, Lara A.
Salisbury, Benjamin A.
Anant, Madan Kumar
Vovis, Gerald F.
Lee, Min Seob
Gomez, Ricardo
Behnke, Ernesto
Oyarzun, Enrique
Tromp, Gerard
Menon, Ramkumar
Williams, Scott M.
TI Polymorphisms in maternal and fetal genes encoding for proteins involved
in extracellular matrix metabolism alter the risk for
small-for-gestational-age
SO JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
LA English
DT Article
DE DNA variants; extracellular matrix; genetic association study; genomics;
genotype; haplotype; high dimensional biology; SNP; intrauterine growth
restriction; genetic epidemiology; complex disease
ID INTRAUTERINE GROWTH RESTRICTION; UTERINE ARTERY DOPPLER;
LOW-BIRTH-WEIGHT; MULTIFACTOR-DIMENSIONALITY REDUCTION; HARDY-WEINBERG
EQUILIBRIUM; FALSE DISCOVERY RATE; SIB-PAIR LINKAGE; PLACENTAL GROWTH;
FACTOR RECEPTOR-1; ANGIOGENIC FACTORS
AB Objective. To examine the association between maternal and fetal genetic variants and small-for-gestational-age (SGA).
Methods. A case-control study was conducted in patients with SGA neonates (530 maternal and 436 fetal) and controls (599 maternal and 628 fetal); 190 candidate genes and 775 SNPs were studied. Single-locus, multi-locus and haplotype association analyses were performed on maternal and fetal data with logistic regression, multifactor dimensionality reduction (MDR) analysis, and haplotype-based association with 2 and 3 marker sliding windows, respectively. Ingenuity pathway analysis (IPA) software was used to assess pathways that associate with SGA.
Results. The most significant single-locus association in maternal data was with a SNP in tissue inhibitor of metalloproteinase 2 (TIMP2) (rs2277698 OR = 1.71, 95% CI [1.26-2.32], p = 0.0006) while in the fetus it was with a SNP in fibronectin 1 isoform 3 preproprotein (FN1) (rs3796123, OR = 1.46, 95% CI [1.20-1.78], p = 0.0001). Both SNPs were adjusted for potential confounders (maternal body mass index and fetal sex). Haplotypc analyses resulted in associations in alpha 1 type I collagen preproprotein (COL1A1, rs1007086-rs2141279-rs17639446, global p = 0.006) in mothers and FN1 (rs2304573-rs1250204-rs1250215, global p = 0.045) in fetuses. Multi-locus analyses with MDR identified a two SNP model with maternal variants collagen type V alpha 2 (COL5A2) and plasminogen activator urokinase (PLAU) predicting SGA outcome correctly 59% of the time (p = 0.035).
Conclusions. Genetic variants in extracellular matrix-related genes showed significant single-locus association with SGA. These data are consistent with other studies that have observed elevated circulating fibronectin concentrations in association with increased risk of SGA. The present study supports the hypothesis that DNA variants can partially explain the risk of SGA in a cohort of Hispanic women.
C1 [Edwards, Digna R. Velez] Vanderbilt Univ, Inst Med & Publ Hlth, Dept Obstet & Gynecol, Vanderbilt Epidemiol Ctr, Nashville, TN USA.
[Romero, Roberto; Kusanovic, Juan Pedro; Hassan, Sonia S.; Mazaki-Tovi, Shali; Vaisbuch, Edi; Kim, Chong Jai; Erez, Offer; Chaiworapongsa, Tinnakorn; Friel, Lara A.] NICHD, Perinatol Res Branch, NIH, DHHS, Bethesda, MD USA.
[Romero, Roberto; Kusanovic, Juan Pedro; Hassan, Sonia S.; Mazaki-Tovi, Shali; Vaisbuch, Edi; Kim, Chong Jai; Erez, Offer; Chaiworapongsa, Tinnakorn; Friel, Lara A.] NICHD, Perinatol Res Branch, NIH, DHHS, Detroit, MI USA.
[Romero, Roberto; Tromp, Gerard] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
[Kim, Chong Jai] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Pearce, Brad D.; Menon, Ramkumar] Emory Univ, Dept Epidemiol, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.
[Bartlett, Jacquelaine; Williams, Scott M.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN USA.
[Salisbury, Benjamin A.; Anant, Madan Kumar] PGxHealth LLC, New Haven, CT USA.
[Vovis, Gerald F.] Helix Therapeut LLC, New Haven, CT USA.
[Lee, Min Seob] GenomeCare Inc, San Diego, CA USA.
[Gomez, Ricardo; Behnke, Ernesto] Hosp Dr Sotero del Rio, CEDIP Ctr Perinatal Diag & Res, Dept Obstet & Gynecol, Santiago, Chile.
[Gomez, Ricardo; Oyarzun, Enrique] Pontificia Univ Catolica Chile, Dept Obstet & Gynecol, Santiago, Chile.
[Williams, Scott M.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
RP Romero, R (reprint author), Wayne State Univ, Perinatol Res Branch, NICHD, NIH,DHHS,Hutzel Womens Hosp, 3990 John R,Box 4, Detroit, MI 48201 USA.
EM prbchiefstaff@med.wayne.edu; smwilliams@chgr.mc.vanderbilt.edu
RI Williams, Scott/B-9491-2012; Velez Edwards, Digna/C-1090-2012; Tromp,
Gerard/B-2677-2017;
OI Tromp, Gerard/0000-0002-7761-0806; Vaisbuch, Edi/0000-0002-8400-9031;
Salisbury, Benjamin/0000-0003-0796-6492
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, NIH, DHHS
FX This research was supported, in part, by the Perinatology Research
Branch, Division of Intramural Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development, NIH, DHHS.
NR 162
TC 6
Z9 9
U1 0
U2 4
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1476-7058
EI 1476-4954
J9 J MATERN-FETAL NEO M
JI J. Matern.-Fetal Neonatal Med.
PD FEB
PY 2011
VL 24
IS 2
BP 362
EP 380
DI 10.3109/14767058.2010.497572
PG 19
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 716XZ
UT WOS:000287008100031
PM 20617897
ER
PT J
AU Liu, XD
Sun, J
Sun, LG
Liu, WQ
Wang, YH
AF Liu, Xiaodong
Sun, Jing
Sun, Liguang
Liu, Wenqi
Wang, Yuhong
TI Reflectance spectroscopy: a new approach for reconstructing penguin
population size from Antarctic ornithogenic sediments
SO JOURNAL OF PALEOLIMNOLOGY
LA English
DT Article
DE Reflectance spectroscopy; Ornithogenic sediments; Historical penguin
populations; Antarctica
ID NEAR-INFRARED SPECTROSCOPY; LAKE-SEDIMENTS; ORGANIC-MATTER; SOIL
PROPERTIES; ARDLEY ISLAND; WATER; CONTAMINATION; FEASIBILITY; MARITIME;
SPECTRA
AB Reflectance spectroscopy has several advantages compared to traditional chemical methods in paleolimnology. It requires little cost, involves minimal or no sample preparation and is rapid. There has, however, been limited use of reflectance spectroscopy in polar paleolimnological studies. This paper explores the application of reflectance spectroscopy to reconstruct historical changes in penguin population size in the maritime Antarctic. Two ornithogenic sediment cores on Ardley Island, Antarctica were analyzed. Penguin droppings and weathered soils were analyzed as reference materials. Principal component analysis and linear mixing modeling were performed on the spectral data to estimate the proportion of penguin guano in the sediments and these values were used to infer historical penguin population numbers. Historical penguin population size versus time, reconstructed from reflectance spectra, and population numbers inferred from previous geochemical analysis of bio-elements, were quite similar. Our results illustrate the feasibility of rapidly inferring historical changes in penguin population size using reflectance spectroscopy on Antarctic ornithogenic sediments. Our findings suggest that this technique has potential for reconstructing past population numbers of other seabirds and mammals using lake sediments influenced by animal excrement.
C1 [Liu, Xiaodong; Sun, Liguang] Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Anhui, Peoples R China.
[Sun, Jing] Columbia Univ, Lamont Doherty Earth Observ, Palisades, NY 10964 USA.
[Liu, Wenqi] Univ Sci & Technol China, Instruments Ctr Phys Sci, Hefei 230026, Anhui, Peoples R China.
[Wang, Yuhong] NIH, Bethesda, MD 20892 USA.
RP Liu, XD (reprint author), Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Anhui, Peoples R China.
EM ycx@ustc.edu.cn
RI Sun, Jing /B-9248-2017
OI Sun, Jing /0000-0002-0129-5184
FU National Natural Science Foundation [40876096, 41076123, 40730107,
40606003]; SOA Key Laboratory for Polar Science [KP2007002]; CAAA
[20070202]; CAS
FX We thank the Chinese Antarctic and Arctic Administration of National
Oceanic Bureau for logistical support. This study was supported by the
National Natural Science Foundation (Grant Nos. 40876096, 41076123,
40730107 and 40606003), open research fund from SOA Key Laboratory for
Polar Science (KP2007002), the young fund for strategic research of the
Chinese Polar Sciences from CAAA (No. 20070202), and the special fund
for excellent PhD theses of CAS. We especially appreciate three
anonymous reviewers for their critical reviews and careful corrections
of this manuscript.
NR 50
TC 9
Z9 10
U1 0
U2 9
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0921-2728
J9 J PALEOLIMNOL
JI J. Paleolimn.
PD FEB
PY 2011
VL 45
IS 2
BP 213
EP 222
DI 10.1007/s10933-010-9493-6
PG 10
WC Environmental Sciences; Geosciences, Multidisciplinary; Limnology
SC Environmental Sciences & Ecology; Geology; Marine & Freshwater Biology
GA 712OV
UT WOS:000286677000007
ER
PT J
AU Huang, T
Sun, LG
Wang, YH
Kong, DM
AF Huang, Tao
Sun, Liguang
Wang, Yuhong
Kong, Deming
TI Late Holocene Ad,lie penguin population dynamics at Zolotov Island,
Vestfold Hills, Antarctica
SO JOURNAL OF PALEOLIMNOLOGY
LA English
DT Article
DE Adelie penguin; Antarctic climates; Ice core; Ornithogenic sediments;
Western Antarctic Peninsula; Little Ice Age
ID SEA-ICE EXTENT; CLIMATE-CHANGE; EASTERN ANTARCTICA; PALEONTOLOGICAL
EVIDENCE; DIATOM ASSEMBLAGES; PENINSULA REGION; ADELIE PENGUINS;
LAKE-SEDIMENTS; TRACE-ELEMENTS; ARDLEY ISLAND
AB We inferred late Holocene Ad,lie penguin occupation history and population dynamics on Zolotov Island, Vestfold Hills, Antarctica, using geochemical data from a dated ornithogenic sediment core (ZOL4). Radiocarbon dates on fossil penguin bones in the core indicate that Ad,lie penguins occupied the island as early as 1,800 years before present (yr BP), following the retreat of the Sorsdal glacier. This occupation began similar to 1,200 years later than that observed at Ardley Island and King George Island, in the South Shetland Islands. Phosphorus was identified as the most indicative bio-element for penguin guano in core ZOL4, and was used to infer past penguin population dynamics. Around 1,800 years ago, the Ad,lie penguin populations at both Zolotov Island and Ardley Island increased rapidly and reached their highest levels similar to 1,000 yr BP. For the past similar to 900 years, the penguin populations at Zolotov Island have shown a general rising trend, with fluctuations, while those at Ardley Island have shown a moderate decreasing trend. The Ad,lie penguin populations at both Ardley Island and Zolotov Island showed a clear decline similar to 300 years ago, which we interpret as a response to the Little Ice Age, or a neoglacial cooling event.
C1 [Huang, Tao; Sun, Liguang; Wang, Yuhong; Kong, Deming] Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Peoples R China.
[Wang, Yuhong] NIH, Bethesda, MD 20892 USA.
RP Sun, LG (reprint author), Univ Sci & Technol China, Inst Polar Environm, Hefei 230026, Peoples R China.
EM slg@ustc.edu.cn
RI Huang, Tao/B-5915-2009
FU National Natural Science Foundation of China [40730107]; National
Science and Technology Supporting Program [2006BAB18B07]; Major State
Basic Research and Development Program of China (973 program)
[2010CB428902]; Australian Antarctic Division Science Project [AAD2873]
FX This study was funded by the National Natural Science Foundation of
China (No. 40730107), the National Science and Technology Supporting
Program (2006BAB18B07), the Major State Basic Research and Development
Program of China (973 program, No. 2010CB428902) and the Australian
Antarctic Division Science Project (AAD2873). We thank the Chinese
Arctic and Antarctic Administration, Polar Research Institute of China,
Australian Antarctic Division for logistical support in field, Dr.
Renbin Zhu for collection of samples and Dr. William Cooper for
assistance with radiocarbon dating. We especially thank the reviewers
for their critical comments and Dr. Dominic Hodgson and Dr. Mark Brenner
for their help in improving this manuscript.
NR 65
TC 9
Z9 10
U1 3
U2 15
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0921-2728
J9 J PALEOLIMNOL
JI J. Paleolimn.
PD FEB
PY 2011
VL 45
IS 2
BP 273
EP 285
DI 10.1007/s10933-011-9497-x
PG 13
WC Environmental Sciences; Geosciences, Multidisciplinary; Limnology
SC Environmental Sciences & Ecology; Geology; Marine & Freshwater Biology
GA 712OV
UT WOS:000286677000011
ER
PT J
AU Simitsopoulou, M
Roilides, E
Georgiadou, E
Paliogianni, F
Walsh, TJ
AF Simitsopoulou, Maria
Roilides, Emmanuel
Georgiadou, Elpiniki
Paliogianni, Fotini
Walsh, Thomas J.
TI Differential transcriptional profiles induced by amphotericin B
formulations on human monocytes during response to hyphae of Aspergillus
fumigatus
SO MEDICAL MYCOLOGY
LA English
DT Article
DE monocytes; cytokines; chemokines; immunoregulation; gene arrays; ELISA
ID INVASIVE PULMONARY ASPERGILLOSIS; HUMAN MONONUCLEAR-CELLS; TOLL-LIKE
RECEPTORS; LIPID FORMULATIONS; HOST-DEFENSE; FUNGAL-INFECTIONS;
CANDIDA-ALBICANS; GENE-EXPRESSION; MICROARRAY ANALYSIS; CYTOKINE BALANCE
AB Amphotericin B formulations possess diverse immunomodulatory properties that may contribute to the activity of phagocytes against invasive aspergillosis. In this work we provide a novel set of data on different gene transcriptional profiles of monocytes exposed to the combination of Aspergillus fumigatus and amphotericin B formulations. We used pathway-specific microarray analysis, RT-PCR analysis and enzyme-linked immunosorbent assays to compare the effects of amphotericin B deoxycholate (DAMB) at 1 mu g/ml and amphotericin B lipid complex (ABLC) at 5 mu g/ml to assess gene expression of immune molecules of THP-1 cells exposed to A. fumigatus hyphae (AF) for 4 h. A. fumigatus hyphae at effector/target ratio 10/1 induced mostly chemotactic factors for monocyte recruitment. DAMB at 1 mu g/ml in the presence or absence of AF induced the most pronounced changes in pro-inflammatory and chemokine gene expression, while ABLC under the same conditions caused less dramatic effect. There was a reciprocal response of increased expression of the genes encoding IL-1 beta and IL-20 and decreased expression of IL-10, IL-2 and IL-3 in response of monocytes to both the hyphae and antifungal agents. These results demonstrate that amphotericin B formulations exert differential effects on genes encoding pro-inflammatory molecules, immunoregulatory molecules and chemokines by human monocytes during response to A. fumigatus and that these molecules may affect antifungal activity.
C1 [Walsh, Thomas J.] Cornell Univ, Weill Cornell Med Coll, Transplantat Oncol Infect Dis Program, Div Infect Dis, New York, NY 10065 USA.
[Walsh, Thomas J.] New York Presbyterian Hosp, New York, NY 10065 USA.
[Simitsopoulou, Maria; Roilides, Emmanuel; Georgiadou, Elpiniki] Aristotle Univ Thessaloniki, Hippokrat Hosp, Sch Med, Infect Dis Lab,Dept Pediat 3, GR-54006 Thessaloniki, Greece.
[Paliogianni, Fotini] Univ Patras, Sch Med, Dept Microbiol, GR-26110 Patras, Greece.
[Roilides, Emmanuel; Walsh, Thomas J.] NCI, Immunocompromised Host Sect, Bethesda, MD 20892 USA.
RP Walsh, TJ (reprint author), Cornell Univ, Weill Cornell Med Coll, Transplantat Oncol Infect Dis Program, Div Infect Dis, 1300 York Ave,Room A-421, New York, NY 10065 USA.
EM thw2003@med.cornell.edu
FU Enzon Pharmaceuticals Inc.; National Cancer Institute
FX This research was supported in part by a research grant from Enzon
Pharmaceuticals Inc. to the Aristotle University of Thessaloniki and by
the intramural research program of the National Cancer Institute.
NR 51
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U1 1
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1369-3786
J9 MED MYCOL
JI Med. Mycol.
PD FEB
PY 2011
VL 49
IS 2
BP 176
EP 185
DI 10.3109/13693786.2010.510539
PG 10
WC Infectious Diseases; Mycology; Veterinary Sciences
SC Infectious Diseases; Mycology; Veterinary Sciences
GA 722RH
UT WOS:000287451500010
PM 20807031
ER
PT J
AU Chen, H
You, MJ
Jiang, Y
Wang, W
Li, L
AF Chen, H.
You, M. J.
Jiang, Y.
Wang, W.
Li, L.
TI RMI1 Attenuates Tumor Development and is Essential for Early Embryonic
Survival
SO MOLECULAR CARCINOGENESIS
LA English
DT Article
DE tumor development; radiation; RMI1; bloom syndrome; genomic instability
ID BLOOMS-SYNDROME GENE; HOMOLOGOUS RECOMBINATION; ESSENTIAL COMPONENT;
P53-DEFICIENT MICE; HOLLIDAY JUNCTIONS; TOPOISOMERASE III; SYNDROME
HELICASE; GENOME STABILITY; SYNDROME PROTEIN; BLM
AB RMI1/BLAP75 (RecQ-mediated genome instability 1/Bloom-associated protein 75) is an OB-fold protein highly conserved from yeast to human. Previous studies showed that RMI1 is required for the stability of the BLM/RMI1/Top3 alpha complex and for the suppression of elevated sister chromatids exchange (SCE). The presence of RMI1 strongly stimulates Holliday dissolution activity of the Bloom helicase in vitro. The in vivo function of RMI1, however, remains largely undefined. To address this question, we generated RMI1 knockout mice through homologous replacement targeting. We found that, while RMI1(+/-) mice showed no obvious developmental phenotype, deletion of both mRMI1 alleles resulted in early embryonic lethality before implantation. To determine whether RMI1 plays a role in tumorigenesis, we generated RMI1/p53 double heterozygous mice and analyzed their onset of ionizing radiation-induced tumor development. RMI1(+/-)/p53(+/-) mice succumbed to tumor with a higher frequency and exhibited a substantially shortened survival when compared to the wild type, RMI1(+/-) and p53(+/-) cohorts. These results demonstrated a dual-role of RMI1 in embryonic development and tumor suppression. (C) 2010 Wiley-Liss, Inc.
C1 [Li, L.] Univ Texas MD Anderson Canc Ctr, Unit 66, Dept Expt Radiat Oncol, Houston, TX 77030 USA.
[You, M. J.] Univ Texas MD Anderson Canc Ctr, Dept Hematopathol, Houston, TX 77030 USA.
[Wang, W.] NIA, Genet Lab, NIH, Baltimore, MD 21224 USA.
[Li, L.] Univ Texas MD Anderson Canc Ctr, Dept Genet, Houston, TX 77030 USA.
RP Li, L (reprint author), Univ Texas MD Anderson Canc Ctr, Unit 66, Dept Expt Radiat Oncol, 1515 Holcombe Blvd, Houston, TX 77030 USA.
RI Jiang, Yingjun/I-8919-2014
FU National Cancer Institute [CA127945, CA097175]; UT MDACC; American
Cancer Society IRG; UT MDACC IRG; Ladies Leukemia League; National
Institute on Aging, National Institute of Health [Z01 AG000657-08]
FX The authors wish to thank Dr. Gigi Lozano (Department of Genetics, UT
MDACC) for critical suggestions to this work. The GEF Core facility
provided ES cell selection and blastocyst injection services for the
generation of the knockout mice. This work was supported, in whole or in
part, by grants from the National Cancer Institute CA127945 and CA097175
(to L.L.) and UT MDACC Physician Scientist Award, American Cancer
Society IRG, UT MDACC IRG and Ladies Leukemia League (to MJ.Y.). This
work was also supported in part by the Intramural Research Program of
the National Institute on Aging (Z01 AG000657-08), National Institute of
Health (to W.W.).
NR 37
TC 4
Z9 5
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0899-1987
J9 MOL CARCINOGEN
JI Mol. Carcinog.
PD FEB
PY 2011
VL 50
IS 2
BP 80
EP 88
DI 10.1002/mc.20694
PG 9
WC Biochemistry & Molecular Biology; Oncology
SC Biochemistry & Molecular Biology; Oncology
GA 715CG
UT WOS:000286857400003
PM 21229605
ER
PT J
AU Moore, NM
Kuhn, NZ
Hanlon, SE
Lee, JSH
Nagahara, LA
AF Moore, N. M.
Kuhn, N. Z.
Hanlon, S. E.
Lee, J. S. H.
Nagahara, L. A.
TI De-convoluting cancer's complexity: using a 'physical sciences lens' to
provide a different (clearer) perspective of cancer PREFACE
SO PHYSICAL BIOLOGY
LA English
DT Editorial Material
ID BIOLOGY
C1 [Moore, N. M.; Kuhn, N. Z.; Hanlon, S. E.; Lee, J. S. H.; Nagahara, L. A.] NCI, Off Phys Sci Oncol, Ctr Strateg Sci Initiat, Bethesda, MD 20892 USA.
RP Moore, NM (reprint author), NCI, Off Phys Sci Oncol, Ctr Strateg Sci Initiat, Bethesda, MD 20892 USA.
RI Lee, Jerry/A-3189-2008; Lee, Jerry/K-4553-2014
OI Lee, Jerry/0000-0003-1515-0952;
NR 5
TC 8
Z9 8
U1 0
U2 1
PU IOP PUBLISHING LTD
PI BRISTOL
PA DIRAC HOUSE, TEMPLE BACK, BRISTOL BS1 6BE, ENGLAND
SN 1478-3967
J9 PHYS BIOL
JI Phys. Biol.
PD FEB
PY 2011
VL 8
IS 1
AR 010302
DI 10.1088/1478-3975/8/1/010302
PG 4
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 717LE
UT WOS:000287044600003
PM 21368346
ER
PT J
AU Guenterberg, KD
Grignol, VP
Relekar, KV
Varker, KA
Chen, HX
Kendra, KL
Olencki, TE
Carson, WE
AF Guenterberg, Kristan D.
Grignol, Valerie P.
Relekar, Kiran V.
Varker, Kimberly A.
Chen, Helen X.
Kendra, Kari L.
Olencki, Thomas E.
Carson, William E., III
TI A Pilot Study of Bevacizumab and Interferon-alpha 2b in Ocular Melanoma
SO AMERICAN JOURNAL OF CLINICAL ONCOLOGY-CANCER CLINICAL TRIALS
LA English
DT Article
DE bevacizumab; vascular endothelial growth factor; angiogenic factor;
interferon-alpha2b; uveal neoplasm
ID ENDOTHELIAL-GROWTH-FACTOR; METASTATIC UVEAL MELANOMA; CUTANEOUS
MELANOMA; COLORECTAL-CANCER; SYSTEMIC THERAPY; DACARBAZINE BOLD;
BREAST-CANCER; CELL LINES; ANGIOGENESIS; EXPRESSION
AB Objectives: We hypothesized that administration of bevacizumab, a monoclonal antibody that neutralizes vascular endothelial growth factor, in combination with high-dose interferon-alpha2b (IFN-alpha 2b), an inhibitor of basic fibroblast growth factor, would have clinical activity in patients with metastatic ocular melanoma.
Methods: Patients with metastatic ocular melanoma received bevacizumab (15 mg/kg intravenously every 2 weeks) plus IFN-alpha 2b (5 MU/m(2) subcutaneously 3 times weekly for 2 weeks followed by a dose of 10 MU/m(2) subcutaneously thereafter). Patients exhibiting a clinical response or stabilization of disease were treated until disease progression.
Results: In this pilot study, 5 patients were treated (3 men, 2 women) with a mean age of 63.8 years (range, 53-71 years). Overall, the regimen was well-tolerated. The following adverse events were noted: grade 3 dyspnea (2 patients), grade 3 and 4 fatigue (2), grade 3 muscle weakness (1), grade 3 anorexia (1), grade 1 and 2 proteinuria (2), and grade 3 diarrhea (1). All adverse events resolved with a treatment holiday or dose reduction. One patient had reduction in tumor burden of 23% by Response Evaluation Criteria in Solid Tumors criteria and 2 patients had stabilization of disease lasting 28 and 36 weeks, respectively. Two patients failed to respond and progressed after 6 and 7 weeks of therapy.
Conclusion: Bevacizumab and IFN-alpha 2b were well tolerated in this patient population, and clinical activity was observed. Further study of high-dose IFN-alpha 2b in combination with bevacizumab in this setting is warranted.
C1 [Guenterberg, Kristan D.; Grignol, Valerie P.; Relekar, Kiran V.; Varker, Kimberly A.; Carson, William E., III] Ohio State Univ, Div Surg Oncol, Columbus, OH 43210 USA.
[Chen, Helen X.] NCI, CTEP, Bethesda, MD 20892 USA.
[Kendra, Kari L.; Olencki, Thomas E.] Ohio State Univ, Div Hematol & Oncol, Columbus, OH 43210 USA.
RP Carson, WE (reprint author), Ohio State Univ, Div Surg Oncol, N924 Doan Hall,410 W 10th Ave, Columbus, OH 43210 USA.
EM william.carson@osumc.edu
RI Carson, William/E-2846-2011
FU National Institutes of Health [U01 CA76576, N01 CM62207, K24 CA093670,
T32 CA009338, CA093071]
FX Supported by National Institutes of Health Grants U01 CA76576, N01
CM62207, K24 CA093670, T32 CA009338, and CA093071.
NR 42
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U1 2
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3732
J9 AM J CLIN ONCOL-CANC
JI Am. J. Clin. Oncol.-Cancer Clin. Trials
PD FEB
PY 2011
VL 34
IS 1
BP 87
EP 91
DI 10.1097/COC.0b013e3181d2ed67
PG 5
WC Oncology
SC Oncology
GA 711XF
UT WOS:000286624100018
PM 20458209
ER
PT J
AU Corbin, M
McLean, D
't Mannetje, A
Dryson, E
Walls, C
McKenzie, F
Maule, M
Cheng, S
Cunningham, C
Kromhout, H
Blair, A
Pearce, N
AF Corbin, Marine
McLean, David
't Mannetje, Andrea
Dryson, Evan
Walls, Chris
McKenzie, Fiona
Maule, Milena
Cheng, Soo
Cunningham, Chris
Kromhout, Hans
Blair, Aaron
Pearce, Neil
TI Lung Cancer and Occupation: A New Zealand Cancer Registry-Based
Case-Control Study
SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE
LA English
DT Article
DE lung cancer; occupation; case-control study; wood workers; metal
workers; welding; machine operators; food process workers
ID DRY-CLEANING WORKERS; ASBESTOS TEXTILE WORKERS; MULTICENTER
CASE-CONTROL; HIGH-RISK OCCUPATIONS; INDUSTRY WORKERS; COHORT MORTALITY;
BRITISH-COLUMBIA; EMPIRICAL-BAYES; MEAT INDUSTRY; EXPOSURES
AB Background There are many proven and suspected occupational causes of lung calico; which will become relatively more important over time, as smoking prevalence decreases.
Methods We interviewed 457 cases aged 20-75 years notified to the New Zealand Cancer Registry during 2007-2008, and 792 population controls. We collected information on demographic details, potential confounders, and employment history. Associations were estimated using logistic regression adjusted for gender; age, ethnicity, smoking, and socio-economic status.
Results Among occupations of a priori interest, elevated odds ratios (ORs) were observed for sawmill, wood panel and related wood-processing plant operators (OR 4.63; 95% CI 1.05-20.29), butchers (OR 8.77, 95% CI 1.06-72.55), rubber and plastics products machine operators (4.27; 1.16-15.66), heavy truck drivers (2.24; 1.19-4.21) and workers in petroleum, coal, chemical and associated product manufacturing (1.80; 1.11-2.90); non-significantly elevated risks were also observed for loggers (4.67; 0.81-27.03), welders and flame-cutters (2.50; 0.86-7.25), pressers (5.74; 0.96-34.42), and electric and electronic equipment assemblers (3.61; 0.96-13.57). Several occupations and industries not of a priori interest also showed increased risks, including nursing associate professionals (5.45; 2.29-12.99), enrolled nurses (7.95; 3.10-20.42), care givers (3.47; 1.40-8.59), plant and machine operators and assemblers (1.61; 1.20-2.16), stationary machine operators and assemblers (1.67; 1.22-2.28), food and related products processing machine operators (1.98; 1.23-3.19), laborers and related elementary service workers (1.45; 1.05-2.00), manufacturing (1.34; 1.02-1.77), car retailing (3.08; 1.36-6.94), and road freight transport (3.02; 1.45-6.27).
Conclusions Certain occupations and industries have increased lung cancer risks in New Zealand, including wood workers, metal workers, meat workers, textile workers and drivers. Am. J. Ind. Med. 54:89-101, 2011. (C) 2010 Wiley-Liss, Inc.
C1 [Corbin, Marine; McLean, David; 't Mannetje, Andrea; Dryson, Evan; Walls, Chris; McKenzie, Fiona; Cheng, Soo; Pearce, Neil] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
[Corbin, Marine; Maule, Milena] Univ Turin, Canc Epidemiol Unit, CeRMS & CPO Piemonte, Turin, Italy.
[Cunningham, Chris] Massey Univ, Res Ctr Maori Hlth & Dev, Wellington, New Zealand.
[Kromhout, Hans] Univ Utrecht, Inst Risk Assessment Sci, Utrecht, Netherlands.
[Blair, Aaron] NCI, Occupat & Environm Epidemiol Branch, Bethesda, MD 20892 USA.
[Blair, Aaron] Occupat Canc Res Ctr, Toronto, ON, Canada.
[Pearce, Neil] London Sch Hyg & Trop Med, Dept Epidemiol & Publ Hlth, London WC1, England.
RP Pearce, N (reprint author), Massey Univ, Ctr Publ Hlth Res, Wellington Campus,Private Box 756, Wellington, New Zealand.
EM n.e.pearce@massey.ac.nz
OI Pearce, Neil/0000-0002-9938-7852
FU Health Research Council of New Zealand; New Zealand Department of
Labour; Lottery Health Research; Cancer Society of New Zealand; Accident
Compensation Corporation (ACC); Health Research Council
FX Contract grant sponsor: Health Research Council of New Zealand; Contract
grant sponsor: New Zealand Department of Labour; Contract grant sponsor:
Lottery Health Research; Contract grant sponsor: Cancer Society of New
Zealand; Contract grant sponsor: Accident Compensation Corporation
(ACC).; This project was funded by the Health Research Council of New
Zealand, by the New Zealand Department of Labour, by Lottery Health
Research, by the Cancer Society of New Zealand, and by the Accident
Compensation Corporation (ACC). Views and/or conclusions in this article
are those of Massey University and may not reflect the position of ACC.
The Centre for Public Health Research is supported by a Programme Grant
from the Health Research Council. We thank Pam Miley-Terry, Joy Stubbs,
Nicky Curran, and Heather Duckett. We also thank the staff of the New
Zealand Cancer Registry at the New Zealand Health Information Service
for collecting and making available information on cancer registrations.
We also thank Miria Hudson for her assistance.
NR 64
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U1 4
U2 12
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0271-3586
J9 AM J IND MED
JI Am. J. Ind. Med.
PD FEB
PY 2011
VL 54
IS 2
BP 89
EP 101
DI 10.1002/ajim.20906
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 712XH
UT WOS:000286699100001
PM 20957667
ER
PT J
AU Meehan, B
Appu, S
St Croix, B
Rak-Poznanska, K
Klotz, L
Rak, J
AF Meehan, Brian
Appu, Sree
St Croix, Brad
Rak-Poznanska, Krystyna
Klotz, Laurence
Rak, Janusz
TI Age-related properties of the tumour vasculature in renal cell carcinoma
SO BJU INTERNATIONAL
LA English
DT Article
DE RCC; angiogenesis; arteriogenesis; ageing; endothelial nitric oxide
synthase
ID ENDOTHELIAL GROWTH-FACTOR; NITRIC-OXIDE SYNTHASE; MICROVESSEL DENSITY;
PROGNOSTIC-SIGNIFICANCE; CLINICAL-SIGNIFICANCE; BLOOD-VESSELS;
ANGIOGENESIS; EXPRESSION; CANCER; ARTERIOGENESIS
AB What's known on the subject? and What does the study add?
Little is known about the impact of vascular ageing on the angiogenic features of clear cell renal cell carcinoma, a disease in which antiangiogenic therapy currently has a well established role. It is also rather surprising that this question has not been raised in a disease context where patients' age may differ by several decades. We provide the first glimpse in to the related vasclar changes, including morphology and some of the molecular features.
OBJECTIVE
To assess whether ageing processes influence angiogenesis in renal cell carcinoma (RCC) we carried out a pilot study of vascular properties in a series of archival primary kidney tumours in patients of different ages.
PATIENTS AND METHODS
A cohort of patients with RCC was identified restrospectively, with an age range of 35-84 years.
Paraffin-embedded, formalin-fixed sections of surgical tumour specimens were stained for endothelial (CD31, von Willebrand factor [vWF]), pericyte (alpha smooth muscle actin [SMA]) and leucocytic (CD45) markers, as well as for proliferative (Ki67) and angiogenic activity (tumour endothelial markers [TEMs], delta-like 4 [Dll4], Dll1, endothelial nitric oxide synthase [eNOS]).
Vascular properties were compared between patients above and below 65 years of age.
RESULTS
Microvascular density (MVD) within capillary hot spots was generally higher in patients with non-metastatic clear-cell RCC (ccRCC; n = 21) than in those with metastatic RCC (mRCC; n = 9).
Patients with ccRCC who were more than 65 years old showed significantly higher MVD than their younger (< 65 years) counterparts. There were dividing (Ki67-positive) endothelial and mural cells in both small (< 20 mu m) capillary and large (> 20 mu m), pre-capillary vessels, suggesting the involvement of both angiogenic and remodelling/arteriogenic processes.
Tumour endothelial markers (TEM1, TEM7, TEM8), Notch ligands (Dll1, Dll4), and other molecular characteristics (eNOS) were analysed. Age-related differences were observed in the frequency of pre-capillary vessels expressing Dll1, which was significantly higher in tumours of younger patients (< 65 years), while eNOS was more prevalent among capillaries associated with ccRCC in older patients (> 65 years).
CONCLUSIONS
The results of the present study suggest that age influences the structural and molecular properties of the tumour vasculature in ccRCC.
We postulate that vascular ageing could also be relevant in the context of anti-angiogenic therapy.
C1 [Meehan, Brian; Rak, Janusz] McGill Univ, Montreal Childrens Hosp, Res Inst, Montreal, PQ H3Z 2Z3, Canada.
[Appu, Sree; Klotz, Laurence] Univ Toronto, Sunnybrook Res Inst, Toronto, ON, Canada.
[St Croix, Brad] NCI, Frederick, MD 21701 USA.
[Rak-Poznanska, Krystyna] Prov Specialist Hosp, Res & Dev Ctr Wroclaw, Wroclaw, Poland.
RP Rak, J (reprint author), McGill Univ, Montreal Childrens Hosp, Res Inst, 4060 Ste Catherine W, Montreal, PQ H3Z 2Z3, Canada.
EM janusz.rak@mcgill.ca
FU Cancer Research Society; Canadian Cancer Society; Jack Cole Chair in
Pediatric Oncology
FX None declared. Source of Funding: this work was supported by grants from
the Cancer Research Society and partially by funds from the Canadian
Cancer Society, both to J.R., who is also a recipient of the Jack Cole
Chair in Pediatric Oncology. Infrastructure support was provided by
Fonds de la Recherche en Sante Quebec.
NR 55
TC 9
Z9 10
U1 1
U2 5
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1464-4096
J9 BJU INT
JI BJU Int.
PD FEB
PY 2011
VL 107
IS 3
BP 416
EP 424
DI 10.1111/j.1464-410X.2010.09569.x
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 711MW
UT WOS:000286596700013
PM 20804487
ER
PT J
AU Pedone, C
Napoli, N
Pozzilli, P
Lauretani, F
Bandinelli, S
Ferrucci, L
Antonelli-Incalzi, R
AF Pedone, Claudio
Napoli, Nicola
Pozzilli, Paolo
Lauretani, Fulvio
Bandinelli, Stefania
Ferrucci, Luigi
Antonelli-Incalzi, Raffaele
TI Quality of diet and potential renal acid load as risk factors for
reduced bone density in elderly women Reply
SO BONE
LA English
DT Letter
C1 [Pedone, Claudio; Antonelli-Incalzi, Raffaele] Univ Campus Biomed, Area Geriatria, I-00128 Rome, Italy.
[Pedone, Claudio; Napoli, Nicola; Pozzilli, Paolo] Fdn Alberto Sordi Onlus, Rome, Italy.
[Napoli, Nicola; Pozzilli, Paolo] Univ Campus Biomed, Area Endocrinol & Malattie Metab, I-00128 Rome, Italy.
[Lauretani, Fulvio] Tuscany Reg Hlth Agcy, Florence, Italy.
[Bandinelli, Stefania] Azienda Sanit Firenze, Geriatr Rehabil Unit, Florence, Italy.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, NIH, Baltimore, MD 21224 USA.
[Antonelli-Incalzi, Raffaele] Fdn San Raffaele Cittadella della Carita, Taranto, Italy.
RP Pedone, C (reprint author), Univ Campus Biomed, Area Geriatria, Via Alvaro del Portillo 21, I-00128 Rome, Italy.
EM c.pedone@unicampus.it
RI Antonelli Incalzi, Raffaele/G-3978-2012;
OI Pedone, Claudio/0000-0003-1847-9032
NR 0
TC 1
Z9 1
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 8756-3282
J9 BONE
JI Bone
PD FEB 1
PY 2011
VL 48
IS 2
BP 416
EP 416
DI 10.1016/j.bone.2010.09.004
PG 1
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 710UY
UT WOS:000286543700032
ER
PT J
AU Kolesar, J
Brundage, RC
Pomplun, M
Alberti, D
Holen, K
Traynor, A
Ivy, P
Wilding, G
AF Kolesar, Jill
Brundage, Richard C.
Pomplun, Marcia
Alberti, Dona
Holen, Kyle
Traynor, Anne
Ivy, Percy
Wilding, George
TI Population pharmacokinetics of 3-aminopyridine-2-carboxaldehyde
thiosemicarbazone (Triapine (R)) in cancer patients
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Triapine (R); 3-Aminopyridine-2-carboxaldehyde thiosemicarbazone;
Population pharmacokinetics; Phase 1
ID RIBONUCLEOTIDE REDUCTASE INHIBITOR; BLOOD MONONUCLEAR-CELLS; ADVANCED
SOLID TUMORS; PHASE-I; 3-AP; TRIAL; GEMCITABINE; COMBINATION;
CONSORTIUM; CARCINOMA
AB The purpose of this study was to develop a population pharmacokinetic (PK) model for 3-AP, to evaluate the effect of ABCB1 polymorphisms on the pharmacokinetic profile of 3-AP, and to assess the relationship between 3AP disposition and patient covariates.
A total of 40 patients with advanced cancer from two phase 1 studies were included in the population PK model building. Patients received 3-AP 25-105 mg/m(2) IV on day 1. 3-AP plasma and erythrocyte levels were sampled at 10 timepoints over a 24-h period and measured by a validated HPLC method. Data were analyzed by a nonlinear mixed-effects modeling approach using the NONMEM system.
3-AP pharmacokinetics were described as a 3-compartment model with first-order elimination, with one compartment representing the plasma and another representing erythrocyte concentrations. Gender was associated with volume of distribution, in which women had a lower V2. The number of cycles administered was associated with clearance; those with decreased clearance were more likely to receive less than 2 cycles before going off study.
This study suggests that monitoring 3-AP plasma concentrations in the first cycle and dose adjustment in those with decreased clearance may be helpful in decreasing toxicity associated with the 3-AP.
C1 [Kolesar, Jill; Pomplun, Marcia; Alberti, Dona; Holen, Kyle; Traynor, Anne; Wilding, George] Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, Madison, WI 53792 USA.
[Kolesar, Jill] Univ Wisconsin, Sch Pharm, Madison, WI 53792 USA.
[Brundage, Richard C.] Univ Minnesota, Ctr Forecasting Drug Response, Minneapolis, MN USA.
[Alberti, Dona; Holen, Kyle; Traynor, Anne; Wilding, George] Univ Wisconsin, Sch Med & Publ Hlth, Dept Med, Madison, WI 53792 USA.
[Ivy, Percy] NCI, Canc Therapy & Evaluat Program, Bethesda, MD 20892 USA.
RP Kolesar, J (reprint author), Univ Wisconsin, Paul P Carbone Comprehens Canc Ctr, 600 Highland Ave,K4-554, Madison, WI 53792 USA.
EM jmkolesar@pharmacy.wisc.edu
FU NCI [U01CA062491]; CTEP Translational Research Initiative [24XS090];
National Center for Research Resources, NIH [1ULRR0 25011]; American
College of Clinical Pharmacy
FX Supported by: U01CA062491 "Early Clinical Trials of Anti-Cancer Agents
with Phase I Emphasis" NCI; CTEP Translational Research Initiative
Funding 24XS090, and 1ULRR0 25011 Clinical and Translational Science
Award of the National Center for Research Resources, NIH and the
American College of Clinical Pharmacy.
NR 21
TC 17
Z9 17
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD FEB
PY 2011
VL 67
IS 2
BP 393
EP 400
DI 10.1007/s00280-010-1331-z
PG 8
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 711YE
UT WOS:000286627400016
PM 20440618
ER
PT J
AU Beumer, JH
Eiseman, JL
Gilbert, JA
Holleran, JL
Yellow-Duke, AE
Clausen, DM
D'Argenio, DZ
Ames, MM
Hershberger, PA
Parise, RA
Bai, L
Covey, JM
Egorin, MJ
AF Beumer, Jan H.
Eiseman, Julie L.
Gilbert, Judith A.
Holleran, Julianne L.
Yellow-Duke, Archibong E.
Clausen, Dana M.
D'Argenio, David Z.
Ames, Matthew M.
Hershberger, Pamela A.
Parise, Robert A.
Bai, Lihua
Covey, Joseph M.
Egorin, Merrill J.
TI Plasma pharmacokinetics and oral bioavailability of the
3,4,5,6-tetrahydrouridine (THU) prodrug, triacetyl-THU (taTHU), in mice
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Tetrahydrouridine; THU; Bioavailability; Metabolism; Mouse; Cytidine
deaminase
ID METHYLTRANSFERASE INHIBITOR 5-FLUORO-2'-DEOXYCYTIDINE; CYTIDINE
DEAMINASE INHIBITOR; CYTOSINE-ARABINOSIDE; DEOXYCYTIDYLATE DEAMINASE;
TETRAHYDROURIDINE THU; CLINICAL-PHARMACOLOGY; PHASE-I; METABOLISM;
URIDINE; PN401
AB Cytidine drugs, such as gemcitabine, undergo rapid catabolism and inactivation by cytidine deaminase (CD). 3,4,5,6-tetrahydrouridine (THU), a potent CD inhibitor, has been applied preclinically and clinically as a modulator of cytidine analogue metabolism. However, THU is only 20% orally bioavailable, which limits its preclinical evaluation and clinical use. Therefore, we characterized THU pharmacokinetics after the administration to mice of the more lipophilic pro-drug triacetyl-THU (taTHU).
Mice were dosed with 150 mg/kg taTHU i.v. or p.o. Plasma and urine THU concentrations were quantitated with a validated LC-MS/MS assay. Plasma and urine pharmacokinetic parameters were calculated non-compartmentally and compartmentally.
taTHU did not inhibit CD. THU, after 150 mg/kg taTHU i.v., had a 235-min terminal half-life and produced plasma THU concentrations > 1 mu g/mL, the concentration shown to inhibit CD, for 10 h. Renal excretion accounted for 40-55% of the i.v. taTHU dose, 6-12% of the p.o. taTHU dose. A two-compartment model of taTHU generating THU fitted the i.v. taTHU data best. taTHU, at 150 mg/kg p.o., produced a concentration versus time profile with a plateau of approximately 10 mu g/mL from 0.5-2 h, followed by a decline with a 122-min half-life. Approximately 68% of i.v. taTHU is converted to THU. Approximately 30% of p.o. taTHU reaches the systemic circulation as THU.
The availability of THU after p.o. taTHU is 30%, when compared to the 20% achieved with p.o. THU. These data will support the clinical studies of taTHU.
C1 [Beumer, Jan H.; Eiseman, Julie L.; Holleran, Julianne L.; Yellow-Duke, Archibong E.; Clausen, Dana M.; Hershberger, Pamela A.; Parise, Robert A.; Bai, Lihua; Egorin, Merrill J.] Univ Pittsburgh, Inst Canc, Drug Discovery Program, Pittsburgh, PA 15213 USA.
[Beumer, Jan H.; Parise, Robert A.] Univ Pittsburgh, Sch Pharm, Dept Pharmaceut Sci, Pittsburgh, PA 15213 USA.
[Eiseman, Julie L.; Hershberger, Pamela A.; Bai, Lihua; Egorin, Merrill J.] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15213 USA.
[Gilbert, Judith A.; Ames, Matthew M.] Mayo Clin, Coll Med, Dept Mol Pharmacol & Expt Therapeut, Rochester, MN 55905 USA.
[D'Argenio, David Z.] Univ So Calif, Dept Biomed Engn, Los Angeles, CA 90089 USA.
[Covey, Joseph M.] NCI, Toxicol & Pharmacol Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Rockville, MD 20852 USA.
[Egorin, Merrill J.] Univ Pittsburgh, Sch Med, Dept Med, Div Hematol Oncol, Pittsburgh, PA 15213 USA.
RP Beumer, JH (reprint author), Univ Pittsburgh, Inst Canc, Drug Discovery Program, Hillman Res Pavil,Room G27D,5117 Ctr Ave, Pittsburgh, PA 15213 USA.
EM beumerjh@upmc.edu
OI Beumer, Jan/0000-0002-8978-9401
FU National Cancer Institute [NO1-CM-52202, P30-CA47904, P41-EB001978];
Hillman Fellows for Innovative Cancer Research Award; American Society
of Clinical Oncology Cancer Foundation
FX We thank Dr. B. Rao Vishnuvajjala for his advice, Dr. Richard M.
Weinshilboum of Mayo Clinic for recombinant human CD preparation, Diane
Mazzei and her colleagues at the University of Pittsburgh Animal
Facility for their expert assistance, and the University of Pittsburgh
Cancer Institute Hematology/Oncology Writing Group for constructive
suggestions regarding the manuscript. This work was supported by
contract NO1-CM-52202 and grants P30-CA47904 and P41-EB001978 from the
National Cancer Institute. JHB is the recipient of a Hillman Fellows for
Innovative Cancer Research Award. MJE is the recipient of an American
Society of Clinical Oncology Cancer Foundation Translational Research
Professorship.
NR 37
TC 5
Z9 6
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD FEB
PY 2011
VL 67
IS 2
BP 421
EP 430
DI 10.1007/s00280-010-1337-6
PG 10
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 711YE
UT WOS:000286627400019
PM 20443002
ER
PT J
AU Sonoda, S
Li, HCA
Tajima, K
AF Sonoda, Shunro
Li, Hong Chuan
Tajima, Kazuo
TI Ethnoepidemiology of HTLV-1 related diseases: Ethnic determinants of
HTLV-1 susceptibility and its worldwide dispersal
SO CANCER SCIENCE
LA English
DT Review
ID T-CELL LEUKEMIA; VIRUS TYPE-I; TROPICAL SPASTIC PARAPARESIS;
PERIPHERAL-BLOOD LYMPHOCYTES; INFECTIVE DERMATITIS; CHILD TRANSMISSION;
MYELOPATHY; LYMPHOMA; RISK; CARRIERS
AB Human T-cell lymphotropic virus type 1 is vertically transmitted in neonatal life and is causatively associated with adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in adults. Persistence of HTLV-1 in host T cells, clonal expansion of the HTLV-1 carrying T cells, and emergence of malignantly transformed T cells are in accord with the multistep model of human cancer and roles for continuous interaction between host genes and environmental factors. This article reviews two lines of HTLV-1 investigation, one regarding worldwide surveillance of HTLV-1 infection foci by serological testing and molecular analysis of HTLV-1 isolates, and the other focusing on genetics of the human leukocyte antigen (HLA) that determines the ethnic background of HTLV-1 permissiveness and susceptibility to ATL or HAM/TSP. The serological surveillance revealed transcontinental dispersal of HTLV-1 in the prehistoric era that started out of Africa, spread to Austro-Melanesia and the Asian continent, then moved to North America and through to the southern edge of South America. This was highlighted by an Andean mummy study that proved ancient migration of paleo-mongoloid HTLV-1 from Asia to South America. Phylogenetic analysis of HLA alleles provided a basis for ethnic susceptibility to HTLV-1 infection and associated diseases, both ATL and HAM/TSP. Ethnicity-based sampling of peripheral blood lymphocytes has great potential for genome-wide association studies to illuminate ethnically defined host factors for viral oncogenesis with reference to HTLV-1 and other pathogenic elements causatively associated with chronic disease and malignancies. (Cancer Sci 2011; 102: 295-301)
C1 [Sonoda, Shunro; Li, Hong Chuan] Kagoshima Univ, Dept Virol, Kagoshima 890, Japan.
[Sonoda, Shunro] Kagoshima Univ, Fac Med, Kagoshima 890, Japan.
[Sonoda, Shunro] So Reg Hosp, Makurazaki, Japan.
[Li, Hong Chuan] NCI, Div Canc Epidemiol & Genet, Frederick, MD 21701 USA.
[Tajima, Kazuo] Aichi Canc Ctr, Res Inst, Nagoya, Aichi 464, Japan.
RP Sonoda, S (reprint author), Kagoshima Univ, Dept Virol, Kagoshima 890, Japan.
EM sumikoshunro@ybb.ne.jp; ktajima@aichi-cc.jp
FU Ministry of Science, Education, Sports and Technology of Japan
FX We greatly thank Drs. V. Zaninovic, A. Blank, M. Blank (Colombia), L.
Cartier, L. Ramirez, L Nunez (Chile), L. Hurtado, L. V. Hurtado, R.
Andrade (Bolivia), B. Hanchard, O. Morgan, B. Cranston (Jamaica), A.
Manns, W. Blattner, P. Levine, N. Mueller, M. Hisada, R. Biggar, J.
Goedert, V. Franchini, S. Jacobson, W. Harrington Jr., J. Byrnes, M.
Hojo (USA), G. de The, A. Gessain (France), B. Kitze (Germany), W. Hall
(Ireland), K. Takahashi, Y.Nagata, K. Kawakami, T. Takezaki, N. Arima,
K. Usuku, S. Yashiki, T. Fujiyoshi, L. Hong, M. Osame, A. Utsunomiya, S.
Kashiwagi, T. Miura, M. Hayami, S. Horai, and M. Moore (Japan) for their
kind collaboration in our field studies and laboratory work, as well as
in preparation of this article. We highly appreciate Drs. I. Danjoh, Y.
Nakamura, and Y. Obata, the Rikken Bio-Resource Center of Japan for
their expertise in preserving peripheral blood lymphocytes collected in
our field studies and in establishing B cell lines for future studies on
human genome diversity and genome-wide scans of disease-susceptible
genes. The present investigation was supported by the Monbusho
International Collaborative Study of Cancer Research and by
Grants-in-Aid from the Ministry of Science, Education, Sports and
Technology of Japan.
NR 79
TC 31
Z9 34
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1347-9032
J9 CANCER SCI
JI Cancer Sci.
PD FEB
PY 2011
VL 102
IS 2
BP 295
EP 301
DI 10.1111/j.1349-7006.2010.01820.x
PG 7
WC Oncology
SC Oncology
GA 711PQ
UT WOS:000286604300001
PM 21205073
ER
PT J
AU Holleley, CE
Nichols, RA
Whitehead, MR
Gunn, MR
Gupta, J
Sherwin, WB
AF Holleley, Clare E.
Nichols, Richard A.
Whitehead, Michael R.
Gunn, Melissa R.
Gupta, Jyoutsna
Sherwin, William B.
TI Induced dispersal in wildlife management: experimental evaluation of the
risk of hybrid breakdown and the benefit of hybrid vigor in the F1
generation
SO CONSERVATION GENETICS
LA English
DT Article
DE Hybrid vigor; Hybrid breakdown; Inbreeding depression; Drosophila
melanogaster; Conservation; Management; Genetic drift
ID CAPTIVE DROSOPHILA POPULATIONS; OUTBREEDING DEPRESSION; INBRED
POPULATIONS; MODELING PROBLEMS; COLLARED LIZARDS; MISSOURI OZARKS;
MELANOGASTER; HETEROSIS; CONSERVATION; DYSGENESIS
AB Management practices often aim to increase the level of gene flow by either: introducing animals from captive breeding programs, translocating animals from abundant areas, or increasing the chance of animals dispersing between populations by creating habitat corridors. These practices provide opportunity for the hybrid offspring of introduced and resident animals to experience either increased fitness (hybrid vigor) or decreased fitness (hybrid breakdown). There is very little quantitative data available to adequately assess whether hybridization is likely to be beneficial or detrimental to populations managed in these ways. Using Drosophila melanogaster populations, we conducted two experiments that simulate the common management practices of translocation and wildlife habitat corridors. We monitored the frequency and magnitude of hybrid vigor and hybrid breakdown in F1 hybrids to assess the relative risks and benefits to populations and also monitored net productivity (number of adults produced from controlled crosses) to assess whether the populations were stable or in decline. In the translocation experiment, we observed instances of both significant hybrid vigor and hybrid breakdown, both occurring at a frequency of 9%. In the habitat corridor experiments, populations with moderate to high dispersal (1-4% per generation) did not develop significant hybrid vigor or hybrid breakdown. However, of the populations experiencing low dispersal (0.25% per generation) for 34 generations, 6% displayed significant hybrid vigor and 6% displayed significant hybrid breakdown. These results suggest that in first generation hybrids there may be limited opportunity to utilize hybrid vigor as a tool to increase the short-term viability of populations because there is an equal likelihood of encountering hybrid breakdown that may drive the population into further decline. However, our results apply only to populations of moderate size (N = 50; N (e) = 14.3) in the absence of deliberate consanguineous mating. Lastly, we observed that net productivity was positively correlated with dispersal rate, suggesting that initial F1 declines in fitness may be temporary and that it is preferable to maintain high levels of selectable variation via induced dispersal to assist the long-term survival of vulnerable populations.
C1 [Holleley, Clare E.] NCI, Lab Genom Divers, Frederick, MD 21702 USA.
[Holleley, Clare E.; Whitehead, Michael R.; Gunn, Melissa R.; Gupta, Jyoutsna; Sherwin, William B.] Univ New S Wales, Evolut & Ecol Res Ctr, Sydney, NSW 2052, Australia.
[Holleley, Clare E.; Whitehead, Michael R.; Gunn, Melissa R.; Gupta, Jyoutsna; Sherwin, William B.] Univ New S Wales, Sch Biol Earth & Environm Sci, Sydney, NSW 2052, Australia.
[Nichols, Richard A.] Queen Mary Univ London, Sch Biol & Chem Sci, London E1 4NS, England.
[Whitehead, Michael R.] Australian Natl Univ, Sch Biol Sci, Canberra, ACT 0200, Australia.
[Gunn, Melissa R.] Food & Environm Res Agcy, York Y041 1LZ, N Yorkshire, England.
RP Holleley, CE (reprint author), NCI, Lab Genom Divers, Frederick, MD 21702 USA.
EM holleleyce@mail.nih.gov
RI Holleley, Clare/C-4629-2011; Sherwin, William B/C-3432-2008;
OI Holleley, Clare/0000-0002-5257-0019; Sherwin, William
B/0000-0002-1578-8473; Whitehead, Michael/0000-0002-9038-5746; Nichols,
Richard Alan/0000-0002-4801-9312
FU Australian Research Council [DP0559363]
FX We acknowledge L. Tsai, E. Ho and J. Chao for fly culture assistance; O.
E. Gaggiotti, A. R. Templeton, J. L. Wang and M. Mariette for comments
on the manuscript and the Ramaciotti Centre for Gene Function Analysis
for DNA fragment size analysis. This research was supported by
Australian Research Council Grant DP0559363 to WBS and RAN.
NR 57
TC 4
Z9 4
U1 1
U2 24
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1566-0621
EI 1572-9737
J9 CONSERV GENET
JI Conserv. Genet.
PD FEB
PY 2011
VL 12
IS 1
BP 31
EP 40
DI 10.1007/s10592-009-9984-z
PG 10
WC Biodiversity Conservation; Genetics & Heredity
SC Biodiversity & Conservation; Genetics & Heredity
GA 703IP
UT WOS:000285971900003
ER
PT J
AU Okuno, T
Hooper, LC
Ursea, R
Smith, J
Nussenblatt, R
Hooks, JJ
Hayashi, K
AF Okuno, Toshiomi
Hooper, Laura C.
Ursea, Roxana
Smith, Janine
Nussenblatt, Robert
Hooks, John J.
Hayashi, Kozaburo
TI Role of Human Herpes Virus 6 in Corneal Inflammation Alone or With Human
Herpesviruses
SO CORNEA
LA English
DT Article
DE human herpesvirus 6; herpes simplex virus; varicella zoster virus;
cornea; inflammation; polymerase chain reaction
ID HUMAN-HERPESVIRUS-6 INFECTION; EXANTHEM-SUBITUM; HHV-6; SUPPRESSION;
HIV-1
AB Purpose: The purpose of this study was to determine the association of human herpes virus 6 (HHV-6) and/or other human herpesviruses in corneal inflammation using polymerase chain reaction (PCR).
Methods: We collected tear films, conjunctival smears, and a corneal button of inflamed cornea, and the presence of HHV-6 and other herpesviruses in these samples were assessed by a nested PCR.
Results: In tear films collected from 3 of 9 patients with dendritic keratitis, HHV-6 DNA was positive twice, together with herpes simplex virus (HSV) or varicella zoster virus DNA most often, during the acute phase of the disease. Two other patients in this group were either positive for HSV-1 and varicella zoster virus or for HSV-1 and Epstein-Barr virus DNA but negative for HHV-6. When another 12 patients' smear samples from corneal ulcer or keratouveitis were examined, 9 were positive for HHV-6 DNA. Of these, 4 were positive for HSV-1 simultaneously, whereas the remaining 5 patients were negative for HSV-1. One patient's smear was positive for HSV-1 but not for HHV-6. In the corneal button, both HSV and HHV-6 DNAs were positive by nested PCR. HHV-6 was also positive by nested PCR in the conjunctival swab obtained from the contralateral inflamed eye of the patient.
Conclusions: In 22 patients with corneal inflammation, HHV-6 was positive in 14 of 22 patients and HSV-1 was found in 9 of those patients. These data indicated that the association of HHV-6 with disease was more frequent than with other herpesviruses and that HHV-6 may be another sole causative agent for corneal inflammation.
C1 [Okuno, Toshiomi] Hyogo Coll Med, Dept Microbiol, Nishinomiya, Hyogo 6638501, Japan.
[Hooper, Laura C.; Nussenblatt, Robert; Hooks, John J.; Hayashi, Kozaburo] Res Inst, Immunol Lab, Lucknow 226001, Uttar Pradesh, India.
[Ursea, Roxana; Smith, Janine; Nussenblatt, Robert] NEI, Ophthalmol Clin, NIH, Bethesda, MD 20892 USA.
RP Okuno, T (reprint author), Hyogo Coll Med, Dept Microbiol, 1-1 Mukogawa Cho, Nishinomiya, Hyogo 6638501, Japan.
EM tmokuno@hyo-med.ac.jp
FU National Eye Institute, National Institutes of Health
FX Supported (in part) by the Intramural Research Program of the National
Eye Institute, National Institutes of Health.
NR 19
TC 7
Z9 9
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0277-3740
J9 CORNEA
JI Cornea
PD FEB
PY 2011
VL 30
IS 2
BP 204
EP 207
DI 10.1097/ICO.0b013e3181e2e9be
PG 4
WC Ophthalmology
SC Ophthalmology
GA 702SD
UT WOS:000285914700019
PM 20847652
ER
PT J
AU Simon, SL
Bouville, A
Beck, HL
Ibrahim, S
AF Simon, Steven L.
Bouville, Andre
Beck, Harold L.
Ibrahim, Shawki
TI 1997 THYROID ABSORBED DOSE ESTIMATES FOR THE NORTHERN MARSHALL ISLANDS
RESPONSE
SO HEALTH PHYSICS
LA English
DT Letter
ID NUCLEAR-WEAPONS TESTS; FALLOUT; BIKINI
C1 [Simon, Steven L.; Bouville, Andre] NCI, Bethesda, MD 20892 USA.
[Ibrahim, Shawki] Colorado State Univ, Ft Collins, CO 80523 USA.
RP Simon, SL (reprint author), NCI, Bethesda, MD 20892 USA.
NR 4
TC 0
Z9 0
U1 1
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0017-9078
EI 1538-5159
J9 HEALTH PHYS
JI Health Phys.
PD FEB
PY 2011
VL 100
IS 2
BP 229
EP 230
DI 10.1097/HP.0b013e3181f8c6a5
PG 2
WC Environmental Sciences; Public, Environmental & Occupational Health;
Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical
Imaging
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA 700BR
UT WOS:000285707600014
ER
PT J
AU Devaney, JM
Gordish-Dressman, H
Harmon, BT
Bradbury, MK
Devaney, SA
Harris, TB
Thompson, PD
Clarkson, PM
Price, TB
Angelopoulos, TJ
Gordon, PM
Moyna, NM
Pescatello, LS
Visich, PS
Zoeller, RF
Seip, RL
Seo, J
Kim, BH
Tosi, LL
Garcia, M
Li, RL
Zmuda, JM
Delmonico, MJ
Lindsay, RS
Howard, BV
Kraus, WE
Hoffman, EP
AF Devaney, Joseph M.
Gordish-Dressman, Heather
Harmon, Brennan T.
Bradbury, Margaret K.
Devaney, Stephanie A.
Harris, Tamara B.
Thompson, Paul D.
Clarkson, Priscilla M.
Price, Thomas B.
Angelopoulos, Theodore J.
Gordon, Paul M.
Moyna, Niall M.
Pescatello, Linda S.
Visich, Paul S.
Zoeller, Robert F.
Seip, Richard L.
Seo, Jinwook
Kim, Bo Hyoung
Tosi, Laura L.
Garcia, Melissa
Li, Rongling
Zmuda, Joseph M.
Delmonico, Matthew J.
Lindsay, Robert S.
Howard, Barbara V.
Kraus, William E.
Hoffman, Eric P.
TI AKT1 polymorphisms are associated with risk for metabolic syndrome
SO HUMAN GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; INSULIN-SECRETION; AMERICAN-INDIANS; DENATURING
HPLC; GLUCOSE-LEVELS; EMERGING ROLE; MUSCLE MASS; PROTEIN; LOCI;
SUSCEPTIBILITY
AB Converging lines of evidence suggest that AKT1 is a major mediator of the responses to insulin, insulin-like growth factor 1 (IGF1), and glucose. AKT1 also plays a key role in the regulation of both muscle cell hypertrophy and atrophy. We hypothesized that AKT1 variants may play a role in the endophenotypes that make up metabolic syndrome. We studied a 12-kb region including the first exon of the AKT1 gene for association with metabolic syndrome-related phenotypes in four study populations [FAMUSS cohort (n = 574; age 23.7 +/- A 5.7 years), Strong Heart Study (SHS) (n = 2,134; age 55.5 +/- A 7.9 years), Dynamics of Health, Aging and Body Composition (Health ABC) (n = 3,075; age 73.6 +/- A 2.9 years), and Studies of a Targeted Risk Reduction Intervention through Defined Exercise (STRRIDE) (n = 175; age 40-65 years)]. We identified a three SNP haplotype that we call H1, which represents the ancestral alleles at the three loci and H2, which represents the derived alleles at the three loci. In young adult European Americans (FAMUSS), H1 was associated with higher fasting glucose levels in females. In middle age Native Americans (SHS), H1 carriers showed higher fasting insulin and HOMA in males, and higher BMI in females. In older African-American and European American subjects (Health ABC) H1 carriers showed a higher incidence of metabolic syndrome. Homozygotes for the H1 haplotype showed about twice the risk of metabolic syndrome in both males and females (p < 0.001). In middle-aged European Americans with insulin resistance (STRRIDE) studied by intravenous glucose tolerance test (IVGTT), H1 carriers showed increased insulin resistance due to the Sg component (p = 0.021). The 12-kb haplotype is a risk factor for metabolic syndrome and insulin resistance that needs to be explored in further populations.
C1 [Devaney, Joseph M.; Gordish-Dressman, Heather; Harmon, Brennan T.; Bradbury, Margaret K.; Devaney, Stephanie A.; Seo, Jinwook; Hoffman, Eric P.] Childrens Natl Med Ctr, Med Genet Res Ctr, Dept Integrat Syst Biol, Washington, DC 20010 USA.
[Harris, Tamara B.; Garcia, Melissa] NIA, NIH, Bethesda, MD 20892 USA.
[Thompson, Paul D.; Price, Thomas B.; Seip, Richard L.] Hartford Hosp, Henry Low Heart Ctr, Div Cardiol, Hartford, CT 06102 USA.
[Clarkson, Priscilla M.] Univ Massachusetts, Dept Kinesiol, Amherst, MA 01003 USA.
[Price, Thomas B.] Yale Univ, Sch Med, Dept Diagnost Radiol, New Haven, CT 06520 USA.
[Angelopoulos, Theodore J.] Univ Cent Florida, Dept Hlth Profess, Ctr Lifestyle Med, Orlando, FL 32816 USA.
[Gordon, Paul M.] Univ Michigan, Lab Phys Act & Exercise Intervent Res, Ann Arbor, MI 48108 USA.
[Moyna, Niall M.] Dublin City Univ, Dept Sport Sci & Hlth, Dublin 9, Ireland.
[Pescatello, Linda S.] Univ Connecticut, Sch Allied Hlth, Storrs, CT 06269 USA.
[Visich, Paul S.] Cent Michigan Univ, Human Performance Lab, Mt Pleasant, MI 48859 USA.
[Zoeller, Robert F.] Florida Atlantic Univ, Dept Exercise Sci & Hlth Promot, Davie, FL 33314 USA.
[Kim, Bo Hyoung] INFINITT Technol, Seoul, South Korea.
[Tosi, Laura L.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Li, Rongling] Univ Tennessee, Dept Prevent Med, Memphis, TN USA.
[Zmuda, Joseph M.] Univ Pittsburgh, Dept Epidemiol & Human Genet, Pittsburgh, PA 15261 USA.
[Delmonico, Matthew J.] Univ Rhode Isl, Dept Kinesiol, Kingston, RI 02881 USA.
[Lindsay, Robert S.] Univ Glasgow, Fac Med, Glasgow, Lanark, Scotland.
[Howard, Barbara V.] MedStar Res Inst, Hyattsville, MD 20783 USA.
[Kraus, William E.] Duke Univ, Med Ctr, Duke Ctr Living, Durham, NC 27710 USA.
RP Hoffman, EP (reprint author), Childrens Natl Med Ctr, Med Genet Res Ctr, Dept Integrat Syst Biol, 111 Michigan Ave NW, Washington, DC 20010 USA.
EM ehoffman@cnmcresearch.org
RI gordon, paul/E-3862-2015
OI Kraus, William E/0000-0003-1930-9684; gordon, paul/0000-0003-4403-0888
FU NHLBI NIH HHS [U01 HL066614-04, U01 HL066614]; NIAMS NIH HHS [R01
AR055100, R01 AR055100-08]; NICHD NIH HHS [R24 HD050846, R24
HD050846-06]
NR 40
TC 12
Z9 13
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
J9 HUM GENET
JI Hum. Genet.
PD FEB
PY 2011
VL 129
IS 2
BP 129
EP 139
DI 10.1007/s00439-010-0910-8
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 706CJ
UT WOS:000286194000002
PM 21061022
ER
PT J
AU Yahiro, K
Satoh, M
Morinaga, N
Tsutsuki, H
Ogura, K
Nagasawa, S
Nomura, F
Moss, J
Noda, M
AF Yahiro, Kinnosuke
Satoh, Mamoru
Morinaga, Naoko
Tsutsuki, Hiroyasu
Ogura, Kohei
Nagasawa, Sayaka
Nomura, Fumio
Moss, Joel
Noda, Masatoshi
TI Identification of Subtilase Cytotoxin (SubAB) Receptors Whose Signaling,
in Association with SubAB-Induced BiP Cleavage, Is Responsible for
Apoptosis in HeLa Cells
SO INFECTION AND IMMUNITY
LA English
DT Article
ID FOCAL ADHESION KINASE; ENDOPLASMIC-RETICULUM STRESS; UNFOLDED PROTEIN
RESPONSE; TOXIGENIC ESCHERICHIA-COLI; ANCHORAGE-DEPENDENT APOPTOSIS;
INTESTINAL EPITHELIAL-CELLS; BREAST-CARCINOMA CELLS; NG2 PROTEOGLYCAN;
DOWN-REGULATION; CHAPERONE BIP
AB Subtilase cytotoxin (SubAB), which is produced by certain strains of Shiga-toxigenic Escherichia coli (STEC), causes the 78-kDa glucose-regulated protein (GRP78/BiP) cleavage, followed by induction of endoplasmic reticulum (ER) stress, leading to caspase-dependent apoptosis via mitochondrial membrane damage by Bax/Bak activation. The purpose of the present study was to identify SubAB receptors responsible for HeLa cell death. Four proteins, NG2, alpha 2 beta 1 integrin (ITG), L1 cell adhesion molecule (L1CAM), and hepatocyte growth factor receptor (Met), were identified to be SubAB-binding proteins by immunoprecipitation and purification, followed by liquid chromatography-tandem mass spectrometry analysis. SubAB-induced Bax conformational change, Bax/Bak complex formation, caspase activation, and cell death were decreased in beta 1 ITG, NG2, and L1CAM small interfering RNA-transfected cells, but unexpectedly, BiP cleavage was still observed. Pretreatment of cells with a function-blocking beta 1 ITG antibody (monoclonal antibody [MAb] P5D2) enhanced SubAB-induced caspase activation; MAb P5D2 alone had no effect on caspase activation. Furthermore, we found that SubAB induced focal adhesion kinase fragmentation, which was mediated by a proteasome-dependent pathway, and caspase activation was suppressed in the presence of proteasome inhibitor. Thus, beta 1 ITG serves as a SubAB-binding protein and may interact with SubAB-signaling pathways, leading to cell death. Our results raise the possibility that although BiP cleavage is necessary for SubAB-induced apoptotic cell death, signaling pathways associated with functional SubAB receptors may be required for activation of SubAB-dependent apoptotic pathways.
C1 [Yahiro, Kinnosuke] Chiba Univ, Grad Sch Med, Dept Mol Infectiol, Chuo Ku, Chiba 2608670, Japan.
[Satoh, Mamoru; Nomura, Fumio] Chiba Univ, Grad Sch Med, Dept Mol Diag, Chiba 2608670, Japan.
[Nagasawa, Sayaka] Chiba Univ, Grad Sch Med, Dept Legal Med, Chiba 2608670, Japan.
[Moss, Joel] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Yahiro, K (reprint author), Chiba Univ, Grad Sch Med, Dept Mol Infectiol, Chuo Ku, 1-8-1 Inohana, Chiba 2608670, Japan.
EM yahirok@faculty.chiba-u.jp
FU Ministry of Education, Science, and Culture of Japan; Japan Science and
Technology Agency; National Heart, Lung, and Blood Institute, National
Institutes of Health
FX This work was supported by grants in aid for Scientific Research from
the Ministry of Education, Science, and Culture of Japan and Improvement
of Research Environment for Young Researchers from the Japan Science and
Technology Agency. Joel Moss was supported by the Intramural Research
Program, National Heart, Lung, and Blood Institute, National Institutes
of Health.
NR 79
TC 13
Z9 13
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD FEB
PY 2011
VL 79
IS 2
BP 617
EP 627
DI 10.1128/IAI.01020-10
PG 11
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 709SP
UT WOS:000286462000007
PM 21098100
ER
PT J
AU Brett, PJ
Burtnick, MN
Heiss, C
Azadi, P
DeShazer, D
Woods, DE
Gherardini, FC
AF Brett, Paul J.
Burtnick, Mary N.
Heiss, Christian
Azadi, Parastoo
DeShazer, David
Woods, Donald E.
Gherardini, Frank C.
TI Burkholderia thailandensis oacA Mutants Facilitate the Expression of
Burkholderia mallei-Like O Polysaccharides
SO INFECTION AND IMMUNITY
LA English
DT Article
ID VIRULENCE DETERMINANT; MURINE MACROPHAGES; PSEUDOMALLEI;
LIPOPOLYSACCHARIDE; ACETYLATION; GLANDERS; ANTIGEN; IDENTIFICATION;
MELIOIDOSIS; STRATEGIES
AB Previous studies have shown that the O polysaccharides (OPS) expressed by Burkholderia mallei are similar to those produced by Burkholderia thailandensis except that they lack the 4-O-acetyl modifications on their 6-deoxy-alpha-L-talopyranosyl residues. In the present study, we describe the identification and characterization of an open reading frame, designated oacA, expressed by B. thailandensis that accounts for this phenomenon. Utilizing the B. thailandensis and B. mallei lipopolysaccharide (LPS)-specific monoclonal antibodies Pp-PS-W and 3D11, Western immunoblot analyses demonstrated that the LPS antigens expressed by the oacA mutant, B. thailandensis ZT0715, were antigenically similar to those produced by B. mallei ATCC 23344. In addition, immunoblot analyses demonstrated that when B. mallei ATCC 23344 was complemented in trans with oacA, it synthesized B. thailandensis-like LPS antigens. To elucidate the structure of the OPS moieties expressed by ZT0715, purified samples were analyzed via nuclear magnetic resonance spectroscopy. As predicted, these studies demonstrated that the loss of OacA activity influenced the O acetylation phenotype of the OPS moieties. Unexpectedly, however, the results indicated that the O methylation status of the OPS antigens was also affected by the loss of OacA activity. Nonetheless, it was revealed that the LPS moieties expressed by the oacA mutant reacted strongly with the B. mallei LPS-specific protective monoclonal antibody 9C1-2. Based on these findings, it appears that OacA is required for the 4-O acetylation and 2-O methylation of B. thailandensis OPS antigens and that ZT0715 may provide a safe and cost-effective source of B. mallei-like OPS to facilitate the synthesis of glanders subunit vaccine candidates.
C1 [Brett, Paul J.; Burtnick, Mary N.] Univ S Alabama, Dept Microbiol & Immunol, Mobile, AL 36688 USA.
[Heiss, Christian; Azadi, Parastoo] Univ Georgia, Complex Carbohydrate Res Ctr, Athens, GA 30602 USA.
[DeShazer, David] USA, Med Res Inst Infect Dis, Bacteriol Div, Ft Detrick, MD 21702 USA.
[Woods, Donald E.] Univ Calgary, Hlth Sci Ctr, Dept Microbiol & Infect Dis, Calgary, AB T2N 4N1, Canada.
[Gherardini, Frank C.] NIAID, Lab Zoonot Pathogens, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Brett, PJ (reprint author), Univ S Alabama, Dept Microbiol & Immunol, 5851 USA Dr N, Mobile, AL 36688 USA.
EM pbrett@jaguar1.usouthal.edu
FU NIH, National Institute of Allergy and Infectious Diseases; Department
of Energy [DE-FG09-93ER-20097]; University of South Alabama
FX This research was supported in part by the Intramural Research Program
of the NIH, National Institute of Allergy and Infectious Diseases, the
Department of Energy-funded (DE-FG09-93ER-20097) Center for Plant and
Microbial Complex Carbohydrates, and lab start-up funds from the
University of South Alabama.
NR 43
TC 12
Z9 12
U1 0
U2 8
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
J9 INFECT IMMUN
JI Infect. Immun.
PD FEB
PY 2011
VL 79
IS 2
BP 961
EP 969
DI 10.1128/IAI.01023-10
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 709SP
UT WOS:000286462000043
PM 21115721
ER
PT J
AU Beachler, DC
Gellert, LL
Jacobson, LP
Ambinder, RF
Breen, EC
Martinez-Maza, O
Rabkin, CC
Kaslow, RA
D'Souza, G
AF Beachler, Daniel C.
Gellert, Lan L.
Jacobson, Lisa P.
Ambinder, Richard F.
Breen, Elizabeth C.
Martinez-Maza, Otoniel
Rabkin, Charles C.
Kaslow, Richard A.
D'Souza, Gypsyamber
TI Kaposi Sarcoma-Associated Herpesvirus Serum DNA and Antibodies Not
Associated With Subsequent Non-Hodgkin Lymphoma Risk
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Article
DE Kaposi sarcoma-associated herpesvirus; non-Hodgkin lymphoma; MACS; human
herpesvirus 8; DNA; AIDS cancer
ID MULTICENTER AIDS COHORT; HUMAN-HERPESVIRUS-8 INFECTION; HIV; VIRUS;
PARTICIPANTS; CANCER; ADULTS
AB Kaposi sarcoma-associated herpes virus (KSHV) infects B-cells and is found in non-Hodgkin lymphoma (NHL) B-cell tumors and could therefore contribute to the occurrence of NHL. We performed a nested case-control study including 155 incident NHL cases and matched noncancer controls. Pre-NHL serum was tested for KSHV DNA and antibodies. Serum KSHV DNA was more common in cases than controls (14% versus 6%, P = 0.03), but after adjustment, the difference was not significant. Epstein-Barr virus serum DNA was similarly unassociated with NHL as were KSHV antibodies. KSHV is not a primary cause of NHL in HIV-infected men who have sex with men.
C1 [Beachler, Daniel C.; Gellert, Lan L.; Jacobson, Lisa P.; D'Souza, Gypsyamber] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Gellert, Lan L.] Mem Sloan Kettering Canc Ctr, Dept Pathol, New York, NY 10021 USA.
[Ambinder, Richard F.] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD USA.
[Breen, Elizabeth C.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Behav Sci, Los Angeles, CA 90095 USA.
[Martinez-Maza, Otoniel] Univ Calif Los Angeles, David Geffen Sch Med, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA 90095 USA.
[Martinez-Maza, Otoniel] Univ Calif Los Angeles, David Geffen Sch Med, Dept Obstet & Gynaecol, Los Angeles, CA 90095 USA.
[Rabkin, Charles C.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Kaslow, Richard A.] Univ Alabama, Dept Epidemiol, Birmingham, AL 35294 USA.
RP D'Souza, G (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, 615 N Wolfe St,Room E6132, Baltimore, MD 21205 USA.
EM gdsouza@jhsph.edu
RI Martinez-Maza, Otoniel/B-2667-2009;
OI Martinez-Maza, Otoniel/0000-0003-1364-0675; Beachler, Daniel
/0000-0003-2788-3061
FU National Institute of Allergy and Infectious Diseases [U01-AI-35043,
1P50 CA96888]; National Cancer Institute [P50 CA96888, UO1-AI-35042,
5-MO1-RR-00052 (GCRC), UO1-AI-35043, UO1-AI-35039, UO1-AI-35040,
UO1-AI-35041]
FX This study was supported by funding from the National Institute of
Allergy and Infectious Diseases (U01-AI-35043, Principal Investigator L.
Jacobson) and (1P50 CA96888, Principal Investigator R. Amibinder).; Data
in this article were collected by the Multicenter AIDS Cohort Study
(MACS) with centers (Principal Investigators) at The Johns Hopkins
Bloomberg School of Public Health (Joseph B. Margolick, Lisa P.
Jacobson), Howard Brown Health Center, Feinberg School of Medicine,
Northwestern University and Cook County Bureau of Health Services (John
P. Phair, Steven M. Wolinsky), University of California, Los Angeles
(Roger Detels, Otoniel Martinez-Maza), and University of Pittsburgh
(Charles R. Rinaldo). The MACS is funded by the National Institute of
Allergy and Infectious Diseases with additional supplemental funding
from the National Cancer Institute P50 CA96888, UO1-AI-35042,
5-MO1-RR-00052 (GCRC), UO1-AI-35043, UO1-AI-35039, UO1-AI-35040,
UO1-AI-35041. Web site located at
http://www.statepi.jhsph.edu/macs/macs.html.
NR 24
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1525-4135
J9 JAIDS-J ACQ IMM DEF
JI JAIDS
PD FEB 1
PY 2011
VL 56
IS 2
BP 188
EP 192
DI 10.1097/QAI.0b013e3181ff976b
PG 5
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 714KE
UT WOS:000286807700020
PM 21116187
ER
PT J
AU Combs, CA
Smirnov, A
Chess, D
McGavern, DB
Schroeder, JL
Riley, J
Kang, SS
Lugar-Hammer, M
Gandjbakhche, A
Knutson, JR
Balaban, RS
AF Combs, C. A.
Smirnov, A.
Chess, D.
McGavern, D. B.
Schroeder, J. L.
Riley, J.
Kang, S. S.
Lugar-Hammer, M.
Gandjbakhche, A.
Knutson, J. R.
Balaban, R. S.
TI Optimizing multiphoton fluorescence microscopy light collection from
living tissue by noncontact total emission detection (epiTED)
SO JOURNAL OF MICROSCOPY
LA English
DT Article
DE Brain; epi-detection; imaging; kidney; light collection improvement;
muscle; photon diffusion simulations; scattering; two-photon microscopy
ID 2-PHOTON EXCITATION MICROSCOPY; NONLINEAR MICROSCOPY; IN-VIVO; INJURY
AB P>A benefit of multiphoton fluorescence microscopy is the inherent optical sectioning that occurs during excitation at the diffraction-limited spot. The scanned collection of fluorescence emission is incoherent; that is, no real image needs to be formed on the detector plane. The nearly isotropic emission of fluorescence excited at the focal spot allows for new detection schemes that efficiently funnel all attainable photons to detector(s). We previously showed [Combs, C.A., et al. (2007) Optimization of multiphoton excitation microscopy by total emission detection using a parabolic light reflector. J. Microsc. 228, 330-337] that parabolic mirrors and condensers could be combined to collect the totality of solid angle around the excitation spot for tissue blocks, leading to similar to 8-fold signal gain. Using a similar approach, we have developed an in vivo total emission detection (epiTED) instrument modified to make noncontact images from outside of living tissue. Simulations suggest that a similar to 4-fold enhancement may be possible (much larger with lower NA objectives than the 0.95 NA used here) with this approach, depending on objective characteristics, imaging depth and the characteristics of the sample being imaged. In our initial prototype, 2-fold improvements were demonstrated in the mouse brain and skeletal muscle as well as the rat kidney, using a variety of fluorophores and no compromise of spatial resolution. These results show this epiTED prototype effectively doubles emission signal in vivo; thus, it will maintain the image signal-to-noise ratio at two times the scan rate or enable full scan rate at approximately 30% reduced laser power (to minimize photo-damage).
C1 [Combs, C. A.] NHLBI, Light Microscopy Facil, NIH, Bethesda, MD 20892 USA.
[Smirnov, A.; Knutson, J. R.] NHLBI, Lab Mol Biophys, NIH, Bethesda, MD 20892 USA.
[Chess, D.; Schroeder, J. L.; Lugar-Hammer, M.; Balaban, R. S.] NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA.
[McGavern, D. B.; Kang, S. S.] NINDS, Viral Immunol & Intravital Imaging Unit, NIH, Bethesda, MD 20892 USA.
[Riley, J.; Gandjbakhche, A.] NICHD, Program Pediat Imaging & Tissue Sci PPITS, Sect Analyt & Funct Biophoton SAFB, NIH, Bethesda, MD USA.
RP Combs, CA (reprint author), 9000 Rockville Pike,10-6N-309, Bethesda, MD 20892 USA.
EM combsc@nih.gov
OI McGavern, Dorian/0000-0001-9568-545X
FU Intramural NIH HHS [ZIC HL006019-01]
NR 22
TC 15
Z9 15
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-2720
J9 J MICROSC-OXFORD
JI J. Microsc..
PD FEB
PY 2011
VL 241
IS 2
BP 153
EP 161
DI 10.1111/j.1365-2818.2010.03411.x
PG 9
WC Microscopy
SC Microscopy
GA 705EA
UT WOS:000286110500006
PM 21118209
ER
PT J
AU Heiss, BL
Maximova, OA
Pletnev, AG
AF Heiss, Brian L.
Maximova, Olga A.
Pletnev, Alexander G.
TI Insertion of MicroRNA Targets into the Flavivirus Genome Alters Its
Highly Neurovirulent Phenotype
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TICK-BORNE ENCEPHALITIS; ATTENUATED VIRUS-VACCINES; DENGUE TYPE-4
VIRUSES; NEURONAL DIFFERENTIATION; EXPRESSION; BRAIN; RNA; DETERMINANTS;
MUTATIONS; MONKEYS
AB Flaviviruses such as West Nile, Japanese encephalitis, and tick-borne encephalitis (TBEV) viruses are important neurotropic human pathogens, causing a devastating and often fatal neuroinfection. Here, we demonstrate that incorporation into the viral genome of a target sequence for cellular microRNAs expressed in the central nervous system (CNS) enables alteration of the neurovirulence of the virus and control of the neuropathogenesis of flavivirus infection. As a model virus for this type of modification, we used a neurovirulent chimeric tick-borne encephalitis/dengue virus (TBEV/DEN4) that contained the structural protein genes of a highly pathogenic TBEV. The inclusion of just a single target copy for a brain tissue-expressed mir-9, mir-124a, mir-128a, mir-218, or let-7c microRNA into the TBEV/DEN4 genome was sufficient to prevent the development of otherwise lethal encephalitis in mice infected intracerebrally with a large dose of virus. Viruses bearing a complementary target for mir-9 or mir-124a were highly restricted in replication in primary neuronal cells, had limited access into the CNS of immunodeficient mice, and retained the ability to induce a strong humoral immune response in monkeys. This work suggests that microRNA targeting to control flavivirus tissue tropism and pathogenesis might represent a rational approach for virus attenuation and vaccine development.
C1 [Heiss, Brian L.; Maximova, Olga A.; Pletnev, Alexander G.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Pletnev, AG (reprint author), NIAID, Infect Dis Lab, NIH, Bldg 33,Room 3W10A,33 North Dr,MSC 3203, Bethesda, MD 20892 USA.
EM apletnev@niaid.nih.gov
FU Division of Intramural Research Program of the National Institute of
Allergy and Infectious Diseases, National Institutes of Health
FX This work was supported by the Division of Intramural Research Program
of the National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 41
TC 26
Z9 29
U1 2
U2 10
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD FEB
PY 2011
VL 85
IS 4
BP 1464
EP 1472
DI 10.1128/JVI.02091-10
PG 9
WC Virology
SC Virology
GA 709EP
UT WOS:000286420900005
PM 21123372
ER
PT J
AU Jones, CP
Datta, SAK
Rein, A
Rouzina, I
Musier-Forsyth, K
AF Jones, Christopher P.
Datta, Siddhartha A. K.
Rein, Alan
Rouzina, Ioulia
Musier-Forsyth, Karin
TI Matrix Domain Modulates HIV-1 Gag's Nucleic Acid Chaperone Activity via
Inositol Phosphate Binding
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; RETROVIRAL NUCLEOCAPSID PROTEINS;
TRANSFER-RNA SYNTHETASE; IN-VITRO; GENOMIC RNA; REVERSE TRANSCRIPTION;
PLASMA-MEMBRANE; CONFORMATIONAL-CHANGES; STRAND TRANSFER; LEUKEMIA-VIRUS
AB Retroviruses replicate by reverse transcribing their single-stranded RNA genomes into double-stranded DNA using specific cellular tRNAs to prime cDNA synthesis. In HIV-1, human tRNA3 Lys serves as the primer and is packaged into virions during assembly. The viral Gag protein is believed to chaperone tRNA3 Lys placement onto the genomic RNA primer binding site; however, the timing and possible regulation of this event are currently unknown. Composed of the matrix (MA), capsid (CA), nucleocapsid (NC), and p6 domains, the multifunctional HIV-1 Gag polyprotein orchestrates the highly coordinated process of virion assembly, but the contribution of these domains to tRNA3 Lys annealing is unclear. Here, we show that NC is absolutely essential for annealing and that the MA domain inhibits Gag's tRNA annealing capability. During assembly, MA specifically interacts with inositol phosphate (IP)-containing lipids in the plasma membrane (PM). Surprisingly, we find that IPs stimulate Gag-facilitated tRNA annealing but do not stimulate annealing in Gag variants lacking the MA domain or containing point mutations involved in PM binding. Moreover, we find that IPs prevent MA from binding to nucleic acids but have little effect on NC or Gag. We propose that Gag binds to RNA either with both NC and MA domains or with NC alone and that MA-IP interactions alter Gag's binding mode. We propose that MA's interactions with the PM trigger the switch between these two binding modes and stimulate Gag's chaperone function, which may be important for the regulation of events such as tRNA primer annealing.
C1 [Jones, Christopher P.; Musier-Forsyth, Karin] Ohio State Univ, Dept Chem, Ctr Retroviral Res, Columbus, OH 43210 USA.
[Jones, Christopher P.; Musier-Forsyth, Karin] Ohio State Univ, Dept Biochem, Ctr Retroviral Res, Columbus, OH 43210 USA.
[Jones, Christopher P.; Musier-Forsyth, Karin] Ohio State Univ, Ctr RNA Biol, Columbus, OH 43210 USA.
[Datta, Siddhartha A. K.; Rein, Alan] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[Rouzina, Ioulia] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Minneapolis, MN 55455 USA.
RP Musier-Forsyth, K (reprint author), Ohio State Univ, Dept Chem, Ctr Retroviral Res, 100 W 18th Ave, Columbus, OH 43210 USA.
EM musier@chemistry.ohio-state.edu
OI Datta, Siddhartha/0000-0002-4098-7490
FU NIH, National Cancer Institute, Center for Cancer Research; NIH
[GM065056, T32 GM008512]
FX This work was supported in part by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research, and by
NIH grant GM065056 (to K.M.-F.). C.P.J. was supported by NIH Training
Grant T32 GM008512.
NR 77
TC 37
Z9 38
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD FEB
PY 2011
VL 85
IS 4
BP 1594
EP 1603
DI 10.1128/JVI.01809-10
PG 10
WC Virology
SC Virology
GA 709EP
UT WOS:000286420900017
PM 21123373
ER
PT J
AU Lee, EG
Roy, J
Jackson, D
Clark, P
Boyer, PL
Hughes, SH
Linial, ML
AF Lee, Eun-Gyung
Roy, Jacqueline
Jackson, Dana
Clark, Patrick
Boyer, Paul L.
Hughes, Stephen H.
Linial, Maxine L.
TI Foamy Retrovirus Integrase Contains a Pol Dimerization Domain Required
for Protease Activation
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID BIMOLECULAR FLUORESCENCE COMPLEMENTATION; VIRUS REVERSE-TRANSCRIPTASE;
LIVING CELLS; CRYSTAL-STRUCTURE; HIV-1 PROTEASE; C-TERMINUS; GAG;
VISUALIZATION; POLYPROTEIN; PRECURSOR
AB Unlike orthoretroviruses, foamy retroviruses (FV) synthesize Pol independently of Gag. The FV Pol precursor is cleaved only once between reverse transcriptase (RT) and integrase (IN) by the protease (PR), resulting in a PR-RT and an IN protein. Only the Pol precursor, not the cleaved subunits, is packaged into virions. Like orthoretroviral PRs, FV PR needs to dimerize to be active. Previously, we showed that a Pol mutant lacking IN has defects in PR activity and Pol packaging into virions. We now show that introduction of a leucine zipper (zip) dimerization motif in an IN truncation mutant can restore PR activity, leading to Pol processing in cells. However, these zip mutants neither cleave Gag nor incorporate Pol into virions. We propose that IN is required for Pol dimerization, which is necessary for the creation of a functional PR active site.
C1 [Lee, Eun-Gyung; Roy, Jacqueline; Jackson, Dana; Linial, Maxine L.] Fred Hutchinson Canc Res Ctr, Div Basic Sci, Seattle, WA 98109 USA.
[Clark, Patrick] SAIC Frederick, Basic Sci Program, Frederick, MD 21702 USA.
[Boyer, Paul L.; Hughes, Stephen H.] Natl Canc Res Inst Frederick, HIV Drug Resistance Program, Frederick, MD 21702 USA.
RP Hughes, SH (reprint author), NCI, POB B, Frederick, MD 21783 USA.
EM hughesst@mail.nih.gov
FU NIH [R01 CA 18282]; NIH (National Cancer Institute)
FX This research was supported by NIH grant R01 CA 18282 to M. L. L. and by
the Intramural Research Program of the NIH (National Cancer Institute).
NR 38
TC 8
Z9 8
U1 0
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD FEB
PY 2011
VL 85
IS 4
BP 1655
EP 1661
DI 10.1128/JVI.01873-09
PG 7
WC Virology
SC Virology
GA 709EP
UT WOS:000286420900023
PM 21123385
ER
PT J
AU Goldner, J
Peters, TL
Richards, MH
Pearce, S
AF Goldner, Jonathan
Peters, Tracy L.
Richards, Maryse H.
Pearce, Steven
TI Exposure to Community Violence and Protective and Risky Contexts Among
Low Income Urban African American Adolescents: A Prospective Study
SO JOURNAL OF YOUTH AND ADOLESCENCE
LA English
DT Article
DE Time sampling technique; Exposure to community violence; African
American; Urban low income
ID INNER-CITY; ROUTINE ACTIVITIES; YOUNG ADOLESCENTS; CHILDREN; YOUTH;
RESILIENCE; VICTIMIZATION; NEIGHBORHOODS; INTERVENTION; DELINQUENCY
AB This study examined protective and risky companionship and locations for exposure to community violence among African American young adolescents living in high crime, urban areas. The Experience Sampling Method (ESM), an in vivo data collection method, was employed to gather information from 233 students (62% female) over 3 years, beginning in the 6th grade. Questionnaire variables of exposure to community violence were regressed onto ESM companionship and location variables, cross-sectionally and longitudinally, separately for boys and girls. At different points, time spent with parents, in school, and outside in private space was associated with less exposure to violence for boys and girls, while time spent with girls was protective for boys. In addition, time spent outside in public and with older peers was associated with increased risk for boys and girls. These findings are discussed in relation to previous and potential future research, and to strategies to prevent exposure to community violence.
C1 [Goldner, Jonathan; Peters, Tracy L.; Richards, Maryse H.; Pearce, Steven] Loyola Univ, Dept Psychol, Chicago, IL 60626 USA.
[Peters, Tracy L.] NIMH, Genet Epidemiol Res Branch, Intramural Res Program, Bethesda, MD 20892 USA.
RP Richards, MH (reprint author), Loyola Univ, Dept Psychol, 6525 N Sheridan Rd, Chicago, IL 60626 USA.
EM mrichar@luc.edu
NR 55
TC 5
Z9 5
U1 4
U2 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0047-2891
J9 J YOUTH ADOLESCENCE
JI J. Youth Adolesc.
PD FEB
PY 2011
VL 40
IS 2
BP 174
EP 186
DI 10.1007/s10964-010-9527-4
PG 13
WC Psychology, Developmental
SC Psychology
GA 705FO
UT WOS:000286114500004
PM 20352310
ER
PT J
AU Brown, P
Gipson, C
AF Brown, Patricia
Gipson, Chester
TI A word from OLAW and USDA
SO LAB ANIMAL
LA English
DT Editorial Material
C1 [Brown, Patricia] NIH, OLAW, OER, OD,HHS, Bethesda, MD 20892 USA.
[Gipson, Chester] USDA, APHIS, Washington, DC USA.
RP Brown, P (reprint author), NIH, OLAW, OER, OD,HHS, Bethesda, MD 20892 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0093-7355
J9 LAB ANIMAL
JI Lab Anim.
PD FEB
PY 2011
VL 40
IS 2
BP 36
EP 36
DI 10.1038/laban0211-36a
PG 1
WC Veterinary Sciences
SC Veterinary Sciences
GA 712DX
UT WOS:000286646000008
PM 21252974
ER
PT J
AU Shi, ZM
Yuan, BJ
Zhang, CL
Zhou, MH
Holmboe-Ottesen, G
AF Shi, Zumin
Yuan, Baojun
Zhang, Cuilin
Zhou, Minghao
Holmboe-Ottesen, Gerd
TI Egg consumption and the risk of diabetes in adults, Jiangsu, China
SO NUTRITION
LA English
DT Article
DE Egg consumption; Diabetes; China
ID HEART-DISEASE RISK; PHYSICIANS HEALTH; CHOLESTEROL; METAANALYSIS;
POPULATION; RESPONSES; PLASMA; TYPE-2
AB Background: Although egg consumption has been associated with elevated plasma levels of cholesterol and triglyceride and with risk of cardiovascular disease in some populations, epidemiologic studies on egg consumption and the risk of diabetes are extremely sparse, particularly in the Chinese population.
Method: Data from a household survey in the year 2002 among 2849 adults aged >= 20 y from a nationally representative sample in Jiangsu Province, China, were used. Dietary information was assessed by a validated food frequency questionnaire and 3 d weighed food records. Fasting blood specimens were collected.
Results: After the adjustment for age, total calorie intake, education, smoking, family history of diabetes, and sedentary activity, egg consumption was significantly and positively associated with diabetes risk, particularly in women. The odds ratios (OR) (95% CI) of diabetes associated with egg consumption <2/wk, 2-6/wk, and >= 1/d in the total sample were 1.00, 1.75, 2.28 (1.14-4.54), respectively (P for trend 0.029). Corresponding ORs (95% CI) in women were 1.00, 1.66, and 3.01 (1.12, 8.12), respectively (P for trend 0.022). Additional adjustment of body mass index attenuated the association, but it remained significant. There was a similar, however, not statistically significant association in men. In addition, plasma triglyceride and total cholesterol levels were significantly higher in women who consumed >= 2 eggs/wk than those who consumed eggs less often.
Conclusion: Egg consumption was positively associated with the risk of diabetes among the Chinese, particularly in women. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Shi, Zumin; Yuan, Baojun; Zhou, Minghao] Jiangsu Prov Ctr Dis Control & Prevention, Nanjing, Peoples R China.
[Shi, Zumin; Holmboe-Ottesen, Gerd] Univ Oslo, Dept Gen Practice & Community Med, Inst Hlth & Soc, Oslo, Norway.
[Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD USA.
RP Shi, ZM (reprint author), Jiangsu Prov Ctr Dis Control & Prevention, Nanjing, Peoples R China.
EM zumins@vip.sina.com
RI Shi, Zumin/A-1093-2009
OI Shi, Zumin/0000-0002-3099-3299
FU Jiangsu Provincial Natural Science Foundation [BK2008464]; Jiangsu
Provincial Health Bureau; Eunice Kennedy Shriver National Institute of
Child Health and Human Development, National Institutes of Health
FX The authors thank the participating Regional Centers for Disease Control
and Prevention in Jiangsu Province, including the Nanjing, Xuzhou,
Jiangyin, Taicang, Suining, Jurong, Sihong, and Haimen Centres for their
support for the data collection. This study was financed by Jiangsu
Provincial Natural Science Foundation (BK2008464) and Jiangsu Provincial
Health Bureau. Dr. Cuilin Zhang is supported by the Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development, National Institutes of Health.
NR 21
TC 20
Z9 20
U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0899-9007
J9 NUTRITION
JI Nutrition
PD FEB
PY 2011
VL 27
IS 2
BP 194
EP 198
DI 10.1016/j.nut.2010.01.012
PG 5
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 710UL
UT WOS:000286542400013
PM 20471806
ER
PT J
AU Boyce, JA
Assa'a, A
Burks, AW
Jones, SM
Sampson, HA
Wood, RA
Plaut, M
Cooper, SE
Fenton, MJ
Arshad, SH
Bahna, SL
Beck, LA
Byrd-Bredbenner, C
Camargo, CA
Eichenfield, L
Furuta, GT
Hanifin, JM
Jones, C
Kraft, M
Levy, BD
Lieberman, P
Luccioli, S
McCall, KM
Schneider, LC
Simon, RA
Simons, FER
Teach, SJ
Yawn, BP
Schwaninger, JM
AF Boyce, Joshua A.
Assa'a, Amal
Burks, A. Wesley
Jones, Stacie M.
Sampson, Hugh A.
Wood, Robert A.
Plaut, Marshall
Cooper, Susan E.
Fenton, Matthew J.
Arshad, S. Hasan
Bahna, Sami L.
Beck, Lisa A.
Byrd-Bredbenner, Carol
Camargo, Carlos A., Jr.
Eichenfield, Lawrence
Furuta, Glenn T.
Hanifin, Jon M.
Jones, Carol
Kraft, Monica
Levy, Bruce D.
Lieberman, Phil
Luccioli, Stefano
McCall, Kathleen M.
Schneider, Lynda C.
Simon, Ronald A.
Simons, F. Estelle R.
Teach, Stephen J.
Yawn, Barbara P.
Schwaninger, Julie M.
TI Guidelines for the diagnosis and management of food allergy in the
United States: Summary of the NIAID-Sponsored Expert Panel Report
SO NUTRITION
LA English
DT Article
C1 [Plaut, Marshall; Cooper, Susan E.; Fenton, Matthew J.; Schwaninger, Julie M.] NIAID, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA.
[Boyce, Joshua A.] Harvard Univ, Brigham & Womens Hosp, Div Rheumatol Immunol & Allergy, Dept Med,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Camargo, Carlos A., Jr.] Harvard Univ, Brigham & Womens Hosp, Dept Emergency Med,Div Rheumatol Allergy & Immuno, Massachusetts Gen Hosp,Dept Med, Boston, MA 02115 USA.
[Levy, Bruce D.] Brigham & Womens Hosp, Partners Asthma Ctr, Pulm & Crit Med Div, Boston, MA 02115 USA.
[Assa'a, Amal] Univ Cincinnati, Div Allergy & Immunol, Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH 45221 USA.
[Burks, A. Wesley] Duke Univ, Med Ctr, Dept Pediat, Div Allergy & Immunol, Durham, NC 27706 USA.
[Kraft, Monica] Duke Univ, Med Ctr, Dept Med, Div Pulm Allergy & Crit Care Med, Durham, NC 27706 USA.
[Jones, Stacie M.] Univ Arkansas Med Sci, Arkansas Childrens Hosp, Div Allergy & Immunol, Dept Pediat, Little Rock, AR 72205 USA.
[Sampson, Hugh A.] Mt Sinai Sch Med, Elliot & Roslyn Jaffe Food Allergy Inst, Div Allergy & Immunol, Dept Pediat, New York, NY USA.
[Wood, Robert A.] Johns Hopkins Univ, Sch Med, Dept Pediat, Div Allergy & Immunol, Baltimore, MD 21205 USA.
[Arshad, S. Hasan] Univ Southampton, Southampton SO9 5NH, Hants, England.
[Arshad, S. Hasan] St Marys Hosp, David Hide Asthma & Allergy Res Ctr, Newport PO30 5TG, Isle Of Wight, England.
[Arshad, S. Hasan] Southampton Univ Hosp NHS Trust, Southampton SO16 6YD, Hants, England.
[Bahna, Sami L.] Louisiana State Univ, Hlth Sci Ctr, Allergy & Immunol Sect, Dept Pediat, Baton Rouge, LA 70803 USA.
[Beck, Lisa A.] Univ Rochester, Med Ctr, Dept Dermatol, Rochester, NY 14642 USA.
[Byrd-Bredbenner, Carol] Rutgers State Univ, Dept Nutr Sci, New Brunswick, NJ 08903 USA.
[Eichenfield, Lawrence] Rady Childrens Hosp, Div Pediat & Adolescent Dermatol, San Diego, CA USA.
[Eichenfield, Lawrence] Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA.
[Eichenfield, Lawrence] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
[Furuta, Glenn T.] Childrens Hosp Denver, Sect Pediat Gastroenterol Hepatol & Nutr, Digest Hlth Inst, Aurora, CO USA.
[Furuta, Glenn T.] Natl Jewish Hlth, Dept Pediat, Denver, CO USA.
Univ Colorado, Denver Sch Med, Dept Pediat, Aurora, CO USA.
Oregon Hlth & Sci Univ, Dept Dermatol, Portland, OR 97201 USA.
Allergy & Asthma Network Mothers Asthmat, Mclean, VA USA.
Univ Tennessee, Coll Med, Dept Med, Div Allergy & Immunol, Knoxville, TN 37996 USA.
US FDA, Off Food Addit Safety, College Pk, MD USA.
Childrens Hosp Orange Cty, Orange, CA USA.
Childrens Hosp Boston, Div Immunol, Boston, MA USA.
Scripps Clin, Div Allergy Asthma & Immunol, San Diego, CA USA.
Univ Manitoba, Fac Med, Dept Pediat, Winnipeg, MB R3T 2N2, Canada.
Univ Manitoba, Fac Med, Dept Child Hlth & Immunol, Winnipeg, MB R3T 2N2, Canada.
Childrens Natl Med Ctr, Div Emergency Med, Washington, DC 20010 USA.
Olmsted Med Ctr, Dept Res, Rochester, MN USA.
Univ Minnesota, Sch Med, Dept Family & Community Hlth, Minneapolis, MN 55455 USA.
RP Fenton, MJ (reprint author), NIAID, Div Allergy Immunol & Transplantat, NIH, 6610 Rockledge Dr,Room 6503, Bethesda, MD 20892 USA.
EM fentonm@niaid.nih.gov
RI Byrd-Bredbenner, Carol/F-8064-2015
OI Byrd-Bredbenner, Carol/0000-0002-8010-3987
FU NIAID; GlaxoSmithKline; Food Allergy and Anaphylaxis Network; Gerber;
Mead Johnson; National Institutes of Health; Food Allergy Initiative;
National Institutes of Health (Division of Receipt and Referral,
National Institute of Allergy and Infectious Diseases, National Center
for Complementary and Alternative Medicine); Phadia AB; Genentech;
National Institutes of Health (National Institute of Allergy and
Infectious Diseases); National Institute of Health Research, UK;
American Academy of Allergy, Asthma, and Immunology; National Eczema
Association; US Department of Agriculture; Canned Food Alliance; New
Jersey Department of Health and Senior Services; Dey; Novartis;
Astellas; Astellas, Ferndale; Johnson Johnson; Sinclair; Stiefel;
Therapeutics Inc.; American Gastrointestinal Association; ALZA; Astellas
Pharma US, Inc; Asubio Pharmaceuticals, Inc.; Centocor, Inc; Corgentech;
Nucryst Pharmaceuticals; Seattle Genetics; Shionogi USA; AllerGen;
Canadian Allergy, Asthma and Immunology Foundation/Anaphylaxis Canada;
Canadian Institutes of Health, Research; AstraZeneca Foundation;
Aventis; Child Health Center Board; CNMC Research Advisory Council;
National Association of Chain Drug Stores Foundation; National
Institutes of Health (National Institute of Allergy and Infectious,
Diseases: National Heart, Lung, and Blood Institute);
Novartis/Genentech; Robert Woods Johnson Foundation; US Centers for
Disease Control and Prevention; US Public Health Service; Washington,
DC, Department of Health
FX NIAID-sponsored Expert Panel; A. Assa'ad holds, or is listed as an
inventor on, US patent application #10/566903, entitled "Genetic markers
of food allergy." She has served as a consultant for GlaxoSmithKline and
as a speaker for the American College of Allergy, Asthma, and,
Immunology, the North East Allergy Society, the Virginia Allergy
Society, the New, England Allergy Society, and the American Academy of
Pediatrics. Dr Assa'ad has, received funding/grant support from
GlaxoSmithKline.; A. W. Burks holds, or is listed as an inventor on,
multiple US patents related to food allergy. He owns stock in Allertein
and MastCell, Inc, and is a minority stockholder in Dannon Co
Probiotics. He has served as a consultant for ActoGeniX NV, McNeil
Nutritionals, Mead Johnson, and Novartis. He has served on the speaker's
bureau for EpiPen/Dey, LP, and has served on the data monitoring
committee for Genentech. He has served on an expert panel for Nutricia.
Dr Burks has received funding/grant support from the Food Allergy and
Anaphylaxis Network, Gerber, Mead Johnson, and the National Institutes
of Health.; H. A. Sampson holds, or is listed as an inventor on,
multiple US patents related to food allergy. He owns stock in Allertein
Therapeutics. He is the immediate past president of the American Academy
of Allergy, Asthma, and Immunology. He has served as a consultant for
Allertein Therapeutics, the American Academy of Allergy, Asthma, and
Immunology, the Food Allergy Initiative, and Schering Plough. He has
received, funding/grant support for research projects from the Food
Allergy Initiative, the National Institutes of Health (Division of
Receipt and Referral, National Institute of Allergy and Infectious
Diseases, National Center for Complementary and Alternative Medicine),
and Phadia AB. He is a co-owner of Herbal Spring, LLC.; R. A. Wood has
served as a speaker/advisory board member for GlaxoSmithKline, Merck,
and Dey. He has received funding/grant support from Genentech and the,
National Institutes of Health (National Institute of Allergy and
Infectious Diseases).; S. H. Arshad has received funding/grant support
from the National Institutes of Health and the National Institute of
Health Research, UK.; L. A. Beck has received funding/grant support from
the American Academy of Allergy, Asthma, and Immunology, the National
Eczema Association, and the National Institutes of Health.; C.
Byrd-Bredbenner owns stock in Johnson & Johnson. She has received
funding/grant support from the US Department of Agriculture, the Canned
Food Alliance, and the New Jersey Department of Health and Senior
Services.; C. A. Camargo Jr has consulted for Dey and Novartis. He has
received funding/grant support from a variety of government agencies and
not-for-profit research foundations, as well as Dey and Novartis.; L.
Eichenfield has received funding/grant support from a variety of
not-for-profit foundations, as well as Astellas, Ferndale, Johnson &
Johnson, Novartis, Sinclair, Stiefel, and Therapeutics Inc.; G. T.
Furuta has served as a consultant and/or speaker to Caption Therapeutics
and TAP. He has received funding/grant support from the American
Gastrointestinal Association and the National Institutes of Health.; J.
M. Hanifin has served as served as a consultant for ALZA, Anesiva, Inc,
Barrier Therapeutics, Inc, Milliken & Company, Nordic Biotech, Novartis
Pharmaceuticals Corporation, Shionogi USA, Taisho Pharmaceutical R&D,
Inc, Teikoku Pharma USA, Inc, UCB, York Pharma, ZARS, Inc, and
ZymoGenetics. He has served as an investigator or received research
funding from ALZA, Astellas Pharma US, Inc, Asubio Pharmaceuticals, Inc.
Centocor, Inc, Corgentech, Novartis, Nucryst Pharmaceuticals, Seattle
Genetics, and Shionogi USA.; F. E. R. Simons holds a patent on
"Fast-disintegrating epinephrine tablets for sublingual administration."
She is a past-president of the American Academy of Allergy, Asthma and
Immunology and of the Canadian Society of Allergy and Clinical
Immunology. She is a member of the advisory boards of Dey, Intelliject,
and ALK-Abello. She has received funding/grant support from AllerGen,
the Canadian Allergy, Asthma and Immunology Foundation/Anaphylaxis
Canada, and the Canadian Institutes of Health, Research.; S.J. Teach has
served as a speaker for AstraZeneca. He has received funding/grant
support from the AstraZeneca Foundation, Aventis, the Child Health
Center Board, the CNMC Research Advisory Council, the National
Association of Chain Drug Stores Foundation, the National Institutes of
Health (National Institute of Allergy and Infectious, Diseases: National
Heart, Lung, and Blood Institute), Novartis/Genentech, the Robert Woods
Johnson Foundation, the US Centers for Disease Control and Prevention,
the US Public Health Service, and the Washington, DC, Department of
Health.
NR 0
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U1 1
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PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0899-9007
EI 1873-1244
J9 NUTRITION
JI Nutrition
PD FEB
PY 2011
VL 27
IS 2
BP 253
EP 267
DI 10.1016/j.nut.2010.12.001
PG 15
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 710UL
UT WOS:000286542400022
PM 21215925
ER
PT J
AU Landon, MB
Mele, L
Spong, CY
Carpenter, MW
Ramin, SM
Casey, B
Wapner, RJ
Varner, MW
Rouse, DJ
Thorp, JM
Sciscione, A
Catalano, P
Harper, M
Saade, G
Caritis, SN
Sorokin, Y
Peaceman, AM
Tolosa, JE
Anderson, GD
AF Landon, Mark B.
Mele, Lisa
Spong, Catherine Y.
Carpenter, Marshall W.
Ramin, Susan M.
Casey, Brian
Wapner, Ronald J.
Varner, Michael W.
Rouse, Dwight J.
Thorp, John M., Jr.
Sciscione, Anthony
Catalano, Patrick
Harper, Margaret
Saade, George
Caritis, Steve N.
Sorokin, Yoram
Peaceman, Alan M.
Tolosa, Jorge E.
Anderson, Garland D.
CA Eunice Kennedy Shriver Natl Inst
TI The Relationship Between Maternal Glycemia and Perinatal Outcome
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID GESTATIONAL DIABETES-MELLITUS; GLUCOSE-TOLERANCE TEST; PREGNANCY
OUTCOMES; SCREENING-TESTS; CRITERIA; INTOLERANCE; TRIAL
AB OBJECTIVE: To examine the relationship between varying degrees of maternal hyperglycemia and pregnancy outcomes.
METHODS: This was a secondary analysis of a treatment trial for mild gestational diabetes including four cohorts: 1) 473 women with untreated mild gestational diabetes; 2) 256 women with a positive 50-g screen and one abnormal oral glucose tolerance test (OGTT) value; 3) 675 women with a positive screen and no abnormal OGTT values; and 4) 437 women with a normal 50-g screen. Groups were compared by test of trend for a composite perinatal outcome (neonatal hypoglycemia, hyperbilirubinemia, elevated cord C-peptide level, and perinatal trauma or death), frequency of large for gestational age neonates, shoulder dystocia, and pregnancy-related hypertension. Three-hour OGTT levels (fasting, 1-, 2-, and 3-hour) levels were divided into categories and analyzed for their relationship to perinatal and maternal outcomes.
RESULTS: There were significant trends by glycemic status among the four cohorts for the composite and all other outcomes (P<.001). Analysis for trend according to OGTT categories showed an increasing relationship between fasting and all postload levels and the various outcomes (P<.05). Fasting glucose 90 mg/dL or greater and 1 hour 165 mg/dL or greater were associated with an increased risk for the composite outcome (odds ratios and 95% confidence intervals of 2.0 [1.03-4.15] and 1.46 [1.02-2.11] to 1.52 [1.08-2.15] for the fasting and 1 hour, respectively). A 1 hour glucose 150 mg/dL or greater was associated with an increased risk for large for gestational age (odds ratios, 1.8 [1.02-3.18] to 2.35 [1.35-4.14]); however, 2- and 3-hour glucose levels did not increase the risk for the composite or large for gestational age until well beyond current gestational diabetes diagnostic thresholds.
CONCLUSION: A monotonic relationship exists between increasing maternal glycemia and perinatal morbidity. Current OGTT criteria require reevaluation in determining thresholds for the diagnosis and treatment of gestational diabetes. (Obstet Gynecol 2011;117:218-24) DOI: 10.1097/AOG.0b013e318203ebe0
C1 [Landon, Mark B.] Ohio State Univ, Coll Med, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
George Washington Univ, Ctr Biostat, Washington, DC USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
Brown Univ, Dept Obstet, Providence, RI 02912 USA.
Brown Univ, Dept Gynecol, Providence, RI 02912 USA.
Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
Columbia Univ, New York, NY USA.
Univ Utah, Salt Lake City, UT USA.
Univ Alabama, Birmingham, AL USA.
Univ N Carolina, Chapel Hill, NC USA.
Drexel Univ, Philadelphia, PA 19104 USA.
Case Western Reserve Univ, Metrohlth Med Ctr, Cleveland, OH USA.
Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
Univ Texas Med Branch, Galveston, TX USA.
Univ Pittsburgh, Pittsburgh, PA USA.
Wayne State Univ, Detroit, MI USA.
Northwestern Univ, Chicago, IL 60611 USA.
Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
RP Landon, MB (reprint author), Ohio State Univ, Coll Med, Dept Obstet & Gynecol, 395 12th Ave,Suite 572, Columbus, OH 43210 USA.
EM Mark.Landon@osumc.edu
RI Varner, Michael/K-9890-2013
OI caritis, steve/0000-0002-2169-0712; Peaceman, Alan/0000-0002-4515-4850;
Varner, Michael/0000-0001-9455-3973
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [HD27915, HD34116, HD40485, HD34208, HD27869, HD40500,
HD40560, HD34136, HD40544, HD27860, HD40545, HD53097, HD21410, HD27917,
HD40512, HD53118, HD36801]; General Clinical Research Centers
[M01-RR00034]; National Center for Research Resources [UL1-RR024989,
M01-RR00080, UL1-RR025764, C06-RR11234]
FX Supported by grants from the Eunice Kennedy Shriver National Institute
of Child Health and Human Development (HD27915, HD34116, HD40485,
HD34208, HD27869, HD40500, HD40560, HD34136, HD40544, HD27860, HD40545,
HD53097, HD21410, HD27917, HD40512, HD53118, HD36801), General Clinical
Research Centers Grant (M01-RR00034), and the National Center for
Research Resources (UL1-RR024989, M01-RR00080, UL1-RR025764,
C06-RR11234) and does not necessarily represent the official views of
the National Institute of Child Health and Human Development or the
National Institutes of Health.
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD FEB
PY 2011
VL 117
IS 2
BP 218
EP 224
DI 10.1097/AOG.0b013e318203ebe0
PN 1
PG 7
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 709SB
UT WOS:000286460600004
PM 21309194
ER
PT J
AU Rouse, DJ
Weiner, SJ
Bloom, SL
Varner, MW
Spong, CY
Ramin, SM
Caritis, SN
Grobman, WA
Sorokin, Y
Sciscione, A
Carpenter, MW
Mercer, BM
Thorp, JM
Malone, FD
Harper, M
Iams, JD
Anderson, GD
AF Rouse, Dwight J.
Weiner, Steven J.
Bloom, Steven L.
Varner, Michael W.
Spong, Catherine Y.
Ramin, Susan M.
Caritis, Steve N.
Grobman, William A.
Sorokin, Yoram
Sciscione, Anthony
Carpenter, Marshall W.
Mercer, Brian M.
Thorp, John M., Jr.
Malone, Fergal D.
Harper, Margaret
Iams, Jay D.
Anderson, Garland D.
CA Eunice Kennedy Shriver Natl Inst
TI Failed Labor Induction Toward an Objective Diagnosis
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID NULLIPAROUS WOMEN; CESAREAN DELIVERY; TERM
AB METHODS: This was a secondary analysis of a randomized multicenter trial in which all cervical examinations from admission were recorded. Inclusion criteria: nulliparas at or beyond 36 weeks of gestation undergoing induction with a cervix of 2 cm or less dilated and less than completely effaced. The latent phase of labor was defined as ending at a cervical dilation of 4 cm and effacement of at least 90%, or at a cervical dilation of 5 cm regardless of effacement.
RESULTS: A total of 1,347 women were analyzed. The overall vaginal delivery rate was 63.2%. Most women had exited the latent phase after 6 hours of oxytocin and membrane rupture (n = 939; 69.7%); only 5% remained in the latent phase after 12 hours. The longer the latent phase, the lower the vaginal delivery rate. Even so, 39.4% of the 71 women who remained in the latent phase after 12 hours of oxytocin and membrane rupture were delivered vaginally. Chorioamnionitis, endometritis, or both, and uterine atony were the only maternal adverse outcomes related to latent-phase duration: adjusted odds ratios (95% confidence intervals) of 1.12 (1.07, 1.17) and 1.13 (1.06, 1.19), respectively, for each additional hour. Neonatal outcomes were not related to latent-phase duration.
CONCLUSION: Almost 40% of the women who remained in the latent phase after 12 hours of oxytocin and membrane rupture were delivered vaginally. Therefore, it is reasonable to avoid deeming labor induction a failure in the latent phase until oxytocin has been administered for at least 12 hours after membrane rupture. (Obstet Gynecol 2011;117:267-72) DOI: 10.1097/AOG.0b013e318207887a
C1 [Rouse, Dwight J.] Brown Univ, Warren Alpert Med Sch, Dept Obstet & Gynecol, Providence, RI 02905 USA.
Univ Alabama, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
Univ Utah, Salt Lake City, UT USA.
Univ Texas Hlth Sci Ctr Houston, Houston, TX USA.
Univ Pittsburgh, Pittsburgh, PA USA.
Northwestern Univ, Chicago, IL 60611 USA.
Wayne State Univ, Detroit, MI USA.
Drexel Univ, Philadelphia, PA 19104 USA.
Case Western Reserve Univ, Metrohlth Med Ctr, Cleveland, OH USA.
Univ N Carolina, Chapel Hill, NC USA.
Columbia Univ, New York, NY USA.
Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
Ohio State Univ, Columbus, OH 43210 USA.
Univ Texas Med Branch, Galveston, TX USA.
George Washington Univ, Ctr Biostat, Washington, DC USA.
Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Rouse, DJ (reprint author), Brown Univ, Warren Alpert Med Sch, Dept Obstet & Gynecol, 101 Dudley St,3rd Floor, Providence, RI 02905 USA.
EM drouse@wihri.org
RI Malone, Fergal/D-6233-2012; 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) [HD21410, HD27860, HD27869, HD27915, HD27917,
HD34116, HD34136, HD34208, HD40485, HD40500, HD40512, HD40544, HD40545,
HD40560, HD36801]
FX Supported by grants from the Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD) [HD21410, HD27860,
HD27869, HD27915, HD27917, HD34116, HD34136, HD34208, HD40485, HD40500,
HD40512, HD40544, HD40545, HD40560, and HD36801] and does not
necessarily represent the official views of the NICHD or the NIH.
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U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD FEB
PY 2011
VL 117
IS 2
BP 267
EP 272
DI 10.1097/AOG.0b013e318207887a
PN 1
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 709SB
UT WOS:000286460600010
PM 21252738
ER
PT J
AU Wakamatsu, K
Hearing, V
AF Wakamatsu, Kazumasa
Hearing, Vincent
TI Shosuke Ito PROFILE
SO PIGMENT CELL & MELANOMA RESEARCH
LA English
DT Biographical-Item
C1 [Wakamatsu, Kazumasa] Fujita Hlth Univ, Sch Hlth Sci, Dept Chem, Aichi, Japan.
[Hearing, Vincent] NIH, Cell Biol Lab, Bethesda, MD 20892 USA.
RP Wakamatsu, K (reprint author), Fujita Hlth Univ, Sch Hlth Sci, Dept Chem, Aichi, Japan.
EM kwaka@fujita-hu.ac.jp; hearingv@nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1755-1471
J9 PIGM CELL MELANOMA R
JI Pigment Cell Melanoma Res.
PD FEB
PY 2011
VL 24
IS 1
BP 247
EP 247
DI 10.1111/j.1755-148X.2010.00739.x
PG 1
WC Oncology; Cell Biology; Dermatology
SC Oncology; Cell Biology; Dermatology
GA 706IA
UT WOS:000286210400032
PM 21232028
ER
PT J
AU Fitzgerald, PJ
AF Fitzgerald, Paul J.
TI A neurochemical yin and yang: does serotonin activate and norepinephrine
deactivate the prefrontal cortex?
SO PSYCHOPHARMACOLOGY
LA English
DT Review
DE Executive function; Impulsivity; Cognitive flexibility; Reversal
learning; Working memory; Fluoxetine; Clonidine; Propranolol; Guanfacine
ID SPATIAL WORKING-MEMORY; ACUTE TRYPTOPHAN DEPLETION;
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY
DISORDER; RECEPTOR KNOCKOUT MICE; AGED RHESUS-MONKEYS;
REACTION-TIME-TASK; COGNITIVE FLEXIBILITY; LOCUS-COERULEUS; IMPULSIVE
BEHAVIOR
AB The prefrontal cortex (PFC) receives serotonergic input from the dorsal raphe nucleus of the brainstem, as well as noradrenergic input from another brainstem nucleus, the locus coeruleus. A large number of studies have shown that these two neurotransmitter systems, and drugs that affect them, modulate the functional properties of the PFC in both humans and animal models.
Here I examine the hypothesis that serotonin (5-HT) plays a general role in activating the PFC, whereas norepinephrine (NE) plays a general role in deactivating this brain region. In this manner, the two neurotransmitter systems may have opposing effects on PFC-influenced behavior. To assess this hypothesis, three primary lines of evidence are examined comprising the effects of 5-HT and NE on impulsivity, cognitive flexibility, and working memory.
While all of the existing data do not unequivocally support the activation/deactivation hypothesis, there is a large body of support for it.
C1 [Fitzgerald, Paul J.] Johns Hopkins Univ, Zanvyl Krieger Mind Brain Inst, Solomon H Snyder Dept Neurosci, Baltimore, MD 21218 USA.
RP Fitzgerald, PJ (reprint author), NIAAA, 5625 Fishers Lane,Room 2N09, Rockville, MD 20852 USA.
EM pfitz@mbi.mb.jhu.edu
NR 129
TC 15
Z9 15
U1 3
U2 14
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD FEB
PY 2011
VL 213
IS 2-3
BP 171
EP 182
DI 10.1007/s00213-010-1856-1
PG 12
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 716AT
UT WOS:000286938000002
PM 20386882
ER
PT J
AU Li, JX
Crocker, C
Koek, W
Rice, KC
France, CP
AF Li, Jun-Xu
Crocker, Caroline
Koek, Wouter
Rice, Kenner C.
France, Charles P.
TI Effects of serotonin (5-HT)(1A) and 5-HT2A receptor agonists on
schedule-controlled responding in rats: drug combination studies
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Serotonin; Receptor; Drug interaction; Additivity; Rat;
Schedule-controlling responding; Agonist; Antagonist
ID ANTAGONIST; EFFICACY; DOI
AB Indirect-acting serotonin (5-HT) receptor agonists (e.g., selective 5-HT reuptake inhibitors [SSRI]) stimulate multiple 5-HT receptors, although the role of particular receptors as well as interaction(s) among different receptors in the therapeutic effects of SSRIs is not fully understood.
Relatively few studies have systematically examined direct-acting agonists in combination. This study examined the 5-HT1A receptor agonists 8-hydroxy-2-(di-n-propylamino) tetralin hydrochloride (8-OH-DPAT; 0.01-10.0 mg/kg) and 3-chloro-4-fluorophenyl-4-fluoro-4-([(5-methyl-6-methylamino-pyridin-2-ylmethyl)-amino]-methyl)-piperidin-1-yl-methanone (F13714; 0.01-1.0 mg/kg) and the 5-HT2A receptor agonists 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM; 0.32-10.0 mg/kg) and dipropyltryptamine (DPT; 1.0-32.0 mg/kg), alone and in combination, in rats responding under a fixed ratio schedule of food presentation.
When administered alone, each drug decreased the rate of responding in a dose-related manner with the potency order being F13714 > 8-OH-DPAT > DOM > DPT. WAY100635 (5-HT1A receptor antagonist; 0.01-0.1 mg/kg) attenuated the rate-decreasing effects of 8-OH-DPAT and F13714 while MDL100907 (5-HT2A receptor antagonist; 0.01-0.1 mg/kg) attenuated the rate-decreasing effects of DOM and DPT. Dose addition analysis showed that the interaction between 8-OH-DPAT and F13714, as well as the interaction between DOM and DPT, was additive. In contrast, the interaction between 8-OH-DPAT and DOM, as well as the interaction between F13714 and DOM, was infra-additive.
This study shows that for some dose combinations, agonist actions at one 5-HT receptor subtype attenuate agonist actions at another 5-HT receptor subtype; thus, the combined neuropharmacological actions and therapeutic effects of indirect-acting agonists are not likely to be adequately characterized by examining in isolation activity at particular 5-HT receptor subtypes.
C1 [Li, Jun-Xu; Crocker, Caroline; Koek, Wouter; France, Charles P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
[Koek, Wouter; France, Charles P.] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
[Rice, Kenner C.] NIDA, Chem Biol Res Lab, Bethesda, MD 20892 USA.
[Rice, Kenner C.] NIAAA, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
RP France, CP (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM france@uthscsa.edu
RI Li, Jun-Xu/K-9192-2013
FU National Institute on Drug Abuse, National Institutes of Health [K05
DA17918]
FX CPF is supported by a Senior Scientist Award from the National Institute
on Drug Abuse, National Institutes of Health (K05 DA17918). This
research was supported, in part, by the Intramural Research Program of
the National Institute on Drug Abuse, National Institutes of Health. The
content of this manuscript is solely the responsibility of the authors
and does not necessarily represent the views of the National Institute
on Drug Abuse or the National Institutes of Health.
NR 21
TC 8
Z9 8
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD FEB
PY 2011
VL 213
IS 2-3
BP 489
EP 497
DI 10.1007/s00213-010-2136-9
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 716AT
UT WOS:000286938000022
PM 21174080
ER
PT J
AU Liu, HJ
Fergusson, MM
Wu, JJ
Rovira, II
Liu, J
Gavrilova, O
Lu, T
Bao, JJ
Han, DH
Sack, MN
Finkel, T
AF Liu, Hongjun
Fergusson, Maria M.
Wu, J. Julie
Rovira, Ilsa I.
Liu, Jie
Gavrilova, Oksana
Lu, Teng
Bao, Jianjun
Han, Donghe
Sack, Michael N.
Finkel, Toren
TI Wnt Signaling Regulates Hepatic Metabolism
SO SCIENCE SIGNALING
LA English
DT Article
ID TRANSCRIPTION FACTOR FOXO1; BETA-CATENIN; GLUCOSE-PRODUCTION; TCF7L2
GENE; LIVER; GLUCONEOGENESIS; RISK; EXPRESSION; MICE; MECHANISMS
AB The contribution of the Wnt pathway has been extensively characterized in embryogenesis, differentiation, and stem cell biology but not in mammalian metabolism. Here, using in vivo gain-and loss-of-function models, we demonstrate an important role for Wnt signaling in hepatic metabolism. In particular, beta-catenin, the downstream mediator of canonical Wnt signaling, altered serum glucose concentrations and regulated hepatic glucose production. beta-Catenin also modulated hepatic insulin signaling. Furthermore, beta-catenin interacted with the transcription factor FoxO1 in livers from mice under starved conditions. The interaction of FoxO1 with beta-catenin regulated the transcriptional activation of the genes encoding glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK), the two rate-limiting enzymes in hepatic gluconeogenesis. Moreover, starvation induced the hepatic expression of mRNAs encoding different Wnt isoforms. In addition, nutrient deprivation appeared to favor the association of beta-catenin with FoxO family members, rather than with members of the T cell factor of transcriptional activators. Notably, in a model of diet-induced obesity, hepatic deletion of beta-catenin improved overall metabolic homeostasis. These observations implicate Wnt signaling in the modulation of hepatic metabolism and raise the possibility that Wnt signaling may play a similar role in the metabolic regulation of other tissues.
C1 [Liu, Hongjun; Fergusson, Maria M.; Wu, J. Julie; Rovira, Ilsa I.; Liu, Jie; Lu, Teng; Bao, Jianjun; Sack, Michael N.; Finkel, Toren] NHLBI, Ctr Mol Med, Bethesda, MD 20892 USA.
[Gavrilova, Oksana] NIDDK, Bethesda, MD 20892 USA.
[Lu, Teng] Emory Univ, Sch Med, Atlanta, GA 30322 USA.
[Han, Donghe] Univ Pittsburgh, Sch Med, Dept Microbiol & Mol Genet, Pittsburgh, PA 15219 USA.
RP Finkel, T (reprint author), NHLBI, Ctr Mol Med, Bldg 10, Bethesda, MD 20892 USA.
EM finkelt@nih.gov
FU NIA NIH HHS [R00 AG032356, R00 AG032356-03]
NR 48
TC 65
Z9 66
U1 0
U2 15
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1937-9145
J9 SCI SIGNAL
JI Sci. Signal.
PD FEB 1
PY 2011
VL 4
IS 158
AR ra6
DI 10.1126/scisignal.2001249
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 714HY
UT WOS:000286801000001
PM 21285411
ER
PT J
AU Collins, BJ
Stout, MD
Levine, KE
Kissling, GE
Melnick, RL
Fennell, TR
Pritchard, JB
Walden, R
Abdo, K
Fernando, RA
Burka, LT
Hooth, MJ
AF Collins, Bradley J.
Stout, Matthew D.
Levine, Keith E.
Kissling, Grace E.
Melnick, Ronald L.
Fennell, Timothy R.
Pritchard, John B.
Walden, Ramsey
Abdo, Kamal
Fernando, Reshan A.
Burka, Leo T.
Hooth, Michelle J.
TI Hexavalent Chromium in Drinking Water, Reply
SO TOXICOLOGICAL SCIENCES
LA English
DT Letter
C1 [Collins, Bradley J.; Stout, Matthew D.; Kissling, Grace E.; Melnick, Ronald L.; Abdo, Kamal; Burka, Leo T.; Hooth, Michelle J.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Levine, Keith E.; Fennell, Timothy R.; Fernando, Reshan A.] RTI Int, Discovery & Analyt Sci, Res Triangle Pk, NC 27709 USA.
[Pritchard, John B.; Walden, Ramsey] NIEHS, Pharmacol Lab, Res Triangle Pk, NC 27709 USA.
RP Collins, BJ (reprint author), NIEHS, Natl Toxicol Program, 111 Alexander Dr,MD K2-13, Res Triangle Pk, NC 27709 USA.
EM collin10@niehs.nih.gov
RI Fennell, Tim/D-9936-2013
NR 0
TC 0
Z9 0
U1 0
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
J9 TOXICOL SCI
JI Toxicol. Sci.
PD FEB
PY 2011
VL 119
IS 2
BP 425
EP 425
DI 10.1093/toxsci/kfq348
PG 1
WC Toxicology
SC Toxicology
GA 710XH
UT WOS:000286549800019
ER
PT J
AU Hunn, JP
Feng, CG
Sher, A
Howard, JC
AF Hunn, Julia P.
Feng, Carl G.
Sher, Alan
Howard, Jonathan C.
TI The immunity-related GTPases in mammals: a fast-evolving cell-autonomous
resistance system against intracellular pathogens
SO MAMMALIAN GENOME
LA English
DT Article
ID INDUCIBLY EXPRESSED GTPASE; TOXOPLASMA-GONDII; IFN-GAMMA; P47 GTPASES;
INTERFERON-GAMMA; HOST-DEFENSE; TRYPANOSOMA-CRUZI; POPULATION BIOLOGY;
NUCLEOTIDE-BINDING; CROHNS-DISEASE
AB The immunity-related GTPases (IRGs) belong to the family of large, interferon-inducible GTPases and constitute a cell-autonomous resistance system essential for the control of vacuolar pathogens like Toxoplasma gondii in mice. Recent results demonstrated that numerous IRG members accumulate collaboratively at the parasitophorous vacuole of invading T. gondii leading to the destruction of the vacuole and the parasite and subsequent necrotic host cell death. Complex regulatory interactions between different IRG proteins are necessary for these processes. Disturbance of this finely balanced system, e.g., by single genetic deficiency for the important negative regulator Irgm1 or the autophagic regulator Atg5, leads to spontaneous activation of the effector IRG proteins when induced by IFN gamma. This activation has cytotoxic consequences resulting in a severe lymphopenia, macrophage defects, and failure of the adaptive immune system in Irgm1-deficient mice. However, alternative functions in phagosome maturation and induction of autophagy have been proposed for Irgm1. The IRG system has been studied primarily in mice, but IRG genes are present throughout the mammalian lineage. Interestingly, the number, type, and diversity of genes present differ greatly even between closely related species, probably reflecting intimate host-pathogen coevolution driven by an armed race between the IRG resistance proteins and pathogen virulence factors. IRG proteins are targets for polymorphic T. gondii virulence factors, and genetic variation in the IRG system between different mouse strains correlates with resistance and susceptibility to virulent T. gondii strains.
C1 [Hunn, Julia P.; Howard, Jonathan C.] Univ Cologne, Inst Genet, D-50674 Cologne, Germany.
[Feng, Carl G.; Sher, Alan] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Howard, JC (reprint author), Univ Cologne, Inst Genet, Zuelpicher Str 47A, D-50674 Cologne, Germany.
EM j.howard@uni-koeln.de
OI Howard, Jonathan/0000-0003-2756-5143
FU Deutsche Forschungsgemeinschaft [SFB635, SFB670, SFB680, SPP1399];
NIAID, NIH
FX JCH and JPH were supported by SFB635, SFB670, SFB680 and SPP1399 from
the Deutsche Forschungsgemeinschaft; and CGF and AS were supported by
the Intramural Research Program of the NIAID, NIH. We are grateful to
our colleague Gregory Taylor for his pioneering work on the IRG system.
NR 85
TC 44
Z9 44
U1 1
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0938-8990
J9 MAMM GENOME
JI Mamm. Genome
PD FEB
PY 2011
VL 22
IS 1-2
BP 43
EP 54
DI 10.1007/s00335-010-9293-3
PG 12
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA 711UG
UT WOS:000286616300005
PM 21052678
ER
PT J
AU Gotts, SJ
Milleville, SC
Bellgowan, PSF
Martin, A
AF Gotts, Stephen J.
Milleville, Shawn C.
Bellgowan, Patrick S. F.
Martin, Alex
TI Broad and Narrow Conceptual Tuning in the Human Frontal Lobes
SO CEREBRAL CORTEX
LA English
DT Article
DE animals; category; fMRI adaptation; semantic memory; visual objects
ID HUMAN VISUAL-CORTEX; POSTERIOR INFEROTEMPORAL CORTEX; RESONANCE-IMAGING
EVIDENCE; PRIMATE PREFRONTAL CORTEX; INFERIOR TEMPORAL CORTEX; NEURAL
MECHANISMS; OBJECT RECOGNITION; SEMANTIC MEMORY; OCCIPITAL CORTEX;
FUNCTIONAL ARCHITECTURE
AB Previous work has implicated prefrontal cortices in selecting among and retrieving conceptual information stored elsewhere. However, recent neurophysiological work in monkeys suggests that prefrontal cortex may play a more direct role in representing conceptual information in a flexible context-specific manner. Here, we investigate the nature of visual object representations from perceptual to conceptual levels in an unbiased data-driven manner using a functional magnetic resonance imaging adaptation paradigm with pictures of animals. Throughout much of occipital cortex, activity was highly sensitive to changes in 2D stimulus form, consistent with tuning to form and position within retinotopic coordinates and matching an automated measure of shape similarity. Broad superordinate conceptual information was represented as early as extrastriate and posterior ventral temporal cortex. These regions were not completely invariant to form, suggesting that form similarity remains an important organizational constraint into the temporal cortex. Separate sites within prefrontal cortex represented broad and narrow conceptual tuning, with more anterior sites tuned narrowly to close conceptual associates in a manner that was invariant to stimulus form/position and that matched independent similarity ratings of the stimuli. The combination of broad and narrow conceptual tuning within prefrontal cortex may support flexible selection, retrieval, and classification of objects at different levels of categorical abstraction.
C1 [Gotts, Stephen J.; Milleville, Shawn C.; Bellgowan, Patrick S. F.; Martin, Alex] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Gotts, SJ (reprint author), NIMH, Lab Brain & Cognit, NIH, Bldg 10,Room 4C-217, Bethesda, MD 20892 USA.
EM gottss@mail.nih.gov
RI martin, alex/B-6176-2009; Gotts, Stephen/J-4842-2012
FU National Institute of Mental Health, Division of Intramural Research
FX National Institute of Mental Health, Division of Intramural Research.
NR 89
TC 12
Z9 12
U1 2
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
J9 CEREB CORTEX
JI Cereb. Cortex
PD FEB
PY 2011
VL 21
IS 2
BP 477
EP 491
DI 10.1093/cercor/bhq113
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 706KK
UT WOS:000286217100025
PM 20562319
ER
PT J
AU Dickstein, LP
Zoghbi, SS
Fujimura, Y
Imaizumi, M
Zhang, Y
Pike, VW
Innis, RB
Fujita, M
AF Dickstein, Leah P.
Zoghbi, Sami S.
Fujimura, Yota
Imaizumi, Masao
Zhang, Yi
Pike, Victor W.
Innis, Robert B.
Fujita, Masahiro
TI Comparison of F-18- and C-11-labeled aryloxyanilide analogs to measure
translocator protein in human brain using positron emission tomography
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Compartment model; Kinetic analysis; Inflammation; Translocator protein
(18 kDa); PET
ID PERIPHERAL BENZODIAZEPINE-RECEPTORS; IN-VIVO; 18 KDA; NONHUMAN-PRIMATES;
PET RADIOLIGAND; NEUROINFLAMMATION; QUANTIFICATION; NOMENCLATURE;
INFLAMMATION; LIGANDS
AB Translocator protein (TSPO) is a promising biomarker for neuroinflammation. We developed two new PET ligands, F-18-PBR06 and C-11-PBR28, to image TSPOs. Although our prior studies suggest that either of the two ligands could be used to quantify TSPOs in human brain, the studies were done in different sets of subjects. In this study, we directly compared F-18-PBR06 and C-11-PBR28 in eight human subjects to determine (1) whether either ligand provides more precise measurements of TSPOs and (2) whether the higher in vitro affinity of PBR06 compared to PBR28 led to higher in vivo binding of F-18-PBR06 compared to C-11-PBR28.
In vivo binding was calculated as total distribution volume (V (T)), using an unconstrained two-tissue compartment model. V (T) was corrected for plasma free fraction (f (P)) to measure ligand binding based on free ligand concentration in brain.
Both ligands measured V (T) with similar precision, as evidenced by similarly good identifiability. However, V (T) for both radioligands increased with increasing lengths of data acquisition, consistent with the accumulation of radiometabolites in brain. Despite its higher lipophilicity and higher in vitro affinity, V (T)/f (P) of F-18-PBR06 was similar to that of C-11-PBR28.
Both F-18-PBR06 and C-11-PBR28 are similar in terms of precision, sensitivity to accumulation of radiometabolites, and magnitude of in vivo binding. Thus, selection between the two radioligands will be primarily determined by the logistical impact of the different half-lives of the two radionuclides (110 vs 20 min).
C1 [Dickstein, Leah P.; Zoghbi, Sami S.; Fujimura, Yota; Imaizumi, Masao; Zhang, Yi; Pike, Victor W.; Innis, Robert B.; Fujita, Masahiro] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
RP Fujita, M (reprint author), NIMH, Mol Imaging Branch, NIH, Bldg 10,Room B1D43,10 Ctr Dr,MSC 1026, Bethesda, MD 20892 USA.
EM FujitaM@intra.nimh.nih.gov
OI Dickstein, Leah/0000-0002-4779-4122
FU NIMH [Z01-MH-002795-07, Z01-MH-002793-07]
FX This research was supported by the Intramural Program of NIMH (project
#Z01-MH-002795-07 and #Z01-MH-002793-07). We thank Kacey Anderson, M.
Desiree Ferraris Araneta, Robert L. Gladding, Kimberly Jenko, William C.
Kreisl, Barbara Scepura, Cheryl Wallisch, and the staff of the PET
Department for successful completion of the studies, PMOD Technologies
(Zurich, Switzerland) for providing its image analysis and modeling
software, and Jussi Hirvonen for assisting statistical analyses.
NR 14
TC 13
Z9 13
U1 1
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD FEB
PY 2011
VL 38
IS 2
BP 352
EP 357
DI 10.1007/s00259-010-1622-y
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 706GC
UT WOS:000286205000017
PM 21085954
ER
PT J
AU Yu, B
Ruman, J
Christman, G
AF Yu, Bo
Ruman, Jane
Christman, Gregory
TI The role of peripheral gonadotropin-releasing hormone receptors in
female reproduction
SO FERTILITY AND STERILITY
LA English
DT Article
DE GnRH; peripheral GnRH receptor; central GnRH receptor; GnRH agonist;
chemotherapy; apoptosis; ovarian damage; implantation; placenta
ID INDUCED OVARIAN DAMAGE; PLACENTAL GNRH RECEPTOR; BREAST-CANCER PATIENTS;
HUMAN ENDOMETRIAL; CHORIONIC-GONADOTROPIN; YOUNG-WOMEN; GENE-EXPRESSION;
FERTILITY PRESERVATION; INDUCED GONADOTOXICITY; EMBRYONIC-DEVELOPMENT
AB Objective: To review the physiologic functions and clinical significance of peripheral GnRH receptors.
Design: Literature review. All peer-reviewed journal articles published before 2010 on peripheral GnRH receptors were searched for in the Pubmed database, and relevant findings were summarized.
Result(s): Peripheral GnRH/GnRH receptor systems may serve as regulators of hCG synthesis and implantation, and play crucial roles in antiproliferation and apoptosis. Currently, GnRH agonists have been used in cancer treatment and ovary protection during chemotherapy, taking advantage of the local direct effect mediated by peripheral GnRH receptors.
Conclusion(s): The ubiquitous GnRH/GnRH receptor system in human tissues has been shown to have some important physiologic functions. Further research to clarify functions of these peripheral GnRH receptors may lead to discovery of new therapeutic options. (Fertil Steril (R) 2011;95:465-73. (C)2011 by American Society for Reproductive Medicine.)
C1 [Yu, Bo] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, CRC, Bethesda, MD 20892 USA.
[Ruman, Jane] Mt Sinai Med Ctr, Dept Obstet & Gynecol, New York, NY 10029 USA.
[Christman, Gregory] Univ Michigan, Med Ctr, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
RP Yu, B (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, CRC, 10 Ctr Dr,1E-3140, Bethesda, MD 20892 USA.
EM yub4@mail.nih.gov
NR 83
TC 16
Z9 20
U1 3
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD FEB
PY 2011
VL 95
IS 2
BP 465
EP 473
DI 10.1016/j.fertnstert.2010.08.045
PG 9
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 709EA
UT WOS:000286419000007
PM 20888559
ER
PT J
AU Kuehn, D
Carter, TC
Aros, S
Conley, MR
Troendle, J
Cassorla, F
Mills, JL
AF Kuehn, D.
Carter, T. C.
Aros, S.
Conley, M. R.
Troendle, J.
Cassorla, F.
Mills, J. L.
TI HEAVY PRENATAL EXPOSURE TO ALCOHOL AND THE RISK FOR GROWTH, FACIAL AND
NEUROLOGIC ABNORMALITIES IN CHILDREN
SO JOURNAL OF INVESTIGATIVE MEDICINE
LA English
DT Meeting Abstract
CT Southern Regional Meeting
CY FEB 17-19, 2011
CL New Orleans, LA
C1 [Kuehn, D.; Carter, T. C.; Conley, M. R.; Troendle, J.; Mills, J. L.] NICHD, Eunice Kennedy Shriver, NIH, DHHS, Bethesda, MD USA.
[Kuehn, D.] USUHS, Bethesda, MD USA.
[Aros, S.; Cassorla, F.] Univ Chile, Santiago, Chile.
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 1081-5589
J9 J INVEST MED
JI J. Invest. Med.
PD FEB
PY 2011
VL 59
IS 2
MA 128
BP 408
EP 408
PG 1
WC Medicine, General & Internal; Medicine, Research & Experimental
SC General & Internal Medicine; Research & Experimental Medicine
GA 709SK
UT WOS:000286461500139
ER
PT J
AU Li, LQ
Jothi, R
Cui, KR
Lee, JY
Cohen, T
Gorivodsky, M
Tzchori, I
Zhao, YG
Hayes, SM
Bresnick, EH
Zhao, KJ
Westphal, H
Love, PE
AF Li, LiQi
Jothi, Raja
Cui, Kairong
Lee, Jan Y.
Cohen, Tsadok
Gorivodsky, Marat
Tzchori, Itai
Zhao, Yangu
Hayes, Sandra M.
Bresnick, Emery H.
Zhao, Keji
Westphal, Heiner
Love, Paul E.
TI Nuclear adaptor Ldb1 regulates a transcriptional program essential for
the maintenance of hematopoietic stem cells
SO NATURE IMMUNOLOGY
LA English
DT Article
ID SELF-RENEWAL; IN-VIVO; PROGENITOR CELLS; PROTEIN LMO2; GATA FACTORS;
MICE; LEUKEMIA; DIFFERENTIATION; IDENTIFICATION; EXPRESSION
AB The nuclear adaptor Ldb1 functions as a core component of multiprotein transcription complexes that regulate differentiation in diverse cell types. In the hematopoietic lineage, Ldb1 forms a complex with the non-DNA-binding adaptor Lmo2 and the transcription factors E2A, Scl and GATA-1 (or GATA-2). Here we demonstrate a critical and continuous requirement for Ldb1 in the maintenance of both fetal and adult mouse hematopoietic stem cells (HSCs). Deletion of Ldb1 in hematopoietic progenitors resulted in the downregulation of many transcripts required for HSC maintenance. Genome-wide profiling by chromatin immunoprecipitation followed by sequencing (ChIP-Seq) identified Ldb1 complex-binding sites at highly conserved regions in the promoters of genes involved in HSC maintenance. Our results identify a central role for Ldb1 in regulating the transcriptional program responsible for the maintenance of HSCs.
C1 [Li, LiQi; Lee, Jan Y.; Love, Paul E.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
[Jothi, Raja] NIEHS, Biostat Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Cui, Kairong; Zhao, Keji] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Cohen, Tsadok; Gorivodsky, Marat; Tzchori, Itai; Zhao, Yangu; Westphal, Heiner] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mammalian Mol Genet, NIH, Bethesda, MD USA.
[Hayes, Sandra M.] SUNY Upstate Med Univ, Dept Microbiol & Immunol, Syracuse, NY USA.
[Bresnick, Emery H.] Univ Wisconsin, Sch Med & Publ Hlth, Paul Carbone Canc Ctr, Wisconsin Inst Med Res, Madison, WI USA.
RP Love, PE (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Cellular & Dev Biol, NIH, Bethesda, MD 20892 USA.
EM lovep@mail.nih.gov
RI Jothi, Raja/G-3780-2015
FU National Institutes of Health [DK068634]
FX We thank D. El-Khoury and A. Grinberg for technical support, and M.
Mukhopadhyay for advice about mouse experiments. Supported by the
Intramural Research Program of the National Institutes of Health (Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, L. L., J.Y.L., T. C., M. G., I. T., Y.Z., H. W. and P. E.
L.; National Institute of Environmental Health Sciences, R.J.; National
Heart, Lung, and Blood Institute, K. C. and K.Z.) and the National
Institutes of Health (DK068634 to E.H.B.).
NR 45
TC 56
Z9 59
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1529-2908
J9 NAT IMMUNOL
JI Nat. Immunol.
PD FEB
PY 2011
VL 12
IS 2
BP 129
EP U38
DI 10.1038/ni.1978
PG 9
WC Immunology
SC Immunology
GA 708QF
UT WOS:000286378400006
PM 21186366
ER
PT J
AU Kannan, P
Telu, S
Shukla, S
Ambudkar, SV
Pike, VW
Halldin, C
Gottesman, MM
Innis, RB
Hall, MD
AF Kannan, Pavitra
Telu, Sanjay
Shukla, Suneet
Ambudkar, Suresh V.
Pike, Victor W.
Halldin, Christer
Gottesman, Michael M.
Innis, Robert B.
Hall, Matthew D.
TI The "Specific" P-Glycoprotein Inhibitor Tariquidar Is Also a Substrate
and an Inhibitor for Breast Cancer Resistance Protein (BCRP/ABCG2)
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Article
DE Positron emission tomography; drug transporters; P-glycoprotein; breast
cancer resistance protein; blood-brain barrier; transport inhibitors;
tariquidar
ID BLOOD-BRAIN-BARRIER; DRUG EFFLUX TRANSPORTERS; MULTIDRUG-RESISTANCE;
XR9576; ABCG2; RADIOTRACERS; LYMPHOCYTES; REVERSAL
AB Tariquidar was developed as a specific inhibitor of the efflux transporter ABCB1. Recent positron emission tomographic brain imaging studies using [(11)C]-tariquidar to measure ABCB1 (P-gp, P-glycoprotein) density in mice indicate that the inhibitor may not be as specific as previously thought. We examined its selectivity as an inhibitor and a substrate for the human transporters P-gp, breast cancer resistance protein (BCRP, ABCG2), and multidrug resistance protein 1 (MRP1, ABCC1). Our results show that at low concentrations, tariquidar acts selectively as an inhibitor of P-gp and also as a substrate of BCRP. At much higher concentrations (>= 100 nM), tariquidar acts as an inhibitor of both P-gp and BCRP. Thus, the in vivo specificity of tariquidar depends on concentration and the relative density and capacity of P-gp vs BCRP.
C1 [Kannan, Pavitra; Telu, Sanjay; Pike, Victor W.; Innis, Robert B.] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
[Kannan, Pavitra; Halldin, Christer] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Shukla, Suneet; Ambudkar, Suresh V.; Gottesman, Michael M.; Hall, Matthew D.] NCI, Cell Biol Lab, Bethesda, MD 20892 USA.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, 10 Ctr Dr,Rm B1D43, Bethesda, MD 20892 USA.
EM robert.innis@nih.gov
RI shukla, suneet/B-4626-2012;
OI Kannan, Pavitra/0000-0002-9170-6062
FU National Institutes of Mental Health [Z01-MH-002852-04, MH002793-09];
National Cancer Institute at the National Institutes of Health
[Z01-BC-005598, Z01-BC-010030-12]
FX This research was supported by the Intramural Research Programs of the
National Institutes of Mental Health (Project Nos. Z01-MH-002852-04 and
MH002793-09) and the National Cancer Institute (Project No.
Z01-BC-005598 and No. Z01-BC-010030-12) at the National Institutes of
Health.
NR 33
TC 60
Z9 62
U1 2
U2 13
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 FEB
PY 2011
VL 2
IS 2
BP 82
EP 89
DI 10.1021/cn100078a
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA 724GU
UT WOS:000287564900004
PM 22778859
ER
PT J
AU Wang, YY
Park, KD
Salome, C
Wilson, SM
Stables, JP
Liu, RH
Khanna, R
Kohn, H
AF Wang, Yuying
Park, Ki Duk
Salome, Christophe
Wilson, Sarah M.
Stables, James P.
Liu, Rihe
Khanna, Rajesh
Kohn, Harold
TI Development and Characterization of Novel Derivatives of the
Antiepileptic Drug Lacosamide That Exhibit Far Greater Enhancement in
Slow Inactivation of Voltage-Gated Sodium Channels
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Article
DE Lacosamide; sodium channel; slow inactivation; affinity bait
ID ANTICONVULSANT ACTIVITIES; OPIOID RECEPTORS; STEM-CELLS; EPILEPSY;
DIFFERENTIATION; NEURONS; BINDING; SITE; CARBAMAZEPINE; MECHANISMS
AB The novel antiepileptic drug (R)-N-benzyl 2-acetamido-3-methoxypropionamide ((R)-lacosamide, Vimpat ((R)-1)) was recently approved in the United States and Europe for adjuvant treatment of partial-onset seizures in adults. (R)-1 preferentially enhances slow inactivation of voltage-gated Na(+) currents, a pharmacological process relevant in the hyperexcitable neuron. We have advanced a strategy to identify lacosamide binding partners by attaching affinity bait (AB) and chemical reporter (CR) groups to (R)-1 to aid receptor detection and isolation. We showed that select lacosamide AB and AB&CR derivatives exhibited excellent activities similar to (R)-1 in the maximal electroshock seizure model in rodents. Here, we examined the effect of these lacosamide AB and AB&CR derivatives and compared them with (R)-1 on Na(+) channel function in central nervous system (CNS) catecholaminergic (CAD) cells. Using whole-cell patch clamp electrophysiology, we demonstrated that the test compounds do not affect the Na+ channel fast inactivation process, that they were far better modulators of slow inactivation than (R)-1, and that modulation of the slow inactivation process was stereospecific. The lacosamide AB agents that contained either an electrophilic isothiocyanate ((R)-5) or a photolabile azide ((R)-8) unit upon AB activation gave modest levels of permanent N(+) channel slow inactivation, providing initial evidence that these compounds may have covalently reacted with their cognate receptor(s). Our findings support the further use of these agents to delineate the (R)-1-mediated Na(+) channel slow inactivation process.
C1 [Wang, Yuying; Khanna, Rajesh] Indiana Univ, Sch Med, Dept Pharmacol, Indianapolis, IN 46202 USA.
[Wang, Yuying; Khanna, Rajesh] Indiana Univ, Sch Med, Dept Toxicol, Indianapolis, IN 46202 USA.
[Wilson, Sarah M.; Khanna, Rajesh] Indiana Univ, Sch Med, Paul & Carole Stark Neurosci Res Inst, Program Med Neurosci, Indianapolis, IN 46202 USA.
[Kohn, Harold] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
[Liu, Rihe] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC 27599 USA.
[Park, Ki Duk; Salome, Christophe; Liu, Rihe; Kohn, Harold] Univ N Carolina, UNC Eshelman Sch Pharm, Div Med Chem & Nat Prod, Chapel Hill, NC 27599 USA.
[Stables, James P.] NINDS, Epilepsy Branch, NIH, Bethesda, MD 20892 USA.
RP Khanna, R (reprint author), Indiana Univ, Sch Med, Dept Pharmacol, Indianapolis, IN 46202 USA.
EM khanna5@iupui.edu; harold_kohn@email.unc.edu
OI Khanna, Rajesh/0000-0002-9066-2969
FU National Institutes of Health (NIH) [R01NS054112]; Indiana State
Department of Health Spinal Cord and Brain Injury Fund [A70-9-079138];
Indiana University [2286501]
FX This work is supported by grants from the National Institutes of Health
(NIH) (R01NS054112 to H.K., R.L.), the Indiana State Department of
Health Spinal Cord and Brain Injury Fund (A70-9-079138 to R.K.), and the
Indiana University Biomedical Committee Research Support Funds (2286501
to R.K). S.M.W. is a Stark Scholar.
NR 58
TC 25
Z9 27
U1 1
U2 2
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 FEB
PY 2011
VL 2
IS 2
BP 90
EP 106
DI 10.1021/cn100089b
PG 17
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA 724GU
UT WOS:000287564900005
PM 21532923
ER
PT J
AU Song, EQ
Hu, J
Wen, CY
Tian, ZQ
Yu, X
Zhang, ZL
Shi, YB
Pang, DW
AF Song, Er-Qun
Hu, Jun
Wen, Cong-Ying
Tian, Zhi-Quan
Yu, Xu
Zhang, Zhi-Ling
Shi, Yun-Bo
Pang, Dai-Wen
TI Fluorescent-Magnetic-Biotargeting Multifunctional Nanobioprobes for
Detecting and Isolating Multiple Types of Tumor Cells
SO ACS NANO
LA English
DT Article
DE tumor; cancer; quantum dot; magnetic; multifunctional nanoparticle;
multifunctional nanosphere; multifunctional nanobioprobe
ID APTAMER-CONJUGATED NANOPARTICLES; SEMICONDUCTOR QUANTUM DOTS; ONE-POT
SYNTHESIS; CANCER-CELLS; BIOMEDICAL APPLICATIONS; PHOTOTHERMAL THERAPY;
GOLD NANOSHELLS; SEPARATION; DIAGNOSIS; NANOSPHERES
AB Fluorescent-magnetic-biotargeting multifunctional nanobioprobes (FMBMNs) have attracted great attention in recent years due to their increasing, important applications in biomedical research, clinical diagnosis, and biomedicine. We have previously developed such nanobioprobes for the detection and isolation of a single kind of tumor cells. Detection and isolation of multiple tumor markers or tumor cells from complex samples sensitively and with high efficiency Is critical for the early diagnosis of tumors, especially malignant tumors or cancers, which will Improve clinical diagnosis outcomes and help to select effective treatment approaches. Here, we expanded the application of the monoclonal antibody (mAb)-coupled FMBMNs for multiplexed assays. Multiple types of cancer cells, such as leukemia cells and prostate cancer cells, were detected and collected from mixed samples within 25 min by using a magnet and an ordinary fluorescence microscope. The capture efficiencies of mAb-coupled FMBMNs for the above-mentioned two types of cells were 96% and 97%, respectively. Furthermore, by using the mAb-coupled FMBMNs, specific and sensitive detection and rapid separation of a small number of spiked leukemia cells and prostate cancer cells in a large population of cultured normal cells (about 0.01% were tumor cells) were achieved simply and inexpensively without any sample pretreatment before cell analysis. Therefore, mAb-coupled multicolor FMBMNs may be used for very sensitive detection and rapid isolation of multiple cancer cells in biomedical research and medical diagnostics.
C1 [Song, Er-Qun; Hu, Jun; Wen, Cong-Ying; Tian, Zhi-Quan; Yu, Xu; Zhang, Zhi-Ling; Pang, Dai-Wen] Wuhan Univ, Key Lab Analyt Chem Biol & Med, Coll Chem & Mol Sci,MOE Innovat Platform 985, Res Ctr Nanobiol & Nanomed,Minist Educ, Wuhan 430072, Peoples R China.
[Song, Er-Qun] Southwest Univ, Coll Pharmaceut Sci, Minist Educ, Key Lab Luminescence & Real Time Anal, Chongqing, Peoples R China.
[Shi, Yun-Bo] NICHHD, Sect Mol Morphogenesis, Program Cell Regulat & Metab, NIH, Bethesda, MD 20892 USA.
RP Pang, DW (reprint author), Wuhan Univ, Key Lab Analyt Chem Biol & Med, Coll Chem & Mol Sci,MOE Innovat Platform 985, Res Ctr Nanobiol & Nanomed,Minist Educ, Wuhan 430072, Peoples R China.
EM dwpang@whu.edu.cn
RI 林, 毅/E-5033-2011; Zhang, Zhi-Ling/B-3135-2010; Yu, Xu /C-9578-2015;
Tian, Zhi-Quan/K-5304-2012
OI Zhang, Zhi-Ling/0000-0001-7807-2264; Yu, Xu /0000-0002-3587-7019;
FU National Key Scientific Program (973)-Nanoscience and Nanotechnology
[2006CB933100, 2011CB933600]; Science Fund for Creative Research Groups
of NSFC [20621502, 20921062]; National Natural Science Foundation of
China [20833006, 20875071, 21005056, 210050641]; Ministry of Public
Health [2009ZX10004-107, 2008ZX10004-004]; NICHD, NIH, USA
FX This work was supported by the National Key Scientific Program
(973)-Nanoscience and Nanotechnology (2006CB933100; 2011CB933600), the
Science Fund for Creative Research Groups of NSFC (20621502; 20921062),
the National Natural Science Foundation of China (20833006; 20875071;
21005056; 210050641, the Ministry of Public Health (2009ZX10004-107;
2008ZX10004-004), and the Intramural Research Program of NICHD, NIH,
USA.
NR 62
TC 123
Z9 130
U1 24
U2 200
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1936-0851
J9 ACS NANO
JI ACS Nano
PD FEB
PY 2011
VL 5
IS 2
BP 761
EP 770
DI 10.1021/nn1011336
PG 10
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA 724CN
UT WOS:000287553800009
PM 21250650
ER
PT J
AU Brion, M
Sanchez-Salorio, M
Corton, M
de la Fuente, M
Pazos, B
Othman, M
Swaroop, A
Abecasis, G
Sobrino, B
Carracedo, A
AF Brion, Maria
Sanchez-Salorio, Manuel
Corton, Marta
de la Fuente, Maria
Pazos, Belen
Othman, Mohammad
Swaroop, Anand
Abecasis, Goncalo
Sobrino, Beatriz
Carracedo, Angel
CA Spanish Multi-Ctr Grp AMD
TI Genetic association study of age-related macular degeneration in the
Spanish population
SO ACTA OPHTHALMOLOGICA
LA English
DT Article
DE ABCA4; age-related macular degeneration; ARMS2; case-control study; CFH;
FGF2; genetic association
ID COMPLEMENT-FACTOR-H; STARGARDT DISEASE GENE; GENOME SCAN; CHOROIDAL
NEOVASCULARIZATION; JAPANESE POPULATION; SUSCEPTIBILITY LOCI;
HEMICENTIN-1 GENES; EXTENDED FAMILIES; GROWTH-FACTORS; MESSENGER-RNA
AB Purpose: To investigate new genetic risk factors and replicate reported associations with advanced age-related macular degeneration (AMD) in a prospective case-control study developed with a Spanish cohort.
Methods: Three hundred and fifty-three unrelated patients with advanced AMD (225 with atrophic AMD, 57 with neovascular AMD, and 71 with mixed AMD) and 282 age-matched controls were included. Functional and tagging SNPs in 55 candidate genes were genotyped using the SNPlex (TM) genotyping system. Single SNP and haplotype association analysis were performed to determine possible genetic associations; interaction effects between SNPs were also investigated.
Results: In agreement with previous reports, ARMS2 and CFH genes were strongly associated with AMD in the studied Spanish population. Moreover, both loci influenced risk independently giving support to different pathways implicated in AMD pathogenesis. No evidence for association of advanced AMD with other previous reported susceptibility genes, such as CST3, CX3CR1, FBLN5, HMCN1, PON1, SOD2, TLR4, VEGF and VLDLR, was detected. However, two additional genes appear to be candidate markers for the development of advanced AMD. A variant located at the 3' UTR of the FGF2 gene (rs6820411) was highly associated with atrophic AMD, and the functional SNP rs3112831 at ABCA4 showed a marginal association with the disease.
Conclusion: We performed a large gene association study in advanced AMD in a Spanish population. Our findings show that CFH and ARMS2 genes seem to be the principal risk loci contributing independently to AMD in our cohort. We report new significant associations that could also influence the development of advanced AMD. These findings should be confirmed in further studies with larger cohorts.
C1 [Brion, Maria] Hospital Univ Complex Santiago CHUS, Santiago De Compostela, Spain.
[Brion, Maria; Corton, Marta; Sobrino, Beatriz; Carracedo, Angel] Univ Santiago de Compostela, CIBERER, Genom Med Grp, Santiago De Compostela, Spain.
[Sanchez-Salorio, Manuel; de la Fuente, Maria; Pazos, Belen] Inst Gallego Oftalmol INGO, Santiago De Compostela, Spain.
[Othman, Mohammad; Swaroop, Anand] Univ Michigan, Dept Ophthalmol, Ann Arbor, MI USA.
[Othman, Mohammad; Swaroop, Anand] Univ Michigan, Dept Visual Sci & Human Genet, Ann Arbor, MI USA.
[Swaroop, Anand] NEI, Natl Inst Hlth, Neurobiol Neurodegenerat & Repair Lab, Bethesda, MD USA.
[Abecasis, Goncalo] Univ Michigan, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Sobrino, Beatriz; Carracedo, Angel] Univ Santiago de Compostela, Natl Genotyping Ctr CEGEN, Santiago De Compostela, Spain.
RP Brion, M (reprint author), Univ Santiago de Compostela, Fac Med, San Francisco S-N, Santiago De Compostela 5782, Spain.
EM maria.brion@usc.es
RI Coco-Martin, Rosa/H-4511-2015;
OI Coco-Martin, Rosa/0000-0002-1811-1417; Brion, Maria/0000-0001-7463-2148;
Abecasis, Goncalo/0000-0003-1509-1825; Swaroop,
Anand/0000-0002-1975-1141; Carracedo, Angel/0000-0003-1085-8986
FU Xunta de Galicia [PGI-DIT06PXIB208204PR]; Instituto de Salud Carlos III
[EMER07/018]; National Institutes of Health, USA
FX This study was supported by grants from the Xunta de Galicia
(PGI-DIT06PXIB208204PR), the Instituto de Salud Carlos III (EMER07/018),
and National Institutes of Health, USA. The sponsor or funding
organization had no role in the design or conduct of this research.
NR 74
TC 19
Z9 22
U1 0
U2 8
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1755-375X
J9 ACTA OPHTHALMOL
JI Acta Ophthalmol.
PD FEB
PY 2011
VL 89
IS 1
BP E12
EP E22
DI 10.1111/j.1755-3768.2010.02040.x
PG 11
WC Ophthalmology
SC Ophthalmology
GA 711YL
UT WOS:000286628100002
PM 21106043
ER
PT J
AU Redon, CE
Nakamura, AJ
Martin, OA
Parekh, PR
Weyemi, US
Bonner, WM
AF Redon, Christophe E.
Nakamura, Asako J.
Martin, Olga A.
Parekh, Palak R.
Weyemi, Urbain S.
Bonner, William M.
TI Recent developments in the use of gamma-H2AX as a quantitative DNA
double-strand break biomarker
SO AGING-US
LA English
DT Article
DE DNA damage; DNA repair; gamma-H2AX; double-strand break; biomarker;
cancer; senescent cells
ID BLOOD-LYMPHOCYTES; DAMAGE RESPONSE; ADIPOSE-TISSUE; RADIATION-EXPOSURE;
TUMOR-CELLS; IN-VIVO; REPAIR; ASSAY; H2AX; POLY(ADP-RIBOSE)
AB The past year has seen considerable developments in the use of the DNA double-strand breaks (DSBs) to evaluate genome alterations in cells undergoing a variety of genotoxic stresses in vitro and in vivo. When the gamma-H2AX foci which mark the DSBs are stained, individual breaks are detectible, making the assay suitable for situations requiring great sensitivity. While the methods for the detection of gamma-H2AX foci are still evolving, particularly for in vivo detection, the basic assay has proven to be useful in several diverse areas of research. We will highlight recent developments of the assay in four areas: radiation biodosimetry, the evaluation or validation of new cancer drugs in clinical studies, chronic inflammation, and environmental genotoxicity.
C1 [Redon, Christophe E.; Nakamura, Asako J.; Martin, Olga A.; Parekh, Palak R.; Weyemi, Urbain S.; Bonner, William M.] NCI, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Bonner, WM (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
EM bonnerw@mail.nih.gov
RI Parekh, Palak/B-7042-2015; Weyemi, Urbain/E-2083-2016
OI Parekh, Palak/0000-0001-9201-5194;
FU National Cancer Institute, NIH
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, NIH.
NR 42
TC 76
Z9 78
U1 1
U2 8
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD FEB
PY 2011
VL 3
IS 2
BP 168
EP 174
PG 7
WC Cell Biology
SC Cell Biology
GA 732FM
UT WOS:000288170400013
PM 21325706
ER
PT J
AU Leggio, L
Addolorato, G
Cippitelli, A
Jerlhag, E
Kampov-Polevoy, AB
Swift, RM
AF Leggio, Lorenzo
Addolorato, Giovanni
Cippitelli, Andrea
Jerlhag, Elisabet
Kampov-Polevoy, Alexei B.
Swift, Robert M.
TI Role of Feeding-Related Pathways in Alcohol Dependence: A Focus on Sweet
Preference, NPY, and Ghrelin
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Review
DE Alcohol Dependence; Alcohol Craving; Appetite; Feeding-Related Pathways;
Sweet Preference; Feeding-Related Peptides; Neuropeptide Y; Ghrelin
ID NEUROPEPTIDE-Y NPY; CORTICOTROPIN-RELEASING-FACTOR; STIMULATES
LOCOMOTOR-ACTIVITY; NUCLEUS-ACCUMBENS; FAMILY-HISTORY; PARAVENTRICULAR
NUCLEUS; HYPOTHALAMIC NUCLEI; DOPAMINE-OVERFLOW; TASTE INTENSITY;
ETHANOL INTAKE
AB Converging research evidence suggests that alcohol and food-seeking behaviors share common neural pathways. There is preclinical and clinical evidence linking the consumption of sweets to alcohol intake in both animals and humans. In addition, a growing body of animal and human literature suggests the involvement of "feeding-related" peptides in alcohol-seeking behavior. In particular, both central and peripheral appetitive peptides have shown a possible role in alcohol dependence. The present mini-review will summarize the literature on the link between sweet preference and alcohol dependence, and on the role of feeding-related peptides in alcohol dependence. Specifically, in an attempt to narrow the field, the present mini-review will focus on 2 specific pathways, the central neuropeptide Y and the peripheral gut peptide ghrelin. Although more research is needed, data available suggest that studying feeding-related pathways in alcohol dependence may have theoretic, biologic, diagnostic, and therapeutic implications.
C1 [Leggio, Lorenzo; Swift, Robert M.] Brown Univ, Ctr Alcohol & Addict Studies, Sch Med, Providence, RI 02912 USA.
[Leggio, Lorenzo; Addolorato, Giovanni] Univ Cattolica Sacro Cuore, Rome, Italy.
[Cippitelli, Andrea] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD USA.
[Jerlhag, Elisabet] Univ Gothenburg, Pharmacol Sect, Inst Neurosci & Physiol, Sahlgrenska Acad, Gothenburg, Sweden.
[Kampov-Polevoy, Alexei B.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
RP Leggio, L (reprint author), Brown Univ, Ctr Alcohol & Addict Studies, Sch Med, Box GS 121-4, Providence, RI 02912 USA.
EM lorenzo_leggio@brown.edu
RI Leggio, Lorenzo/M-2972-2016;
OI Addolorato, Giovanni/0000-0002-1522-9946
NR 83
TC 29
Z9 29
U1 0
U2 18
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD FEB
PY 2011
VL 35
IS 2
BP 194
EP 202
DI 10.1111/j.1530-0277.2010.01334.x
PG 9
WC Substance Abuse
SC Substance Abuse
GA 710KH
UT WOS:000286510000002
PM 21058960
ER
PT J
AU Liu, JX
Zhou, ZF
Hodgkinson, CA
Yuan, QP
Shen, PH
Mulligan, CJ
Wang, A
Gray, RR
Roy, A
Virkkunen, M
Goldman, D
Enoch, MA
AF Liu, Jixia
Zhou, Zhifeng
Hodgkinson, Colin A.
Yuan, Qiaoping
Shen, Pei-Hong
Mulligan, Connie J.
Wang, Alex
Gray, Rebecca R.
Roy, Alec
Virkkunen, Matti
Goldman, David
Enoch, Mary-Anne
TI Haplotype-Based Study of the Association of Alcohol-Metabolizing Genes
With Alcohol Dependence in Four Independent Populations
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Dependence; Alcohol Dehydrogenases; Aldehyde Dehydrogenases;
Haplotype Association; ALDH1A1
ID ALDEHYDE DEHYDROGENASE-DEFICIENCY; WHITE COLLEGE-STUDENTS; PROMOTER
POLYMORPHISMS; LINKAGE DISEQUILIBRIUM; EUROPEAN AMERICANS; MISSION
INDIANS; BINGE DRINKING; ALDH GENES; RISK; JAPANESE
AB Background:
Ethanol is metabolized by 2 rate-limiting reactions: alcohol dehydrogenases (ADH) convert ethanol to acetaldehyde that is subsequently metabolized to acetate by aldehyde dehydrogenases (ALDH). Approximately 50% of East Asians have genetic variants that significantly impair this pathway and influence alcohol dependence (AD) vulnerability. We investigated whether variation in alcohol metabolism genes might alter the AD risk in four non-East Asian populations by performing systematic haplotype association analyses to maximize the chances of capturing functional variation.
Methods:
Haplotype-tagging SNPs were genotyped using the Illumina GoldenGate platform. Genotypes were available for 40 SNPs across the ADH genes cluster and 24 SNPs across the two ALDH genes in four diverse samples that included cases (lifetime AD) and controls (no Axis 1 disorders). The case control sample sizes were the following: Finnish Caucasians: 232, 194; African Americans: 267, 422; Plains American Indians: 226, 110; and Southwestern American (SW) Indians: 317, 72.
Results:
In all four populations, as well as HapMap populations, 5 haplotype blocks were identified across the ADH gene cluster: (i) ADH5-ADH4; (ii) ADH6-ADH1A-ADH1B; (iii) ADH1C; (iv) intergenic; (v) ADH7. The ALDH1A1 gene was defined by 4 blocks and ALDH2 by 1 block. No haplotype or SNP association results were significant after correction for multiple comparisons; however, several results, particularly for ALDH1A1 and ADH4, replicated earlier findings. There was an ALDH1A1 block 1 and 2 (extending from intron 5 to the 3' UTR) yin yang haplotype (haplotypes that have opposite allelic configuration) association with AD in the Finns driven by SNPs rs3764435 and rs2303317, respectively, and an ALDH1A1 block 3 (including the promoter region) yin yang haplotype association in SW Indians driven by 5 SNPs, all in allelic identity. The ADH4 SNP rs3762894 was associated with AD in Plains Indians.
Conclusions:
The systematic evaluation of alcohol-metabolizing genes in four non-East Asian populations has shown only modest associations with AD, largely for ALDH1A1 and ADH4. A concentration of signals for AD with ALDH1A1 yin yang haplotypes in several populations warrants further study.
C1 [Liu, Jixia; Zhou, Zhifeng; Hodgkinson, Colin A.; Yuan, Qiaoping; Shen, Pei-Hong; Wang, Alex; Goldman, David; Enoch, Mary-Anne] NIAAA, NIH, LNG, Bethesda, MD 20892 USA.
[Mulligan, Connie J.; Wang, Alex; Gray, Rebecca R.] Univ Florida, Dept Anthropol, Gainesville, FL 32611 USA.
[Roy, Alec] New Jersey Hlth Care Syst, Dept Vet Affairs, E Orange, NJ USA.
[Virkkunen, Matti] Univ Helsinki, Dept Psychiat, Inst Clin Med, FIN-00014 Helsinki, Finland.
[Virkkunen, Matti] Kellokoski Hosp, Kellokoski, Finland.
RP Liu, JX (reprint author), NIAAA, NIH, LNG, 5625 Fishers Lane,Room 3S32,MSC 9412, Bethesda, MD 20892 USA.
EM liujixia@mail.nih.gov
RI Goldman, David/F-9772-2010
OI Goldman, David/0000-0002-1724-5405
FU National Institute on Alcohol Abuse and Alcoholism, NIH [RO1 DA
10336-02]; National Institute of Drug Abuse, NIH; NIH [R03 AA12906]
FX This research was supported by the Intramural Research Program of the
National Institute on Alcohol Abuse and Alcoholism, NIH and in part by
grant RO1 DA 10336-02 to AR from the National Institute of Drug Abuse,
NIH and by NIH grant R03 AA12906 to C.J.M. We gratefully acknowledge the
work performed by Robert Robin and Bernard Albaugh in recruiting and
interviewing the SW Indians and Plains Indians, respectively. Longina
Akhtar and Elisa Moore provided technical support. Danielle Muchnik,
Angelica Gonzalez-Oliver, David Mayorga, Ben Burkley, and Jena
Chojnowski assisted in genotyping samples.
NR 63
TC 25
Z9 25
U1 3
U2 23
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0145-6008
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD FEB
PY 2011
VL 35
IS 2
BP 304
EP 316
DI 10.1111/j.1530-0277.2010.01346.x
PG 13
WC Substance Abuse
SC Substance Abuse
GA 710KH
UT WOS:000286510000014
PM 21083667
ER
PT J
AU Li, JS
Colan, SD
Sleeper, LA
Newburger, JW
Pemberton, VL
Atz, AM
Cohen, MS
Golding, F
Klein, GL
Lacro, RV
Radojewski, E
Richmond, ME
Minich, LL
AF Li, Jennifer S.
Colan, Steven D.
Sleeper, Lynn A.
Newburger, Jane W.
Pemberton, Victoria L.
Atz, Andrew M.
Cohen, Meryl S.
Golding, Fraser
Klein, Gloria L.
Lacro, Ronald V.
Radojewski, Elizabeth
Richmond, Marc E.
Minich, L. LuAnn
CA Pediat Heart Network Investigators
TI Lessons learned from a pediatric clinical trial: The Pediatric Heart
Network Angiotensin-Converting Enzyme Inhibition in Mitral Regurgitation
Study
SO AMERICAN HEART JOURNAL
LA English
DT Article
ID ATRIOVENTRICULAR-CANAL DEFECTS; SURGICAL REPAIR; OFF-LABEL;
SEPTAL-DEFECT; CHILDREN; ECHOCARDIOGRAPHY; REPRESENTATION; MULTICENTER;
ENALAPRIL; DISEASE
AB Background Mitral regurgitation is the most common indication for reoperation in children following repair of atrioventricular septal defect (AVSD). We hypothesized that angiotensin-converting enzyme inhibitor therapy would decrease the severity of mitral regurgitation and limit left ventricular volume overload in children following AVSD repair.
Methods The Pediatric Heart Network designed a placebo-controlled randomized trial of enalapril in this population. The primary aim was to test the effect of enalapril on the change in left ventricular end-diastolic dimension body surface area-adjusted z score. Before the launch of the trial, a feasibility study was performed to estimate the number of patients with at least moderate mitral regurgitation following AVSD repair.
Trial experience Seventeen months after the start of the study, 349 patients were screened, 8 were trial eligible, and only 5 were enrolled. The study was subsequently terminated because of low patient accrual. Several factors led to the problems with patient accrual, including (1) the use of criteria to assess disease severity in the feasibility study that were not identical to those used in the trial, (2) failure to achieve equipoise for the study among clinicians and referring physicians, (3) reliance on methodology developed in adult populations with different disease mechanisms, and (4) absence of adequate data to define the natural history of the disease process under study. Progress in the treatment of children with cardiovascular disease will depend on the future of multicenter collaborative clinical trials. The lessons learned from this study may contribute to improvements in this research. (Am Heart J 2011;161:233-40.)
C1 [Li, Jennifer S.] Duke Univ, Med Ctr, Duke Clin Res Inst, Div Cardiol,Dept Pediat, Durham, NC 27715 USA.
[Colan, Steven D.; Sleeper, Lynn A.; Klein, Gloria L.] New England Res Inst, Watertown, MA 02172 USA.
[Newburger, Jane W.; Lacro, Ronald V.] Childrens Hosp, Boston, MA 02115 USA.
[Pemberton, Victoria L.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Atz, Andrew M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Cohen, Meryl S.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Golding, Fraser; Radojewski, Elizabeth] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Richmond, Marc E.] Columbia Univ, New York, NY USA.
[Minich, L. LuAnn] Univ Utah, Salt Lake City, UT USA.
RP Li, JS (reprint author), Duke Univ, Med Ctr, Duke Clin Res Inst, Div Cardiol,Dept Pediat, POB 17969, Durham, NC 27715 USA.
EM jennifer.li@duke.edu
FU National Heart, Lung, and Blood Institute [HL068269, HL068270, HL068279,
HL068281, HL068285, HL068292, HL068290, HL068288, HL085057]
FX Supported by U01 grants from the National Heart, Lung, and Blood
Institute (HL068269, HL068270, HL068279, HL068281, HL068285, HL068292,
HL068290, HL068288, HL085057).
NR 32
TC 9
Z9 9
U1 0
U2 2
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 FEB
PY 2011
VL 161
IS 2
BP 233
EP 240
DI 10.1016/j.ahj.2010.10.030
PG 8
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 719FX
UT WOS:000287188000005
PM 21315203
ER
PT J
AU Shen, JA
Johnson, VM
Sullivan, LM
Jacques, PF
Magnani, JW
Lubitz, SA
Pandey, S
Levy, D
Vasan, RS
Quatromoni, PA
Junyent, M
Ordovas, JM
Benjamin, EJ
AF Shen, Jian
Johnson, Victor M.
Sullivan, Lisa M.
Jacques, Paul F.
Magnani, Jared W.
Lubitz, Steven A.
Pandey, Shivda
Levy, Daniel
Vasan, Ramachandran S.
Quatromoni, Paula A.
Junyent, Mireia
Ordovas, Jose M.
Benjamin, Emelia J.
TI Dietary factors and incident atrial fibrillation: the Framingham Heart
Study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID POLYUNSATURATED-FATTY-ACIDS; ALCOHOL-CONSUMPTION; FISH-OIL; BLOOD
INSTITUTE; NATIONAL HEART; RISK-FACTORS; DANISH DIET; WHOLE-GRAIN;
DISEASE; HEALTH
AB Background: There have been conflicting reported associations between dietary factors and incident atrial fibrillation (AF).
Objective: We evaluated associations between consumption of alcohol, caffeine, fiber, and polyunsaturated fatty acids (PUFAs) and incident AF in the Framingham Heart Study.
Design: Participants without AF (n = 4526; 9640 examinations; mean age: 62 y; 56% women) from the original and offspring cohorts completed food-frequency questionnaires and were followed prospectively for 4 y. We examined the associations between dietary exposures and AF with Cox proportional hazards regression.
Results: A total of 296 individuals developed AF (177 men, 119 women). In multivariable analyses, there were no significant associations between examined dietary exposures and AF risk. Hazard ratios (HRs) for increasing quartiles of dietary factors were as follows: for alcohol, 0.73 (95% CI: 0.5, 1.05), 0.85 (95% CI: 0.61, 1.18), and 1.12 (95% CI: 0.83, 1.51) (P for trend = 0.48); for caffeine, 0.84 (95% CI: 0.62, 1.15), 0.87 (95% CI: 0.64, 1.2), and 0.98 (95% CI: 0.7, 1.39) (P for trend = 0.84); for total fiber, 0.86 (95% CI: 0.61, 1.2), 0.64 (95% CI: 0.44, 0.92), and 0.81 (95% CI: 0.54, 1.2) (P for trend = 0.16); and for n-3 (omega-3) PUFAs, 1.11 (95% CI: 0.81, 1.54), 0.92 (95% CI: 0.65, 1.29), and 1.18 (95% CI: 0.85, 1.64) (P for trend = 0.57; quartile 1 was the reference group). In exploratory analyses, consumption of >4 servings of dark fish/wk (5 cases and 21 individuals at risk) was significantly associated with AF risk compared with the consumption of,1 serving of dark fish/wk (HR: 6.53; 95% CI: 2.65, 16.06; P < 0.0001).
Conclusions: Consumption of alcohol, caffeine, fiber, and fish-derived PUFAs was not significantly associated with AF risk. The observed adverse association between the consumption of dark fish and AF merits further investigation. Our findings suggest that the dietary exposures examined convey limited attributable risk of AF in the general population. Am J Clin Nutr 2011;93:261-6.
C1 [Magnani, Jared W.; Levy, Daniel; Benjamin, Emelia J.] NHLBI, Farmingham Heart Study, Framingham, MA 01702 USA.
[Shen, Jian; Jacques, Paul F.; Junyent, Mireia; Ordovas, Jose M.] Tufts Univ, Human Nutr Res Ctr Aging, Jean Mayer US Dept Agr, Boston, MA 02111 USA.
[Johnson, Victor M.; Sullivan, Lisa M.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Quatromoni, Paula A.; Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Magnani, Jared W.; Pandey, Shivda; Levy, Daniel; Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Evans Mem Dept Med, Cardiol Sect, Boston, MA 02215 USA.
[Vasan, Ramachandran S.; Benjamin, Emelia J.] Boston Univ, Evans Mem Dept Med, Sect Prevent Med, Boston, MA 02215 USA.
[Quatromoni, Paula A.] Boston Univ, Sargent Coll Hlth & Rehabil Sci, Dept Hlth Sci, Boston, MA 02215 USA.
[Lubitz, Steven A.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
RP Benjamin, EJ (reprint author), NHLBI, Farmingham Heart Study, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM emelia@bu.edu
OI Ramachandran, Vasan/0000-0001-7357-5970; Sullivan,
Lisa/0000-0003-0726-7149; Benjamin, Emelia/0000-0003-4076-2336
FU Heart, Lung, and Blood Institute [HL-54776]; National Institute of
Diabetes and Digestive and Kidney Diseases [DK075030]; US Department of
Agriculture Research [53-K06-5-10, 58-1950-9-001]; American Heart
Association [09FTF2190028]; National Institutes of Health [N01-HC 25195,
6R01-NS 17950, RC1HL101056, HL092577, 1R01HL102214]
FX Supported by the National Heart, Lung, and Blood Institute (grants
HL-54776; to JS and JMO), the National Institute of Diabetes and
Digestive and Kidney Diseases (grant DK075030; to JMO), the US
Department of Agriculture Research (contracts 53-K06-5-10 and
58-1950-9-001; to JS and JMO), the American Heart Association (award
09FTF2190028; to JWM), and the National Institutes of Health (grants
N01-HC 25195, 6R01-NS 17950, RC1HL101056, HL092577, and 1R01HL102214; to
EJB).
NR 47
TC 44
Z9 44
U1 0
U2 14
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
EI 1938-3207
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD FEB
PY 2011
VL 93
IS 2
BP 261
EP 266
DI 10.3945/ajcn.110.001305
PG 6
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 709DQ
UT WOS:000286417900006
PM 21106919
ER
PT J
AU Persson, C
Canedo, P
Machado, JC
El-Omar, EM
Forman, D
AF Persson, Christina
Canedo, Paulo
Machado, Jose C.
El-Omar, Emad M.
Forman, David
TI Polymorphisms in Inflammatory Response Genes and Their Association With
Gastric Cancer: A HuGE Systematic Review and Meta-Analyses
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Review
DE epidemiology; genetics; Helicobacter pylori; interleukins;
meta-analysis; polymorphism; genetic; stomach neoplasms
ID HELICOBACTER-PYLORI INFECTION; NECROSIS-FACTOR-ALPHA; RECEPTOR
ANTAGONIST GENE; SQUAMOUS-CELL CARCINOMA; EPSTEIN-BARR-VIRUS; TNF-A
GENES; INCREASED RISK; CHINESE POPULATION; INTERLEUKIN-1 POLYMORPHISMS;
PROMOTER POLYMORPHISM
AB To evaluate the association between gastric cancer susceptibility and inflammation-related gene polymorphisms, the authors conducted a series of meta-analyses using a predefined protocol. Genes investigated were those coding for the interleukin (IL) proteins (IL1B, IL1RN, IL8, and IL10) and for tumor necrosis factor-alpha. Gastric cancers were stratified by histologic subtype and anatomic subsite, by Helicobacter pylori infection status, by geographic location (Asian or non-Asian study population), and by a quantitative index of study quality. All published literature and meeting abstracts from the period 1990-2006 were considered. Results consistently supported increased cancer risk for IL1RN2 carriers; the increased risk was specific to non-Asian populations and was seen for intestinal and diffuse cancers, distal cancers, and, to a lesser extent, cardia cancers. Analyses restricted to high-quality studies or H. pylori-positive cases and controls also showed significant associations with both carrier status and homozygosity status. In Asian populations, reduced risk was observed in association with IL1B-31C carrier status. This effect was also observed in analyses restricted to high-quality studies. These results indicate the importance of stratification by anatomic site, histologic type, H. pylori infection, and country of origin. Study quality considerations, both laboratory and epidemiologic, can also affect results and may explain, in part, the variability in results published to date.
C1 [Persson, Christina] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Persson, Christina] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Canedo, Paulo; Machado, Jose C.] Univ Porto, Inst Mol Pathol & Immunol, P-4100 Oporto, Portugal.
[El-Omar, Emad M.] Univ Aberdeen, Dept Med, Aberdeen, Scotland.
[Forman, David] Int Agcy Res Canc, Sect Canc Informat, F-69372 Lyon, France.
RP Persson, C (reprint author), NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
EM christina.persson@nih.gov
RI Machado, Jose Carlos/C-5907-2009; Kim, Seongman/N-6910-2014; Canedo,
Paulo/C-4947-2008
OI Machado, Jose Carlos/0000-0003-4741-8415; Canedo,
Paulo/0000-0001-6838-5726
FU Marie Curie Training in Molecular Epidemiology fellowship
FX This review was supported by a Marie Curie Training in Molecular
Epidemiology fellowship award.
NR 73
TC 91
Z9 96
U1 1
U2 18
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 FEB 1
PY 2011
VL 173
IS 3
BP 259
EP 270
DI 10.1093/aje/kwq370
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 709TC
UT WOS:000286463300002
PM 21178102
ER
PT J
AU Hsu, WL
Yu, KJ
Chien, YC
Chiang, CJ
Cheng, YJ
Chen, JY
Liu, MY
Chou, SP
You, SL
Hsu, MM
Lou, PJ
Wang, CP
Hong, JH
Leu, YS
Tsai, MH
Su, MC
Tsai, ST
Chao, WY
Ger, LP
Chen, PR
Yang, CS
Hildesheim, A
Diehl, SR
Chen, CJ
AF Hsu, Wan-Lun
Yu, Kelly J.
Chien, Yin-Chu
Chiang, Chun-Ju
Cheng, Yu-Juen
Chen, Jen-Yang
Liu, Mei-Ying
Chou, Sheng-Ping
You, San-Lin
Hsu, Mow-Ming
Lou, Pei-Jen
Wang, Cheng-Ping
Hong, Ji- Hong
Leu, Yi-Shing
Tsai, Ming-Hsui
Su, Mao-Chang
Tsai, Sen-Tien
Chao, Wen-Yuan
Ger, Luo-Ping
Chen, Peir-Rong
Yang, Czau-Siung
Hildesheim, Allan
Diehl, Scott R.
Chen, Chien-Jen
TI Familial Tendency and Risk of Nasopharyngeal Carcinoma in Taiwan:
Effects of Covariates on Risk
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE carcinoma; cohort studies; herpesvirus 4; human
ID EPSTEIN-BARR-VIRUS; CIGARETTE-SMOKING; CHINA; CANCER; COHORT; INFECTION;
GUANGZHOU; AREA
AB In the present study, the authors compared the long-term risk of nasopharyngeal carcinoma (NPC) of male participants in an NPC multiplex family cohort with that of controls in a community cohort in Taiwan after adjustment for anti-Epstein-Barr virus (EBV) seromarkers and cigarette smoking. A total of 43 incident NPC cases were identified from the 1,019 males in the NPC multiplex family cohort and the 9,622 males in the community cohort, for a total of 8,061 person-years and 185,587 person-years, respectively. The adjusted hazard ratio was 6.8 (95% confidence interval (CI): 2.3, 20.1) for the multiplex family cohort compared with the community cohort. In the evaluation of anti-EBV viral capsid antigen immunoglobulin A and anti-EBV deoxyribonuclease, the adjusted hazard ratios were 2.8 (95% CI: 1.3, 6.0) and 15.1 (95% CI: 4.2, 54.1) for those positive for 1 EBV seromarker and positive for both seromarkers, respectively, compared with those negative for both EBV seromarkers. The adjusted hazard ratio was 31.0 (95% CI: 9.7, 98.7) for participants who reported a family history of NPC and who were anti-EBV-seropositive compared with individuals without such a history who were anti-EBV-seronegative. The findings suggest that both family history of NPC and anti-EBV seropositivity are important determinants of subsequent NPC risk and that the effect of family history on NPC risk cannot be fully explained by mediation through EBV serologic responses.
C1 [Hsu, Wan-Lun; Chien, Yin-Chu; You, San-Lin; Chen, Chien-Jen] Acad Sinica, Genom Res Ctr, Taipei 115, Taiwan.
[Hsu, Wan-Lun; Chiang, Chun-Ju; Cheng, Yu-Juen; Chen, Chien-Jen] Natl Taiwan Univ, Coll Publ Hlth, Grad Inst Epidemiol, Taipei 10764, Taiwan.
[Yu, Kelly J.; Hildesheim, Allan] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Chen, Jen-Yang; Chou, Sheng-Ping] Natl Hlth Res Inst, Natl Inst Canc Res, Chunan, Taiwan.
[Chen, Jen-Yang; Yang, Czau-Siung] Natl Taiwan Univ, Coll Med, Grad Inst Microbiol, Taipei 10764, Taiwan.
[Liu, Mei-Ying] Natl Taipei Coll Nursing, Ctr Gen Educ, Taipei, Taiwan.
[Hsu, Mow-Ming; Lou, Pei-Jen; Wang, Cheng-Ping] Natl Taiwan Univ Hosp, Dept Otolaryngol, Taipei, Taiwan.
[Wang, Cheng-Ping] Natl Taiwan Univ, Coll Med, Inst Biomed Engn, Taipei 10764, Taiwan.
[Wang, Cheng-Ping] Natl Taiwan Univ, Coll Engn, Taipei 10764, Taiwan.
[Hong, Ji- Hong] Chang Gung Mem Hosp, Dept Radiat Oncol, Tao Yuan, Taiwan.
[Leu, Yi-Shing] MacKay Mem Hosp, Dept Otolaryngol, Taipei, Taiwan.
[Tsai, Ming-Hsui] China Med Univ Hosp, Dept Otolaryngol, Taichung, Taiwan.
[Su, Mao-Chang] Chung Shan Med Univ Hosp, Dept Otorhinolaryngol Head & Neck Surg, Taichung, Taiwan.
[Su, Mao-Chang] Chung Shan Med Univ Hosp, Dept Speech Language Pathol & Audiol, Taichung, Taiwan.
[Su, Mao-Chang] Chung Shan Med Univ Hosp, Sch Med, Taichung, Taiwan.
[Tsai, Sen-Tien; Chao, Wen-Yuan] Natl Cheng Kung Univ Hosp, Dept Otolaryngol, Tainan 70428, Taiwan.
[Ger, Luo-Ping] Kaohsiung Vet Gen Hosp, Dept Educ & Res, Kaohsiung, Taiwan.
[Chen, Peir-Rong] Buddhist Tzu Chi Gen Hosp, Dept Otolaryngol, Hualien, Taiwan.
[Diehl, Scott R.] New Jersey Dent, Ctr Pharmacogenom & Complex Dis Res, Newark, NJ USA.
RP Chen, CJ (reprint author), Acad Sinica, Genom Res Ctr, 128 Acad Rd,Sect 2, Taipei 115, Taiwan.
EM cjchen@ntu.edu.tw
RI Chen, Chien-Jen/C-6976-2008; Chen, Jen-Yang/D-2085-2010; Hildesheim,
Allan/B-9760-2015;
OI Hildesheim, Allan/0000-0003-0257-2363; WANG,
CHENG-PING/0000-0001-7872-1463; LOU, PEI-JEN/0000-0002-3383-8593
FU Intramural NIH HHS
NR 35
TC 11
Z9 12
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 FEB 1
PY 2011
VL 173
IS 3
BP 292
EP 299
DI 10.1093/aje/kwq358
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 709TC
UT WOS:000286463300005
PM 21148719
ER
PT J
AU Quinlan, SC
Pfeiffer, RM
Morton, LM
Engels, EA
AF Quinlan, Scott C.
Pfeiffer, Ruth M.
Morton, Lindsay M.
Engels, Eric A.
TI Risk factors for early-onset and late-onset post-transplant
lymphoproliferative disorder in kidney recipients in the United States
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Article
ID NON-HODGKIN-LYMPHOMA; EPSTEIN-BARR-VIRUS; SOLID-ORGAN TRANSPLANTATION;
RENAL-TRANSPLANTATION; DISTINCT ENTITY; IMMUNOSUPPRESSION; EPIDEMIOLOGY;
DISEASE; MALIGNANCY; INFECTION
AB Solid-organ transplant recipients have an elevated risk for some malignancies because of the requirement for immunosuppression [1]. In particular, non-Hodgkin's lymphoma (NHL) is common and comprises one end of a spectrum of post-transplant lymphoproliferative disorder (PTLD) ranging from benign hyperplasia to lymphoid malignancy [2]. PTLD risk is influenced by the type of organ transplanted, the age and Epstein-Barr virus (EBV) serostatus of the transplant recipient, and the intensity of immunosuppression [3-9]. PTLD incidence is high immediately after transplantation, decreases subsequently, and then rises again 4-5 years from transplantation [10,11]. This incidence pattern suggests the presence of separate early-onset and late-onset PTLD subtypes. Early-onset PTLDs tend to be EBV-positive and, when extranodal, are more likely than late-onset PTLDs to be localized to the transplanted organ [12,13]. Late-onset PTLD is less likely to be associated with EBV and, overall, is more likely than early-onset PTLD to be extranodal [13,14]. The Scientific Registry of Transplant Recipients (SRTR) includes data on a large number of solid-organ transplant recipients in the United States and information on malignancies diagnosed post-transplantation. We used these data to conduct a retrospective cohort study among kidney transplant recipients to examine differences in risk factors between early-onset PTLD and late-onset PTLD.
C1 [Engels, Eric A.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, DHHS, Rockville, MD 20892 USA.
RP Engels, EA (reprint author), NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, DHHS, 6120 Execut Blvd,EPS 7076, Rockville, MD 20892 USA.
EM engelse@exchange.nih.gov
RI Pfeiffer, Ruth /F-4748-2011; Morton, Lindsay/B-5234-2015
OI Morton, Lindsay/0000-0001-9767-2310
FU The National Cancer Institute; HRSA is part of the U.S. Department of
Health and Human Services [231-00-0116]
FX Grant sponsor: Intramural Research Program of The National Cancer
Institute. Grant sponsor: HRSA is part of the U.S. Department of Health
and Human Services; Grant number: 231-00-0116 [to The Scientific
Registry of Transplant Recipients (SRTR)]
NR 29
TC 56
Z9 57
U1 0
U2 6
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD FEB
PY 2011
VL 86
IS 2
BP 206
EP 209
DI 10.1002/ajh.21911
PG 4
WC Hematology
SC Hematology
GA 718UL
UT WOS:000287151700015
PM 21264909
ER
PT J
AU Huson, SM
Acosta, MT
Belzberg, AJ
Bernards, A
Chernoff, J
Cichowski, K
Evans, DG
Ferner, RE
Giovannini, M
Korf, BR
Listernick, R
North, KN
Packer, RJ
Parada, LF
Peltonen, J
Ramesh, V
Reilly, KM
Risner, JW
Schorry, EK
Upadhyaya, M
Viskochil, DH
Zhu, YA
Hunter-Schaedle, K
Giancotti, FG
AF Huson, Susan M.
Acosta, Maria T.
Belzberg, Allan J.
Bernards, Andre
Chernoff, Jonathan
Cichowski, Karen
Evans, D. Gareth
Ferner, Rosalie E.
Giovannini, Marco
Korf, Bruce R.
Listernick, Robert
North, Kathryn N.
Packer, Roger J.
Parada, Luis F.
Peltonen, Juha
Ramesh, Vijaya
Reilly, Karlyne M.
Risner, John W.
Schorry, Elizabeth K.
Upadhyaya, Meena
Viskochil, David H.
Zhu, Yuan
Hunter-Schaedle, Kim
Giancotti, Filippo G.
TI Back to the Future: Proceedings From the 2010 NF Conference
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE neurofibromatosis; schwannomatosis; NF1; NF2; neurofibroma; learning
disabilities; bone dysplasia; MPNST
ID GROWTH-FACTOR RECEPTOR; PERIPHERAL-NERVE; NEUROFIBROMATOSIS TYPE-2;
PHENOTYPE; TUMORIGENESIS; EXPRESSION; PLEXIFORM; MUTATIONS; SPRED1;
TUMORS
AB The neurofibromatoses (NF) encompass the rare diseases NF1, NF2, and schwannomatosis. The NFs affect 100,000 Americans; over 2 million persons worldwide; and are caused by mutation of tumor suppressor genes. Individuals with NF1 in particular may develop tumors anywhere in the nervous system; additional manifestations can include learning disabilities, bone dysplasia, cardiovascular defects, unmanageable pain, and physical disfigurement. Ultimately, the NFs can cause blindness, deafness, severe morbidity, and increased mortality and NF1 includes a risk of malignant cancer. Today there is no treatment for the NFs (other than symptomatic); however, research efforts to understand these genetic conditions have made tremendous strides in the past few years. Progress is being made on all fronts, from discovery studies-understanding the molecular signaling deficits that cause the manifestations of NF-to the growth of preclinical drug screening initiatives and the emergence of a number of clinical trials. An important element in fuelling this progress is the sharing of knowledge, and to this end, for over 20 years the Children's Tumor Foundation has convened an annual NF Conference, bringing together NF professionals to share ideas and build collaborations. The 2010 NF Conference held in Baltimore, MD June 5-8, 2010 hosted over 300 NF researchers and clinicians. This paper provides a synthesis of the highlights presented at the Conference and as such, is a "state-of-the-field" for NF research in 2010. (C) 2010 Wiley-Liss, Inc.
C1 [Risner, John W.; Hunter-Schaedle, Kim] Childrens Tumor Fdn, New York, NY 10005 USA.
[Huson, Susan M.; Evans, D. Gareth] Univ Manchester, St Marys Hosp, Manchester M13 0JH, Lancs, England.
[Acosta, Maria T.; Packer, Roger J.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Belzberg, Allan J.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Bernards, Andre; Ramesh, Vijaya] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Chernoff, Jonathan] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Cichowski, Karen] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Ferner, Rosalie E.] Guys & St Thomas NHS Hosp Trust, London, England.
[Giovannini, Marco] House Ear Res Inst, Los Angeles, CA USA.
[Korf, Bruce R.] Univ Alabama, Birmingham, AL USA.
[Listernick, Robert] Childrens Mem Hosp, Chicago, IL 60614 USA.
[North, Kathryn N.] Univ Sydney, Sydney, NSW 2006, Australia.
[Parada, Luis F.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Peltonen, Juha] Inst Biomed, Helsinki, Finland.
[Reilly, Karlyne M.] NCI, NIH, Frederick, MD 21701 USA.
[Schorry, Elizabeth K.] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Upadhyaya, Meena] Cardiff Univ, Cardiff, S Glam, Wales.
[Viskochil, David H.] Univ Utah, Salt Lake City, UT USA.
[Zhu, Yuan] Univ Michigan, Ann Arbor, MI 48109 USA.
[Giancotti, Filippo G.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
RP Hunter-Schaedle, K (reprint author), Childrens Tumor Fdn, 95 Pine St, New York, NY 10005 USA.
EM khs@ctf.org
RI Peltonen, Juha/C-2817-2008; Parada, luis/B-9400-2014; Chernoff,
Jonathan/I-7631-2014; North, Kathryn/K-6476-2012;
OI Peltonen, Juha/0000-0002-5732-4167; Chernoff,
Jonathan/0000-0002-4803-7836; North, Kathryn/0000-0003-0841-8009; Evans,
Gareth/0000-0002-8482-5784
FU National Institutes of Health [1R13NS070505-01]
FX Grant sponsor: National Institutes of Health; Grant number:
1R13NS070505-01.
NR 31
TC 11
Z9 11
U1 1
U2 7
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD FEB
PY 2011
VL 155A
IS 2
BP 307
EP 321
DI 10.1002/ajmg.a.33804
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 718VE
UT WOS:000287153700009
PM 21271647
ER
PT J
AU Conde-Agudelo, A
Romero, R
Kusanovic, JP
AF Conde-Agudelo, Agustin
Romero, Roberto
Kusanovic, Juan Pedro
TI Nifedipine in the management of preterm labor: a systematic review and
metaanalysis
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Review
DE calcium channel blocker; neonatal morbidity; pregnancy; premature birth;
preterm birth; tocolysis; uterine contractility
ID RANDOMIZED CONTROLLED-TRIAL; CALCIUM-CHANNEL BLOCKERS;
MAGNESIUM-SULFATE; ORAL NIFEDIPINE; INFLAMMATORY RESPONSE;
MYOCARDIAL-INFARCTION; CLINICAL-SIGNIFICANCE; ANTAGONIST ATOSIBAN; ACUTE
TOCOLYSIS; RITODRINE
AB OBJECTIVE: To determine the efficacy and safety of nifedipine as a tocolytic agent in women with preterm labor.
STUDY DESIGN: A systematic review and metaanalysis of randomized controlled trials.
RESULTS: Twenty-six trials (2179 women) were included. Nifedipine was associated with a significant reduction in the risk of delivery within 7 days of initiation of treatment and before 34 weeks' gestation, respiratory distress syndrome, necrotizing enterocolitis, intraventricular hemorrhage, neonatal jaundice, and admission to the neonatal intensive care unit when compared with beta(2)-adrenergic-receptor agonists. There was no difference between nifedipine and magnesium sulfate in tocolytic efficacy. Nifedipine was associated with significantly fewer maternal adverse events than beta(2)-adrenergic-receptor agonists and magnesium sulfate. Maintenance nifedipine tocolysis was ineffective in prolonging gestation or improving neonatal outcomes when compared with placebo or no treatment.
CONCLUSION: Nifedipine is superior to beta(2)-adrenergic-receptor agonists and magnesium sulfate for tocolysis in women with preterm labor.
C1 [Conde-Agudelo, Agustin; Romero, Roberto; Kusanovic, Juan Pedro] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Conde-Agudelo, Agustin; Romero, Roberto; Kusanovic, Juan Pedro] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI USA.
[Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI USA.
[Romero, Roberto; Kusanovic, Juan Pedro] Wayne State Univ, Dept Obstet & Gynecol, Detroit, MI USA.
RP Conde-Agudelo, A (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services
FX This study was supported in part by the Intramural Research Program of
the Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services.
NR 79
TC 7
Z9 9
U1 1
U2 10
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 FEB
PY 2011
VL 204
IS 2
AR 134.e1
DI 10.1016/j.ajog.2010.11.038
PG 20
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 715HV
UT WOS:000286874900017
PM 21284967
ER
PT J
AU Mittal, P
Romero, R
Tarca, AL
Draghici, S
Nhan-Chang, CL
Chaiworapongsa, T
Hotra, J
Gomez, R
Kusanovic, JP
Lee, DC
Kim, CJ
Hassan, SS
AF Mittal, Pooja
Romero, Roberto
Tarca, Adi L.
Draghici, Sorin
Nhan-Chang, Chia-Ling
Chaiworapongsa, Tinnakorn
Hotra, John
Gomez, Ricardo
Kusanovic, Juan Pedro
Lee, Deug-Chan
Kim, Chong Jai
Hassan, Sonia S.
TI A molecular signature of an arrest of descent in human parturition
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE adenosine triphosphatase; Na plus /K plus transporting; alpha 1
polypeptide; ATP1A1; COX2; HIF1A; hypoxia inducible factor-1;
inflammation; interleukin-6; myometrium; parturition; pregnancy;
prostaglandin-endoperoxide synthase 2; PTGS2; spontaneous term labor;
systems biology; transcriptomics
ID TUMOR-NECROSIS-FACTOR; SMOOTH-MUSCLE-CELLS; HUMAN-FETAL MEMBRANES; HUMAN
MYOMETRIAL CELLS; CORTICOTROPIN-RELEASING HORMONE; MESSENGER-RNA
EXPRESSION; AMNIOTIC-FLUID INTERLEUKIN-6; SPONTANEOUS PRETERM LABOR;
PROSTAGLANDIN-E SYNTHASE; HUMAN UTERINE MYOCYTES
AB OBJECTIVE: This study was undertaken to identify the molecular basis of an arrest of descent.
STUDY DESIGN: Human myometrium was obtained from women in term labor (TL; n = 29) and arrest of descent (AODes; n = 21). Gene expression was characterized using Illumina HumanHT-12 microarrays. A moderated Student t test and false discovery rate adjustment were applied for analysis. Confirmatory quantitative reverse transcription-polymerase chain reaction and immunoblot were performed in an independent sample set.
RESULTS: Four hundred genes were differentially expressed between women with an AODes compared with those with TL. Gene Ontology analysis indicated enrichment of biological processes and molecular functions related to inflammation and muscle function. Impacted pathways included inflammation and the actin cytoskeleton. Overexpression of hypoxia inducible factor-1a, interleukin -6, and prostaglandin-endoperoxide synthase 2 in AODes was confirmed.
CONCLUSION: We have identified a stereotypic pattern of gene expression in the myometrium of women with an arrest of descent. This represents the first study examining the molecular basis of an arrest of descent using a genome-wide approach.
C1 [Mittal, Pooja; Romero, Roberto; Tarca, Adi L.; Draghici, Sorin; Nhan-Chang, Chia-Ling; Chaiworapongsa, Tinnakorn; Hotra, John; Kusanovic, Juan Pedro; Lee, Deug-Chan; Kim, Chong Jai; Hassan, Sonia S.] NICHHD, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Mittal, Pooja; Romero, Roberto; Tarca, Adi L.; Draghici, Sorin; Nhan-Chang, Chia-Ling; Chaiworapongsa, Tinnakorn; Hotra, John; Kusanovic, Juan Pedro; Lee, Deug-Chan; Kim, Chong Jai; Hassan, Sonia S.] NICHHD, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI USA.
[Mittal, Pooja; Nhan-Chang, Chia-Ling; Chaiworapongsa, Tinnakorn; Kusanovic, Juan Pedro; Hassan, Sonia S.] Wayne State Univ, Sch Med, Dept Obstet & Gynecol, Detroit, MI 48201 USA.
[Romero, Roberto; Tarca, Adi L.] Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI USA.
[Gomez, Ricardo] Univ Catolica Chile, Sotero Rio Hosp, Ctr Perinatal Diag & Res, Dept Obstet & Gynecol, Puente Alto, Chile.
RP Mittal, P (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, 3990 John R,Box 4, Detroit, MI 48201 USA.
EM pmittal@med.wayne.edu
RI Draghici, Sorin/B-3074-2013
OI Draghici, Sorin/0000-0002-0786-8377
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services
FX This study was supported in part by the Perinatology Research Branch,
Division of Intramural Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health, Department of Health and Human Services.
NR 308
TC 3
Z9 3
U1 0
U2 6
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
EI 1097-6868
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD FEB
PY 2011
VL 204
IS 2
AR 177.e15
DI 10.1016/j.ajog.2010.09.025
PG 19
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 715HV
UT WOS:000286874900040
PM 21284969
ER
PT J
AU Vaisbuch, E
Whitty, JE
Hassan, SS
Romero, R
Kusanovic, JP
Cotton, DB
Sorokin, Y
Karumanchi, SA
AF Vaisbuch, Edi
Whitty, Janice E.
Hassan, Sonia S.
Romero, Roberto
Kusanovic, Juan Pedro
Cotton, David B.
Sorokin, Yoram
Karumanchi, S. Ananth
TI Circulating angiogenic and antiangiogenic factors in women with
eclampsia
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE placental growth factor; preeclampsia; pregnancy; soluble endoglin;
soluble fms-like tyrosine kinase 1; soluble vascular endothelial growth
factor receptor-1
ID ENDOTHELIAL GROWTH-FACTOR; UTERINE ARTERY DOPPLER; FOR-GESTATIONAL-AGE;
LATE-ONSET PREECLAMPSIA; TYROSINE KINASE-1; FACTOR RECEPTOR-1; MATERNAL
SERUM; EARLY-PREGNANCY; DEVELOP PREECLAMPSIA; SOLUBLE ENDOGLIN
AB OBJECTIVE: The objective of the study was to determine whether eclampsia has a different circulating profile of angiogenic (placental growth factor [PlGF]) and antiangiogenic factors (soluble vascular endothelial growth factor receptor-1 [sVEGFR-1] and soluble endoglin [sEng]) from severe preeclampsia.
STUDY DESIGN: This cross-sectional study included pregnant women in the following groups: (1) normal pregnancy (n = 40); (2) severe preeclampsia (n = 40); and (3) eclampsia (n = 20). Maternal serum PlGF, sVEGFR-1, and sEng concentrations were determined using an enzyme-linked immunosorbent assay.
RESULTS: The study results included the following: (1) the median concentration of sVEGFR-1 and sEng was higher and of PlGF was lower in severe preeclampsia or eclampsia than in normal pregnancy (P<.001 for all); and (2) the median concentrations of these 3 analytes did not differ significantly between patients with severe preeclampsia and those with eclampsia.
CONCLUSION: Eclampsia is associated with higher maternal circulating concentrations of sVEGFR-1 and sEng and lower concentrations of PlGF than normal pregnancy but with similar concentrations to severe preeclampsia. These findings suggest that eclampsia shares a common pathogenic pathway as severe preeclampsia.
C1 [Vaisbuch, Edi; Hassan, Sonia S.; Romero, Roberto; Kusanovic, Juan Pedro] Wayne State Univ, Perinatol Res Branch, Intramural Div,Dept Hlth & Human Serv,NIH, Hutzel Womens Hosp,Eunice Kennedy Shriver Natl In, Detroit, MI 48201 USA.
[Vaisbuch, Edi; Hassan, Sonia S.; Kusanovic, Juan Pedro; Cotton, David B.; Sorokin, Yoram] Wayne State Univ, Dept Obstet & Gynecol, Hutzel Womens Hosp, Detroit, MI 48201 USA.
[Romero, Roberto] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
[Whitty, Janice E.] Hubbard Hosp, Meharry Med Coll, Dept Obstet & Gynecol, Nashville, TN USA.
[Karumanchi, S. Ananth] Beth Israel Deaconess Med Ctr, Howard Hughes Med Inst, Boston, MA 02215 USA.
[Karumanchi, S. Ananth] Harvard Univ, Sch Med, Boston, MA USA.
RP Romero, R (reprint author), Wayne State Univ, Perinatol Res Branch, Intramural Div,Dept Hlth & Human Serv,NIH, Hutzel Womens Hosp,Eunice Kennedy Shriver Natl In, 3990 John R,Box 4, Detroit, MI 48201 USA.
EM prbchiefstaff@med.wayne.edu
OI Vaisbuch, Edi/0000-0002-8400-9031
FU Perinatology Research Branch, Division of Intramural Research, Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services; Burroughs Welcome Fund
FX This study was supported in part by the Perinatology Research Branch,
Division of Intramural Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health, Department of Health and Human Services. S.A.K. is an
investigator of the Howard Hughes Medical Institute and is supported by
the Burroughs Welcome Fund Clinical Scientist Award. S.A.K. is a
coinventor on multiple patents held by the Beth Israel Deaconess Medical
Center for the diagnosis/therapy of preeclampsia that has been
outlicensed to multiple companies. In addition, S.A.K. is a consultant
to Beckman Coulter, Abbott Diagnostics, Roche Diagnostics, and Johnson &
Johnson.
NR 100
TC 8
Z9 8
U1 0
U2 3
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 FEB
PY 2011
VL 204
IS 2
AR 152.e1
DI 10.1016/j.ajog.2010.08.049
PG 9
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 715HV
UT WOS:000286874900025
PM 21062661
ER
PT J
AU Sei, Y
Lu, XP
Liou, A
Zhao, XL
Wank, SA
AF Sei, Yoshitatsu
Lu, Xinping
Liou, Alice
Zhao, Xilin
Wank, Stephen A.
TI A stem cell marker-expressing subset of enteroendocrine cells resides at
the crypt base in the small intestine
SO AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
LA English
DT Article
DE green fluorescent protein; leucine-rich repeat-containing G
protein-coupled receptor 5; organoid
ID PROGENITOR CELLS; ENDOCRINE-CELLS; CHROMOGRANIN-A; ADULT-MOUSE;
DIFFERENTIATION; EPITHELIUM; FATE; SPECIFICATION; NEUROGENIN-3; SIGNALS
AB Sei Y, Lu X, Liou A, Zhao X, Wank SA. A stem cell marker-expressing subset of enteroendocrine cells resides at the crypt base in the small intestine. Am J Physiol Gastrointest Liver Physiol 300: G345-G356, 2011. First published November 18, 2010; doi:10.1152/ajpgi.00278.2010.-The spatial orientation of the enteroendocrine cells along the crypt-villus axis is closely associated with their differentiation in the intestine. Here we studied this relationship using primary duodenal crypts and an ex vivo organoid system established from cholecystokinin-green fluorescent protein (CCK-GFP) transgenic mice. In the primary duodenal crypts, GFP+ cells were found not only in the upper crypt but also at the crypt base, where the stem cells reside. Many GFP+ cells below +4 position were positive for the putative intestinal stem cell markers, leucine-rich repeat-containing G protein-coupled receptor 5, CD133, and doublecortin and CaM kinase-like-1, and also for the neuroendocrine transcription factor neurogenin 3. However, these cells were neither stem nor transient amplifying precursor cells because they were negative for both Ki-67 and phospho-Histone H3 and positive for the mature endocrine marker chromogranin A. Furthermore, these cells expressed multiple endocrine hormones. Tracking of GFP+ cells in the organoids from CCK-GFP mice indicated that GFP+ cells were first observed around the +4 position, some of which localized to the crypt base later in the culture period. These results suggest that a subset of enteroendocrine cells migrates down to the crypt base or stays localized at the crypt base, where they express stem and postmitotic endocrine markers. Further investigation of the function of this subset may provide novel insights into the genesis and development of enteroendocrine cells as well as enteroendocrine tumorigenesis.
C1 [Sei, Yoshitatsu; Lu, Xinping; Liou, Alice; Zhao, Xilin; Wank, Stephen A.] NIDDK, Digest Dis Branch, NIH, Bethesda, MD USA.
RP Sei, Y (reprint author), Natl Inst Diabet Digest & Kidney Dis, Gastroenterol Sect, 10 Ctr Dr,Bldg 10,Rm 9C-112,MSC1804, Bethesda, MD 20892 USA.
EM seiy@mail.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases, NIH
FX This research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases, NIH.
NR 34
TC 26
Z9 26
U1 0
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1857
J9 AM J PHYSIOL-GASTR L
JI Am. J. Physiol.-Gastroint. Liver Physiol.
PD FEB
PY 2011
VL 300
IS 2
BP G345
EP G356
DI 10.1152/ajpgi.00278.2010
PG 12
WC Gastroenterology & Hepatology; Physiology
SC Gastroenterology & Hepatology; Physiology
GA 713GX
UT WOS:000286724600017
PM 21088235
ER
PT J
AU Miller, RL
AF Miller, R. Lance
TI Transgenic mice: beyond the knockout
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Review
DE Cre; enhanced green fluorescent protein; high-throughput;
renal-specific; transgenics
ID TRANSLATIONAL PROFILING APPROACH; DESIGNED G(I)-COUPLED RECEPTOR; GREEN
FLUORESCENT PROTEIN; CNS CELL-TYPES; CONDITIONAL EXPRESSION; CRE
RECOMBINASE; IN-VIVO; COUPLED RECEPTORS; STEM-CELLS; MOUSE
AB Miller RL. Transgenic mice: beyond the knockout. Am J Physiol Renal Physiol 300: F291-F300, 2011. First published November 10, 2010; doi: 10.1152/ajprenal.00082.2010.-Transgenic mice have had a tremendous impact on biomedical research. Most researchers are familiar with transgenic mice that carry Cre recombinase (Cre) and how they are used to create conditional knockouts. However, some researchers are less familiar with many of the other types of transgenic mice and their applications. For example, transgenic mice can be used to study biochemical and molecular pathways in primary cultures and cell suspensions derived from transgenic mice, cell-cell interactions using multiple fluorescent proteins in the same mouse, and the cell cycle in real time and in the whole animal, and they can be used to perform deep tissue imaging in the whole animal, follow cell lineage during development and disease, and isolate large quantities of a pure cell type directly from organs. These novel transgenic mice and their applications provide the means for studying of molecular and biochemical events in the whole animal that was previously limited to cell cultures. In conclusion, transgenic mice are not just for generating knockouts.
C1 NHLBI, Epithelial Syst Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Miller, RL (reprint author), NHLBI, Epithelial Syst Biol Lab, NIH, 10 Ctr Dr,Bldg 10,Rm 6N312, Bethesda, MD 20892 USA.
EM lance.miller@nih.gov
NR 62
TC 9
Z9 11
U1 0
U2 18
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD FEB
PY 2011
VL 300
IS 2
BP F291
EP F300
DI 10.1152/ajprenal.00082.2010
PG 10
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 715XQ
UT WOS:000286929200001
PM 21068085
ER
PT J
AU Schnermann, J
AF Schnermann, Jurgen
TI Maintained tubuloglomerular feedback responses during acute inhibition
of P2 purinergic receptors in mice
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE PPADS; suramin; stop-flow pressure; proximal reabsorption; micropuncture
ID DEFICIENT MICE; GLOMERULAR HEMODYNAMICS; ADENOSINE; FLOW; PRESSURE; ATP;
ACTIVATION; BLOCKADE; RELEASE; RENIN
AB Schnermann J. Maintained tubuloglomerular feedback responses during acute inhibition of P2 purinergic receptors in mice. Am J Physiol Renal Physiol 300: F339-F344, 2011. First published December 8, 2010; doi:10.1152/ajprenal.00637.2010.-Tubuloglomerular feedback (TGF), the change of afferent arteriolar resistance initiated by changes of luminal NaCl concentration, is thought to be related to NaCl-dependent release of ATP by macula densa cells. In the present study, we have explored the possibility that the released ATP may directly interact with vasoconstrictor P2 purinergic receptors in the vicinity of the glomerular vascular pole. In two different strains of wild-type mice (SWR/J and FVB), TGF responses were determined in vivo by measuring the stop flow pressure (P-SF) change caused by a saturating increase in loop of Henle flow rate before and during the administration of the P2 receptor inhibitors PPADS (12 mg/kg + 35 mg.kg(-1).h(-1) iv) or suramin (50 mg/kg + 150 mg.kg(-1).h(-1)). Both agents significantly reduced the blood pressure response to the P2X agonist alpha,beta-methylene ATP. In SWR/J and FVB mice, elevating flow to 30 nl/min reduced P-SF by 16.4 +/- 2.2 and 17.1 +/- 1.8%. During infusion of PPADS, P-SF fell by 18.8 +/- 2 (P = 0.4) and 16.5 +/- 1.5% (P = 0.82) in the two strains of mice. During suramin infusion, P-SF decreased by 14.7 +/- 2.4 (P = 0.62) and 15 +/- 1.3% (P = 0.4) in SWR/J and FVB mice, respectively. Including PPADS (10(-4) M) in the loop perfusate did not significantly alter the P-SF response (18.9 +/- 1.8%; P = 0.54). Arterial blood pressure was not systematically affected by the P2 inhibitors. As measured by free-flow micropuncture, PPADS significantly reduced proximal tubular fluid reabsorption in both fractional and absolute terms. These results indicate that the direct activation of P2 purinergic receptors by ATP is not a major cause of TGF-induced vasoconstriction in vivo.
C1 NIDDK, Kidney Dis Branch, NIH, Bethesda, MD 20892 USA.
RP Schnermann, J (reprint author), NIDDK, Kidney Dis Branch, NIH, Bldg 10,Rm 4D51,10 Ctr Dr,MSC 1370, Bethesda, MD 20892 USA.
EM jurgens@intra.niddk.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health, Bethesda, MD
FX This work was supported by the intramural research program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health, Bethesda, MD.
NR 34
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U1 0
U2 6
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD FEB
PY 2011
VL 300
IS 2
BP F339
EP F344
DI 10.1152/ajprenal.00637.2010
PG 6
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 715XQ
UT WOS:000286929200006
PM 21147842
ER
PT J
AU Leibenluft, E
AF Leibenluft, Ellen
TI Severe Mood Dysregulation, Irritability, and the Diagnostic Boundaries
of Bipolar Disorder in Youths
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Review
ID DEFICIT HYPERACTIVITY DISORDER; OPPOSITIONAL DEFIANT DISORDER;
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PLACEBO-CONTROLLED TRIAL;
HOSPITALIZED AGGRESSIVE-CHILDREN; ADOLESCENT PSYCHIATRIC-DISORDERS;
VENTROMEDIAL PREFRONTAL CORTEX; DISRUPTIVE BEHAVIOR DISORDERS;
DOUBLE-BLIND; CONDUCT DISORDER
AB In recent years, increasing numbers of children have been diagnosed with bipolar disorder. In some cases, children with unstable mood clearly meet current diagnostic criteria for bipolar disorder, and in others, the diagnosis is unclear. Severe mood dysregulation is a syndrome defined to capture the symptomatology of children whose diagnostic status with respect to bipolar disorder is uncertain, that is, those who have severe, nonepisodic irritability and the hyperarousal symptoms characteristic of mania but who lack the well-demarcated periods of elevated or irritable mood characteristic of bipolar disorder. Levels of impairment are comparable between youths with bipolar disorder and those with severe mood dysregulation. An emerging literature compares children with severe mood dysregulation and those with bipolar disorder in longitudinal course, family history, and pathophysiology. Longitudinal data in both clinical and community samples indicate that nonepisodic irritability in youths is common and is associated with an elevated risk for anxiety and unipolar depressive disorders, but not bipolar disorder, in adulthood. Data also suggest that youths with severe mood dysregulation have lower familial rates of bipolar disorder than do those with bipolar disorder. While youths in both patient groups have deficits in face emotion labeling and experience more frustration than do normally developing children, the brain mechanisms mediating these pathophysiologic abnormalities appear to differ between the two patient groups. No specific treatment for severe mood dysregulation currently exists, but verification of its identity as a syndrome distinct from bipolar disorder by further research should include treatment trials.
C1 NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, Bethesda, MD 20892 USA.
RP Leibenluft, E (reprint author), NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, Bldg 15K,MSC-2670, Bethesda, MD 20892 USA.
EM leibs@mail.nih.gov
FU NIMH
FX Supported by the NIMH Intramural Research Program.
NR 105
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U1 17
U2 50
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD FEB
PY 2011
VL 168
IS 2
BP 129
EP 142
DI 10.1176/appi.ajp.2010.10050766
PG 14
WC Psychiatry
SC Psychiatry
GA 716MI
UT WOS:000286972800007
PM 21123313
ER
PT J
AU Shaw, P
Gilliam, M
Liverpool, M
Weddle, C
Malek, M
Sharp, W
Greenstein, D
Evans, A
Rapoport, J
Giedd, J
AF Shaw, Philip
Gilliam, Mary
Liverpool, Maria
Weddle, Catherine
Malek, Meaghan
Sharp, Wendy
Greenstein, Deanna
Evans, Alan
Rapoport, Judith
Giedd, Jay
TI Cortical Development in Typically Developing Children With Symptoms of
Hyperactivity and Impulsivity: Support for a Dimensional View of
Attention Deficit Hyperactivity Disorder
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID AUTOMATED 3-D EXTRACTION; REVISED CONNERS PARENT; DEFICIT/HYPERACTIVITY
DISORDER; LATENT CLASS; BRAIN ABNORMALITIES; CEREBRAL-CORTEX; MATTER
VOLUME; RATING-SCALE; GREY-MATTER; ADOLESCENTS
AB Objective: There is considerable epidemiological and neuropsychological evidence that attention deficit hyperactivity disorder (ADHD) is best considered dimensionally, lying at the extreme end of a continuous distribution of symptoms and underlying cognitive impairments. The authors investigated whether cortical brain development in typically developing children with symptoms of hyperactivity and impulsivity resembles that found in the syndrome of ADHD. Specifically, they examined whether a slower rate of cortical thinning during late childhood and adolescence, which they previously found in ADHD, is also linked to the severity of symptoms of hyperactivity and impulsivity in typically developing children.
Method: In a longitudinal analysis, a total of 193 typically developing children with 389 neuroanatomic magnetic resonance images and varying levels of symptoms of hyperactivity and impulsivity (measured with the Conners' Parent Rating Scale) were contrasted with 197 children with ADHD with 337 imaging scans. The relationship between the rates of regional cortical thinning and severity of symptoms of hyperactivity/impulsivity was determined.
Results: Youth with higher levels of hyperactivity/impulsivity had a slower rate of cortical thinning, predominantly in prefrontal cortical regions, bilaterally in the middle frontal/premotor gyri, extending down the medial prefrontal wall to the anterior cingulate; the orbitofrontal cortex; and the right inferior frontal gyrus. For each increase of one point in the hyperactivity/impulsivity score, there was a decrease in the rate of regional cortical thinning of 0.0054 mm/year (SE=0.0019 mm/year). Children with ADHD had the slowest rate of cortical thinning.
Conclusions: Slower cortical thinning during adolescence characterizes the presence of both the symptoms and syndrome of ADHD, providing neurobiological evidence for dimensionality of the disorder.
C1 [Shaw, Philip] NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA.
McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada.
RP Shaw, P (reprint author), NIMH, Child Psychiat Branch, Rm 3N202,Bldg 10,Ctr Dr, Bethesda, MD 20892 USA.
EM shawp@mail.nih.gov
RI Giedd, Jay/B-7302-2012; Giedd, Jay/J-9644-2015; Giedd, Jay/A-3080-2008
OI Giedd, Jay/0000-0003-0827-3460; Giedd, Jay/0000-0003-2002-8978;
FU National Institute of Mental Health
FX Supported by the Intramural Research Program of the National Institute
of Mental Health.
NR 53
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U1 2
U2 28
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD FEB
PY 2011
VL 168
IS 2
BP 143
EP 151
DI 10.1176/appi.ajp.2010.10030385
PG 9
WC Psychiatry
SC Psychiatry
GA 716MI
UT WOS:000286972800008
PM 21159727
ER
PT J
AU Finger, EC
Marsh, AA
Blair, KS
Reid, ME
Sims, C
Ng, P
Pine, DS
Blair, RJR
AF Finger, Elizabeth C.
Marsh, Abigail A.
Blair, Karina S.
Reid, Marguerite E.
Sims, Courtney
Ng, Pamela
Pine, Daniel S.
Blair, R. James R.
TI Disrupted Reinforcement Signaling in the Orbitofrontal Cortex and
Caudate in Youths With Conduct Disorder or Oppositional Defiant Disorder
and a High Level of Psychopathic Traits
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID CALLOUS-UNEMOTIONAL TRAITS; VENTROMEDIAL PREFRONTAL CORTEX;
PROBABILISTIC RESPONSE REVERSAL; DORSAL ANTERIOR CINGULATE; COMMON
STEREOTACTIC SPACE; PASSIVE-AVOIDANCE; BASOLATERAL AMYGDALA; DISSOCIABLE
ROLES; HUMAN BRAIN; CHILDREN
AB Objective: Dysfunction in the amygdala and orbitofrontal cortex has been reported in youths and adults with psychopathic traits. The specific nature of the functional irregularities within these structures remains poorly understood. The authors used a passive avoidance task to examine the responsiveness of these systems to early stimulus-reinforcement exposure, when prediction errors are greatest and learning maximized, and to reward in youths with psychopathic traits and comparison youths.
Method: While performing the passive avoidance learning task, 15 youths with conduct disorder or oppositional defiant disorder plus a high level of psychopathic traits and 15 healthy subjects completed a 3.0-T fMRI scan.
Results: Relative to the comparison youths, the youths with a disruptive behavior disorder plus psychopathic traits showed less orbitofrontal responsiveness both to early stimulus-reinforcement exposure and to rewards, as well as less caudate response to early stimulus-reinforcement exposure. There were no group differences in amygdala responsiveness to these two task measures, but amygdala responsiveness throughout the task was lower in the youths with psychopathic traits.
Conclusions: Compromised sensitivity to early reinforcement information in the orbitofrontal cortex and caudate and to reward outcome information in the orbitofrontal cortex of youths with conduct disorder or oppositional defiant disorder plus psychopathic traits suggests that the integrated functioning of the amygdala, caudate, and orbitofrontal cortex may be disrupted. This provides a functional neural basis for why such youths are more likely to repeat disadvantageous decisions. New treatment possibilities are raised, as pharmacologic modulations of serotonin and dopamine can affect this form of learning.
C1 [Finger, Elizabeth C.] Univ Western Ontario, Dept Clin Neurol Sci, Schulich Sch Med, London, ON N6A 5A5, Canada.
NIMH, Mood & Anxiety Program, Bethesda, MD 20892 USA.
Georgetown Univ, Dept Psychol, Washington, DC 20057 USA.
RP Finger, EC (reprint author), Univ Western Ontario, Dept Clin Neurol Sci, Schulich Sch Med, B10-004,339 Windermere Rd, London, ON N6A 5A5, Canada.
EM elizabeth.finger@lhsc.on.ca
RI Finger, Elizabeth/B-6453-2015
FU NIMH; School of Psychiatry, University of New South Wales, Sydney,
Australia
FX Supported by the NIMH Intramural Research Program and by sponsorship of
Ms. Ng by the School of Psychiatry, University of New South Wales,
Sydney, Australia.
NR 63
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U1 6
U2 29
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD FEB
PY 2011
VL 168
IS 2
BP 152
EP 162
DI 10.1176/appi.ajp.2010.10010129
PG 11
WC Psychiatry
SC Psychiatry
GA 716MI
UT WOS:000286972800009
PM 21078707
ER
PT J
AU Brown, TM
Fee, E
AF Brown, Theodore M.
Fee, Elizabeth
TI Milton Terris (1915-2002): Outspoken Advocate for Progressive Public
Health Policy
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
C1 [Brown, Theodore M.] Univ Rochester, Dept Hist, Rochester, NY 14627 USA.
[Brown, Theodore M.] Univ Rochester, Dept Community & Prevent Med, Rochester, NY 14627 USA.
[Fee, Elizabeth] NIH, Hist Med Div, Natl Lib Med, Bethesda, MD 20892 USA.
RP Brown, TM (reprint author), Univ Rochester, Dept Hist, 601 Elmwood Ave, Rochester, NY 14627 USA.
EM Theodore_Brown@urmc.rochester.edu
NR 2
TC 0
Z9 0
U1 0
U2 4
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD FEB
PY 2011
VL 101
IS 2
BP 253
EP 253
DI 10.2105/AJPH.2010.196667
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 707QH
UT WOS:000286300600015
PM 21228289
ER
PT J
AU Parry, M
AF Parry, Manon
TI Ralph Nader: Public Health Advocate and Political Agitator
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
C1 [Parry, Manon] Univ Maryland, College Pk, MD 20742 USA.
RP Parry, M (reprint author), Natl Lib Med, Exhibit Program, 8600 Rockville Pike,Bldg 38,Room 1E-21, Bethesda, MD 20894 USA.
EM parrym@mail.nlm.nih.gov
NR 4
TC 0
Z9 0
U1 0
U2 3
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD FEB
PY 2011
VL 101
IS 2
BP 257
EP 257
DI 10.2105/AJPH.2009.191163
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 707QH
UT WOS:000286300600017
PM 21228291
ER
PT J
AU Gulley, SP
Rasch, EK
Chan, L
AF Gulley, Stephen P.
Rasch, Elizabeth K.
Chan, Leighton
TI Ongoing Coverage for Ongoing Care: Access, Utilization, and
Out-of-Pocket Spending Among Uninsured Working-Aged Adults with Chronic
Health Care Needs
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID DISABILITIES; INSURANCE; SERVICES; MEDICARE; POPULATION; PHYSICIAN;
AMERICANS; QUALITY; PEOPLE; SYSTEM
AB Objectives. We sought to determine how part-year and full-year gaps in health insurance coverage affected working-aged persons with chronic health care needs.
Methods. We conducted multivariate analyses of the 2002-2004 Medical Expenditure Panel Survey to compare access, utilization, and out-of-pocket spending burden among key groups of persons with chronic conditions and disabilities. The results are generalizable to the US community-dwelling population aged 18 to 64 years.
Results. Among 92 million adults with chronic conditions, 21% experienced at least 1 month uninsured during the average year (2002-2004). Among the 25 million persons reporting both chronic conditions and disabilities, 23% were uninsured during the average year. These gaps in coverage were associated with significantly higher levels of access problems, lower rates of ambulatory visits and prescription drug use, and higher levels of out-of-pocket spending.
Conclusions. Implementation of health care reform must focus not only on the prevention of chronic conditions and the expansion of insurance coverage but also on the long-term stability of the coverage to be offered. (Am J Public Health. 2011;101:368-375. doi:10.2105/AJPH.2010.191569)
C1 [Gulley, Stephen P.; Rasch, Elizabeth K.; Chan, Leighton] NIH, Mark O Hatfield Clin Res Ctr, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Gulley, Stephen P.] Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA USA.
RP Gulley, SP (reprint author), NIH, Mark O Hatfield Clin Res Ctr, Dept Rehabil Med, Bldg 10 CRC,Room 1-1469,10 Ctr Dr,MSC 1604, Bethesda, MD 20892 USA.
EM gulley@brandeis.edu
FU National Institutes of Health Clinical Research Center, Rehabilitation
Medicine Department
FX This research was supported by the Intramural Research Program of the
National Institutes of Health Clinical Research Center, Rehabilitation
Medicine Department.
NR 43
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U1 1
U2 8
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD FEB
PY 2011
VL 101
IS 2
BP 368
EP 375
DI 10.2105/AJPH.2010.191569
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 707QH
UT WOS:000286300600035
PM 21164090
ER
PT J
AU Cardenas, I
Mor, G
Aldo, P
Lang, SM
Stabach, P
Sharp, A
Romero, R
Mazaki-Tovi, S
Gervasi, M
Means, RE
AF Cardenas, Ingrid
Mor, Gil
Aldo, Paulomi
Lang, Sabine M.
Stabach, Paul
Sharp, Andrew
Romero, Roberto
Mazaki-Tovi, Shali
Gervasi, MariaTeresa
Means, Robert E.
TI Placental Viral Infection Sensitizes to Endotoxin-Induced Pre-Term
Labor: A Double Hit Hypothesis
SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
LA English
DT Article
DE Double hit hypothesis; lipopolysaccharide; placenta; toll-like
receptors; trophoblast; viral infection
ID BARR-VIRUS INFECTIONS; HERPES-SIMPLEX-VIRUS; TOLL-LIKE RECEPTORS;
INTRAUTERINE INFECTION; PREGNANCY; TROPHOBLAST; INFLAMMATION; DELIVERY;
LIPOPOLYSACCHARIDE
AB Problem
Among pregnant women, acquired viral infections with a concurrent bacterial infection is a detrimental factor associated to poor prognosis. We evaluate the effect of a viral infection that does not lead to pre-term labor on the response to low doses of lipopolysaccharide (LPS). Our objectives were (i) to characterize the effect of a viral infection concurrent with exposure to microbial products on pregnancy outcome and (ii) to characterize the placental and fetal immune responses to the viral sensitization to LPS.
Method
C57B/6 wild-type mice were injected with murine gammaherpesvirus 68 (MHV68) at E8.5. Either PBS or LPS was injected i.p. at E15.5. Pregnancy outcome and cytokine/chemokine profile from implantation sites were analyzed by multiplex.
Results
LPS treatment of MHV-68-infected animals induced pre-term delivery and fetal death in 100% of the mice. Pre-term labor was characterized by a upregulation of pro-inflammatory cytokines and chemokines in both placenta and decidua. Similar profiles were observed from MHV-68-infected human primary trophoblast and trophoblast cell lines in response to LPS.
Conclusion
We describe for the first time that a sub-clinical viral infection in pregnant mice might sensitize to a bacterial infection leading to pre-term delivery. We propose the 'Double Hit Hypothesis' where the presence of a viral infection enhances the effect of bacterial products during pregnancy leading not only to pre-term labor but likely larger adverse outcomes.
C1 [Cardenas, Ingrid; Mor, Gil; Aldo, Paulomi; Sharp, Andrew] Yale Univ, Sch Med, Dept Obstet Gynecol & Reprod Sci, Reprod Immunol Unit, New Haven, CT 06520 USA.
[Lang, Sabine M.; Stabach, Paul; Means, Robert E.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06520 USA.
[Romero, Roberto; Mazaki-Tovi, Shali] Wayne State Univ, Perinatol Res Branch, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH,DHHS, Detroit, MI USA.
[Gervasi, MariaTeresa] Azienda Osped Padova, Dept Obstet & Gynecol, Padua, Italy.
RP Mor, G (reprint author), Yale Univ, Sch Med, Dept Obstet Gynecol & Reprod Sci, Reprod Immunol Unit, 333 Cedar St,LSOG 305A, New Haven, CT 06520 USA.
EM gil.mor@yale.edu
FU National Institutes of Health, NICDH [P01HD054713, 3N01 HD23342]; Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services
FX This study is in part funded by grants from the National Institutes of
Health, NICDH P01HD054713 and 3N01 HD23342 and the Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development, National Institutes of Health, Department of
Health and Human Services.
NR 31
TC 48
Z9 49
U1 0
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1046-7408
J9 AM J REPROD IMMUNOL
JI Am. J. Reprod. Immunol.
PD FEB
PY 2011
VL 65
IS 2
BP 110
EP 117
DI 10.1111/j.1600-0897.2010.00908.x
PG 8
WC Immunology; Reproductive Biology
SC Immunology; Reproductive Biology
GA 703TA
UT WOS:000286003000004
PM 20712808
ER
PT J
AU Aaron, CP
Tandri, H
Barr, RG
Johnson, WC
Bagiella, E
Chahal, H
Jain, A
Kizer, JR
Bertoni, AG
Lima, JAC
Bluemke, DA
Kawut, SM
AF Aaron, Carrie P.
Tandri, Harikrishna
Barr, R. Graham
Johnson, W. Craig
Bagiella, Emilia
Chahal, Harjit
Jain, Aditya
Kizer, Jorge R.
Bertoni, Alain G.
Lima, Joao A. C.
Bluemke, David A.
Kawut, Steven M.
TI Physical Activity and Right Ventricular Structure and Function The
MESA-Right Ventricle Study
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE exercise; pulmonary heart disease; pulmonary hypertension; magnetic
resonance imaging
ID ATHLETES HEART; PULMONARY-HYPERTENSION; STRENUOUS EXERCISE; CARDIAC
STRUCTURE; ATHEROSCLEROSIS; MASS; HYPERTROPHY; LUNG; RAT; PERFORMANCE
AB Rationale: Intense exercise in elite athletes is associated with increased left ventricular (LV) and right ventricular (RV) mass and volumes. However, the effect of physical activity on the RV in an older community-based population is unknown. Objectives: We studied the association between levels of physical activity in adults and RV mass and volumes.
Methods: The Multi-Ethnic Study of Atherosclerosis (MESA) performed cardiac magnetic resonance imaging on community-based participants without clinical cardiovascular disease. RV volumes were determined from manually contoured endocardial margins. RV mass was determined from the difference between epicardial and endocardial volumes multiplied by the specific gravity of myocardium. Metabolic equivalent-minutes/day were calculated from the self-reported frequency, duration, and intensity of physical activity.
Measurements and Main Results: The study sample (n = 1,867) was aged 61.8 +/- 10 years, 48% male, 44% white, 27% African American, 20% Hispanic, and 9% Chinese. Higher levels of moderate and vigorous physical activity were linearly associated with higher RV mass (P = 0.02) after adjusting for demographics, anthropometrics, smoking, cholesterol, diabetes mellitus, hypertension, and LV mass. Higher levels of intentional exercise (physical activity done for the sole purpose of conditioning or fitness) were nonlinearly associated with RV mass independent of LV mass (P = 0.03). There were similar associations between higher levels of physical activity and larger RV volumes.
Conclusions: Higher levels of physical activity in adults were associated with greater RV mass independent of the associations with LV mass; similar results were found for RV volumes. Exercise-associated RV remodeling may have important clinical implications.
C1 [Kawut, Steven M.] Univ Penn, Sch Med, Penn Cardiovasc Inst, Dept Med, Philadelphia, PA 19104 USA.
[Kawut, Steven M.] Univ Penn, Sch Med, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Aaron, Carrie P.; Barr, R. Graham] Columbia Univ, Coll Phys & Surg, Dept Med, New York, NY USA.
[Bagiella, Emilia] Columbia Univ, Dept Biostat, Mailman Sch Publ Hlth, New York, NY USA.
[Tandri, Harikrishna; Chahal, Harjit; Jain, Aditya; Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[Johnson, W. Craig] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Kizer, Jorge R.] Weill Cornell Med Ctr, Dept Med, New York, NY USA.
[Kizer, Jorge R.] Weill Cornell Med Ctr, Dept Publ Hlth, New York, NY USA.
[Bertoni, Alain G.] Wake Forest Univ Hlth Sci, Dept Epidemiol & Prevent, Winston Salem, NC USA.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Kawut, SM (reprint author), Univ Penn, Sch Med, Penn Cardiovasc Inst, Dept Med, 711 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM kawut@mail.med.upenn.edu
OI Bluemke, David/0000-0002-8323-8086
FU National Institute of Health [R01-HL086719, R01-HL077612, N01-HC95159,
HC95165, N01-HC95169]; Tethys Bioscience; Gilead; Novartis; Pfizer;
Actelion; Gileac; United Therapeutics; Lung Rx; Merck
FX Supported by National Institute of Health grants R01-HL086719 (S.M.K.),
R01-HL077612 (R.G.B.), N01-HC95159 through HC95165; and N01-HC95169.;
C.P.A. does not have a financial relationship with a commercial entity
that has an interest in the subject of this manuscript. H.T. does not
have a financial relationship with a commercial entity that has an
interest in the subject of this manuscript. R.G.B. received a sponsored
grant from National Institutes of Health (NIH) for more than $100,001.
W.C.J. received a sponsored grant from NIH for $50,001-$100,000. E.B.
does not have a financial relationship with a commercial entity that has
an interest in the subject of this manuscript. H.C. does not have a
financial relationship with a commercial entity that has an interest in
the subject of this manuscript. A.J. does not have a financial
relationship with a commercial entity that has an interest in the
subject of this manuscript. J.K. received a sponsored grant from NIH for
more than $100,001. A.B. received consultancy fees from Tethys
Bioscience for $1,001-$5,000 and a sponsored grant for $50,001-8100,000,
both for diabetic research. A.B. also received a sponsored research
grant from NIH for more than $100,001. J.A.C.L. does not have a
financial relationship with a commercial entity that has an interest in
the subject of this manuscript. D.A.B. is a full-time employee of NIH
Clinical Center. S.M.K. received consultancy fees from Gilead and
Novartis for $1,001-$5,000 each and served on the advisory board of
Bayer for $1,001-$5,000, Gilead for $1,001-$5,000 and (twice) for
$10,001-$50,000, and Pfizer for $5001-$10,000. S.M.K. also received
lecture fees from Gilead for $1,001-$5,000 and Actelion for
$1,001-$5,000. S.M.K. received sponsored grants from Actelion, Gileac,
United Therapeutics, Lung Rx, Merck, and Pfizer, all for $10,001-$50,000
each, and from Bayer for $5,001-$10,000 and Pfizer for 850,001-$100,000.
S.M.K. served on the advisory board of NIH for less than $1,000, and the
American Lung Association for $1,001-$5,000. S.M.K. received a sponsored
grant from NIH for more than $100,001.
NR 34
TC 24
Z9 24
U1 1
U2 5
PU AMER THORACIC SOC
PI NEW YORK
PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD FEB 1
PY 2011
VL 183
IS 3
BP 396
EP 404
DI 10.1164/rccm.201003-0469OC
PG 9
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 720QD
UT WOS:000287294300017
PM 20813888
ER
PT J
AU Valderrama-Aguirre, A
Zuniga-Soto, E
Marino-Ramirez, L
Moreno, LA
Escalante, AA
Arevalo-Herrera, M
Herrera, S
AF Valderrama-Aguirre, Augusto
Zuniga-Soto, Evelin
Marino-Ramirez, Leonardo
Angela Moreno, Luz
Escalante, Ananias A.
Arevalo-Herrera, Myriam
Herrera, Socrates
TI Polymorphism of the Pv200L Fragment of Merozoite Surface Protein-1 of
Plasmodium vivax in Clinical Isolates from the Pacific Coast of Colombia
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID SEQUENCE ALIGNMENT; DNA POLYMORPHISM; MALARIA; VACCINE; MSP1;
IMMUNOGENICITY; RECOMBINATION; SAFETY
AB Merozoite surface protein 1 (MSP-1) is a polymorphic malaria protein with functional domains involved in parasite erythrocyte interaction. Plasmodium vivax MSP-1 has a fragment (Pv200L) that has been identified as a potential subunit vaccine because it is highly immunogenic and induces partial protection against infectious parasite challenge in vaccinated monkeys. To determine the extent of genetic polymorphism and its effect on the translated protein, we sequenced the Pv200L coding region from isolates of 26 P vivax-infected patients in a malaria-endemic area of Colombia. The extent of nucleotide diversity (pi) in these isolates (0.061 +/- 0.004) was significantly lower (P <= 0.001) than that observed in Thai and Brazilian isolates; 0.083 +/- 0.006 and 0.090 +/- 0.006, respectively. We found two new alleles and several previously unidentified dimorphic substitutions and significant size polymorphism. The presence of highly conserved blocks in this fragment has important implications for the development of Pv200L as a subunit vaccine candidate.
C1 [Valderrama-Aguirre, Augusto; Zuniga-Soto, Evelin; Angela Moreno, Luz; Arevalo-Herrera, Myriam; Herrera, Socrates] Malaria Vaccine & Drug Dev Ctr, Cali, Colombia.
[Valderrama-Aguirre, Augusto; Zuniga-Soto, Evelin; Angela Moreno, Luz; Arevalo-Herrera, Myriam; Herrera, Socrates] Univ Valle, Fac Salud, Inst Inmunol, Cali, Colombia.
[Marino-Ramirez, Leonardo] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Computat Biol Branch, Bethesda, MD 20892 USA.
[Escalante, Ananias A.] Arizona State Univ, Sch Life Sci, Tempe, AZ USA.
RP Herrera, S (reprint author), Malaria Vaccine & Drug Dev Ctr, Carrera 37,2Bis 5E-08, Cali, Colombia.
EM avalderrama@inmuno.org; ezuniga@inmuno.org; marino@ncbi.nlm.nih.gov;
luzangelmo@hotmail.com; Ananias.Escalante@asu.edu; marevalo@inmuno.org;
sherrera@inmuno.org
RI Marino-Ramirez, Leonardo/I-5759-2013;
OI Marino-Ramirez, Leonardo/0000-0002-5716-8512; Valderrama-Aguirre,
Augusto/0000-0002-5255-1440
FU National Institute of Allergy and Infectious Diseases (NIAID) [A1-49486/
TMRC]; National Bureau of Sciences; University of Valle State
[245-2004]; COLCIENCIAS [1106-04-16489]; Colombian Ministry of Social
Protection [2304-04-19524, 253-2005]; National Institutes of Health, USA
[R01GM080586]; International Center of Excellence for Malaria Research
NIAID/ICEMR [U 19AI089702]
FX This study was supported through a P. vivax vaccine research program
granted by the National Institute of Allergy and Infectious Diseases
(NIAID grant no. A1-49486/ TMRC), National Bureau of Sciences,
University of Valle State (contract no. 245-2004), COLCIENCIAS (grant
1106-04-16489), and the Colombian Ministry of Social Protection (grant
2304-04-19524) (contract no. 253-2005). Ananias A. Escalante is
supported by the grant R01GM080586 from the National Institutes of
Health, USA and through an International Center of Excellence for
Malaria Research NIAID/ICEMR grant no U 19AI089702.
NR 25
TC 3
Z9 3
U1 0
U2 2
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 FEB
PY 2011
VL 84
IS 2
SU 2
BP 64
EP 70
DI 10.4269/ajtmh.2011.09-0517
PG 7
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 716WL
UT WOS:000287004100010
PM 21292880
ER
PT J
AU Gu, DY
Ma, Y
Niu, G
Yan, YJ
Lang, LX
Aisaand, HA
Gao, HK
Kiesewetter, DO
Chen, XY
AF Gu, Dongyu
Ma, Ying
Niu, Gang
Yan, Yongjun
Lang, Lixin
Aisaand, Haji Akber
Gao, Haokao
Kiesewetter, Dale O.
Chen, Xiaoyuan
TI LC/MS evaluation of metabolism and membrane transport of bombesin
peptides
SO AMINO ACIDS
LA English
DT Article
DE LC/MS/MS; Gastrin-releasing peptide receptor (GRPR); Bombesin (BBN);
Agonist; Antagonist
ID HUMAN PROSTATE ADENOCARCINOMA; IN-VITRO; RECEPTOR EXPRESSION; CANCER;
HETERODIMER; ANTAGONISTS; ANALOGS; TUMORS; PET
AB Two bombsin peptides, GRPR agonist [Aca-QWAVGHLM-NH(2)] and antagonist [fQWAVGHL-NHEthyl] were evaluated. We employed the highly sensitive Waters Q-Tof Premier MS coupled with a UPLC system to identify the metabolites produced by rat hepatocytes or PC-3 human prostate cancer cells; and we utilized the AB/MDS 4000 Q-Trap LC/MS/MS system with highly sensitive quantitative and qualitative performance, to quantitatively analyze the internalization of GRPR agonist and antagonist in PC-3 cells. The major metabolites of both GRPR agonist and antagonist were the result of peptide bond hydrolysis between W and A which was demonstrated by observation of the N-terminal fragment m/z 446 (Aca-QW-OH) for agonist and m/z 480 (fQW-OH) for antagonist. Both peptides were also hydrolyzed between A and V which formed peaks m/z 517 [Aca-QWA-OH] and m/z 555 (VGHLM-NH2) for the agonist and m/z 551 [fQWA-OH] and m/z 452 (VGHL-NHEthyl) for the antagonist. The peptide agonist also formed a unique metabolite that resulted from hydrolysis of the C-terminal amide. The antagonist showed significantly slower metabolism as compared to the agonist in both rat hepatocytes and PC-3 cells. The antagonist also showed significantly lower PC-3 cell internalization rate than that of the agonist. In conclusion, the metabolism profiles of both GRPR agonist and antagonist peptides were identified by LC/MS. The antagonist peptide was more stable than the agonist peptide in rat hepatocyte incubation. One major factor could be the hydrolysis-resistant C-terminal L-NHEthyl group compared with the unsubstituted amide of the agonist. Another factor could be different amino acid sequences of the agonist and antagonist that may also influence the enzymatic hydrolysis. The antagonist ligand is potentially more useful for receptor-targeted imaging due primarily to its higher metabolic stability.
C1 [Gu, Dongyu; Ma, Ying; Niu, Gang; Yan, Yongjun; Lang, Lixin; Gao, Haokao; Kiesewetter, Dale O.; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
[Gu, Dongyu; Aisaand, Haji Akber] Chinese Acad Sci, Xinjiang Tech Inst Phys & Chem, Urumqi, Peoples R China.
[Gu, Dongyu] Chinese Acad Sci, Grad Univ, Beijing, Peoples R China.
RP Chen, XY (reprint author), NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, 31 Ctr Dr,Suite 1C14, Bethesda, MD 20892 USA.
EM dk7k@nih.gov; shawn.chen@nih.gov
FU National Institute of Biomedical Imaging and Bioengineering (NIBIB),
National Institutes of Health (NIH)
FX The research was supported by Intramural Research Program of the
National Institute of Biomedical Imaging and Bioengineering (NIBIB),
National Institutes of Health (NIH).
NR 21
TC 8
Z9 8
U1 0
U2 19
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0939-4451
J9 AMINO ACIDS
JI Amino Acids
PD FEB
PY 2011
VL 40
IS 2
BP 669
EP 675
DI 10.1007/s00726-010-0696-y
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 706BK
UT WOS:000286189600035
PM 20676905
ER
PT J
AU Park, SS
Maudsley, S
AF Park, Sung-Soo
Maudsley, Stuart
TI Discontinuous pH gradient-mediated separation of TiO2-enriched
phosphopeptides
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE Titanium dioxide; Phosphoproteomics; Mass spectrometry; pH-dependent
elution
ID MASS-SPECTROMETRY; TITANIUM-DIOXIDE; PHOSPHORYLATED PEPTIDES; SIGNALING
PATHWAYS; FEMTOMOLE LEVEL; RECEPTOR; ENRICHMENT; CELLS; IDENTIFICATION;
STRATEGY
AB Global profiling of phosphoproteomes has proven to be a great challenge due to the relatively low stoichiometry of protein phosphorylation and poor ionization efficiency in mass spectrometers. Effective, physiologically relevant, phosphoproteome research relies on the efficient phosphopeptide enrichment from complex samples. Immobilized metal affinity chromatography and titanium dioxide chromatography can greatly assist selective phosphopeptide enrichment. However, the complexity of resultant enriched samples is often still high, suggesting that further separation of enriched phosphopeptides is required. We have developed a pH gradient elution technique for enhanced phosphopeptide identification in conjunction with titanium dioxide chromatography. Using this process, we demonstrated its superiority to the traditional "one-pot" strategies for differential protein identification. Our technique generated a highly specific separation of phosphopeptides by an applied pH gradient between 9.2 and 11.3. The most efficient elution range for high-resolution phosphopeptide separation was between pHs 9.2 and 9.4. High-resolution separation of multiply phosphorylated peptides was primarily achieved using elution ranges greater than pH 9.4. Investigation of phosphopeptide sequences identified in each pH fraction indicated that phosphopeptides with phosphorylated residues proximal to acidic residues, including glutamic acid, aspartic acid, and other phosphorylated residues, were preferentially eluted at higher pH values. Published by Elsevier Inc.
C1 [Park, Sung-Soo; Maudsley, Stuart] NIA, Receptor Pharmacol Unit, NIH, Baltimore, MD 21224 USA.
RP Maudsley, S (reprint author), NIA, Receptor Pharmacol Unit, NIH, Baltimore, MD 21224 USA.
EM maudsleyst@mail.nih.gov
FU National Institutes of Health
FX This work was carried out entirely with the support of the Intramural
Research Program of the National Institutes of Health.
NR 36
TC 19
Z9 19
U1 0
U2 12
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0003-2697
EI 1096-0309
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD FEB 1
PY 2011
VL 409
IS 1
BP 81
EP 88
DI 10.1016/j.ab.2010.10.003
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 705KE
UT WOS:000286126500012
PM 20946866
ER
PT J
AU Ferrer, RA
Huedo-Medina, TB
Johnson, BT
Ryan, S
Pescatello, LS
AF Ferrer, Rebecca A.
Huedo-Medina, Tania B.
Johnson, Blair T.
Ryan, Stacey
Pescatello, Linda S.
TI Exercise Interventions for Cancer Survivors: A Meta-Analysis of Quality
of Life Outcomes
SO ANNALS OF BEHAVIORAL MEDICINE
LA English
DT Article
DE Cancer; Oncology; Exercise; Behavioral interventions; Quality of life;
Meta-analysis; Exercise interventions; Cancer survivors
ID RANDOMIZED CONTROLLED-TRIAL; RECEIVING ADJUVANT CHEMOTHERAPY;
PHYSICAL-ACTIVITY INTERVENTION; ANDROGEN DEPRIVATION THERAPY; STEM-CELL
TRANSPLANTATION; BREAST-CANCER; PROSTATE-CANCER; FUNCTIONAL ASSESSMENT;
AEROBIC EXERCISE; RESISTANCE EXERCISE
AB Exercise improves quality of life (QOL) in cancer survivors, although characteristics of efficacious exercise interventions for this population have not been identified.
The present meta-analysis examines the efficacy of exercise interventions in improving QOL in cancer survivors, as well as features that may moderate such effects.
Studies were identified and coded, and QOL effect sizes were calculated and analyzed for trends.
Overall, exercise interventions increased QOL, but this tendency depended to some extent on exercise and patient features. Although several features were associated with effect sizes, models revealed that interventions were particularly successful if they targeted more intense aerobic exercise and addressed women. These tendencies emerged over longer periods of time and were more prominent in studies with higher methodological quality.
Appropriately designed exercise interventions enhance QOL for cancer survivors and this pattern is especially evident for women. Limitations are discussed.
C1 [Ferrer, Rebecca A.] NCI, Div Canc Control & Populat, Behav Res Program, Rockville, MD 20852 USA.
[Huedo-Medina, Tania B.; Johnson, Blair T.] Univ Connecticut, Dept Psychol, Storrs, CT USA.
[Huedo-Medina, Tania B.; Johnson, Blair T.; Ryan, Stacey; Pescatello, Linda S.] Univ Connecticut, Ctr Hlth Intervent & Prevent, Storrs, CT USA.
[Ryan, Stacey; Pescatello, Linda S.] Univ Connecticut, Dept Kinesiol, Storrs, CT USA.
RP Ferrer, RA (reprint author), NCI, Div Canc Control & Populat, Behav Res Program, 6130 Executive Blvd,MSC 7326,Room 4089A, Rockville, MD 20852 USA.
EM ferrerra@mail.nih.gov
FU NIMH NIH HHS [R01 MH058563-13, F31 MH080626, F31MH080626, R01 MH058563,
R01-MH58563]
NR 142
TC 92
Z9 93
U1 4
U2 13
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0883-6612
J9 ANN BEHAV MED
JI Ann. Behav. Med.
PD FEB
PY 2011
VL 41
IS 1
BP 32
EP 47
DI 10.1007/s12160-010-9225-1
PG 16
WC Psychology, Multidisciplinary
SC Psychology
GA 717KB
UT WOS:000287041400004
PM 20931309
ER
PT J
AU Cohen, SS
Gammon, MD
Signorello, LB
North, KE
Lange, EM
Fowke, JH
Hargreaves, MK
Cai, QY
Zheng, W
Blot, WJ
Matthews, CE
AF Cohen, Sarah S.
Gammon, Marilie D.
Signorello, Lisa B.
North, Kari E.
Lange, Ethan M.
Fowke, Jay H.
Hargreaves, Margaret K.
Cai, Qiuyin
Zheng, Wei
Blot, William J.
Matthews, Charles E.
TI Serum Adiponectin in Relation to Body Mass Index and Other Correlates in
Black and White Women
SO ANNALS OF EPIDEMIOLOGY
LA English
DT Article
DE Adiponectin; African Americans; Obesity
ID FOOD FREQUENCY QUESTIONNAIRE; SOUTHERN COMMUNITY COHORT; INSULIN
SENSITIVITY; AFRICAN-AMERICANS; FAT DISTRIBUTION; GLYCEMIC LOAD;
UNITED-STATES; PLASMA; RISK; HYPERTENSION
AB PURPOSE: Adiponectin is a promising biomarker linking obesity and disease risk; however, limited data are available regarding adiponectin in black women among whom obesity is highly prevalent.
METHODS: A cross-sectional analysis was conducted to assess racial differences and correlates of serum adiponectin measured in 996 black and 996 white women enrolled in the Southern Community Cohort Study through Community Health Centers in 12 southeastern states from 2002 to 2006.
RESULTS: Black subjects had significantly lower adiponectin levels than white subjects (median 10.9 vs 14.9 mu g/mL, Wilcoxonp < .0001). Among black subjects, adiponectin was lower among overweight and obese women compared with healthy weight women but showed no clear decreasing trend with increasing severity of obesity; adjusted geometric means (95% confidence interval) were 15.0 [13.8-16.4], 11.5 [10.6-12.5], 9.7 [9.0-10.6], 11.4 [10.3-12.6], and 10.9 [9.5-12.6] mu g/mL for body mass index [BMI] categories of 18.5-24.9, 25-29.9, 30-34.9, 35-39.9, and 40-45, p for trend < .0001). In contrast, among whites there was a monotonic reduction in adiponectin over increasing BMI (adjusted geometric means = 19.9 [18.3-21.7], 15.1 [13.9-16.4], 14.3 [13.2-15.5], 12.5 [11.2-13.9], and 11.0 [9.7-12.5] mu g/mL, p for trend < .0001). BMI, age, high-density lipoprotein cholesterol, and hypertension were important correlates of adiponectin in both groups.
CONCLUSIONS: Among women, racial differences exist in both the magnitude and form of the adiponectin-BMI association. Ann Epidemiol 2011;21:86-94. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Cohen, Sarah S.; Signorello, Lisa B.; Blot, William J.] Int Epidemiol Inst, Rockville, MD 20850 USA.
[Cohen, Sarah S.; Gammon, Marilie D.; North, Kari E.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Signorello, Lisa B.; Fowke, Jay H.; Cai, Qiuyin; Zheng, Wei; Blot, William J.] Vanderbilt Univ, Med Ctr, Dept Med, Div Epidemiol, Nashville, TN USA.
[Signorello, Lisa B.; Fowke, Jay H.; Cai, Qiuyin; Zheng, Wei; Blot, William J.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[North, Kari E.] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC USA.
[Lange, Ethan M.] Univ N Carolina, Dept Biostat, Chapel Hill, NC USA.
[Lange, Ethan M.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Hargreaves, Margaret K.] Meharry Med Coll, Dept Internal Med, Nashville, TN 37208 USA.
[Matthews, Charles E.] NCI, Nutr Epidemiol Branch, Rockville, MD USA.
RP Cohen, SS (reprint author), Int Epidemiol Inst, 1455 Res Blvd,Suite 550, Rockville, MD 20850 USA.
EM sarah@ieixmail.com
RI matthews, Charles/E-8073-2015
OI matthews, Charles/0000-0001-8037-3103
FU Susan G. Komen for the Cure [OP05-0927-DR1]; National Cancer Institute
(NCI) [R01 CA92447, T32 GA09330-26, 5-R25-CA057726]; National Institute
of Environmental Health Sciences [P30ES10126]; Vanderbilt-Ingram Cancer
Center [P30 CA68485]
FX This project was funded in part by grant OP05-0927-DR1 from Susan G.
Komen for the Cure. The Southern Community Cohort Study is funded by
grant R01 CA92447 from the National Cancer Institute (NCI). Dr. Cohen
also received support from NCI Training Grants T32 GA09330-26 and
5-R25-CA057726. Dr. Gammon is supported in part from P30ES10126 from the
National Institute of Environmental Health Sciences.; Serum sample
preparation was conducted at the Survey and Biospecimen Shared Resource
that is supported in part by the Vanderbilt-Ingram Cancer Center (P30
CA68485).
NR 38
TC 21
Z9 22
U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1047-2797
J9 ANN EPIDEMIOL
JI Ann. Epidemiol.
PD FEB
PY 2011
VL 21
IS 2
BP 86
EP 94
DI 10.1016/j.annepidem.2010.10.011
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 708FR
UT WOS:000286348200003
PM 21109453
ER
PT J
AU Kiesewetter, DO
Jacobson, O
Lang, LX
Chen, XY
AF Kiesewetter, Dale O.
Jacobson, Orit
Lang, Lixin
Chen, Xiaoyuan
TI Automated radiochemical synthesis of [F-18]FBEM: A thiol reactive
synthon for radiofluorination of peptides and proteins
SO APPLIED RADIATION AND ISOTOPES
LA English
DT Article
DE PET; Fluorine-18; Thiol reactive synthon; [F-18]FBEM
ID F-18-LABELING AGENT; RGD PEPTIDE; F-18; PACLITAXEL
AB The automated radiochemical synthesis of N-[2-(4-[F-18]fluorobenzamido)ethyl]maleimide ([F-18]FBEM, IUPAC name: N-maleoylethyl-4-[F-18]fluorobenzamide), a prosthetic group for radiolabeling the free sulfhydryl groups of peptides and proteins, is herein described. 4-[F-18]fluorobenzoic acid was first prepared by nucleophilic displacement of a trimethylammonium moiety on a pentamethylbenzyl benzoate ester with [F-18]fluoride. In the second step the ester was cleaved under acidic conditions. Finally, 4-[F-18]fluorobenzoic acid was coupled to N-(2-aminoethyl)maleimide using diethylcyanophosphate and diisopropylethyl amine. Following high-performance liquid chromatography (HPLC) purification, [F-18]FBEM was obtained in 17.3 +/- 7.1% yield (not decay corrected) in approximately 95 min. Isolation from the HPLC eluate and preparation for subsequent use, which was conducted manually, required an additional 10-15 min. The measured specific activity for three batches was 181.3, 251.6, and 351.5 GBq/ mu mol at the end of bombardment (EOB). Published by Elsevier Ltd.
C1 [Kiesewetter, Dale O.; Jacobson, Orit; Lang, Lixin; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
RP Kiesewetter, DO (reprint author), NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bldg 10,Room 1C401,MSC 1180, Bethesda, MD 20892 USA.
EM dk7k@nih.gov
FU National Institute of Biomedical Imaging and Bioengineering, National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Biomedical Imaging and Bioengineering, National
Institutes of Health. Technical assistance was provided by Eckert &
Ziegler Eurotope GmbH for programming suggestions.
NR 14
TC 26
Z9 26
U1 4
U2 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0969-8043
J9 APPL RADIAT ISOTOPES
JI Appl. Radiat. Isot.
PD FEB
PY 2011
VL 69
IS 2
BP 410
EP 414
DI 10.1016/j.apradiso.2010.09.023
PG 5
WC Chemistry, Inorganic & Nuclear; Nuclear Science & Technology; Radiology,
Nuclear Medicine & Medical Imaging
SC Chemistry; Nuclear Science & Technology; Radiology, Nuclear Medicine &
Medical Imaging
GA 717QY
UT WOS:000287063700021
PM 20965741
ER
PT J
AU Mickey, BJ
Zhou, ZF
Heitzeg, MM
Heinz, E
Hodgkinson, CA
Hsu, DT
Langenecker, SA
Love, TM
Pecina, M
Shafir, T
Stohler, CS
Goldman, D
Zubieta, JK
AF Mickey, Brian J.
Zhou, Zhifeng
Heitzeg, Mary M.
Heinz, Elizabeth
Hodgkinson, Colin A.
Hsu, David T.
Langenecker, Scott A.
Love, Tiffany M.
Pecina, Marta
Shafir, Tal
Stohler, Christian S.
Goldman, David
Zubieta, Jon-Kar
TI Emotion Processing, Major Depression, and Functional Genetic Variation
of Neuropeptide Y
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID PREFRONTAL CORTEX; TRAUMA EXPOSURE; NEURAL BASIS; PEPTIDE-YY; NPY;
STRESS; BRAIN; DISORDER; PAIN; NEUROCIRCUITRY
AB Context: Despite recent progress in describing the common neural circuitry of emotion and stress processing, the bases of individual variation are less well understood. Genetic variants that underlie psychiatric disease have proven particularly difficult to elucidate. Functional genetic variation of neuropeptide Y (NPY) was recently identified as a source of individual differences in emotion. Low NPY levels have been reported in major depressive disorder (MDD).
Objective: To determine whether low-expression NPY genotypes are associated with negative emotional processing at 3 levels of analysis.
Design: Cross-sectional, case-control study.
Setting: Academic medical center.
Participants: Among 44 individuals with MDD and 137 healthy controls, 152 (84%) had an NPY genotype classified as low, intermediate, or high expression according to previously established haplotype-based expression data.
Main Outcome Measures: Healthy subjects participated in functional magnetic resonance imaging while viewing negative (vs neutral) words (n=58) and rated positive and negative affect during a pain-stress challenge (n=78). Genotype distribution was compared between 113 control subjects and 39 subjects with MDD.
Results: Among healthy individuals, negatively valenced words activated the medial prefrontal cortex. Activation within this region was inversely related to genotype predicted NPY expression (P=. 03). Whole-brain regression of responses to negative words showed that the rostral anterior cingulate cortex activated in the low-expression group and deactivated in the high-expression group (P<.05). During the stress challenge, individuals with low-expression NPY genotypes reported more negative affective experience before and after pain (P=. 002). Low-expression NPY genotypes were overrepresented in subjects with MDD after controlling for age and sex (P=.004). Population stratification did not account for the results.
Conclusions: These findings support a model in which NPY genetic variation predisposes certain individuals to low NPY expression, thereby increasing neural responsivity to negative stimuli within key affective circuit elements, including the medial prefrontal and anterior cingulate cortices. These genetically influenced neural response patterns appear to mediate risk for some forms of MDD.
C1 [Mickey, Brian J.; Heitzeg, Mary M.; Hsu, David T.; Langenecker, Scott A.; Love, Tiffany M.; Pecina, Marta; Shafir, Tal; Zubieta, Jon-Kar] Univ Michigan, Mol & Behav Neurosci Inst, Ann Arbor, MI 48109 USA.
[Mickey, Brian J.; Heitzeg, Mary M.; Hsu, David T.; Langenecker, Scott A.; Shafir, Tal; Zubieta, Jon-Kar] Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA.
[Zhou, Zhifeng; Heinz, Elizabeth; Hodgkinson, Colin A.; Goldman, David] Natl Inst Alcohol Abuse & Alcoholism, Neurogenet Lab, Rockville, MD USA.
[Stohler, Christian S.] Univ Maryland, Sch Dent, Baltimore, MD 21201 USA.
RP Mickey, BJ (reprint author), Univ Michigan, Mol & Behav Neurosci Inst, 205 Zina Pitcher Pl, Ann Arbor, MI 48109 USA.
EM bmickey@umich.edu
RI Langenecker, Scott/F-3548-2012; Mickey, Brian/J-1756-2014; Hsu,
David/J-5814-2014; Goldman, David/F-9772-2010;
OI Langenecker, Scott/0000-0002-7932-5494; Mickey,
Brian/0000-0002-7847-7680; Goldman, David/0000-0002-1724-5405; Love,
Tiffany/0000-0001-9299-3190
FU National Institute of Mental Health [P01 MH42251, R25 MH6374, K23
MH074459]; National Institute on Drug Abuse [R01 DA016423, R01 DA
022520]; National Institute on Alcohol Abuse and Alcoholism; Phil F.
Jenkins Research Fund
FX This work was supported by grants P01 MH42251, R25 MH6374, and K23
MH074459 from the National Institute of Mental Health, grants R01
DA016423 and R01 DA 022520 from the National Institute on Drug Abuse,
the Intramural Research Program of the National Institute on Alcohol
Abuse and Alcoholism, and the Phil F. Jenkins Research Fund.
NR 50
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U2 9
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-990X
J9 ARCH GEN PSYCHIAT
JI Arch. Gen. Psychiatry
PD FEB
PY 2011
VL 68
IS 2
BP 158
EP 166
DI 10.1001/archgenpsychiatry.2010.197
PG 9
WC Psychiatry
SC Psychiatry
GA 717KC
UT WOS:000287041500007
PM 21300944
ER
PT J
AU Wang, H
O'Reilly, EJ
Weisskopf, MG
Logroscino, G
McCullough, ML
Thun, MJ
Schatzkin, A
Kolonel, LN
Ascherio, A
AF Wang, Hao
O'Reilly, Eilis J.
Weisskopf, Marc G.
Logroscino, Giancarlo
McCullough, Marji L.
Thun, Michael J.
Schatzkin, Arthur
Kolonel, Laurence N.
Ascherio, Alberto
TI Smoking and Risk of Amyotrophic Lateral Sclerosis A Pooled Analysis of 5
Prospective Cohorts
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID MOTOR-NEURON DISEASE; RECREATIONAL PHYSICAL-ACTIVITY; POSTMENOPAUSAL
BREAST-CANCER; BASE-LINE CHARACTERISTICS; WESTERN WASHINGTON-STATE; II
NUTRITION COHORT; CIGARETTE-SMOKING; ALCOHOL-CONSUMPTION; MULTIETHNIC
COHORT; ANTECEDENT EVENTS
AB Background: Cigarette smoking has been proposed as a risk factor for amyotrophic lateral sclerosis (ALS), but epidemiological studies supporting this hypothesis have been small and mostly retrospective.
Objective: To prospectively examine the relation between smoking and ALS in 5 well-established large cohorts.
Design: Five prospective cohorts with study-specific follow-up ranging from 7 to 28 years.
Setting: Academic research.
Patients: Participants in the Nurses' Health Study, the Health Professionals Follow-up Study, the Cancer Prevention Study II Nutrition Cohort, the Multiethnic Cohort, and the National Institutes of Health-AARP (formerly known as the American Association of Retired Persons) Diet and Health Study.
Main Outcome Measures: Amyotrophic lateral sclerosis deaths identified through the National Death Index. In the Nurses' Health Study and the Health Professionals Follow-up Study, confirmed nonfatal incident ALS was also included.
Results: A total of 832 participants with ALS were documented among 562 804 men and 556 276 women. Smokers had a higher risk of ALS than never smokers, with age- and sex-adjusted relative risks of 1.44 (95% confidence interval, 1.23-1.68; P <.001) for former smokers and 1.42(95% confidence interval, 1.07-1.88; P=.02) for current smokers. Although the risk of ALS was positively associated with pack-years smoked(P <.001), duration of smoking(9% increase for each 10 years of smoking, P=.006), and the number of cigarettes smoked per day (10% increase for each increment of 10 cigarettes smoked per day, P <.001), these associations did not persist when never smokers were excluded. However, among ever smokers, the risk of ALS increased as age at smoking initiation decreased (P=.03).
Conclusions: Results of this large longitudinal study support the hypothesis that cigarette smoking increases the risk of ALS. The potential importance of age at smoking initiation and the lack of a dose response deserve further investigation. Arch Neurol. 2011; 68(2):207-213
C1 [Wang, Hao; O'Reilly, Eilis J.; Ascherio, Alberto] Harvard Univ, Dept Nutr, Sch Publ Hlth, Boston, MA 02115 USA.
[O'Reilly, Eilis J.; Ascherio, Alberto] Harvard Univ, Dept Epidemiol, Sch Publ Hlth, Boston, MA 02115 USA.
[Weisskopf, Marc G.] Harvard Univ, Dept Environm Hlth, Sch Publ Hlth, Boston, MA 02115 USA.
[Ascherio, Alberto] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Ascherio, Alberto] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Logroscino, Giancarlo] Univ Bari, Dept Neurol & Psychiat, Sch Med, Bari, Italy.
[McCullough, Marji L.; Thun, Michael J.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Schatzkin, Arthur] NCI, Nutrit Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Kolonel, Laurence N.] Univ Hawaii, Canc Res Ctr Hawaii, Canc Epidemiol Program, Honolulu, HI 96813 USA.
RP O'Reilly, EJ (reprint author), Harvard Univ, Dept Nutr, Sch Publ Hlth, 665 Huntington Ave, Boston, MA 02115 USA.
EM eoreilly@hsph.harvard.edu
RI LOGROSCINO, GIANCARLO/K-5148-2016
OI LOGROSCINO, GIANCARLO/0000-0003-0423-3242
FU National Institute of Neurological Diseases and Stroke [R01 NS045893]
FX This work was supported by grant R01 NS045893 from the National
Institute of Neurological Diseases and Stroke (Dr Ascherio).
NR 50
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U2 7
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD FEB
PY 2011
VL 68
IS 2
BP 207
EP 213
DI 10.1001/archneurol.2010.367
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 721CY
UT WOS:000287330300008
PM 21320987
ER
PT J
AU Lin, FR
Metter, EJ
O'Brien, RJ
Resnick, SM
Zonderman, AB
Ferrucci, L
AF Lin, Frank R.
Metter, E. Jeffrey
O'Brien, Richard J.
Resnick, Susan M.
Zonderman, Alan B.
Ferrucci, Luigi
TI Hearing Loss and Incident Dementia
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; ALZHEIMERS-DISEASE; OLDER-ADULTS; COGNITIVE DECLINE;
IMPAIRMENT; PREVALENCE; AGE; HEALTH; DYSFUNCTION; POPULATION
AB Objective: To determine whether hearing loss is associated with incident all-cause dementia and Alzheimer disease (AD).
Design: Prospective study of 639 individuals who underwent audiometric testing and were dementia free in 1990 to 1994. Hearing loss was defined by a pure-tone average of hearing thresholds at 0.5, 1, 2, and 4 kHz in the better-hearing ear (normal, < 25 dB [n=455]; mild loss, 25-40 dB [n=125]; moderate loss, 41-70 dB [n=53]; and severe loss, > 70 dB [n=6]). Diagnosis of incident dementia was made by consensus diagnostic conference. Cox proportional hazards models were used to model time to incident dementia according to severity of hearing loss and were adjusted for age, sex, race, education, diabetes mellitus, smoking, and hypertension.
Setting: Baltimore Longitudinal Study of Aging.
Participants: Six hundred thirty-nine individuals aged 36 to 90 years.
Main Outcome Measure: Incident caces of all-cause dementia and AD until May 31, 2008.
Results: During a median follow-up of 11.9 years, 58 cases of incident all-cause dementia were diagnosed, of which 37 cases were AD. The risk of incident all-cause dementia increased log linearly with the severity of baseline hearing loss (1.27 per 10-dB loss; 95% confidence interval, 1.06-1.50). Compared with normal hearing, the hazard ratio (95% confidence interval) for incident all-cause dementia was 1.89 (1.00-3.58) for mild hearing loss, 3.00 (1.43-6.30) for moderate hearing loss, and 4.94 (1.09-22.40) for severe hearing loss. The risk of incident AD also increased with baseline hearing loss (1.20 per 10 dB of hearing loss) but with a wider confidence interval (0.94-1.53).
Conclusions: Hearing loss is independently associated with incident all-cause dementia. Whether hearing loss is a marker for early-stage dementia or is actually a modifiable risk factor for dementia deserves further study. Arch Neurol. 2011; 68(2):214-220
C1 [Lin, Frank R.] Johns Hopkins Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21287 USA.
[Lin, Frank R.] Johns Hopkins Med Inst, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
[Metter, E. Jeffrey; Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Clin Res Branch, Baltimore, MD 21224 USA.
[O'Brien, Richard J.] Johns Hopkins Bayview Med Ctr, Dept Neurol, Baltimore, MD USA.
[O'Brien, Richard J.] Johns Hopkins Bayview Med Ctr, Dept Med, Baltimore, MD USA.
[Resnick, Susan M.; Zonderman, Alan B.] NIA, Lab Behav Neurosci, Intramural Res Program, Bethesda, MD 20892 USA.
RP Lin, FR (reprint author), Johns Hopkins Sch Med, Dept Otolaryngol Head & Neck Surg, JHOC 6120,601 N Caroline St, Baltimore, MD 21287 USA.
EM flin1@jhmi.edu
OI Zonderman, Alan B/0000-0002-6523-4778
FU National Institute on Aging; National Institute on Deafness and Other
Communication Disorders [1K23DC011279-01]
FX This work was supported by the Intramural Research Program of the
National Institute on Aging and grant 1K23DC011279-01 from the National
Institute on Deafness and Other Communication Disorders (Dr Lin).
NR 44
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U1 12
U2 57
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD FEB
PY 2011
VL 68
IS 2
BP 214
EP 220
DI 10.1001/archneurol.2010.362
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 721CY
UT WOS:000287330300009
PM 21320988
ER
PT J
AU Sojkova, J
Driscoll, I
Iacono, D
Zhou, Y
Codispoti, KE
Kraut, MA
Ferrucci, L
Pletnikova, O
Mathis, CA
Klunk, WE
O'Brien, RJ
Wong, DF
Troncoso, JC
Resnick, SM
AF Sojkova, Jitka
Driscoll, Ira
Iacono, Diego
Zhou, Yun
Codispoti, Kari-Elise
Kraut, Michael A.
Ferrucci, Luigi
Pletnikova, Olga
Mathis, Chester A.
Klunk, William E.
O'Brien, Richard J.
Wong, Dean F.
Troncoso, Juan C.
Resnick, Susan M.
TI In Vivo Fibrillar beta-Amyloid Detected Using [C-11]PiB Positron
Emission Tomography and Neuropathologic Assessment in Older Adults
SO ARCHIVES OF NEUROLOGY
LA English
DT Article
ID PITTSBURGH COMPOUND-B; REFERENCE TISSUE MODEL; ALZHEIMERS-DISEASE;
COGNITIVE IMPAIRMENT; SPATIAL CONSTRAINT; DIAGNOSIS; PET; MARKER; PIB
AB Background: In demented older adults, in vivo amyloid imaging shows agreement with diagnostic neuropathologic assessment of beta-amyloid (A beta). However, the extent of agreement in nondemented older adults remains unclear.
Objective: To compare A beta quantified using in vivo carbon 11-labeled Pittsburgh Compound B positron emission tomography and postmortem neuropathologic assessment of A beta in older adults.
Design: Case series.
Setting: Community-dwelling older adults who came to autopsy.
Participants: Five nondemented and 1 demented participant from the Baltimore Longitudinal Study of Aging.
Main Outcome Measure: Agreement between the mean cortical distribution volume ratio and the Consortium to Establish a Registry for AD (CERAD) neuritic plaque (NP) score used for pathologic diagnosis of Alzheimer disease.
Results: Of the 6 participants, 4 had moderate NPs, 2 had sparse or no detectable NPs, and 3 had microscopic findings of cerebral amyloid angiopathy at autopsy. On in vivo imaging, the mean cortical distribution volume ratio ranged from 0.96 to 1.59. Although there was agreement between in vivo amyloid imaging and CERAD NP scores in participants with either high or negligible A beta levels in vivo, only limited agreement was observed among those with intermediate levels of A beta. The best overall agreement was achieved at a distribution volume ratio of 1.2.
Conclusions: In older adults, variable agreement between in vivo imaging and CERAD NP score was observed. The limited agreement may, in part, reflect differences in typical measurements of A beta using imaging compared with the CERAD neuropathologic protocol. Direct quantification of regional A beta in relation to in vivo imaging is necessary to further enhance our understanding of the imaging-pathologic assessment correlation. Arch Neurol. 2011; 68(2):232-240
C1 [Resnick, Susan M.] NIA, Lab Behav Neurosci, Biomed Res Ctr, NIH, Baltimore, MD 21224 USA.
[Sojkova, Jitka; Zhou, Yun; Codispoti, Kari-Elise; Kraut, Michael A.; Wong, Dean F.] Johns Hopkins Univ, Sch Med, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD USA.
[Iacono, Diego; Codispoti, Kari-Elise; Pletnikova, Olga; Troncoso, Juan C.] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA.
[Troncoso, Juan C.] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA.
[Wong, Dean F.] Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA.
[Mathis, Chester A.] Univ Pittsburgh, Dept Radiol, Pittsburgh, PA 15260 USA.
[Klunk, William E.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA.
[O'Brien, Richard J.] Johns Hopkins Bayview Med Ctr, Dept Neurol, Baltimore, MD USA.
[Wong, Dean F.] Johns Hopkins Univ, Dept Environm Hlth Sci, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
RP Resnick, SM (reprint author), NIA, Lab Behav Neurosci, Biomed Res Ctr, NIH, 251 Bayview Blvd,Room 4B317, Baltimore, MD 21224 USA.
EM resnicks@grc.nia.nih.gov
OI Klunk, William/0000-0001-5512-0251
FU National Institute on Aging, National Institutes of Health; Johns
Hopkins University Alzheimer's Disease Research Center [N01-AG-3-2124,
K24 DA00412, P50 AG005133, R37 AG025516, P01 AG025204, P50 AG05146]
FX This research was supported in part by the Intramural Research Program
of the National Institute on Aging, National Institutes of Health, and
N01-AG-3-2124 and extramural grants K24 DA00412 (Dr Wong), P50 AG005133,
R37 AG025516 (Dr Klunk), and P01 AG025204 (Dr Klunk) and by grant P50
AG05146 from The Johns Hopkins University Alzheimer's Disease Research
Center.
NR 22
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U1 0
U2 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-9942
J9 ARCH NEUROL-CHICAGO
JI Arch. Neurol.
PD FEB
PY 2011
VL 68
IS 2
BP 232
EP 240
DI 10.1001/archneurol.2010.357
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 721CY
UT WOS:000287330300011
PM 21320990
ER
PT J
AU Gavrielides, MA
Gallas, BD
Lenz, P
Badano, A
Hewitt, SM
AF Gavrielides, Marios A.
Gallas, Brandon D.
Lenz, Petra
Badano, Aldo
Hewitt, Stephen M.
TI Observer Variability in the Interpretation of HER2/neu
Immunohistochemical Expression With Unaided and Computer-Aided Digital
Microscopy
SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE
LA English
DT Article
ID CELLULAR IMAGING-SYSTEM; IN-SITU HYBRIDIZATION; BREAST-CANCER; TISSUE
MICROARRAYS; VIRTUAL MICROSCOPY; INTEROBSERVER REPRODUCIBILITY;
QUANTITATIVE-ANALYSIS; PROTEIN EXPRESSION; HER-2/NEU STATUS; RECEPTOR
STATUS
AB Context.-Observer variability in digital microscopy and the effect of computer-aided digital microscopy are underexamined areas in need of further research, considering the increasing use and future role of digital imaging in pathology. A reduction in observer variability using computer aids could enhance the statistical power of studies designed to determine the utility of new biomarkers and accelerate their incorporation in clinical practice.
Objectives.-To quantify interobserver and intraobserver variability in immunohistochemical analysis of HER2/neu with digital microscopy and computer-aided digital microscopy, and to test the hypothesis that observer agreement in the quantitative assessment of HER2/neu immunohistochemical expression is increased with the use of computer-aided microscopy.
Design.-A set of 335 digital microscopy images extracted from 64 breast cancer tissue slides stained with a HER2 antibody, were read by 14 observers in 2 reading modes: the unaided mode and the computer-aided mode. In the unaided mode, HER2 images were displayed on a calibrated color monitor with no other information, whereas in the computer-aided mode, observers were shown a HER2 image along with a corresponding feature plot showing computer-extracted values of membrane staining intensity and membrane completeness for the particular image under examination and, at the same time, mean feature values of the different HER2 categories. In both modes, observers were asked to provide a continuous score of HER2 expression.
Results.-Agreement analysis performed on the output of the study showed significant improvement in both interobserver and intraobserver agreement when the computer-aided reading mode was used to evaluate preselected image fields.
Conclusion.-The role of computer-aided digital microscopy in reducing observer variability in immunohistochemistry is promising. (Arch Pathol Lab Med. 2011;135:233-242)
C1 [Gavrielides, Marios A.; Gallas, Brandon D.; Badano, Aldo] US FDA, Div Imaging & Appl Math, Off Sci & Engn Labs, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
[Lenz, Petra; Hewitt, Stephen M.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Gavrielides, MA (reprint author), US FDA, Div Imaging & Appl Math, Off Sci & Engn Labs, Ctr Devices & Radiol Hlth, 10903 New Hampshire Ave,Bldg 62,Room 4114, Silver Spring, MD 20993 USA.
EM marios.gavrielides@fda.hhs.gov
OI Gallas, Brandon/0000-0001-7332-1620; Hewitt,
Stephen/0000-0001-8283-1788; badano, aldo/0000-0003-3712-6670
NR 43
TC 30
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U1 1
U2 7
PU COLLEGE AMER PATHOLOGISTS
PI NORTHFIELD
PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 USA
SN 0003-9985
J9 ARCH PATHOL LAB MED
JI Arch. Pathol. Lab. Med.
PD FEB
PY 2011
VL 135
IS 2
BP 233
EP 242
PG 10
WC Medical Laboratory Technology; Medicine, Research & Experimental;
Pathology
SC Medical Laboratory Technology; Research & Experimental Medicine;
Pathology
GA 722KG
UT WOS:000287430500017
PM 21284444
ER
PT J
AU Rossouw, J
Bray, P
Liu, JM
Kooperberg, C
Hsia, J
Lewis, C
Cushman, M
Bonds, D
Hendrix, S
Papanicolaou, G
Howard, T
Herrington, D
AF Rossouw, Jacques
Bray, Paul
Liu, Jingmin
Kooperberg, Charles
Hsia, Judith
Lewis, Cora
Cushman, Mary
Bonds, Denise
Hendrix, Susan
Papanicolaou, George
Howard, Timothy
Herrington, David
TI Estrogen Receptor Polymorphisms and the Vascular Effects of Hormone
Therapy
SO ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
LA English
DT Article
DE blood coagulation; clinical trials; coronary artery disease;
epidemiology; pulmonary embolism; receptors; stroke; estrogen
ID ALPHA GENE POLYMORPHISMS; CORONARY-HEART-DISEASE; C-REACTIVE PROTEIN;
RANDOMIZED CONTROLLED-TRIAL; CONJUGATED EQUINE ESTROGEN; POSTMENOPAUSAL
WOMEN; PLUS PROGESTIN; CARDIOVASCULAR-DISEASE; MYOCARDIAL-INFARCTION;
REPLACEMENT THERAPY
AB Objective-To test whether estrogen receptor polymorphisms modify the effects of postmenopausal hormone therapy on biomarkers and on risk of coronary heart disease events, stroke, or venous thromboembolism.
Methods and Results-The design was a nested case-control study in the Women's Health Initiative trials of postmenopausal hormone therapy. The study included all cases in the first 4 years: 359 cases of coronary heart disease, 248 of stroke, and 217 of venous thromboembolism. Six estrogen receptor-alpha polymorphisms and 1 estrogen receptor-beta polymorphism were genotyped; 8 biomarkers known to be affected by hormone therapy were measured at baseline and 1 year after randomization. The polymorphisms were not associated with risk of vascular events and did not modify the increased risks of coronary heart disease, stroke, or venous thromboembolism due to hormone therapy. However, a reduced response of plasmin-antiplasmin to hormone therapy was noted for estrogen receptor-1 IVS1 (intron number 1)-354 (interaction P<0.0001, corrected for multiple comparisons P=0.014) and estrogen receptor-1 IVS1-1415 (interaction P<0.0001, corrected P=0.014).
Conclusion-Estrogen receptor polymorphisms reduce the effect of postmenopausal hormone therapy on plasmin-antiplasmin, a marker of coagulation and fibrinolysis. However, screening for estrogen receptor polymorphisms to identify women at less risk of adverse cardiovascular outcomes is not likely to be useful in making decisions about hormone therapy treatment. (Arterioscler Thromb Vasc Biol. 2011;31:464-469.)
C1 [Rossouw, Jacques; Bonds, Denise; Papanicolaou, George] NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
[Bray, Paul] Thomas Jefferson Univ, Dept Hematol, Philadelphia, PA 19107 USA.
[Liu, Jingmin] Canc Res Ctr, Fred Hutchinson Publ Hlth Sci Div, Seattle, WA USA.
[Hsia, Judith] George Washington Univ, Dept Cardiol, Washington, DC USA.
[Lewis, Cora] Univ Alabama, Div Prevent Med, Birmingham, AL USA.
[Cushman, Mary] Univ Vermont, Dept Med, Burlington, VT USA.
[Hendrix, Susan] Detroit Med Ctr, Dept Obstet & Gynecol, Detroit, MI USA.
[Howard, Timothy] Wake Forest Univ, Bowman Gray Sch Med, Ctr Genom & Pesonalized Med Res, Winston Salem, NC USA.
[Herrington, David] Wake Forest Univ, Bowman Gray Sch Med, Dept Cardiol, Winston Salem, NC USA.
RP Rossouw, J (reprint author), NHLBI, Div Cardiovasc Sci, Rockledge 2,Rm 9192,6701 Rockledge Ave, Bethesda, MD 20892 USA.
EM rossouwj@nih.gov
FU National Heart, Lung, and Blood Institute, National Institutes of Health
[N01WH 2211, 2452, 32100, 32101, 32102, 32105, 32106, 32107, 32108,
32109, 32111, 32112, 32113, 32115, 32118, 32119, 32122, 42107, 42108,
42109, 42110, 42112, 42113, 42115, 42116, 42117, 42118, 42119, 42120,
42121, 42122, 42123, 42124, 42125, 42126, 42129, 42130, 42131, 42132,
44221]
FX The Women's Health Initiative is funded by contracts N01WH 2211, 2452,
32100 to 32102, 32105 to 32106, 32108 to 32109, 32111 to 32113, 32115,
32118 to 32119, 32122, 42107 to 42126, 42129 to 42132, and 44221 from
the National Heart, Lung, and Blood Institute, National Institutes of
Health. Study drugs were donated by Wyeth Research, St. Davids, Pa.
NR 35
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U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1079-5642
J9 ARTERIOSCL THROM VAS
JI Arterioscler. Thromb. Vasc. Biol.
PD FEB
PY 2011
VL 31
IS 2
BP 464
EP U433
DI 10.1161/ATVBAHA.110.215087
PG 9
WC Hematology; Peripheral Vascular Disease
SC Hematology; Cardiovascular System & Cardiology
GA 708PS
UT WOS:000286376800034
PM 21106950
ER
PT J
AU Alevizos, I
Alexander, S
Turner, RJ
Illei, GG
AF Alevizos, Ilias
Alexander, Stefanie
Turner, R. James
Illei, Gabor G.
TI MicroRNA Expression Profiles as Biomarkers of Minor Salivary Gland
Inflammation and Dysfunction in Sjogren's Syndrome
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; FIBROBLAST-LIKE SYNOVIOCYTES;
RHEUMATOID-ARTHRITIS; IMMUNE-SYSTEM; LUNG-CANCER; DISEASE; PROGNOSIS;
DIAGNOSIS; BIOPSIES; PLAYERS
AB Objective. MicroRNA reflect physiologic and pathologic processes and may be used as biomarkers of concurrent pathophysiologic events in complex settings such as autoimmune diseases. We generated microRNA microarray profiles from the minor salivary glands of control subjects without Sjogren's syndrome (SS) and patients with SS who had low-grade or high-grade inflammation and impaired or normal saliva production, to identify microRNA patterns specific to salivary gland inflammation or dysfunction.
Methods. MicroRNA expression profiles were generated by Agilent microRNA arrays. We developed a novel method for data normalization by identifying housekeeping microRNA. MicroRNA profiles were compared by unsupervised mathematical methods to test how well they distinguish between control subjects and various subsets of patients with SS. Several bioinformatics methods were used to predict the messenger RNA targets of the differentially expressed microRNA.
Results. MicroRNA expression patterns accurately distinguished salivary glands from control subjects and patients with SS who had low-degree or high-degree inflammation. Using real-time quantitative polymerase chain reaction, we validated 2 microRNA as markers of inflammation in an independent cohort. Comparing microRNA from patients with preserved or low salivary flow identified a set of differentially expressed microRNA, most of which were up-regulated in the group with decreased salivary gland function, suggesting that the targets of microRNA may have a protective effect on epithelial cells. The predicted biologic targets of microRNA associated with inflammation or salivary gland dysfunction identified both overlapping and distinct biologic pathways and processes.
Conclusion. Distinct microRNA expression patterns are associated with salivary gland inflammation and dysfunction in patients with SS, and microRNA represent a novel group of potential biomarkers.
C1 [Illei, Gabor G.] Natl Inst Dent & Craniofacial Res, Sjogrens Clin, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
RP Illei, GG (reprint author), Natl Inst Dent & Craniofacial Res, Sjogrens Clin, Mol Physiol & Therapeut Branch, NIH, 10 Ctr Dr,1N110, Bethesda, MD 20892 USA.
EM illeig@mail.nih.gov
FU National Institute of Dental and Craniofacial Research, NIH
FX Supported by the Intramural Research Program of the National Institute
of Dental and Craniofacial Research, NIH.
NR 27
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U1 2
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0004-3591
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD FEB
PY 2011
VL 63
IS 2
BP 535
EP 544
DI 10.1002/art.30131
PG 10
WC Rheumatology
SC Rheumatology
GA 719KC
UT WOS:000287202600031
PM 21280008
ER
PT J
AU Parks, CG
Walitt, BT
Pettinger, M
Chen, JC
de Roos, AJ
Hunt, J
Sarto, G
Howard, BV
AF Parks, Christine G.
Walitt, Brian T.
Pettinger, Mary
Chen, Jiu-Chiuan
de Roos, Anneclaire J.
Hunt, Julie
Sarto, Gloria
Howard, Barbara V.
TI Insecticide Use and Risk of Rheumatoid Arthritis and Systemic Lupus
Erythematosus in the Women's Health Initiative Observational Study
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID UNITED-STATES; OCCUPATIONAL EXPOSURES; ORGANOCHLORINE PESTICIDES;
SOCIOECONOMIC-STATUS; DISEASE; MORTALITY; FARMERS; DETERMINANTS;
AUTOIMMUNITY; ASSOCIATIONS
AB Objective. Farming and agricultural pesticide use has been associated with 2 autoimmune rheumatic diseases, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). However, risk associated with other residential or work place insecticide use is unknown.
Methods. We analyzed data from the Women's Health Initiative Observational Study (n = 76,861 postmenopausal women, ages 50-79 years). Incident cases (n = 213: 178 for RA, 27 for SLE, and 8 for both) were identified based on self-report and use of disease-modifying antirheumatic drugs at year 3 of followup. We examined self-reported residential or work place insecticide use (personally mixing/applying by self and application by others) in relation to RA/SLE risk, overall and in relation to farm history. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were adjusted for age, race, region, education, occupation, smoking, reproductive factors, asthma, other autoimmune diseases, and comorbidities.
Results. Compared with never used, personal use of insecticides was associated with increased RA/SLE risk, with significant trends for greater frequency (HR 2.04, 95% CI 1.17-3.56 for >= 6 times/year) and duration (HR 1.97, 95% CI 1.20-3.23 for >= 20 years). Risk was also associated with long-term insecticide application by others (HR 1.85, 95% CI 1.07-3.20 for >= 20 years) and frequent application by others among women with a farm history (HR 2.73, 95% CI 1.10-6.78 for >= 6 times/year).
Conclusion. These results suggest residential and work place insecticide exposure is associated with the risk of autoimmune rheumatic diseases in postmenopausal women. Although these findings require replication in other populations, they support a role for environmental pesticide exposure in the development of autoimmune rheumatic diseases.
C1 [Parks, Christine G.] NIEHS, Durham, NC USA.
[Walitt, Brian T.] Washington Hosp Ctr, Washington, DC 20010 USA.
[Pettinger, Mary; de Roos, Anneclaire J.; Hunt, Julie] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Chen, Jiu-Chiuan] Univ Calif Los Angeles, Keck Sch Med, Los Angeles, CA USA.
[Sarto, Gloria] Univ Wisconsin, Med Ctr, Madison, WI 53706 USA.
[Howard, Barbara V.] MedStar Hlth Res Inst, Washington, DC USA.
RP Parks, CG (reprint author), NIEHS, Epidemiol Branch, A3-05,POB 12233, Res Triangle Pk, NC 27599 USA.
EM parks1@mail.nih.gov
RI Chen, JC/I-2261-2016;
OI Parks, Christine/0000-0002-5734-3456
FU NIH, National Institute of Environmental Health Sciences; National
Heart, Lung, and Blood Institute; NIH; US Department of Health and Human
Services [N01-WH-22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13,
32115, 32118-32119, 32122, 42107-26, 42129-32, 44221];
Merck/Schering-Plough
FX Supported in part by the Intramural Research Program of the NIH,
National Institute of Environmental Health Sciences. The Women's Health
Initiative is funded by the National Heart, Lung, and Blood Institute,
the NIH, and the US Department of Health and Human Services (contracts
N01-WH-22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115,
32118-32119, 32122, 42107-26, 42129-32, and 44221).; Dr. Howard has
received consultant fees and speaking fees (less than $10,000) and
research support in the form of drug donation from
Merck/Schering-Plough.
NR 42
TC 30
Z9 30
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 2151-464X
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD FEB
PY 2011
VL 63
IS 2
BP 184
EP 194
DI 10.1002/acr.20335
PG 11
WC Rheumatology
SC Rheumatology
GA 719ML
UT WOS:000287208800003
PM 20740609
ER
PT J
AU Louie, GH
Tektonidou, MG
Caban-Martinez, AJ
Ward, MM
AF Louie, Grant H.
Tektonidou, Maria G.
Caban-Martinez, Alberto J.
Ward, Michael M.
TI Sleep Disturbances in Adults With Arthritis: Prevalence, Mediators, and
Subgroups at Greatest Risk. Data From the 2007 National Health Interview
Survey
SO ARTHRITIS CARE & RESEARCH
LA English
DT Article
ID QUALITY-OF-LIFE; RHEUMATOID-ARTHRITIS; CHRONIC PAIN; DAYTIME SLEEPINESS;
UNITED-STATES; OLDER-ADULTS; INSOMNIA; DISORDERS; POPULATION; DEPRESSION
AB Objective. To examine the prevalence of sleep disturbances in adults with arthritis in a nationally representative sample, mediators of sleep difficulties, and subgroups of individuals with arthritis at greatest risk.
Methods. Using data on US adults ages >= 18 years participating in the 2007 National Health Interview Survey, we computed the prevalence of 3 measures of sleep disturbance (insomnia, excessive daytime sleepiness, and sleep duration <6 hours) among persons with arthritis. We used logistic regression analysis to examine if the association of arthritis and sleep disturbances was independent of sociodemographic characteristics and comorbidities, and to identify potential mediators. We used classification trees to identify subgroups at higher risk.
Results. The adjusted prevalence of insomnia was higher among adults with arthritis than those without arthritis (23.1% versus 16.4%; P < 0.0001), but was similar to those with other chronic diseases. Adults with arthritis were more likely than those without arthritis to report insomnia (unadjusted odds ratio 2.92, 95% confidence interval 2.68-3.17), but adjustment for sociodemographic characteristics and comorbidities attenuated this association. Joint pain and limitation due to pain mediated the association between arthritis and insomnia. Among adults with arthritis, those with depression and anxiety were at highest risk for sleep disturbance. Results for excessive daytime sleepiness and sleep duration < 6 hours were similar.
Conclusion. Sleep disturbance affects up to 10.2 million US adults with arthritis, and is mediated by joint pain and limitation due to pain. Among individuals with arthritis, those with depression and anxiety are at greatest risk.
C1 [Louie, Grant H.; Ward, Michael M.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Tektonidou, Maria G.] Natl Univ Athens, Athens, Greece.
[Caban-Martinez, Alberto J.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
RP Louie, GH (reprint author), Johns Hopkins Univ, Sch Med, 5200 Eastern Ave,Mason F Lord Bldg,Ctr Tower,Suit, Baltimore, MD 21224 USA.
EM glouie2@jhmi.edu
OI Caban-Martinez, Alberto/0000-0002-5960-1308
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases at
the NIH
FX Supported by the Intramural Research Program of the National Institute
of Arthritis and Musculoskeletal and Skin Diseases at the NIH.
NR 50
TC 21
Z9 21
U1 2
U2 5
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 2151-464X
J9 ARTHRIT CARE RES
JI Arthritis Care Res.
PD FEB
PY 2011
VL 63
IS 2
BP 247
EP 260
DI 10.1002/acr.20362
PG 14
WC Rheumatology
SC Rheumatology
GA 719ML
UT WOS:000287208800011
PM 20890980
ER
PT J
AU Yang, M
Perry, K
Weber, MD
Katz, AM
Crawley, JN
AF Yang, Mu
Perry, Kayla
Weber, Michael D.
Katz, Adam M.
Crawley, Jacqueline N.
TI Social Peers Rescue Autism-Relevant Sociability Deficits in Adolescent
Mice
SO AUTISM RESEARCH
LA English
DT Article
DE autism; BTBR inbred strain; mouse model; peer enrichment; social
enrichment; behavioral intervention
ID FRAGILE-X-SYNDROME; INTENSIVE BEHAVIORAL TREATMENT; INTEGRATED PLAY
GROUPS; BTBR-T+TF/J MICE; SPECTRUM DISORDERS; REPETITIVE BEHAVIOR;
INBRED STRAINS; EARLY-CHILDHOOD; TASKS RELEVANT; MOUSE MODELS
AB Behavioral therapies are currently the most effective interventions for treating the diagnostic symptoms of autism. We employed a mouse model of autism to evaluate components of behavioral interventions that improve sociability in mice. BTBR T+tf/J (BTBR) is an inbred mouse strain that exhibits prominent behavioral phenotypes with face validity to all three diagnostic symptom categories of autism, including robust and well-replicated deficits in social approach and reciprocal social interactions. To investigate the role of peer interactions in the development of sociability, BTBR juvenile mice were reared in the same home cage with juvenile mice of a highly social inbred strain, C57BL/6J (B6). Subject mice were tested as young adults for sociability and repetitive behaviors. B6 controls reared with B6 showed their strain-typical high sociability. BTBR controls reared with BTBR showed their strain-typical lack of sociability. In contrast, BTBR reared with B6 as juveniles showed significant sociability as young adults. A 20-day intervention was as effective as a 40-day intervention for improving social approach behavior. High levels of repetitive self-grooming in BTBR were not rescued by peer-rearing with B6, indicating specificity of the intervention to the social domain. These results from a robust mouse model of autism support the interpretation that social enrichment with juvenile peers is a beneficial intervention for improving adult outcome in the social domain. This novel paradigm may prove useful for discovering factors that are essential for effective behavioral treatments, and biological mechanisms underlying effective behavioral interventions.
C1 [Yang, Mu] NIMH, Lab Behav Neurosci, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Yang, M (reprint author), NIMH, Lab Behav Neurosci, Intramural Res Program, NIH, Bldg 35,Room 1C-909,Mail Code 3730, Bethesda, MD 20892 USA.
EM yangmu@mail.nih.gov
OI Perry, Kayla/0000-0002-2629-1083
FU National Institute of Mental Health
FX Grant sponsor: National Institute of Mental Health Intramural Research
Program.
NR 80
TC 44
Z9 44
U1 1
U2 4
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 FEB
PY 2011
VL 4
IS 1
SI SI
BP 17
EP 27
DI 10.1002/aur.163
PG 11
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 729JP
UT WOS:000287945900003
PM 20928844
ER
PT J
AU Carter, MD
Shah, CR
Muller, CL
Crawley, JN
Carneiro, AMD
Veenstra-VanderWeele, J
AF Carter, Michelle D.
Shah, Charisma R.
Muller, Christopher L.
Crawley, Jacqueline N.
Carneiro, Ana M. D.
Veenstra-VanderWeele, Jeremy
TI Absence of Preference for Social Novelty and Increased Grooming in
Integrin beta 3 Knockout Mice: Initial Studies and Future Directions
SO AUTISM RESEARCH
LA English
DT Article
DE autism; genetic; integrin; cell adhesion; serotonin; social memory;
grooming; obsessive-compulsive disorder
ID WHOLE-BLOOD SEROTONIN; AUTISM SPECTRUM DISORDER; PERVASIVE DEVELOPMENTAL
DISORDERS; RECEPTOR GENE OXTR; COPY NUMBER VARIATION; MOUSE MODEL;
1ST-DEGREE RELATIVES; MENTAL-RETARDATION; ULTRASONIC VOCALIZATIONS;
BEHAVIORAL PHENOTYPES
AB Elevated whole blood serotonin 5-HT, or hyperserotonemia, is a common biomarker in autism spectrum disorder (ASD). The integrin beta 3 receptor subunit gene (ITGB3) is a quantitative trait locus for whole blood 5-HT levels. Recent work shows that integrin beta 3 interacts with the serotonin transporter (SERT) in both platelets and in the midbrain. Furthermore, multiple studies have now reported gene gene interaction between the integrin beta 3 and SERT genes in association with ASD. Given the lack of previous data on the impact of integrin beta 3 on brain or behavioral phenotypes, we sought to compare mice with decreased or absent expression of the integrin beta 3 receptor subunit (Itgb3+/- and -/-) with wildtype littermate controls in behavioral tasks relevant to ASD. These mice did not show deficits in activity level in the open field or anxiety-like behavior on the elevated plus maze, two potential confounds in the evaluation of mouse social behavior. In the three-chamber social test, mice lacking integrin beta 3 were shown to have normal sociability but did not show a preference for social novelty. Importantly, the absence of integrin beta 3 did not impair olfaction or the ability to recall familiar social odors. Additionally, mice lacking integrin beta 3 showed increased grooming behavior in novel environments. These preliminary studies reveal altered social and repetitive behavior in these mice, which suggests that the integrin beta 3 subunit may be involved in brain systems relevant to ASD. Further work is needed to fully characterize these behavioral changes and the underlying brain mechanisms.
C1 [Carter, Michelle D.; Shah, Charisma R.; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Psychiat, Nashville, TN USA.
[Muller, Christopher L.; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN USA.
[Crawley, Jacqueline N.] NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA.
[Carneiro, Ana M. D.; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pharmacol, Nashville, TN USA.
[Carneiro, Ana M. D.; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Kennedy Ctr Res Human Dev, Nashville, TN USA.
[Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pediat, Nashville, TN USA.
RP Veenstra-VanderWeele, J (reprint author), 465 21st Ave S,7158 MRB 3, Nashville, TN 37232 USA.
EM j.vvw@vanderbilt.edu
RI Veenstra-VanderWeele, Jeremy/K-1935-2015
OI Veenstra-VanderWeele, Jeremy/0000-0002-6349-1076
FU Seaside Therapeutics; Roche Pharmaceuticals; Novartis; NIH
[K08-MH081066, T32-MH065215, HD15052]; NIH (Vanderbilt Kennedy Center)
[T32-MH065215, HD15052, MH081066]
FX Dr. Veenstra-VanderWeele receives research support from Seaside
Therapeutics, Roche Pharmaceuticals, and Novartis, for clinical trials
unrelated to the current research.; Grant sponsor: NIH; Grant numbers:
K08-MH081066; T32-MH065215; HD15052.; We are especially grateful to the
families who participated in the original genetic studies. We also thank
Randy Blakely for helpful advice and generous mentorship. This work was
supported, in part, by NIH grants MH081066 (JV), T32-MH065215 (JV), and
HD15052 (Vanderbilt Kennedy Center).
NR 97
TC 42
Z9 42
U1 3
U2 9
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 FEB
PY 2011
VL 4
IS 1
SI SI
BP 57
EP 67
DI 10.1002/aur.180
PG 11
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 729JP
UT WOS:000287945900006
PM 21254450
ER
PT J
AU Kidd, LR
Hein, DW
Woodson, K
Taylor, PR
Albanes, D
Virtamo, J
Tangrea, JA
AF Kidd, LaCreis R.
Hein, David W.
Woodson, Karen
Taylor, Philip R.
Albanes, Demetrius
Virtamo, Jarmo
Tangrea, Joseph A.
TI Lack of Association of the N-acetyltransferase NAT1*10 Allele with
Prostate Cancer Incidence, Grade, or Stage Among Smokers in Finland
SO BIOCHEMICAL GENETICS
LA English
DT Article
DE N-acetyltransferase 1; Prostate cancer; Disease progression; Arylamine
carcinogens
ID NON-HODGKIN-LYMPHOMA; NAT2 GENETIC POLYMORPHISMS; DNA ADDUCT FORMATION;
HAIR DYE USE; N-ACETYLTRANSFERASE-1 NAT1; CIGARETTE-SMOKING; MEAT
INTAKE; COLORECTAL-CANCER; PANCREATIC-CANCER; EPITHELIAL-CELLS
AB Genetic variations in xenobiotic metabolizing genes can influence susceptibility to many environmentally induced cancers. Inheritance of the N-acetyltransferase 1 allele (NAT1*10), linked with increased metabolic activation of pro-carcinogens, is associated with an increased susceptibility to many cancers in which cigarette- or meat-derived carcinogens have been implicated in their etiology. The role of NAT1*10 in prostate cancer is under studied. Although cigarette smoking is not considered a risk factor for prostate cancer, a recent review suggests it may play a role in disease progression. Consequently, we examined the association of NAT1*10 with prostate cancer risk, grade, and stage among 400 Finnish male smokers using a case-control study design. Following genotyping of 206 patients and 196 healthy controls, our results do not support the role of NAT1*10 in relation to prostate cancer risk (OR = 1.28; 95% CI, 0.66-2.47), aggressive disease (OR = 0.58; 95% CI, 0.13-2.67), or advanced disease (OR = 1.19; 95% CI, 0.49-2.91).
C1 [Kidd, LaCreis R.; Hein, David W.] Univ Louisville, Dept Pharmacol & Toxicol, James Graham Brown Canc Ctr, Hlth Sci Ctr, Louisville, KY 40292 USA.
[Kidd, LaCreis R.; Woodson, Karen; Taylor, Philip R.; Tangrea, Joseph A.] NCI, Canc Prevent Studies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Virtamo, Jarmo] Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland.
RP Kidd, LR (reprint author), Univ Louisville, Dept Pharmacol & Toxicol, James Graham Brown Canc Ctr, Hlth Sci Ctr, 306 Clin & Translat Res Bldg,505 S Hancock St, Louisville, KY 40292 USA.
EM lrkidd01@louisville.edu
RI Hein, David/A-9707-2008; Albanes, Demetrius/B-9749-2015
FU National Cancer Institute, United States Department of Health and Human
Services [NO1 CN45165, 45035]
FX We thank Rama Modali and Kirsten Taylor for technical support and Mike
Barrett, Kirk Snyder, and Tan Carly for data management. This study was
supported in part by Public Health Service contracts NO1 CN45165 and
45035 from the National Cancer Institute, United States Department of
Health and Human Services.
NR 58
TC 4
Z9 4
U1 0
U2 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0006-2928
J9 BIOCHEM GENET
JI Biochem. Genet.
PD FEB
PY 2011
VL 49
IS 1-2
BP 73
EP 82
DI 10.1007/s10528-010-9386-4
PG 10
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 732ES
UT WOS:000288168400008
PM 20931357
ER
PT J
AU Kendrick, AA
Choudhury, M
Rahman, SM
McCurdy, CE
Friederich, M
Van Hove, JLK
Watson, PA
Birdsey, N
Bao, JJ
Gius, D
Sack, MN
Jing, EX
Kahn, CR
Friedman, JE
Jonscher, KR
AF Kendrick, Agnieszka A.
Choudhury, Mahua
Rahman, Shaikh M.
McCurdy, Carrie E.
Friederich, Marisa
Van Hove, Johan L. K.
Watson, Peter A.
Birdsey, Nicholas
Bao, Jianjun
Gius, David
Sack, Michael N.
Jing, Enxuan
Kahn, C. Ronald
Friedman, Jacob E.
Jonscher, Karen R.
TI Fatty liver is associated with reduced SIRT3 activity and mitochondrial
protein hyperacetylation
SO BIOCHEMICAL JOURNAL
LA English
DT Article
DE cellular metabolism; mitochondrial metabolism; NAD; non-alcoholic fatty
liver disease; obesity; proteomics; sirtuin
ID LYSINE ACETYLATION; INSULIN-RESISTANCE; OXIDATIVE STRESS;
PYRUVATE-CARBOXYLASE; DEACETYLASE ACTIVITY; HISTONE DEACETYLASE;
GENE-EXPRESSION; ACID OXIDATION; OBESITY; METABOLISM
AB Acetylation has recently emerged as an important mechanism for controlling a broad array of proteins mediating cellular adaptation to metabolic fuels. Acetylation is governed, in part, by SIRTs (sirtuins), class III NAD(+)-dependent deacetylases that regulate lipid and glucose metabolism in liver during fasting and aging. However, the role of acetylation or SIRTs in pathogenic hepatic fuel metabolism under nutrient excess is unknown. In the present study, we isolated acetylated proteins from total liver proteome and observed 193 preferentially acetylated proteins in mice fed on an HFD (high-fat diet) compared with controls, including 11 proteins not previously identified in acetylation studies. Exposure to the HFD led to hyperacetylation of proteins involved in gluconeogenesis, mitochondrial oxidative metabolism, methionine metabolism, liver injury and the ER (endoplasmic reticulum) stress response. Livers of mice fed on the HFD had reduced SIRT3 activity, a 3-fold decrease in hepatic NAD(+) levels and increased mitochondrial protein oxidation. In contrast, neither SIRT1 nor histone acetyltransferase activities were altered, implicating SIRT3 as a dominant factor contributing to the observed phenotype. In Sirt3(-/-) mice, exposure to the HFD further increased the acetylation status of liver proteins and reduced the activity of respiratory complexes III and IV. This is the first study to identify acetylation patterns in liver proteins of HFD-fed mice. Our results suggest that SIRT3 is an integral regulator of mitochondrial function and its depletion results in hyperacetylation of critical mitochondrial proteins that protect against hepatic lipotoxicity under conditions of nutrient excess.
C1 [Kendrick, Agnieszka A.; Friedman, Jacob E.; Jonscher, Karen R.] Univ Colorado, Sch Med, Dept Anesthesiol, NORC,Mass Spectrometry Core Facil, Aurora, CO 80045 USA.
[Choudhury, Mahua; Rahman, Shaikh M.; McCurdy, Carrie E.; Friederich, Marisa; Van Hove, Johan L. K.; Friedman, Jacob E.] Univ Colorado, Sch Med, Dept Pediat, Aurora, CO 80045 USA.
[Watson, Peter A.; Birdsey, Nicholas] Denver VA Med Ctr, Denver, CO 80220 USA.
[Bao, Jianjun; Sack, Michael N.] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
[Gius, David] NCI, Radiat Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Jing, Enxuan; Kahn, C. Ronald] Harvard Univ, Sch Med, Joslin Diabet Ctr, Boston, MA 02215 USA.
RP Friedman, JE (reprint author), Univ Colorado, Sch Med, Dept Anesthesiol, NORC,Mass Spectrometry Core Facil, Aurora, CO 80045 USA.
EM jed.friedman@ucdenver.edu
OI Jonscher, Karen/0000-0002-7929-4886
FU National Institutes of Health [DK59767, P30-DK48520, K12 HD057022];
University of Colorado, Center for Human Nutrition [P30-DK048520-09];
American Heart Association [09BGIA2060705]; American Diabetes
Mentor-based Post-Doctoral Fellowship [7-08-MN-17]; Veterans
Administration; National Heart, Lung, and Blood Institute; Center for
Cancer Research, National Cancer Institute
FX This work was supported by the National Institutes of Health [grant
numbers DK59767, P30-DK48520 (to J.E.F.)]; a Pilot & Feasibility Award
from the University of Colorado, Center for Human Nutrition [grant
number P30-DK048520-09 to K.R.J.)]; the National Institutes of Health
Office of Research in Women's Health BIRCWH Program [grant number K12
HD057022 (to C.E.M.)]; a Beginning Grant in Aid from the American Heart
Association [grant number 09BGIA2060705 (to S.M.R.)]; and an American
Diabetes Mentor-based Post-Doctoral Fellowship [grant number 7-08-MN-17
(to MC.)]. P.W. was supported by Veterans Administration Merit Awards.
J.B. and M.N.S. were funded by the National Heart, Lung, and Blood
Institute. D.G. was supported by the Center for Cancer Research,
National Cancer Institute.
NR 53
TC 122
Z9 129
U1 4
U2 28
PU PORTLAND PRESS LTD
PI LONDON
PA THIRD FLOOR, EAGLE HOUSE, 16 PROCTER STREET, LONDON WC1V 6 NX, ENGLAND
SN 0264-6021
J9 BIOCHEM J
JI Biochem. J.
PD FEB 1
PY 2011
VL 433
BP 505
EP 514
DI 10.1042/BJ20100791
PN 3
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 757AJ
UT WOS:000290055900012
PM 21044047
ER
PT J
AU Keppler, BR
Archer, TK
Kinyamu, HK
AF Keppler, Brian R.
Archer, Trevor K.
Kinyamu, H. Karimi
TI Emerging roles of the 26S proteasome in nuclear hormone
receptor-regulated transcription
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE REGULATORY MECHANISMS
LA English
DT Review
DE Proteasome; Nuclear hormone receptor; Transcription; Chromatin
ID RNA-POLYMERASE-II; CHROMATIN-REMODELING COMPLEX; BREAST-CANCER CELLS;
GLUCOCORTICOID-RECEPTOR; ESTROGEN-RECEPTOR; DEPENDENT TRANSCRIPTION;
ANDROGEN RECEPTOR; TARGET GENES; IN-VIVO; MOLECULAR CHAPERONES
AB The mechanisms by which nuclear hormone receptors (NHRs) regulate transcription are highly dynamic and require interplay between a myriad of regulatory protein complexes including the 26S proteasome. Protein degradation is the most well-established role of the proteasome; however, an increasing body of evidence suggests that the 26S proteasome may regulate transcription in proteolytic and nonproteolytic mechanisms. Here we review how these mechanisms may apply to NHR-mediated transcriptional regulation. This article is part of a Special Issue entitled The 26S Proteasome: When degradation is just not enough! Published by Elsevier B.V.
C1 [Keppler, Brian R.; Archer, Trevor K.; Kinyamu, H. Karimi] NIEHS, Chromatin & Gene Express Sect, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Kinyamu, HK (reprint author), NIEHS, Chromatin & Gene Express Sect, Mol Carcinogenesis Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM Kinyamu@niehs.nih.gov
OI Keppler, Bernhard/0000-0003-0877-1822
FU National Institute of Environmental Health Sciences, NIH [Z01
ES071006-10]
FX This research was supported by the Intramural Research Program of the
National Institute of Environmental Health Sciences, NIH (project no.
Z01 ES071006-10, to T.A.). We thank Drs. Heather King, Paul Wade, and
Sergei Nechaev for critically reviewing the manuscript.
NR 106
TC 8
Z9 8
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-9399
J9 BBA-GENE REGUL MECH
JI Biochim. Biophys. Acta-Gene Regul. Mech.
PD FEB
PY 2011
VL 1809
IS 2
SI SI
BP 109
EP 118
DI 10.1016/j.bbagrm.2010.08.005
PG 10
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 722LR
UT WOS:000287434200006
PM 20728592
ER
PT J
AU Kim, HW
Rao, JS
Rapoport, SI
Igarashi, M
AF Kim, Hyung-Wook
Rao, Jagadeesh S.
Rapoport, Stanley I.
Igarashi, Miki
TI Dietary n-6 PUFA deprivation downregulates arachidonate but upregulates
docosahexaenoate metabolizing enzymes in rat brain
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
LA English
DT Article
DE Arachidonic; Brain; PUFA; Phospholipase; Lipoxygenase; SREBP
ID POLYUNSATURATED FATTY-ACIDS; INDEPENDENT PHOSPHOLIPASE A(2); DESATURASE
MESSENGER-RNA; AIN-93 PURIFIED DIETS; GROUP-SPECIFIC ASSAYS;
ALPHA-LINOLENIC ACID; GENE-EXPRESSION; FRONTAL-CORTEX; CANCER CELLS;
INHIBITORS
AB Background: Dietary n-3 polyunsaturated fatty acid (PUFA) deprivation increases expression of arachidonic acid (AA 20:4n-6)-selective cytosolic phospholipase A(2) (cPLA(2)) IVA and cyclooxygenase (COX)-2 in rat brain, while decreasing expression of docosahexaenoic acid (DHA 22:6n-3)-selective calcium-independent iPLA(2) VIA. Assuming that these enzyme changes represent brain homeostatic responses to deprivation, we hypothesized that dietary n-6 PUFA deprivation would produce changes in the opposite directions. Methods: Brain expression of PUFA-metabolizing enzymes and their transcription factors was quantified in male rats fed an n-6 PUFA adequate or deficient diet for 15 weeks post-weaning. Results: The deficient compared with adequate diet increased brain mRNA, protein and activity of iPLA(2) VIA and 15-lipoxygenase (LOX), but decreased cPLA(2) IVA and COX-2 expression. The brain protein level of the iPLA(2) transcription factor SREBP-1 was elevated, while protein levels were decreased for AP-2 alpha and NF-kappa B p65, cPLA(2) and COX-2 transcription factors, respectively. Conclusions: With dietary n-6 PUFA deprivation, rat brain PUFA metabolizing enzymes and some of their transcription factors change in a way that would homeostatically dampen reductions in brain n-6 PUFA concentrations and metabolism, while n-3 PUFA metabolizing enzyme expression is increased. The changes correspond to reported in vitro enzyme selectivities for AA compared with DHA. Published by Elsevier B.V.
C1 [Kim, Hyung-Wook; Rao, Jagadeesh S.; Rapoport, Stanley I.; Igarashi, Miki] NIA, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA.
RP Kim, HW (reprint author), NIA, Brain Physiol & Metab Sect, NIH, Bldg 9,Room 1S126, Bethesda, MD 20892 USA.
EM kimhyung@mail.nih.gov
FU National Institute on Aging, NIH
FX This research was supported entirely by the Intramural Research Program
of the National Institute on Aging, NIH. The authors thank the NIH
Fellows' Editorial Board and Dr. Eugene Streicher for editorial
assistance.
NR 54
TC 20
Z9 21
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1388-1981
EI 0006-3002
J9 BBA-MOL CELL BIOL L
JI Biochim. Biophys. Acta Mol. Cell Biol. Lipids
PD FEB
PY 2011
VL 1811
IS 2
BP 111
EP 117
DI 10.1016/j.bbalip.2010.10.005
PG 7
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 716UH
UT WOS:000286998500007
PM 21070866
ER
PT J
AU Lee, S
Choi, KY
Chung, H
Ryu, JH
Lee, A
Koo, H
Youn, IC
Park, JH
Kim, IS
Kim, SY
Chen, X
Jeong, SY
Kwon, IC
Kim, K
Choi, K
AF Lee, Seulki
Choi, Ki Young
Chung, Hyunjin
Ryu, Ju Hee
Lee, Aeju
Koo, Heebeom
Youn, In-Chan
Park, Jae Hyung
Kim, In-San
Kim, Sang Yoon
Chen, Xiaoyuan
Jeong, Seo Young
Kwon, Ick Chan
Kim, Kwangmeyung
Choi, Kuiwon
TI Real Time, High Resolution Video Imaging of Apoptosis in Single Cells
with a Polymeric Nanoprobe
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID PROBES
AB We report a new apoptosis nanoprobe (Apo-NP) designed on the basis of a polymer nanoparticle platform. This simple one-step technique is capable of boosting fluorescence signals upon apoptosis in living cells, enabling real-time imaging of apoptosis in single cells and in vivo. The Apo-NP efficiently delivers chemically labeled, dual-quenched caspase-3-sensitive fluorogenic peptides into cells, allowing caspase-3-dependent strong fluorescence amplification to be imaged in apoptotic cells in real-time and at high resolution. The design platform of the Apo-NP is flexible and can be fine-tuned for a wide array of applications such as identification of caspase-related apoptosis in pathologies and for monitoring therapeutic efficacy of apoptotic drugs in cancer treatment.
C1 [Lee, Seulki; Choi, Ki Young; Chung, Hyunjin; Ryu, Ju Hee; Lee, Aeju; Koo, Heebeom; Youn, In-Chan; Kwon, Ick Chan; Kim, Kwangmeyung; Choi, Kuiwon] Korea Inst Sci & Technol, Biomed Res Ctr, Seoul 136791, South Korea.
[Lee, Seulki; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
[Choi, Ki Young; Park, Jae Hyung] Kyung Hee Univ, Coll Engn, Dept Chem Engn, Gyeonggi Do 449701, South Korea.
[Choi, Ki Young; Lee, Aeju; Park, Jae Hyung; Jeong, Seo Young] Kyung Hee Univ, Dept Life & Nanopharmaceut Sci, Seoul 130701, South Korea.
[Kim, In-San] Kyungpook Natl Univ, Daeggu 700422, South Korea.
[Kim, Sang Yoon] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Otolaryngol, Seoul 138736, South Korea.
RP Kim, K (reprint author), Korea Inst Sci & Technol, Biomed Res Ctr, 39-1 Haweolgog Dong, Seoul 136791, South Korea.
EM kim@kist.re.kr; choi@kist.re.kr
RI byun, jaehyun/G-5584-2014; 김, 인산/I-8988-2014; CHOI, KI
YOUNG/Q-7177-2016; Kim, In-San/D-3956-2017
FU MEST; KIST, Theragnosis; Korea Health 21 RD Project [A062254]; NIH/NIST
NRC
FX This work was financially supported by the Real-Time Molecular Imaging
Project and Global Research Laboratory Project of MEST and by a grant to
the Intramural Research Program of the KIST, Theragnosis, and by a grant
(A062254) of the Korea Health 21 R&D Project. S.L. was partially funded
by the NIH/NIST NRC fellowship.
NR 18
TC 26
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U1 1
U2 16
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD FEB
PY 2011
VL 22
IS 2
BP 125
EP 131
DI 10.1021/bc1004119
PG 7
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 720RE
UT WOS:000287297000003
PM 21218786
ER
PT J
AU Doughty, E
Kertesz-Farkas, A
Bodenreider, O
Thompson, G
Adadey, A
Peterson, T
Kann, MG
AF Doughty, Emily
Kertesz-Farkas, Attila
Bodenreider, Olivier
Thompson, Gary
Adadey, Asa
Peterson, Thomas
Kann, Maricel G.
TI Toward an automatic method for extracting cancer- and other
disease-related point mutations from the biomedical literature
SO BIOINFORMATICS
LA English
DT Article
ID PROSTATE-CANCER; GROWTH-FACTOR; GENE; SYSTEM; VALIDATION; DATABASE; TEXT
AB Motivation: A major goal of biomedical research in personalized medicine is to find relationships between mutations and their corresponding disease phenotypes. However, most of the disease-related mutational data are currently buried in the biomedical literature in textual form and lack the necessary structure to allow easy retrieval and visualization. We introduce a high-throughput computational method for the identification of relevant disease mutations in PubMed abstracts applied to prostate (PCa) and breast cancer (BCa) mutations.
Results: We developed the extractor of mutations (EMU) tool to identify mutations and their associated genes. We benchmarked EMU against MutationFinder-a tool to extract point mutations from text. Our results show that both methods achieve comparable performance on two manually curated datasets. We also benchmarked EMU's performance for extracting the complete mutational information and phenotype. Remarkably, we show that one of the steps in our approach, a filter based on sequence analysis, increases the precision for that task from 0.34 to 0.59 (PCa) and from 0.39 to 0.61 (BCa). We also show that this high-throughput approach can be extended to other diseases.
Discussion: Our method improves the current status of disease-mutation databases by significantly increasing the number of annotated mutations. We found 51 and 128 mutations manually verified to be related to PCa and Bca, respectively, that are not currently annotated for these cancer types in the OMIM or Swiss-Prot databases. EMU's retrieval performance represents a 2-fold improvement in the number of annotated mutations for PCa and BCa. We further show that our method can benefit from full-text analysis once there is an increase in Open Access availability of full-text articles.
C1 [Doughty, Emily; Kertesz-Farkas, Attila; Thompson, Gary; Adadey, Asa; Peterson, Thomas; Kann, Maricel G.] Univ Maryland Baltimore Cty, Baltimore, MD 21250 USA.
[Kertesz-Farkas, Attila] US FDA, Div Imaging & Appl Math, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
[Bodenreider, Olivier] Natl Lib Med, Bethesda, MD 20894 USA.
RP Kann, MG (reprint author), Univ Maryland Baltimore Cty, Baltimore, MD 21250 USA.
EM mkann@umbc.edu
RI Kann, Maricel/E-5701-2012
FU National Institutes of Health (NIH) [1K22CA143148, R01LM009722]; Centre
for Devices and Radiological Health; US Food and Drug Administration;
NIH, National Library of Medicine
FX This work was supported by the National Institutes of Health (NIH)
[1K22CA143148, MGK (PI) and R01LM009722, MGK (collaborator)]. A. K. F.
acknowledges funding from the Research Fellowship Program of the Centre
for Devices and Radiological Health, administrated by the Oak Ridge
Associated Universities through a contact with the US Food and Drug
Administration. Additional funding (OB) was provided by the Intramural
Research Program of the NIH, National Library of Medicine.
NR 32
TC 26
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U1 0
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1367-4803
J9 BIOINFORMATICS
JI Bioinformatics
PD FEB 1
PY 2011
VL 27
IS 3
BP 408
EP 415
DI 10.1093/bioinformatics/btq667
PG 8
WC Biochemical Research Methods; Biotechnology & Applied Microbiology;
Computer Science, Interdisciplinary Applications; Mathematical &
Computational Biology; Statistics & Probability
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Computer Science; Mathematical & Computational Biology; Mathematics
GA 716RN
UT WOS:000286991300016
PM 21138947
ER
PT J
AU Garces-Ramirez, L
Green, JL
Hiranita, T
Kopajtic, TA
Mereu, M
Thomas, AM
Mesangeau, C
Narayanan, S
McCurdy, CR
Katz, JL
Tanda, G
AF Garces-Ramirez, Linda
Green, Jennifer L.
Hiranita, Takato
Kopajtic, Theresa A.
Mereu, Maddalena
Thomas, Alexandra M.
Mesangeau, Christophe
Narayanan, Sanju
McCurdy, Christopher R.
Katz, Jonathan L.
Tanda, Gianluigi
TI Sigma Receptor Agonists: Receptor Binding and Effects on Mesolimbic
Dopamine Neurotransmission Assessed by Microdialysis
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Abuse liability; addiction; cocaine; dopamine microdialysis; nucleus
accumbens; reinforcing effects; sigma receptors
ID CENTRAL-NERVOUS-SYSTEM; NUCLEUS-ACCUMBENS; IN-VIVO; EXTRACELLULAR
CONCENTRATION; COCAINE BINDING; GUINEA-PIG; LIGANDS; RAT; DRUGS;
TRANSMISSION
AB Background: Subtypes of sigma (sigma) receptors, sigma(1) and sigma(2), can be pharmacologically distinguished, and each may be involved in substance-abuse disorders. sigma-Receptor antagonists block cocaine place conditioning and sigma-receptor agonists are self-administered in rats that previously self-administered cocaine. Self-administration of abused drugs has been related to increased dopamine (DA) neurotransmission, however, sigma-receptor agonist effects on mesolimbic DA are not fully characterized.
Methods: Receptor-binding studies assessed affinities of sigma-receptor ligands for sigma-receptor subtypes and the DA transporter; effects on DA transmission in the rat nucleus accumbens shell were assessed using in vivo microdialysis.
Results: Cocaine (.1-1.0 mg/kg intravenous [IV]), the nonselective sigma(1/2)-receptor agonist DTG (1.0-5.6 mg/kg IV), and the selective sigma(1)-receptor agonist PRE-084 (.32-10 mg/kg IV) dose-dependently increased DA to similar to 275%, similar to 150%, and similar to 160% maxima, respectively. DTG-induced stimulation of DA was antagonized by the nonselective sigma(1/2)-receptor antagonist BD 1008 (10 mg/kg intraperitoneal [IP]) and the preferential sigma(2)-receptor antagonist SN 79 (1-3 mg/kg IP), but not by the preferential sigma(1)-receptor antagonist, BD 1063 (10-30 mg/kg IP). Neither PRE-084 nor cocaine was antagonized by BD 1063 or BD 1008.
Conclusions: sigma-Receptor agonists stimulated DA in a brain area critical for reinforcing effects of cocaine. DTG effects on DA appear to be mediated by sigma(2)-receptors rather than sigma(1)-receptors. However, DA stimulation by cocaine or PRE-084 does not likely involve sigma-receptors. The relatively low potency on DA transmission of the selective sigma(1)-receptor agonist, PRE-084, and its previously reported potent reinforcing effects, suggest a dopamine-independent reinforcing pathway that may contribute to substance-abuse disorders.
C1 [Garces-Ramirez, Linda; Green, Jennifer L.; Hiranita, Takato; Kopajtic, Theresa A.; Mereu, Maddalena; Thomas, Alexandra M.; Katz, Jonathan L.; Tanda, Gianluigi] NIDA, NIH, Dept Hlth & Human Serv, Intramural Res Program,Psychobiol Sect,Medicat Di, Baltimore, MD 21224 USA.
[Hiranita, Takato] NIH, Japan Soc Promot Sci, Baltimore, MD USA.
[Garces-Ramirez, Linda] Inst Politecn Nacl, Escuela Nacl Ciencias Biol, Mexico City, DF, Mexico.
[Mesangeau, Christophe; Narayanan, Sanju; McCurdy, Christopher R.] Univ Mississippi, Dept Med Chem, Oxford, MS USA.
RP Tanda, G (reprint author), NIDA, NIH, Dept Hlth & Human Serv, Intramural Res Program,Psychobiol Sect,Medicat Di, Bldg C,Room 321,5500 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM gtanda@intra.nida.nih.gov
RI Tanda, Gianluigi/B-3318-2009; Hiranita, Takato/G-6567-2011;
OI Tanda, Gianluigi/0000-0001-9526-9878; Katz, Jonathan/0000-0002-1068-1159
FU National Institute on Drug Abuse (NIDA), National Institutes of Health,
Department of Health and Human Services; NIDA [DA023205 [CRM]]; Consejo
Nacional de Ciencia y Tecnologia, Mexico
FX This work was supported by the Intramural Research Program of the
National Institute on Drug Abuse (NIDA), National Institutes of Health,
Department of Health and Human Services, and in part by NIDA Grant
(DA023205 [CRM]). LG-R was recipient of a scholarship from Consejo
Nacional de Ciencia y Tecnologia, Mexico.
NR 51
TC 27
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U1 1
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD FEB 1
PY 2011
VL 69
IS 3
BP 208
EP 217
DI 10.1016/j.biopsych.2010.07.026
PG 10
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 708PZ
UT WOS:000286377600004
PM 20950794
ER
PT J
AU Pantin, JM
Tian, X
Keyvanfar, K
Zerfas, P
Eckhaus, M
Childs, RW
AF Pantin, J. M.
Tian, X.
Keyvanfar, K.
Zerfas, P.
Eckhaus, M.
Childs, R. W.
TI SUPERIOR ENGRAFTMENT AND SURVIVAL AND LESS GVHD IN NOD-SCID IL2RG(NULL)
(NSG) MICE RECEIVING INTRABONE COMPARED WITH IV TRANSPLANTS OF HUMAN
T-CELL REPLETE G-CSF MOBILIZED PERIPHERAL BLOOD STEM CELLS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT Annual Meeting of the
American-Society-for-Blood-and-Marrow-Transplantation(BMT) Tandem
CY FEB 17-21, 2011
CL Honolulu, HI
SP Amer Soc Blood & Marrow Transplant, Ctr Int Blood & Marrow Transplant Res Tandem
C1 [Pantin, J. M.; Tian, X.; Keyvanfar, K.; Childs, R. W.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2011
VL 17
IS 2
SU 2
MA 41
BP S166
EP S167
DI 10.1016/j.bbmt.2010.12.047
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 721JX
UT WOS:000287350500042
ER
PT J
AU Chatterjee, K
Sun, LM
Chow, LC
Young, MF
Simon, CG
AF Chatterjee, Kaushik
Sun, Limin
Chow, Laurence C.
Young, Marian F.
Simon, Carl G., Jr.
TI Combinatorial screening of osteoblast response to 3D calcium
phosphate/poly(is an element of-caprolactone) scaffolds using gradients
and arrays
SO BIOMATERIALS
LA English
DT Article
DE 3D scaffolds; Calcium phosphate; Combinatorial screening; Nanoparticles;
Osteoblast; Tissue engineering
ID STEM-CELLS; BONE REGENERATION; PHOSPHATE; DIFFERENTIATION; BIOMATERIALS;
BIOCERAMICS; INTERFACES; COMPOSITE; CULTURE; MODEL
AB There is a need for combinatorial and high-throughput methods for screening cell-biomaterial interactions to maximize tissue generation in scaffolds. Current methods employ a flat two-dimensional (2D) format even though three-dimensional (3D) scaffolds are more representative of the tissue environment in vivo and cells are responsive to topographical differences of 2D substrates and 3D scaffolds. Thus, combinatorial libraries of 3D porous scaffolds were developed and used to screen the effect of nano-amorphous calcium phosphate (nACP) particles on osteoblast response. Increasing nACP content in poly (is an element of-caprolactone) (PCL) scaffolds promoted osteoblast adhesion and proliferation. The nACP-containing scaffolds released calcium and phosphate ions which are known to activate osteoblast function. Scaffold libraries were fabricated in two formats, gradients and arrays, and the magnitude of the effect of nACP on osteoblast proliferation was greater for arrays than gradients. The enhanced response in arrays can be explained by differences in cell culture designs, diffusional effects and differences in the ratio of "scaffold mass to culture medium". These results introduce a gradient library approach for screening large pore 3D scaffolds and demonstrate that inclusion of the nACP particles enhances osteoblast proliferation in 3D scaffolds. Further, comparison of gradients and arrays suggests that gradients were more sensitive for detecting effects of scaffold composition on cell adhesion (short time points, 1 day) whereas arrays were more sensitive at detecting effects on cell proliferation (longer time points, 14 day). Published by Elsevier Ltd.
C1 [Chatterjee, Kaushik; Simon, Carl G., Jr.] Natl Inst Stand & Technol, Div Polymers, Gaithersburg, MD 20899 USA.
[Chatterjee, Kaushik; Young, Marian F.] Natl Inst Dent & Craniofacial Res, Craniofacial & Skeletal Dis Branch, NIH, Bethesda, MD USA.
[Sun, Limin; Chow, Laurence C.] Natl Inst Stand & Technol, Amer Dent Assoc Fdn, Paffenbarger Res Ctr, Gaithersburg, MD 20899 USA.
RP Simon, CG (reprint author), Natl Inst Stand & Technol, Div Polymers, 100 Bur Dr, Gaithersburg, MD 20899 USA.
EM carl.simon@nist.gov
RI Sanders, Susan/G-1957-2011
FU National Research Council of the National Academy of Sciences in the
Joint NIH-NIBIB/NIST; NIST; NIH-NIDCR (National Institute of Dental and
Craniofacial Research) [NIH-NIBIB R21 EB006497-01, NIH-NIDCR R01DE16416]
FX K.C. acknowledges support from a Research Associateship Award from the
National Research Council of the National Academy of Sciences in the
Joint NIH-NIBIB/NIST Postdoctoral Program (National Institutes of
Health-National Institute of Biomedical Imaging and
Bioengineering/National Institute of Standards and Technology). This
work was supported by NIST, the Intramural Program of the NIH-NIDCR
(National Institute of Dental and Craniofacial Research), NIH-NIBIB R21
EB006497-01 and NIH-NIDCR R01DE16416. The standard deviation (S.D.) is
the same as the "combined standard uncertainty of the mean" for the
purposes of this work. The content is solely the responsibility of the
authors and does not necessarily represent the official views of NIH,
NIBIB, NIDCR, NIST or ADA (American Dental Association). This article, a
contribution of NIST and NIH, is not subject to US copyright. Certain
equipment and instruments or materials are identified in the paper to
adequately specify the experimental details. Such identification does
not imply recommendation by NIST, nor does it imply the materials are
necessarily the best available for the purpose.
NR 40
TC 25
Z9 25
U1 1
U2 33
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0142-9612
J9 BIOMATERIALS
JI Biomaterials
PD FEB
PY 2011
VL 32
IS 5
BP 1361
EP 1369
DI 10.1016/j.biomaterials.2010.10.043
PG 9
WC Engineering, Biomedical; Materials Science, Biomaterials
SC Engineering; Materials Science
GA 717UN
UT WOS:000287073000012
PM 21074846
ER
PT J
AU Sawyer, RT
Maier, LA
AF Sawyer, Richard T.
Maier, Lisa A.
TI Chronic beryllium disease: an updated model interaction between innate
and acquired immunity
SO BIOMETALS
LA English
DT Article
DE Beryllium; Chronic beryllium disease; Granuloma; Innate immunity;
Acquired immunity
ID CD4(+) T-CELLS; MHC-CLASS-II; PERIPHERAL-BLOOD MONONUCLEAR;
ANTIGEN-PRESENTING CELLS; HUMAN-LEUKOCYTE ANTIGEN;
NECROSIS-FACTOR-ALPHA; HLA-DP; TNF-ALPHA; DENDRITIC CELLS;
LYMPHOCYTE-PROLIFERATION
AB During the last decade, there have been concerted efforts to reduce beryllium (Be) exposure in the workplace and thereby reduce potential cases of this occupational lung disorder. Despite these efforts, it is estimated that there are at least one million Be-exposed individuals in the U.S. who are potentially at risk for developing chronic beryllium disease (CBD). Previously, we reviewed the current CBD literature and proposed that CBD represents a model interaction between innate and acquired immunity (Sawyer et al., Int Immunopharmacol 2:249-261, 2002). We closed this review with a section on "future directions" that identified key gaps in our understanding of the pathogenesis of CBD. In the intervening period, progress has been made to fill in some of these gaps, and the current review will provide an update on that progress. Based on recent findings, we provide a new hypothesis to explain how Be drives sustained chronic inflammation and granuloma formation in CBD leading to progressive compromised lung function in CBD patients. This paradigm has direct implications for our understanding of the development of an immune response to Be, but is also likely applicable to other immune-mediated lung diseases of known and unknown etiology.
C1 [Maier, Lisa A.] Natl Jewish Hlth, Robert H Hollis Lab Environm & Occupat Hlth Sci, Div Environm & Occupat Hlth Sci, Dept Med, Denver, CO USA.
[Sawyer, Richard T.] NIAID, Asthma Allergy & Inflammat Branch, Div Allergy Immunol & Transplantat, NIH, Bethesda, MD 20892 USA.
[Maier, Lisa A.] Univ Colorado, Sch Med, Dept Med, Div Pulm Sci & Crit Care Med, Denver, CO USA.
[Maier, Lisa A.] Univ Colorado, Dept Environm & Occupat Hlth, Colorado Sch Publ Hlth, Denver, CO USA.
RP Maier, LA (reprint author), Natl Jewish Hlth, Robert H Hollis Lab Environm & Occupat Hlth Sci, Div Environm & Occupat Hlth Sci, Dept Med, Denver, CO USA.
EM maierl@njc.org
FU NIEHS NIH HHS [P01 ES011810-06A1, P01 ES011810]
NR 120
TC 9
Z9 10
U1 0
U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0966-0844
J9 BIOMETALS
JI Biometals
PD FEB
PY 2011
VL 24
IS 1
BP 1
EP 17
DI 10.1007/s10534-010-9376-3
PG 17
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 707WW
UT WOS:000286322800001
PM 20981472
ER
PT J
AU Jugessur, A
Shi, M
Gjessing, HK
Lie, RT
Wilcox, AJ
Weinberg, CR
Christensen, K
Boyles, AL
Daack-Hirsch, S
Nguyen, TT
Christiansen, L
Lidral, AC
Murray, JC
AF Jugessur, Astanand
Shi, Min
Gjessing, Hakon Kristian
Lie, Rolv Terje
Wilcox, Allen James
Weinberg, Clarice Ring
Christensen, Kaare
Boyles, Abee Lowman
Daack-Hirsch, Sandra
Nguyen, Truc Trung
Christiansen, Lene
Lidral, Andrew Carl
Murray, Jeffrey Clark
TI Fetal Genetic Risk of Isolated Cleft Lip Only versus Isolated Cleft Lip
and Palate: A Subphenotype Analysis using Two Population-Based Studies
of Orofacial Clefts in Scandinavia
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Article
DE birth defects; orofacial cleft; cleft lip; cleft palate; genetic
epidemiology
ID CASE-PARENT TRIADS; ORAL CLEFTS; CRANIOFACIAL DEVELOPMENT; CANDIDATE
GENES; FACIAL CLEFTS; AND/OR PALATE; FLIP-FLOP; PHENOTYPE; ASSOCIATION;
MUTATIONS
AB BACKGROUND: Cleft lip only (CLO) and cleft lip and palate (CLP) are commonly regarded as variants of the same defect and are traditionally combined to form the single group of cleft lip with or without cleft palate (CL/P) prior to analysis. However, recent data have suggested that at least a subgroup of isolated CLO may be etiologically distinct from isolated CLP. METHODS: To explore fetal genetic risk of isolated CLO separately from isolated CLP, we performed a subphenotype analysis using two population-based studies of clefts in Scandinavia. One hundred twenty-one isolated CLO, 190 isolated CLP, and 592 control triads were available from Norway (1996-2001), and a further 76 isolated CLO and 107 isolated CLP triads were available from Denmark (19912001). Genotypes for 1315 SNPs in 334 autosomal cleft candidate genes were analyzed using two complementary statistical methods, Triad Multi-Marker (TRIMM; Shi et al., 2007)) and HAPLIN (Gjessing and Lie, 2006), to look for genetic associations across the two national samples. RESULTS: Both TRIMM and HAPLIN identified strong associations between FGF12 and isolated CLO in both populations. In addition, only TRIMM identified associations with IRF6 and VCL, and only HAPLIN found an association with CX43. When analyses were repeated on the larger sample of isolated CLP, no significant associations were found with FGF12, IRF6, VCL, or CX43. CONCLUSIONS: Despite some inconsistency in the pattern of associations across the two populations, the associations themselves were phenotype-specific. While both IRF6 and FGF12 have previously shown strong associations with isolated CL/P, the associations with VCL and CX43 are novel and warrant further investigation in other isolated CLO samples. Birth Defects Research (Part A) 91:85-92, 2011. (C) 2010 Wiley-Liss, Inc.
C1 [Jugessur, Astanand; Gjessing, Hakon Kristian] Norwegian Inst Publ Hlth, Div Epidemiol, N-0403 Oslo, Norway.
[Jugessur, Astanand] Royal Childrens Hosp, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia.
[Shi, Min; Weinberg, Clarice Ring] NIEHS, Biostat Branch, Durham, NC USA.
[Gjessing, Hakon Kristian; Lie, Rolv Terje] Univ Bergen, Fac Med & Dent, Dept Publ Hlth & Primary Hlth Care, N-5018 Bergen, Norway.
[Lie, Rolv Terje; Nguyen, Truc Trung] Norwegian Inst Publ Hlth, Med Birth Registry Norway, N-5018 Bergen, Norway.
[Wilcox, Allen James; Boyles, Abee Lowman] NIEHS, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Christensen, Kaare; Christiansen, Lene; Murray, Jeffrey Clark] Univ So Denmark, Dept Epidemiol, DK-5000 Odense, Denmark.
[Christensen, Kaare] Odense Univ Hosp, Dept Clin Biochem & Pharmacol, DK-5000 Odense, Denmark.
[Christensen, Kaare] Odense Univ Hosp, Dept Clin Genet, DK-5000 Odense, Denmark.
[Daack-Hirsch, Sandra] Univ Iowa, Coll Nursing, Iowa City, IA 52242 USA.
[Lidral, Andrew Carl; Murray, Jeffrey Clark] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Lidral, Andrew Carl; Murray, Jeffrey Clark] Univ Iowa, Dept Epidemiol, Iowa City, IA 52242 USA.
[Lidral, Andrew Carl; Murray, Jeffrey Clark] Univ Iowa, Dept Biol Sci, Iowa City, IA 52242 USA.
RP Jugessur, A (reprint author), Norwegian Inst Publ Hlth, Div Epidemiol, POB 4404 Nydalen, N-0403 Oslo, Norway.
EM astanand.jugessur@fhi.no
RI Christensen, Kaare/C-2360-2009; Gjessing, Hakon/A-5871-2012;
OI Christensen, Kaare/0000-0002-5429-5292; Boyles,
Abee/0000-0002-8711-2077; Wilcox, Allen/0000-0002-3376-1311
FU U.S. National Institute of Environmental Health Sciences (NIEHS); U.S.
National Institutes of Health (NIH) [P60 DE13076, DE08559, DE11948, P30
ES05605, RO1 DE-11948-04]; Norwegian Research Council [NFR 177522];
National Institutes of Health (NIH) [N01-HG-65403]
FX Supported by a grant from: This research was supported in part by the
Intramural Research Program of the U.S. National Institute of
Environmental Health Sciences (NIEHS); by U.S. National Institutes of
Health (NIH) grants DE08559, P60 DE13076, DE08559, DE11948, P30 ES05605,
and RO1 DE-11948-04; and by the Norwegian Research Council (NFR
177522).; We thank all participating families who made this study
possible. Special thanks go to the following individuals for their input
in candidate gene selection and sample preparation: Kathy Frees,
Ecaterina Dragan, Adela Mansilla, Bridget Riley, Dorthe Grosen, Brian
Schutte, Edward Lammer, Temis Felix, Michael Lovett, Satoshi Suzuki,
Andrew Olshan, Rulang Jiang, Diana Caprau, Richard Finnell, Christine
Jewell, John Cidlowski, Fedik Rahimov, Jack Taylor, and Alexandre
Vieira. We are particularly grateful to Susie McConnell and Jacqueline
Leung-Heras for outstanding secretarial support. Genotyping services
were provided by the Center for Inherited Disease Research (CIDR), which
is funded through a federal contract from the National Institutes of
Health (NIH) to the Johns Hopkins University (grant N01-HG-65403). We
thank Ivy McMullen, Corinne Boehm, Kim Doheny, and other CIDR staff
involved in this project. We also thank the U.S. National Institute of
Dental and Craniofacial Research (NIDCR) for underwriting a significant
proportion of the genotyping costs by CIDR.
NR 59
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U1 0
U2 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD FEB
PY 2011
VL 91
IS 2
BP 85
EP 92
DI 10.1002/bdra.20747
PG 8
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 730LU
UT WOS:000288035600003
PM 21319277
ER
PT J
AU Sanford, TH
Storey, BB
Linehan, WM
Rogers, CA
Pinto, PA
Bratslavsky, G
AF Sanford, Thomas H.
Storey, Benjamin Barckley
Linehan, William Marston
Rogers, Craig A.
Pinto, Peter A.
Bratslavsky, Gennady
TI Outcomes and timing for intervention of partial adrenalectomy in
patients with a solitary adrenal remnant and history of bilateral
phaeochromocytomas
SO BJU INTERNATIONAL
LA English
DT Article
DE adrenal-sparing surgery; complications; partial adrenalectomy; treatment
outcome
ID ENDOCRINE NEOPLASIA TYPE-2; HEREDITARY PHEOCHROMOCYTOMA;
SURGICAL-MANAGEMENT; SPARING SURGERY; EXPERIENCE; TUMORS
AB What's known on the subject? and What does the study add?
At the present time, outcomes of the patients treated with partial adrenalectomy on a solitary adrenal are described in less than 100 patients in the world literature. In patients with bilateral pheochromocytomas, the timing for intervention as well as size threshold to allow for steroid independence is not known. This manuscript provides evidence that staged adrenal surgery as well as operating on the solitary adrenal before the largest tumour reaches 4 cm may allow for best functional outcomes and steroid independence.
OBJECTIVE
To evaluate the outcomes and timing of intervention for adrenal-sparing surgery in patients left with a solitary adrenal remnant after bilateral adrenal surgeries.
PATIENTS AND METHODS
Patients were included in the study if they had undergone bilateral adrenal surgery as a treatment for phaeochromocytoma and were left with a solitary adrenal remnant.
Perioperative, functional and oncological outcomes were evaluated in 21 patients who met the inclusion criteria.
RESULTS
There was minimal perioperative morbidity and no perioperative mortality.
After a median (range) follow-up of 21 (3-143) months, there were two cases of persistent disease.
Ten patients (48%) required steroid supplementation upon discharge, with four subsequently discontinuing this treatment. Patients were more likely to require steroid supplementation after surgery if they underwent simultaneous adrenalectomy and contralateral partial adrenalectomy, rather than staged procedures (86 vs 40%, P = 0.02).
Patients who underwent surgery for tumours > 4 cm were more likely to require long-term steroids than patients who underwent surgery for lesions < 4 cm (75 vs 18%, P = 0.05).
CONCLUSIONS
Patients left with a solitary adrenal remnant after bilateral adrenal surgery have low surgical morbidity, reasonable functional outcomes and low rates of recurrence at an intermediate follow-up period.
A staged approach could decrease the immediate postoperative need for steroids, and intervention before the largest tumour reaches 4 cm could decrease the rate of long-term steroid dependence.
C1 [Sanford, Thomas H.; Storey, Benjamin Barckley; Linehan, William Marston; Pinto, Peter A.; Bratslavsky, Gennady] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Rogers, Craig A.] Henry Ford Hosp, Dept Urol, Detroit, MI 48202 USA.
RP Bratslavsky, G (reprint author), NCI, Urol Oncol Branch, NIH, Bldg 10,Room 1-5940, Bethesda, MD 20892 USA.
EM bratslag@mail.nih.gov
FU NIH, National Cancer Institute, Center for Cancer Research
FX None declared. Source of Funding: Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 19
TC 8
Z9 10
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1464-4096
J9 BJU INT
JI BJU Int.
PD FEB
PY 2011
VL 107
IS 4
BP 571
EP 575
DI 10.1111/j.1464-410X.2010.09568.x
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 713WE
UT WOS:000286767300009
PM 20726977
ER
PT J
AU Tanno, T
Rabel, A
Alleyne, M
Lee, YT
Dahut, WL
Gulley, JL
Miller, JL
AF Tanno, Toshihiko
Rabel, Antoinette
Alleyne, Michael
Lee, Y. Terry
Dahut, William L.
Gulley, James L.
Miller, Jeffery L.
TI HEPCIDIN, ANAEMIA, AND PROSTATE CANCER
SO BJU INTERNATIONAL
LA English
DT Letter
ID GENE-EXPRESSION
C1 [Tanno, Toshihiko; Rabel, Antoinette; Alleyne, Michael; Lee, Y. Terry; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
[Alleyne, Michael; Dahut, William L.; Gulley, James L.] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Gulley, James L.] NCI, Tumor Immunol & Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Tanno, T (reprint author), NIDDK, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
FU Intramural NIH HHS [ZIA DK025100-04]
NR 7
TC 11
Z9 12
U1 1
U2 7
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1464-4096
J9 BJU INT
JI BJU Int.
PD FEB
PY 2011
VL 107
IS 4
BP 678
EP 679
DI 10.1111/j.1464-410X.2011.10108.x
PG 2
WC Urology & Nephrology
SC Urology & Nephrology
GA 713WE
UT WOS:000286767300024
PM 21276178
ER
PT J
AU Valenti, RM
Amodio, E
Nam, JM
Preiss, L
Graubard, BI
Romano, N
Goedert, JJ
AF Valenti, R. M.
Amodio, E.
Nam, J-M
Preiss, L.
Graubard, B. I.
Romano, N.
Goedert, J. J.
TI Delayed-type hypersensitivity in classic Kaposi sarcoma patients and
controls
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE delayed-type hypersensitivity; Kaposi sarcoma; herpesviruses; human
immunodeficiency virus (HIV); transplantation; Italy
ID RISK-FACTORS; HERPESVIRUS; PROGRESSION; RESPONSES
AB BACKGROUND: Immune perturbation likely affects the development of Kaposi sarcoma (KS) among people infected with the KS-associated herpesvirus (KSHV). We tested whether KSHV-seropositive individuals or cases of classic KS (cKS), which typically originates in the leg, had differing delayed-type hypersensitivity (DTH) in the forearm or leg.
METHODS: Mantoux DTH with three antigens (Candida, tetanus, PPD) was performed on the forearm and leg of 15 cKS cases, 14 KSHV-positives without KS, and 15 KSHV-negative controls. The diameters of induration responses were compared by group and body site.
RESULTS: Leg DTH was greater than forearm DTH among controls (mean difference 5.6 mm, P=0.0004), whereas this was not observed in cKS cases (-2.2 mm, P=0.32) or KSHV-positives (0.5 mm, P=0.56). Leg-minus-forearm DTH difference was greater in controls compared with cKS cases (P=0.004) and KSHV-positives (P=0.002). Leg-plus-forearm DTH was similar in controls (mean 28.2 mm) and cKS cases (24.5 mm, P=0.60), but it was reduced in KSHV-positives (11.8 mm, P=0.02), particularly in the leg (P=0.004) and marginally in the forearm (P=0.07).
CONCLUSION: KS cases had weaker DTH only in the leg, whereas both body sites appeared weaker in KSHV-positives without KS. Both systemic and regional immune alterations may influence the development of this malignancy. British Journal of Cancer (2011) 104, 433-436. doi:10.1038/sj.bjc.6606088 www.bjcancer.com Published online 18 January 2011 (C) 2011 Cancer Research UK
C1 [Nam, J-M; Graubard, B. I.; Goedert, J. J.] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Valenti, R. M.; Amodio, E.; Romano, N.] Univ Palermo, Sect Hyg, Dept Sci Hlth Promot G DAlessandro, I-90127 Palermo, Italy.
[Preiss, L.] RTI Int, Rockville, MD 20852 USA.
RP Goedert, JJ (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,Room 7068, Rockville, MD 20852 USA.
EM goedertj@mail.nih.gov
FU National Cancer Institute, NIH
FX This work was supported in part by the Intramural Research Program of
the National Cancer Institute, NIH. We thank Enza Viviano, MD, for
performing the DTH; Charles Rabkin, MD, and Eric Engels, MD, for
comments on the paper; James M Schmitt, MD, Division of Occupational
Safety and Health, National Institutes of Health, for the ball-point pen
measurement method and for helping with pilot assessment of DTH in the
leg; and the study participants.
NR 20
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U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0007-0920
EI 1532-1827
J9 BRIT J CANCER
JI Br. J. Cancer
PD FEB 1
PY 2011
VL 104
IS 3
BP 433
EP 436
DI 10.1038/sj.bjc.6606088
PG 4
WC Oncology
SC Oncology
GA 722IY
UT WOS:000287427100009
PM 21245864
ER
PT J
AU Lew, JQ
Chow, WH
Hollenbeck, AR
Schatzkin, A
Park, Y
AF Lew, J. Q.
Chow, W-H
Hollenbeck, A. R.
Schatzkin, A.
Park, Y.
TI Alcohol consumption and risk of renal cell cancer: the NIH-AARP diet and
health study
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE alcohol; renal cell cancer; cohort
ID KIDNEY CANCER; CARCINOMA; WOMEN; DRINKING; COHORT; BEVERAGES; GENDER
AB BACKGROUND: The effect of moderate to heavy drinking (>15 g per day) on renal cell cancer (RCC) risk is unclear.
METHOD The relationship between alcohol consumption and RCC was examined in the NIH-AARP Diet and Health Study (n = 49 2187, 1814 cases).
RESULTS: Compared with >0 to <5 g per day of alcohol consumption, the multivariate relative risk (95% confidence intervals) for 15 to <3C and >= 30g per day was, 0.75 (0.63-0.90) and 0.71 (0.59-0.85), respectively, in men and 0.67 (0.42-1.07) and 0.43 (0.22-0.84), respectively, in women.
CONCLUSION: Alcohol consumption was inversely associated with RCC in a dose-response manner. The inverse association may be extended to >= 30 g per day of alcohol intake. British Journal of Cancer (2011) 104, 537-541. doi:10.1038/sj.bjc.6606089 www.bjcancer.com Published online 18 January 2011 (C) 2011 Cancer Research UK
C1 [Lew, J. Q.; Chow, W-H; Schatzkin, A.; Park, Y.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Lew, J. Q.] Washington Univ, St Louis Childrens Hosp, Med Ctr, St Louis, MO 63110 USA.
[Hollenbeck, A. R.] AARP, Washington, DC USA.
RP Park, Y (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Bethesda, MD 20892 USA.
EM parkyik@mail.nih.gov
OI Park, Yikyung/0000-0002-6281-489X
FU Florida Department of Health (FDOH)
FX Cancer incidence data from the Atlanta metropolitan area were collected
by the Georgia Center for Cancer Statistics, Department of Epidemiology,
Rollins School of Public Health, Emory University. Cancer incidence data
from California were collected by the California Department of Health
Services, Cancer Surveillance Section. Cancer incidence data from the
Detroit metropolitan area were collected by the Michigan Cancer
Surveillance Program, Community Health Administration, State of
Michigan. The Florida cancer incidence data used in this report were
collected by the Florida Cancer Data System (FCDC) under contract with
the Florida Department of Health (FDOH). The views expressed herein are
solely those of the authors and do not necessarily reflect those of the
FCDC or FDOH. Cancer incidence data from Louisiana were collected by the
Louisiana Tumor Registry, Louisiana State University Medical Center in
New Orleans. Cancer incidence data from New Jersey were collected by the
New Jersey State Cancer Registry, Cancer Epidemiology Services, New
Jersey State Department of Health and Senior Services. Cancer incidence
data from North Carolina were collected by the North Carolina Central
Cancer Registry. Cancer incidence data from Pennsylvania were supplied
by the Division of Health Statistics and Research, Pennsylvania
Department of Health, Harrisburg, Pennsylvania. The Pennsylvania
Department of Health specifically disclaims responsibility for any
analyses, interpretations, or conclusions. Cancer incidence data from
Arizona were collected by the Arizona Cancer Registry, Division of
Public Health Services, Arizona Department of Health Services. Cancer
incidence data from Texas were collected by the Texas Cancer Registry,
Cancer Epidemiology and Surveillance Branch, Texas Department of State
Health Services. We are indebted to the participants in the NIH-AARP
Diet and Health Study for their outstanding cooperation. We also thank
Sigurd Hermansen and Kerry Grace Morrissey from Westat for study
outcomes ascertainment and management and Leslie Carroll at Information
Management Services for data support and analysis.
NR 21
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U2 2
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 FEB 1
PY 2011
VL 104
IS 3
BP 537
EP 541
DI 10.1038/sj.bjc.6606089
PG 5
WC Oncology
SC Oncology
GA 722IY
UT WOS:000287427100024
PM 21245859
ER
PT J
AU Hartge, P
AF Hartge, Patricia
TI Reducing Ovarian Cancer Death Rates Through Screening
SO CANCER
LA English
DT Editorial Material
C1 NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20852 USA.
RP Hartge, P (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd,EPS 8090, Rockville, MD 20852 USA.
EM hartgep@mail.nih.gov
NR 4
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0008-543X
J9 CANCER-AM CANCER SOC
JI Cancer
PD FEB 1
PY 2011
VL 117
IS 3
BP 449
EP 450
DI 10.1002/cncr.25622
PG 2
WC Oncology
SC Oncology
GA 709JC
UT WOS:000286433300007
PM 21254048
ER
PT J
AU Li, DH
Tang, HW
Hassan, MM
Holly, EA
Bracci, PM
Silverman, DT
AF Li, Donghui
Tang, Hongwei
Hassan, Manal M.
Holly, Elizabeth A.
Bracci, Paige M.
Silverman, Debra T.
TI Diabetes and risk of pancreatic cancer: a pooled analysis of three large
case-control studies
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Diabetes; Pancreatic cancer; Case-control study; Epidemiology
ID FRANCISCO-BAY AREA; DIRECT INTERVIEWS; CIGARETTE-SMOKING; MELLITUS;
ASSOCIATION; MORTALITY; GLUCOSE; METAANALYSIS; HISTORY; WOMEN
AB Racial differences in diabetes-associated pancreatic cancer (PC) and the interaction of diabetes with other risk factors are not well established. We determined the association between diabetes and risk of PC in 2,192 cases and 5,113 controls in three large case-control studies conducted at the National Cancer Institute, the University of California San Francisco, and the M.D. Anderson Cancer Center. In multivariable analyses, diabetes was associated with a 1.8-fold risk of PC [95% confidence interval (CI) = 1.5-2.1]. Risk estimates decreased with increasing years with diabetes (a parts per thousand currency sign2 years OR = 2.9, 95% CI = 2.1-3.9; 3-5 years OR = 1.9, 95% CI = 1.3-2.6; 6-10 years OR = 1.6, 95% CI = 1.2-2.3; 11-15 years OR = 1.3, 95% CI = 0.9-2.0; > 15 years OR = 1.4, 95% CI = 1.0-2.0 (p for trend < 0.0001). Among diabetics, risk was higher in insulin ever users compared with nonusers (OR = 2.2, 95% CI = 1.6-3.7) and was restricted to insulin use of a parts per thousand currency sign3 years (OR = 2.4). Insulin use of > 10 years was associated with a reduced risk of pancreatic cancer (OR = 0.5, 95% CI = 0.3-0.9; p for trend < 0.0001). Hispanic men and Asians had a higher risk of diabetes-associated PC than did whites and blacks, but the differences were not statistically significant. No significant interaction between diabetes and cigarette smoking, alcohol consumption and body mass index was observed. Although reverse causation may explain the association between diabetes diagnosed in close temporal proximity to PC, our results show that long-term diabetes, even though risk diminishes over time, remains a risk factor for PC independent of obesity and smoking.
C1 [Li, Donghui; Tang, Hongwei; Hassan, Manal M.] Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, Houston, TX 77030 USA.
[Holly, Elizabeth A.; Bracci, Paige M.] Univ Calif San Francisco, Sch Med, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Silverman, Debra T.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Li, DH (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Gastrointestinal Med Oncol, 1515 Holcombe Blvd,Unit 426, Houston, TX 77030 USA.
EM dLi@mdanderson.org
FU National Institute of Health, NCI [CA59706, CA89726, CA108370, CA109767,
CA98380]; Rombauer Pancreatic Cancer Research Fund (UCSF); Lockton
Pancreatic Cancer Research Fund (MDACC); Division of Cancer Epidemiology
and Genetics of the National Cancer institute
FX Grant support is given by National Institute of Health, NCI grants
CA59706, CA89726, CA108370, CA109767 (Holly E.A.: PI), CA98380 (Li D.:
PI), The Rombauer Pancreatic Cancer Research Fund (UCSF) and The Lockton
Pancreatic Cancer Research Fund (MDACC). The NCI study was supported by
the intramural program of the Division of Cancer Epidemiology and
Genetics of the National Cancer institute (Silverman D.T.: PI).
NR 42
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U2 5
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD FEB
PY 2011
VL 22
IS 2
BP 189
EP 197
DI 10.1007/s10552-010-9686-3
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 709TT
UT WOS:000286465000004
PM 21104117
ER
PT J
AU Byun, W
Sui, XM
Hebert, JR
Church, TS
Lee, IM
Matthews, CE
Blair, SN
AF Byun, Wonwoo
Sui, Xuemei
Hebert, James R.
Church, Timothy S.
Lee, I-Min
Matthews, Charles E.
Blair, Steven N.
TI Cardiorespiratory fitness and risk of prostate cancer: Findings from the
Aerobics Center Longitudinal Study
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Cardiorespiratory fitness; Prostate cancer; Cohort studies; Attitude to
health; Screening/detection bias
ID RECREATIONAL PHYSICAL-ACTIVITY; ALL-CAUSE MORTALITY; UNITED-STATES;
HYPERTENSION INCIDENCE; ASYMPTOMATIC WOMEN; BODY-MASS; FOLLOW-UP; MEN;
EPIDEMIOLOGY; PREDICTOR
AB Objective: To examine the association between cardiorespiratory fitness (CRF) and risk of incident prostate cancer (PrCA). Methods: Participants were 19,042 male subjects in the Aerobics Center Longitudinal Study (ACLS), ages 20-82 years, who received a baseline medical examination including a maximal treadmill exercise test between 1976 and 2003. CRF levels were defined as low (lowest 20%), moderate (middle 40%), and high (upper 40%) according to age-specific distribution of treadmill duration from the overall ACLS population. PrCA was assessed from responses to mail-back health surveys during 1982-2004. Cox proportional hazards regression models, adjusted for potential confounders, were used to compute hazard ratios (HRs), 95% confidence intervals (95% CIs), and incidence rates (per 10,000 person-years of follow-up). Results: A total of 634 men reported a diagnosis of incident PrCA during an average of 9.3 +/- 7.1 years of follow-up. Adjusted HRs (95% CIs) in men with moderate and high CRF relative to low CRF were, 1.68 (1.13-2.48) and 1.74 (1.15-2.62), respectively. The positive association between CRF and PrCA was observed only in the strata of men who were not obese, had >= 1 follow-up examination, or who were diagnosed <= 1995. Conclusions: Rather than revealing a causal relationship, the unexpected positive association observed between CRF and incident PrCA is most likely due to a screening/detection bias in more fit men who also are more health-conscious. Results have important implications for understanding the health-related factors that predispose men to receive PrCA screening that may lead to over-detection of indolent disease. Published by Elsevier Ltd.
C1 [Byun, Wonwoo] Univ S Carolina, Publ Hlth Res Ctr, Arnold Sch Publ Hlth, Dept Exercise Sci, Columbia, SC 29208 USA.
[Hebert, James R.; Blair, Steven N.] Univ S Carolina, Arnold Sch Publ Hlth, Dept Epidemiol & Biostat, Columbia, SC 29208 USA.
[Hebert, James R.; Blair, Steven N.] Univ S Carolina, Canc Prevent & Control Program, Columbia, SC 29208 USA.
[Church, Timothy S.] Pennington Biomed Res Ctr, Prevent Med Lab, Baton Rouge, LA USA.
[Lee, I-Min] Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA.
[Lee, I-Min] Harvard Univ, Sch Med, Boston, MA USA.
[Matthews, Charles E.] NCI, Div Canc Epidemiol & Genet, Nutr Epidemiol Branch, Rockville, MD USA.
RP Byun, W (reprint author), Univ S Carolina, Publ Hlth Res Ctr, Arnold Sch Publ Hlth, Dept Exercise Sci, 921 Assembly St, Columbia, SC 29208 USA.
EM byun@email.sc.edu
RI matthews, Charles/E-8073-2015
OI matthews, Charles/0000-0001-8037-3103
FU National Institutes of Health [AG06945, HL62508, K05 CA136975, R21
DK088195]; Coca-Cola Company
FX This study was supported by National Institutes of Health grants
AG06945, HL62508, K05 CA136975 (to JR Hebert from the Cancer Training
Branch of the National Cancer Institute), R21 DK088195 (to X Sui from
the National Institute of Diabetes and Digestive and Kidney Diseases)
and an unrestricted research fund from The Coca-Cola Company. We thank
all the Cooper Clinic physicians and technicians for collecting the
baseline data, and staff at the Cooper Institute for data entry and data
management.
NR 58
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U1 4
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PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1877-7821
J9 CANCER EPIDEMIOL
JI Cancer Epidemiol.
PD FEB
PY 2011
VL 35
IS 1
BP 59
EP 65
DI 10.1016/j.canep.2010.07.013
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 736CL
UT WOS:000288467500010
PM 20708996
ER
PT J
AU Weaver, KE
Rowland, JH
Augustson, E
Atienza, AA
AF Weaver, Kathryn E.
Rowland, Julia H.
Augustson, Erik
Atienza, Audie A.
TI Smoking Concordance in Lung and Colorectal Cancer Patient-Caregiver
Dyads and Quality of Life
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID HEALTH BEHAVIORS; TOBACCO USE; SHORT-FORM; SURVIVORS; WOMEN; DEPENDENCE;
CESSATION; RELATIVES; ADULTS
AB Background: Distress may be heightened among members of cancer patient-caregiver dyads that are mismatched on smoking status (either the patient or caregiver smokes, but the other does not), negatively affecting quality of life (QoL). The purpose of this study was to examine associations between patient-caregiver smoking concordance, caregiver psychological adjustment, and caregiver and patient mental and physical QoL.
Methods: Lung and colorectal patient-caregiver dyads (N = 742) were identified from the Cancer Care Outcomes Research and Surveillance (CanCORS) and CanCORS Caregiver studies. The majority of the cancer patients were male (67.0%) with local (45.6%) or regional (12.9%) disease. The majority of the informal caregivers were females (78.6%), under 65 years of age (69.6%), and often spouses (57.8%) of the patients.
Results: Lung and colorectal cancer caregivers, who were members of dyads where one or both members continued to smoke, reported worse mental health QoL than nonsmoking dyads. For colorectal cancer patients, continuing to smoke when the caregiver did not was associated with worse mental health QoL compared with nonsmoking dyads. Dyad smoking was less strongly associated with physical QoL for both caregivers and patients.
Conclusion: Results highlight the importance of assessing smoking in both cancer patients and their caregivers and referring families to appropriate psychosocial and smoking cessation services.
Impact: This is the first study to show associations between cancer patient-caregiver smoking status and QoL for both dyad members. Future studies will need to confirm these associations longitudinally and investigate potential mechanisms linking dyad smoking and QoL. Cancer Epidemiol Biomarkers Prev; 20(2); 239 48. (C) 2010 AACR.
C1 [Weaver, Kathryn E.] Wake Forest Univ, Bowman Gray Sch Med, Dept Social Sci & Hlth Policy, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
[Weaver, Kathryn E.; Rowland, Julia H.; Augustson, Erik; Atienza, Audie A.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Weaver, Kathryn E.] NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, Dept Hlth & Human Serv,NIH, Bethesda, MD 20892 USA.
RP Weaver, KE (reprint author), Wake Forest Univ, Bowman Gray Sch Med, Dept Social Sci & Hlth Policy, Div Publ Hlth Sci, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM keweaver@wfubmc.edu
FU National Cancer Institute (NCI) [U01 CA093344, U01 CA093332, U01
CA093324, U01 CA093348, U01 CA093329, U01 CA01013, U01 CA093326];
Department of Veteran's Affairs [U01 CDA093344, HARQ 03-438MO-03]
FX This work from the Cancer Care Outcomes Research and Surveillance
(CanCORS) Consortium was supported by grants from the National Cancer
Institute (NCI) to the Statistical Coordinating Center (U01 CA093344)
and the NCI-supported Primary Data Collection and Research Centers (Dana
Farber Cancer Institute/Cancer Research NetworkU01 CA093332, Harvard
Medical School/Northern California Cancer CenterU01 CA093324, RAND/UCLA
U01 CA093348, University of Alabama at BirminghamU01 CA093329,
University of IowaU01 CA01013, University of North CarolinaU01
CA093326), and by a Department of Veteran's Affairs grant to the Durham
VA Medical CenterU01 CDA093344 (MOU) and HARQ 03-438MO-03).
NR 38
TC 15
Z9 15
U1 1
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD FEB
PY 2011
VL 20
IS 2
BP 239
EP 248
DI 10.1158/1055-9965.EPI-10-0666
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 717CU
UT WOS:000287021400005
PM 21177426
ER
PT J
AU Vergati, M
Cereda, V
Madan, RA
Gulley, JL
Huen, NY
Rogers, CJ
Hance, KW
Arlen, PM
Schlom, J
Tsang, KY
AF Vergati, Matteo
Cereda, Vittore
Madan, Ravi A.
Gulley, James L.
Huen, Ngar-Yee
Rogers, Connie J.
Hance, Kenneth W.
Arlen, Philip M.
Schlom, Jeffrey
Tsang, Kwong Y.
TI Analysis of circulating regulatory T cells in patients with metastatic
prostate cancer pre- versus post-vaccination
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Cancer vaccine; Prostate cancer; Immunotherapy; Regulatory T cells;
Vaccination
ID CHRONIC LYMPHOCYTIC-LEUKEMIA; TRANSCRIPTION FACTOR FOXP3;
PERIPHERAL-BLOOD; TRYPTOPHAN CATABOLISM; SUPPRESSIVE FUNCTION; CARCINOMA
PATIENTS; OVARIAN-CANCER; BREAST-CANCER; EXPRESSION; MELANOMA
AB We have previously shown that the suppressive function of regulatory T cells (Tregs) from peripheral blood mononuclear cells (PBMCs) is enhanced in patients with prostate cancer when compared with healthy individuals. Two phase II studies using the PSA-TRICOM vaccine in patients with metastatic castration-resistant prostate cancer (mCRPC) showed evidence of patient benefit in terms of enhanced survival. The Halabi nomogram has been used to predict survival (HPS) of patients with mCRPC treated with conventional chemotherapy or second-line hormonal therapy. Tregs from PBMCs of patients (n = 23) with mCRPC were obtained pre- and post-three monthly vaccinations, and analyzed for number, phenotype, and suppressive function. Changes post- versus pre-vaccination in these parameters were compared with 3-year survival and HPS. No differences in Treg numbers were observed post- versus pre-vaccination. Trends (P = 0.029) were observed between overall survival (OS) and a decrease in Treg suppressive function post- versus pre-vaccination. Trends were also observed in analyzing effector:Treg (CD4(+)CD25(+)CD127(-)FoxP3(+)CTLA4(+)) ratio post- versus pre-vaccination with OS versus HPS. These data provide preliminary evidence for a possible association between improved OS and a decrease in Treg function when PBMCs are analyzed after three monthly vaccinations. Patients with an OS > HPS were more likely to have decreased Treg function following vaccine. Larger studies to confirm and extend these findings are warranted.
C1 [Vergati, Matteo; Cereda, Vittore; Madan, Ravi A.; Gulley, James L.; Huen, Ngar-Yee; Rogers, Connie J.; Hance, Kenneth W.; Arlen, Philip M.; Schlom, Jeffrey; Tsang, Kwong Y.] NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Madan, Ravi A.; Gulley, James L.; Arlen, Philip M.] NCI, Med Oncol Branch, 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,Room 8B09, Bethesda, MD 20892 USA.
EM js141c@nih.gov
RI Gulley, James/K-4139-2016
OI Gulley, James/0000-0002-6569-2912
FU Intramural NIH HHS [Z01 BC010666-04, ZIA BC010973-03, Z01 BC010973-01]
NR 58
TC 31
Z9 32
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD FEB
PY 2011
VL 60
IS 2
BP 197
EP 206
DI 10.1007/s00262-010-0927-9
PG 10
WC Oncology; Immunology
SC Oncology; Immunology
GA 709TD
UT WOS:000286463400005
PM 20976449
ER
PT J
AU Limburg, PJ
Mahoney, MR
Ziegler, KLA
Sontag, SJ
Schoen, RE
Benya, R
Lawson, MJ
Weinberg, DS
Stoffel, E
Chiorean, M
Heigh, R
Levine, J
Della'Zanna, G
Rodriguez, L
Richmond, E
Gostout, C
Mandrekar, SJ
Smyrk, TC
AF Limburg, Paul J.
Mahoney, Michelle R.
Ziegler, Katie L. Allen
Sontag, Stephen J.
Schoen, Robert E.
Benya, Richard
Lawson, Michael J.
Weinberg, David S.
Stoffel, Elena
Chiorean, Michael
Heigh, Russell
Levine, Joel
Della'Zanna, Gary
Rodriguez, Luz
Richmond, Ellen
Gostout, Christopher
Mandrekar, Sumithra J.
Smyrk, Thomas C.
CA Canc Prevention Network
TI Randomized Phase II Trial of Sulindac, Atorvastatin, and Prebiotic
Dietary Fiber for Colorectal Cancer Chemoprevention
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID ABERRANT CRYPT FOCI; FAMILIAL ADENOMATOUS POLYPOSIS; COLON-CANCER;
RISK-FACTORS; STATINS; HUMANS; CARCINOGENESIS; METAANALYSIS; PREVENTION;
HISTORY
AB Sulindac, atorvastatin, or prebiotic dietary fiber may reduce colorectal cancer (CRC) risk. However, clinical trial data are currently limited. We conducted a randomized, phase II chemoprevention trial involving subjects 40 years or older, with previously resected colon cancer or multiple/advanced colorectal adenomas. Magnification chromoendoscopy (MCE) was performed to identify and characterize rectal aberrant crypt foci (ACF); eligibility criteria required five or more rectal ACFs at baseline. Intervention assignments were as follows: (a) atorvastatin 20 mg qd; (b) sulindac 150 mg bid; (c) oligofructose-enriched inulin (as ORAFTI (R) Synergy1) 6 gm bid; or (d) control (maltodextrin) 6 gm bid, for 6 months. Percent change in rectal ACF number (%Delta ACF) within arm was the primary endpoint. Secondary endpoints included changes in proliferation (Ki67) and apoptosis (caspase-3), as measured from normal mucosa biopsy samples. Among 85 eligible randomized subjects, 76 (86%) completed the trial per protocol. The median (range) of rectal ACF was 9 (5-34) and 8 (0-37) at baseline and postintervention, respectively. The median (SD) for %Delta ACF was 5.6 (-69% to 143%), -18.6 (-83% to 160%), -3.6 (-88% to 83%), and -10.0 (-100% to 117%) in the atorvastatin, sulindac, ORAFTI (R) Synergy1 and control arms, respectively. Neither within-arm (P = 0.12-0.59) nor between-arm (P = 0.30-0.92) comparisons of %Delta ACF were statistically significant. The active and control interventions also seemed to have similar effects on mucosal proliferation and apoptosis (P > 0.05 for each comparison). Data from this multicenter, phase II trial do not provide convincing evidence of CRC risk reduction from 6-month interventions with atorvastatin, sulindac, or ORAFTI (R) Synergy1, although statistical power was limited by the relatively small sample size. Cancer Prev Res; 4(2); 259-69. (C)2011 AACR.
C1 [Limburg, Paul J.; Mahoney, Michelle R.; Ziegler, Katie L. Allen; Gostout, Christopher; Mandrekar, Sumithra J.; Smyrk, Thomas C.] Mayo Clin, Rochester, MN USA.
[Sontag, Stephen J.] Hines Vet Adm, Hines, IL USA.
[Schoen, Robert E.] Univ Pittsburgh, Pittsburgh, PA USA.
[Benya, Richard] Univ Illinois, Chicago, IL USA.
[Lawson, Michael J.] Kaiser Permanente Med Grp, Sacramento, CA USA.
[Weinberg, David S.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Stoffel, Elena] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Chiorean, Michael] Indiana Univ, Indianapolis, IN 46204 USA.
[Heigh, Russell] Mayo Clin Arizona, Scottsdale, AZ USA.
[Levine, Joel] Univ Connecticut, Farmington, CT USA.
[Della'Zanna, Gary; Rodriguez, Luz; Richmond, Ellen] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
RP Limburg, PJ (reprint author), 200 1st St SW, Rochester, MN 55905 USA.
EM limburg.paul@mayo.edu
FU National Cancer Institute, Division of Cancer Prevention [N01-CN-35000];
Beneo Group; Olympus America; [M01-RR00585]
FX This work was sponsored by the National Cancer Institute, Division of
Cancer Prevention (contract no. N01-CN-35000). Mayo Clinic Clinical
Research Unit is supported by grant M01-RR00585. Research support (study
supplies, equipment and/or meeting support) was also provided by the
Beneo Group and Olympus America.
NR 37
TC 28
Z9 29
U1 1
U2 13
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 FEB
PY 2011
VL 4
IS 2
BP 259
EP 269
DI 10.1158/1940-6207.CAPR-10-0215
PG 11
WC Oncology
SC Oncology
GA 715KH
UT WOS:000286882900010
PM 21209397
ER
PT J
AU Zhang, Q
Pan, J
Zhang, JJ
Liu, PY
Chen, R
Chen, DR
Lubet, R
Wang, YA
You, M
AF Zhang, Qi
Pan, Jing
Zhang, Jingjie
Liu, Pengyuan
Chen, Ruth
Chen, Da-ren
Lubet, Ronald
Wang, Yian
You, Ming
TI Aerosolized Bexarotene Inhibits Lung Tumorigenesis without Increasing
Plasma Triglyceride and Cholesterol Levels in Mice
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID A/J MICE; CANCER CHEMOPREVENTION; MAMMARY CANCERS; CLINICAL-TRIAL;
PREVENTION; TARGRETIN; LGD1069; CARCINOGENESIS; PROGRESSION; BUDESONIDE
AB Prior studies have shown the retinoid X receptor (RXR) agonist bexarotene has preventive efficacy in rodent models of mammary and lung tumorigenesis albeit causing hypertriglyceridemia and hypercholesterolemia. We reasoned that bexarotene delivered by inhalation may provide sufficient dose directly to the respiratory tract to achieve efficacy while avoiding these side effects. In this study, the chemopreventive activity of aerosolized bexarotene was investigated in the benzo(a) pyrene [B(a)P]-induced mouse lung tumor model as assessed by tumor multiplicity and tumor load. Aerosolized bexarotene significantly decreased tumor multiplicity and tumor load by 43% and 74%, respectively. Our data showed that bexarotene can both inhibit proliferation and promote apoptosis in vivo. Our data also show that aerosolized bexarotene did not increase plasma total cholesterol and triglyceride level compared with diet group. These results indicate that aerosolization may be a safe and effective route of administering bexarotene for chemoprevention of lung cancer. Cancer Prev Res; 4(2); 270-6. (C)2010 AACR.
C1 [Zhang, Qi; Pan, Jing; Liu, Pengyuan; Wang, Yian; You, Ming] Washington Univ, Dept Surg, Sch Med, St Louis, MO 63110 USA.
[Zhang, Jingjie; Chen, Ruth; Chen, Da-ren] Washington Univ, Dept Energy Environm & Chem Engn, St Louis, MO 63110 USA.
[Lubet, Ronald] NCI, Chemoprevent Branch, Bethesda, MD 20892 USA.
RP You, M (reprint author), Washington Univ, Dept Surg, Sch Med, Campus Box 8109,660 S Euclid Ave, St Louis, MO 63110 USA.
EM youm@wustl.edu
NR 28
TC 10
Z9 10
U1 0
U2 3
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 FEB
PY 2011
VL 4
IS 2
BP 270
EP 276
DI 10.1158/1940-6207.CAPR-10-0246
PG 7
WC Oncology
SC Oncology
GA 715KH
UT WOS:000286882900011
PM 21163938
ER
PT J
AU Saydam, O
Senol, O
Wurdinger, T
Mizrak, A
Ozdener, GB
Stemmer-Rachamimov, AO
Yi, M
Stephens, RM
Krichevsky, AM
Saydam, N
Brenner, GJ
Breakefield, XO
AF Saydam, Okay
Senol, Ozlem
Wuerdinger, Thomas
Mizrak, Arda
Ozdener, Gokhan Baris
Stemmer-Rachamimov, Anat O.
Yi, Ming
Stephens, Robert M.
Krichevsky, Anna M.
Saydam, Nurten
Brenner, Gary J.
Breakefield, Xandra O.
TI miRNA-7 Attenuation in Schwannoma Tumors Stimulates Growth by
Upregulating Three Oncogenic Signaling Pathways
SO CANCER RESEARCH
LA English
DT Article
ID P21-ACTIVATED KINASES; CANCER-CELLS; PROSTATE-CANCER; SUPPRESSOR GENE;
FACTOR RECEPTOR; NEUROFIBROMATOSIS; MICRORNAS; EXPRESSION; MERLIN;
INHIBITOR
AB Micro RNAs (miRNA) negatively regulate protein-coding genes at the posttranscriptional level and are critical in tumorigenesis. Schwannomas develop from proliferation of dedifferentiated Schwann cells, which normally wrap nerve fibers to help support and insulate nerves. In this study, we carried out high-throughput miRNA expression profiling of human vestibular schwannomas by using an array representing 407 known miRNAs to explore the role of miRNAs in tumor growth. Twelve miRNAs were found to be significantly deregulated in tumor samples as compared with control nerve tissue, defining a schwannoma-typical signature. Among these miRNAs, we focused on miR-7, which was one of the most downregulated in these tumors and has several known oncogene targets, including mRNAs for epidermal growth factor receptor (EGFR) and p21-activated kinase 1 (Pak1). We found that overexpression of miR-7 inhibited schwannoma cell growth both in culture and in xenograft tumor models in vivo, which correlated with downregulation of these signaling pathways. Furthermore, we identified a novel direct target of miR-7, the mRNA for associated cdc42 kinase 1 (Ack1), with the expression levels of miR-7 and Ack1 being inversely correlated in human schwannoma samples. These results represent the first miRNA profiling of schwannomas and the first report of a tumor suppressor function for miR-7 in these tumors that is mediated by targeting the EGFR, Pak1, and Ack1 oncogenes. Our findings suggest miR-7 as a potential therapeutic molecule for schwannoma treatment, and they prompt clinical evaluation of drugs that can inhibit the EGFR, Pak1, and Ack1 signaling pathways to treat this tumor type. Cancer Res; 71(3); 852-61. (C) 2010 AACR.
C1 [Saydam, Okay; Saydam, Nurten] Med Univ Vienna, Dept Pediat, A-1090 Vienna, Austria.
[Stemmer-Rachamimov, Anat O.] Harvard Univ, Sch Med, Dept Pathol, Mol Neurooncol Lab,Massachusetts Gen Hosp, Boston, MA 02115 USA.
[Brenner, Gary J.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Anesthesia & Crit Care, Boston, MA 02115 USA.
[Krichevsky, Anna M.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Neurol, Boston, MA 02115 USA.
[Yi, Ming; Stephens, Robert M.] NCI, Adv Biomed Comp Ctr, Bethesda, MD 20892 USA.
[Saydam, Okay; Senol, Ozlem; Wuerdinger, Thomas; Mizrak, Arda; Ozdener, Gokhan Baris; Breakefield, Xandra O.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA USA.
[Saydam, Okay; Senol, Ozlem; Wuerdinger, Thomas; Mizrak, Arda; Ozdener, Gokhan Baris; Breakefield, Xandra O.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA USA.
RP Saydam, O (reprint author), Med Univ Vienna, Dept Pediat, A-1090 Vienna, Austria.
EM okay.saydam@meduniwien.ac.at
FU NIH/NINDS [P01 NS24279]; DOD [W81XWH-091-0476]; Children's Tumor
Foundation [2007-01-043]
FX NIH/NINDS P01 NS24279 (X.O. Breakefield/O. Saydam), DOD W81XWH-091-0476
(X.O. Breakefield/O. Saydam), and Children's Tumor Foundation
2007-01-043 (O. Saydam).
NR 38
TC 80
Z9 91
U1 0
U2 11
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD FEB 1
PY 2011
VL 71
IS 3
BP 852
EP 861
DI 10.1158/0008-5472.CAN-10-1219
PG 10
WC Oncology
SC Oncology
GA 714SW
UT WOS:000286830300025
PM 21156648
ER
PT J
AU Solier, S
Pommier, Y
AF Solier, Stephanie
Pommier, Yves
TI MDC1 Cleavage by Caspase-3: A Novel Mechanism for Inactivating the DNA
Damage Response during Apoptosis
SO CANCER RESEARCH
LA English
DT Article
ID DOUBLE-STRAND BREAKS; HISTONE H2AX; S-PHASE; ACTIVATION; CANCER;
GAMMA-H2AX; RECOGNITION; CHECKPOINT; MEDIATORS; REPAIR
AB Recently, we identified the "apoptotic ring," containing phosphorylated histone H2AX (gamma-H2AX), as an early chromatin modification during apoptosis. Because gamma-H2AX initiates the DNA damage response (DDR), we tested whether the apoptotic H2AX response leads to the full recruitment of the DDR factors that normally coordinate DNA repair and cell-cycle checkpoints. We show that the apoptotic H2AX response does not recruit the DDR factors because MDC1 (mediator of DNA damage checkpoint protein 1), which normally binds to gamma-H2AX in response to DNA damage and amplifies the DDR, is cleaved by caspase-3. This cleavage separates the BRCT and FHA domains of MDC1 and constitutes a novel mechanism for the inactivation of DNA repair in apoptotic cells. Also, we show that downregulation of MDC1 increases the apoptotic response to TRAIL. Together, these results implicate MDC1 in the cellular apoptotic response. Cancer Res; 71(3); 906-13. (C)2010 AACR.
C1 [Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Pommier, Y (reprint author), NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bldg 37,Rm 5068, Bethesda, MD 20892 USA.
EM pommier@nih.gov
FU Intramural NIH HHS [Z01 BC006150-26]
NR 33
TC 12
Z9 15
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD FEB 1
PY 2011
VL 71
IS 3
BP 906
EP 913
DI 10.1158/0008-5472.CAN-10-3297
PG 8
WC Oncology
SC Oncology
GA 714SW
UT WOS:000286830300030
PM 21148072
ER
PT J
AU Moore, LE
Baris, DR
Figueroa, JD
Garcia-Closas, M
Karagas, MR
Schwenn, MR
Johnson, AT
Lubin, JH
Hein, DW
Dagnall, CL
Colt, JS
Kida, M
Jones, MA
Schned, AR
Cherala, SS
Chanock, SJ
Cantor, KP
Silverman, DT
Rothman, N
AF Moore, L. E.
Baris, D. R.
Figueroa, J. D.
Garcia-Closas, M.
Karagas, M. R.
Schwenn, M. R.
Johnson, A. T.
Lubin, J. H.
Hein, D. W.
Dagnall, C. L.
Colt, J. S.
Kida, M.
Jones, M. A.
Schned, A. R.
Cherala, S. S.
Chanock, S. J.
Cantor, K. P.
Silverman, D. T.
Rothman, N.
TI GSTM1 null and NAT2 slow acetylation genotypes, smoking intensity and
bladder cancer risk: results from the New England bladder cancer study
and NAT2 meta-analysis
SO CARCINOGENESIS
LA English
DT Article
ID GENETIC POLYMORPHISMS; SUSCEPTIBILITY; ASSOCIATION; POPULATION;
EXPOSURE; TOBACCO; GSTT1
AB Associations between bladder cancer risk and NAT2 and GSTM1 polymorphisms have emerged as some of the most consistent findings in the genetic epidemiology of common metabolic polymorphisms and cancer, but their interaction with tobacco use, intensity and duration remain unclear. In a New England population-based case-control study of urothelial carcinoma, we collected mouthwash samples from 1088 of 1171 cases (92.9%) and 1282 of 1418 controls (91.2%) for genotype analysis of GSTM1, GSTT1 and NAT2 polymorphisms. Odds ratios and 95% confidence intervals of bladder cancer among New England Bladder Cancer Study subjects with one or two inactive GSTM1 alleles (i.e. the 'null' genotype) were 1.26 (0.85-1.88) and 1.54 (1.05-2.25), respectively (P-trend = 0.008), compared with those with two active copies. GSTT1 inactive alleles were not associated with risk. NAT2 slow acetylation status was not associated with risk among never (1.04; 0.71-1.51), former (0.95; 0.75-1.20) or current smokers (1.33; 0.91-1.95); however, a relationship emerged when smoking intensity was evaluated. Among slow acetylators who ever smoked at least 40 cigarettes/day, risk was elevated among ever (1.82; 1.14-2.91, P-interaction = 0.07) and current heavy smokers (3.16; 1.22-8.19, P-interaction = 0.03) compared with rapid acetylators in each category; but was not observed at lower intensities. In contrast, the effect of GSTM1-null genotype was not greater among smokers, regardless of intensity. Meta-analysis of the NAT2 associations with bladder cancer showed a highly significant relationship. Findings from this large USA population-based study provided evidence that the NAT2 slow acetylation genotype interacts with tobacco smoking as a function of exposure intensity.
C1 [Moore, L. E.; Baris, D. R.; Figueroa, J. D.; Garcia-Closas, M.; Lubin, J. H.; Dagnall, C. L.; Colt, J. S.; Chanock, S. J.; Cantor, K. P.; Silverman, D. T.; Rothman, N.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20852 USA.
[Karagas, M. R.; Schned, A. R.] Dartmouth Med Sch, Dept Community & Family Med, Lebanon, NH 03756 USA.
[Schwenn, M. R.] ME Ctr Dis Control, Maine Canc Registry, Augusta, ME 04333 USA.
[Johnson, A. T.] Vermont Canc Registry, Burlington, VT 05401 USA.
[Hein, D. W.] Univ Louisville, Dept Pharmacol & Toxicol, Sch Med, Louisville, KY 40202 USA.
[Kida, M.] Vermont Coll Med Pathol, Dept Anat & Phys Pathol, Burlington, VT 05401 USA.
[Jones, M. A.] So Maine Med Ctr, Dept Clin Pathol, Portland, ME 04102 USA.
[Cherala, S. S.] New Hampshire Canc Registry, Div Publ Hlth Serv, Concord, NH 03301 USA.
[Dagnall, C. L.] NCI Frederick, Core Genotyping Facil, SAIC Frederick Inc, Bethesda, MD 20892 USA.
RP Moore, LE (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,EPS Room 8102, Bethesda, MD 20852 USA.
EM moorele@mail.nih.gov
RI Hein, David/A-9707-2008; Garcia-Closas, Montserrat /F-3871-2015;
OI Garcia-Closas, Montserrat /0000-0003-1033-2650; Dagnall,
Casey/0000-0001-7334-4718
FU National Institutes of Health, National Cancer Institute, Division of
Cancer Epidemiology and Genetics, Occupational and Environmental
Epidemiology Branch
FX Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Division of Cancer Epidemiology and Genetics,
Occupational and Environmental Epidemiology Branch.
NR 27
TC 60
Z9 64
U1 0
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD FEB
PY 2011
VL 32
IS 2
BP 182
EP 189
DI 10.1093/carcin/bgq223
PG 8
WC Oncology
SC Oncology
GA 712OP
UT WOS:000286676400008
PM 21037224
ER
PT J
AU Wang, HS
Yamamoto, JF
Caberto, C
Saltzman, B
Decker, R
Vogt, TM
Yokochi, L
Chanock, S
Wilkens, LR
Le Marchand, L
AF Wang, Hansong
Yamamoto, Jennifer F.
Caberto, Christian
Saltzman, Barbara
Decker, Robert
Vogt, Thomas M.
Yokochi, Lance
Chanock, Stephen
Wilkens, Lynne R.
Le Marchand, Loic
TI Genetic variation in the bioactivation pathway for polycyclic
hydrocarbons and heterocyclic amines in relation to risk of colorectal
neoplasia
SO CARCINOGENESIS
LA English
DT Article
ID SINGLE-NUCLEOTIDE POLYMORPHISMS; DONE RED MEAT; METABOLIZING-ENZYMES;
DIET HISTORY; AH RECEPTOR; CANCER RISK; PHASE-I; CYP1A1; HAWAII;
N-ACETYLTRANSFERASE-2
AB Animal work implicates chemical carcinogens, such as polycyclic aromatic hydrocarbons (PAHs) and heterocyclic aromatic amines (HAAs) as contributing to the development of colorectal cancer (CRC). The epidemiologic evidence, however, remains inconsistent possibly due to intra-individual variation in bioactivation of these compounds. We conducted a case-control study of colorectal adenoma (914 cases, 1185 controls) and CRC (496 cases, 607 controls) among Japanese Americans, European Americans and Native Hawaiians to investigate the association of genetic variation in the PAH and HAA bioactivation pathway (CYP1A1, CYP1A2, CYP1B1, AHR and ARNT) identified through sequencing with risk of colorectal neoplasia, as well as their interactions with smoking and intakes of red meat and HAAs. The A allele for ARNT rs12410394 was significantly inversely associated with CRC [odds ratios (ORs) and 95% confidence intervals (CIs) for GG, AG and AA genotypes: 1.00, 0.66 (0.48-0.89), 0.54 (0.37-0.78), P-trend = 0.0008] after multiple comparison adjustment. CYP1A2 rs11072508 was marginally significantly associated with CRC, where each copy of the T allele was associated with reduced risk (OR: 0.72, 95% CI: 0.58-0.88, P-trend = 0.0017). No heterogeneity of genetic effects across racial/ethnic groups was detected. In addition, no significant interaction was observed after adjusting for multiple testing between genetic variants and pack-years of smoking, intake of red meat or HAAs (PhIP, MeIQx, Di-MeIQx or total HAAs) or NAT2 genotype (Rapid versus Slow or Intermediate). This study suggests that the genomic region around ARNT rs12410394 may harbor variants associated with CRC.
C1 [Wang, Hansong; Yamamoto, Jennifer F.; Caberto, Christian; Saltzman, Barbara; Wilkens, Lynne R.; Le Marchand, Loic] Univ Hawaii, Program Epidemiol, Canc Res Ctr Hawaii, Honolulu, HI 96813 USA.
[Decker, Robert; Vogt, Thomas M.] Kaiser Permanente Hawaii, Honolulu, HI 96819 USA.
[Yokochi, Lance] Pacific Hlth Res Inst, Honolulu, HI 96813 USA.
[Chanock, Stephen] NCI, Bethesda, MD 20892 USA.
RP Le Marchand, L (reprint author), Univ Hawaii, Program Epidemiol, Canc Res Ctr Hawaii, 1236 Lauhala St,Suite 407, Honolulu, HI 96813 USA.
EM loic@crch.hawaii.edu
FU National Cancer Institute [R01 CA60987, CA72520]; Hawaii Tumor Registry
(National Cancer Institute) [N01-PC-35137]
FX National Cancer Institute (R01 CA60987, CA72520).; The authors thank
Jean Sato for coordinating the data collection, Maj Earle and Anne Tome
for data management and Annette Lum-Jones and Ann Seifried for
performing the laboratory assays. We also thank the Hawaii Tumor
Registry (National Cancer Institute contract N01-PC-35137) for
assistance in CRC case identification.
NR 40
TC 34
Z9 34
U1 1
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD FEB
PY 2011
VL 32
IS 2
BP 203
EP 209
DI 10.1093/carcin/bgq237
PG 7
WC Oncology
SC Oncology
GA 712OP
UT WOS:000286676400011
PM 21081473
ER
PT J
AU Loukili, N
Rosenblatt-Velin, N
Li, JH
Clerc, S
Pacher, P
Feihl, F
Waeber, B
Liaudet, L
AF Loukili, Noureddine
Rosenblatt-Velin, Nathalie
Li, Jianhui
Clerc, Stephanie
Pacher, Pal
Feihl, Francois
Waeber, Bernard
Liaudet, Lucas
TI Peroxynitrite induces HMGB1 release by cardiac cells in vitro and HMGB1
upregulation in the infarcted myocardium in vivo
SO CARDIOVASCULAR RESEARCH
LA English
DT Article
DE Myocardial infarction; Peroxynitrite; High-mobility group box 1;
Inflammation; Cardiomyocytes
ID ISCHEMIA-REPERFUSION INJURY; MOBILITY GROUP BOX-1; FACTOR-KAPPA-B;
ISCHEMIA/REPERFUSION INJURY; NITRIC-OXIDE; DECOMPOSITION CATALYSTS;
HYDROGEN-PEROXIDE; HEART-FAILURE; POSTINFARCTION; INFLAMMATION
AB Aims High-mobility group box 1 (HMGB1) is a nuclear protein actively secreted by immune cells and passively released by necrotic cells that initiates pro-inflammatory signalling through binding to the receptor for advance glycation end-products. HMGB1 has been established as a key inflammatory mediator during myocardial infarction, but the proximal mechanisms responsible for myocardial HMGB1 expression and release in this setting remain unclear. Here, we investigated the possible involvement of peroxynitrite, a potent cytotoxic oxidant formed during myocardial infarction, on these processes.
Methods and results The ability of peroxynitrite to induce necrosis and HMGB1 release in vitro was evaluated in H9c2 cardiomyoblasts and in primary murine cardiac cells (myocytes and non-myocytes). In vivo, myocardial HMGB1 expression and nitrotyrosine content (a marker of peroxynitrite generation) were determined following myocardial ischaemia and reperfusion in rats, whereas peroxynitrite formation was inhibited by two different peroxynitrite decomposition catalysts: 5,10,15,20-tetrakis(4-sulphonatophenyl) porphyrinato iron (III) (FeTPPS) or Mn(III)-tetrakis(4-benzoic acid) porphyrin chloride (MnTBAP). In all types of cells studied, peroxynitrite (100 mu M) elicited significant necrosis, the loss of intracellular HMGB1, and its passive release into the medium. In vivo, myocardial ischaemia-reperfusion induced significant myocardial necrosis, cardiac nitrotyrosine formation, and marked overexpression of myocardial HMGB1. FeTPPS reduced nitrotyrosine, decreased infarct size, and suppressed HMGB1 overexpression, an effect that was similarly obtained with MnTBAP.
Conclusion These findings indicate that peroxynitrite represents a key mediator of HMGB1 overexpression and release by cardiac cells and provide a novel mechanism linking myocardial oxidative/nitrosative stress with post-infarction myocardial inflammation.
C1 [Loukili, Noureddine; Li, Jianhui; Liaudet, Lucas] Univ Hosp Ctr, Dept Intens Care Med, CH-1011 Lausanne, Switzerland.
[Loukili, Noureddine; Rosenblatt-Velin, Nathalie; Li, Jianhui; Clerc, Stephanie; Feihl, Francois; Waeber, Bernard; Liaudet, Lucas] Fac Biol & Med, CH-1011 Lausanne, Switzerland.
[Rosenblatt-Velin, Nathalie; Clerc, Stephanie; Feihl, Francois; Waeber, Bernard; Liaudet, Lucas] Univ Hosp Ctr, Div Clin Pathophysiol, CH-1011 Lausanne, Switzerland.
[Li, Jianhui] Zhejiang Univ, Affiliated Hosp 1, Dept Hepatobiliary Surg, Coll Med, Hangzhou 310003, Zhejiang, Peoples R China.
[Pacher, Pal] NIAA, Lab Physiol Studies, NIH, Bethesda, MD USA.
RP Liaudet, L (reprint author), Univ Hosp Ctr, Dept Intens Care Med, CH-1011 Lausanne, Switzerland.
EM lucas.liaudet@chuv.ch
RI Pacher, Pal/B-6378-2008; Liaudet, Lucas/E-1322-2017
OI Pacher, Pal/0000-0001-7036-8108; Liaudet, Lucas/0000-0003-2670-4930
FU Swiss National Fund for Scientific Research [320000-118174/1]; Lausanne
CardioMet Foundation [2007-R07-15]; NIAAA, National Institutes of Health
FX This work was supported by a Grant from the Swiss National Fund for
Scientific Research (No. 320000-118174/1) and a Grant from The Lausanne
CardioMet Foundation (No. 2007-R07-15) to L.L. This work was also
supported by the Intramural Research Program of the NIAAA, National
Institutes of Health to P.P.
NR 49
TC 31
Z9 32
U1 2
U2 11
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0008-6363
J9 CARDIOVASC RES
JI Cardiovasc. Res.
PD FEB
PY 2011
VL 89
IS 3
BP 586
EP 594
DI 10.1093/cvr/cvq373
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 712OT
UT WOS:000286676800016
PM 21113057
ER
PT J
AU Cleland, MM
Norris, KL
Karbowski, M
Wang, C
Suen, DF
Jiao, S
George, NM
Luo, X
Li, Z
Youle, RJ
AF Cleland, M. M.
Norris, K. L.
Karbowski, M.
Wang, C.
Suen, D-F
Jiao, S.
George, N. M.
Luo, X.
Li, Z.
Youle, R. J.
TI Bcl-2 family interaction with the mitochondrial morphogenesis machinery
SO CELL DEATH AND DIFFERENTIATION
LA English
DT Article
DE Bax; mitochondria fusion; Bak; apoptosis; Mfn2
ID MAMMALIAN-CELLS; BAX ACTIVATION; APOPTOSIS; FUSION; FISSION; PROTEIN;
DOMAIN; MORPHOLOGY; DYNAMICS; NEURONS
AB The regulation of both mitochondrial dynamics and apoptosis is key for maintaining the health of a cell. Bcl-2 family proteins, central in apoptosis regulation, also have roles in the maintenance of the mitochondrial network. Here we report that Bax and Bak participate in the regulation of mitochondrial fusion in mouse embryonic fibroblasts, primary mouse neurons and human colon carcinoma cells. To assess how Bcl-2 family members may regulate mitochondrial morphogenesis, we determined the binding of a series of chimeras between Bcl-xL and Bax to the mitofusins, mitofusin 1 (Mfn1) and mitofusin 2 (Mfn2). One chimera (containing helix 5 (H5) of Bax replacing H5 of Bcl-xL (Bcl-xL/Bax H5)) co-immunoprecipitated with Mfn1 and Mfn2 significantly better than either wild-type Bax or Bcl-xL. Expression of Bcl-xL/Bax H5 in cells reduced the mobility of Mfn1 and Mfn2 and colocalized with ectopic Mfn1 and Mfn2, as well as endogenous Mfn2 to a greater extent than wild-type Bax. Ultimately, Bcl-xL/Bax H5 induced substantial mitochondrial fragmentation in healthy cells. Therefore, we propose that Bcl-xL/Bax H5 disturbs mitochondrial morphology by binding and inhibiting Mfn1 and Mfn2 activity, supporting the hypothesis that Bcl-2 family members have the capacity to regulate mitochondrial morphology through binding to the mitofusins in healthy cells. Cell Death and Differentiation (2011) 18, 235-247; doi: 10.1038/cdd.2010.89; published online 30 July 2010
C1 [Cleland, M. M.; Norris, K. L.; Wang, C.; Suen, D-F; Youle, R. J.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Karbowski, M.] Univ Maryland, Inst Biotechnol, Ctr Med Biotechnol, Bethesda, MD USA.
[Jiao, S.; Li, Z.] NIMH, Clin Brain Disorders Branch, NIH, Bethesda, MD 20892 USA.
[George, N. M.; Luo, X.] Univ Nebraska, Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE USA.
RP Youle, RJ (reprint author), 35 Convent Dr,Room 2C917, Bethesda, MD 20892 USA.
EM youler@ninds.nih.gov
RI Li, Zheng/I-8016-2014; Wang, Chunxin/B-9312-2016; Jiao,
Song/L-2803-2015;
OI Li, Zheng/0000-0002-2978-2531; Wang, Chunxin/0000-0001-6015-6806; Jiao,
Song/0000-0003-0496-6454; Harwig, Megan/0000-0003-2140-5739
FU National Institute of General Medical Science [RO1-GM083131,
RO1-GM76237]; NINDS, NIH
FX We would like to thank Drs. David Huang and Kym Lowes for the C57BL/6 WT
and Bax-/-Bak-/- cells and their comments on the
manuscript; Dr. Kuan Hong Wang for his thoughtful reading of the
manuscript; Susan Smith for her tissue culture assistance; and the NINDS
DNA sequencing facility, the NINDS imaging facility and Sungyoung Auh
for her assistance with statistical analysis. We would also like to
thank Dr. Fred Bunz for the pSEPT vector and advice on gene targeting
strategy; Dr. Seung-Wook Ryu for cloning FLAG-Mfn2; Dr. Liqiang Zhang
for cloning GFP-Bax/Bcl-xL H5; and Dr. Benoit Pierrat for the gift of
anti-endophilin B2. MK and XL thankfully acknowledge financial support
from National Institute of General Medical Science (RO1-GM083131 to MK
and RO1-GM76237 to XL). This work was supported in part by the
Intramural Research Program, NINDS, NIH.
NR 39
TC 51
Z9 52
U1 4
U2 16
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1350-9047
J9 CELL DEATH DIFFER
JI Cell Death Differ.
PD FEB
PY 2011
VL 18
IS 2
BP 235
EP 247
DI 10.1038/cdd.2010.89
PG 13
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 704IW
UT WOS:000286045800005
PM 20671748
ER
PT J
AU Goldberg, ME
Torjman, MC
Schwartzman, RJ
Mager, DE
Wainer, IW
AF Goldberg, Michael E.
Torjman, Marc C.
Schwartzman, Robert J.
Mager, Donald E.
Wainer, Irving W.
TI Enantioselective Pharmacokinetics of (R)- and (S)-Ketamine After a 5-Day
Infusion in Patients with Complex Regional Pain Syndrome
SO CHIRALITY
LA English
DT Article
DE ketamine; norketamine; CRPS; pharmacokinetics; pharmacodynamics;
enantioselective; liquid chromatography; mass spectrometry
ID HUMAN LIVER-MICROSOMES; REFLEX SYMPATHETIC DYSTROPHY; COMPARATIVE
PHARMACOLOGY; MASS-SPECTROMETRY; N-DEMETHYLATION; KETAMINE; NORKETAMINE;
ENANTIOMERS; METABOLITES; VOLUNTEERS
AB Introduction: This study determined the pharmacokinetics and pharmacodynamics of (R)- and (S)-ketamine and (R)- and (S)-norketamine following a 5-day moderate dose, as a continuous (R, S)-ketamine infusion in complex regional pain syndrome (CRPS) patients. Materials and methods: Ketamine was titrated to 10-40 mg/h and maintained for 5 days. (R)and (S)-Ketamine and (R)- and (S)-norketamine pharmacokinetic and pharmacodynamic studies were performed. Blood samples were obtained on Day 1 preinfusion, and at 60-90, 120-150, 180-210, and 240-300 min after the start of the infusion, on Days 2, 3, 4, 5, and on Day 5 at 60 min after the end of infusion. The plasma concentrations of (R)- and (S)-ketamine and (R)- and (S)-norketamine were determined using enantioselective liquid chromatography-mass spectrometry. Results: Ketamine and norketamine levels stabilized 5 h after the start of the infusion. (R)-Ketamine clearance was significantly lower resulting in higher steady-state plasma concentrations than (S)-ketamine. The first-order elimination for (S)-norketamine was significantly greater than that of (R)-enantiomer. When comparing the pharmacokinetic parameters of the patients who responded to ketamine treatment with those who did not, no differences were observed in ketamine clearance and the first-order elimination of norketamine. Conclusion: The results indicate that (R)- and (S)-ketamine and (R)- and (S)-norketamine plasma concentrations do not explain the antinociceptive activity of the drug in patients suffering from CRPS. Chirality 23:138-143, 2011. (C) 2010 Wiley-Liss, Inc.
C1 [Goldberg, Michael E.; Torjman, Marc C.] UMDNJ Robert Wood Johnson Med Sch, Dept Anesthesiol, Cooper Univ Hosp, Camden, NJ 08103 USA.
[Schwartzman, Robert J.] Drexel Univ, Coll Med, Dept Neurol, Philadelphia, PA 19104 USA.
[Mager, Donald E.] SUNY Buffalo, Dept Pharmaceut Sci, Buffalo, NY 14260 USA.
[Wainer, Irving W.] NIA, Bioanalyt Chem & Drug Discovery Sect, Clin Invest Lab, Intramural Res Program, Baltimore, MD 21224 USA.
RP Goldberg, ME (reprint author), UMDNJ Robert Wood Johnson Med Sch, Dept Anesthesiol, Cooper Univ Hosp, 1 Cooper Plaza, Camden, NJ 08103 USA.
EM Goldberg-Mike@Cooperhealth.edu
FU National Institute on Aging/NIH
FX Contract grant sponsor: National Institute on Aging/NIH (Intramural
Research Program)
NR 30
TC 8
Z9 8
U1 1
U2 10
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0899-0042
J9 CHIRALITY
JI Chirality
PD FEB
PY 2011
VL 23
IS 2
BP 138
EP 143
DI 10.1002/chir.20890
PG 6
WC Chemistry, Medicinal; Chemistry, Analytical; Chemistry, Organic;
Pharmacology & Pharmacy
SC Pharmacology & Pharmacy; Chemistry
GA 703KM
UT WOS:000285976800008
PM 20803495
ER
PT J
AU Wirka, RC
Gore, S
Van Wagoner, DR
Arking, DE
Lubitz, SA
Lunetta, KL
Benjamin, EJ
Alonso, A
Ellinor, PT
Barnard, J
Chung, MK
Smith, JD
AF Wirka, Robert C.
Gore, Shamone
Van Wagoner, David R.
Arking, Dan E.
Lubitz, Steven A.
Lunetta, Kathryn L.
Benjamin, Emelia J.
Alonso, Alvaro
Ellinor, Patrick T.
Barnard, John
Chung, Mina K.
Smith, Jonathan D.
TI A Common Connexin-40 Gene Promoter Variant Affects Connexin-40
Expression in Human Atria and Is Associated With Atrial Fibrillation
SO CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY
LA English
DT Article
DE atrial fibrillation; ion channels; genetics; allelic expression
imbalance
ID HAPLOTYPE RECONSTRUCTION; HEART-DISEASE; GENOTYPE; RISK; MICE
AB Background-A common single-nucleotide polymorphism (SNP) in the promoter of the Connexin-40 (Cx40) gene GJA5 was suggested to affect Cx40 promoter activity and the risk of atrial fibrillation (AF), but the role of other common Cx40 polymorphisms is unknown.
Methods and Results-Eight SNPs within the Cx40 gene region were tested for association with Cx40 levels measured in atrial tissue from 61 individuals. The previously described Cx40 promoter SNP (rs35594137, -44G -> A) was not associated with Cx40 mRNA levels. However, a common SNP (rs10465885) located in the TATA box of an alternative Cx40 promoter was strongly associated with Cx40 mRNA expression (P < 0.0001) and displayed strong and consistent allelic expression imbalance in human atrial tissue. A promoter-luciferase assay in cultured murine cardiomyocytes demonstrated reduced activity of the promoter containing the minor allele of this SNP (P < 0.0001). Both rs35594137 and rs10465885 were tested for association with early-onset lone AF (<= 60 years of age) in 384 cases and 3010 population control subjects. rs10465885 was associated with the AF phenotype (odds ratio, 1.18; P=0.046). This result was confirmed in a meta-analysis including 2 additional early-onset lone AF case-control cohorts (odds ratio, 1.16, P=0.022). rs35594137 was not associated with the lone AF phenotype in any of the cohorts studied or in a combined analysis.
Conclusions-A previously described Cx40 promoter SNP was not found to influence Cx40 expression or risk of AF. We describe an alternate promoter polymorphism that directly affects levels of Cx40 mRNA in vivo and is associated with early-onset lone AF. (Circ Arrhythm Electrophysiol. 2011;4:87-93.)
C1 [Wirka, Robert C.] Case Western Reserve Univ, Cleveland Clin, Lerner Coll Med, Cleveland, OH 44106 USA.
[Smith, Jonathan D.] Cleveland Clin, Dept Cell Biol & Cardiovasc Med, Cleveland, OH 44195 USA.
[Gore, Shamone] Cleveland Clin, Dept Cell Biol, Cleveland, OH 44195 USA.
[Van Wagoner, David R.] Cleveland Clin, Dept Mol Cardiol & Cardiovasc Med, Cleveland, OH 44195 USA.
[Barnard, John] Cleveland Clin, Dept Quantitat Hlth Sci, Cleveland, OH 44195 USA.
[Chung, Mina K.] Cleveland Clin, Dept Cardiovasc Med & Mol Cardiol, Cleveland, OH 44195 USA.
[Arking, Dan E.] Johns Hopkins Univ, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
[Lubitz, Steven A.; Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiac Arrhythmia Serv, Boston, MA 02114 USA.
[Lunetta, Kathryn L.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Benjamin, Emelia J.] NHLBI, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Cardiol Sect, Dept Med, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Prevent Med Sect, Dept Med, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Alonso, Alvaro] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
RP Smith, JD (reprint author), Cleveland Clin, Dept Cell Biol & Cardiovasc Med, 9500 Euclid Ave,NC-10, Cleveland, OH 44195 USA.
EM barnarj@ccf.org; chungm@ccf.org; smithj4@ccf.org
RI Alonso, Alvaro/A-4917-2010;
OI Alonso, Alvaro/0000-0002-2225-8323; Lunetta,
Kathryn/0000-0002-9268-810X; Benjamin, Emelia/0000-0003-4076-2336
FU CCR NIH HHS [RC1 HL099452-02]; Howard Hughes Medical Institute; NCRR NIH
HHS [1UL-RR024989, UL1 RR024989, UL1 RR024989-05, UL1 RR025005, UL1
RR025005-05, UL1RR025005]; NHGRI NIH HHS [U01 HG004402, U01 HG004402-01,
U01HG004402]; NHLBI NIH HHS [RC1 HL101056, 1RC1HL099452, HL090620,
HL092577, N01 HC055015, N01 HC055016, N01 HC055018, N01 HC055019, N01
HC055020, N01 HC055021, N01 HC055022, N01-HC-55015, N01-HC-55016,
N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, N01-HC-55022,
N01HC55015, N01HC55016, N01HC55018, N01HC55019, N01HC55020, N01HC55021,
N01HC55022, R01 HL059367, R01 HL059367-10, R01 HL086694, R01
HL086694-03, R01 HL087641, R01 HL087641-03, R01 HL090620, R01
HL090620-04, R01 HL092577, R01 HL092577-03, R01 HL104156, R01HL086694,
R01HL087641, R01HL59367, RC1 HL099452, RC1 HL099452-02, RC1 HL101056-02,
T32 HL007575, T32 HL007575-26A1, T32HL007575]; NIDA NIH HHS [DA027021,
R21 DA027021, R21 DA027021-02]; PHS HHS [HHSN268200625226C]
NR 26
TC 41
Z9 44
U1 0
U2 3
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 FEB
PY 2011
VL 4
IS 1
BP 87
EP +
DI 10.1161/CIRCEP.110.959726
PG 21
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 721LL
UT WOS:000287356000015
PM 21076161
ER
PT J
AU Kelly, RJ
Draper, D
Chen, CC
Robey, RW
Figg, WD
Piekarz, RL
Chen, XH
Gardner, ER
Balis, FM
Venkatesan, AM
Steinberg, SM
Fojo, T
Bates, SE
AF Kelly, Ronan J.
Draper, Deborah
Chen, Clara C.
Robey, Robert W.
Figg, William D.
Piekarz, Richard L.
Chen, Xiaohong
Gardner, Erin R.
Balis, Frank M.
Venkatesan, Aradhana M.
Steinberg, Seth M.
Fojo, Tito
Bates, Susan E.
TI A Pharmacodynamic Study of Docetaxel in Combination with the
P-glycoprotein Antagonist Tariquidar (XR9576) in Patients with Lung,
Ovarian, and Cervical Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID METASTATIC BREAST-CANCER; MEDIATED MULTIDRUG-RESISTANCE; IN-VIVO
REVERSAL; PHASE-I; CHEMOTHERAPY RESPONSE; TC-99M TETROFOSMIN; VALSPODAR
PSC-833; CELL CARCINOMA; SOLID TUMORS; PSC 833
AB Purpose: P-glycoprotein (Pgp) antagonists have been difficult to develop because of complex pharmacokinetic interactions and a failure to show meaningful results. Here we report the results of a pharmacokinetic and pharmacodynamic trial using a third-generation, potent, noncompetitive inhibitor of Pgp, tariquidar (XR9576), in combination with docetaxel.
Experimental Design: In the first treatment cycle, the pharmacokinetics of docetaxel (40 mg/m(2)) were evaluated after day 1 and day 8 doses, which were administered with or without tariquidar (150 mg). 99m Tc-sestamibi scanning and CD56(+) mononuclear cell rhodamine efflux assays were conducted to assess Pgp inhibition. In subsequent cycles, 75 mg/m2 docetaxel was administered with 150 mg tariquidar every 3 weeks.
Results: Forty-eight patients were enrolled onto the trial. Nonhematologic grade 3/4 toxicities in 235 cycles were minimal. Tariquidar inhibited Pgp-mediated rhodamine efflux from CD56(+) cells and reduced 99m Tc-sestamibi clearance from the liver. There was striking variability in basal sestamibi uptake; a 12% to 24% increase in visible lesions was noted in 8 of 10 patients with lung cancer. No significant difference in docetaxel disposition was observed in pairwise comparison with and without tariquidar. Four partial responses (PR) were seen (4/48); 3 in the non-small cell lung cancer (NSCLC) cohort, measuring 40%, 57%, and 67% by RECIST, and 1 PR in a patient with ovarian cancer.
Conclusions: Tariquidar is well tolerated, with less observed systemic pharmacokinetic interaction than previous Pgp antagonists. Variable effects of tariquidar on retention of sestamibi in imageable lung cancers suggest that follow-up studies assessing tumor drug uptake in this patient population would be worthwhile. Clin Cancer Res; 17(3); 569-80. (C) 2010 AACR.
C1 [Kelly, Ronan J.; Draper, Deborah; Robey, Robert W.; Figg, William D.; Piekarz, Richard L.; Chen, Xiaohong; Fojo, Tito; Bates, Susan E.] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Chen, Clara C.] NIH, Dept Nucl Med, Warren G Magnuson Clin Ctr, Bethesda, MD USA.
[Chen, Clara C.] NIH, Dept Radiol, Warren G Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Gardner, Erin R.] NCI, SAIC Frederick, Clin Pharmacol Program, Frederick, MD 21701 USA.
[Balis, Frank M.] Childrens Hosp Philadelphia, Ctr Childhood Canc Res, Philadelphia, PA 19104 USA.
[Venkatesan, Aradhana M.] NCI, Dept Radiol & Imaging Sci, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, CCR, Bethesda, MD 20892 USA.
RP Bates, SE (reprint author), NCI, Med Oncol Branch, Ctr Canc Res, 9000 Rockville Pike,Bldg 10,Rm 12N226, Bethesda, MD 20892 USA.
EM sebates@helix.nih.gov
RI Figg Sr, William/M-2411-2016
FU National Cancer Institute, NIH [HHSN261200800001E]; NIH, National Cancer
Institute, Center for Cancer Research
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, NIH, under contract HHSN261200800001E
(E.R.G.). This work was supported by the Intramural Research Program of
the NIH, National Cancer Institute, Center for Cancer Research.
NR 50
TC 67
Z9 70
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD FEB 1
PY 2011
VL 17
IS 3
BP 569
EP 580
DI 10.1158/1078-0432.CCR-10-1725
PG 12
WC Oncology
SC Oncology
GA 715HI
UT WOS:000286873400019
PM 21081657
ER
PT J
AU Bagatell, R
Herzog, CE
Trippett, M
Grippo, JF
Cirrincione-Dall, G
Fox, E
Macy, M
Bish, J
Whitcomb, P
Aikin, A
Wright, G
Yurasov, S
Balis, FM
Gore, L
AF Bagatell, R.
Herzog, C. E.
Trippett, M.
Grippo, J. F.
Cirrincione-Dall, G.
Fox, E.
Macy, M.
Bish, J.
Whitcomb, P.
Aikin, A.
Wright, G.
Yurasov, S.
Balis, F. M.
Gore, L.
TI Pharmacokinetically Guided Phase 1 Trial of the IGF-1 Receptor
Antagonist RG1507 in Children with Recurrent or Refractory Solid Tumors
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID EWINGS-SARCOMA CELLS; I RECEPTOR; RHABDOMYOSARCOMA CELLS;
ANTITUMOR-ACTIVITY; GROWTH; EXPRESSION; ANTIBODY; INHIBITION; INCREASES;
MICE
AB Purpose: This pediatric phase I study was designed to identify the doses of RG1507, a monoclonal antibody against the Type 1 Insulin-like Growth Factor Receptor (IGF1R), that achieves exposures equivalent to those achieved in adults at recommended doses.
Experimental Design: Children with relapsed or refractory solid tumors were treated using the same doses and administration schedules of RG1507 (3 and 9 mg/kg/wk, and 16 mg/kg every 3 weeks [q3W]) as those studied in adults. Detailed pharmacokinetic (PK) sampling was performed after the first dose; selected peak and trough levels were subsequently obtained. Target exposures were >= 85% of mean areas under concentration x time curves (AUCs) in adults at doses of 9 mg/kg/wk and 16 mg/kg q3W. A maximum tolerated dose could be identified if dose-limiting toxicities (DLT) occurred.
Results: Thirty-one evaluable patients aged 3-17 years were enrolled at 3 mg/kg/wk (n = 3), 9 mg/kg/wk (n 18), or 16 mg/kg q3W (n 10). There were no DLTs. At 9 mg/kg/wk the mean AUC(0-7d) (21,000 mu g h/mL) exceeded the target (16,000 mg h/mL). At 16 mg/kg q3W, the mean AUC(021d) (70,000 mg h/mL) exceeded the target (59,400 mg h/mL). Clearance normalized to body weight was age dependent. There were no objective responses. Seven patients had stable disease for > 12 weeks, including two patients with osteosarcoma with stable disease for 52+ and 78+ weeks.
Conclusions: The recommended doses of RG1507 in children with solid tumors are 9 mg/kg/wk and 16 mg/kg q3W. This flexible design is well suited for trials of agents associated with limited toxicity. Clin Cancer Res; 17(3); 611-9. (C) 2010 AACR.
C1 [Bagatell, R.; Fox, E.; Bish, J.; Balis, F. M.] Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19066 USA.
[Herzog, C. E.] Univ Texas MD Anderson Canc Ctr, Dept Pediat, Houston, TX 77030 USA.
[Trippett, M.; Wright, G.] Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
[Grippo, J. F.; Cirrincione-Dall, G.; Yurasov, S.] Hoffmann La Roche Inc, Nutley, NJ 07110 USA.
[Macy, M.; Gore, L.] Childrens Hosp, Dept Pediat, Aurora, CO USA.
[Macy, M.; Gore, L.] Univ Colorado Denver, Aurora, CO USA.
[Whitcomb, P.; Aikin, A.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
RP Bagatell, R (reprint author), Childrens Hosp Philadelphia, Dept Pediat, CTRB 4022,3501 Civ Ctr Blvd, Philadelphia, PA 19066 USA.
EM bagatellr@email.chop.edu
FU Hoffmann-La Roche Inc; NIH (National Cancer Institute, Center for Cancer
Research); Alex's Lemonade Stand Foundation; Caitlin Robb Foundation;
Morgan Adams Foundation
FX The research support was provided by Hoffmann-La Roche Inc. This
research was also supported in part by the Intramural Research Program
of the NIH (National Cancer Institute, Center for Cancer Research),
Alex's Lemonade Stand Foundation, the Caitlin Robb Foundation, and the
Morgan Adams Foundation.
NR 19
TC 21
Z9 21
U1 0
U2 1
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 FEB 1
PY 2011
VL 17
IS 3
BP 611
EP 619
DI 10.1158/1078-0432.CCR-10-1731
PG 9
WC Oncology
SC Oncology
GA 715HI
UT WOS:000286873400023
PM 21127194
ER
PT J
AU Alsarraj, J
Walker, RC
Webster, JD
Simpson, RM
Ozato, K
Hunter, KW
AF Alsarraj, Jude
Walker, Renard C.
Webster, Joshua D.
Simpson, R. Mark
Ozato, Keiko
Hunter, Kent W.
TI A mutant of the metastasis susceptibility gene Brd4 promotes EMT, stem
cell-like conversion, and metastatic progression in a mouse mammary
tumor model
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Alsarraj, Jude; Walker, Renard C.; Webster, Joshua D.; Simpson, R. Mark; Hunter, Kent W.] NCI, NIH, Bethesda, MD 20892 USA.
[Ozato, Keiko] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 159
EP 160
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200013
ER
PT J
AU Winter, SF
Hunter, KW
AF Winter, Scott F.
Hunter, Kent W.
TI Arid4b: a candidate breast cancer progression modifier gene
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Winter, Scott F.; Hunter, Kent W.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 166
EP 166
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200030
ER
PT J
AU Guedez, L
Kwityn, CJ
Stetler-Stevenson, WG
AF Guedez, Liliana
Kwityn, Clifford J.
Stetler-Stevenson, William G.
TI Inflammation linked to the deficiency of tissue inhibitor of
metalloproteinase-2 accelerates tumorogenesis of Lewis-lung carcinoma
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Guedez, Liliana; Kwityn, Clifford J.; Stetler-Stevenson, William G.] NCI, Bethesda, MD 20892 USA.
RI Stetler-Stevenson, William/H-6956-2012
OI Stetler-Stevenson, William/0000-0002-5500-5808
NR 0
TC 0
Z9 0
U1 0
U2 3
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 171
EP 171
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200048
ER
PT J
AU Tsai, YC
Weissman, AM
Maditz, R
AF Tsai, Yien Che
Weissman, Allan M.
Maditz, Rhyan
TI Regulation of ER-associated degradation and ER stress in metastasis:
insights from studies on an ER ubiquitin ligase
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Tsai, Yien Che; Weissman, Allan M.; Maditz, Rhyan] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 190
EP 190
PG 1
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200106
ER
PT J
AU Goldberger, NE
Tran, B
Hunter, K
AF Goldberger, Natalie E.
Bao Tran
Hunter, Kent
TI Identification of candidate microRNAs regulating breast cancer
metastasis
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Goldberger, Natalie E.; Hunter, Kent] NCI, Bethesda, MD 20892 USA.
[Bao Tran] SAIC, Frederick, MD USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 212
EP 213
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200171
ER
PT J
AU Marino, N
Marshall, JCA
Collins, J
Veenstra, T
Zhou, M
Steeg, PS
AF Marino, Natascia
Marshall, Jean-Claude A.
Collins, Joshua
Veenstra, Timothy
Zhou, Ming
Steeg, Patricia S.
TI The actin-binding protein Gelsolin as a potential binding partner of
Nm23
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Marino, Natascia; Marshall, Jean-Claude A.; Collins, Joshua; Steeg, Patricia S.] NIH, Bethesda, MD 20892 USA.
[Veenstra, Timothy; Zhou, Ming] NIH, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 228
EP 229
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200221
ER
PT J
AU Sourbier, C
Kim, YS
Lee, S
Trepel, J
Neckers, L
Linehan, M
AF Sourbier, Carole
Kim, Yeono-Sang
Lee, Sunmin
Trepel, Jane
Neckers, Len
Linehan, Marston
TI Invasion of HLRCC tumors: assessing the contribution of HIF, ROS, and
lipids
SO CLINICAL & EXPERIMENTAL METASTASIS
LA English
DT Meeting Abstract
C1 [Sourbier, Carole; Kim, Yeono-Sang; Lee, Sunmin; Trepel, Jane; Neckers, Len; Linehan, Marston] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0262-0898
J9 CLIN EXP METASTAS
JI Clin. Exp. Metastasis
PD FEB
PY 2011
VL 28
IS 2
BP 257
EP 258
PG 2
WC Oncology
SC Oncology
GA 753RB
UT WOS:000289796200305
ER
PT J
AU Desai, V
Donsante, A
Swoboda, KJ
Martensen, M
Thompson, J
Kaler, SG
AF Desai, V.
Donsante, A.
Swoboda, K. J.
Martensen, M.
Thompson, J.
Kaler, S. G.
TI Favorably skewed X-inactivation accounts for neurological sparing in
female carriers of Menkes disease
SO CLINICAL GENETICS
LA English
DT Article
DE ATP7A; junction fragment; Menkes disease; skewing; X-inactivation
ID OCCIPITAL-HORN-SYNDROME; CHROMOSOME INACTIVATION; CANDIDATE GENE;
NEONATAL DIAGNOSIS; LINKED DISEASE; PROTEIN; PLASMA; MICE;
TRANSLOCATION; ACTIVATION
AB Classical Menkes disease is an X-linked recessive neurodegenerative disorder caused by mutations in ATP7A, which is located at Xq13.1-q21. ATP7A encodes a copper-transporting P-type ATPase and plays a critical role in development of the central nervous system. With rare exceptions involving sex chromosome aneuploidy or X-autosome translocations, female carriers of ATP7A mutations are asymptomatic except for subtle hair and skin abnormalities, although the mechanism for this neurological sparing has not been reported. We studied a three-generation family in which a severe ATP7A mutation, a 5.5-kb genomic deletion spanning exons 13 and 14, segregated. The deletion junction fragment was amplified from the proband by long-range polymerase chain reaction and sequenced to characterize the breakpoints. We screened at-risk females in the family for this junction fragment and analyzed their X-inactivation patterns using the human androgen-receptor (HUMARA) gene methylation assay. We detected the junction fragment in the proband, two obligate heterozygotes, and four of six at-risk females. Skewed inactivation of the X chromosome harboring the deletion was noted in all female carriers of the deletion (n = 6), whereas random X-inactivation was observed in all non-carriers (n = 2). Our results formally document one mechanism for neurological sparing in female carriers of ATP7A mutations. Based on review of X-inactivation patterns in female carriers of other X-linked recessive diseases, our findings imply that substantial expression of a mutant ATP7A at the expense of the normal allele could be associated with neurologic symptoms in female carriers of Menkes disease and its allelic variants, occipital horn syndrome, and ATP7A-related distal motor neuropathy.
C1 [Desai, V.; Donsante, A.; Kaler, S. G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Human Copper Metab, Program Mol Med, NIH, Bethesda, MD 20892 USA.
[Swoboda, K. J.; Martensen, M.; Thompson, J.] Univ Utah, Sch Med, Dept Neurol, Pediat Motor Disorders Res Program, Salt Lake City, UT USA.
[Swoboda, K. J.; Martensen, M.; Thompson, J.] Univ Utah, Sch Med, Dept Pediat, Pediat Motor Disorders Res Program, Salt Lake City, UT USA.
RP Kaler, SG (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Human Copper Metab, Program Mol Med, NIH, Bldg 10,Room 5-2571,10 Ctr Dr,MSC 1832, Bethesda, MD 20892 USA.
EM kalers@mail.nih.gov
FU NIH
FX We are grateful to the family for their participation and to Sarah
Godwin for mutation identification in the proband. This work was
supported by the NIH Intramural Research Program.
NR 40
TC 15
Z9 16
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0009-9163
J9 CLIN GENET
JI Clin. Genet.
PD FEB
PY 2011
VL 79
IS 2
BP 176
EP 182
DI 10.1111/j.1399-0004.2010.01451.x
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 703HE
UT WOS:000285968200011
PM 20497190
ER
PT J
AU Vinh, DC
Schwartz, B
Hsu, AP
Miranda, DJ
Valdez, PA
Fink, D
Lau, KP
Long-Priel, D
Kuhns, DB
Uzel, G
Pittaluga, S
Hoover, S
Galgiani, JN
Holland, SM
AF Vinh, Donald C.
Schwartz, Brian
Hsu, Amy P.
Miranda, David J.
Valdez, Patricia A.
Fink, Danielle
Lau, Karen P.
Long-Priel, Debra
Kuhns, Douglas B.
Uzel, Gulbu
Pittaluga, Stefania
Hoover, Susan
Galgiani, John N.
Holland, Steven M.
TI Interleukin-12 Receptor beta 1 Deficiency Predisposing to Disseminated
Coccidioidomycosis
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Editorial Material
ID CHRONIC MUCOCUTANEOUS CANDIDIASIS; INTERFERON; IMMITIS
C1 [Vinh, Donald C.; Hsu, Amy P.; Miranda, David J.; Uzel, Gulbu; Holland, Steven M.] NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Schwartz, Brian] Univ Calif San Francisco, Div Infect Dis, San Francisco, CA 94143 USA.
[Valdez, Patricia A.] NIAID, Bacterial Pathogenesis Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Fink, Danielle; Lau, Karen P.; Long-Priel, Debra; Kuhns, Douglas B.] SAIC Frederick, Neutrophil Monitoring Lab, Clin Serv Program, Frederick, MD USA.
[Pittaluga, Stefania] NCI, Pathol Lab, NIH, Frederick, MD 21701 USA.
[Hoover, Susan; Galgiani, John N.] Univ Arizona, Valley Fever Ctr Excellence, Tucson, AZ USA.
RP Holland, SM (reprint author), NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, Bldg 10CRC,Rm B3-4141,MSC 1684, Bethesda, MD 20892 USA.
EM smh@nih.gov
RI Hoover, Susan/F-8580-2015;
OI VINH, DONALD/0000-0003-1347-7767
FU Canadian Institutes of Health Research; Intramural NIH HHS
NR 14
TC 31
Z9 31
U1 0
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD FEB
PY 2011
VL 52
IS 4
BP E99
EP E102
DI 10.1093/cid/ciq215
PG 4
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 712PD
UT WOS:000286677800003
PM 21258095
ER
PT J
AU Tamura, MK
Xie, DW
Yaffe, K
Cohen, DL
Teal, V
Kasner, SE
Messe, SR
Sehgal, AR
Kusek, J
DeSalvo, KB
Cornish-Zirker, D
Cohan, J
Seliger, SL
Chertow, GM
Go, AS
AF Tamura, Manjula Kurella
Xie, Dawei
Yaffe, Kristine
Cohen, Debbie L.
Teal, Valerie
Kasner, Scott E.
Messe, Steven R.
Sehgal, Ashwini R.
Kusek, John
DeSalvo, Karen B.
Cornish-Zirker, Denise
Cohan, Janet
Seliger, Stephen L.
Chertow, Glenn M.
Go, Alan S.
TI Vascular Risk Factors and Cognitive Impairment in Chronic Kidney
Disease: The Chronic Renal Insufficiency Cohort (CRIC) Study
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID CARDIOVASCULAR HEALTH COGNITION; HEMODIALYSIS-PATIENTS; DIALYSIS
PATIENTS; DEMENTIA; BRAIN; ANEMIA; ADULTS; PERFORMANCE; COMMUNITY;
OUTCOMES
AB Background and objectives Cognitive impairment is common among persons with chronic kidney disease, but the extent to which nontraditional vascular risk factors mediate this association is unclear.
Design, setting, participants, & measurements We conducted cross-sectional analyses of baseline data collected from adults with chronic kidney disease participating in the Chronic Renal Insufficiency Cohort study. Cognitive impairment was defined as a Modified Mini-Mental State Exam score >1 SD below the mean score.
Results Among 3591 participants, the mean age was 58.2 +/- 11.0 years, and the mean estimated GFR (eGFR) was 43.4 +/- 13.5 ml/min per 1.73 m(2). Cognitive impairment was present in 13%. After adjustment for demographic characteristics, prevalent vascular disease (stroke, coronary artery disease, and peripheral arterial disease) and traditional vascular risk factors (diabetes, hypertension, smoking, and elevated cholesterol), an eGFR <30 ml /min per 1.73 m(2) was associated with a 47% increased odds of cognitive impairment (odds ratio 1.47, 95% confidence interval 1.05, 2.05) relative to those with an eGFR 45 to 59 ml/min per 1.73 m(2). This association was attenuated and no longer significant after adjustment for hemoglobin concentration. While other nontraditional vascular risk factors including C-reactive protein, homocysteine, serum albumin, and albuminuria were correlated with cognitive impairment in unadjusted analyses, they were not significantly associated with cognitive impairment after adjustment for eGFR and other confounders.
Conclusions The prevalence of cognitive impairment was higher among those with lower eGFR, independent of traditional vascular risk factors. This association may be explained in part by anemia. Clin J Am Soc Nephrol 6: 248-256, 2011. doi: 10.2215/CJN.02660310
C1 [Tamura, Manjula Kurella; Chertow, Glenn M.] Stanford Univ, Sch Med, Div Nephrol, Palo Alto, CA 94304 USA.
[Tamura, Manjula Kurella] Vet Affairs Palo Alto Geriatr Res & Educ Clin Ctr, Palo Alto, CA USA.
[Xie, Dawei; Teal, Valerie; Kasner, Scott E.] Univ Penn, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Yaffe, Kristine] San Francisco VA Med Ctr, Dept Psychiat, San Francisco, CA USA.
[Yaffe, Kristine] San Francisco VA Med Ctr, Dept Neurol, San Francisco, CA USA.
[Yaffe, Kristine] San Francisco VA Med Ctr, Dept Epidemiol, San Francisco, CA USA.
[Go, Alan S.] Univ Calif San Francisco, Dept Epidemiol, San Francisco, CA 94143 USA.
[Cohen, Debbie L.] Univ Penn, Renal Electrolyte Div, Philadelphia, PA 19104 USA.
[Kasner, Scott E.; Messe, Steven R.] Univ Penn, Dept Neurol, Philadelphia, PA 19104 USA.
[Sehgal, Ashwini R.] Case Western Reserve Univ, Div Nephrol, Cleveland, OH 44106 USA.
[Kusek, John] NIDDK, Div Kidney Urol & Hematol Dis, NIH, Bethesda, MD USA.
[DeSalvo, Karen B.] Tulane Univ, Sect Gen Internal Med & Geriatr, New Orleans, LA 70118 USA.
[Cornish-Zirker, Denise] Univ Michigan, Div Cardiovasc Med & Hypertens, Ann Arbor, MI 48109 USA.
[Cohan, Janet] Univ Illinois, Dept Med, Chicago, IL USA.
[Seliger, Stephen L.] Univ Maryland, Div Nephrol, Baltimore, MD 21201 USA.
[Go, Alan S.] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
[Go, Alan S.] Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA.
[Go, Alan S.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
[Yaffe, Kristine] San Francisco VA Med Ctr, Dept Biostat, San Francisco, CA USA.
RP Tamura, MK (reprint author), Stanford Univ, Sch Med, Div Nephrol, 780 Welch Rd,Suite 106, Palo Alto, CA 94304 USA.
EM mktamura@stanford.edu
RI Kasner, Scott/C-6109-2011; Kurella Tamura, Manjula/C-8284-2014
OI Kurella Tamura, Manjula/0000-0001-5227-2479
FU National Institute of Diabetes and Digestive and Kidney Diseases
[5U01DK060990, 5U01DK060984, 5U01DK06102, 5U01DK061021, 5U01DK061028,
5U01DK60980, 5U01DK060963, 5U01DK060902, R01DK069406]; National
Institutes of Health [UL1RR024134, UL1RR025005, M01RR16500, UL1RR024989,
M01RR000042, UL1RR024986, UL1RR029879, RR05096, UL1RR024131]; National
Institute of Aging [K23AG028952]; Amgen
FX The CRIC Study is supported by cooperative agreement project grants
5U01DK060990, 5U01DK060984, 5U01DK06102, 5U01DK061021, 5U01DK061028,
5U01DK60980, 5U01DK060963, and 5U01DK060902 from the National Institute
of Diabetes and Digestive and Kidney Diseases and by grants UL1RR024134,
UL1RR025005, M01RR16500, UL1RR024989, M01RR000042, UL1RR024986,
UL1RR029879, RR05096, and UL1RR024131 from the National Institutes of
Health. Dr. Kurella Tamura received support from the National Institute
of Aging (grant K23AG028952). Dr. Yaffe was supported by R01DK069406,
also from the National Institute of Diabetes and Digestive and Kidney
Diseases. These results were presented in abstract form at the American
Society of Nephrology Meeting.; Dr. Kurella Tamura has previously
received grant support from Amgen.
NR 36
TC 41
Z9 47
U1 1
U2 9
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 FEB
PY 2011
VL 6
IS 2
BP 248
EP 256
DI 10.2215/CJN.02660310
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 722KJ
UT WOS:000287430800004
ER
PT J
AU Onumah, C
Kimmel, PL
Rosenberg, ME
AF Onumah, Chavon
Kimmel, Paul L.
Rosenberg, Mark E.
TI Race Disparities in US Nephrology Fellowship Training
SO CLINICAL JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
LA English
DT Article
ID GRADUATE MEDICAL-EDUCATION; STAGE RENAL-DISEASE; CHRONIC KIDNEY-DISEASE;
HEALTH-CARE-SYSTEM; RACIAL-DIFFERENCES; UNITED-STATES; TRUST; PATIENT;
DISCRIMINATION; RECRUITMENT
AB Background and objectives Renal disease disproportionately affects African-American patients. Trust has been implicated as an important factor in patient outcomes. Higher levels of trust and better interpersonal care have been reported when race of patient and physician are concordant. The purpose of this analysis was to examine trends in the racial background of U.S. medical school graduates, internal medicine residents, nephrology fellows, and patients with ESRD.
Design, setting, participants, & measurements Data for medical school graduates were obtained from the Association of American Medical Colleges and data for internal medicine and nephrology trainees from GME Track. ESRD data were obtained from U.S. Renal Data System (USRDS) annual reports.
Results A significant disparity continues to exist between the proportional race makeup of African-American nephrology fellows (3.8%) and ESRD patients (32%). The low numbers of African-American nephrology fellows, and consequently new nephrologists, in light of the increase in ESRD patients has important implications for patient-centered nephrology care.
Conclusions Efforts are needed to increase minority recruitment into nephrology training programs, to more closely balance the racial background of trainees and patients in hopes of fostering improved trust between ESRD caregivers and patients, increasing access to care, alleviating ESRD health care disparities, and improving patient care. Clin J Am Soc Nephrol 6: 390-394, 2011. doi: 10.2215/CJN.04450510
C1 [Onumah, Chavon; Rosenberg, Mark E.] Univ Minnesota, Minneapolis VA Med Ctr, Dept Med, Minneapolis, MN 55417 USA.
[Kimmel, Paul L.] NIDDK, Bethesda, MD USA.
RP Rosenberg, ME (reprint author), Univ Minnesota, Minneapolis VA Med Ctr, Dept Med, 1 Vet Dr, Minneapolis, MN 55417 USA.
EM rosen001@umn.edu
NR 42
TC 3
Z9 3
U1 0
U2 2
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 FEB
PY 2011
VL 6
IS 2
BP 390
EP 394
DI 10.2215/CJN.04450510
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA 722KJ
UT WOS:000287430800022
PM 21273375
ER
PT J
AU Visvader, JE
Smith, GH
AF Visvader, Jane E.
Smith, Gilbert H.
TI Murine Mammary Epithelial Stem Cells: Discovery, Function, and Current
Status
SO COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY
LA English
DT Article
ID ESTROGEN-RECEPTOR-ALPHA; PROGENITOR CELLS; GLAND DEVELOPMENT;
BREAST-CANCER; IN-VIVO; CHEMICAL CARCINOGENESIS; TGF-BETA-1 EXPRESSION;
SELF-RENEWAL; MOUSE; DIFFERENTIATION
AB An entire mammary epithelial outgrowth, capable of full secretory differentiation, may comprise the progeny of a single cellular antecedent, i.e., may be generated from a single mammary epithelial stem cell. Early studies showed that any portion of an intact murine mammary gland containing epithelium could recapitulate an entire mammary epithelial tree on transplantation into an epithelium-free mammary fat pad. More recent studies have shown that a hierarchy of mammary stem/progenitor cells exists among the mammary epithelium and that their behavior and maintenance is dependent on signals generated both locally and systemically. In this review, we have attempted to develop the scientific saga surrounding the discovery and characterization of the murine mammary stem/progenitor cell hierarchy and to suggest further approaches that will enhance our knowledge and understanding of these cells and their role in both normal development and neoplasia.
C1 [Smith, Gilbert H.] NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Visvader, Jane E.] Walter & Eliza Hall Inst Med Res, Stem Cells & Canc Div, Parkville, Vic 3050, Australia.
RP Smith, GH (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
EM gs4d@nih.gov
NR 85
TC 33
Z9 35
U1 0
U2 4
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1943-0264
J9 CSH PERSPECT BIOL
JI Cold Spring Harbor Perspect. Biol.
PD FEB
PY 2011
VL 3
IS 2
AR a004879
DI 10.1101/cshperspect.a004879
PG 14
WC Cell Biology
SC Cell Biology
GA 714LD
UT WOS:000286810200009
ER
PT J
AU Yang, YN
Remmers, EF
Ogunwole, CB
Kastner, DL
Gregersen, PK
Li, WT
AF Yang, Yaning
Remmers, Elaine F.
Ogunwole, Chukwuma B.
Kastner, Daniel L.
Gregersen, Peter K.
Li, Wentian
TI Effective sample size: Quick estimation of the effect of related samples
in genetic case-control association analyses
SO COMPUTATIONAL BIOLOGY AND CHEMISTRY
LA English
DT Article
DE Genetic association; Correlation; Variance inflation; Effective sample
size
ID GENOME-WIDE ASSOCIATION; COMPLEX HUMAN-DISEASES; CASE-CONTROL DESIGNS;
LINKAGE DISEQUILIBRIUM; RHEUMATOID-ARTHRITIS; POPULATION STRATIFICATION;
ESTIMATING EQUATIONS; ALLELE FREQUENCIES; CORRELATED DATA; INDIVIDUALS
AB Affected relatives are essential for pedigree linkage analysis, however, they cause a violation of the independent sample assumption in case-control association studies. To avoid the correlation between samples, a common practice is to take only one affected sample per pedigree in association analysis. Although several methods exist in handling correlated samples, they are still not widely used in part because these are not easily implemented, or because they are not widely known. We advocate the effective sample size method as a simple and accessible approach for case-control association analysis with correlated samples. This method modifies the chi-square test statistic, p-value, and 95% confidence interval of the odds-ratio by replacing the apparent number of allele or genotype counts with the effective ones in the standard formula, without the need for specialized computer programs. We present a simple formula for calculating effective sample size for many types of relative pairs and relative sets. For allele frequency estimation, the effective sample size method captures the variance inflation exactly. For genotype frequency, simulations showed that effective sample size provides a satisfactory approximation. A gene which is previously identified as a type 1 diabetes susceptibility locus, the interferon-induced helicase gene (IFIH1), is shown to be significantly associated with rheumatoid arthritis when the effective sample size method is applied. This significant association is not established if only one affected sib per pedigree were used in the association analysis. Relationship between the effective sample size method and other methods - the generalized estimation equation, variance of eigenvalues for correlation matrices, and genomic controls - are discussed. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Gregersen, Peter K.; Li, Wentian] N Shore LIJ Hlth Syst, Feinstein Inst Med Res, Robert S Boas Ctr Genom & Human Genet, Manhasset, NY 11030 USA.
[Yang, Yaning] Univ Sci & Technol China, Dept Stat & Finance, Hefei 230026, Anhui, Peoples R China.
[Remmers, Elaine F.; Ogunwole, Chukwuma B.; Kastner, Daniel L.] NIAMSD, Genet & Genom Branch, NIH, Bethesda, MD 20892 USA.
RP Li, WT (reprint author), N Shore LIJ Hlth Syst, Feinstein Inst Med Res, Robert S Boas Ctr Genom & Human Genet, 350 Community Dr, Manhasset, NY 11030 USA.
EM wli@nslij-genetics.org
OI Li, Wentian/0000-0003-1155-110X
FU National Institute of Health [R01-AR44422, NO1-AR22263]; National
Natural Science Foundation of China [10671189]; Chinese Academy of
Science [KJCX3-SYW-S02]; National Institute of Arthritis and
Musculoskeletal and Skin Diseases of the National Institutes of Health
FX WL and PKG are supported by the National Institute of Health grant
R01-AR44422, NO1-AR22263. YY is supported by the National Natural
Science Foundation of China Grant 10671189 and the Chinese Academy of
Science Grant No. KJCX3-SYW-S02. EFR, CBO and DLK was supported in part
by the Intramural Research Program of the National Institute of
Arthritis and Musculoskeletal and Skin Diseases of the National
Institutes of Health. We would like to thank Chris Amos, Yongchao Ge,
Jianxin Shi, Jan Freudenberg for helpful discussion.
NR 76
TC 7
Z9 7
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1476-9271
J9 COMPUT BIOL CHEM
JI Comput. Biol. Chem.
PD FEB
PY 2011
VL 35
IS 1
BP 40
EP 49
DI 10.1016/j.compbiolchem.2010.12.006
PG 10
WC Biology; Computer Science, Interdisciplinary Applications
SC Life Sciences & Biomedicine - Other Topics; Computer Science
GA 741EI
UT WOS:000288845500006
PM 21333602
ER
PT J
AU Moody, TW
Ito, T
Osefo, N
Jensen, RT
AF Moody, Terry W.
Ito, Tetsuhide
Osefo, Nuramy
Jensen, Robert T.
TI VIP and PACAP: recent insights into their functions/roles in physiology
and disease from molecular and genetic studies
SO CURRENT OPINION IN ENDOCRINOLOGY DIABETES AND OBESITY
LA English
DT Article
DE circadian rhythm; depression; diabetes; motility; neuroprotection;
neurotransmitter; obesity; PACAP; schizophrenia; VIP
ID CYCLASE-ACTIVATING POLYPEPTIDE; VASOACTIVE-INTESTINAL-PEPTIDE;
ADENYLATE-CYCLASE; DEFICIENT MICE; SUPRACHIASMATIC NUCLEI; RECEPTOR
AGONIST; NEUROPROTECTIVE PEPTIDE; SUSTAINED RELAXATION; EXTRACELLULAR
DOMAIN; VPAC(1) RECEPTORS
AB Purpose of review
Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) as well as the three classes of G-protein-coupled receptors mediating their effects, are widely distributed in the central nervous system (CNS) and peripheral tissues. These peptides are reported to have many effects in different tissues, which are physiological or pharmacological, and which receptor mediates which effect, has been difficult to determine, primarily due to lack of potent, stable, selective agonists/antagonists. Recently the use of animals with targeted knockout of the peptide or a specific receptor has provided important insights into their role in normal physiology and disease states.
Recent findings
During the review period, considerable progress and insights has occurred in the understanding of the role of VIP/PACAP as well as their receptors in a number of different disorders/areas. Particularly, insights into their roles in energy metabolism, glucose regulation, various gastrointestinal processes including gastrointestinal inflammatory conditions and motility and their role in the CNS as well as CNS diseases has greatly expanded.
Summary
PACAP/VIP as well as their three classes of receptors are important in many physiological/pathophysiological processes, some of which are identified in these studies using knockout animals. These studies may lead to new novel treatment approaches. Particularly important are their roles in glucose metabolism and on islets leading to possible novel approaches in diabetes; their novel anti-inflammatory, cytoprotective effects, their CNS neuroprotective effects, and their possible roles in diseases such as schizophrenia and chronic depression.
C1 [Jensen, Robert T.] NIDDK, Digest Dis Branch, NIH, Bethesda, MD 20892 USA.
[Moody, Terry W.; Osefo, Nuramy] NCI, Dept Hlth & Human Serv, Natl Canc Inst Off Director, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Ito, Tetsuhide] Kyushu Univ, Dept Med & Bioregulatory Sci, Grad Sch Med Sci, Fukuoka 812, Japan.
RP Jensen, RT (reprint author), NIDDK, Digest Dis Branch, NIH, Bldg 10,Room 9C-103, Bethesda, MD 20892 USA.
EM robertj@bdg10.niddk.nih.gov
FU NIDDK; NCI
FX The work was partially supported by intramural funds of NIDDK and NCI.
NR 92
TC 30
Z9 38
U1 2
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1752-296X
J9 CURR OPIN ENDOCRINOL
JI Curr. Opin. Endocrinol. Diabetes Obes.
PD FEB
PY 2011
VL 18
IS 1
BP 61
EP 67
DI 10.1097/MED.0b013e328342568a
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 697TW
UT WOS:000285542100012
PM 21157320
ER
PT J
AU Athar, M
Elmets, CA
Kopelovich, L
AF Athar, Mohammad
Elmets, Craig A.
Kopelovich, Levy
TI Pharmacological Activation of p53 in Cancer Cells
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Review
DE p53; cancer therapeutics; mutant p53 refolding; restoration of tumor
suppressor functions; mdm2
ID WILD-TYPE P53; SMALL-MOLECULE ANTAGONISTS; PRIMA-1 INDUCES APOPTOSIS;
MYELOID-LEUKEMIA CELLS; REGRESSION IN-VIVO; MUTANT P53; DEPENDENT
APOPTOSIS; TUMOR-SUPPRESSOR; GENE-THERAPY; COLORECTAL-CANCER
AB Tumor suppressor p53 is a transcription factor that regulates a large number of genes and guards against genomic instability. Under multiple cellular stress conditions, p53 functions to block cell cycle progression transiently unless proper DNA repair occurs. Failure of DNA repair mechanisms leads to p53-mediated induction of cell death programs. p53 also induces permanent cell cycle arrest known as cellular senescence. During neoplastic progression, p53 is often mutated and fails to efficiently perform these functions. It has been observed that cancers carrying a wild-type p53 may also have interrupted downstream p53 regulatory signaling leading to disruption in p53 functions. Therefore, strategies to reactivate p53 provide an attractive approach for blocking tumor pathogenesis and its progression. p53 activation may also lead to regression of existing early neoplastic lesions and therefore may be important in developing cancer chemoprevention protocols. A large number of small molecules capable of reactivating p53 have been developed and some are progressing through clinical trials for prospective human applications. However, several questions remain to be answered at this stage. For example, it is not certain if pharmacological activation of p53 will restore all of its multifaceted biological responses, assuming that the targeted cell is not killed following p53 activation. It remains to be demonstrated whether the distinct biological effects regulated by specific post-translationally modified p53 can effectively be restored by refolding mutant p53. Mutant p53 can be classified as a loss-of-function or gain-of-function protein depending on the type of mutation. It is also unclear whether reactivation of mutant p53 has similar consequences in cells carrying gain-of-function and loss-of-function p53 mutants. This review provides a description of various pharmacological approaches tested to activate p53 (both wild-type and mutant) and to assess the effects of activated p53 on neoplastic progression.
C1 [Athar, Mohammad; Elmets, Craig A.] Univ Alabama Birmingham, Dept Dermatol, Birmingham, AL 35294 USA.
[Athar, Mohammad; Elmets, Craig A.] Univ Alabama Birmingham, Skin Dis Res Ctr, Birmingham, AL 35294 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Athar, M (reprint author), Univ Alabama Birmingham, Dept Dermatol, Volker Hall,Room 509,1530 3rd Ave S, Birmingham, AL 35294 USA.
EM mathar@uab.edu
FU [R01 ES015323]; [R21ES017494]; [NCI NO1-CN-43300
261200433001C-521958]; [P30AR050948]
FX Grant Support from the following awards, R01 ES015323, R21ES017494, NCI
NO1-CN-43300 261200433001C-521958, P30AR050948.
NR 118
TC 20
Z9 20
U1 1
U2 18
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y26, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD FEB
PY 2011
VL 17
IS 6
BP 631
EP 639
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 768PI
UT WOS:000290947000010
PM 21391904
ER
PT J
AU Schelonka, RL
Maheshwari, A
Carlo, WA
Taylor, S
Hansen, NI
Schendel, DE
Thorsen, P
Skogstrand, K
Hougaard, DM
Higgins, RD
AF Schelonka, Robert L.
Maheshwari, Akhil
Carlo, Waldemar A.
Taylor, Sarah
Hansen, Nellie I.
Schendel, Diana E.
Thorsen, Poul
Skogstrand, Kristin
Hougaard, David M.
Higgins, Rosemary D.
CA NICHD Neonatal Res Network
TI T cell cytokines and the risk of blood stream infection in extremely low
birth weight infants
SO CYTOKINE
LA English
DT Article
DE Cytokine; Infection; Sepsis; Neonate
ID ONSET NEONATAL SEPSIS; DIAGNOSTIC MARKERS; INTERLEUKIN-6; DIVERSITY;
IMMUNITY; RECEPTOR; NETWORK; INNATE; HELPER
AB Cytokines mediate the host immune response to infectious micro-organisms. The objective of this study was to determine whether immune regulatory interleukins (IL-4, IL-5, IL-6, and IL-10) and inflammatory cytokines (Interferon-gamma [INF-gamma], tumor necrosis factor-beta [TNF-beta], IL-2, and IL-17) are associated with an increased risk of developing blood stream bacterial/fungal infection (BSI) in extremely low birth weight (ELBW) infants. ELBW infants from 17 NICHD Neonatal Research Network centers without early onset sepsis were studied. Cytokines were measured from blood on days 1, 3, 7, 14, and 21 after birth. 996 ELBW infants contributed a minimum of 4080 unique measurements for each cytokine during the five sampling periods. Infants with BSI had lower levels of the inflammatory cytokines IL-17 (p = 0.01), and higher levels of the regulatory cytokines, IL-6 (p = 0.01) and IL-10 (p < 0.001). Higher levels of regulatory cytokines relative to pro-inflammatory cytokines were associated with increased risk of BSI even after adjusting for confounding variables. In ELBW infants, the ratio of immune regulatory cytokines to inflammatory cytokines was associated with development of BSI. Altered maturation of regulatory and inflammatory cytokines may increase the risk of serious infection in this population. (C) 2010 Elsevier Ltd. All rights reserved.
C1 [Schelonka, Robert L.; Maheshwari, Akhil; Carlo, Waldemar A.] Univ Alabama Birmingham, Dept Pediat, Birmingham, AL USA.
[Taylor, Sarah; Hansen, Nellie I.] RTI Int, Stat & Epidemiol Unit, Res Triangle Pk, NC USA.
[Schendel, Diana E.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Thorsen, Poul] Lillebaelt Hosp, Dept Obstet & Gynecol, Kolding, Denmark.
[Skogstrand, Kristin; Hougaard, David M.] Statens Serum Inst, Dept Clin Biochem & Immunol, Sect Neonatal Screening & Hormones, DK-2300 Copenhagen, Denmark.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Schelonka, RL (reprint author), Oregon Hlth & Sci Univ, Mail Code CDRCP,707 SW Gaines St, Portland, OR 97239 USA.
EM schelonk@ohsu.edu
OI Skogstrand, Kristin/0000-0002-0026-3711
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
of Child Health and Human Development; Centers for Disease Control and
Prevention [Y1-HD-5000-01]
FX The National Institutes of Health, the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, and the Centers for
Disease Control and Prevention (via an Interagency Agreement
Y1-HD-5000-01) provided grant support for recruitment during 1999-2001
and data analysis for the Neonatal Research Network's Cytokines Study.
The funding agencies provided overall oversight for study conduct, but
all data analyses and interpretation were independent of the funding
agencies. We are indebted to our medical and nursing colleagues and the
infants and their parents who agreed to take part in this study.
NR 30
TC 21
Z9 22
U1 0
U2 6
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1043-4666
J9 CYTOKINE
JI Cytokine
PD FEB
PY 2011
VL 53
IS 2
BP 249
EP 255
DI 10.1016/j.cyto.2010.11.003
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Immunology
SC Biochemistry & Molecular Biology; Cell Biology; Immunology
GA 720HX
UT WOS:000287272700020
PM 21145756
ER
PT J
AU Roederer, M
AF Roederer, Mario
TI Interpretation of Cellular Proliferation Data: Avoid the Panglossian
SO CYTOMETRY PART A
LA English
DT Editorial Material
DE CFSE; mathematical modeling; precursor frequency; cell division
ID LYMPHOCYTE-PROLIFERATION; DIVISION
AB There are several statistics that may be calculated to characterize a cellular proliferation experiment. By far, the most commonly-reported statistic is the percent of cells in the final culture that have divided; however, this statistic has significant limitations. Other statistics provided by software modeling provide a much richer characterization of the biological response; however, their use also comes with caveats. Here, I discuss the practical application of these statistics, including their limitations and interdependencies, using hypothetical data. The goal of this perspective is to prevent the blind reliance or overly optimistic ("panglossian") interpretation of the statistics generated by software, so that researchers and reviewers have a more-informed basis for drawing conclusions from the data. Published 2011 Wiley-Liss, Inc.(dagger)
C1 NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Roederer, M (reprint author), NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, NIH, 40 Convent Dr,Room 5509, Bethesda, MD 20892 USA.
EM Roederer@nih.gov
NR 10
TC 40
Z9 40
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4922
J9 CYTOM PART A
JI Cytom. Part A
PD FEB
PY 2011
VL 79A
IS 2
BP 95
EP 101
DI 10.1002/cyto.a.21010
PG 7
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 715SW
UT WOS:000286908900003
PM 21265003
ER
PT J
AU Roederer, M
Nozzi, JL
Nason, MC
AF Roederer, Mario
Nozzi, Joshua L.
Nason, Martha C.
TI SPICE: Exploration and Analysis of Post-Cytometric Complex Multivariate
Datasets
SO CYTOMETRY PART A
LA English
DT Article
DE immunophenotyping; data analysis; subsets; multivariate; polyfunctional
ID T-CELL RESPONSES; FLOW-CYTOMETRY; HIV-1 INFECTION; REPLICATION;
PROTECTION; CORRELATE; AVIDITY; DISEASE; QUALITY; FUTURE
AB Polychromatic flow cytometry results in complex, multivariate datasets. To date, tools for the aggregate analysis of these datasets across multiple specimens grouped by different categorical variables, such as demographic information, have not been optimized. Often, the exploration of such datasets is accomplished by visualization of patterns with pie charts or bar charts, without easy access to statistical comparisons of measurements that comprise multiple components. Here we report on algorithms and a graphical interface we developed for these purposes. In particular, we discuss thresholding necessary for accurate representation of data in pie charts, the implications for display and comparison of normalized versus unnormalized data, and the effects of averaging when samples with significant background noise are present. Finally, we define a statistic for the nonparametric comparison of complex distributions to test for difference between groups of samples based on multi-component measurements. While originally developed to support the analysis of T cell functional profiles, these techniques are amenable to a broad range of datatypes. Published 2011 Wiley-Liss, Inc.(dagger)
C1 [Roederer, Mario] NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Nozzi, Joshua L.] NIAID, Bioinformat & Computat Biosci Branch, NIH, Bethesda, MD 20892 USA.
[Nason, Martha C.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
RP Roederer, M (reprint author), NIAID, ImmunoTechnol Sect, Vaccine Res Ctr, NIH, 40 Convent Dr,Room 5509, Bethesda, MD 20892 USA.
EM Roederer@nih.gov
FU NIAID; NIH
FX Grant sponsors: NIAID, NIH
NR 25
TC 297
Z9 297
U1 1
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4922
J9 CYTOM PART A
JI Cytom. Part A
PD FEB
PY 2011
VL 79A
IS 2
BP 167
EP 174
DI 10.1002/cyto.a.21015
PG 8
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 715SW
UT WOS:000286908900011
PM 21265010
ER
PT J
AU Kim, L
Brzostowski, J
Majithia, A
Lee, NS
McMains, V
Kimmel, AR
AF Kim, Leung
Brzostowski, Joseph
Majithia, Amit
Lee, Nam-Sihk
McMains, Vanessa
Kimmel, Alan R.
TI Combinatorial cell-specific regulation of GSK3 directs cell
differentiation and polarity in Dictyostelium
SO DEVELOPMENT
LA English
DT Article
DE cAMP; Cell polarity; Receptors; Protein phosphorylation; Chemotaxis;
Dictyostelium
ID GLYCOGEN-SYNTHASE KINASE-3; WNT SIGNAL-TRANSDUCTION; NEURONAL POLARITY;
TERMINAL DIFFERENTIATION; FATE SPECIFICATION; MITOTIC SPINDLE;
BETA-CATENIN; C. ELEGANS; DISCOIDEUM; PATHWAY
AB In Dictyostelium, the interaction of secreted cAMP with specific cell surface receptors regulates the activation/de-activation of GSK3, which mediates developmental cell patterning. In addition, Dictyostelium cells polarize in response to extracellular cAMP, although a potential role for GSK3 in this pathway has not been investigated. Previously, we had shown that ZAK1 was an activating tyrosine kinase for GSK3 function in Dictyostelium and we now identify ZAK2 as the other tyrosine kinase in the cAMP-activation pathway for GSK3; no additional family members exist. We also now show that tyrosine phosphorylation/activation of GSK3 by ZAK2 and ZAK1 separately regulate GSK3 in distinct differentiated cell populations, and that ZAK2 acts in both autonomous and non-autonomous pathways to regulate these cell-type differentiations. Finally, we demonstrate that efficient polarization of Dictyostelium towards cAMP depends on ZAK1-mediated tyrosine phosphorylation of GSK3. Combinatorial regulation of GSK3 by ZAK kinases in Dictyostelium guides cell polarity, directional cell migration and cell differentiation, pathways that extend the complexity of GSK3 signaling throughout the development of Dictyostelium.
C1 [Kim, Leung; Brzostowski, Joseph; Majithia, Amit; McMains, Vanessa; Kimmel, Alan R.] NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
[Kim, Leung; Lee, Nam-Sihk] Florida Int Univ, Dept Biol Sci, Miami, FL 33199 USA.
RP Kimmel, AR (reprint author), NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
EM ark1@helix.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX Ms J. Liu deserves appreciation for superb technical support. We thank
Dr A. Kuspa for advice on prespore purification and Dr B. Raaka for use
of the FACS. We are indebted to Drs Shaulsky, Kuspa and Zupan, and their
co-workers for their generosity in providing RNA-seq data prior to
publication (Parikh et al., 2010) and access to dictyExpress (Rot et
al., 2009) (http://www.ailab.si/dictyexpress/). Finally, we are grateful
for discussions with Drs T. Khruana and D. Rosel. This work was
supported by the Intramural Research Program of the National Institute
of Diabetes and Digestive and Kidney Diseases, National Institutes of
Health. A. M. is a Howard Hughes Medical Institute-National Institutes
of Health Research Scholar. Deposited in PMC for release after 6 months.
NR 57
TC 8
Z9 12
U1 3
U2 8
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0950-1991
J9 DEVELOPMENT
JI Development
PD FEB 1
PY 2011
VL 138
IS 3
BP 421
EP 430
DI 10.1242/dev.055335
PG 10
WC Developmental Biology
SC Developmental Biology
GA 702CS
UT WOS:000285872800004
PM 21205787
ER
PT J
AU Song, JK
Giniger, E
AF Song, Jeong K.
Giniger, Edward
TI Noncanonical Notch Function in Motor Axon Guidance Is Mediated by Rac
GTPase and the GEF1 Domain of Trio
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE Notch; Trio; Rac; Abl; axon guidance; Drosophila
ID ABL TYROSINE KINASE; NUCLEOTIDE-EXCHANGE FACTORS; ACTIN STRESS FIBERS;
RHO FAMILY GTPASES; GENETIC INTERACTIONS; C. ELEGANS; DROSOPHILA;
RECEPTOR; PROTEIN; MIDLINE
AB The receptor Notch interacts with the Abl tyrosine kinase signaling pathway to control axon growth and guidance in Drosophila motor neurons. In part, this is mediated by binding to Trio, a guanine nucleotide exchange factor (GEF) for Rho GTPases. We show here that one of the two GEF domains of Trio, the Rac-specific GEF1, is essential for Trio-dependent motor axon guidance and for the genetic suppression of Notch function in motor axon patterning, but the Rho-specific GEF2 domain is not. Consistent with this, we show that Rac, and not Rho1 or Cdc42, interacts genetically with Notch in a manner indistinguishable from that of bona fide Abl signaling components. We infer, therefore, that Rac is a key component of Abl signaling in Drosophila motor axons, and specifically that it is the crucial Rho GTPase in "noncanonical" Notch/Abl signaling. Developmental Dynamics 240:324-332, 2011. (C) 2011 Wiley-Liss, Inc.
C1 [Song, Jeong K.; Giniger, Edward] NINDS, Axon Guidance & Neural Connect Unit, Basic Neurosci Program, NIH, Bethesda, MD 20892 USA.
RP Giniger, E (reprint author), Room 1016,37 Convent Dr, Bethesda, MD 20892 USA.
EM ginigere@ninds.nih.gov
RI Giniger, Edward/C-1764-2015
OI Giniger, Edward/0000-0002-8340-6158
FU NIH [NINDS: Z01NS003013]
FX We thank K. Zinn, L. Belluscio and the members of the Giniger Lab for
comments on the manuscript, D. Crowner and Z. Liu for technical
assistance, the Bloomington Drosophila Stock Center for fly lines, and
Developmental Studies Hybridoma Bank for antibody reagents. E.G. was
funded in part by the Intramural Research Program of the NIH (NINDS:
Z01NS003013).
NR 51
TC 20
Z9 20
U1 0
U2 11
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1058-8388
J9 DEV DYNAM
JI Dev. Dyn.
PD FEB
PY 2011
VL 240
IS 2
BP 324
EP 332
DI 10.1002/dvdy.22525
PG 9
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 717VQ
UT WOS:000287075900003
PM 21246649
ER
PT J
AU Kang, L
Ayala, JE
Lee-Young, RS
Zhang, ZH
James, FD
Neufer, PD
Pozzi, A
Zutter, MM
Wasserman, DH
AF Kang, Li
Ayala, Julio E.
Lee-Young, Robert S.
Zhang, Zhonghua
James, Freyja D.
Neufer, P. Darrell
Pozzi, Ambra
Zutter, Mary M.
Wasserman, David H.
TI Diet-Induced Muscle Insulin Resistance Is Associated With Extracellular
Matrix Remodeling and Interaction With Integrin alpha(2)beta(1) in Mice
SO DIABETES
LA English
DT Article
ID TUMOR-NECROSIS-FACTOR; SKELETAL-MUSCLE; GENE-EXPRESSION; INDIVIDUAL
TISSUES; COLLAGEN GENE; ACTIVATION; ALPHA-2-BETA-1; ALPHA-1-BETA-1;
MECHANISM; RECEPTOR
AB OBJECTIVE-The hypothesis that high-fat (HF) feeding causes skeletal muscle extracellular matrix (ECM) remodeling in C57BL/6J mice and that this remodeling contributes to diet-induced muscle insulin resistance (IR) through the collagen receptor integrin alpha(2)beta(1) was tested.
RESEARCH DESIGN AND METHODS-The association between IR and ECM remodeling was studied in mice fed chow or HF diet. Specific genetic and pharmacological murine models were used to study effects of HF feeding on ECM in the absence of IR. The role of ECM-integrin interaction in IR was studied using hyperinsulinemic-euglycemic clamps on integrin alpha(2)beta(1)-null (itga2(-/-)), integrin alpha(1)beta(1)-null (itga1(-/-)), and wild-type littermate mice fed chow or HF. Integrin alpha(2)beta(1) and integrin alpha(1)beta(1) signaling pathways have opposing actions.
RESULTS-HF-fed mice had IR and increased muscle collagen (Col) III and ColIV protein; the former was associated with increased transcript, whereas the latter was associated with reduced matrix metalloproteinase 9 activity. Rescue of muscle IR by genetic muscle-specific mitochondria-targeted catalase overexpression or by the phosphodiesterase 5a inhibitor, sildenafil, reversed HF feeding effects on ECM remodeling and increased muscle vascularity. Collagen remained elevated in HF-fed itga2(-/-) mice. Nevertheless, muscle insulin action and vascularity were increased. Muscle IR in HF-fed itga1(-/-) mice was unchanged. Insulin sensitivity in chow-fed itga1(-/-) and itga2(-/-) mice was not different from wild-type littermates.
CONCLUSIONS-ECM collagen expansion is tightly associated with muscle IR. Studies with itga2(-/-) mice provide mechanistic insight for this association by showing that the link between muscle IR and increased collagen can be uncoupled by the absence of collagen-integrin alpha(2)beta(1) interaction. Diabetes 60:416-426, 2011
C1 [Kang, Li; Ayala, Julio E.; Lee-Young, Robert S.; James, Freyja D.; Wasserman, David H.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
[Ayala, Julio E.; Wasserman, David H.] Vanderbilt Univ, Mouse Metab Phenotyping Ctr, Nashville, TN 37232 USA.
[Zhang, Zhonghua; Zutter, Mary M.] Vanderbilt Univ, Dept Pathol, Nashville, TN 37232 USA.
[Neufer, P. Darrell] E Carolina Univ, Dept Exercise & Sport Sci & Physiol, Greenville, NC USA.
[Pozzi, Ambra] Vanderbilt Univ, Div Nephrol, Nashville, TN 37232 USA.
RP Kang, L (reprint author), Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
EM li.kang@vanderbilt.edu
FU National Institutes of Health [DK-54902, DK-59637]
FX This work was supported by National Institutes of Health Grants DK-54902
and DK-59637 (Mouse Metabolic Phenotyping Center).
NR 41
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U1 0
U2 4
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD FEB
PY 2011
VL 60
IS 2
BP 416
EP 426
DI 10.2337/db10-1116
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 719AR
UT WOS:000287172100009
PM 21270253
ER
PT J
AU Yanovski, JA
Krakoff, J
Salaita, CG
McDuffie, JR
Kozlosky, M
Sebring, NG
Reynolds, JC
Brady, SM
Calis, KA
AF Yanovski, Jack A.
Krakoff, Jonathan
Salaita, Christine G.
McDuffie, Jennifer R.
Kozlosky, Merel
Sebring, Nancy G.
Reynolds, James C.
Brady, Sheila M.
Calis, Karim A.
TI Effects of Metformin on Body Weight and Body Composition in Obese
Insulin-Resistant Children A Randomized Clinical Trial
SO DIABETES
LA English
DT Article
ID DEPENDENT DIABETES-MELLITUS; POLYCYSTIC-OVARY-SYNDROME; LIFE-STYLE
INTERVENTION; FAMILY-BASED TREATMENT; METABOLIC SYNDROME; CHILDHOOD
OBESITY; PEDIATRIC OBESITY; GLUCOSE-TOLERANCE; RISK-FACTORS; MASS INDEX
AB OBJECTIVE-Metformin can decrease adiposity and ameliorate obesity-related comorbid conditions, including abnormalities in glucose homeostasis in adolescents, but there are few data evaluating the efficacy of metformin among younger children. Our objective was to determine whether metformin treatment causes weight loss and improves obesity-related comorbidities in obese children, who are insulin-resistant.
RESEARCH DESIGN AND METHODS-This study was a randomized double-blind placebo-controlled trial consisting of 100 severely obese (mean BMI 34.6 +/- 6.6 kg/m(2)) insulin-resistant children aged 6-12 years, randomized to 1,000 mg metformin (n = 53) or placebo (n = 47) twice daily for 6 months, followed by open-label metformin treatment for 6 months. All children and their parents participated in a monthly dietitian-administered weight-reduction program.
RESULTS-Eighty-five percent completed the 6-month randomized phase. Children prescribed metformin had significantly greater decreases in BMI (difference -1.09 kg/m(2), CI -1.87 to -0.31, P = 0.006), body weight (difference -3.38 kg, CI -5.2 to -1.57, P < 0.001), BMI Z score (difference between metformin and placebo groups -0.07, CI -0.12 to -0.01, P = 0.02), and fat mass (difference -1.40 kg, CI -2.74 to -0.06, P = 0.04). Fasting plasma glucose (P = 0.007) and homeostasis model assessment (HOMA) insulin resistance index (P = 0.006) also improved more in metformin-treated children than in placebo-treated children. Gastrointestinal symptoms were significantly more prevalent in metformin-treated children, which limited maximal tolerated dosage in 17%. During the 6-month open-label phase, children treated previously with placebo decreased their BMI Z score; those treated continuously with metformin did not significantly change BMI Z score furl her.
CONCLUSIONS-Metformin had modest but favorable effects on body weight, body composition, and glucose homeostasis in obese insulin-resistant children participating in a low-intensity weight-reduction program. Diabetes 60:477-485, 2011
C1 [Yanovski, Jack A.; McDuffie, Jennifer R.; Brady, Sheila M.; Calis, Karim A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Growth & Obes, Program Dev Endocrinol & Genet, Bethesda, MD 20892 USA.
[Krakoff, Jonathan] Natl Inst Diabet & Digest & Kidney Dis NIDDK, Phoenix Epidemiol & Clin Res Branch, Bethesda, MD USA.
[Salaita, Christine G.; Kozlosky, Merel; Sebring, Nancy G.] NIH, Dept Nutr, Hatfield Clin Res Ctr, Bethesda, MD 20892 USA.
[Reynolds, James C.] NIH, Dept Diagnost Radiol & Imaging Sci, Hatfield Clin Res Ctr, Bethesda, MD 20892 USA.
[Calis, Karim A.] NIH, Dept Pharm, Hatfield Clin Res Ctr, Bethesda, MD 20892 USA.
RP Yanovski, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Growth & Obes, Program Dev Endocrinol & Genet, Bethesda, MD 20892 USA.
EM jy15i@nih.gov
OI Yanovski, Jack/0000-0001-8542-1637
FU Eunice Kennedy Shriver NICHD, NIH [Z01-HD-000641]; NCMHD, NIH; NIDDK;
Obecure
FX This study was supported by the Intramural Research Program of the
Eunice Kennedy Shriver NICHD, NIH (Grant Z01-HD-000641), and NCMHD, NIH
(both to J.A.Y.), and in part by NIDDK (J.K.).; J.A.Y. received a grant
from Obecure and has a material transfer agreement with Roche for
support of other obesity-medication treatment studies. No other
potential conflicts of interest relevant to this article were reported.
NR 51
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U1 0
U2 8
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD FEB
PY 2011
VL 60
IS 2
BP 477
EP 485
DI 10.2337/db10-1185
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 719AR
UT WOS:000287172100016
PM 21228310
ER
PT J
AU Palmer, ND
Hester, JM
An, SS
Adeyemo, A
Rotimi, C
Langefeld, CD
Freedman, BI
Ng, MCY
Bowden, DW
AF Palmer, Nicholette D.
Hester, Jessica M.
An, S. Sandy
Adeyemo, Adebowale
Rotimi, Charles
Langefeld, Carl D.
Freedman, Barry I.
Ng, Maggie C. Y.
Bowden, Donald W.
TI Resequencing and Analysis of Variation in the TCF7L2 Gene in African
Americans Suggests That SNP rs7903146 Is the Causal Diabetes
Susceptibility Variant
SO DIABETES
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; STAGE RENAL-DISEASE; COMMON VARIANTS; RISK
LOCI; TYPE-2; POPULATION; POLYMORPHISMS; REPLICATION; NEPHROPATHY;
FAMILY
AB OBJECTIVE-Variation in the transcription factor 7-like 2 (TCF7L2) locus is associated with type 2 diabetes across multiple ethnicities. The aim of this study was to elucidate which variant in TCF7L2 confers diabetes susceptibility in African Americans.
RESEARCH DESIGN AND METHODS-Through the evaluation of tagging single nucleotide polymorphisms (SNPs), type 2 diabetes susceptibility was limited to a 4.3-kb interval, which contains the YRI (African) linkage disequilibrium (LD) block containing rs7903146. To better define the relationship between type 2 diabetes risk and genetic variation we resequenced this 4.3-kb region in 96 African American DNAs. Thirty-three novel and 13 known SNPs were identified: 20 with minor allele frequencies (MAF) >0.05 and 12 with MAF >0.10. These polymorphisms and the previously identified DG10S478 microsatellite were evaluated in African American type 2 diabetic cases (n = 1,033) and controls (n = 1,106).
RESULTS-Variants identified from direct sequencing and databases were genotyped or imputed. Fifteen SNPs showed association with type 2 diabetes (P < 0.05) with rs7903146 being the most significant (P = 6.32 x 10(-6)). Results of imputation, haplotype, and conditional analysis of SNPs were consistent with rs7903146 being the trait-defining SNP. Analysis of the DG10S478 microsatellite, which is outside the 4.3-kb LD block, revealed consistent association of risk allele 8 with type 2 diabetes (odds ratio [OR] = 1.33; P = 0.022) as reported in European populations; however, allele 16 (MAF = 0.016 cases and 0.032 controls) was strongly associated with reduced risk (OR = 0.39; P = 5.02 x 10(-6)) in contrast with previous studies.
CONCLUSIONS-In African Americans, these observations suggest that rs7903146 is the trait-defining polymorphism associated with type 2 diabetes risk. Collectively, these results support ethnic differences in type 2 diabetes associations. Diabetes 60:662-668, 2011
C1 [Palmer, Nicholette D.; An, S. Sandy; Bowden, Donald W.] Wake Forest Univ, Dept Biochem, Winston Salem, NC 27109 USA.
[Palmer, Nicholette D.; Hester, Jessica M.; An, S. Sandy; Ng, Maggie C. Y.; Bowden, Donald W.] Wake Forest Univ, Ctr Human Genom, Winston Salem, NC 27109 USA.
[Palmer, Nicholette D.; Hester, Jessica M.; An, S. Sandy; Ng, Maggie C. Y.; Bowden, Donald W.] Wake Forest Univ, Ctr Diabet Res, Winston Salem, NC 27109 USA.
[Hester, Jessica M.] Wake Forest Univ, Program Mol Genet & Genom, Winston Salem, NC 27109 USA.
[Adeyemo, Adebowale; Rotimi, Charles] NHGRI, Ctr Res Genom & Global Hlth, Bethesda, MD 20892 USA.
[Langefeld, Carl D.] Wake Forest Univ, Dept Biostat Sci, Winston Salem, NC 27109 USA.
[Freedman, Barry I.] Wake Forest Univ, Dept Internal Med, Nephrol Sect, Winston Salem, NC 27109 USA.
[Ng, Maggie C. Y.] Wake Forest Univ, Dept Pediat, Winston Salem, NC 27109 USA.
RP Bowden, DW (reprint author), Wake Forest Univ, Dept Biochem, Winston Salem, NC 27109 USA.
EM dbowden@wfubmc.edu
OI Adeyemo, Adebowale/0000-0002-3105-3231
FU National Institutes of Health [K99-DK081350, R01-DK066358, R01-DK053591,
R01-HL56266, R01-DK070941]; General Clinical Research Center of the Wake
Forest University School of Medicine [M01-RR07122]
FX This work was supported by National Institutes of Health grants
K99-DK081350 (to N.D.P.), R01-DK066358 (to D.W.B.), R01-DK053591 (to
D.W.B.), R01-HL56266 (to B.I.F.), and R01-DK070941 (to B.I.F.), and in
part by the General Clinical Research Center of the Wake Forest
University School of Medicine Grant M01-RR07122.
NR 34
TC 38
Z9 39
U1 1
U2 4
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0012-1797
J9 DIABETES
JI Diabetes
PD FEB
PY 2011
VL 60
IS 2
BP 662
EP 668
DI 10.2337/db10-0134
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 719AR
UT WOS:000287172100037
PM 20980453
ER
PT J
AU Liu, JK
Fox, CS
Hickson, DA
May, WL
Ding, JZ
Carr, JJ
Taylor, HA
AF Liu, Jiankang
Fox, Caroline S.
Hickson, DeMarc A.
May, Warren L.
Ding, Jingzhong
Carr, J. Jeffery
Taylor, Herman A.
TI Pericardial Fat and Echocardiographic Measures of Cardiac Abnormalities
The Jackson Heart Study
SO DIABETES CARE
LA English
DT Article
ID EPICARDIAL ADIPOSE-TISSUE; LEFT-VENTRICULAR HYPERTROPHY; DISEASE
RISK-FACTORS; OBESITY; ATHEROSCLEROSIS; DYSFUNCTION; POPULATION;
ASSOCIATION; GUIDELINES; COMMUNITY
AB OBJECTIVE-Pericardial adipose tissue (PAT), a regional fat depot adjacent to the myocardium, may mediate the complex relation between obesity and cardiac left ventricular (LV) abnormalities. We sought to evaluate the association of PAT with echocardiographic measures of LV abnormalities in the Jackson Heart Study (JHS).
RESEARCH DESIGN AND METHODS-A total of 1,414 African Americans (35% men; mean age 58 years) from the JHS underwent computed tomographic assessment of PAT and abdominal visceral adipose tissue (VAT) from 2007 to 2009 and echocardiography examination between 2000 and 2004. Echocardiographic measures of left atrial (LA) internal diameter, LV mass, LV ejection fraction (LVEF), and E-wave velocity-to-A-wave velocity ratio (E/A ratio) were examined in relation to PAT, VAT, BMI, and waist circumference (WC).
RESULTS-All adiposity measures were positively correlated with LA diameter and LV mass and negatively correlated with E/A ratio (P = 0.02 to 0.0001) and were not with LVEF (P = 0.36-0.61). In women, per 1-SD increment of PAT, we observed association with higher LV mass (9.0 +/- 1.7 gm, P = 0.0001) and LA diameter (1.0 +/- 0.1 mm, P = 0.0001). However, the magnitude of the association between PAT and cardiac measures was similar compared with VAT (P = 0.65 [LV mass]; P = 0.26 [LA diameter]) and was smallercompared with BM I (P = 0.002 [LV mass]; P = 0.01 [LA diameter]) and WC (P = 0.009 [LA diameter]).
CONCLUSIONS-PAT is correlated with echocardiographic measures of cardiac LV abnormalities, but the association is not stronger than other adiposity measures.
C1 [Liu, Jiankang; Hickson, DeMarc A.; May, Warren L.; Taylor, Herman A.] Jackson State Univ, Univ Mississippi, Med Ctr, Jackson Heart Study, Jackson, MS USA.
[Fox, Caroline S.] Brigham & Womens Hosp, Dept Med, Div Endocrinol Diabet & Metab, NHLBI,Framingham Heart Study, Boston, MA 02115 USA.
[Fox, Caroline S.] Harvard Univ, Sch Med, Boston, MA USA.
[Ding, Jingzhong] Wake Forest Univ, Bowman Gray Sch Med, Sticht Ctr Aging, Winston Salem, NC USA.
[Carr, J. Jeffery] Wake Forest Univ, Bowman Gray Sch Med, Dept Radiol, Winston Salem, NC USA.
RP Liu, JK (reprint author), Jackson State Univ, Univ Mississippi, Med Ctr, Jackson Heart Study, Jackson, MS USA.
EM jliu@umc.edu
RI Carr, John/A-1938-2012
OI Carr, John/0000-0002-4398-8237
FU National Heart, Lung, and Blood Institute (NHLBI) [N01-HC-95170,
N01-HC-95171, N01-C-95172]; National Center on Minority Health and
Health Disparities (NCMHD)
FX The JHS is supported by the National Heart, Lung, and Blood Institute
(NHLBI) and the National Center on Minority Health and Health
Disparities (NCMHD). Funding for H.A.T. was provided under contracts
N01-HC-95170, N01-HC-95171, and N01-C-95172 from the NHLBI and the
NCMHD.
NR 25
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U1 0
U2 2
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD FEB
PY 2011
VL 34
IS 2
BP 341
EP 346
DI 10.2337/dc10-1312
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 722LO
UT WOS:000287433900018
PM 21228247
ER
PT J
AU Wang, WY
Lee, ET
Howard, BV
Fabsitz, RR
Devereux, RB
Welty, TK
AF Wang, Wenyu
Lee, Elisa T.
Howard, Barbara V.
Fabsitz, Richard R.
Devereux, Richard B.
Welty, Thomas K.
TI Fasting Plasma Glucose and Hemoglobin A(1c) in Identifying and
Predicting Diabetes The Strong Heart Study
SO DIABETES CARE
LA English
DT Article
ID OPERATING CHARACTERISTIC CURVES; CARDIOVASCULAR-DISEASE;
AMERICAN-INDIANS; HIGH-RISK; METABOLIC SYNDROME; PREVALENCE; MELLITUS;
AREAS; POPULATION; TOLERANCE
AB OBJECTIVE-To compare fasting plasma glucose (FPG) and HbA(1c) in identifying and predicting type 2 diabetes in a population with high rates of diabetes.
RESEARCH DESIGN AND METHODS-Diabetes was defined as an FPG level >= 126 mg/dL or an HbA(1c) level >= 6.5%. Data collected from the baseline and second exams (1989-1995) of the Strong Heart Study were used.
RESULTS-For cases of diabetes identified by FPG >= 126 mg/dL, using HbA(1c) >= 6.5% at the initial and 4-year follow-up diabetes screenings (or in identifying incident cases in 4 years) among undiagnosed participants left 46% and 59% of cases of diabetes undetected, respectively, whereas for cases identified by HbA(1c) >= 6.5%, using FPG >= 126 mg/dL left 11% and 59% unidentified, respectively. Age, waist circumference, urinary albumin-to-creatinine ratio, and baseline FPG and HbA(1c) levels were common significant risk factors for incident diabetes defined by either FPG or HbA(1c); triglyceride levels were significant for diabetes defined by HbA(1c) alone, and blood pressure and sibling history of diabetes were significant for diabetes defined by FPG alone. Using both the baseline FPG and HbA(1c) in diabetes prediction identified more people at risk than using either measure alone.
CONCLUSIONS-Among undiagnosed participants, using HbA(1c) alone in initial diabetes screening identifies fewer cases of diabetes than FPG, and using either FPG or HbA(1c) alone cannot effectively identify diabetes in a 4-year periodic successive diabetes screening or incident cases of diabetes in 4 years. Using both criteria may identify more people at risk. The proposed models using the commonly available clinical measures can be applied to assessing the risk of incident diabetes using either criterion.
C1 [Wang, Wenyu; Lee, Elisa T.] Univ Oklahoma, Hlth Sci Ctr, Coll Publ Hlth, Ctr Amer Indian Hlth Res, Oklahoma City, OK USA.
[Howard, Barbara V.] MedStar Hlth Res Inst, Washington, DC USA.
[Fabsitz, Richard R.] NHLBI, Epidemiol & Biometry Program, Bethesda, MD 20892 USA.
[Devereux, Richard B.] Weill Cornell Med Coll, New York, NY USA.
[Welty, Thomas K.] Missouri Breaks Ind Res Inc, Timber Lake, SD USA.
RP Wang, WY (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Publ Hlth, Ctr Amer Indian Hlth Res, Oklahoma City, OK USA.
EM wenyu-wang@ouhsc.edu
FU National Heart, Lung, and Blood Institute [UO1 HL-41642, UO1 HL-41652,
UO1 HL-41654, U01-HL65521]; American Indian tribes/communities; Indian
Health Service
FX This study was supported by grants UO1 HL-41642, UO1 HL-41652, UO1
HL-41654, and U01-HL65521 from the National Heart, Lung, and Blood
Institute.; The authors express their appreciation to the 13
participating American Indian tribes/communities, the Indian Health
Service, and the participants for their support and assistance.
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PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD FEB
PY 2011
VL 34
IS 2
BP 363
EP 368
DI 10.2337/dc10-1680
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 722LO
UT WOS:000287433900022
PM 21270194
ER
PT J
AU James, C
Bullard, KM
Rolka, DB
Geiss, LS
Williams, DE
Cowie, CC
Albright, A
Gregg, EW
AF James, Cherie
Bullard, Kai McKeever
Rolka, Deborah B.
Geiss, Linda S.
Williams, Desmond E.
Cowie, Catherine C.
Albright, Ann
Gregg, Edward W.
TI Implications of Alternative Definitions of Prediabetes for Prevalence in
US Adults
SO DIABETES CARE
LA English
DT Article
ID IMPAIRED GLUCOSE-TOLERANCE; INCIDENT CARDIOVASCULAR EVENTS; DIABETES
PREVENTION PROGRAM; LIFE-STYLE; GLYCATED HEMOGLOBIN; FASTING GLYCEMIA;
RISK; DIAGNOSIS; MELLITUS; IMPACT
AB OBJECTIVE-To compare the prevalence of prediabetes using A1C, fasting plasma glucose (FPG), and oral glucose tolerance test (OGTT) criteria, and to examine the degree of agreement between the measures.
RESEARCH DESIGN AND METHODS-We used the 2005-2008 National Health and Nutrition Examination Surveys to classify 3,627 adults aged >= 18 years without diabetes according to their prediabetes status using A1C, FPG, and OGTT. We compared the prevalence of prediabetes according to different measures and used conditional probabilities to examine agreement between measures.
RESULTS-In 2005-2008, the crude prevalence of prediabetes in adults >= 18 aged years was 14.2% for A1C 5.7-6.4% (A1C5.7), 26.2% for FPG 100-125 mg/dL (IFG100), 7.0% for FPG 110-125 mg/dL (IFG110), and 13.7% for OGTT 140-199 mg/dL (IGT). Prediabetes prevalence varied by age, sex, and race/ethnicity, and there was considerable discordance between measures of prediabetes. Among those with IGT, 58.2, 23.4, and 32.3% had IFG100, IFG110, and A1C5.7, respectively, and 67.1% had the combination of either A1C5.7 or IFG100.
CONCLUSIONS-The prevalence of prediabetes varied by the indicator used to measure risk; there was considerable discordance between indicators and the characteristics of individuals with prediabetes. Programs to prevent diabetes may need to consider issues of equity, resources, need, and efficiency in targeting their efforts.
C1 [Bullard, Kai McKeever; Rolka, Deborah B.; Geiss, Linda S.; Williams, Desmond E.; Albright, Ann; Gregg, Edward W.] Ctr Dis Control & Prevent, Div Diabet Translat, Atlanta, GA 30333 USA.
[James, Cherie] RTI Int, Atlanta Reg Off, Atlanta, GA USA.
[Cowie, Catherine C.] NIDDK, NIH, Bethesda, MD USA.
RP Geiss, LS (reprint author), Ctr Dis Control & Prevent, Div Diabet Translat, Atlanta, GA 30333 USA.
EM lgeiss@cdc.gov
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U1 0
U2 5
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD FEB
PY 2011
VL 34
IS 2
BP 387
EP 391
DI 10.2337/dc10-1314
PG 5
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 722LO
UT WOS:000287433900026
PM 21270196
ER
PT J
AU Bankoski, A
Harris, TB
McClain, JJ
Brychta, RJ
Caserotti, P
Chen, KY
Berrigan, D
Troiano, RP
Koster, A
AF Bankoski, Andrea
Harris, Tamara B.
McClain, James J.
Brychta, Robert J.
Caserotti, Paolo
Chen, Kong Y.
Berrigan, David
Troiano, Richard P.
Koster, Annemarie
TI Sedentary Activity Associated With Metabolic Syndrome Independent of
Physical Activity
SO DIABETES CARE
LA English
DT Article
ID CARDIOVASCULAR-DISEASE; UNITED-STATES; TIME; RISK; ADULTS; INDIVIDUALS;
BEHAVIOR; OBESITY
AB OBJECTIVE-This study examined the association between objectively measured sedentary activity and metabolic syndrome among older adults.
RESEARCH DESIGN AND METHODS-Data were from 1,367 men and women, aged a >= 60 years who participated in the 2003-2006 National Health and Nutrition Examination Survey (NHANES). Sedentary time during waking hours was measured by an accelerometer (<100 counts per minute). A sedentary bout was defined as a period of time >5 mm. A sedentary break was defined as an interruption in sedentary time (>= 100 counts per minute). Metabolic syndrome was defined according to the Adult Treatment Panel (ATP) III criteria.
RESULTS-On average, people spent 9.5 h (65% of wear time) as sedentary. Compared with people without metabolic syndrome, people with metabolic syndrome spent a greater percentage of time as sedentary (67.3 vs. 62.2%), had longer average sedentary bouts (17.7 vs. 16.7 min), had lower intensity during sedentary time (14.8 vs. 15.8 average counts per minute), and had fewer sedentary breaks (82.3 vs. 86.7), adjusted for age and sex (all P < 0.01). A higher percentage of time sedentary and fewer sedentary breaks were associated with a significantly greater likelihood of metabolic syndrome after adjustment for age, sex, ethnicity, education, alcohol consumption, smoking, BMI, diabetes, heart disease, and physical activity. The association between intensity during sedentary time and metabolic syndrome was borderline significant.
CONCLUSIONS-The proportion of sedentary time was strongly related to metabolic risk, independent of physical activity. Current results suggest older people may benefit from reducing total sedentary time and avoiding prolonged periods of sedentary time by increasing the number of breaks during sedentary time.
C1 [Bankoski, Andrea; Harris, Tamara B.; Caserotti, Paolo; Koster, Annemarie] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Bankoski, Andrea] George Mason Univ, Global & Community Hlth Dept, Fairfax, VA 22030 USA.
[McClain, James J.] NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, Bethesda, MD 20892 USA.
[Brychta, Robert J.; Chen, Kong Y.] NIDDK, Bethesda, MD USA.
[Koster, Annemarie] Maastricht Univ Med Ctr, Dept Internal Med, Sch Publ Hlth & Primary Care, Maastricht, Netherlands.
RP Koster, A (reprint author), NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
EM kostera@mail.nih.gov
RI Koster, Annemarie/E-7438-2010;
OI Troiano, Richard/0000-0002-6807-989X; Chen, Kong/0000-0002-0306-1904
FU National Institutes of Health, National Institute on Aging
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Institute on Aging.
NR 24
TC 150
Z9 155
U1 2
U2 32
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD FEB
PY 2011
VL 34
IS 2
BP 497
EP 503
DI 10.2337/dc10-0987
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 722LO
UT WOS:000287433900047
PM 21270206
ER
PT J
AU Sacks, DB
AF Sacks, David B.
TI A1C Versus Glucose Testing: A Comparison
SO DIABETES CARE
LA English
DT Review
ID NUTRITION EXAMINATION SURVEY; IRON-DEFICIENCY ANEMIA; 3RD
NATIONAL-HEALTH; DIABETES-MELLITUS; HEMOGLOBIN A(1C); BLOOD-GLUCOSE;
BIOLOGICAL VARIATION; GLYCATED HEMOGLOBIN; TOLERANCE TESTS; HEPARINIZED
PLASMA
C1 NIH, Dept Lab Med, Bethesda, MD 20892 USA.
RP Sacks, DB (reprint author), NIH, Dept Lab Med, Bldg 10, Bethesda, MD 20892 USA.
EM sacksdb@mail.nih.gov
OI Sacks, David/0000-0003-3100-0735
NR 60
TC 115
Z9 119
U1 2
U2 16
PU AMER DIABETES ASSOC
PI ALEXANDRIA
PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0149-5992
J9 DIABETES CARE
JI Diabetes Care
PD FEB
PY 2011
VL 34
IS 2
BP 518
EP 523
DI 10.2337/dc10-1546
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 722LO
UT WOS:000287433900051
PM 21270207
ER
PT J
AU Gong, Q
Gregg, EW
Wang, J
An, Y
Zhang, P
Yang, W
Li, H
Li, H
Jiang, Y
Shuai, Y
Zhang, B
Zhang, J
Gerzoff, RB
Roglic, G
Hu, Y
Li, G
Bennett, PH
AF Gong, Q.
Gregg, E. W.
Wang, J.
An, Y.
Zhang, P.
Yang, W.
Li, H.
Li, H.
Jiang, Y.
Shuai, Y.
Zhang, B.
Zhang, J.
Gerzoff, R. B.
Roglic, G.
Hu, Y.
Li, G.
Bennett, P. H.
TI Long-term effects of a randomised trial of a 6-year lifestyle
intervention in impaired glucose tolerance on diabetes-related
microvascular complications: the China Da Qing Diabetes Prevention
Outcome Study
SO DIABETOLOGIA
LA English
DT Article
DE Diabetic retinopathy; Impaired glucose tolerance; Lifestyle
intervention; Nephropathy; Neuropathy
ID PIMA-INDIANS; VASCULAR-DISEASE; FOLLOW-UP; PREVALENCE; RETINOPATHY;
MORTALITY; MELLITUS; PROGRAM; AGE; IGT
AB We determined the effects of 6 years of lifestyle intervention in persons with impaired glucose tolerance (IGT) on the development of retinopathy, nephropathy and neuropathy over a 20 year period.
In 1986, 577 adults with IGT from 33 clinics in Da Qing, China were randomly assigned by clinic to a control group or one of three lifestyle intervention groups (diet, exercise, and diet plus exercise). Active intervention was carried out from 1986 to 1992. In 2006 we conducted a 20 year follow-up study of the original participants to compare the incidence of microvascular complications in the combined intervention group vs the control group.
Follow-up information was obtained on 542 (94%) of the 577 original participants. The cumulative incidence of severe retinopathy was 9.2% in the combined intervention group and 16.2% in the control group (p = 0.03, log-rank test). After adjusting for clinic and age, the incidence of severe retinopathy was 47% lower in the intervention group than the control group (hazard rate ratio 0.53, 95% CI 0.29-0.99, p = 0.048). No significant differences were found in the incidence of severe nephropathy (hazard rate ratio 1.05, 95% CI 0.16-7.05, intervention vs control, p = 0.96) or in the prevalence of neuropathy (8.6% vs 9.1%, p = 0.89) among the 20 year survivors.
Lifestyle intervention for 6 years in IGT was associated with a 47% reduction in the incidence of severe, vision-threatening retinopathy over a 20 year interval, primarily due to the reduced incidence of diabetes in the intervention group. However, similar benefits were not seen for nephropathy or neuropathy.
C1 [Gong, Q.; An, Y.; Yang, W.; Shuai, Y.; Zhang, B.; Li, G.] China Japan Friendship Hosp, Dept Endocrinol, Beijing 100029, Peoples R China.
[Gregg, E. W.; Zhang, P.; Gerzoff, R. B.] Ctr Dis Control & Prevent, Div Diabet Translat, Atlanta, GA USA.
[Wang, J.; Jiang, Y.; Zhang, J.; Hu, Y.] Da Qing First Hosp, Dept Cardiol, Da Qing, Peoples R China.
[Roglic, G.] World Hlth Org, Dept Chron Dis & Hlth Promot, Geneva, Switzerland.
[Gong, Q.; Bennett, P. H.] NIDDKD, Diabet Epidemiol & Clin Res Sect, NIH, Phoenix, AZ USA.
RP Li, G (reprint author), China Japan Friendship Hosp, Dept Endocrinol, Beijing 100029, Peoples R China.
EM guangwei_li@medmail.com.cn
FU CDC/WHO [U58/CCU424123-01-02]; China-Japan Friendship Hospital; Da Qing
First Hospital; American Diabetes Association; National Institute of
Diabetes and Digestive and Kidney Diseases
FX We thank the participants in the original Da Qing Diabetes Prevention
Study and the Da Qing Diabetes Prevention Outcome Study. We thank L.
Zhang and H. Zhang of the China-Japan Friendship Hospital for grading
the fundus photographs. We thank M. M. Engelgau for assistance in
acquiring funding and B.V. Howard for help in the design of the original
study. We also acknowledge L. Kong, the China Ministry of Health, the
leadership of the China-Japan Friendship Hospital, Da Qing First
Hospital, the Da Qing City Health Bureau and the Beijing and West
Pacific Regional Office of WHO for their general support. We thank W.C.
Knowler, C.C. Mason, R.G. Nelson and S. Kobes of the Diabetes
Epidemiology and Clinical Research Section, NIDDK, for statistical
assistance. Special thanks are due to the late Professor X. Pan as this
study would not have been possible without his leadership in the
original Da Qing Diabetes Prevention Study. This study was supported by
CDC/WHO Cooperative Agreement No. U58/CCU424123-01-02, China-Japan
Friendship Hospital and Da Qing First Hospital. Q. Gong received a
Mentor-based Postdoctoral Research Fellowship from the American Diabetes
Association and partial support from Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases. The
sponsors had no role in any aspect of the study design, in the
collection, analysis and interpretation of data, or in the development
of the manuscript.
NR 27
TC 92
Z9 100
U1 1
U2 20
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD FEB
PY 2011
VL 54
IS 2
BP 300
EP 307
DI 10.1007/s00125-010-1948-9
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 703SO
UT WOS:000286001800014
PM 21046360
ER
PT J
AU Jiang, XL
Gonzalez, FJ
Yu, AM
AF Jiang, Xi-Ling
Gonzalez, Frank J.
Yu, Ai-Ming
TI Drug-metabolizing enzyme, transporter, and nuclear receptor genetically
modified mouse models
SO DRUG METABOLISM REVIEWS
LA English
DT Review
DE Transgenic; knockout; humanized; drug metabolism; pharmacokinetics; drug
interaction; toxicity; cancer
ID CANCER RESISTANCE PROTEIN; NADPH-CYTOCHROME-P450 REDUCTASE GENE; HEPATIC
CYTOCHROME-P450 REDUCTASE; UDP-GLUCURONOSYLTRANSFERASE-1 UGT1 LOCUS;
LIVER-SPECIFIC EXPRESSION; ORGANIC ANION TRANSPORT; MDR1A
P-GLYCOPROTEIN; BLOOD-BRAIN-BARRIER; TRANSGENIC MICE; TARGETED
DISRUPTION
AB Determining the in vivo significance of a specific enzyme, transporter, or xenobiotic receptor in drug metabolism and pharmacokinetics may be hampered by gene multiplicity and complexity, levels of expression, and interaction between various components involved. The development of knockout (loss-of-function) and transgenic (gain-of-function) mouse models opens the door to the improved understanding of gene function in a whole-body system. There is also growing interest in the development of humanized mice to overcome species differences in drug metabolism and disposition. This review, therefore, aims to summarize and discuss some successful examples of drug-metabolizing enzyme, transporter, and nuclear-receptor genetically modified mouse models. These genetically modified mouse models have been proven as invaluable models for understanding in vivo function of drug-metabolizing enzymes, transporters, and xenobiotic receptors in drug metabolism and transport, as well as predicting potential drug-drug interaction and toxicity in humans. Nevertheless, concerns remain about interpretation of data obtained from such genetically modified mouse models, in which the expression of related genes is altered significantly.
C1 [Yu, Ai-Ming] SUNY Buffalo, Dept Pharmaceut Sci, Sch Pharm & Pharmaceut Sci, Buffalo, NY 14260 USA.
[Gonzalez, Frank J.] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
RP Yu, AM (reprint author), SUNY Buffalo, Dept Pharmaceut Sci, Sch Pharm & Pharmaceut Sci, 541 Cooke Hall, Buffalo, NY 14260 USA.
EM aimingyu@buffalo.edu
RI Jiang, Xiling/E-9197-2012
FU National Institute On Drug Abuse, National Institutes of Health (NIH;
Bethesda, Maryland, USA [R01DA021172]; Pfizer (New York, New York, USA)
FX AMY wants to thank the support (award number R01DA021172) from the
National Institute On Drug Abuse, National Institutes of Health (NIH;
Bethesda, Maryland, USA). XLJ is supported by a Pfizer (New York, New
York, USA) fellowship.
NR 139
TC 17
Z9 17
U1 0
U2 11
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0360-2532
J9 DRUG METAB REV
JI Drug Metab. Rev.
PD FEB
PY 2011
VL 43
IS 1
BP 27
EP 40
DI 10.3109/03602532.2010.512294
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 734PO
UT WOS:000288348000002
PM 20854191
ER
PT J
AU Kuhar, DT
Henderson, DK
AF Kuhar, David T.
Henderson, David K.
TI Pandemic (H1N1) 2009 and HIV Co-infection
SO EMERGING INFECTIOUS DISEASES
LA English
DT Letter
C1 [Kuhar, David T.] Ctr Dis Control & Prevent, Atlanta, GA 30333 USA.
[Henderson, David K.] NIH, Bethesda, MD 20892 USA.
RP Kuhar, DT (reprint author), Ctr Dis Control & Prevent, 1600 Clifton Rd NE,Mailstop A31, Atlanta, GA 30333 USA.
EM dkuhar@cdc.gov
NR 4
TC 0
Z9 0
U1 0
U2 1
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD FEB
PY 2011
VL 17
IS 2
BP 328
EP 328
DI 10.3201/eid1702.101775
PG 1
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 722MM
UT WOS:000287436400045
PM 21291627
ER
PT J
AU Eisenhofer, G
Pacak, K
Huynh, TT
Qin, N
Bratslavsky, G
Linehan, WM
Mannelli, M
Friberg, P
Grebe, SK
Timmers, HJ
Bornstein, SR
Lenders, JWM
AF Eisenhofer, Graeme
Pacak, Karel
Thanh-Truc Huynh
Qin, Nan
Bratslavsky, Gennady
Linehan, W. Marston
Mannelli, Massimo
Friberg, Peter
Grebe, Stefan K.
Timmers, Henri J.
Bornstein, Stefan R.
Lenders, Jacques W. M.
TI Catecholamine metabolomic and secretory phenotypes in phaeochromocytoma
SO ENDOCRINE-RELATED CANCER
LA English
DT Article
AB Phaeochromocytomas and paragangliomas (PPGLs) are highly heterogeneous tumours with variable catecholamine biochemical phenotypes and diverse hereditary backgrounds. This analysis of 18 catecholamine-related plasma and urinary biomarkers in 365 patients with PPGLs and 846 subjects without PPGLs examined how catecholamine metabolomic profiles are impacted by hereditary background and relate to variable hormone secretion. Catecholamine secretion was assessed in a subgroup of 156 patients from whom tumour tissue was available for measurements of catecholamine contents. Among all analytes, the free catecholamine O-methylated metabolites measured in plasma showed the largest tumour-related increases relative to the reference group. Patients with tumours due to multiple endocrine neoplasia type 2 and neurofibromatosis type 1 (NF1) showed similar catecholamine metabolite and secretory profiles to patients with adrenaline-producing tumours and no evident hereditary background. Tumours from these three patient groups contained higher contents of catecholamines, but secreted the hormones at lower rates than tumours that did not contain appreciable adrenaline, the latter including PPGLs due to von Hippel-Lindau (VHL) and succinate dehydrogenase (SDH) gene mutations. Large increases of plasma dopamine and its metabolites additionally characterised patients with PPGLs due to the latter mutations, whereas patients with NF1 were characterised by large increases in plasma dihydroxyphenylglycol and dihydroxyphenylacetic acid, the deaminated metabolites of noradrenaline and dopamine. This analysis establishes the utility of comprehensive catecholamine metabolite profiling for characterising the distinct and highly diverse catecholamine metabolomic and secretory phenotypes among different groups of patients with PPGLs. The data further suggest developmental origins of PPGLs from different populations of chromaffin cell progenitors.
C1 [Eisenhofer, Graeme; Qin, Nan] Univ Dresden, Inst Clin Chem & Lab Med, D-01307 Dresden, Germany.
[Eisenhofer, Graeme; Bornstein, Stefan R.; Lenders, Jacques W. M.] Univ Dresden, Dept Med, D-01307 Dresden, Germany.
[Pacak, Karel; Thanh-Truc Huynh] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Reprod & Adult Endocrinol Program, Bethesda, MD 20892 USA.
[Bratslavsky, Gennady; Linehan, W. Marston] NCI, Urol Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Mannelli, Massimo] Univ Florence, Dept Clin Pathophysiol, I-50139 Florence, Italy.
[Friberg, Peter] Univ Gothenburg, Sahlgrenska Acad & Univ Hosp, Dept Clin Physiol, SE-41345 Gothenburg, Sweden.
[Grebe, Stefan K.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN 55905 USA.
[Timmers, Henri J.] Radboud Univ Nijmegen, Med Ctr, Dept Endocrinol, NL-6525 GA Nijmegen, Netherlands.
[Lenders, Jacques W. M.] Radboud Univ Nijmegen, Med Ctr, Dept Internal Med, NL-6525 GA Nijmegen, Netherlands.
RP Eisenhofer, G (reprint author), Univ Dresden, Inst Clin Chem & Lab Med, Fetscherstr 74, D-01307 Dresden, Germany.
EM graeme.eisenhofer@uniklinikum-dresden.de
RI Lenders, J.W.M./L-4487-2015;
OI Mannelli, Massimo/0000-0002-8001-9857
FU Deutsche Forschungsgesellschaft (DFG) [515/6-1]; Center for Regenerative
Therapies Dresden; Dresden Tumour Center; Eunice Kennedy Shriver
National Institute of Child Health and Human Development and the Center
for Cancer Research, National Cancer Institute, at the National
Institutes of Health
FX This work was supported by the Deutsche Forschungsgesellschaft (DFG
grant no: 515/6-1), the Center for Regenerative Therapies Dresden and
the Dresden Tumour Center. Support from the intramural programs of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development and the Center for Cancer Research, National Cancer
Institute, at the National Institutes of Health, was not in the form of
any specific grant.
NR 45
TC 44
Z9 44
U1 0
U2 1
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 1351-0088
EI 1479-6821
J9 ENDOCR-RELAT CANCER
JI Endocr.-Relat. Cancer
PD FEB
PY 2011
VL 18
IS 1
BP 97
EP 111
DI 10.1677/ERC-10-0211
PG 15
WC Oncology; Endocrinology & Metabolism
SC Oncology; Endocrinology & Metabolism
GA V30ED
UT WOS:000208798400012
PM 21051559
ER
PT J
AU Martiniova, L
Perera, SM
Brouwers, FM
Alesci, S
Abu-Asab, M
Marvelle, AF
Kiesewetter, DO
Thomasson, D
Morris, JC
Kvetnansky, R
Tischler, AS
Reynolds, JC
Fojo, AT
Pacak, K
AF Martiniova, Lucia
Perera, Shiromi M.
Brouwers, Frederieke M.
Alesci, Salvatore
Abu-Asab, Mones
Marvelle, Amanda F.
Kiesewetter, Dale O.
Thomasson, David
Morris, John C.
Kvetnansky, Richard
Tischler, Arthur S.
Reynolds, James C.
Fojo, Antonio Tito
Pacak, Karel
TI Increased uptake of [I-123]meta-iodobenzylguanidine,
[F-18]fluorodopamine, and [H-3]norepinephrine in mouse pheochromocytoma
cells and tumors after treatment with the histone deacetylase inhibitors
SO ENDOCRINE-RELATED CANCER
LA English
DT Article
ID CHROMOBACTERIUM-VIOLACEUM NO-968; MALIGNANT PHEOCHROMOCYTOMA; I-131
METAIODOBENZYLGUANIDINE; METASTATIC PHEOCHROMOCYTOMA; THYROID-CANCER;
PHASE-II; SIGNAL THERAPY; MURINE MODEL; DEPSIPEPTIDE; EXPRESSION
AB [I-131]meta-iodobenzylguanidine ([I-131]MIBG) is the most commonly used treatment for metastatic pheochromocytoma and paraganglioma. It enters the chromaffin cells via the membrane norepinephrine transporter; however, its success has been modest. We studied the ability of histone deacetylase (HDAC) inhibitors to enhance [I-123]MIBG uptake by tumors in a mouse metastatic pheochromocytoma model. HDAC inhibitors are known to arrest growth, induce differentiation and apoptosis in various cancer cells, and further inhibit tumor growth. We report the in vitro and in vivo effects of two HDAC inhibitors, romidepsin and trichostatin A, on the uptake of [H-3]norepinephrine, [I-123]MIBG, and [F-18]fluorodopamine in a mouse model of metastatic pheochromocytoma. The effects of both inhibitors on norepinephrine transporter activity were assessed in mouse pheochromocytoma (MPC) cells by using the transporter-blocking agent desipramine and the vesicular-blocking agent reserpine. HDAC inhibitors increased [H-3] norepinephrine, [I-123]MIBG, and [F-18]fluorodopamine uptake through the norepinephrine transporter in MPC cells. In vivo, inhibitor treatment resulted in significantly increased uptake of [F-18]fluorodopamine positron emission tomography (PET) in pheochromocytoma liver metastases (19.1 +/- 3.2% injected dose per gram of tumor (%ID/g) compared to liver metastases in pretreatment scans 5.9 +/- 0.6%; P < 0.001). Biodistribution analysis after inhibitors treatment confirmed the PET results. The uptake of [I-123]MIBG was significantly increased in liver metastases 9.5 +/- 1.1% compared to 3.19 +/- 0.4% in untreated control liver metastases (P < 0.05). We found that HDAC inhibitors caused an increase in the amount of norepinephrine transporter expressed in tumors. HDAC inhibitors may enhance the therapeutic efficacy of [I-131]MIBG treatment in patients with advanced malignant pheochromocytoma and paraganglioma. Endocrine-Related Cancer (2011) 18 143-157
C1 [Martiniova, Lucia; Perera, Shiromi M.; Brouwers, Frederieke M.; Marvelle, Amanda F.; Pacak, Karel] NIH, E Kennedy Shriver Natl Inst Child Human & Dev, Sect Med Neuroendocrinol, Bethesda, MD 20892 USA.
[Alesci, Salvatore] NIMH, Clin Neuroendocrinol Branch, NIH, Bethesda, MD 20892 USA.
[Abu-Asab, Mones] NCI, Lab Pathol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kiesewetter, Dale O.] Natl Inst Biomed Imaging & Bioengn, Intramural Sci PRGMS, NIH, Bethesda, MD 20892 USA.
[Thomasson, David] Warren Grant Magnuson Clin Ctr, Lab Diagnost Radiol, Bethesda, MD 20892 USA.
[Morris, John C.] NCI, Metab Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Martiniova, Lucia; Kvetnansky, Richard] Slovak Acad Sci, Inst Expt Endocrinol, SK-83306 Bratislava, Slovakia.
[Tischler, Arthur S.] Tufts Univ, Dept Pathol, Sch Med & Tufts Med Ctr, Boston, MA 02111 USA.
[Reynolds, James C.] NIH, Dept Nucl Med, Clin Ctr, Bethesda, MD 20892 USA.
[Fojo, Antonio Tito] NCI, Med Oncol Branch, NIH, Ctr Canc Res, Bethesda, MD USA.
RP Pacak, K (reprint author), NIH, E Kennedy Shriver Natl Inst Child Human & Dev, Sect Med Neuroendocrinol, Bldg 10,Room 1E-3140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
OI Abu-Asab, Mones/0000-0002-4047-1232
FU NIH [R01-CA48017]; Pheo Para Alliance; National Institute of Child
Health and Human Development; National Cancer Institute; National
Institute of Biomedical Imaging and Bioengineering; National Institute
of Mental Health at the National Institutes of Health; [APVV-0148-06]
FX This research was supported in part by the NIH grant R01-CA48017 and a
grant from the Pheo Para Alliance (to A S Tischler) and APVV-0148-06 (to
R Kvetnansky). This work also was supported by the intramural program of
the National Institute of Child Health and Human Development, the
National Cancer Institute, the National Institute of Biomedical Imaging
and Bioengineering, and the National Institute of Mental Health at the
National Institutes of Health.
NR 69
TC 19
Z9 19
U1 0
U2 1
PU BIOSCIENTIFICA LTD
PI BRISTOL
PA EURO HOUSE, 22 APEX COURT WOODLANDS, BRADLEY STOKE, BRISTOL BS32 4JT,
ENGLAND
SN 1351-0088
EI 1479-6821
J9 ENDOCR-RELAT CANCER
JI Endocr.-Relat. Cancer
PD FEB
PY 2011
VL 18
IS 1
BP 143
EP 157
DI 10.1677/ERC-10-0090
PG 15
WC Oncology; Endocrinology & Metabolism
SC Oncology; Endocrinology & Metabolism
GA 709LP
UT WOS:000286439800015
PM 21098082
ER
PT J
AU Lee, HW
Muniyappa, R
Yan, X
Yue, LQ
Linden, EH
Chen, H
Hansen, BC
Quon, MJ
AF Lee, Ho-Won
Muniyappa, Ranganath
Yan, Xu
Yue, Lilly Q.
Linden, Ellen H.
Chen, Hui
Hansen, Barbara C.
Quon, Michael J.
TI Comparison between Surrogate Indexes of Insulin Sensitivity/Resistance
and Hyperinsulinemic Euglycemic Glucose Clamps in Rhesus Monkeys
SO ENDOCRINOLOGY
LA English
DT Article
ID HOMEOSTASIS MODEL ASSESSMENT; DEPENDENT DIABETES-MELLITUS; FASTING
PLASMA-GLUCOSE; REDUCES BLOOD-PRESSURE; GREEN TEA POLYPHENOL; METABOLIC
SYNDROME; NONHUMAN-PRIMATES; ISLET AMYLOIDOSIS; MACACA-MULATTA; CHECK
INDEX
AB The euglycemic glucose clamp is the reference method for assessing insulin sensitivity in humans and animals. However, clamps are ill-suited for large studies because of extensive requirements for cost, time, labor, and technical expertise. Simple surrogate indexes of insulin sensitivity/resistance including quantitative insulin-sensitivity check index (QUICKI) and homeostasis model assessment (HOMA) have been developed and validated in humans. However, validation studies of QUICKI and HOMA in both rats and mice suggest that differences in metabolic physiology between rodents and humans limit their value in rodents. Rhesus monkeys are a species more similar to humans than rodents. Therefore, in the present study, we evaluated data from 199 glucose clamp studies obtained from a large cohort of 86 monkeys with a broad range of insulin sensitivity. Data were used to evaluate simple surrogate indexes of insulin sensitivity/resistance (QUICKI, HOMA, Log HOMA, 1/HOMA, and 1/Fasting insulin) with respect to linear regression, predictive accuracy using a calibration model, and diagnostic performance using receiver operating characteristic. Most surrogates had modest linear correlations with SI(Clamp) (r approximate to 0.4-0.64) with comparable correlation coefficients. Predictive accuracy determined by calibration model analysis demonstrated better predictive accuracy of QUICKI than HOMA and Log HOMA. Receiver operating characteristic analysis showed equivalent sensitivity and specificity of most surrogate indexes to detect insulin resistance. Thus, unlike in rodents but similar to humans, surrogate indexes of insulin sensitivity/resistance including QUICKI and log HOMA may be reasonable to use in large studies of rhesus monkeys where it may be impractical to conduct glucose clamp studies. (Endocrinology 152: 414-423, 2011)
C1 [Lee, Ho-Won; Muniyappa, Ranganath; Chen, Hui; Quon, Michael J.] NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Yan, Xu; Yue, Lilly Q.] US FDA, Div Biostat, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
[Linden, Ellen H.; Hansen, Barbara C.] Univ S Florida, Obes Diabet & Aging Res Ctr, Dept Pediat, Coll Med, St Petersburg, FL 33701 USA.
[Linden, Ellen H.; Hansen, Barbara C.] Univ S Florida, Dept Internal Med, Coll Med, St Petersburg, FL 33701 USA.
RP Lee, HW (reprint author), NIH, Diabet Unit, Natl Ctr Complementary & Alternat Med, Bldg 10, Bethesda, MD 20892 USA.
RI Hansen, Barbara/J-8723-2012;
OI Hansen, Barbara/0000-0001-9646-3525; Quon, Michael/0000-0002-9601-9915;
Quon , Michael /0000-0002-5289-3707
FU National Center for Complementary and Alternative Medicine, National
Institutes of Health; American Diabetes Association
FX This work was supported in part by the Intramural Research Program,
National Center for Complementary and Alternative Medicine, National
Institutes of Health, and in part by a Clinical Research Award from the
American Diabetes Association (to M.J.Q.). The primate colony support
was via National Institutes of Health National Institute on Aging N01AG3
1012 and continues under National Institutes of Health
HHSN263200800022C, institutional, and private funds (to B.C.H.).
NR 42
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U1 0
U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
J9 ENDOCRINOLOGY
JI Endocrinology
PD FEB
PY 2011
VL 152
IS 2
BP 414
EP 423
DI 10.1210/en.2010-1164
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 709FA
UT WOS:000286422100012
PM 21209021
ER
PT J
AU Vlaanderen, J
Lan, Q
Kromhout, H
Rothman, N
Vermeulen, R
AF Vlaanderen, Jelle
Lan, Qing
Kromhout, Hans
Rothman, Nathaniel
Vermeulen, Roel
TI Occupational Benzene Exposure and the Risk of Lymphoma Subtypes: A
Meta-analysis of Cohort Studies Incorporating Three Study Quality
Dimensions
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Review
DE acute lymphocytic leukemia; benzene; chronic lymphocytic leukemia;
Hodgkin lymphoma; leukemia; meta-analysis; multiple myeloma; non-Hodgkin
lymphoma; occupational exposure
ID NON-HODGKIN-LYMPHOMA; PETROLEUM DISTRIBUTION WORKERS; INDUSTRY WIDE
MORTALITY; DOSE-RELATED INCIDENCE; OIL REFINERY WORKERS;
MULTIPLE-MYELOMA; FOLLOW-UP; UNITED-STATES; HEMATOLOGIC NEOPLASMS;
INTERLYMPH-CONSORTIUM
AB BACKGROUND: The use of occupational cohort studies to assess the association of benzene and lymphoma is complicated by problems with exposure misclassification, outcome classification, and low statistical power.
OBJECTIVE: We performed meta-analyses of occupational cohort studies for five different lymphoma categories: Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL), multiple myeloma (MM), acute lymphocytic leukemia (ALL), and chronic lymphocytic leukemia (CLL).
DATA EXTRACTION: We assessed three study quality dimensions to evaluate the impact of study quality variations on meta-relative risks (mRRs): stratification by the year of start of follow-up, stratification by the strength of the reported acute myelogenous leukemia association, and stratification by the quality of benzene exposure assessment.
DATA SYNTHESIS: mRRs for MM, ALL, and CLL increased with increasing study quality, regardless of the study quality dimension. mRRs for NHL also increased with increasing study quality, although this effect was less pronounced. We observed no association between occupational benzene exposure and HL.
CONCLUSIONS: Our meta-analysis provides support for an association between occupational benzene exposure and risk of MM, ALL, and CLL. The evidence for an association with NHL is less clear, but this is likely complicated by the etiologic heterogeneity of this group of diseases. Further consideration of the association between benzene and NHL will require delineation of risks by NHL subtype.
C1 [Vermeulen, Roel] Univ Utrecht, Inst Risk Assessment Sci, Div Environm Epidemiol, NL-3584 CK Utrecht, Netherlands.
[Lan, Qing; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RP Vermeulen, R (reprint author), Univ Utrecht, Inst Risk Assessment Sci, Div Environm Epidemiol, Jenalaan 18D, NL-3584 CK Utrecht, Netherlands.
EM R.C.H.Vermeulen@uu.nl
RI Vermeulen, Roel/F-8037-2011
OI Vermeulen, Roel/0000-0003-4082-8163
FU European Union [FOOD-CT-2005-513943]
FX This work was performed as part of the work package "Integrated Risk
Assessment" of the Environmental Cancer Risk, Nutrition, and Individual
Susceptibility Network of Excellence, operating within the European
Union 6th Framework Program, Priority 5: "Food Quality and Safety"
(FOOD-CT-2005-513943).
NR 99
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U1 0
U2 14
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD FEB
PY 2011
VL 119
IS 2
BP 159
EP 167
DI 10.1289/ehp.1002318
PG 9
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA 714IP
UT WOS:000286803400016
PM 20880796
ER
PT J
AU Metcalf, CJE
Klepac, P
Ferrari, M
Grais, RF
Djibo, A
Grenfell, BT
AF Metcalf, C. J. E.
Klepac, P.
Ferrari, M.
Grais, R. F.
Djibo, A.
Grenfell, B. T.
TI Modelling the first dose of measles vaccination: the role of maternal
immunity, demographic factors, and delivery systems
SO EPIDEMIOLOGY AND INFECTION
LA English
DT Article
DE Mathematical modelling; measles (rubeola); vaccine policy development
ID RUBELLA MMR VACCINE; AGE; MUMPS; EPIDEMICS; DYNAMICS; INFANTS;
IMMUNOGENICITY; TRANSMISSION; ANTIBODIES; EFFICACY
AB Measles vaccine efficacy is higher at 12 months than 9 months because of maternal immunity, but delaying vaccination exposes the children most vulnerable to measles mortality to infection. We explored how this trade-off changes as a function of regionally varying epidemiological drivers, e. g. demography, transmission seasonality, and vaccination coverage. High birth rates and low coverage both favour early vaccination, and initiating vaccination at 9-11 months, then switching to 12-14 months can reduce case numbers. Overall however, increasing the age-window of vaccination decreases case numbers relative to vaccinating within a narrow age-window (e. g. 9-11 months). The width of the age-window that minimizes mortality varies as a function of birth rate, vaccination coverage and patterns of access to care. Our results suggest that locally age-targeted strategies, at both national and sub-national scales, tuned to local variation in birth rate, seasonality, and access to care may substantially decrease case numbers and fatalities for routine vaccination.
C1 [Metcalf, C. J. E.; Klepac, P.; Grenfell, B. T.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Ferrari, M.] Penn State Univ, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Ferrari, M.; Grenfell, B. T.] NIH, Fogarty Int Ctr, Bethesda, MD USA.
[Grais, R. F.] Epictr, Paris, France.
RP Metcalf, CJE (reprint author), Princeton Univ, Dept Ecol & Evolutionary Biol, Eno Hall, Princeton, NJ 08544 USA.
EM cmetcalf@princeton.edu
FU Bill and Melinda Gates Foundation; Science and Technology Directorate,
Department of Homeland Security; Fogarty International Center, National
Institutes of Health
FX We thank Justin Lessler and two anonymous reviewers for comments on the
manuscript. This work was funded by the Bill and Melinda Gates
Foundation (C.J.E.M., P.K., B.T.G.); B.T.G. and M.F. were also supported
by the Research and Policy for Infectious Disease Dynamics Program
(RAPIDD) of the Science and Technology Directorate, Department of
Homeland Security, and the Fogarty International Center, National
Institutes of Health.
NR 29
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Z9 9
U1 1
U2 9
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0950-2688
J9 EPIDEMIOL INFECT
JI Epidemiol. Infect.
PD FEB
PY 2011
VL 139
IS 2
BP 265
EP 274
DI 10.1017/S0950268810001329
PG 10
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 703WU
UT WOS:000286012800013
PM 20525415
ER
PT J
AU Bae, EH
Theodore, WH
Fregni, F
Cantello, R
Pascual-Leone, A
Rotenberg, A
AF Bae, Erica Hyunji
Theodore, William H.
Fregni, Felipe
Cantello, Roberto
Pascual-Leone, Alvaro
Rotenberg, Alexander
TI An estimate of placebo effect of repetitive transcranial magnetic
stimulation in epilepsy
SO EPILEPSY & BEHAVIOR
LA English
DT Article
DE Repetitive transcranial magnetic stimulation; Epilepsy; Placebo
ID REFRACTORY EPILEPSY; CORTICAL DYSPLASIA; TRIAL; EEG
AB Objective: Low-frequency repetitive transcranial magnetic stimulation (rTMS) is emerging as a therapeutic tool in epilepsy. In recent years, several open-label trials have shown an encouraging reduction in seizure frequency in patients with epilepsy. However, the data from controlled trials are mixed with respect to antiepileptic rTMS efficacy, and the field would benefit from further carefully controlled trials. Prior to initiating new trials, it is important assess the magnitude of the placebo effect of presently used sham rTMS methods.
Methods: We systematically analyzed individual subject data from three placebo-controlled trials and measured the placebo effect at follow-up intervals of 2, 4, and 8 weeks after sham rTMS treatment. Given the relatively small subgroup sample size, placebo condition data were pooled for analysis.
Results: Three methods for sham rTMS were employed in the reviewed studies: (1) coil positioning orthogonal to the scalp, (2) a spring-loaded sham coil, and (3) a double active-sham coil. The placebo response overall was consistently low across follow-up intervals, both for median change in seizure frequency (Kruskal-Wallis, P > 0.4, df=2) and for responder (defined as >= 50% seizure frequency reduction) rate (Fisher's exact rest, P > 0.9, df = 2). The aggregate effect of the placebo condition was a 0-2% median seizure reduction rate and a responder rate of 16-20%.
Conclusion: We anticipate that these data will contribute to future power analysis as well as selection and design of sham rTMS methods for controlled rTMS trials. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Bae, Erica Hyunji; Rotenberg, Alexander] Harvard Univ, Sch Med, Dept Neurol, Childrens Hosp, Boston, MA 02115 USA.
[Bae, Erica Hyunji; Fregni, Felipe; Pascual-Leone, Alvaro; Rotenberg, Alexander] Harvard Univ, Sch Med, Berenson Allen Ctr Noninvas Brain Stimulat, Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA.
[Theodore, William H.] NIH, Bethesda, MD 20892 USA.
[Fregni, Felipe] Harvard Univ, Sch Med, Lab Neuromodulat, Spaulding Rehabil Hosp, Boston, MA 02115 USA.
[Cantello, Roberto] Amedeo Avogadro Univ, Dept Clin & Expt Med, Neurol Sect, Novara, Italy.
RP Rotenberg, A (reprint author), Harvard Univ, Sch Med, Dept Neurol, Childrens Hosp, Boston, MA 02115 USA.
EM alexander.rotenberg@childrens.harvard.edu
RI Cantello, Roberto/L-3786-2016
OI Cantello, Roberto/0000-0001-6999-5729
FU Siegel Family Fund for Epilepsy Research; National Institutes of Health
[K24 RR018875, UL1 RR025758]
FX A.R. acknowledges the Siegel Family Fund for Epilepsy Research for
support. A.P.L. received support through National Institutes of Health
Grants K24 RR018875 and UL1 RR025758.
NR 13
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U1 0
U2 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1525-5050
J9 EPILEPSY BEHAV
JI Epilepsy Behav.
PD FEB
PY 2011
VL 20
IS 2
BP 355
EP 359
DI 10.1016/j.yebeh.2010.12.005
PG 5
WC Behavioral Sciences; Clinical Neurology; Psychiatry
SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry
GA 727WN
UT WOS:000287833700033
PM 21216200
ER
PT J
AU Rossler, W
Angst, J
Gamma, A
Haker, H
Stulz, N
Merikangas, KR
Ajdacic-Gross, V
AF Roessler, Wulf
Angst, Jules
Gamma, Alex
Haker, Helene
Stulz, Niklaus
Merikangas, Kathleen R.
Ajdacic-Gross, Vladeta
TI Reappraisal of the interplay between psychosis and depression symptoms
in the pathogenesis of psychotic syndromes: results from a twenty-year
prospective community study
SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
LA English
DT Article
DE Subclinical psychosis; Schizotypy; Schizotypal personality disorder;
Depression; Community study; Epidemiological cohort
ID GENERAL-POPULATION; SCHIZOTYPAL PERSONALITY; SEPARATE DISEASES; ZURICH
COHORT; SCHIZOPHRENIA; EXPERIENCES; MODELS; DISORDER; EPISODES; SCL-90
AB The interplay of psychotic and affective symptoms is a crucial challenge in understanding the pathogenesis of psychosis. In this study, we analyzed the interplay between two subclinical psychosis symptoms dimensions, and one depression symptoms dimension, using longitudinal data from Zurich. The Zurich study started in 1979 with a representative sample of 591 participants who were aged 20/21. Follow-up interviews were conducted at age 23, 28, 30, 35, and 41. The psychiatric symptoms were assessed with a semi-structured interview and the SCL 90-R. In this study, we analyzed three SCL-90-R subscales: the depression symptoms dimension and two distinct symptoms dimensions of subclinical psychosis, one representing a schizophrenia nuclear symptom dimension, the other representing a schizotypal symptoms dimension. Modeling was done with hybrid latent growth models, thereby including simultaneous and cross-lagged effects. The interplay between the two subclinical psychosis symptoms dimensions and the depression symptoms dimension includes several intertwined pathways. The schizotypal symptoms dimension has strong direct effects on the schizophrenia nuclear symptoms dimension, but also on the depression symptoms dimension. The latter has for its part an effect on the schizophrenia nuclear symptoms dimension. The main driving force within the dynamic interplay between depression and psychosis symptoms is a schizotypal symptoms dimension, which represents social and interpersonal deficiencies, ideas of reference, suspiciousness, paranoid ideation, and odd behavior. It does not only directly influence subclinical nuclear schizophrenia symptoms but also the symptoms of depression.
C1 [Roessler, Wulf; Angst, Jules; Gamma, Alex; Haker, Helene; Stulz, Niklaus; Ajdacic-Gross, Vladeta] Univ Zurich, Psychiat Univ Hosp, Dept Gen & Social Psychiat, CH-8021 Zurich, Switzerland.
[Roessler, Wulf] Swiss Fed Inst Technol, Zurich, Switzerland.
[Merikangas, Kathleen R.] NIMH, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RP Rossler, W (reprint author), Univ Zurich, Psychiat Univ Hosp, Dept Gen & Social Psychiat, Militarstr 8, CH-8021 Zurich, Switzerland.
EM roessler@dgsp.uzh.ch
OI Ajdacic-Gross, Vladeta/0000-0002-7032-9237
FU Swiss National Science Foundation [32-50881.97]
FX The study was supported by the Swiss National Science Foundation (grant
# 32-50881.97).
NR 46
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U1 3
U2 16
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0940-1334
J9 EUR ARCH PSY CLIN N
JI Eur. Arch. Psych. Clin. Neurosci.
PD FEB
PY 2011
VL 261
IS 1
BP 11
EP 19
DI 10.1007/s00406-010-0123-0
PG 9
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 712KI
UT WOS:000286665200003
PM 20625755
ER
PT J
AU Ho, M
Kim, H
AF Ho, Mitchell
Kim, Heungnam
TI Glypican-3: A new target for cancer immunotherapy
SO EUROPEAN JOURNAL OF CANCER
LA English
DT Review
DE Glypicans; Immunotherapy; Biological markers; Liver neoplasms; Melanoma;
Ovarian neoplasms; Endodermal sinus tumour; Neuroblastoma; Wilms tumour
ID HUMAN HEPATOCELLULAR-CARCINOMA; GOLABI-BEHMEL-SYNDROME;
DEVELOPMENTALLY-REGULATED TRANSCRIPT; HUMAN LIVER-CANCER; CLEAR-CELL;
ONCOFETAL PROTEIN; TUMOR-MARKER; MOUSE MODEL; 3 ANTIBODY; EXPRESSION
AB Hepatocellular carcinoma (HCC) remains a common malignant cancer worldwide. There is an urgent need to identify new molecular targets for the development of novel therapeutic approaches. Herein, we review the structure, function and biology of glypican-3 (GPC3) and its role in human cancer with a focus on its potential as a therapeutic target for immunotherapy. GPC3 is a cell-surface protein that is over-expressed in HCC. Loss-of-function mutations of GPC3 cause Simpson-Golabi-Behmel syndrome (SGBS), a rare X-linked over-growth condition. GPC3 binds Wnt and Hedgehog (Hh) signalling proteins. GPC3 is also able to bind basic growth factors such as fibroblast growth factor 2 through its heparan sulphate glycan chains. GPC3 is a promising candidate for liver cancer therapy given that it shows high expression in HCC. An anti-GPC3 monoclonal antibody has shown anti-cancer activity in mice and its humanised IgG molecule is currently undergoing clinical evaluation in patients with HCC. There is also evidence that soluble GPC3 may be a useful serum biomarker for HCC. Published by Elsevier Ltd.
C1 [Ho, Mitchell; Kim, Heungnam] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Ho, M (reprint author), NCI, Mol Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Room 5002, Bethesda, MD 20892 USA.
EM homi@mail.nih.gov
RI Ho, Mitchell/F-5059-2015
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. We thank the
NIH Fellows Editorial Board for their review of the manuscript, and Yen
Phung and Anna Mazzuca for editorial assistance. 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 organisations imply endorsement by the US
Government.
NR 52
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U1 3
U2 33
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0959-8049
J9 EUR J CANCER
JI Eur. J. Cancer
PD FEB
PY 2011
VL 47
IS 3
BP 333
EP 338
DI 10.1016/j.ejca.2010.10.024
PG 6
WC Oncology
SC Oncology
GA 727ER
UT WOS:000287780900001
PM 21112773
ER
PT J
AU Artym, VV
Matsumoto, K
Mueller, SC
Yamada, KM
AF Artym, Vira V.
Matsumoto, Kazue
Mueller, Susette C.
Yamada, Kenneth M.
TI Dynamic membrane remodeling at invadopodia differentiates invadopodia
from podosomes
SO EUROPEAN JOURNAL OF CELL BIOLOGY
LA English
DT Article
DE Invadopodia; Podosomes; Cortactin; Focal adhesions; Invasion
ID EXTRACELLULAR-MATRIX DEGRADATION; ADHESION STRUCTURES; CELL STRUCTURES;
INVASION; OSTEOCLASTS; CORTACTIN; FIBROBLASTS; SITES; ORGANIZATION;
PROTEINS
AB Invadopodia are specialized actin-rich protrusions of metastatic tumor and transformed cells with crucial functions in ECM degradation and invasion. Although early electron microscopy studies described invadopodia as long filament-like protrusions of the cell membrane adherent to the matrix, fluorescence microscopy studies have focused on invadopodia as actin-cortactin aggregates localized to areas of ECM degradation. The absence of a clear conceptual integration of these two descriptions of invadopodial structure has impeded understanding of the regulatory mechanisms that govern invadopodia. To determine the relationship between the membrane filaments identified by electron microscopy and the actin-cortactin aggregates of invadopodia, we applied rapid live-cell high-resolution TIRF microscopy to examine cell membrane dynamics at the cortactin core of the invadopodia of human carcinoma cells. We found that cortactin docking to the cell membrane adherent to 2D fibronectin matrix initiates invadopodium assembly associated with the formation of an invadopodial membrane process that extends from a ventral cell membrane lacuna toward the ECM. The tip of the invadopodial process flattens as it interacts with the 2D matrix, and it undergoes constant rapid ruffling and dynamic formation of filament-like protrusions as the invadopodium matures. To describe this newly discovered dynamic relationship between the actin-cortactin core and invadopodial membranes, we propose a model of the invadopodial complex. Using TIRF microscopy, we also established that - in striking contrast to the invadopodium - membrane at the podosome of a macrophage fails to form any process- or filament-like membrane protrusions. Thus, the undulation and ruffling of the invadopodial membrane together with the formation of dynamic filament-like extensions from the invadopodial cortactin core defines invadopodia as invasive superstructures that are distinct from the podosomes. (C) 2010 Elsevier GmbH. All rights reserved.
C1 [Artym, Vira V.; Matsumoto, Kazue; Yamada, Kenneth M.] NIDCR, Lab Cell & Dev Biol, NIH, Bethesda, MD 20892 USA.
[Artym, Vira V.; Mueller, Susette C.] Georgetown Univ, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20057 USA.
RP Artym, VV (reprint author), NIDCR, Lab Cell & Dev Biol, NIH, 30 Convent Dr,Room 408, Bethesda, MD 20892 USA.
EM vartym@mail.nih.gov
OI Yamada, Kenneth/0000-0003-1512-6805
FU NCI [K99CA129205]; NIH/NIDCR [DE 000719]; NIH [R01 CA112673]
FX This work was supported by Pathway to Independence Award K99CA129205
from NCI (V.V.A.), NIH/NIDCR Intramural project DE 000719 (K.M.Y.), and
NIH R01 CA112673 (S.C.M.).
NR 26
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U1 2
U2 13
PU ELSEVIER GMBH, URBAN & FISCHER VERLAG
PI JENA
PA OFFICE JENA, P O BOX 100537, 07705 JENA, GERMANY
SN 0171-9335
J9 EUR J CELL BIOL
JI Eur. J. Cell Biol.
PD FEB-MAR
PY 2011
VL 90
IS 2-3
BP 172
EP 180
DI 10.1016/j.ejcb.2010.06.006
PG 9
WC Cell Biology
SC Cell Biology
GA 733UG
UT WOS:000288288100010
PM 20656375
ER
PT J
AU Windelinckx, A
De Mars, G
Huygens, W
Peeters, MW
Vincent, B
Wijmenga, C
Lambrechts, D
Delecluse, C
Roth, SM
Metter, EJ
Ferrucci, L
Aerssens, J
Vlietinck, R
Beunen, GP
Thomis, MA
AF Windelinckx, An
De Mars, Gunther
Huygens, Wim
Peeters, Maarten W.
Vincent, Barbara
Wijmenga, Cisca
Lambrechts, Diether
Delecluse, Christophe
Roth, Stephen M.
Metter, E. Jeffrey
Ferrucci, Luigi
Aerssens, Jeroen
Vlietinck, Robert
Beunen, Gaston P.
Thomis, Martine A.
TI Comprehensive fine mapping of chr12q12-14 and follow-up replication
identify activin receptor 1B (ACVR1B) as a muscle strength gene
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE complex trait; combined linkage and association analyses; family-based
association; genotype/phenotype association
ID GROWTH-FACTOR-BETA; MYOSTATIN PATHWAY GENES; FAMILY-BASED TESTS; WIDE
LINKAGE SCAN; SKELETAL-MUSCLE; QUANTITATIVE TRAITS; MUSCULAR STRENGTH;
MESSENGER-RNA; ASSOCIATION; MEN
AB Muscle strength is important in functional activities of daily living and the prevention of common pathologies. We describe the two-staged fine mapping of a previously identified linkage peak for knee strength on chr12q12-14. First, 209 tagSNPs in/around 74 prioritized genes were genotyped in 500 Caucasian brothers from the Leuven Genes for Muscular Strength study (LGfMS). Combined linkage and family-based association analyses identified activin receptor 1B (ACVR1B) and inhibin beta C (INHBC), part of the transforming growth factor beta pathway regulating myostatin - a negative regulator of muscle mass - signaling, for follow-up. Second, 33 SNPs, selected in these genes based on their likelihood to functionally affect gene expression/function, were genotyped in an extended sample of 536 LGfMS siblings. Strong associations between ACVR1B genotypes and knee muscle strength (P-values up to 0.00002) were present. Of particular interest was the association with rs2854464, located in a putative miR-24-binding site, as miR-24 was implicated in the inhibition of skeletal muscle differentiation. Rs2854464 AA individuals were similar to 2% stronger than G-allele carriers. The strength increasing effect of the A-allele was also observed in an independent replication sample (n=266) selected from the Baltimore Longitudinal Study of Aging and a Flemish Policy Research Centre Sport, Physical Activity and Health study. However, no genotype-related difference in ACVR1B mRNA expression in quadriceps muscle was observed. In conclusion, we applied a two-stage fine mapping approach, and are the first to identify and partially replicate genetic variants in the ACVR1B gene that account for genetic variation in human muscle strength. European Journal of Human Genetics (2011) 19, 208-215; doi:10.1038/ejhg.2010.173; published online 10 November 2010
C1 [Windelinckx, An; De Mars, Gunther; Huygens, Wim; Peeters, Maarten W.; Vincent, Barbara; Delecluse, Christophe; Beunen, Gaston P.; Thomis, Martine A.] Katholieke Univ Leuven, Res Ctr Exercise & Hlth, Dept Biomed Kinesiol, Fac Kinesiol & Rehabil Sci, B-3001 Leuven, Belgium.
[Wijmenga, Cisca] Univ Med Ctr Utrecht, Dept Med Genet, Complex Genet Sect, Utrecht, Netherlands.
[Lambrechts, Diether] VIB, Vesalius Res Ctr, Leuven, Belgium.
[Roth, Stephen M.] Univ Maryland, Sch Publ Hlth, Dept Kinesiol, College Pk, MD 20742 USA.
[Metter, E. Jeffrey; Ferrucci, Luigi] NIA, Clin Res Branch, Longitudinal Studies Sect, Baltimore, MD 21224 USA.
[Aerssens, Jeroen] Tibotec Bvba, Dept Translat Med Res, Mechelen, Belgium.
[Vlietinck, Robert] Katholieke Univ Leuven, Fac Med, Dept Human Genet, Clin Genet Sect, B-3001 Leuven, Belgium.
RP Thomis, MA (reprint author), Katholieke Univ Leuven, Res Ctr Exercise & Hlth, Dept Biomed Kinesiol, Fac Kinesiol & Rehabil Sci, Tervuursevest 101, B-3001 Leuven, Belgium.
EM Martine.Thomis@faber.kuleuven.be
RI Verdrengh, Evelien/H-4571-2012; Wijmenga, Cisca/D-2173-2009;
OI Wijmenga, Cisca/0000-0002-5635-1614; Roth, Stephen/0000-0002-7841-3695
FU KU Leuven [OT/04/44, OT/98/39]; Research Foundation Flanders (FWO)
[G.0496.05]; FWO [G.0496.05]; National Institute on Aging, National
Institutes of Health [AG022791]; Flemish Government
FX AW and WH were funded by the Research Fund of the KU Leuven (OT/04/44
and OT/98/39, respectively). The Research Foundation Flanders (FWO)
funded GDM by grant G.0496.05 and MP as post-doctoral researcher. The
fine mapping phase of the LGfMS is funded by OT/04/44 and FWO grant
G.0496.05. The BLSA research was conducted as a component of the
Intramural Research Program of the National Institute on Aging and
further supported by AG022791 from the National Institutes of Health.
Strength phenotyping of the SPAH cohort was supported by the Flemish
Government in the Flemish Policy Research Centre Sport, Physical
Activity and Health and genotyping by a FWO Research grant to Martine
Thomis. We thank Ivo Salden for his support during the preparation of
DNA samples, Ruben van 't Slot, Bart Claes, Gilian Peuteman, Ricardo
Lima and Andrew Ludlow for the genotyping, Monique Ramaekers and Els Van
den Eede for assistance in the biopsy study and Karolina Szlufcik for
support during the mRNA expression analyses. We would like to dedicate
this paper to Gunther De Mars, who deceased on 28/02/2010 (age 34) and
greatly contributed to the LGfMS study and to earlier versions of this
manuscript.
NR 47
TC 12
Z9 14
U1 0
U2 9
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD FEB
PY 2011
VL 19
IS 2
BP 208
EP 215
DI 10.1038/ejhg.2010.173
PG 8
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 705YK
UT WOS:000286176500016
PM 21063444
ER
PT J
AU Tripathi, L
Singh, R
Stables, JP
AF Tripathi, Laxmi
Singh, Ranjit
Stables, James P.
TI Design & synthesis of N '-[substituted] pyridine-4-carbohydrazides as
potential anticonvulsant agents
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE N '-[substituted]pyridine-4-carohydrazides; Anticonvulsant activity;
Neurotoxicity; Computational study
ID MAXIMAL ELECTROSHOCK SCREEN; ANTIEPILEPTIC DRUGS; ARYL SEMICARBAZONES;
PHARMACOPHORE; DISCOVERY; TARGETS
AB A series of N'-[substituted] pyridine-4-carbohydrazides were designed and synthesized keeping in view the structural requirement of pharmacophore and evaluated for anticonvulsant activity and neurotoxicity. The anticonvulsant activity of the titled compounds was established after intraperitoneal administration in three seizure models, which include MES, scMET and 6 Hz model. The most active compound of the series was N'-[4-(4-fluorophenoxy)benzylidene]pyridine-4-carbohydrazide PCH 6, which showed a MES ED50 value of 128.3 mg/kg and 6 Hz ED50 value of 53.3 mg/kg in mice. The median toxic dose (TD50) was 343.6 mg/kg, providing compound PCH 6 with a protection index of 2.67 in the MES test and 6.44 in 6 Hz test. A computational study was also carried out, including calculation of pharmacophore pattern, prediction of pharmacokinetic properties and docking studies. (C) 2010 Elsevier Masson SAS. All rights reserved.
C1 [Tripathi, Laxmi; Singh, Ranjit] Shobhit Univ, Sch Pharmaceut Sci, Meerut 250110, Uttar Pradesh, India.
[Stables, James P.] NIH, Preclin Pharmacol Sect, Epilepsy Branch, Bethesda, MD 20892 USA.
RP Tripathi, L (reprint author), Shobhit Univ, Sch Pharmaceut Sci, Meerut 250110, Uttar Pradesh, India.
EM tripathilaxmi@rediffmail.com
NR 27
TC 13
Z9 14
U1 0
U2 2
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 FEB
PY 2011
VL 46
IS 2
BP 509
EP 518
DI 10.1016/j.ejmech.2010.11.030
PG 10
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 725AL
UT WOS:000287617500006
PM 21167624
ER
PT J
AU Balboni, G
Salvadori, S
Marczak, ED
Knapp, BI
Bidlack, JM
Lazarus, LH
Peng, XM
Si, YG
Neumeyer, JL
AF Balboni, Gianfranco
Salvadori, Severo
Marczak, Ewa D.
Knapp, Brian I.
Bidlack, Jean M.
Lazarus, Lawrence H.
Peng, Xuemei
Si, Yu Gui
Neumeyer, John L.
TI Opioid bifunctional ligands from morphine and the opioid pharmacophore
Dmt-Tic
SO EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
DE Bifunctional ligands; Dmt-Tic pharmacophore; Opioid receptors
ID DESIGNED MULTIPLE LIGAND; BIVALENT LIGANDS; INVERSE AGONISM; RECEPTORS;
ANTAGONIST; ANALOGS; NALTRINDOLE; EVOLUTION; BINDING
AB Bifunctional ligands containing an ester linkage between morphine and the delta-selective pharmacophore Dmt-Tic were synthesized, and their binding affinity and functional bioactivity at the mu, delta and kappa opioid receptors determined. Bifunctional ligands containing or not a spacer of beta-alanine between the two pharmacophores lose the mu agonism deriving from morphine becoming partial p agonists mu or mu antagonists 5. Partial kappa agonism is evidenced only for compound 4. Finally, both compounds showed potent delta antagonism. (C) 2010 Elsevier Masson SAS. All rights reserved.
C1 [Balboni, Gianfranco] Univ Cagliari, Dept Toxicol, I-09124 Cagliari, Italy.
[Salvadori, Severo] Univ Ferrara, Dept Pharmaceut Sci, I-44100 Ferrara, Italy.
[Salvadori, Severo] Univ Ferrara, Ctr Biotechnol, I-44100 Ferrara, Italy.
[Knapp, Brian I.; Bidlack, Jean M.] Univ Rochester, Dept Pharmacol & Physiol, Sch Med & Dent, Rochester, NY 14642 USA.
[Marczak, Ewa D.; Lazarus, Lawrence H.] Natl Inst Environm Hlth Sci, Med Chem Grp, Lab Toxicol & Pharmacol, Res Triangle Pk, NC 27709 USA.
[Peng, Xuemei; Si, Yu Gui; Neumeyer, John L.] Harvard Univ, McLean Hosp, Sch Med, Alcohol & Drug Abuse Res Ctr, Belmont, MA 02478 USA.
RP Balboni, G (reprint author), Univ Cagliari, Dept Toxicol, Via Osped 72, I-09124 Cagliari, Italy.
EM gbalboni@unica.it; jneumeyer@mclean.harvard.edu
OI SALVADORI, Severo/0000-0002-8224-2358
FU NIH [RO1-DA14251, K05-DA 00360]; University of Cagliari; University of
Ferrara; NIEHS
FX This work was supported in part by NIH Grants RO1-DA14251 (to J.L.N.),
K05-DA 00360 (to J.M.B.), University of Cagliari (to G.B.), University
of Ferrara (to S.S.), and the Intramural Research Program of the NIH and
NIEHS (to L.H.L.).
NR 27
TC 9
Z9 10
U1 0
U2 8
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 FEB
PY 2011
VL 46
IS 2
BP 799
EP 803
DI 10.1016/j.ejmech.2010.12.001
PG 5
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 725AL
UT WOS:000287617500036
PM 21216504
ER
PT J
AU Michalski, MH
Chen, XY
AF Michalski, Mark H.
Chen, Xiaoyuan
TI Molecular imaging in cancer treatment
SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING
LA English
DT Article
DE Molecular imaging; Therapy response; Metabolism; Proliferation;
Angiogenesis; Hypoxia; Apoptosis
ID POSITRON-EMISSION-TOMOGRAPHY; ENDOTHELIAL GROWTH-FACTOR; CELL
LUNG-CANCER; INTEGRIN ALPHA(V)BETA(3) EXPRESSION;
MATRIX-METALLOPROTEINASE INHIBITORS; FACTOR RECEPTOR EXPRESSION; HYPOXIC
TISSUE TRACER; IN-VIVO DETECTION; BREAST-CANCER; TUMOR HYPOXIA
AB The success of cancer therapy can be difficult to predict, as its efficacy is often predicated upon characteristics of the cancer, treatment, and individual that are not fully understood or are difficult to ascertain. Monitoring the response of disease to treatment is therefore essential and has traditionally been characterized by changes in tumor volume. However, in many instances, this singular measure is insufficient for predicting treatment effects on patient survival. Molecular imaging allows repeated in vivo measurement of many critical molecular features of neoplasm, such as metabolism, proliferation, angiogenesis, hypoxia, and apoptosis, which can be employed for monitoring therapeutic response. In this review, we examine the current methods for evaluating response to treatment and provide an overview of emerging PET molecular imaging methods that will help guide future cancer therapies.
C1 [Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
[Michalski, Mark H.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
RP Chen, XY (reprint author), NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, 31 Ctr Dr,Suite 1C14, Bethesda, MD 20892 USA.
EM shawn.chen@nih.gov
FU NIH, NIBIB
FX This research was supported by the Intramural Research Program of the
NIH, NIBIB.
NR 203
TC 48
Z9 53
U1 5
U2 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1619-7070
J9 EUR J NUCL MED MOL I
JI Eur. J. Nucl. Med. Mol. Imaging
PD FEB
PY 2011
VL 38
IS 2
BP 358
EP 377
DI 10.1007/s00259-010-1569-z
PG 20
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 706GC
UT WOS:000286205000018
PM 20661557
ER
PT J
AU Huff, J
AF Huff, James
TI Occupational cancer and social inequities
SO EUROPEAN JOURNAL OF PUBLIC HEALTH
LA English
DT Letter
ID PRIMARY PREVENTION
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
RP Huff, J (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA.
EM huff1@niehs.nih.gov
NR 5
TC 0
Z9 0
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1101-1262
J9 EUR J PUBLIC HEALTH
JI Eur. J. Public Health
PD FEB
PY 2011
VL 21
IS 1
BP 129
EP 129
DI 10.1093/eurpub/ckq026
PG 1
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 709TA
UT WOS:000286463100023
PM 20375025
ER
PT J
AU Kleykamp, BA
Jennings, JM
Eissenberg, T
AF Kleykamp, Bethea A.
Jennings, Janine M.
Eissenberg, Thomas
TI Effects of Transdermal Nicotine and Concurrent Smoking on Cognitive
Performance in Tobacco-Abstinent Smokers
SO EXPERIMENTAL AND CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE nicotine; tobacco; smoking; cognition; performance
ID REPLACEMENT THERAPY; CIGARETTE-SMOKING; WORKING-MEMORY; PSYCHOMOTOR
PERFORMANCE; ADMINISTERED NICOTINE; WITHDRAWAL SYNDROME; NEVER-SMOKERS;
PATCH; CESSATION; ATTENTION
AB Smokers experience cognitive decrements during tobacco abstinence and boosts in performance on resumption of smoking. Few studies have examined whether smoking cessation treatments such as transdermal nicotine (TN) ameliorate these decrements or attenuate the cognitive effects of smoking. Identifying the effects of nicotine on these tobacco-related changes in performance could guide the development of more efficacious treatments. The purpose of this double-blind, randomized, laboratory study was to use process-specific cognitive tasks to examine the effects of TN and tobacco smoking on attention and working memory in overnight-abstinent smokers (N = 124; 54 women). Each participant completed 4 sessions lasting 6.5 hr corresponding to 0-, 7-, 14-, or 21-mg TN doses, and smoked a single cigarette 4 hr after TN administration. Outcome measures were administered before and after smoking and included tasks measuring attention (alerting, orienting, and executive function), working memory (verbal and spatial), and psychomotor function. Analysis of variance (p < .05) revealed that TN improved verbal and spatial working memory performance, as well as psychomotor function. Smoking, independent of TN dose, improved alerting, verbal working memory, and psychomotor function. Lastly, TN partially attenuated the effects of smoking on some working memory outcomes. These findings lend evidence to the idea that TN ameliorates some abstinence-related cognitive decrements and suggest that TN does not completely attenuate the cognitive effects of a concurrently smoked cigarette. Consequently, TN's efficacy as a smoking cessation treatment might be improved if these limitations are better addressed by either modifying or supplementing existing treatments.
C1 [Kleykamp, Bethea A.] NIDA, Nicotine Psychopharmacol Sect, Clin Pharmacol & Therapeut Branch, Intramural Res Program,NIH,Dept Hlth & Human Serv, Baltimore, MD 21224 USA.
[Jennings, Janine M.] Wake Forest Univ, Dept Psychol, Winston Salem, NC 27109 USA.
[Eissenberg, Thomas] Virginia Commonwealth Univ, Dept Psychol, Richmond, VA 23284 USA.
[Eissenberg, Thomas] Virginia Commonwealth Univ, Inst Drug & Alcohol Studies, Richmond, VA 23284 USA.
RP Kleykamp, BA (reprint author), NIDA, Nicotine Psychopharmacol Sect, Clin Pharmacol & Therapeut Branch, Intramural Res Program,NIH,Dept Hlth & Human Serv, 251 Bayview Blvd,Room 01A941, Baltimore, MD 21224 USA.
EM annie.kleykamp@nih.gov
FU Public Health Service [R01DA11082, F31DA017437]
FX Portions of this work were presented at the 11th and 12th Annual
Meetings of the Society for Research on Nicotine and Tobacco and the
67th and 68th Annual Meetings of the College on Problems of Drug
Dependence. This work was supported by Public Health Service Grants
R01DA11082 and F31DA017437. This article is based on dissertation
research that was conducted, completed, and defended at Virginia
Commonwealth University by Bethea A. Kleykamp under the guidance of
Thomas Eissenberg.
NR 61
TC 8
Z9 8
U1 2
U2 5
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1064-1297
J9 EXP CLIN PSYCHOPHARM
JI Exp. Clin. Psychopharmacol.
PD FEB
PY 2011
VL 19
IS 1
BP 75
EP 84
DI 10.1037/a0022417
PG 10
WC Psychology, Biological; Psychology, Clinical; Pharmacology & Pharmacy;
Psychiatry
SC Psychology; Pharmacology & Pharmacy; Psychiatry
GA 722WM
UT WOS:000287466000008
PM 21341925
ER
PT J
AU Aguilera, G
AF Aguilera, Greti
TI HPA axis responsiveness to stress: Implications for healthy aging
SO EXPERIMENTAL GERONTOLOGY
LA English
DT Article; Proceedings Paper
CT 10th International Symposium on the Neurobiology and Neuroendocrinology
of Aging
CY JUL 25-30, 2010
CL Bregenz, AUSTRIA
DE Stress; Hypothalamic pituitary adrenal axis (HPA); Corticotropin
releasing hormone (CRH); Vasopressin (VP); Glucocorticoids
ID CORTICOTROPIN-RELEASING HORMONE; PITUITARY-ADRENAL AXIS; FACTOR
MESSENGER-RNA; GLUCOCORTICOID-RECEPTOR GENE; AGE-RELATED-CHANGES;
PARAVENTRICULAR NUCLEUS; ADRENOCORTICOTROPIN SECRETION; SUPRACHIASMATIC
NUCLEI; FISCHER-344 RATS; CIRCADIAN-RHYTHM
AB The major neuroendocrine response mediating stress adaptation is activation of the hypothalamic pituitary adrenal axis, with stimulation of corticotropin releasing hormone (CRH) and vasopressin (VP) from parvocellular neurons of the hypothalamic paraventricular nucleus, leading to stimulation of pituitary ACTH secretion and increases in glucocorticoid secretion from the adrenal cortex. Basal production and transient increases during stress of glucocorticoids and its hypothalamic regulators are essential for neuronal plasticity and normal brain function. While activation of the HPA axis is essential for survival during stress, chronic exposure to stress hormones can predispose to psychological, metabolic and immune alterations. Thus, prompt termination of the stress response is essential to prevent negative effects of inappropriate levels of CRH and glucocorticoids. This review addresses the regulation of HPA axis activity with emphasis on the mechanisms of termination of CRH transcription, which is a critical step in this process. In addition, the actions by which glucocorticoids, CRH and VP can affect the aging process will be discussed. Published by Elsevier Inc.
C1 [Aguilera, Greti] NIH, Eunice Kennedy Shiver Inst Child Hlth & Human Dev, Program Dev Endocrinol & Genet, Sect Endocrine Physiol, Bethesda, MD 20892 USA.
RP Aguilera, G (reprint author), NICHD, Sect Endocrine Psysiol DEB, CRC, NIH Bldg 10,Rm 11E-3330 10 Ctr Dr, Bethesda, MD 20892 USA.
EM Greti_Aguilera@nih.gov
FU Intramural NIH HHS [Z01 HD000631-18, Z99 HD999999]
NR 89
TC 72
Z9 75
U1 1
U2 13
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0531-5565
J9 EXP GERONTOL
JI Exp. Gerontol.
PD FEB-MAR
PY 2011
VL 46
IS 2-3
SI SI
BP 90
EP 95
DI 10.1016/j.exger.2010.08.023
PG 6
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA 720OQ
UT WOS:000287290400002
PM 20833240
ER
PT J
AU DeJesus, CE
Egen, J
Metzger, M
Alvarez, X
Combs, CA
Malide, D
Yu, ZX
Tian, X
Donahue, RE
AF DeJesus, Catherine E.
Egen, Jackson
Metzger, Mark
Alvarez, Xavier
Combs, Christian A.
Malide, Daniela
Yu, Zu Xi
Tian, Xin
Donahue, Robert E.
TI Transient neutropenia after granulocyte-colony stimulating factor
administration is associated with neutrophil accumulation in pulmonary
vasculature
SO EXPERIMENTAL HEMATOLOGY
LA English
DT Article
ID G-CSF; DONORS; MACROPHAGES; SPLEEN; LUNGS
AB Objective. To better define the nature of the transient neutropenia shortly following granulocyte-colony stimulating factor (G-CSF) administration.
Materials and Methods. To evaluate the disappearance of neutrophils, we investigated neutrophil trafficking. Ratios of neutrophil number to background cellularity for C57BL/6 LysM-EGFP knock-in mice and rhesus macaques were determined in the lung, liver, spleen, and kidney after G-CSF administration.
Results. For the C57BL/6 LysM-EGFP knock-in mice, the enhanced green fluorescent protein expression (EGFP(+)) cells increased in the lung and spleen within 15 minutes of administering 50 mu g/kg G-CSF subcutaneously, and continued to increase in the lung and spleen from 15 minutes to 30 minutes. At 240 minutes, the pulmonary infiltrate declined to a level comparable to the level at 15 minutes, while in the spleen EGFP(+) cells continued to increase. For rhesus macaques, CD18(+) cells also significantly increased in the lung 30 minutes after administration of 10 mu g/kg G-CSF subcutaneously compared to the control level.
Conclusions. These results suggest that the transient neutropenia following G-CSF administration in the mouse and nonhuman primate is associated with an accumulation of neutrophils within pulmonary and splenic vasculature. Published by Elsevier Inc. on behalf of the ISEH - Society for Hematology and Stem Cells.
C1 [DeJesus, Catherine E.; Metzger, Mark; Donahue, Robert E.] NHLBI, Hematol Branch, NIH, Rockville, MD 20850 USA.
[Egen, Jackson] NIAID, Bethesda, MD 20892 USA.
[Alvarez, Xavier] Tulane Natl Primate Res Ctr, Covington, LA USA.
[Combs, Christian A.; Malide, Daniela] NHLBI, Light Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
[Yu, Zu Xi] NHLBI, Pathol Core Facil, NIH, Bethesda, MD 20892 USA.
[Tian, Xin] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RP Donahue, RE (reprint author), NHLBI, Hematol Branch, NIH, 5 Res Court, Rockville, MD 20850 USA.
EM donahuer@nhlbi.nih.gov
OI Egen, Jackson/0000-0003-2053-0837
FU National Institutes of Health (NIH), National Heart, Lung, and Blood
Institute; NIH [RR00164]
FX The authors wish to thank the veterinary and laboratory animal staff at
5 Research Court and National Insitute of Allergy and Infectious
Diseases (Bethesda, MD, USA) for maintaining the animals used in this
study. In addition, we would like the veterinary pathology staff of the
Division of Veterinary Resources for their help in performing the
necropsies. This research was supported by the Intramural Research
Program of the National Institutes of Health (NIH), National Heart,
Lung, and Blood Institute. Xavier Alvarez is supported partially by NIH
grant RR00164 to the Tulane National Primate Research Center.
NR 21
TC 6
Z9 6
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0301-472X
J9 EXP HEMATOL
JI Exp. Hematol.
PD FEB
PY 2011
VL 39
IS 2
BP 142
EP 150
DI 10.1016/j.exphem.2010.11.004
PG 9
WC Hematology; Medicine, Research & Experimental
SC Hematology; Research & Experimental Medicine
GA 716JE
UT WOS:000286964100002
PM 21087652
ER
PT J
AU Dodson, HC
Lyda, TA
Chambers, JW
Morris, MT
Christensen, KA
Morris, JC
AF Dodson, Heidi C.
Lyda, Todd A.
Chambers, Jeremy W.
Morris, Meredith T.
Christensen, Kenneth A.
Morris, James C.
TI Quercetin, a fluorescent bioflavanoid, inhibits Trypanosoma brucei
hexokinase 1
SO EXPERIMENTAL PARASITOLOGY
LA English
DT Article
DE Trypanosoma brucei; Hexokinase; Quercetin; Glycolysis
ID BLOOD-STREAM FORM; AGENT LONIDAMINE; TUMOR-CELLS; ANTI-TUMOR;
GLYCOLYSIS; MITOCHONDRIA; EXPRESSION; FLAVONOIDS; APOPTOSIS; IMPORT
AB Hexokinases from the African trypanosome, Trypanosome brucei, are attractive targets for the development of anti-parasitic drugs, in part because the parasite utilizes glycolysis exclusively for ATP production during the mammalian infection. Here, we have demonstrated that the bioflavanoid quercetin (QCN), a known trypanocide, is a mixed inhibitor of Trypanosome brucei hexokinase 1 (TbHK1) (IC(50) = 4.1 +/- 0.8 mu M). Spectroscopic analysis of QCN binding to TbHK1, taking advantage of the intrinsically fluorescent single tryptophan (Trp177) in TbHK1, revealed that QCN quenches emission of Trp177, which is located near the hinge region of the enzyme. ATP similarly quenched Trp177 emission, while glucose had no impact on fluorescence.
Supporting the possibility that QCN toxicity is a consequence of inhibition of the essential hexokinase, in live parasites QCN fluorescence localizes to glycosomes, the subcellular home of TbHK1. Additionally, RNAi-mediated silencing of TbHK1 expression expedited QCN induced death, while over-expressing TbHK1 protected trypanosomes from the compound. In summary, these observations support the suggestion that QCN toxicity is in part attributable to inhibition of the essential TbHK1. (C) 2010 Elsevier Inc. All rights reserved.
C1 [Dodson, Heidi C.; Lyda, Todd A.; Chambers, Jeremy W.; Morris, Meredith T.; Morris, James C.] Clemson Univ, Dept Biochem & Genet, Clemson, SC 29634 USA.
[Christensen, Kenneth A.] Clemson Univ, Dept Chem, Clemson, SC 29634 USA.
[Lyda, Todd A.] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Chambers, Jeremy W.] Scripps Res Inst, Dept Mol Therapeut, Jupiter, FL 33458 USA.
RP Morris, JC (reprint author), Clemson Univ, Dept Biochem & Genet, 214 BRC,51 New Cherry St, Clemson, SC 29634 USA.
EM jmorri2@clemson.edu
RI Christensen, Kenneth/D-3460-2017;
OI Chambers, Jeremy/0000-0002-6143-3091
FU US National Institutes of Health [1R15AI075326]
FX The authors would like to thank Stephen Carek and Tom Caldwell for their
technical assistance. This work was supported in part by the US National
Institutes of Health 1R15AI075326 to JCM.
NR 32
TC 14
Z9 14
U1 2
U2 9
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4894
J9 EXP PARASITOL
JI Exp. Parasitol.
PD FEB
PY 2011
VL 127
IS 2
BP 423
EP 428
DI 10.1016/j.exppara.2010.10.011
PG 6
WC Parasitology
SC Parasitology
GA 712CW
UT WOS:000286643300016
PM 20971104
ER
PT J
AU Davis, CD
Milner, JA
AF Davis, Cindy D.
Milner, John A.
TI Vitamin D and colon cancer
SO EXPERT REVIEW OF GASTROENTEROLOGY & HEPATOLOGY
LA English
DT Review
DE colon cancer; CYP24A1; CYP27B1; vitamin D; vitamin D receptor
ID D-RECEPTOR EXPRESSION; EPITHELIAL-CELL PROLIFERATION; RANDOMIZED
CLINICAL-TRIAL; CALCIUM-SENSING RECEPTOR; COLORECTAL ADENOMA RISK;
DIETARY CALCIUM; UNITED-STATES; SERUM 25-HYDROXYVITAMIN-D;
CARCINOMA-CELLS; PROSPECTIVE COHORT
AB A wealth of scientific evidence supports a role for vitamin D in decreasing colorectal cancer incidence, and possibly mortality. This reduction in risk is related to inhibition of cellular proliferation and stimulation of differentiation. The minimal amount and duration needed to bring about these effects necessitate additional studies. Furthermore, a critical evaluation of physiologically relevant biomarkers of vitamin D status, including 25-hydroxyvitamin D, is needed. Several dietary components and the balance between energy intake and expenditure influence vitamin D metabolism. Scientists need to identify confounders and modifiers of the biological response to vitamin D, including dietary factors, lifestyle factors such as exercise, race or ethnicity, and genetic background.
C1 [Davis, Cindy D.; Milner, John A.] NCI, Nutr Sci Res Grp, Canc Prevent Div, Rockville, MD 20892 USA.
RP Davis, CD (reprint author), NCI, Nutr Sci Res Grp, Canc Prevent Div, 6130 Execut Blvd,Suite 3159,MSC 7328, Rockville, MD 20892 USA.
EM davisci@mail.nih.gov
NR 122
TC 9
Z9 10
U1 0
U2 6
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1747-4124
EI 1747-4132
J9 EXPERT REV GASTROENT
JI Expert Rev. Gastroenterol. Hepatol.
PD FEB
PY 2011
VL 5
IS 1
BP 67
EP 81
DI 10.1586/EGH.10.89
PG 15
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 861SL
UT WOS:000298039400013
PM 21309673
ER
PT J
AU Dey, AK
Srivastava, IK
AF Dey, Antu K.
Srivastava, Indresh K.
TI Novel adjuvants and delivery systems for enhancing immune responses
induced by immunogens
SO EXPERT REVIEW OF VACCINES
LA English
DT Review
DE adjuvant; immunogen; MF59; MPL; nanoemulsions; PAMPs; PLG
microparticles; PRR; SMIP
ID MONOPHOSPHORYL-LIPID-A; HEPATITIS-B-VACCINE; HEAT-LABILE ENTEROTOXIN;
VIRUS-LIKE PARTICLES; CELLS IN-VIVO; RECONSTITUTED INFLUENZA VIROSOMES;
IMMUNOSTIMULATING COMPLEX ISCOM; ADP-RIBOSYLTRANSFERASE ACTIVITY;
CROSS-PROTECTIVE IMMUNITY; SERUM ANTIBODY-RESPONSE
AB Vaccines are the most important preventive measure against infectious diseases. In developing an effective vaccine, besides the primary challenge of identifying the most relevant immunogen and efficient regime of immunization, selection of a potent adjuvant and delivery method is equally critical. The formulation of immunogens with different adjuvants may affect the affinity maturation of antibody responses differently, suggesting that the structure of specific epitopes within the immunogen may be influenced by different adjuvants. Thus, developing adjuvants that can efficiently activate both the innate and adaptive arms of the immune system is a major challenge for vaccine researchers. The use of novel adjuvants in combination with novel immunogen design holds great promise towards the goal of enhancing the potency, breadth and durability of vaccines. This article summarizes the different immunopotentiators (and immunomodulators) as well as the delivery systems that are available for vaccine generation and the types of immune responses that each of them induces. Also discussed are adjuvants that have a combination of both immunomodulatory and delivery properties.
C1 [Dey, Antu K.; Srivastava, Indresh K.] Novartis Vaccines & Diagnost Inc, Cambridge, MA 02139 USA.
RP Srivastava, IK (reprint author), NIAID, VPPL, Vaccine Res Ctr, NIH, 942 Clopper Rd, Gaithersburg, MD 20877 USA.
EM srivastavai@mail.nih.gov
RI Dey, Antu/A-1305-2013
FU National Institute of Allergy and Infectious Diseases, NIH (Bethesda,
MD, USA) [AI-9536Z, I-AI-05397, 5PO1-AI48225-03]
FX Some of the work reported in this article was supported by grants and
contracts (AI-9536Z, I-AI-05397 and 5PO1-AI48225-03) from the National
Institute of Allergy and Infectious Diseases, 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 272
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U1 2
U2 14
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
ENGLAND
SN 1476-0584
J9 EXPERT REV VACCINES
JI Expert Rev. Vaccines
PD FEB
PY 2011
VL 10
IS 2
BP 227
EP 251
DI 10.1586/ERV.10.142
PG 25
WC Immunology
SC Immunology
GA 732NM
UT WOS:000288192200014
PM 21105782
ER
PT J
AU Wang, Y
Wang, VM
Chan, CC
AF Wang, Y.
Wang, V. M.
Chan, C-C
TI The role of anti-inflammatory agents in age-related macular degeneration
(AMD) treatment
SO EYE
LA English
DT Review
DE age-related macular degeneration; inflammation; corticosteroid;
nonsteoridal anti-inflammatory drug; immunosuppressant; biologics
ID INTRAVITREAL TRIAMCINOLONE ACETONIDE; RANDOMIZED CLINICAL-TRIAL;
CHLAMYDIA-PNEUMONIAE INFECTION; PIGMENT EPITHELIAL DETACHMENT; CHOROIDAL
NEOVASCULARIZATION; PHOTODYNAMIC THERAPY; TRIPLE THERAPY;
RHEUMATOID-ARTHRITIS; RETINAL DEGENERATION; ENDOTHELIAL-CELLS
AB Although age-related macular degeneration (AMD) is not a classic inflammatory disease like uveitis, inflammation has been found to have an important role in disease pathogenesis and progression. Innate immunity and autoimmune components, such as complement factors, chemokines, cytokines, macrophages, and ocular microglia, are believed to be heavily involved in AMD development. Targeting these specific inflammatory molecules has recently been explored in an attempt to better understand and treat AMD. Although antivascular endothelial growth factor therapy is the first line of defence against neovascular AMD, anti-inflammatory agents such as corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), immunosuppressive agents (eg, methotrexate and rapamycin), and biologics (eg, infliximab, daclizumab, and complement inhibitors) may provide an adjunct or alternative mechanism to suppress the inflammatory processes driving AMD progression. Further investigation is required to evaluate the long-term safety and efficacy of these drugs for both neovascular and non-neovascular AMD. Eye (2011) 25, 127-139; doi: 10.1038/eye.2010.196; published online 24 December 2010
C1 [Wang, Y.; Wang, V. M.; Chan, C-C] NEI, Immunol Lab, Immunopathol Sect, NIH, Bethesda, MD 20892 USA.
[Wang, Y.] Sun Yat Sen Univ, Zhongshan Ophthalm Ctr, Guangzhou 510275, Guangdong, Peoples R China.
RP Chan, CC (reprint author), NEI, Immunol Lab, Immunopathol Sect, NIH, 10 Ctr Dr,10-10N103, Bethesda, MD 20892 USA.
EM chanc@nei.nih.gov
RI wang, yujuan/C-8428-2016
FU NEI
FX The NEI Intramural Research Program provided the funding support. Mrs
Pamela Sieving provided helpful editing assistance.
NR 108
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U1 2
U2 13
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-222X
J9 EYE
JI Eye
PD FEB
PY 2011
VL 25
IS 2
BP 127
EP 139
DI 10.1038/eye.2010.196
PG 13
WC Ophthalmology
SC Ophthalmology
GA 719FR
UT WOS:000287187300001
PM 21183941
ER
PT J
AU Wang, XQ
Hawkins, BT
Miller, DS
AF Wang, Xueqian
Hawkins, Brian T.
Miller, David S.
TI Aryl hydrocarbon receptor-mediated up-regulation of ATP-driven
xenobiotic efflux transporters at the blood-brain barrier
SO FASEB JOURNAL
LA English
DT Article
DE P-glycoprotein; multidrug resistance-associated protein 2; breast cancer
resistance protein; dioxin; brain capillaries
ID CANCER RESISTANCE PROTEIN; P-GLYCOPROTEIN; ENDOTHELIAL-CELLS;
DNA-BINDING; IN-VITRO; ALPHA-NAPHTHOFLAVONE; DRUG TRANSPORTER; ABC
TRANSPORTERS; CYTOCHROMES P450; DIOXIN RECEPTOR
AB Many widespread and persistent organic pollutants, e.g., 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), activate the aryl hydrocarbon receptor (AhR), causing it to translocate to the cell nucleus, where it transactivates target genes. AhR's ability to target the blood-brain barrier is essentially unexplored. We show here that exposing isolated rat brain capillaries to 0.05-0.5 nM TCDD roughly doubled transport activity and protein expression of P-glycoprotein, an ATP-driven drug efflux pump and a critical determinant of drug entry into the CNS. These effects were abolished by actinomycin D or cycloheximide or by the AhR antagonists resveratrol and alpha-naphthoflavone. Brain capillaries from TCDD-dosed rats (1-5 mu g/kg, i.p.) exhibited increased transport activity and protein expression of 3 xenobiotic efflux pumps, P-glycoprotein, multidrug resistance-associated protein 2, and breast cancer resistance polypeptide, as well as expression of Cyp1a1 and Cyp1b1, both AhR target genes. Consistent with increased P-glycoprotein expression in capillaries from TCDD-dosed rats, in situ brain perfusion indicated significantly reduced brain accumulation of verapamil, a P-glycoprotein substrate. These findings suggest a new paradigm for the field of environmental toxicology: toxicants acting through AhR to target xenobiotic efflux transporters at the blood-brain barrier and thus reduce brain accumulation of CNS-acting therapeutic drugs.-Wang, X., Hawkins, B. T., Miller, D. S. Aryl hydrocarbon receptor-mediated up-regulation of ATP-driven xenobiotic efflux transporters at the blood-brain barrier. FASEB J. 25, 644-652 (2011). www.fasebj.org
C1 [Wang, Xueqian; Hawkins, Brian T.; Miller, David S.] NIEHS, Lab Toxicol & Pharmacol, NIH, Res Triangle Pk, NC 27709 USA.
RP Miller, DS (reprint author), NIEHS, Lab Toxicol & Pharmacol, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM miller@niehs.nih.gov
OI Hawkins, Brian/0000-0001-6719-5402
FU National Institute of Environmental Health Sciences, National Institutes
of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Environmental Health Sciences, National Institutes
of Health.
NR 50
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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 FEB
PY 2011
VL 25
IS 2
BP 644
EP 652
DI 10.1096/fj.10-169227
PG 9
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 713GZ
UT WOS:000286724800022
PM 21048045
ER
PT J
AU Deng, YM
Edin, ML
Theken, KN
Schuck, RN
Flake, GP
Kannon, MA
DeGraff, LM
Lih, FB
Foley, J
Bradbury, JA
Graves, JP
Tomer, KB
Falck, JR
Zeldin, DC
Lee, CR
AF Deng, Yangmei
Edin, Matthew L.
Theken, Katherine N.
Schuck, Robert N.
Flake, Gordon P.
Kannon, M. Alison
DeGraff, Laura M.
Lih, Fred B.
Foley, Julie
Bradbury, J. Alyce
Graves, Joan P.
Tomer, Kenneth B.
Falck, John R.
Zeldin, Darryl C.
Lee, Craig R.
TI Endothelial CYP epoxygenase overexpression and soluble epoxide hydrolase
disruption attenuate acute vascular inflammatory responses in mice
SO FASEB JOURNAL
LA English
DT Article
DE CYP2J2; CYP2C8; EPHX2; EETs; eicosanoids; inflammation
ID NF-KAPPA-B; ACUTE LUNG INJURY; ACUTE PSEUDOMONAS PNEUMONIA;
BLOOD-PRESSURE REGULATION; ARACHIDONIC-ACID; CYTOCHROME-P450
EPOXYGENASES; CORONARY-ARTERIES; EPOXYEICOSATRIENOIC ACIDS; THERAPEUTIC
TARGET; MOLECULAR-CLONING
AB Cytochrome P-450 (CYP)-derived epoxyeicosatrienoic acids (EETs) possess potent anti-inflammatory effects in vitro. However, the effect of increased CYP-mediated EET biosynthesis and decreased soluble epoxide hydrolase (sEH, Ephx2)-mediated EET hydrolysis on vascular inflammation in vivo has not been rigorously investigated. Consequently, we characterized acute vascular inflammatory responses to endotoxin in transgenic mice with endothelial expression of the human CYP2J2 and CYP2C8 epoxygenases and mice with targeted disruption of Ephx2. Compared to wild-type controls, CYP2J2 transgenic, CYP2C8 transgenic, and Ephx2(-/-) mice each exhibited a significant attenuation of endotoxin-induced activation of nuclear factor (NF)-kappa B signaling, cellular adhesion molecule, chemokine and cytokine expression, and neutrophil infiltration in lung in vivo. Furthermore, attenuation of endotoxin-induced NF-kappa B activation and cellular adhesion molecule and chemokine expression was observed in primary pulmonary endothelial cells isolated from CYP2J2 and CYP2C8 transgenic mice. This attenuation was inhibited by a putative EET receptor antagonist and CYP epoxygenase inhibitor, directly implicating CYP epoxygenase-derived EETs with the observed anti-inflammatory phenotype. Collectively, these data demonstrate that potentiation of the CYP epoxygenase pathway by either increased endothelial EET biosynthesis or globally decreased EET hydrolysis attenuates NF-kappa B-dependent vascular inflammatory responses in vivo and may serve as a viable anti-inflammatory therapeutic strategy.-Deng, Y., Edin, M. L., Theken, K. N., Schuck, R. N., Flake, G. P., Kannon, M. A., DeGraff, L. M., Lih, F. B., Foley, J., Bradbury, J. A., Graves, J. P., Tomer, K. B., Falck, J. R., Zeldin, D. C., Lee, C. R. Endothelial CYP epoxygenase overexpression and soluble epoxide hydrolase disruption attenuate acute vascular inflammatory responses in mice. FASEB J. 25, 703-713 (2011). www.fasebj.org
C1 [Deng, Yangmei; Theken, Katherine N.; Schuck, Robert N.; Kannon, M. Alison; Lee, Craig R.] UNC, Eshelman Sch Pharm, Div Pharmacotherapy & Expt Therapeut, Chapel Hill, NC 27599 USA.
[Edin, Matthew L.; Flake, Gordon P.; DeGraff, Laura M.; Lih, Fred B.; Foley, Julie; Bradbury, J. Alyce; Graves, Joan P.; Tomer, Kenneth B.; Zeldin, Darryl C.] Natl Inst Environm Hlth Sci, Natl Inst Hlth, Div Intramural Res, Res Triangle Pk, NC USA.
[Falck, John R.] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA.
RP Lee, CR (reprint author), UNC, Eshelman Sch Pharm, Div Pharmacotherapy & Expt Therapeut, CB 7569,Kerr Hall, Chapel Hill, NC 27599 USA.
EM craig_lee@unc.edu
RI Theken, Katherine/H-1098-2012; Tomer, Kenneth/E-8018-2013;
OI Falck, John/0000-0002-9219-7845; Edin, Matthew/0000-0002-7042-500X; Lee,
Craig/0000-0003-3595-5301
FU American Foundation for Pharmaceutical Education; NIH [GM31278,
GM088199, P30 DK34987]; Robert A. Welch Foundation; NIH, NIEHS [Z01
ES050167, Z01 ES025034]; American Heart Association
FX This publication was made possible by a predoctoral fellowship from the
American Foundation for Pharmaceutical Education to K.N.T., NIH grant
GM31278 and support from the Robert A. Welch Foundation to J.R.F., funds
from the Intramural Research Program of the NIH, NIEHS, to K. B. T. (Z01
ES050167) and D.C.Z. (Z01 ES025034), a Beginning Grant-in-Aid from the
American Heart Association and NIH grant GM088199 to C. R. L., and NIH
grant P30 DK34987. The contents of this article are solely the
responsibility of the authors and do not necessarily represent the
official views of the NIEHS, National Institute of General Medical
Sciences, or NIH. D. C. Z. is a coinventor on U.S. Patent No. 6,531,506
B1 (issued March 11, 2003), Inhibition of Epoxide Hydrolases for the
Treatment of Hypertension, and on U. S. Patent No. 6,916,843 B1 (issued
July 12, 2005), Anti-inflammatory Actions of Cytochrome P450
Epoxygenase-Derived Eicosanoids. No other authors declare conflicts of
interest.
NR 52
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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 FEB
PY 2011
VL 25
IS 2
BP 703
EP 713
DI 10.1096/fj.10-171488
PG 11
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA 713GZ
UT WOS:000286724800028
PM 21059750
ER
PT J
AU Beydoun, HA
Sicignano, N
Beydoun, MA
Bocca, S
Stadtmauer, L
Oehninger, S
AF Beydoun, Hind A.
Sicignano, Nicholas
Beydoun, May A.
Bocca, Silvina
Stadtmauer, Laurel
Oehninger, Sergio
TI Pubertal development of the first cohort of young adults conceived by in
vitro fertilization in the United States
SO FERTILITY AND STERILITY
LA English
DT Article
DE Body mass index; infertility; in vitro fertilization; puberty
ID CHILDREN BORN; ASSISTED REPRODUCTION; CONCEPTION; PARENTS; HEALTH
AB Objective: To characterize pubertal development of the first generation of young adults born as a result of in vitro fertilization (IVF). Demographic, clinical, and body size characteristics were examined regarding developmental milestones.
Design: Cross-sectional.
Setting: Academic center.
Patient(s): Young adults (18-26 years) conceived by IVF (no gamete/embryo manipulation) 1981-1990.
Intervention(s): Self-administered questionnaire.
Main Outcome Measure(s): Age at puberty onset, body size.
Result(s): Of 560 eligible young adults, 173 completed the survey (response rate 30.9%). We analyzed data on 166 respondents (71 male and 95 female). No cases of delayed or precocious puberty were observed in the study sample. As expected, age at puberty onset was significantly higher among male subjects (12.3 years) compared with female subjects (11.5 years). A few developmental milestones were predicted by maternal age and infertility diagnoses. For both genders, a direct association was noted between age at puberty onset and height achieved in young adulthood. Structural equation models suggested an inverse relationship of female gender with age at puberty onset and body mass index.
Conclusion(s): In vitro fertilization-conceived young adults did not exhibit pubertal abnormalities. Female gender and age at puberty onset independently predicted body mass index of IVF offspring in young adulthood. (Fertil Steril (R) 2011;95:528-33. (C)2011 by American Society for Reproductive Medicine.)
C1 [Bocca, Silvina; Stadtmauer, Laurel; Oehninger, Sergio] Eastern Virginia Med Sch, Jones Inst Reprod Med, Norfolk, VA 23507 USA.
[Beydoun, Hind A.; Sicignano, Nicholas] Eastern Virginia Med Sch, Grad Program Publ Hlth, Norfolk, VA 23507 USA.
[Beydoun, May A.] NIA, Intramural Res Program, Baltimore, MD 21224 USA.
RP Oehninger, S (reprint author), Eastern Virginia Med Sch, Jones Inst Reprod Med, 601 Colley Ave,4th Floor, Norfolk, VA 23507 USA.
EM oehninsc@evms.edu
FU National Institute on Aging, National Institutes of Health
FX Supported in part by the Intramural Research Program of the National
Institute on Aging, National Institutes of Health.
NR 26
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U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD FEB
PY 2011
VL 95
IS 2
BP 528
EP 533
DI 10.1016/j.fertnstert.2010.04.057
PG 6
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 709EA
UT WOS:000286419000022
PM 20547390
ER
PT J
AU Nieman, LK
Blocker, W
Nansel, T
Mahoney, S
Reynolds, J
Blithe, D
Wesley, R
Armstrong, A
AF Nieman, Lynnette K.
Blocker, Wendy
Nansel, Tonja
Mahoney, Sheila
Reynolds, James
Blithe, Diana
Wesley, Robert
Armstrong, Alicia
TI Efficacy and tolerability of CDB-2914 treatment for symptomatic uterine
fibroids: a randomized, double-blind, placebo-controlled, phase IIb
study
SO FERTILITY AND STERILITY
LA English
DT Article
DE Selective progestin receptor modulator; ulipristal acetate; fibroids;
UFS-QOL
ID QUALITY-OF-LIFE; GONADOTROPIN-RELEASING-HORMONE; PROGESTERONE-RECEPTOR
MODULATORS; LOW-DOSE MIFEPRISTONE; CONTROLLED-TRIAL; LEIOMYOMATA
TREATMENT; WOMEN; DIAGNOSIS; AGONIST; MYOMAS
AB Objective: To evaluate the efficacy and tolerability of the P receptor modulator CDB-2914 (Ulipristal, CDB).
Design: Randomized, placebo-controlled double-blind clinical trial.
Setting: Clinical research center.
Patient(s): Premenopausal women with symptomatic uterine fibroids.
Intervention(s): Once-daily oral CDB (10 or 20 mg) or placebo (PLC) for 12 weeks (treatment 1). A second 3-month treatment with CDB (treatment 2) was offered. A computer-generated blocked randomization was used.
Main Outcome Measure(s): Magnetic resonance imaging (MRI)-determined total fibroid volume (TFV) change was the primary outcome; amenorrhea and quality of life (QOL) were secondary end points.
Result(s): Treatment 1 TFV increased 7% in the PLC group, but decreased 17% and 24% in the CDB10 and CDB20 groups. The TFV decreased further in treatment 2 (-11%). Amenorrhea occurred in 20/26 women taking CDB and none on PLC. Ovulation resumed after CDB. Hemoglobin improved only with CDB (11.9 +/- 1.5 to 12.9 +/- 1.0 g/dL) as did the Fibroid QOL Questionnaire symptom severity, energy/mood, and concern subscores, and overall QOL scores. The CDB was well tolerated, with no serious adverse events. Adverse events were unchanged during treatments.
Conclusion(s): Administration of CDB-2914 for 3-6 months controls bleeding, reduces fibroid size, and improves QOL. (Fertil Steril(R) 2011;95:767-72. (C) 2011 by American Society for Reproductive Medicine.)
C1 [Nieman, Lynnette K.; Blocker, Wendy; Mahoney, Sheila; Armstrong, Alicia] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, Bethesda, MD USA.
[Nansel, Tonja] NICHHD, Div Epidemiol Stat & Populat Res, Bethesda, MD 20892 USA.
[Reynolds, James] Mark O Hatfield Clin Res Ctr, Dept Radiol, Bethesda, MD USA.
[Blithe, Diana] NICHHD, Contracept & Reprod Hlth Branch, Bethesda, MD 20892 USA.
[Wesley, Robert] NIH, Biostat & Clin Epidemiol Serv, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
RP Nieman, LK (reprint author), CRC, Bldg 10,1 East,Room 1-3140,10 Ctr Dr,MSC 1109, Bethesda, MD 20892 USA.
EM NiemanL@nih.gov
OI Nansel, Tonja/0000-0002-8298-7595
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; National Institutes of Health Clinical Center, National
Institutes of Health, Bethesda, MD; Laboratoire HRA-Pharma, Paris,
France
FX Supported by in part by the Intramural Program in Reproductive and Adult
Endocrinology, Eunice Kennedy Shriver National Institute of Child Health
and Human Development, and by the National Institutes of Health Clinical
Center, National Institutes of Health, Bethesda, MD. Under a Cooperative
Research and Development Agreement, Laboratoire HRA-Pharma, Paris,
France, provided study drug and placebo as well as salary support for
one member of the research team. The research team analyzed the data and
drafted the manuscript, and Laboratoire HRA-Pharma agreed to the final
submission, NCT00290251.
NR 32
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U1 0
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
J9 FERTIL STERIL
JI Fertil. Steril.
PD FEB
PY 2011
VL 95
IS 2
BP 767
EP U769
DI 10.1016/j.fertnstert.2010.09.059
PG 8
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 709EA
UT WOS:000286419000071
PM 21055739
ER
PT J
AU Davis, RM
Matsumoto, S
Bernardo, M
Sowers, A
Matsumoto, KI
Krishna, MC
Mitchell, JB
AF Davis, Ryan M.
Matsumoto, Shingo
Bernardo, Marcelino
Sowers, Anastasia
Matsumoto, Ken-Ichiro
Krishna, Murali C.
Mitchell, James B.
TI Magnetic resonance imaging of organic contrast agents in mice: capturing
the whole-body redox landscape
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Magnetic resonance imaging; Nitroxides; Redox; Radioprotection; Electron
paramagnetic resonance spectroscopy; Free radicals
ID IN-VIVO MEASUREMENT; SUPEROXIDE-DISMUTASE; SOLUBLE NITROXIDES; MURINE
TUMOR; TEMPOL; OXYGEN; AMIFOSTINE; RADIOTHERAPY; METABOLISM; PROTECTION
AB Nitroxides are a class of stable free radicals that have several biomedical applications including radioprotection and noninvasive assessment of tissue redox status. For both of these applications, it is necessary to understand the in vivo biodistribution and reduction of nitroxides. In this study, magnetic resonance imaging was used to compare tissue accumulation (concentration) and reduction of two commonly studied nitroxides: the piperidine nitroxide Tempol and the pyrrolidine nitroxide 3-CP. It was found that 3-CP was reduced 3 to 11 times slower (depending on the tissue) than Tempol in vivo and that maximum tissue concentration varies substantially between tissues (0.6-7.2 mM). For a given tissue, the maximum concentration usually did not vary between the two nitroxides. Furthermore, using electron paramagnetic resonance spectroscopy, we showed that the nitroxide reduction rate depends only weakly on cellular pO(2) in the oxygen range expected in vivo. These observations, taken with the marked variation in nitroxide reduction rates observed between tissues, suggest that tissue pO(2) is not a major determinant of the nitroxide reduction rate in vivo. For the purpose of redox imaging, 3-CP was shown to be an optimal choice based on the achievable concentrations and bioreduction observed in vivo. Published by Elsevier Inc.
C1 [Davis, Ryan M.; Matsumoto, Shingo; Sowers, Anastasia; Krishna, Murali C.; Mitchell, James B.] NIH, Radiat Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Bernardo, Marcelino] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Bernardo, Marcelino] NCI, SAIC Frederick, Frederick, MD 21702 USA.
[Matsumoto, Ken-Ichiro] Natl Inst Radiol Sci, Mol Imaging Ctr, Chiba 260, Japan.
RP Davis, RM (reprint author), NIH, Radiat Biol Branch, Ctr Canc Res, Bldg 10, Bethesda, MD 20892 USA.
EM davisrm2@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. We thank Dr. Pete Choyke for his provision of
imaging resources. We thank Dr. Brenda Klaunberg for her assistance in
identifying murine tissues on MR images.
NR 45
TC 26
Z9 27
U1 4
U2 17
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD FEB 1
PY 2011
VL 50
IS 3
BP 459
EP 468
DI 10.1016/j.freeradbiomed.2010.11.028
PG 10
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 722JX
UT WOS:000287429600006
PM 21130158
ER
PT J
AU Ko, SU
Ling, SM
Schreiber, C
Nesbitt, M
Ferrucci, L
AF Ko, Seung-uk
Ling, Shari M.
Schreiber, Catherine
Nesbitt, Mark
Ferrucci, Luigi
TI Gait patterns during different walking conditions in older adults with
and without knee osteoarthritis-Results from the Baltimore Longitudinal
Study of Aging
SO GAIT & POSTURE
LA English
DT Article
DE Gait; Knee osteoarthritis; Challenging walking; Mechanical work
expenditure
ID MUSCLE; STRATEGIES; FATIGUE; HIP
AB Biomechanical analysis of lower extremity activities while walking at different speeds and in challenging conditions may help to identify specific gait patterns associated with knee osteoarthritis (knee-OA). We hypothesized that individuals with asymptomatic knee-OA have lower ankle activity, while individuals with symptomatic knee-OA have similar or higher ankle activity compared to individuals without knee-OA, and that such differences are enhanced during challenging gait tasks. We tested this hypothesis by examining gait characteristics in multiple gait tasks using data from 153 Baltimore Longitudinal Study of Aging (BLSA) participants (112 without knee-OA, 41 with knee-OA: 53-87 years, 52% women). All participants who could walk unassisted were evaluated in the BLSA gait lab while walking at self-selected speed (usual-walking), at maximum speed (fast-walking) and again at self-selected speed after 30-min of walking activities (usual-walking-after-30 min). Knee range of motion was lower for knee-OA participants in the fast-walking and usual-walking-after-30 min tasks (p < 0.030). Ankle range of motion for symptomatic knee-OA was greater compared to asymptomatic knee-OA for all walking tasks (p < 0.050). Symptomatic knee-OA had greater generative MWE of the ankle compared to asymptomatic knee-OA (p = 0.034), while keeping similar absorptive MWE of the knee when compared to no-OA controls (p = 0.151). Symptomatic knee-OA individuals seem to adapt an ankle kinematic gait pattern aimed at avoiding knee pain, by enhancing forward propulsion so to minimize knee joint load. Whether these conditions represent subsequent steps in the causal pathway from knee-OA to changes in gait is still not clear. Published by Elsevier B.V.
C1 [Ko, Seung-uk] Harbor Hosp, NIA, Clin Res Branch, Baltimore, MD 21225 USA.
RP Ko, SU (reprint author), Harbor Hosp, NIA, Clin Res Branch, 3001 S Hanover St, Baltimore, MD 21225 USA.
EM kos2@mail.nih.gov
FU NIH, National Institute on Aging
FX This research was supported entirely by the Intramural Research Program
of the NIH, National Institute on Aging. Data for these analyses were
obtained from the Baltimore Longitudinal Study of Aging, a study
performed by the National Institute on Aging.
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PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0966-6362
J9 GAIT POSTURE
JI Gait Posture
PD FEB
PY 2011
VL 33
IS 2
BP 205
EP 210
DI 10.1016/j.gaitpost.2010.11.006
PG 6
WC Neurosciences; Orthopedics; Sport Sciences
SC Neurosciences & Neurology; Orthopedics; Sport Sciences
GA 737LF
UT WOS:000288569600011
PM 21145241
ER
PT J
AU Lochhead, P
Frank, B
Hold, GL
Rabkin, CS
Ng, MTH
Vaughan, TL
Risch, HA
Gammon, MD
Lissowska, J
Weck, MN
Raum, E
Muller, H
Illig, T
Klopp, N
Dawson, A
McColl, KE
Brenner, H
Chow, WH
El-Omar, EM
AF Lochhead, Paul
Frank, Bernd
Hold, Georgina L.
Rabkin, Charles S.
Ng, Michael T. H.
Vaughan, Thomas L.
Risch, Harvey A.
Gammon, Marilie D.
Lissowska, Jolanta
Weck, Melanie N.
Raum, Elke
Mueller, Heiko
Illig, Thomas
Klopp, Norman
Dawson, Alan
McColl, Kenneth E.
Brenner, Hermann
Chow, Wong-Ho
El-Omar, Emad M.
TI Genetic Variation in the Prostate Stem Cell Antigen Gene and Upper
Gastrointestinal Cancer in White Individuals
SO GASTROENTEROLOGY
LA English
DT Article
DE Stomach Cancer; Esophageal Cancer; Genetic Polymorphisms; Cancer
Genetics
ID CHRONIC ATROPHIC GASTRITIS; HELICOBACTER-PYLORI INFECTION; INCREASED
RISK; STOMACH-CANCER; GLEASON SCORE; OLDER-ADULTS; LY-6 FAMILY;
CARCINOMA; EXPRESSION; ADENOCARCINOMA
AB BACKGROUND & AIMS: An association between gastric cancer and the rs2294008 (C > T) polymorphism in the prostate stem cell antigen (PSCA) gene has been reported for several Asian populations. We set out to determine whether such an association exists in white individuals. METHODS: We genotyped 166 relatives of gastric cancer patients, including 43 Helicobacter pylori-infected subjects with hypochlorhydria and gastric atrophy, 65 infected subjects without these abnormalities, 58 H pylori-negative relatives, and 100 population controls. Additionally, a population-based study of chronic atrophic gastritis provided 533 cases and 1054 controls. We then genotyped 2 population-based, case-control studies of upper gastrointestinal cancer: the first included 312 gastric cancer cases and 383 controls; the second included 309 gastric cancer cases, 159 esophageal cancer cases, and 211 controls. Odds ratios were computed from logistic models and adjusted for confounding variables. RESULTS: Carriage of the risk allele (T) of rs2294008 in PSCA was associated with chronic atrophic gastritis (adjusted odds ratio [OR], 1.5; 95% confidence interval [CI]: 1.1-1.9) and noncardia gastric cancer (OR, 1.9; 95% CI: 1.3-2.8). The association was strongest for the diffuse histologic type (OR, 3.2; 95% CI: 1.2-10.7). An inverse association was observed between carriage of the risk allele and gastric cardia cancer (OR, 0.5; 95% CI: 0.3-0.9), esophageal adenocarcinoma (OR, 0.5; 95% CI: 0.3-0.9), and esophageal squamous cell carcinoma (OR, 0.4; 95% CI: 0.2-0.9). CONCLUSIONS: The rs2294008 polymorphism in PSCA increases the risk of noncardia gastric cancer and its precursors in white individuals but protects against proximal cancers.
C1 [El-Omar, Emad M.] Univ Aberdeen, Div Appl Med, Sch Med & Dent, Inst Med Sci,Gastrointestinal Res Grp, Aberdeen AB25 2ZD, Scotland.
[Frank, Bernd; Weck, Melanie N.; Raum, Elke; Mueller, Heiko; Brenner, Hermann] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-6900 Heidelberg, Germany.
[Rabkin, Charles S.; Chow, Wong-Ho] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Vaughan, Thomas L.] Fred Hutchinson Canc Res Ctr, Program Epidemiol, Seattle, WA 98104 USA.
[Vaughan, Thomas L.] Univ Washington, Sch Publ Hlth, Dept Epidemiol, Seattle, WA 98195 USA.
[Risch, Harvey A.] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06510 USA.
[Gammon, Marilie D.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Div Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Illig, Thomas; Klopp, Norman] Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany.
[McColl, Kenneth E.] Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland.
RP El-Omar, EM (reprint author), Univ Aberdeen, Div Appl Med, Sch Med & Dent, Inst Med Sci,Gastrointestinal Res Grp, Foresterhill, Aberdeen AB25 2ZD, Scotland.
EM e.el-omar@abdn.ac.uk
RI Brenner, Hermann/B-4627-2017;
OI Brenner, Hermann/0000-0002-6129-1572; Lissowska,
Jolanta/0000-0003-2695-5799
FU Baden-Wuerttemberg Ministry of Science, Research, and the Arts; Scottish
Government Chief Scientist Office; United States Public Health Service
[U01-CA57983, U01-CA57949, U01-CA57923, P30ES10126]; National Cancer
Institute, National Institutes of Health, and Department of Health and
Human Services [N02-CP40501, N01-CN05230]
FX Supported by grants from the Baden-Wuerttemberg Ministry of Science,
Research, and the Arts for The ESTHER study baseline examination and the
German analyses on atrophic gastritis; by a Scottish Government Chief
Scientist Office fellowship (to P. L.); by the United States Public
Health Service (U01-CA57983, U01-CA57949, U01-CA57923, P30ES10126) for
the US multicenter esophageal and gastric cancer study; and by the
National Cancer Institute, National Institutes of Health, and Department
of Health and Human Services (N02-CP40501, N01-CN05230).
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PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD FEB
PY 2011
VL 140
IS 2
BP 435
EP 441
DI 10.1053/j.gastro.2010.11.001
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 711LR
UT WOS:000286593600022
PM 21070776
ER
PT J
AU Schwarz, KB
Gonzalez-Peralta, RP
Murray, KF
Molleston, JP
Haber, BA
Jonas, MM
Rosenthal, P
Mohan, P
Balistreri, WF
Narkewicz, MR
Smith, L
Lobritto, SJ
Rossi, S
Valsamakis, A
Goodman, Z
Robuck, PR
Barton, BA
AF Schwarz, Kathleen B.
Gonzalez-Peralta, Regino P.
Murray, Karen F.
Molleston, Jean P.
Haber, Barbara A.
Jonas, Maureen M.
Rosenthal, Philip
Mohan, Parvathi
Balistreri, William F.
Narkewicz, Michael R.
Smith, Lesley
Lobritto, Steven J.
Rossi, Stephen
Valsamakis, Alexandra
Goodman, Zachary
Robuck, Patricia R.
Barton, Bruce A.
CA Peds-C Clinical Res Network
TI The Combination of Ribavirin and Peginterferon Is Superior to
Peginterferon and Placebo for Children and Adolescents With Chronic
Hepatitis C
SO GASTROENTEROLOGY
LA English
DT Article
DE Antiviral Therapy; Pediatric Liver Disease; Multicenter Pediatric Trial
ID ALPHA-2B PLUS RIBAVIRIN; VIROLOGICAL RESPONSE RATES; VIRUS-INFECTION;
PEGYLATED INTERFERON; INITIAL TREATMENT; EFFICACY; SAFETY; TRIAL;
PHARMACOKINETICS; THERAPY
AB BACKGROUND & AIMS: Although randomized trials of adults infected with hepatitis C virus (HCV) have shown that ribavirin increases the efficacy of pegylated interferon (PEG), such trials have not been performed in children. We conducted a randomized controlled trial of PEG and ribavirin, compared with PEG and placebo, in children 5 to 17 years old with chronic hepatitis C. METHODS: HCV RNA-positive children from 11 university medical centers were randomly assigned to receive either PEG alfa-2a (PEG-2a; 180 mu g/1.73 m(2) body surface area, subcutaneously each week; n = 55) and ribavirin (15 mg/kg orally in 2 doses daily) or PEG-2a and placebo (n = 59) for 48 weeks. The primary end point was sustained virologic response (SVR; lack of detectable HCV RNA at least 24 weeks after stopping therapy). RESULTS: SVR was achieved in 53% of children treated with PEG-2a and ribavirin, compared with 21% of children who received PEG-2a and placebo (P < .001). Early virologic response (HCV RNA reduction >2 log(10) IU at 12 weeks) had a negative predictive value of only 0.89 in children with genotype 1, indicating that these children might benefit from 24 weeks of therapy before stopping treatment. Side effects, especially neutropenia, led to dose modification in 40% of children. Eighty-two percent of the PEG/ribavirin and 86% of the PEG/placebo group were in compliance with the year 2 follow-up visit; the durability of virologic response was 100% in both groups. CONCLUSIONS: The combination of PEG and ribavirin is superior to PEG and placebo as therapy for chronic hepatitis C in children and adolescents.
C1 [Schwarz, Kathleen B.] Johns Hopkins Univ, Sch Med, Dept Pediat, Div Gastroenterol & Nutr, Baltimore, MD 21205 USA.
[Valsamakis, Alexandra] Johns Hopkins Univ, Sch Med, Johns Hopkins Clin Virol Lab, Baltimore, MD USA.
[Gonzalez-Peralta, Regino P.] Univ Florida, Coll Med, Dept Pediat, Sect Hepatol & Liver Transplantat, Gainesville, FL USA.
[Gonzalez-Peralta, Regino P.] Shands Childrens Hosp, Gainesville, FL USA.
[Murray, Karen F.] Seattle Childrens Hosp, Div Gastroenterol & Hepatol, Seattle, WA USA.
[Molleston, Jean P.] Indiana Univ Sch Med, Sect Pediat Gastroenterol Hepatol & Nutr, Indianapolis, IN USA.
[Haber, Barbara A.] Univ Penn, Childrens Hosp Philadelphia, Clin & Translat Sci Award Res Ctr, Philadelphia, PA 19104 USA.
[Jonas, Maureen M.] Childrens Hosp Boston, Div Gastroenterol, Boston, MA USA.
[Rosenthal, Philip] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA.
[Mohan, Parvathi] Childrens Natl Med Ctr, Div Gastroenterol Hepatol & Nutr, Washington, DC 20010 USA.
[Balistreri, William F.] Cincinnati Childrens Med Ctr, Cincinnati, OH USA.
[Narkewicz, Michael R.] Univ Colorado, Sect Pediat Gastroenterol Hepatol & Nutr, Dept Pediat, Denver Sch Med, Aurora, CO USA.
[Narkewicz, Michael R.] Childrens Hosp, Aurora, CO USA.
[Smith, Lesley; Lobritto, Steven J.] Columbia Univ, Med Ctr, New York, NY USA.
[Rossi, Stephen] Roche Mol Syst, Pleasanton, CA USA.
[Goodman, Zachary] Armed Forces Inst Pathol, Washington, DC 20306 USA.
[Robuck, Patricia R.] NIDDK, NIH, Washington, DC USA.
[Barton, Bruce A.] Maryland Med Res Inst, Baltimore, MD USA.
RP Schwarz, KB (reprint author), Brady 320,600 N Wolfe St, Baltimore, MD 21287 USA.
EM kschwarz@jhmi.edu
OI Barton, Bruce/0000-0001-7878-8895
FU Roche; Bristol-Myers Squibb; Gilead; Novartis; Boehringer-Ingelheim;
Digestive Care Inc; National Institute of Diabetes and Digestive and
Kidney Diseases and the Food and Drug Administration [1UO1DK067767-01];
National Institutes of Health/National Center for Research Resources
Colorado CTSI [UL1 RR025780]; Children's Hospital, Aurora
[M01-RR-02172]; Children's Hospital Boston, Boston, MA [M01-RR-01271];
University of California, San Francisco, CA [5-M01-RR-020359-01];
Children's National Medical Center, Washington, DC [M01-RR-00645];
Columbia University Medical Center, New York, NY [M01-RR-00082];
University of Florida, Gainesville, FL [M01-RR-00037]; University of
Washington, Seattle, WA [5-M01-RR-000240]; Children's Hospital of
Philadelphia, University of Pennsylvania, Philadelphia, PA
[U01-DK-067767-02]; Johns Hopkins Medical Center, Baltimore, MD
[M01-RR-08084]; University of Cincinnati, Cincinnati, OH; Indiana
University, Indianapolis, IN [M01-RR-00750]; [M01-RR-00069]
FX The authors disclose the following: Dr Schwarz is supported by Roche
(grant/research support), Bristol-Myers Squibb (grant/research support),
Gilead (grant/research support), and Novartis (consultant). Dr
Gonzalez-Peralta is supported by Boehringer-Ingelheim (grant/research
support), Roche (grant/research support), Bristol Myers-Squibb
(grant/research support), and Novartis (consultant). Dr Murray is
supported by Roche (grant/research support), Bristol-Myers Squibb
(grant/research support), and Novartis. Dr Molleston, Dr Haber, Dr
Jonas, Dr Rosenthal, Dr Smith, Dr Lobritto, and Dr Valsamakis are
supported by Roche (grant/research support). Dr Mohan is supported by
Roche (grant/research support) and Gilead (grant/research support). Dr
Balistreri is supported by Digestive Care Inc (consultant) and Roche
(grant/research support). Dr Narkewicz is supported by Novartis
(consultant) and Roche (grant/research support). Dr Rossi is an employee
of Roche Molecular Systems. The remaining authors disclose no
conflicts.; Supported by a cooperative agreement between the National
Institute of Diabetes and Digestive and Kidney Diseases and the Food and
Drug Administration (contract no. 1UO1DK067767-01. CRC) and in part by
National Institutes of Health/National Center for Research Resources
Colorado CTSI grant no. UL1 RR025780 and the following study sites:
M01-RR-00069, Children's Hospital, Aurora, CO; M01-RR-02172, Children's
Hospital Boston, Boston, MA; M01-RR-01271, University of California, San
Francisco, CA; 5-M01-RR-020359-01, Children's National Medical Center,
Washington, DC; M01-RR-00645, Columbia University Medical Center, New
York, NY; M01-RR-00082, University of Florida, Gainesville, FL;
M01-RR-00037, University of Washington, Seattle, WA; 5-M01-RR-000240,
Children's Hospital of Philadelphia, University of Pennsylvania,
Philadelphia, PA; U01-DK-067767-02, Johns Hopkins Medical Center,
Baltimore, MD; M01-RR-08084, University of Cincinnati, Cincinnati, OH;
and M01-RR-00750, Indiana University, Indianapolis, IN. The contents of
this report are the authors' sole responsibility and do not necessarily
represent the official views of the National Institutes of Health.
Additional support was provided by Hoffmann-La Roche for study
medications, the data coordinating center, and central laboratory costs.
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PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD FEB
PY 2011
VL 140
IS 2
BP 450
EP U148
DI 10.1053/j.gastro.2010.10.047
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 711LR
UT WOS:000286593600024
PM 21036173
ER
PT J
AU Ruhl, CE
Everhart, JE
AF Ruhl, Constance E.
Everhart, James E.
TI Gallstone Disease Is Associated With Increased Mortality in the United
States
SO GASTROENTEROLOGY
LA English
DT Article
DE Gallstone Disease; Epidemiology; Gallbladder; Cholelithiasis
ID GALLBLADDER-DISEASE; CARDIOVASCULAR-DISEASE; CANCER; POPULATION;
CHOLECYSTECTOMY; CHOLELITHIASIS; CONSUMPTION; INSULIN; COFFEE; LIVER
AB BACKGROUND & AIMS: Gallstones are common and contribute to morbidity and health care costs, but their effects on mortality are unclear. We examined whether gallstone disease was associated with overall and cause-specific mortalities in a prospective national population-based sample. METHODS: We analyzed data from 14,228 participants in the third US National Health and Nutrition Examination Survey (20-74 years old) who underwent gallbladder ultrasonography from 1988 to 1994. Gallstone disease was defined as ultrasound-documented gallstones or evidence of cholecystectomy. The underlying cause of death was identified from death certificates collected through 2006 (mean follow-up, 14.3 years). Mortality hazard ratios (HR) were calculated using Cox proportional hazards regression analysis to adjust for multiple demographic and cardiovascular disease risk factors. RESULTS: The prevalence of gallstones was 7.1% and of cholecystectomy was 5.3%. During a follow-up period of 18 years or more, the cumulative mortality was 16.5% from all causes (2389 deaths), 6.7% from cardiovascular disease (886 deaths), and 4.9% from cancer (651 deaths). Participants with gallstone disease had higher all-cause mortality in age-adjusted (HR = 1.3; 95% confidence interval [CI]: 1.2-1.5) and multivariate-adjusted analysis (HR = 1.3; 95% CI: 1.1-1.5). A similar increase was observed for cardiovascular disease mortality (multivariate-adjusted HR = 1.4; 95% CI: 1.2-1.7), and cancer mortality (multivariate-adjusted HR = 1.3; 95% CI: 0.98 - 1.8). Individuals with gallstones had a similar increase in risk of death as those with cholecystectomy (multivariate-adjusted HR = 1.1; 95% CI: 0.92-1.4). CONCLUSIONS: In the US population, persons with gallstone disease have increased mortality overall and mortalities from cardiovascular disease and cancer. This relationship was found for both ultrasound-diagnosed gallstones and cholecystectomy.
C1 [Ruhl, Constance E.] Social & Sci Syst Inc, Silver Spring, MD 20910 USA.
[Everhart, James E.] NIDDK, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
RP Ruhl, CE (reprint author), Social & Sci Syst Inc, 8757 Georgia Ave,12th Floor, Silver Spring, MD 20910 USA.
EM cruhl@s-3.com
FU National Institute of Diabetes and Digestive and Kidney Diseases
[HHSN267200700001G]
FX This work was supported by a contract from the National Institute of
Diabetes and Digestive and Kidney Diseases (HHSN267200700001G).
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PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD FEB
PY 2011
VL 140
IS 2
BP 508
EP 516
DI 10.1053/j.gastro.2010.10.060
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 711LR
UT WOS:000286593600030
PM 21075109
ER
PT J
AU Veerapu, NS
Raghuraman, S
Liang, TJ
Heller, T
Rehermann, B
AF Veerapu, Naga Suresh
Raghuraman, Sukanya
Liang, T. Jake
Heller, Theo
Rehermann, Barbara
TI Sporadic Reappearance of Minute Amounts of Hepatitis C Virus RNA After
Successful Therapy Stimulates Cellular Immune Responses
SO GASTROENTEROLOGY
LA English
DT Article
DE Interferon; IFN; Liver Disease; Virology
ID BLOOD MONONUCLEAR-CELLS; ALANINE AMINOTRANSFERASE LEVELS; SUSTAINED
VIROLOGICAL RESPONSE; HCV RNA; OCCULT INFECTION; CULTURE; LIVER;
PERSISTENCE; INTERFERON; RIBAVIRIN
AB BACKGROUND & AIMS: Several studies have reported hepatitis C virus (HCV) RNA sequences in the circulation after treatment-induced or spontaneous recovery. We investigated whether the HCV RNA represents persistence of HCV infection or reinfection. METHODS: We studied 117 patients who recovered from HCV infection (98 following therapy and 19 spontaneously). A reverse-transcription polymerase chain reaction assay was used to detect the 5'-untranslated region of HCV. T-cell responses were studied by enzyme-linked immunospot for interferon-gamma. RESULTS: Plasma samples from 15% of treatment-recovered patients and no spontaneously recovered patient tested positive for HCV RNA. Lymphocytes from 3 patients who responded to therapy and 1 who recovered spontaneously tested positive. The frequency of HCV RNA detection in plasma correlated inversely with the time after the end of treatment. Post-treatment HCV 5'-untranslated region sequences matched pretreatment sequences in 85% of cases. T-cell responses were significantly greater at time points with detectable trace amounts of HCV RNA than at time points without detectable HCV RNA (P = .035) and were primarily against nonstructural HCV antigens. The immune hierarchy was preserved over 5 years in patients whose post-treatment HCV RNA sequences matched pretreatment sequences, indicating HCV RNA persistence. An altered immune hierarchy with dominant immune responses, shifting from nonstructural to structural antigens, was observed in a single patient whose post-treatment HCV genotype differed from that of the pretreatment genotype, indicating HCV reinfection. CONCLUSIONS: Trace amounts of HCV RNA of pretreatment sequence persisted and reappeared sporadically in the circulation within 8 years after recovery from hepatitis C but not thereafter, indicating that patients are cured of HCV infection. Reappearance of HCV RNA induced HCV-specific T-cell responses.
C1 [Veerapu, Naga Suresh; Raghuraman, Sukanya; Rehermann, Barbara] NIDDK, Immunol Sect, Liver Dis Branch, NIH,DHHS, Bethesda, MD 20892 USA.
RP Rehermann, B (reprint author), NIDDK, Immunol Sect, Liver Dis Branch, NIH,DHHS, 10 Ctr Dr,Bldg 10,Room 9B16C, Bethesda, MD 20892 USA.
EM Rehermann@nih.gov
RI Veerapu, Naga Suresh/F-4338-2011
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX Supported by the intramural research program of the National Institute
of Diabetes and Digestive and Kidney Diseases, National Institutes of
Health.
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PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD FEB
PY 2011
VL 140
IS 2
BP 676
EP U422
DI 10.1053/j.gastro.2010.10.048
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 711LR
UT WOS:000286593600046
PM 21040725
ER
PT J
AU Kim, AY
Kuntzen, T
Timm, J
Nolan, BE
Baca, MA
Reyor, LL
Berical, AC
Feller, AJ
Johnson, KL
Zur Wiesch, JS
Robbins, GK
Chung, RT
Walker, BD
Carrington, M
Allen, TM
Lauer, GM
AF Kim, Arthur Y.
Kuntzen, Thomas
Timm, Joerg
Nolan, Brian E.
Baca, Melanie A.
Reyor, Laura L.
Berical, Andrew C.
Feller, Andrea J.
Johnson, Kristin L.
Zur Wiesch, Julian Schulze
Robbins, Gregory K.
Chung, Raymond T.
Walker, Bruce D.
Carrington, Mary
Allen, Todd M.
Lauer, Georg M.
TI Spontaneous Control of HCV Is Associated With Expression of HLA-B*57 and
Preservation of Targeted Epitopes
SO GASTROENTEROLOGY
LA English
DT Article
DE CD8 T Cell; HLA-B57; Spontaneous Clearance; Viral Escape
ID C VIRUS-INFECTION; T-CELL RESPONSES; ANTIGEN CLASS-I; DISEASE
PROGRESSION; IMMUNE-RESPONSES; HIV-INFECTION; P24 GAG; EVOLUTION; HLA;
ALLELES
AB BACKGROUND & AIMS: HLA class I alleles are linked to spontaneous control of hepatitis C virus (HCV) and human immunodeficiency virus-1, but for HCV the roles of particular alleles and corresponding CD8(+) T-cell responses remain incompletely defined. We aimed to determine the correlations between these alleles and natural outcomes of HCV and determine associated key T-cell responses. METHODS: In a cohort of HCV individuals, we determined HLA class I alleles, HCV outcomes, T-cell responses, and examined sequence data for mutational changes within key epitopes. RESULTS: Carriage of HLA-B*57 was associated with a higher rate of viral clearance (risk ratio = 2.0; 95% confidence interval: 1.2-3.4), while HLA-B*08 was associated with a lower rate (risk ratio = 0.34; 95% confidence interval: 0.1-0.9]. Two HLA-B*57-restricted T-cell epitopes were targeted in spontaneous clearance; subjects with chronic viremia expressing HLA-B*57 harbored HCV strains with a high frequency of mutations in key residues. HLAB*57-mediated escape was supported by diminished immune recognition of these variants and acute HCV infection revealing viral evolution toward less recognized variants. Analysis of a genotype 1b strain from a single-source HCV outbreak in which HLA-B*57 was not protective revealed sequence variations that interfere with immunogenicity, thereby preventing HLA-B*57-mediated immune pressure. CONCLUSIONS: Our data indicate a role of HLA-B*57-restricted CD8(+) T-cell responses in mediating spontaneous clearance and evolution in HCV infection, and viral strains containing epitope variants that are less recognized abrogate the protective effects of HLA-B*57. The finding that HLAB*57-mediated antiviral immunity is associated with control of both human immunodeficiency virus-1 and HCV suggests a common shared mechanism of a successful immune response against persistent viruses.
C1 [Kim, Arthur Y.; Reyor, Laura L.; Johnson, Kristin L.; Robbins, Gregory K.; Walker, Bruce D.; Allen, Todd M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, Boston, MA 02114 USA.
[Nolan, Brian E.; Reyor, Laura L.; Chung, Raymond T.; Lauer, Georg M.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Gastrointestinal Unit, Boston, MA 02114 USA.
[Kim, Arthur Y.; Kuntzen, Thomas; Baca, Melanie A.; Berical, Andrew C.; Feller, Andrea J.; Walker, Bruce D.; Carrington, Mary; Allen, Todd M.] Ragon Inst MGH Massachusetts Inst Technol & Harva, Boston, MA USA.
[Timm, Joerg] Univ Essen Gesamthsch, Inst Virol, Essen, Germany.
[Zur Wiesch, Julian Schulze] Univ Med Ctr Hamburg Eppendorf, Div Med, Hamburg, Germany.
[Zur Wiesch, Julian Schulze; Walker, Bruce D.] Howard Hughes Med Inst, Chevy Chase, MD USA.
[Carrington, Mary] NCI, Canc & Inflammat Program, Expt Immunol Lab, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Kim, AY (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, GRB-504, Boston, MA 02114 USA.
EM akim1@partners.org
RI Robbins, Gregory/F-7988-2011; Allen, Todd/F-5473-2011
FU National Institutes of Health [AI 054379, AI 066345, AI 031563, AI
042851, AI 067926, AI 069939, DK 078772, AI 062435]; Harvard Medical
School Center for AIDS Research [P30 AI060354]; Campbell Foundation;
Liver Foundation; Doris Duke Charitable Foundation; Howard Hughes
Medical Institute; Deutsche Forschungsgemeinschaft [DFG KU2250/1-1]
FX This work was funded by the National Institutes of Health (AI 054379 to
AYK, AI 066345 to AYK, GML, TMA, BDW; AI 031563, AI 042851 and AI 054379
to BDW; AI 067926 to TMA; AI 069939 and DK 078772 to RTC, AI 062435 to
GKR), the Harvard Medical School Center for AIDS Research (P30
AI060354), the Campbell Foundation (GML), the Liver Foundation (GML),
the Doris Duke Charitable Foundation and Howard Hughes Medical Institute
(BDW), Deutsche Forschungsgemeinschaft grant DFG KU2250/1-1 (TK).
NR 32
TC 66
Z9 72
U1 0
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0016-5085
J9 GASTROENTEROLOGY
JI Gastroenterology
PD FEB
PY 2011
VL 140
IS 2
BP 686
EP U434
DI 10.1053/j.gastro.2010.09.042
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 711LR
UT WOS:000286593600047
PM 20875418
ER
PT J
AU Wohr, M
Roullet, FI
Crawley, JN
AF Woehr, M.
Roullet, F. I.
Crawley, J. N.
TI Reduced scent marking and ultrasonic vocalizations in the BTBR T plus
tf/J mouse model of autism
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Autism; communication; mice; olfaction; scent marking; social behavior;
ultrasonic vocalizations
ID MICE MUS-DOMESTICUS; BENZODIAZEPINE RECEPTOR COMPLEX; MALE HOUSE MICE;
URINE MARKING; INDIVIDUAL RECOGNITION; INBRED STRAINS; SEX-PHEROMONE;
C57BL/6J MICE; SOCIAL-STATUS; T+TF/J MICE
AB Qualitative impairments in communication, such as delayed language and poor interactive communication skills, are fundamental to the diagnosis of autism. Investigations into social communication in adult BTBR T+tf/J (BTBR) mice are needed to determine whether this inbred strain incorporates phenotypes relevant to the second diagnostic symptom of autism, communication deficits, along with its strong behavioral phenotypes relevant to the first and third diagnostic symptoms, impairments in social interactions and high levels of repetitive behavior. The aim of the present study was to simultaneously measure female urine-elicited scent marking and ultrasonic vocalizations in adult male BTBR mice, in comparison with a standard control strain with high sociability, C57BL/6J (B6), for the assessment of a potential communication deficit in BTBR. Adult male BTBR mice displayed lower scent marking and minimal ultrasonic vocalization responses to female urine obtained from both B6 and BTBR females. Lower scent marking and ultrasonic vocalizations in a social setting by BTBR, as compared with B6, are consistent with the well-replicated social deficits in this inbred mouse strain. Our findings support the interpretation that BTBR incorporate communication deficits, and suggest that scent marking and ultrasonic vocalizations offer promising measures of interest in social cues that may be widely applicable to investigations of mouse models of autism.
C1 [Woehr, M.] Univ Marburg, D-35032 Marburg, Germany.
[Woehr, M.; Roullet, F. I.; Crawley, J. N.] NIMH, Lab Behav Neurosci, Intramural Res Program, NIH,Porter Neurosci Res Ctr, Bethesda, MD 20892 USA.
RP Wohr, M (reprint author), Univ Marburg, Gutenbergstr 18, D-35032 Marburg, Germany.
EM markus.woehr@staff.uni-marburg.de
FU National Institute of Mental Health
FX This work was supported by the National Institute of Mental Health
Intramural Research Program.
NR 68
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Z9 69
U1 1
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1601-1848
EI 1601-183X
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD FEB
PY 2011
VL 10
IS 1
BP 35
EP 43
DI 10.1111/j.1601-183X.2010.00582.x
PG 9
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 709VG
UT WOS:000286468900005
PM 20345893
ER
PT J
AU Scattoni, ML
Ricceri, L
Crawley, JN
AF Scattoni, M. L.
Ricceri, L.
Crawley, J. N.
TI Unusual repertoire of vocalizations in adult BTBR T plus tf/J mice
during three types of social encounters
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Autism; communication; social approach; social motivation; ultrasonic
vocalizations
ID ULTRASONIC VOCALIZATIONS; FEMALE MICE; MUS-MUSCULUS; AUTISTIC-CHILDREN;
INBRED STRAINS; MOUSE MODELS; T+TF/J MICE; HOUSE MICE; BEHAVIOR;
COMMUNICATION
AB BTBR T+tf/J (BTBR) is an inbred mouse strain that displays social deficits and repetitive behaviors analogous to the first and third diagnostic symptoms of autism. We previously reported an unusual pattern of ultrasonic vocalizations in BTBR pups that may represent a behavioral homolog to the second diagnostic symptom of autism, impaired communication. This study investigated the social and vocal repertoire in adult BTBR mice, to evaluate the role of ultrasonic vocalizations in multiple social situations at the adult stage of development. Three different social contexts were considered: male-female, male-male (resident-intruder) and female-female interactions. Behavioral responses and ultrasonic vocalizations were recorded for BTBR and for the highly social control strain C57BL/6J (B6). No episodes of overt fighting or mating were observed during the short durations of the three different experimental encounters. BTBR displayed lower levels of vocalizations and social investigation in all three social contexts as compared with B6. In addition, the correlation analyses between social investigation and ultrasonic vocalization emission rate showed that in B6 mice, the two variables were positively correlated in all the three different social settings, whereas in BTBR mice, the positive correlation was significant only in the male-female interactions. These findings strongly support the value of simultaneously recording two aspects of the mouse social repertoire: social motivation and bioacoustic communication. Moreover, our findings in adults are consistent with previous results in pups, showing an unusual vocal repertoire in BTBR as compared with B6.
C1 [Scattoni, M. L.; Ricceri, L.] Ist Super Sanita, Neurotoxicol & Neuroendocrinol Sect, Dept Cell Biol & Neurosci, I-00161 Rome, Italy.
[Scattoni, M. L.; Crawley, J. N.] NIMH, Lab Behav Neurosci, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Scattoni, ML (reprint author), Ist Super Sanita, Neurotoxicol & Neuroendocrinol Sect, Dept Cell Biol & Neurosci, Viale Regina Elena 299, I-00161 Rome, Italy.
EM marialuisa.scattoni@iss.it
RI Scattoni, Maria Luisa/K-4116-2016
OI Scattoni, Maria Luisa/0000-0002-6659-0280
FU National Institute of Mental Health; Istituto Superiore di Sanita
[530F/52]
FX We are grateful for the excellent technical contributions of our
students Maria Adelaide Marconi, Ludovica De Benedetti, Gloria Matte
Bon, ISS, and Mark Harris, NIMH. Special thanks go to Professor Stefan
Brudzynsky, Brock University, Dr Markus Wohr, University of Marburg, and
Raimund Specht, Avisoft Bioacoustics, for their expert advice concerning
the unstructured call categorization. We thank Adam Katz, NIMH, for the
editing of the supplementary movies. This work was supported by the
National Institute of Mental Health Intramural Research Program and
Istituto Superiore di Sanita 530F/52 'Neurobehavioral phenotyping of
genetically modified mouse models of mental retardation'.
NR 59
TC 100
Z9 102
U1 4
U2 13
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD FEB
PY 2011
VL 10
IS 1
BP 44
EP 56
DI 10.1111/j.1601-183X.2010.00623.x
PG 13
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 709VG
UT WOS:000286468900006
PM 20618443
ER
PT J
AU Coutellier, L
Logemann, A
Kuo, J
Rusnak, M
Usdin, TB
AF Coutellier, L.
Logemann, A.
Kuo, J.
Rusnak, M.
Usdin, T. B.
TI TIP39 modulates effects of novelty-induced arousal on memory
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Noradrenergic system; novelty-induced arousal; short-term memory; TIP39;
working memory
ID OBJECT RECOGNITION MEMORY; ADRENAL STRESS HORMONES; TUBEROINFUNDIBULAR
PEPTIDE; 39 RESIDUES; PARATHYROID-HORMONE-2 RECEPTOR; EMOTIONAL AROUSAL;
LOCUS-COERULEUS; MICE; BRAIN; COGNITION
AB Tuberoinfundibular peptide of 39 residues (TIP39) is a neuropeptide localized to neural circuits subserving emotional processing. Recent work showed that mice with null mutation for the gene coding TIP39 (TIP39-KO mice) display increased susceptibility to environmental provocation. Based on this stressor-dependent phenotype, the neuroanatomical distribution of TIP39, and knowledge that novelty-induced arousal modulates memory functions via noradrenergic activation, we hypothesized that exposure to a novel environment differently affects memory performance of mice with or without TIP39 signaling, potentially by differences in sensitivity of the noradrenergic system. We tested TIP39-KO mice and mice with null mutation of its receptor, the parathyroid hormone 2 receptor (PTH2-R), in tasks of short-term declarative and social memory (object recognition and social recognition tests, respectively), and of working memory (Y-maze test) under conditions of novelty-induced arousal or acclimation to the test conditions. Mice lacking TIP39 signaling showed memory impairment selectively under conditions of novelty-induced arousal. Acute administration of a PTH2-R antagonist in wild-type mice had a similar effect. The restoration of memory functions in TIP39-KO mice after injection of a beta-adrenoreceptor-blocker, propranolol, suggested involvement of the noradrenergic system. Collectively, these results suggest that the TIP39/PTH2-R system modulates the effects of novelty exposure on memory performance, potentially by acting on noradrenergic signaling.
C1 [Coutellier, L.; Logemann, A.; Kuo, J.; Rusnak, M.; Usdin, T. B.] NIMH, Sect Fundamental Neurosci, NIH, Bethesda, MD 20892 USA.
RP Usdin, TB (reprint author), NIMH, Sect Fundamental Neurosci, NIH, 35 Convent Dr,Room 1B-215, Bethesda, MD 20892 USA.
EM usdint@mail.nih.gov
FU NIH, National Institute of Mental Health
FX We thank Jim Pickel for generation of knockout mice, Elka Scordalakes
and Eugene Dimitrov for help and advice, and Andrew Holmes for advice
and helpful comments on the manuscript. This research was supported by
the Intramural Program of the NIH, National Institute of Mental Health.
The authors declare that there are no potential conflicts of interest.
NR 44
TC 5
Z9 5
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD FEB
PY 2011
VL 10
IS 1
BP 90
EP 99
DI 10.1111/j.1601-183X.2010.00643.x
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 709VG
UT WOS:000286468900010
PM 20796031
ER
PT J
AU Yang, JD
Sun, ZF
Hu, CL
Lai, JP
Dove, R
Nakamura, I
Lee, JS
Thorgeirsson, SS
Kang, KJ
Chu, IS
Roberts, LR
AF Yang, Ju Dong
Sun, Zhifu
Hu, Chunling
Lai, Jinping
Dove, Rebecca
Nakamura, Ikuo
Lee, Ju-Seog
Thorgeirsson, Snorri S.
Kang, Koo Jeong
Chu, In-Sun
Roberts, Lewis R.
TI Sulfatase 1 and Sulfatase 2 in Hepatocellular Carcinoma: Associated
Signaling Pathways, Tumor Phenotypes, and Survival
SO GENES CHROMOSOMES & CANCER
LA English
DT Article
ID IQGAP1 INTEGRATES CA2+/CALMODULIN; HEPARAN-SULFATE; IN-VIVO;
TRANSFORMING GROWTH-FACTOR-BETA-1; BREAST-CANCER; GROWTH; HSULF-1;
CELLS; EXPRESSION; BINDING
AB The heparin-degrading endosulfatases sulfatase 1 (SULF1) and sulfatase 2 (SULF2) have opposing effects in hepatocarcinogenesis despite structural similarity. Using mRNA expression arrays, we analyzed the correlations of SULF expression with signaling networks in human hepatocellular carcinomas (HCCs) and the associations of SULF expression with tumor phenotype and patient survival. Data from two mRNA microarray analyses of 139 and 36 HCCs and adjacent tissues were used as training and validation sets. Partek and Metacore software were used to identify SULF correlated genes and their associated signaling pathways. Associations between SULF expression, the hepatoblast subtype of HCC, and survival were examined. Both SULF1 and 2 had strong positive correlations with periostin, IQGAP1, TGFB1, and vimentin and inverse correlations with HNF4A and IQGAP2. Genes correlated with both SULFs were highly associated with the cell adhesion, cytoskeletal remodeling, blood coagulation, TGFB, and Wnt/beta-catenin and epithelial mesenchymal transition signaling pathways. Genes uniquely correlated with SULF2 were more associated with neoplastic processes than genes uniquely correlated with SULF1. High SULF expression was associated with the hepatoblast subtype of HCC. There was a bimodal effect of SULF1 expression on prognosis, with patients in the lowest or highest tertile having a worse prognosis than those in the middle tertile. SULFs have complex effects on HCC signaling and patient survival. There are functionally similar associations with cell adhesion, ECM remodeling, TGFB, and WNT pathways, but also unique associations of SULF1 and SULF2. The roles and targeting of the SULFs in cancer require further investigation. (C) 2010 Wiley-Liss, Inc.
C1 [Yang, Ju Dong; Hu, Chunling; Lai, Jinping; Dove, Rebecca; Nakamura, Ikuo; Roberts, Lewis R.] Mayo Clin, Miles Shirley Fiterman Ctr Digest Dis, Coll Med, Rochester, MN 55905 USA.
[Yang, Ju Dong; Sun, Zhifu; Hu, Chunling; Lai, Jinping; Dove, Rebecca; Nakamura, Ikuo; Roberts, Lewis R.] Mayo Clin, Ctr Canc, Rochester, MN 55905 USA.
[Sun, Zhifu] Mayo Clin, Dept Biomed Stat & Informat, Coll Med, Rochester, MN 55905 USA.
[Lee, Ju-Seog] Univ Texas MD Anderson Canc Ctr, Dept Syst Biol, Houston, TX 77030 USA.
[Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, Bethesda, MD 20892 USA.
[Kang, Koo Jeong] Keimyung Univ, Sch Med, Taegu, South Korea.
[Chu, In-Sun] Korea Res Inst Biosci & Biotechnol, Korean Bioinformat Ctr, Taejon, South Korea.
RP Roberts, LR (reprint author), Mayo Clin, Miles Shirley Fiterman Ctr Digest Dis, Coll Med, 200 1st St SW, Rochester, MN 55905 USA.
EM chu@kribb.re.kr; Roberts.lewis@mayo.edu
OI Sun, Zhifu/0000-0001-8461-7523; Roberts, Lewis/0000-0001-7885-8574
FU National Institutes of Health [CA100882, CA128633]; Mayo Clinic Center
for Cell Signaling in Gastroenterology [NIDDK P30DK084567]; Mayo Clinic
Cancer Center; Mayo Foundation; 21C Frontier Functional Human Genome
Project [MEST FG-4-2]; KRIBB
FX Supported by: National Institutes of Health, Grant numbers: CA100882,
CA128633; Mayo Clinic Center for Cell Signaling in Gastroenterology,
Grant number: NIDDK P30DK084567; Mayo Clinic Cancer Center; Mayo
Foundation; 21C Frontier Functional Human Genome Project (MEST FG-4-2);
KRIBB.
NR 50
TC 21
Z9 22
U1 0
U2 18
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1045-2257
J9 GENE CHROMOSOME CANC
JI Gene Chromosomes Cancer
PD FEB
PY 2011
VL 50
IS 2
BP 122
EP 135
DI 10.1002/gcc.20838
PG 14
WC Oncology; Genetics & Heredity
SC Oncology; Genetics & Heredity
GA 693ZL
UT WOS:000285263800006
PM 21104785
ER
PT J
AU Lacey, JV
Yang, HN
Gaudet, MM
Dunning, A
Lissowska, J
Sherman, ME
Peplonska, B
Brinton, LA
Healey, CS
Ahmed, S
Pharoah, P
Easton, D
Chanock, S
Garcia-Closas, M
AF Lacey, James V., Jr.
Yang, Hannah
Gaudet, Mia M.
Dunning, Alison
Lissowska, Jolanta
Sherman, Mark E.
Peplonska, Beata
Brinton, Louise A.
Healey, Catherine S.
Ahmed, Shahana
Pharoah, Paul
Easton, Douglas
Chanock, Stephen
Garcia-Closas, Montserrat
TI Endometrial cancer and genetic variation in PTEN, PIK3CA, AKT1, MLH1,
and MSH2 within a population-based case-control study
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE SNPs; Uterine cancer; Epidemiology; Haplotypes
ID COWDEN-SYNDROME; HIGH-FREQUENCY; BREAST-CANCER; MUTATIONS; RISK;
CARCINOMA; PATHWAY; VARIANTS; EPIDEMIOLOGY; ASSOCIATION
AB Objective. We assessed whether common genetic variation in PTEN, PIK3CA,AKT1, MLH1, and MSH2-genes that reportedly are frequently altered in endometrial cancer-was associated with risk of endometrial cancer.
Methods. Using data from a population-based case-control study in Poland (PECS) of 417 cases and 407 matched controls, we genotyped 76 tagging single nucleotide polymorphisms (tagSNPs; located in or within 10 kb upstream or 5 kb downstream of the gene of interest, minor allele frequency >=5% among various ethnic groups, and not already represented by another tagSNP at a LD of r(2) >=0.80) on an Illumina Custom Infinium iSelect assay that included over 29,000 SNPs in 1316 genes. For individual SNPs, we used unconditional logistic regression models, adjusted for age and site, to generate odds ratios (ORs) and 95% confidence intervals (CIs). To replicate the one statistically significant association in PECS, we independently genotyped that tagSNP among 1141 endometrial cancer cases and 2275 controls from the SEARCH study in the UK. We assessed haplotypes via extended haplotype blocks and the sequential haplotype scan method.
Results. The rs2677764 tagSNP in PIK3CA was statistically significantly associated with endometrial cancer in PECS (OR = 1.42, 95% Cl, 1.03-1.95; P = 0.03) but not SEARCH (OR=0.98, 95% Cl = 0.82-1.17). Of the 25 haplotypes observed in at least 5% of cases and controls in PECS, only 1, in PIK3CA, was statistically significantly associated with endometrial cancer (OR=1.39, 95% Cl. 1.00-1.93). All haplotype global p-values were null.
Conclusion. Common genetic variation in PTEN, PIK3CA, AIM MLH1, or MSH2 was not statistically significantly associated with endometrial cancer. Published by Elsevier Inc.
C1 [Lacey, James V., Jr.; Yang, Hannah; Gaudet, Mia M.; Lissowska, Jolanta; Sherman, Mark E.; Peplonska, Beata; Brinton, Louise A.; Chanock, Stephen; Garcia-Closas, Montserrat] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Gaudet, Mia M.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Dunning, Alison; Healey, Catherine S.; Ahmed, Shahana; Pharoah, Paul] Univ Cambridge, Canc Res UK Human Canc Genet Res Grp, Dept Oncol, Cambridge, England.
[Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Peplonska, Beata] Nofer Inst Occupat Med, Dept Occupat & Environm Epidemiol, Lodz, Poland.
[Easton, Douglas] Univ Cambridge, Canc Res UK Genet Epidemiol Unit, Dept Publ Hlth & Primary Care, Cambridge, England.
[Chanock, Stephen] NCI, Core Genotyping Facil, Adv Technol Ctr, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Chanock, Stephen] NCI, Lab Translat Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Lacey, JV (reprint author), 1500 E Duarte Rd, Duarte, CA 91010 USA.
EM jlacey@coh.org
RI Peplonska, Beata/F-6004-2010; Garcia-Closas, Montserrat /F-3871-2015;
Brinton, Louise/G-7486-2015;
OI Garcia-Closas, Montserrat /0000-0003-1033-2650; Brinton,
Louise/0000-0003-3853-8562; Lissowska, Jolanta/0000-0003-2695-5799;
Dunning, Alison Margaret/0000-0001-6651-7166
FU National Cancer Institute; National Institutes of Health; Department of
Health and Human Services
FX Supported by the Intramural Research Program of the National Cancer
Institute, the National Institutes of Health, and the Department of
Health and Human Services.
NR 32
TC 7
Z9 9
U1 0
U2 0
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD FEB
PY 2011
VL 120
IS 2
BP 167
EP 173
DI 10.1016/j.ygyno.2010.10.016
PG 7
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 715CA
UT WOS:000286856800002
PM 21093899
ER
PT J
AU Kamath, GS
Zareba, W
Delaney, J
Koneru, JN
McKenna, W
Gear, K
Polonsky, S
Sherrill, D
Bluemke, D
Marcus, F
Steinberg, JS
AF Kamath, Ganesh S.
Zareba, Wojciech
Delaney, Jessica
Koneru, Jayanthi N.
McKenna, William
Gear, Kathleen
Polonsky, Slava
Sherrill, Duane
Bluemke, David
Marcus, Frank
Steinberg, Jonathan S.
TI Value of the signal-averaged electrocardiogram in arrhythmogenic right
ventricular cardiomyopathy/dysplasia
SO HEART RHYTHM
LA English
DT Article
DE Arrhythmogenic right ventricular cardiomyopathy/dysplasia;
Signal-averaged electrocardiogram
ID TERM-FOLLOW-UP; RISK STRATIFICATION; MAGNETIC-RESONANCE; LATE
POTENTIALS; DYSPLASIA/CARDIOMYOPATHY; DYSPLASIA; DIAGNOSIS; TACHYCARDIA;
CRITERIA; ARRHYTHMIAS
AB BACKGROUND Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is an inherited disease that causes structural and functional abnormalities of the right ventricle (RV). The presence of late potentials as assessed by the signal-averaged electrocardiogram (SAECG) is a minor task force criterion.
OBJECTIVE The purpose of this study was to examine the diagnostic and clinical value of the SAECG in a large population of genotyped ARVC/D probands.
METHODS We compared the SAECGs of 87 ARVC/D probands (age 37 +/- 13 years, 47 males) diagnosed as affected or borderline by task force criteria without using the SAECG criterion with 103 control subjects. The association of SAECG abnormalities was also correlated with clinical presentation, surface ECG, ventricular tachycardia (VT) inducibility at electrophysiologic testing, implantable cardioverter-defibrillator therapy for VT, and RV abnormalities as assessed by cardiac magnetic resonance imaging (cMRI).
RESULTS Compared with controls, all three components of the SAECG were highly associated with the diagnosis of ARVC/D (P <.001). They include the filtered QRS duration (97.8 +/- 8.7 ms vs 119.6 +/- 23.8 ms), low-amplitude signal (24.4 +/- 9.2 ms vs 46.2 +/- 23.7 ms), and root mean square amplitude of the last 40 ms of the QRS (50.4 +/- 26.9 +/- mu V vs 27.9 +/- 36.3 mu V). The sensitivity of using SAECG for diagnosis of ARVC/D was increased from 47% using the established 2 of 3 criteria (i.e., late potentials) to 69% by using a modified criterion of any 1 of 3 criteria, while maintaining a high specificity of 95%. Abnormal SAECG as defined by this modified criterion was associated with a dilated RV volume and decreased RV ejection fraction detected by cMRI (P <.05). SAECG abnormalities did not vary with clinical presentation or reliably predict spontaneous or inducible VT and had limited correlation with ECG findings.
CONCLUSION Using 1 of 3 SAECG criteria contributed to increased sensitivity and specificity for the diagnosis of ARVC/D. This finding is incorporated in the recent modification of the task force criteria.
C1 [Steinberg, Jonathan S.] St Lukes Hosp, Div Cardiol, Al Sabah Arrhythmia Inst, New York, NY 10025 USA.
Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
[Zareba, Wojciech; Polonsky, Slava] Univ Rochester, Sch Med, Rochester, NY USA.
[McKenna, William] Heart Hosp, London, England.
[Gear, Kathleen; Marcus, Frank] Univ Arizona, Sarver Heart Ctr, Tucson, AZ USA.
[Sherrill, Duane] Univ Arizona, Mel & Enid Zuckerman Coll Publ Hlth, Tucson, AZ USA.
[Bluemke, David] NIH Clin Ctr, Bethesda, MD USA.
[Steinberg, Jonathan S.] Roosevelt Hosp, Div Cardiol, Al Sabah Arrhythmia Inst, New York, NY 10025 USA.
RP Steinberg, JS (reprint author), St Lukes Hosp, Div Cardiol, Al Sabah Arrhythmia Inst, 1111 Amsterdam Ave, New York, NY 10025 USA.
EM jss7@columbia.edu
RI McKenna, William/C-3243-2008;
OI McKenna, William/0000-0001-7994-2460; Bluemke, David/0000-0002-8323-8086
FU National Heart, Lung, and Blood Institute (NHLBI) [U01 HL65594, HL65652,
HL65691]
FX Funded by National Heart, Lung, and Blood Institute (NHLBI) Grants U01
HL65594, HL65652, and HL65691. Dr. Steinberg is the Al-Sabah Endowed
Director of the Arrhythmia Institute at St. Luke's and Roosevelt
Hospitals.
NR 43
TC 24
Z9 24
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1547-5271
J9 HEART RHYTHM
JI Heart Rhythm
PD FEB
PY 2011
VL 8
IS 2
BP 256
EP 262
DI 10.1016/j.hrthm.2010.10.007
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 712GC
UT WOS:000286652900018
PM 20933608
ER
PT J
AU Guo, XC
Zhang, Y
Li, J
Ma, JC
Wei, ZL
Tan, WJ
O'Brien, SJ
AF Guo, Xiuchan
Zhang, Yong
Li, Ji
Ma, Jingchen
Wei, Zuli
Tan, Wenjie
O'Brien, Stephen J.
TI Strong Influence of Human Leukocyte Antigen (HLA)-DP Gene Variants on
Development of Persistent Chronic Hepatitis B Virus Carriers in the Han
Chinese Population
SO HEPATOLOGY
LA English
DT Article
ID CHRONIC VIRAL-HEPATITIS; HEPATOCELLULAR-CARCINOMA; INFECTIOUS-DISEASES;
ASSOCIATION; HLA; POLYMORPHISMS; CLEARANCE; SUSCEPTIBILITY; BINDING;
KOREA
AB Chronic hepatitis B virus (HBV) infection is a major health issue, especially in Asia. A recent genome-wide association study (GWAS) implicated genetic variants in the human leukocyte antigen (HLA)-DP locus associated with chronic hepatitis B in Japanese and Thai populations. To confirm whether the polymorphisms at the HLA-DP genes are associated with persistent chronic HBV infection in Han Chinese, we conducted an independent casecontrol study using 521 persistent chronic HBV carriers and 819 controls that included 571 persons with HBV natural clearance and 248 never HBV-infected (healthy) individuals. Eleven single nucleotide polymorphisms (SNPs) in a region including HLA-DPA and HLA-DPB and an adjacent SNP in strong linkage disequilibrium (LD) with a neighboring HLA-DR13 locus were genotyped using the TaqMan SNP genotyping assay. Eleven variants at HLA-DP showed a strong association with persistent chronic HBV carrier status (P = 1.82 X 10(-12) to 0.01). We also stratified the analysis by HBV clearance status to test the association between these polymorphisms and HBV natural clearance; similar results were obtained (P = 2.70 x 10(-1)1 to 0.003). Included SNPs define highly structured haplotypes that were also strongly associated with HBV chronic infection (block 1: odds ratio [OR] = 0.54, P = 8.73 x 10(-7); block 2: OR = 1.98, P = 1.37 x 10(-10)). These results further confirm that genetic variants in the HLA-DP locus are strongly associated with persistent HBV infection in the Han Chinese population. (HEPATOLOGY 2011;53:422-428)
C1 [Guo, Xiuchan] Wenzhou Med Coll, Zhejiang Prov Key Lab Med Genet, Sch Lab Med & Life Sci, Wenzhou, Zhejiang, Peoples R China.
[Guo, Xiuchan; Zhang, Yong] Chinese Ctr Dis Control & Prevent, State Key Lab Infect Dis Prevent & Control, Inst Viral Dis Control & Prevent, Beijing, Peoples R China.
[Guo, Xiuchan; Li, Ji; O'Brien, Stephen J.] NCI, Lab Genom Divers, Ctr Canc Res, NIH, Frederick, MD 21701 USA.
[Ma, Jingchen] Hebei Prov Ctr Dis Control & Prevent, Shijiazhuang, Peoples R China.
[Wei, Zuli] Luohes Ctr Dis Control & Prevent, Luohe City, Henan, Peoples R China.
[Tan, Wenjie] Chinese Ctr Dis Control & Prevent, Biotech Ctr Viral Dis Emergency, Inst Viral Dis Control & Prevent, Beijing, Peoples R China.
RP Guo, XC (reprint author), Wenzhou Med Coll, Zhejiang Prov Key Lab Med Genet, Sch Lab Med & Life Sci, Wenzhou, Zhejiang, Peoples R China.
EM xguo1@cdc.gov
FU National Cancer Institute, National Institutes of Health [N01-CO-12400];
NIH, National Cancer Institute, Center for Cancer Research
FX Funded in whole or in part with federal fiends from the National Cancer
Institute, National Institutes of Health, under contract N01-CO-12400.
The content of this publication does not necessarily reflect the views
or policies of the U.S. Department of Health and Human Services, nor
does mention of trade names, commercial products, or organizations imply
endorsement by the U.S. Government. This research was supported in part
by the Intramural Research Program of the NIH, National Cancer
Institute, Center for Cancer Research.
NR 25
TC 82
Z9 96
U1 0
U2 6
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD FEB
PY 2011
VL 53
IS 2
BP 422
EP 428
DI 10.1002/hep.24048
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 715BO
UT WOS:000286855600008
PM 21274863
ER
PT J
AU Nelson, JE
Wilson, L
Brunt, EM
Yeh, MM
Kleiner, DE
Unalp-Arida, A
Kowdley, KV
AF Nelson, James E.
Wilson, Laura
Brunt, Elizabeth M.
Yeh, Matthew M.
Kleiner, David E.
Unalp-Arida, Aynur
Kowdley, Kris V.
CA Nonalcoholic Steatohepatitis Clini
TI Relationship Between the Pattern of Hepatic Iron Deposition and
Histological Severity in Nonalcoholic Fatty Liver Disease
SO HEPATOLOGY
LA English
DT Article
ID NF-KAPPA-B; HEREDITARY HEMOCHROMATOSIS PROTEIN; KUPFFER CELLS; HEPCIDIN
EXPRESSION; OXIDATIVE STRESS; GENETIC HEMOCHROMATOSIS;
MOLECULAR-MECHANISM; INSULIN-RESISTANCE; STEATOHEPATITIS; HFE
AB Previous studies examining the relationship between hepatic iron deposition and histological severity in nonalcoholic fatty liver disease (NAFLD) have been inconclusive. The goal of this study was to examine the relationship between hepatic iron deposition and liver histology in 849 patients enrolled in the Nonalcoholic Steatohepatitis Clinical Research Network. Hepatic iron staining was performed in a central laboratory, and the stains were scored for grade and cellular and parenchymal localization by a central pathology committee; the relationship between the grade and pattern of iron deposition and the clinical, laboratory, and histological variables was examined with univariate and multivariate analyses. Stainable hepatic iron was present in 293 of 849 patients (34.5%) in one of three histological patterns: a hepatocellular (HC) pattern [63/849 (7.4%)], a reticuloendothelial system (RES) cell pattern [91/849 (10.7%)], or a mixed RFS/HC pattern [139/849 (16.4%)]. Patients with the RES iron-staining pattern were more likely to have advanced fibrosis compared to those with those with HC iron (P = 0.01). Patients with RES iron were also more likely to have advanced histological features such as fibrosis (P = 0.049), portal inflammation (P = 0.002), HC ballooning (P = 0.006), and definite nonalcoholic steatohepatitis (P = 0.007) compared to those with patients with HC or mixed iron patterns. The presence of RES iron (odds ratio = 1.60, 95% confidence interval = 1.10-2.33, P = 0.015) was independently associated with advanced hepatic fibrosis on multiple regression analysis after adjustments for age, gender, diabetes status, and body mass index. Conclusion: The presence and pattern of hepatic iron deposition are associated with distinct histological features in patients with NAFLD and may have implications for pathophysiology and therapy. (HEPATOLOGY 2011;53:448-457)
C1 [Kowdley, Kris V.] Virginia Mason Med Ctr, Ctr Liver Dis, Inst Digest Dis, Seattle, WA 98101 USA.
[Nelson, James E.; Kowdley, Kris V.] Virginia Mason Med Ctr, Benaroya Res Inst, Seattle, WA 98101 USA.
[Wilson, Laura; Unalp-Arida, Aynur] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Brunt, Elizabeth M.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA.
[Yeh, Matthew M.] Univ Washington, Med Ctr, Dept Pathol, Seattle, WA 98195 USA.
[Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RP Kowdley, KV (reprint author), Virginia Mason Med Ctr, Ctr Liver Dis, Inst Digest Dis, 1201 9th Ave, Seattle, WA 98101 USA.
EM kkowdley@benaroyaresearch.org
OI Kleiner, David/0000-0003-3442-4453
FU National Institute of Diabetes and Digestive and Kidney Diseases
[U01DK061718, U01DK061728, U01DK061731, U01DK061732, U01DK061734,
U01DK061737, U01DK061738, U01DK061730, U01DK061713]; National Institute
of Child Health and Human Development; National Institutes of Health
[DK-02957]; General Clinical Research Centers [UL1RR024989, M01RR000750,
M01RR00188, UL1RR02413101, M01RR000827, ULIRR02501401, M01RR000065,
M01RR020359]; National Cancer Institute
FX The Nonalcoholic Steatohepatitis Clinical Research Network is supported
by the National Institute of Diabetes and Digestive and Kidney Diseases
(grants U01DK061718, U01DK061728, U01DK061731, U01DK061732, U01DK061734,
U01DK061737, U01DK061738, U01DK061730, and U01DK061713) and by the
National Institute of Child Health and Human Development. Kris V Kowdley
is supported by the National Institutes of Health (K24 grant DK-02957).
Several clinical centers use support from General Clinical Research
Centers or Clinical and Translational Science Awards to conduct studies
for the Nonalcoholic Steatohepatitis Clinical Research Network (grants
UL1RR024989, M01RR000750, M01RR00188, UL1RR02413101, M01RR000827,
ULIRR02501401, M01RR000065, and M01RR020359). This work was supported in
part by the Intramural Research Program of the National Cancer
Institute.
NR 50
TC 78
Z9 85
U1 0
U2 6
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD FEB
PY 2011
VL 53
IS 2
BP 448
EP 457
DI 10.1002/hep.24038
PG 10
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 715BO
UT WOS:000286855600011
PM 21274866
ER
PT J
AU Ohmine, K
Li, Y
Bauer, TR
Hickstein, DD
Russell, DW
AF Ohmine, Ken
Li, Yi
Bauer, Thomas R., Jr.
Hickstein, Dennis D.
Russell, David W.
TI Tracking of Specific Integrant Clones in Dogs Treated with Foamy Virus
Vectors
SO HUMAN GENE THERAPY
LA English
DT Article
ID NIJMEGEN-BREAKAGE-SYNDROME; CHRONIC GRANULOMATOUS-DISEASE; ACUTE
LYMPHOBLASTIC-LEUKEMIA; NOD/SCID-REPOPULATING CELLS; HEMATOPOIETIC
STEM-CELLS; RETROVIRAL GENE MARKING; LONG-TERM; THERAPY; ACTIVATION;
TRANSDUCTION
AB Vector integration can lead to proto-oncogene activation and malignancies during hematopoietic stem cell gene therapy. We previously used foamy virus vectors to deliver the CD18 gene under the control of an internal murine stem cell virus promoter and successfully treated dogs with canine leukocyte adhesion deficiency. Here we have tracked the copy numbers of 11 specific proviruses found in these animals for 36-42 months after transplantation, including examples within or near proto-oncogenes, tumor suppressor genes, and genes unrelated to cancer. We found no evidence for clonal expansion of any of the clones, including those with proviruses in the MECOM gene (MDS1-EVI1 complex). These results suggest that although foamy virus vectors may integrate near proto-oncogenes, this does not necessarily lead to clonal expansion and malignancies. Additionally, we show that copy number estimates of these specific proviruses based on linker-mediated PCR results are different from those obtained by quantitative PCR, but can provide a qualitative assessment of provirus levels.
C1 [Ohmine, Ken; Li, Yi; Russell, David W.] Univ Washington, Dept Med, Div Hematol, Seattle, WA 98195 USA.
[Bauer, Thomas R., Jr.; Hickstein, Dennis D.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Russell, David W.] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
RP Russell, DW (reprint author), Univ Washington, Dept Med, Div Hematol, Seattle, WA 98195 USA.
EM hicksted@mail.nih.gov; drussell@u.washington.edu
FU U.S. National Institutes of Health, National Cancer Institute, Center
for Cancer Research; U.S. National Institutes of Health [HL53750,
HL085107]
FX This research was supported by the Intramural Research Program of the
U.S. National Institutes of Health, National Cancer Institute, Center
for Cancer Research, and by U.S. National Institutes of Health grants
HL53750 and HL085107. We thank Laura Tuschong for processing blood
samples and Mehreen Hai for assistance with LM-PCR.
NR 45
TC 5
Z9 5
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1043-0342
J9 HUM GENE THER
JI Hum. Gene Ther.
PD FEB
PY 2011
VL 22
IS 2
BP 217
EP 224
DI 10.1089/hum.2010.072
PG 8
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 722PQ
UT WOS:000287447200012
PM 20738155
ER
EF