FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Young, J
Zhang, M
Tavora, F
Oliveira, JB
Burke, A
AF Young, J.
Zhang, M.
Tavora, F.
Oliveira, J. B.
Burke, A.
TI DSG2 Mutations in ARVC: A Molecular Autopsy Study
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Univ Maryland, Med Ctr, Baltimore, MD 21201 USA.
Fudan Univ, Shanghai Med Coll, Shanghai 200433, Peoples R China.
NIH, Bethesda, MD 20892 USA.
Messejana Heart & Lung Hosp, Fortaleza, Ceara, Brazil.
NR 0
TC 0
Z9 0
U1 1
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 2012
VL 25
SU 2
MA 17
BP 7A
EP 7A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986900018
ER
PT J
AU Siddiqui, SW
Dunleavy, K
Arthur, DC
Filie, AC
AF Siddiqui, S. W.
Dunleavy, K.
Arthur, D. C.
Filie, A. C.
TI Utility of Fine Needle Aspiration for c-MYC Interphase Fluorescence
In-Situ Hybridization Analysis of Aggressive B-Cell Lymphomas
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Siddiqui, S. W.; Dunleavy, K.; Arthur, D. C.; Filie, A. C.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 432
BP 106A
EP 106A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986900433
ER
PT J
AU Hudson, J
Duncavage, E
Wells, S
Tamburrino, A
Salerno, P
Xi, L
Raffeld, M
Moley, J
Chernock, R
AF Hudson, J.
Duncavage, E.
Wells, S.
Tamburrino, A.
Salerno, P.
Xi, L.
Raffeld, M.
Moley, J.
Chernock, R.
TI Characterization of microRNA Expression in Medullary Thyroid Carcinoma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Washington Univ, Sch Med, St Louis, MO USA.
NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 600
BP 146A
EP 146A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986900601
ER
PT J
AU Jung, CK
Lubin, JH
Brenner, AV
Little, MP
Sigurdson, AJ
Nikiforov, YE
AF Jung, C. K.
Lubin, J. H.
Brenner, A. V.
Little, M. P.
Sigurdson, A. J.
Nikiforov, Y. E.
TI The Increase in Papillary Thyroid Cancer Incidence in the US during the
Last Four Decades Is Accompanied by a High and Stable Frequency of BRAF
Mutations and a Sharp Increase in NRAS Mutations
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Univ Pittsburgh, Pittsburgh, PA USA.
Catholic Univ Korea, Seoul, South Korea.
NIH, Bethesda, MD 20892 USA.
NR 0
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 0893-3952
J9 MODERN PATHOL
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PD FEB
PY 2012
VL 25
SU 2
MA 602
BP 146A
EP 146A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986900603
ER
PT J
AU Shuch, B
Linehan, M
Merino, MJ
AF Shuch, B.
Linehan, M.
Merino, M. J.
TI Are Adrenal Lesions Part of the Hereditary Leiomyomatosis and Renal Cell
Carcinoma Syndrome (HLRCC)?
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Shuch, B.; Linehan, M.; Merino, M. J.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 621
BP 150A
EP 150A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986900622
ER
PT J
AU Walter, BA
Barak, S
Fojo, A
Merino, MJ
AF Walter, B. A.
Barak, S.
Fojo, A.
Merino, M. J.
TI The Role of MicroRNA Expression in the Diagnosis of Adrenocortical
Carcinomas. A Marker of Poor Prognostic Tumors
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Walter, B. A.; Barak, S.; Fojo, A.; Merino, M. J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 626
BP 151A
EP 151A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986900627
ER
PT J
AU Lai, JP
Aung, PP
Khangura, S
Kamal, N
Gallin, JI
Holland, SM
Malech, HL
Heller, T
Quezado, M
AF Lai, J-P
Aung, P. P.
Khangura, S.
Kamal, N.
Gallin, J. I.
Holland, S. M.
Malech, H. L.
Heller, T.
Quezado, M.
TI Chronic Granulomatous Disease Involving Gastrointestinal Tract
(Pathology Study of 87 Cases)
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Lai, J-P; Aung, P. P.; Khangura, S.; Kamal, N.; Gallin, J. I.; Holland, S. M.; Malech, H. L.; Heller, T.; Quezado, M.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 690
BP 166A
EP 166A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986900691
ER
PT J
AU Aung, PP
Linehan, WM
Poropatich, CO
Merino, MJ
AF Aung, P. P.
Linehan, W. M.
Poropatich, C. O.
Merino, M. J.
TI Primary Neuroendocrine Tumors of the Kidney. Morphological and Molecular
Alterations of an Uncommon Malignancy
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI, NIH, Bethesda, MD 20892 USA.
Virginia Hosp Ctr, Arlington, VA 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 2012
VL 25
SU 2
MA 792
BP 191A
EP 191A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901069
ER
PT J
AU Hipp, JD
Monaco, J
Kunju, PL
Cheng, J
Yagi, Y
Rodriguez-Canales, J
Emmert-Buck, MR
Hewitt, S
Feldman, MD
Tomaszewski, JE
Toner, M
Tompkins, RG
Flotte, T
Lucas, D
Gilbertson, JR
Madabhushi, A
Balis, UJ
AF Hipp, J. D.
Monaco, J.
Kunju, P. L.
Cheng, J.
Yagi, Y.
Rodriguez-Canales, J.
Emmert-Buck, M. R.
Hewitt, S.
Feldman, M. D.
Tomaszewski, J. E.
Toner, M.
Tompkins, R. G.
Flotte, T.
Lucas, D.
Gilbertson, J. R.
Madabhushi, A.
Balis, U. J.
TI Integration of Architectural and Cytologic Driven Image Algorithms for
Prostate Adenocarcinoma Identification
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology (USCAP)
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol (USCAP)
C1 Univ Michigan, Ann Arbor, MI 48109 USA.
Rutgers State Univ, Piscataway, NJ USA.
Harvard, Boston, MA USA.
NCI, NIH, Bethesda, MD 20892 USA.
Univ Penn, Perlman Sch Med, Philadelphia, PA 19104 USA.
Mayo Clin, Rochester, MN USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
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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 2012
VL 25
SU 2
MA 890
BP 213A
EP 214A
PG 2
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901167
ER
PT J
AU Jin-Ping, L
Rodriguez, BAW
Aung, PP
Linehan, M
Merino, MJ
AF Jin-Ping, L.
Rodriguez, B. A. Walter
Aung, P. P.
Linehan, M.
Merino, M. J.
TI Mixed Epithelial and Stromal Tumor of Kidney, Molecular and IHC Findings
of a Possible New Hereditary Syndrome
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Jin-Ping, L.; Rodriguez, B. A. Walter; Aung, P. P.; Linehan, M.; Merino, M. J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 899
BP 215A
EP 216A
PG 2
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901176
ER
PT J
AU Navaei, AH
Aung, PP
Walter, BA
Pinto, P
Merino, MJ
AF Navaei, A. H.
Aung, P. P.
Walter, B. A.
Pinto, P.
Merino, M. J.
TI Correlation between ERG Fusion Protein and Androgen Receptor Expression
in Prostate Cancer; Possible Role in Diagnosis and Therapy
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Navaei, A. H.; Aung, P. P.; Walter, B. A.; Pinto, P.; Merino, M. J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 963
BP 230A
EP 230A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901240
ER
PT J
AU Biancotto, A
Dagur, PK
Fuchs, JC
Wiestner, A
Bagwell, CB
Mccoy, JP
AF Biancotto, Angelique
Dagur, Pradeep K.
Fuchs, John C.
Wiestner, Adrian
Bagwell, C. Bruce
McCoy, J. Philip, Jr.
TI Phenotypic complexity of T regulatory subsets in patients with B-chronic
lymphocytic leukemia
SO MODERN PATHOLOGY
LA English
DT Article
DE chronic lymphocytic leukemia; immunophenotyping; T-reg
ID CD38 EXPRESSION; SUPPRESSIVE FUNCTION; CELL RESPONSES; EXPANSION;
FREQUENCY; ZAP-70; CD4; DIFFERENTIATION; INTERLEUKIN-7; SURVIVAL
AB Increased numbers of T regulatory (T-reg) cells are found in B-chronic lymphocytic leukemia, but the nature and function of these T-regs remains unclear. Detailed characterization of the T-regs in chronic lymphocytic leukemia has not been performed and the degree of heterogeneity of among these cells has not been studied to date. Using 15-color flow cytometry we show that T-reg, cells, defined using CD4, CD25, and forkhead box P3 (FOXP3), can be divided into multiple complex subsets based on markers used for naive, memory, and effector delineation as well as markers of T-reg activation. Furthermore FOXP3 cells can be identified among CD4(+)CD25(-) as well as CD8(+)CD4(-) populations in increased proportions in patients with chronic lymphocytic leukemia compared with healthy donors. Significantly different frequencies of naive and effector T-regs populations are found in healthy donor controls compared with donors with chronic lymphocytic leukemia. A population of CCR7(+)CD39(+) T-regs was significantly associated with chronic lymphocytic leukemia. This population demonstrated slightly reduced suppressive activity compared with total T-regs Or T-regs of healthy donors. These data suggest that FOXP3-expressing cells, particularly in patients with chronic lymphocytic leukemia are much more complex for T-reg sub-populations and transitions than previously reported. These findings demonstrate the complexity of regulation of T-cell responses in chronic lymphocytic leukemia and illustrate the use of high-dimensional analysis of cellular phenotypes in facilitating understanding of the intricacies of cellular immune responses and their dysregulation in cancer. Modern Pathology (2012) 25, 246-259; doi:10.1038/modpathol.2011.164; published online 18 November 2011
C1 [McCoy, J. Philip, Jr.] NHLBI, Ctr Human Immunol Autoimmun & Inflammat, NIH, Bethesda, MD 20892 USA.
[Dagur, Pradeep K.; McCoy, J. Philip, Jr.] NHLBI, Flow Cytometiy Core Lab, Bethesda, MD 20892 USA.
[Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Bagwell, C. Bruce] Ver Software House, Topsham, ME USA.
RP Mccoy, JP (reprint author), NHLBI, Ctr Human Immunol Autoimmun & Inflammat, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM mccoyjp@mail.nih.gov
FU NHLBI; CHI, NIH, Bethesda, MD, USA
FX We are grateful to Dr. M. Roederer and Dr. P. Chattopadhyay for their
generous assistance. This research was supported by the Intramural
Research Program of the NHLBI and by the CHI, NIH, Bethesda, MD, USA.
NR 49
TC 10
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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
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VL 25
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BP 246
EP 259
DI 10.1038/modpathol.2011.164
PG 14
WC Pathology
SC Pathology
GA 888EK
UT WOS:000299986400010
PM 22101351
ER
PT J
AU Romero, VAV
Rodriguez, BAW
Merino, MJ
AF Romero, V. A. Valera
Rodriguez, B. A. Walter
Merino, M. J.
TI Molecular Classification Helps Discriminate between Oncocytomas and
Chromophobe Renal Carcinomas Using Meta-Analysis of Gene Expression
Microarrays
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Romero, V. A. Valera; Rodriguez, B. A. Walter; Merino, M. J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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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
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PD FEB
PY 2012
VL 25
SU 2
MA 1039
BP 247A
EP 247A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901316
ER
PT J
AU Rodriguez, BAW
Romero, VAV
Linehan, M
Merino, MJ
AF Rodriguez, B. A. Walter
Romero, V. A. Valera
Linehan, M.
Merino, M. J.
TI Mitochondria Respiratory Chain Gene Expression Analysis in Renal Cell
Carcinoma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI NIN, Bethesda, MD 20892 USA.
NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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U1 0
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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 2012
VL 25
SU 2
MA 1047
BP 249A
EP 249A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901324
ER
PT J
AU Walter, BA
Valera, VA
Pacak, K
Linehan, M
Merino, MJ
AF Walter, B. A.
Valera, V. A.
Pacak, K.
Linehan, M.
Merino, M. J.
TI How Immunohistochemistry Can Help To Identify Renal Tumors Associated
with SDHB Syndrome
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Walter, B. A.; Valera, V. A.; Pacak, K.; Linehan, M.; Merino, M. J.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 1046
BP 249A
EP 249A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901323
ER
PT J
AU Davidson, B
Abeler, V
Hellesylt, E
Holth, A
Shih, IM
Kristensen, GB
Skeie-Jensen, T
Yang, Y
Wang, TL
AF Davidson, B.
Abeler, V.
Hellesylt, E.
Holth, A.
Shih, I-M
Kristensen, G. B.
Skeie-Jensen, T.
Yang, Y.
Wang, T-L
TI Gene Expression Signatures Differentiate Uterine Leiomyosarcoma and
Endometrial Stromal Sarcoma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Norwegian Radium Hosp, Oslo, Norway.
Johns Hopkins Med Inst, Baltimore, MD USA.
NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 1112
BP 265A
EP 265A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901389
ER
PT J
AU Gomez-Macias, GS
Stratton, P
Rodriguez, BAW
Merino, MJ
AF Gomez-Macias, G. S.
Stratton, P.
Rodriguez, B. A. Walter
Merino, M. J.
TI Does GVHD Involve the Gyn Tract? Immunohistochemical Expression of
Elafin as a Marker of Graft-Versus-Host Disease in Gynecological
Biopsies
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI, NIH, Bethesda, MD 20892 USA.
NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
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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 2012
VL 25
SU 2
MA 1142
BP 272A
EP 273A
PG 2
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901419
ER
PT J
AU Bajor-Dattilo, EB
Leung, A
Dunleavy, K
Pack, S
Arthur, D
Raffeld, M
Wilson, W
Jaffe, ES
Pittaluga, S
AF Bajor-Dattilo, E. B.
Leung, A.
Dunleavy, K.
Pack, S.
Arthur, D.
Raffeld, M.
Wilson, W.
Jaffe, E. S.
Pittaluga, S.
TI Correlation of MYC Gene Translocation Status with MYC Protein Expression
in Burkitt Lymphoma and Diffuse Large B Cell Lymphoma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Bajor-Dattilo, E. B.; Leung, A.; Dunleavy, K.; Pack, S.; Arthur, D.; Raffeld, M.; Wilson, W.; Jaffe, E. S.; Pittaluga, S.] NIH, Bethesda, MD 20892 USA.
NR 0
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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 2012
VL 25
SU 2
MA \1359
BP 324A
EP 324A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901636
ER
PT J
AU Calvo, KR
Corrigan-Cummins, M
Costello, R
Tembhare, P
Yuan, CM
Stetler-Stevenson, M
Korde, N
Kwok, M
Yancey, MA
Mulquin, M
Simakova, O
Adriana, Z
Landgren, O
Maric, I
AF Calvo, K. R.
Corrigan-Cummins, M.
Costello, R.
Tembhare, P.
Yuan, C. M.
Stetler-Stevenson, M.
Korde, N.
Kwok, M.
Yancey, M. A.
Mulquin, M.
Simakova, O.
Adriana, Z.
Landgren, O.
Maric, I.
TI Immunophenotypic Profiles of Plasma Cells in Myeloma Precursor Disease
Correlate with the Extent of Disease and Risks for Progression
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology (USCAP)
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol (USCAP)
C1 NIH CC, Bethesda, MD 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 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2012
VL 25
SU 2
MA 1368
BP 326A
EP 326A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901645
ER
PT J
AU Calvo, KR
Wang, W
Corrigan-Cummins, M
Zingone, A
Costello, R
Korde, N
Ghobrial, I
Landgren, O
AF Calvo, K. R.
Wang, W.
Corrigan-Cummins, M.
Zingone, A.
Costello, R.
Korde, N.
Ghobrial, I.
Landgren, O.
TI MicroRNA Profiles of the Bone Marrow Microenvironment and Serum in
Multiple Myeloma Reveal Micrornas in the Serum Associated with Myeloma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology (USCAP)
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol (USCAP)
C1 NIH, Ctr Clin, Bethesda, MD 20892 USA.
NCI, Bethesda, MD 20892 USA.
Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 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 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2012
VL 25
SU 2
MA 1369
BP 326A
EP 326A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901646
ER
PT J
AU Carvajal-Cuenca, A
Salaverria, I
Royo, C
Clot, G
Navarro, A
Hartmann, EM
Trim, N
Woroniecka, R
Erber, W
Gaulard, P
Wlodarska, I
Rymkiewicz, G
Ott, G
Rosenwald, A
Lopez-Guillermo, A
Quintanilla-Fend, L
Ferry, JA
Harris, NL
Jaffe, ES
Siebert, R
Campo, E
Bea, S
AF Carvajal-Cuenca, A.
Salaverria, I.
Royo, C.
Clot, G.
Navarro, A.
Hartmann, E. M.
Trim, N.
Woroniecka, R.
Erber, W.
Gaulard, P.
Wlodarska, I.
Rymkiewicz, G.
Ott, G.
Rosenwald, A.
Lopez-Guillermo, A.
Quintanilla-Fend, L.
Ferry, J. A.
Harris, N. L.
Jaffe, E. S.
Siebert, R.
Campo, E.
Bea, S.
TI Clinicopathologic Characterization of Cyclin D1-Negative Mantle Cell
Lymphoma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Univ Barcelona, Hosp Clin, Barcelona, Spain.
Univ Wurzburg, Inst Pathol, D-8700 Wurzburg, Germany.
Addenbrookes Hosp, Cambridge, England.
MSCM Canc Ctr & Inst, Warsaw, Poland.
Hop Henri Mondor, F-94010 Creteil, France.
Catholic Univ Louvain, Ctr Human Genet, B-3000 Louvain, Belgium.
Robert Bosch Krankenhaus, Stuttgart, Germany.
Univ Tubingen, Inst Pathol, D-7400 Tubingen, Germany.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
NCI, Bethesda, MD 20892 USA.
Univ Kiel, Kiel, Germany.
RI Navarro, Alba/H-2611-2015; Royo, Cristina/H-3193-2015
OI Navarro, Alba/0000-0002-4041-0974; Royo, Cristina/0000-0002-1214-4656
NR 0
TC 1
Z9 1
U1 2
U2 5
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 2012
VL 25
SU 2
MA 1370
BP 326A
EP 327A
PG 2
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901647
ER
PT J
AU Climent, F
Pittaluga, S
Martinez, D
Gonzalez-Barca, E
Romagosa, V
Raffeld, M
Campo, E
Jaffe, ES
AF Climent, F.
Pittaluga, S.
Martinez, D.
Gonzalez-Barca, E.
Romagosa, V.
Raffeld, M.
Campo, E.
Jaffe, E. S.
TI Clinicopathologic Study of Mature T-Cell Lymphoma with B-Cell Markers: A
Review of 21 Cases
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Bellvitge Hosp, Barcelona, Spain.
NCI, NIH, Bethesda, MD 20892 USA.
Hosp Clin Barcelona, Barcelona, Spain.
Inst Catala Oncol, Barcelona, 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 2012
VL 25
SU 2
MA 1384
BP 330A
EP 330A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901661
ER
PT J
AU Huppmann, AR
Pittaluga, S
Raffeld, M
Xi, L
Jaffe, ES
AF Huppmann, A. R.
Pittaluga, S.
Raffeld, M.
Xi, L.
Jaffe, E. S.
TI Subcutaneous Panniculitis-Like T-Cell Lymphoma in Children
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Huppmann, A. R.; Pittaluga, S.; Raffeld, M.; Xi, L.; 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 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2012
VL 25
SU 2
MA 1433
BP 342A
EP 342A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901710
ER
PT J
AU Liu, Q
Davies-Hill, T
Pakzad, K
Raffeld, M
Xi, L
Pittaluga, S
Jaffe, ES
AF Liu, Q.
Davies-Hill, T.
Pakzad, K.
Raffeld, M.
Xi, L.
Pittaluga, S.
Jaffe, E. S.
TI Increased CD5 Positive Polyclonal B-Cells in Castleman Disease, and
Lymphoid Hyperplasia with Castleman-Like Features: A Diagnostic Pitfall
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 [Liu, Q.; Davies-Hill, T.; Pakzad, K.; Raffeld, M.; Xi, L.; 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 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2012
VL 25
SU 2
MA 1478
BP 352A
EP 352A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901755
ER
PT J
AU Maric, I
Liu, QY
Korde, N
Simakova, O
Calvo, K
Zingone, A
Costello, R
Yancey, MA
Tembhare, P
Yuan, C
Stetler-Stevenson, M
Landgren, O
AF Maric, I.
Liu, Q. Y.
Korde, N.
Simakova, O.
Calvo, K.
Zingone, A.
Costello, R.
Yancey, M. A.
Tembhare, P.
Yuan, C.
Stetler-Stevenson, M.
Landgren, O.
TI Mature Megakaryocytes Display High-Level CD34 Expression in a Subset of
Patients with Myeloma Precursor Disease
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NIH, CC, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 2012
VL 25
SU 2
MA 1488
BP 354A
EP 354A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986901765
ER
PT J
AU Menon, MP
Jegalion, A
Raffeld, M
Pittaluga, S
Xi, L
Jaffe, ES
AF Menon, M. P.
Jegalion, A.
Raffeld, M.
Pittaluga, S.
Xi, L.
Jaffe, E. S.
TI Primary CNS T-Cell Lymphomas: Clinical, Morphologic, Immunophenotypic
and Molecular Analysis
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI, NIH, Bethesda, MD 20892 USA.
Cleveland Clin, Cleveland, OH 44106 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 2012
VL 25
SU 2
MA 1491
BP 355A
EP 355A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902003
ER
PT J
AU Simakova, O
Wilson, T
Wang, M
Olivares, N
Klion, A
Metcalfe, DD
Maric, I
AF Simakova, O.
Wilson, T.
Wang, M.
Olivares, N.
Klion, A.
Metcalfe, D. D.
Maric, I.
TI Differential Expression of Activation-Related Antigens on Masts Cells
and Eosinophils in Patients with Systemic Mastocytosis and
Hypereosinophilic Syndrome
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & 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 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2012
VL 25
SU 2
MA 1548
BP 369A
EP 370A
PG 2
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902060
ER
PT J
AU Song, JY
Eberle, FC
Xi, L
Raffeld, M
Harris, NL
Wilson, WH
Pittaluga, S
Jaffe, ES
AF Song, J. Y.
Eberle, F. C.
Xi, L.
Raffeld, M.
Harris, N. L.
Wilson, W. H.
Pittaluga, S.
Jaffe, E. S.
TI Nodal Involvement by Transformed Cutaneous CD30-Positive T-Cell Lymphoma
Mimicking Classical Hodgkin Lymphoma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Massachusetts Gen Hosp, Boston, MA 02114 USA.
Harvard Univ, Sch Med, Boston, MA 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 2012
VL 25
SU 2
MA 1556
BP 372A
EP 372A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902068
ER
PT J
AU Valera, A
Colomo, L
Martinez, A
de Jong, D
Balague, O
Matheu, G
Martinez, M
Taddesse-Heath, L
Jaffe, ES
Bacchi, CE
Campo, E
AF Valera, A.
Colomo, L.
Martinez, A.
de Jong, D.
Balague, O.
Matheu, G.
Martinez, M.
Taddesse-Heath, L.
Jaffe, E. S.
Bacchi, C. E.
Campo, E.
TI ALK Positive Large B-Cell Lymphomas (ALK plus LBCL) Express the Terminal
Plasma Cell Differentiation Program but Lack MYC Rearrangements
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Hosp Clin Barcelona, Barcelona, Spain.
Netherlands Canc Inst, Amsterdam, Netherlands.
Hosp Manacor, Manacor, Spain.
Lab Hematopatol, Mendoza, Argentina.
Howard Univ Hosp, Washington, DC 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 2012
VL 25
SU 2
MA 1578
BP 377A
EP 377A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902090
ER
PT J
AU Yang, HC
Morden, A
Pastan, I
Matsusaka, T
Ichikawa, I
Fogo, AB
AF Yang, H-C
Morden, A.
Pastan, I.
Matsusaka, T.
Ichikawa, I.
Fogo, A. B.
TI Absence of PAI-1 Results in Direct Podocyte Protection In Vivo
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Vanderbilt Univ, Med Ctr, Nashville, TN USA.
Florida State Univ, Tallahassee, FL 32306 USA.
NCI, Bethesda, MD 20892 USA.
Tokai Univ, Sch Med, Isehara, Kanagawa 25911, 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 2012
VL 25
SU 2
MA 1710
BP 409A
EP 409A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902222
ER
PT J
AU Guy, CD
Brunt, EM
Behling, C
Torbenson, M
Yeh, MM
Belt, P
Neuschwander-Tetri, BA
Murray, KF
Kleiner, DE
AF Guy, C. D.
Brunt, E. M.
Behling, C.
Torbenson, M.
Yeh, M. M.
Belt, P.
Neuschwander-Tetri, B. A.
Murray, K. F.
Kleiner, D. E.
TI Hepatic Glycogenosis in Children with Nonalcoholic Fatty Liver Disease
(NAFLD): A Different Disease Than Glycogenic Hepatopathy
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Duke Univ, Durham, NC USA.
Washington Univ, St Louis, MO USA.
Sharp Hosp, San Diego, CA USA.
Johns Hopkins Sch Med, Baltimore, MD USA.
Univ Washington, Seattle, WA 98195 USA.
Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
St Louis Univ, Sch Med, St Louis, MO USA.
Seattle Childrens Hosp, Seattle, WA USA.
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 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2012
VL 25
SU 2
MA 1728
BP 414A
EP 414A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902240
ER
PT J
AU Kleiner, DE
Behling, C
Guy, CD
Torbenson, M
Yeh, MM
Belt, P
Neuschwander-Tetri, BA
Brunt, EM
AF Kleiner, D. E.
Behling, C.
Guy, C. D.
Torbenson, M.
Yeh, M. M.
Belt, P.
Neuschwander-Tetri, B. A.
Brunt, E. M.
TI Glycogenosis Is Associated with Measures of Insulin Resistance in Adults
with Non-Alcoholic Fatty Liver Disease (NAFLD)
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI, Bethesda, MD 20892 USA.
Sharp Hosp, San Diego, CA USA.
Duke Univ, Durham, NC USA.
Johns Hopkins Sch Med, Baltimore, MD USA.
Univ Washington, Seattle, WA 98195 USA.
Johns Hopkins Sch Publ Hlth, Baltimore, MD USA.
St Louis Univ, St Louis, MO 63103 USA.
Washington Univ, St Louis, MO 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 2012
VL 25
SU 2
MA 1737
BP 416A
EP 416A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902249
ER
PT J
AU Lai, JP
Aung, PP
Wang, Z
Rosenberg, A
Kleiner, D
Roberts, LR
Miettinen, M
AF Lai, J-P
Aung, P. P.
Wang, Z.
Rosenberg, A.
Kleiner, D.
Roberts, L. R.
Miettinen, M.
TI Oncogenic SULF2 Protein Expression Is Associated with Pathogenesis of
Cirrhosis and Hepatobiliary Carcinoma
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI, NIH, Bethesda, MD 20892 USA.
Mayo Clin, Rochester, MN 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 2012
VL 25
SU 2
MA 1742
BP 417A
EP 417A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902254
ER
PT J
AU Nobrega, R
Patrocinio, R
Aung, PP
Lai, JP
Wang, Z
Miettinen, M
Warren, K
Quezado, M
AF Nobrega, R.
Patrocinio, R.
Aung, P. P.
Lai, J-P
Wang, Z.
Miettinen, M.
Warren, K.
Quezado, M.
TI Expression Status of IDH1 Mutant and SDHB Genes in Adult and Pediatric
Gliomas
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 NCI, NIH, Bethesda, MD 20892 USA.
BIOPSE Lab, Fortaleza, Ceara, Brazil.
Fac Med Christus, Fortaleza, Ceara, Brazil.
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 2012
VL 25
SU 2
MA 1806
BP 433A
EP 433A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902318
ER
PT J
AU Arora, K
Zhang, W
Fukuoka, J
Kitano, H
Jagirdar, J
AF Arora, K.
Zhang, W.
Fukuoka, J.
Kitano, H.
Jagirdar, J.
TI Detection of EGFR Mutations in Lung Adenocarcinoma by
Immunohistochemistry Using Mutant Specific Antibodies: Are We There Yet?
SO MODERN PATHOLOGY
LA English
DT Meeting Abstract
CT 101st Annual Meeting of the
United-States-and-Canadian-Academy-of-Pathology
CY MAR 17-23, 2012
CL Vancouver, CANADA
SP US & Canadian Acad Pathol
C1 Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
Toyama Univ, Toyama 930, Japan.
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 0893-3952
J9 MODERN PATHOL
JI Mod. Pathol.
PD FEB
PY 2012
VL 25
SU 2
MA 1961
BP 471A
EP 471A
PG 1
WC Pathology
SC Pathology
GA 888EP
UT WOS:000299986902473
ER
PT J
AU Cherkasova, V
Maury, LL
Bacikova, D
Pridham, K
Bahler, J
Maraia, RJ
AF Cherkasova, Vera
Maury, Luis Lopez
Bacikova, Dagmar
Pridham, Kevin
Baehler, Juerg
Maraia, Richard J.
TI Altered nuclear tRNA metabolism in La-deleted Schizosaccharomyces pombe
is accompanied by a nutritional stress response involving Atf1p and
Pcr1p that is suppressible by Xpo-t/Los1p
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID POLYMERASE-III TRANSCRIPTS; PRECURSOR TRANSFER-RNAS; MEIOTIC
RECOMBINATION HOTSPOT; METHIONYL-TRANSFER-RNA; CELL-CYCLE CHECKPOINT;
FISSION YEAST; SACCHAROMYCES-CEREVISIAE; NITROGEN STARVATION;
GENE-EXPRESSION; GCN4 TRANSLATION
AB Deletion of the sla1(+) gene, which encodes a homologue of the human RNA-binding protein La in Schizosaccharomyces pombe, causes irregularities in tRNA processing, with altered distribution of pre-tRNA intermediates. We show, using mRNA profiling, that cells lacking sla1(+) have increased mRNAs from amino acid metabolism (AAM) genes and, furthermore, exhibit slow growth in Edinburgh minimal medium. A subset of these AAM genes is under control of the AP-1-like, stress-responsive transcription factors Atf1p and Pcr1p. Although S. pombe growth is resistant to rapamycin, sla1-Delta cells are sensitive, consistent with deficiency of leucine uptake, hypersensitivity to NH4, and genetic links to the target of rapamycin (TOR) pathway. Considering that perturbed intranuclear pre-tRNA metabolism and apparent deficiency in tRNA nuclear export in sla1-Delta cells may trigger the AAM response, we show that modest overexpression of S. pombe los1(+) (also known as Xpo-t), encoding the nuclear exportin for tRNA, suppresses the reduction in pre-tRNA levels, AAM gene up-regulation, and slow growth of sla1-Delta cells. The conclusion that emerges is that sla1(+) regulates AAM mRNA production in S. pombe through its effects on nuclear tRNA processing and probably nuclear export. Finally, the results are discussed in the context of stress response programs in Saccharomyces cerevisiae.
C1 [Cherkasova, Vera; Bacikova, Dagmar; Pridham, Kevin; Maraia, Richard J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
[Maury, Luis Lopez; Baehler, Juerg] UCL, Dept Genet Evolut & Environm, London WC1E 6BT, England.
[Maury, Luis Lopez; Baehler, Juerg] UCL Canc Inst, London WC1E 6BT, England.
[Maraia, Richard J.] US PHS, Rockville, MD 20852 USA.
RP Maraia, RJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program Genom Differentiat, NIH, Bethesda, MD 20892 USA.
EM maraiar@mail.nih.gov
RI Bahler, Jurg/B-4572-2009; Lopez-Maury, Luis/B-3715-2015
OI Bahler, Jurg/0000-0003-4036-1532; Lopez-Maury, Luis/0000-0002-3510-0621
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development
FX We thank Shiv Grewal, Vincent Geli, and Henry Levin for strains and/or
plasmids, Mike Cashel for advice on analysis of media components, Bob
Intine for RNA preparation for one of the microarray experiments, Shelly
Sazer for a los1-mutant allele used during an early phase of this work,
Marty Blum for media preparation, Nate Blewett for discussion, and Alan
Hinnebusch and anonymous reviewers for critical reading of an earlier
version of the manuscript. This work was supported by the Intramural
Research Program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development.
NR 103
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U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD FEB 1
PY 2012
VL 23
IS 3
BP 480
EP 491
DI 10.1091/mbc.E11-08-0732
PG 12
WC Cell Biology
SC Cell Biology
GA 894EN
UT WOS:000300409900007
PM 22160596
ER
PT J
AU Chen, M
Shabashvili, D
Nawab, A
Yang, SX
Dyer, LM
Brown, KD
Hollingshead, M
Hunter, KW
Kaye, FJ
Hochwald, SN
Marquez, VE
Steeg, P
Zajac-Kaye, M
AF Chen, Min
Shabashvili, Daniel
Nawab, Akbar
Yang, Sherry X.
Dyer, Lisa M.
Brown, Kevin D.
Hollingshead, Melinda
Hunter, Kent W.
Kaye, Frederic J.
Hochwald, Steven N.
Marquez, Victor E.
Steeg, Patricia
Zajac-Kaye, Maria
TI DNA Methyltransferase Inhibitor, Zebularine, Delays Tumor Growth and
Induces Apoptosis in a Genetically Engineered Mouse Model of Breast
Cancer
SO MOLECULAR CANCER THERAPEUTICS
LA English
DT Article
ID FREQUENT EPIGENETIC INACTIVATION; P53-MEDIATED G(1) ARREST; CYCLIN D2
EXPRESSION; TRANSGENIC MICE; PROMOTER HYPERMETHYLATION; P53-DEPENDENT
APOPTOSIS; EPITHELIAL-CELLS; MAMMARY-TUMORS; SFRP GENES; IN-VITRO
AB Zebularine is a novel potent inhibitor of both cytidine deaminase and DNA methylation. We examined the effect of zebularine on mammary tumor growth in genetically engineered MMTV-PyMT transgenic mice that develop mammary tumors at 60 days of age with 100% penetrance. The MMTV-PyMT transgenic mice were randomized at 46 days of age into control (n = 25) and zebularine (n = 25) treatment groups and monitored for parameters of tumor growth. Zebularine was administered at 5 mg/mL in drinking water. We observed a significant delay in the growth of mammary tumors in zebularine-treated mice with a statistically significant reduction (P = 0.0135) in total tumor burden at 94 days of age when the mice were sacrificed. After 48 days of zebularine treatment, the tumors were predominantly necrotic compared with untreated animals. In addition, a high apoptotic index by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay was observed as early as 13 days following treatment. Immunoblot analysis showed depletion of DNMT1 and partial depletion of DNMT3b after zebularine treatment. Microarray analyses of global gene expression identified upregulation of twelve methylation-regulated genes as well as a set of candidate cancer genes that participate in cell growth and apoptosis. In summary, zebularine inhibits the growth of spontaneous mammary tumors and causes early onset of tumor cell necrosis and apoptosis in a genetically engineered mouse model of breast cancer. Defining the parameters of zebularine-mediated tumor inhibition may advance the future development of DNA methyltransferase inhibitors as an effective cancer treatment. Mol Cancer Ther; 11(2); 370-82. (C) 2011 AACR.
C1 [Zajac-Kaye, Maria] Univ Florida, Coll Med, Dept Anat & Cell Biol, Gainesville, FL 32610 USA.
[Chen, Min; Kaye, Frederic J.; Zajac-Kaye, Maria] Univ Florida, Dept Med, Gainesville, FL 32610 USA.
[Dyer, Lisa M.; Brown, Kevin D.] Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA.
[Hochwald, Steven N.] Univ Florida, Dept Surg, Gainesville, FL 32610 USA.
[Yang, Sherry X.] NCI Frederick, Natl Clin Target Validat Lab, Frederick, MD USA.
[Hollingshead, Melinda] NCI Frederick, Dev Therapeut Program, Frederick, MD USA.
[Hunter, Kent W.] NCI, Lab Canc Biol & Genet, Bethesda, MD 20892 USA.
[Marquez, Victor E.] NCI, Med Chem Lab, Bethesda, MD 20892 USA.
[Steeg, Patricia] NCI, Mol Pharmacol Lab, Bethesda, MD 20892 USA.
RP Zajac-Kaye, M (reprint author), Univ Florida, Coll Med, Dept Anat & Cell Biol, Canc & Genet Res Complex,Room 360,2033 Mowry Rd, Gainesville, FL 32610 USA.
EM mzajackaye@ufl.edu
FU National Cancer Institute; Department of Medicine at the University of
Florida; Department of Anatomy and Cell Biology at the University of
Florida
FX This work was supported by National Cancer Institute intramural program
and by the Department of Medicine and Department of Anatomy and Cell
Biology at the University of Florida.
NR 58
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U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1535-7163
J9 MOL CANCER THER
JI Mol. Cancer Ther.
PD FEB
PY 2012
VL 11
IS 2
BP 370
EP 382
DI 10.1158/1535-7163.MCT-11-0458
PG 13
WC Oncology
SC Oncology
GA 894GO
UT WOS:000300415300012
PM 22203734
ER
PT J
AU Buxton, DB
AF Buxton, Denis B.
TI The impact of nanotechnology on myocardial infarction treatment
SO NANOMEDICINE
LA English
DT Editorial Material
DE diagnostics; myocardial infarction; nanotechnology; regenerative
medicine; therapeutic delivery
ID SELF-ASSEMBLING PEPTIDES; DELIVERY; MONOCYTES; TISSUE; HEART
AB "Nanotechnology has the potential to play a role in improving outcomes from MI at multiple points in the disease process. These include earlier and more sensitive diagnosis of developing MI, improved treatments of acute MI with drugs, cell therapy and siRNA, and tissue engineering approaches for preventing infarct expansion and the development of heart failure."
RP Buxton, DB (reprint author), NHLBI, Basic & Early Translat Res Program, Div Cardiovasc Sci, 6701 Rockledge Dr, Bethesda, MD 20892 USA.
EM db225a@nih.gov
OI Buxton, Denis/0000-0003-3077-6435
NR 15
TC 3
Z9 3
U1 0
U2 4
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1743-5889
J9 NANOMEDICINE-UK
JI Nanomedicine
PD FEB
PY 2012
VL 7
IS 2
BP 173
EP 175
DI 10.2217/NNM.11.184
PG 3
WC Biotechnology & Applied Microbiology; Nanoscience & Nanotechnology
SC Biotechnology & Applied Microbiology; Science & Technology - Other
Topics
GA 893DM
UT WOS:000300335800002
PM 22339129
ER
PT J
AU Trcek, T
Chao, JA
Larson, DR
Park, HY
Zenklusen, D
Shenoy, SM
Singer, RH
AF Trcek, Tatjana
Chao, Jeffrey A.
Larson, Daniel R.
Park, Hye Yoon
Zenklusen, Daniel
Shenoy, Shailesh M.
Singer, Robert H.
TI Single-mRNA counting using fluorescent in situ hybridization in budding
yeast
SO NATURE PROTOCOLS
LA English
DT Article
ID ACTIN GENE-EXPRESSION; LABELED PROBES; LOCALIZATION; MOLECULES;
VISUALIZATION; PROTEIN; CELLS; TRANSCRIPTION; COMPLEX
AB Fluorescent in situ hybridization (FISH) allows the quantification of single mRNAs in budding yeast using fluorescently labeled single-stranded DNA probes, a wide-field epifluorescence microscope and a spot-detection algorithm. Fixed yeast cells are attached to coverslips and hybridized with a mixture of FISH probes, each conjugated to several fluorescent dyes. Images of cells are acquired in 3D and maximally projected for single-molecule analysis. Diffraction-limited labeled mRNAs are observed as bright fluorescent spots and can be quantified using a spot-detection algorithm. FISH preserves the spatial distribution of cellular RNA distribution within the cell and the stochastic fluctuations in individual cells that can lead to phenotypic differences within a clonal population. This information, however, is lost if the RNA content is measured on a population of cells by using reverse transcriptase PCR, microarrays or high-throughput sequencing. The FISH procedure and image acquisition described here can be completed in 3 d.
C1 [Trcek, Tatjana; Chao, Jeffrey A.; Park, Hye Yoon; Shenoy, Shailesh M.; Singer, Robert H.] Albert Einstein Coll Med, Dept Anat & Struct Biol, Bronx, NY 10467 USA.
[Larson, Daniel R.] NCI, US Natl Inst Hlth, Bethesda, MD 20892 USA.
[Zenklusen, Daniel] Univ Montreal, Dept Biochim, Montreal, PQ H3C 3J7, Canada.
[Singer, Robert H.] Albert Einstein Coll Med, Gruss Lipper Biophoton Ctr, Bronx, NY 10467 USA.
RP Singer, RH (reprint author), Albert Einstein Coll Med, Dept Anat & Struct Biol, Bronx, NY 10467 USA.
EM robert.singer@einstein.yu.edu
RI Larson, Daniel/B-9829-2008; Zenklusen, Daniel/C-4503-2008; Park, Hye
Yoon/N-9618-2014;
OI Larson, Daniel/0000-0001-9253-3055; Zenklusen,
Daniel/0000-0002-0067-0093; Park, Hye Yoon/0000-0003-4704-8178; Shenoy,
Shailesh/0000-0002-5132-7236
FU US National Institutes of Health [GM57071, GM86217]; Canadian Institutes
of Health Research
FX We thank the Singer laboratory members for critical review of this
manuscript. This work was supported by US National Institutes of Health
grants GM57071 and GM86217 (awarded to R.H.S.) and a grant from the
Canadian Institutes of Health Research (awarded to D.Z.)
NR 35
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U1 1
U2 44
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1754-2189
J9 NAT PROTOC
JI Nat. Protoc.
PD FEB
PY 2012
VL 7
IS 2
BP 408
EP 419
DI 10.1038/nprot.2011.451
PG 12
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 894BP
UT WOS:000300402300016
PM 22301778
ER
PT J
AU Skinner, M
AF Skinner, Mhairi
TI CANCER STEM CELLS TAZ takes centre stage
SO NATURE REVIEWS CANCER
LA English
DT News Item
C1 NCI Nat Pathway Interact Database, Rockville, MD 20852 USA.
RP Skinner, M (reprint author), NCI Nat Pathway Interact Database, Rockville, MD 20852 USA.
NR 0
TC 2
Z9 3
U1 0
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-175X
J9 NAT REV CANCER
JI Nat. Rev. Cancer
PD FEB
PY 2012
VL 12
IS 2
BP 82
EP 82
DI 10.1038/nrc3210
PG 1
WC Oncology
SC Oncology
GA 892BN
UT WOS:000300261700005
PM 22257952
ER
PT J
AU Hunter, KW
AF Hunter, Kent W.
TI Mouse models of cancer: does the strain matter?
SO NATURE REVIEWS CANCER
LA English
DT Review
ID BREAST-CANCER; INTESTINAL NEOPLASIA; TUMOR-SUSCEPTIBILITY;
GENETIC-ANALYSIS; COMPLEX TRAITS; MICE; POLYMORPHISMS; METASTASIS;
CANDIDATE; MODIFIER
AB Mouse models are indispensible tools for understanding the molecular basis of cancer. However, despite the invaluable data provided regarding tumour biology, owing to inbreeding, current mouse models fail to accurately model human populations. Polymorphism is the essential characteristic that makes each of us unique humans, with different disease susceptibility, presentation and progression. Therefore, as we move closer towards designing clinical treatment that is based on an individual's unique biological makeup, it is imperative that we understand how inherited variability influences cancer phenotypes, how it can confound experiments and how it can be exploited to reveal new truths about cancer biology.
C1 NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Hunter, KW (reprint author), NCI, Lab Canc Biol & Genet, NIH, 37-5046,37 Convent Dr, Bethesda, MD 20892 USA.
EM hunterk@mail.nih.gov
FU US National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX I would like to thank J. Alsarraj and D. Threadgill for their insightful
comments on this article. I would also like to apologize to the many
investigators whose work was not discussed in this article owing to
space constraints. This work was supported by the Intramural Research
Program of the US National Institutes of Health, National Cancer
Institute, Center for Cancer Research.
NR 31
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U1 0
U2 10
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-175X
J9 NAT REV CANCER
JI Nat. Rev. Cancer
PD FEB
PY 2012
VL 12
IS 2
BP 144
EP U1
DI 10.1038/nrc3206
PG 6
WC Oncology
SC Oncology
GA 892BN
UT WOS:000300261700013
PM 22257951
ER
PT J
AU Sfanos, KS
Aloia, AL
De Marzo, AM
Rein, A
AF Sfanos, Karen S.
Aloia, Amanda L.
De Marzo, Angelo M.
Rein, Alan
TI XMRV and prostate cancer-a 'final' perspective
SO NATURE REVIEWS UROLOGY
LA English
DT Article
ID MURINE LEUKEMIA-VIRUS; CHRONIC-FATIGUE-SYNDROME; NO EVIDENCE; RETROVIRUS
XMRV; INFECTIOUS RETROVIRUS; SEQUENCE VARIATION; INTEGRATION SITES;
UNITED-STATES; BLOOD-DONORS; MOUSE DNA
AB XMRV was first described in 2006, when it was identified in samples isolated from prostate cancer tissues. However, studies have since shown that XMRV arose in the laboratory and was formed by genetic recombination between two viral genomes carried in the germline DNA of mice used during serial transplantation of the CWR22 prostate cancer xenograft. These new findings strongly imply that XMRV does not circulate in humans, but is only present in the laboratory. Thus, there is no reason to believe that it has any role in the etiology of prostate cancer or other diseases.
C1 [Sfanos, Karen S.] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21231 USA.
[Aloia, Amanda L.; Rein, Alan] NCI, HIV Drug Resistance Program, Frederick, MD 21702 USA.
[De Marzo, Angelo M.] Johns Hopkins Univ, Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21231 USA.
[De Marzo, Angelo M.] Johns Hopkins Univ, Sch Med, Brady Urol Res Inst, Baltimore, MD 21231 USA.
RP Sfanos, KS (reprint author), Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21231 USA.
EM ksfanos@jhmi.edu
OI De Marzo, Angelo/0000-0003-4847-5307
FU NIH, National Cancer Institute, Center for Cancer Research
FX The authors would like to acknowledge Dr Saraswati Sukumar for helpful
discussions. Research by A. Aloia and A. Rein is supported by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 67
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PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4812
J9 NAT REV UROL
JI Nat. Rev. Urol.
PD FEB
PY 2012
VL 9
IS 2
BP 111
EP 118
DI 10.1038/nrurol.2011.225
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 894HA
UT WOS:000300416500010
PM 22231291
ER
PT J
AU Rao, M
Mottl, AK
Cole, SA
Umans, JG
Freedman, BI
Bowden, DW
Langefeld, CD
Fox, CS
Yang, Q
Cupples, A
Iyengar, SK
Hunt, SC
Trikalinos, TA
AF Rao, Madhumathi
Mottl, Amy K.
Cole, Shelley A.
Umans, Jason G.
Freedman, Barry I.
Bowden, Donald W.
Langefeld, Carl D.
Fox, Caroline S.
Yang, Qiong
Cupples, Adrienne
Iyengar, Sudha K.
Hunt, Steven C.
Trikalinos, Thomas A.
TI Meta-analysis of genome-wide linkage scans for renal function traits
SO NEPHROLOGY DIALYSIS TRANSPLANTATION
LA English
DT Article
DE albuminuria; chronic kidney disease; glomerular filtration rate; linkage
scans; meta-analysis
ID GLOMERULAR-FILTRATION-RATE; CHRONIC KIDNEY-DISEASE; GENES-CONTROLLING
VARIATION; URINARY ALBUMIN EXCRETION; TYPE-2 DIABETES-MELLITUS;
COMMUNITY-BASED SAMPLE; SEARCH METAANALYSIS; AFRICAN-AMERICANS; SERUM
CREATININE; MEXICAN-AMERICANS
AB Several genome scans have explored the linkage of chronic kidney disease phenotypes to chromosomic regions with disparate results. Genome scan meta-analysis (GSMA) is a quantitative method to synthesize linkage results from independent studies and assess their concordance.
We searched PubMed to identify genome linkage analyses of renal function traits in humans, such as estimated glomerular filtration rate (GFR), albuminuria, serum creatinine concentration and creatinine clearance. We contacted authors for numerical data and extracted information from individual studies. We applied the GSMA nonparametric approach to combine results across 14 linkage studies for GFR, 11 linkage studies for albumin creatinine ratio, 11 linkage studies for serum creatinine and 4 linkage studies for creatinine clearance.
No chromosomal region reached genome-wide statistical significance in the main analysis which included all scans under each phenotype; however, regions on Chromosomes 7, 10 and 16 reached suggestive significance for linkage to two or more phenotypes. Subgroup analyses by disease status or ethnicity did not yield additional information.
While heterogeneity across populations, methodologies and study designs likely explain this lack of agreement, it is possible that linkage scan methodologies lack the resolution for investigating complex traits. Combining family-based linkage studies with genome-wide association studies may be a powerful approach to detect private mutations contributing to complex renal phenotypes.
C1 [Trikalinos, Thomas A.] Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Ctr Clin Evidence Synth, Boston, MA 02111 USA.
[Rao, Madhumathi] Tufts Med Ctr, Div Nephrol, Boston, MA 02111 USA.
[Mottl, Amy K.] Univ N Carolina, Sch Med, UNC Kidney Ctr, Chapel Hill, NC USA.
[Cole, Shelley A.] SW Fdn Biomed Res, San Antonio, TX 78284 USA.
[Umans, Jason G.] Georgetown Univ, Med Ctr, Dept Med Obstet & Gynecol, Gen Clin Res Ctr, Washington, DC 20007 USA.
[Freedman, Barry I.; Bowden, Donald W.; Langefeld, Carl D.] Wake Forest Univ, Bowman Gray Sch Med, Ctr Human Genom & Publ Hlth Sci, Winston Salem, NC USA.
[Fox, Caroline S.] NHLBI, NHLBIs Framingham Heart Study, Framingham, MA USA.
[Fox, Caroline S.] NHLBI, Ctr Populat Sci, Framingham, MA USA.
[Yang, Qiong; Cupples, Adrienne] Boston Univ, Dept Biostat, Boston, MA 02215 USA.
[Iyengar, Sudha K.] Case Western Reserve Univ, Div Genet & Mol Epidemiol, Cleveland, OH 44106 USA.
[Hunt, Steven C.] Univ Utah, Dept Internal Med, Cardiovasc Genet Div, Salt Lake City, UT 84112 USA.
RP Trikalinos, TA (reprint author), Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Ctr Clin Evidence Synth, Boston, MA 02111 USA.
EM ttrikalinos@tuftsmedicalcenter.org
RI Yang, Qiong/G-5438-2014;
OI Mottl, Amy/0000-0002-4258-1726
FU National Institutes of Health [DK066992, R01 DK053591, R01 HL56266, R01
DK070941, DK084149, N01-HG-65403]; Tufts Clinical and Translational
Science Institute [1 UL1 RR025752-02]; National Heart, Lung and Blood
Institute's Framingham Heart Study [N01-HC-25195]; General Clinical
Research Center of the Wake Forest University School of Medicine [M01
RR07122]; HyperGEN study [HL54471, HL54472, HL54473, HL54495, HL54496,
HL54497, HL54509, HL54515, HL55673]; NIDDK [U01DK57292, U01DK57249,
U01DK57295, U01DK57298, U01DK57300, U01DK57303, U01DK57304, U01DK57329];
National Center for Research Resources for the General Clinical Research
Center: Case Western Reserve University [M01-RR-000080]; National Center
for Research Resources for the General Clinical Research Center: Wake
Forest University [M01-RR-07122]; National Center for Research Resources
for the General Clinical Research Center: Harbor-UCLA Medical Center
[M01-RR-00425]; National Center for Research Resources for the General
Clinical Research Center: College of Medicine-University of California
Irvine [M01-RR-00827-29]; National Center for Research Resources for the
General Clinical Research Center: University of New Mexico HSC
[M01-RR-00997]; National Center for Research Resources for the General
Clinical Research Center: [M01-RR-01346]; [R01-AG18734]
FX This work was supported by (i) National Institutes of Health (DK066992)
to Dr Rao; (ii) Grant 1 UL1 RR025752-02, Tufts Clinical and
Translational Science Institute; (iii) the National Heart, Lung and
Blood Institute's Framingham Heart Study (N01-HC-25195); (iv) Wake
Forest analyses were supported by National Institutes of Health grants
(R01 DK053591 to D. W. B.), (R01 HL56266 to B. I. F.), (R01 DK070941 to
B. I. F.), (DK084149 to B. I. F.) and, in part, by the General Clinical
Research Center of the Wake Forest University School of Medicine grant
M01 RR07122; (v) HyperGEN study (HL54471, HL54472, HL54473, HL54495,
HL54496, HL54497, HL54509, HL54515 and HL55673); (vi) (R01-AG18734);
(vii) The FIND study was supported by Research Grants (U01DK57292,
U01DK57249, U01DK57295, U01DK57298, U01DK57300, U01DK57303, U01DK57304
and U01DK57329) from the NIDDK and, in part, by the Intramural Research
Program of the NIDDK. This work was also supported by the National
Center for Research Resources for the General Clinical Research Center
grants: Case Western Reserve University (M01-RR-000080), Wake Forest
University (M01-RR-07122), Harbor-UCLA Medical Center (M01-RR-00425),
College of Medicine-University of California Irvine (M01-RR-00827-29),
University of New Mexico HSC (M01-RR-00997) and Frederic C. Bartter
(M01-RR-01346).; Genotyping for the original studies was performed by
the Center for Inherited Disease Research (CIDR). CIDR is fully funded
through a federal contract from the National Institutes of Health to the
Johns Hopkins University, contract no. N01-HG-65403.
NR 57
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U1 1
U2 7
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0931-0509
J9 NEPHROL DIAL TRANSPL
JI Nephrol. Dial. Transplant.
PD FEB
PY 2012
VL 27
IS 2
BP 647
EP 656
DI 10.1093/ndt/gfr255
PG 10
WC Transplantation; Urology & Nephrology
SC Transplantation; Urology & Nephrology
GA 894IV
UT WOS:000300421300029
PM 21622988
ER
PT J
AU Amlin-Van Schaick, JC
Kim, S
DiFabio, C
Lee, MH
Broman, KW
Reilly, KM
AF Amlin-Van Schaick, Jessica C.
Kim, Sungjin
DiFabio, Christina
Lee, Min-Hyung
Broman, Karl W.
Reilly, Karlyne M.
TI Arlm1 is a male-specific modifier of astrocytoma resistance on mouse Chr
12
SO NEURO-ONCOLOGY
LA English
DT Article
DE astrocytoma; glioblastoma; modifier; sex differences
ID INTEGRATED GENOMIC ANALYSIS; GLIOBLASTOMA-MULTIFORME; INCREASED
EXPRESSION; MONOAMINE-OXIDASE; WIDE ASSOCIATION; IMMUNE-RESPONSE;
BREAST-CANCER; CONDENSIN-II; ADULT GLIOMA; GENES
AB While many cancers show a sex bias, the genetic basis and molecular mechanisms underlying sex bias are not always clear. Astrocytoma and glioblastoma show male predominance in humans. We have shown previously that glial tumors forming in the Nf1-/+; Trp53-/+cis (NPcis) mouse model also show a sex bias in some genetic contexts. Using cross-species comparisons we have identified candidate male-specific modifiers of astrocytoma/glioblastoma. Linkage analysis of B6X(B6X129)-NPcis mice identifies a modifier of astrocytoma resistance specific to males, named Arlm1, on distal mouse Chr 12. Arlm1 is syntenic to human Chr 7p15, 7p21, 7q36, and 14q32 regions that are altered in human glioblastoma. A subset of these genes shows male-specific correlations to glioblastoma patient survival time and represents strong candidates for the Arlm1 modifier gene. Identification of male-specific modifier genes will lead to a better understanding of the molecular basis of male predominance in astrocytoma and glioblastoma.
C1 [Amlin-Van Schaick, Jessica C.; DiFabio, Christina; Lee, Min-Hyung; Reilly, Karlyne M.] NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA.
[Amlin-Van Schaick, Jessica C.] George Washington Univ, Inst Biomed Sci, Washington, DC USA.
[Kim, Sungjin; Broman, Karl W.] Univ Wisconsin, Sch Med & Publ Hlth, Dept Biostat & Med Informat, Madison, WI USA.
RP Reilly, KM (reprint author), NCI, Mouse Canc Genet Program, W 7th St,POB B, Frederick, MD 21702 USA.
EM reillyk@mail.nih.gov
OI Broman, Karl/0000-0002-4914-6671
FU National Institutes of Health, National Cancer Institute [ZIA BC
010539]; National Cancer Institute [N01-CO-12400]; National Institutes
of Health [HHSN268200782096C, R01 GM074244]
FX Intramural Research Program of the National Institutes of Health,
National Cancer Institute [ZIA BC 010539 to K. M. R.]; federal funds
from the National Cancer Institute to SAIC Frederick [contract
N01-CO-12400]; federal contract from the National Institutes of Health
to The Johns Hopkins University [contract HHSN268200782096C]; extramural
funding from the National Institutes of Health [R01 GM074244 to K.W.B.].
NR 68
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U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD FEB
PY 2012
VL 14
IS 2
BP 160
EP 174
DI 10.1093/neuonc/nor206
PG 15
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 892QO
UT WOS:000300300900004
PM 22234937
ER
PT J
AU Tuo, JS
Grob, S
Zhang, K
Chan, CC
AF Tuo, Jingsheng
Grob, Seanna
Zhang, Kang
Chan, Chi-Chao
TI Genetics of Immunological and Inflammatory Components in Age-related
Macular Degeneration
SO OCULAR IMMUNOLOGY AND INFLAMMATION
LA English
DT Article
DE age-related macular degeneration (AMD); complement factor;
cytokine/chemokine; gene; innate immunity
ID COMPLEMENT-FACTOR-H; POLYPOIDAL CHOROIDAL VASCULOPATHY;
SYSTEMIC-LUPUS-ERYTHEMATOSUS; GENOME-WIDE ASSOCIATION; COPY-NUMBER
VARIATION; HTRA1 PROMOTER POLYMORPHISM; TOLL-LIKE RECEPTOR-3;
PHOTODYNAMIC THERAPY; SUSCEPTIBILITY LOCI; LOC387715 GENOTYPES
AB Age-related macular degeneration (AMD), affecting 30 to 50 million elder individuals worldwide, is a disease affecting the macular retina and choroid that can lead to irreversible central vision loss and blindness. Recent findings support a role for immunologic processes in AMD pathogenesis, including generation of inflammatory related molecules in the Bruch's membrane, recruitment of macrophages, complement activation, microglial activation and accumulation in the macular lesions. Pro-inflammatory effects of chronic inflammation and oxidative stress can result in abnormal retinal pigment epithelium, photoreceptor atrophy and choroidal neovascularization. The associations of immunological and inflammatory genes, in particular the genes related to innate immunity with AMD support the involvement of various immunological pathways in the AMD pathogenesis. We review the literature on the involvements of inflammatory genes in AMD, highlight recent genetic discoveries, and discuss the potential application of such knowledge in the management of patients with AMD.
C1 [Tuo, Jingsheng; Chan, Chi-Chao] NEI, Immunopathol Sect, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Grob, Seanna; Zhang, Kang] Univ Calif San Diego, Dept Ophthalmol, La Jolla, CA 92093 USA.
RP Chan, CC (reprint author), NEI, Immunopathol Sect, Immunol Lab, NIH, 10 Ctr Dr,10-10N103, Bethesda, MD 20892 USA.
EM chanc@nei.nih.gov
OI Tuo, Jingsheng/0000-0002-1372-7810
FU NEI
FX The NEI Intramural Research program provided funding.
NR 119
TC 40
Z9 42
U1 1
U2 11
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0927-3948
J9 OCUL IMMUNOL INFLAMM
JI Ocul. Immunol. Inflamm.
PD FEB
PY 2012
VL 20
IS 1
BP 27
EP 36
DI 10.3109/09273948.2011.628432
PG 10
WC Ophthalmology
SC Ophthalmology
GA 892AO
UT WOS:000300259000006
PM 22324898
ER
PT J
AU Bellizzi, K
Smith, A
Schmidt, S
Keegan, T
Zebrack, B
Lynch, C
Deapen, D
Shnorhavorian, M
AF Bellizzi, K.
Smith, A.
Schmidt, S.
Keegan, T.
Zebrack, B.
Lynch, C.
Deapen, D.
Shnorhavorian, M.
TI Positive and Negative Life Impact of Being Diagnosed With Cancer as an
Adolescent or Young Adult
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Bellizzi, K.; Schmidt, S.] Univ Connecticut, Storrs, CT USA.
[Smith, A.] NCI, Bethesda, MD 20892 USA.
[Keegan, T.] Canc Prevent Inst Calif, Fremont, CA USA.
[Keegan, T.] Stanford Univ, Sch Med, Palo Alto, CA 94304 USA.
[Zebrack, B.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Lynch, C.] Univ Iowa, Iowa City, IA USA.
[Deapen, D.] Univ So Calif, Los Angeles, CA USA.
[Shnorhavorian, M.] Seattle Childrens Hosp, Seattle, WA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 5
EP 6
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800010
ER
PT J
AU Kent, EE
Smith, AW
Keegan, THM
Lynch, C
Wu, XC
Hamilton, AS
Kato, I
Schwartz, S
Harlan, LC
AF Kent, E. E.
Smith, A. W.
Keegan, T. H. M.
Lynch, C.
Wu, X.-C.
Hamilton, A. S.
Kato, I.
Schwartz, S.
Harlan, L. C.
TI Social Support Needs in Adolescents and Young Adults Diagnosed With
Cancer
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Kent, E. E.] NCI, Off Canc Survivorship, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Smith, A. W.] NCI, Outcomes Res Branch, Appl Res Program, Div Canc Control & Populat Sci,NIH, Bethesda, MD 20892 USA.
[Keegan, T. H. M.] Canc Prevent Inst Calif, Fremont, CA USA.
[Keegan, T. H. M.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Lynch, C.] Univ Iowa, Iowa City, IA USA.
[Wu, X.-C.] Louisiana State Univ, Hlth Sci Ctr, Sch Publ Hlth, Epidemiol Program,Louisiana Tumor Registry, New Orleans, LA USA.
[Hamilton, A. S.] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Kato, I.] Wayne State Univ, Sch Med, Karmanos Canc Inst, Detroit, MI USA.
[Kato, I.] Wayne State Univ, Sch Med, Dept Pathol, Detroit, MI USA.
[Schwartz, S.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Harlan, L. C.] NCI, Hlth Serv & Econ Branch, Appl Res Program, Div Canc Control & Populat Sci,NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 5
EP 5
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800009
ER
PT J
AU Ludi, E
Margolis, R
Wiener, L
Pao, M
AF Ludi, E.
Margolis, R.
Wiener, L.
Pao, M.
TI Understanding the Biopsychosocial Experience of International Families:
Adaptation and Challenges
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Ludi, E.; Pao, M.] NIMH, NIH, Bethesda, MD 20892 USA.
[Margolis, R.] NIH, Ctr Clin, Dept Social Work, Bethesda, MD 20892 USA.
[Wiener, L.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 8
EP 8
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800013
ER
PT J
AU Zadeh, S
Wiener, L
Battles, H
Mullins, L
Friebert, S
Patenaude, AF
Phipps, S
Sherman-Bien, S
Elkin, TD
Madan-Swain, A
Kearney, J
Bartell, A
Kupst, MJ
AF Zadeh, S.
Wiener, L.
Battles, H.
Mullins, L.
Friebert, S.
Patenaude, A. F.
Phipps, S.
Sherman-Bien, S.
Elkin, T. D.
Madan-Swain, A.
Kearney, J.
Bartell, A.
Kupst, M. J.
TI Health Disparities Related to Marital Status and Perceived Financial
Burden
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Zadeh, S.; Wiener, L.; Battles, H.] NCI, NIH, Bethesda, MD 20892 USA.
[Mullins, L.] Oklahoma State Univ, Stillwater, OK 74078 USA.
[Friebert, S.] Akron Childrens Hosp, Akron, OH USA.
[Patenaude, A. F.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Phipps, S.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Sherman-Bien, S.] Miller Childrens Hosp, Long Beach, CA USA.
[Elkin, T. D.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Madan-Swain, A.] Univ Alabama, Tuscaloosa, AL USA.
[Kearney, J.; Bartell, A.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Kupst, M. J.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 8
EP 9
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800014
ER
PT J
AU Horowitz, L
AF Horowitz, L.
TI When Race Really Does Matter: Racial and Ethnic Disparities in the Bone
Marrow Registry
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Horowitz, L.] NIMH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 9
EP 10
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800016
ER
PT J
AU Wiener, L
Zadeh, S
Battles, H
Pao, M
AF Wiener, L.
Zadeh, S.
Battles, H.
Pao, M.
TI Can an Adapted Distress Thermometer in the Pediatric Population Be Valid
and Clinically Meaningful?
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Wiener, L.; Zadeh, S.; Battles, H.] NCI, NIH, Bethesda, MD 20892 USA.
[Pao, M.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 27
EP 27
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800047
ER
PT J
AU Zadeh, S
Wiener, L
Battles, H
Pao, M
AF Zadeh, S.
Wiener, L.
Battles, H.
Pao, M.
TI Parent and Provider Ratings of Patient Distress: Are They Valid and/or
Meaningful?
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Zadeh, S.; Wiener, L.; Battles, H.] NCI, NIH, Bethesda, MD 20892 USA.
[Pao, M.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 27
EP 28
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800048
ER
PT J
AU Bevans, M
AF Bevans, M.
TI Distress Screening in Transplant Family Caregivers: What Have We
Learned?
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Bevans, M.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 28
EP 28
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800049
ER
PT J
AU Lichtenthal, W
Wiener, L
Sweeney, C
Roberts, K
Farberov, M
AF Lichtenthal, W.
Wiener, L.
Sweeney, C.
Roberts, K.
Farberov, M.
TI Disparities in Prolonged Grief, Mental Health Service Use, and Barriers
to Use in Racial/Ethnic Minority Parents Bereaved by Cancer
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Lichtenthal, W.; Sweeney, C.; Roberts, K.; Farberov, M.] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Wiener, L.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 40
EP 40
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800070
ER
PT J
AU Snyder, D
Horowitz, L
Ludi, E
Kohn, J
Rosenstein, D
Pao, M
AF Snyder, D.
Horowitz, L.
Ludi, E.
Kohn, J.
Rosenstein, D.
Pao, M.
TI Just ASQ'em: Screening for Suicide in Hospitalized Cancer Patients
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Snyder, D.; Horowitz, L.; Ludi, E.; Pao, M.] NIMH, Bethesda, MD 20892 USA.
[Kohn, J.] NIH, Clin Res Ctr, Bethesda, MD 20892 USA.
[Rosenstein, D.] Univ N Carolina, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 47
EP 48
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800082
ER
PT J
AU Chuang, PY
Conley, Y
Kuo, CWJ
Sherwood, P
AF Chuang, P-Y
Conley, Y.
Kuo, C. W-J
Sherwood, P.
TI Functional Interleukin 1 beta and 6 Proteins and Their Genetic
Variations Associated With Psycho-behavioral Responses in the Caregivers
of Patients With Malignant Brain Tumors
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Chuang, P-Y] NINR, NIH, Bethesda, MD 20892 USA.
[Conley, Y.; Kuo, C. W-J; Sherwood, P.] Univ Pittsburgh, Sch Nursing, Pittsburgh, PA 15261 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 66
EP 67
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800117
ER
PT J
AU Wiener, L
McConnell, D
Latella, L
Ludi, E
AF Wiener, L.
McConnell, D.
Latella, L.
Ludi, E.
TI Cultural and Religious Considerations in Pediatric Palliative Care
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Wiener, L.] NCI, NIH, Bethesda, MD 20892 USA.
[Latella, L.] Cornell Univ, Ithaca, NY USA.
[Ludi, E.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 90
EP 90
PG 1
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800159
ER
PT J
AU Zadeh, S
Wiener, L
AF Zadeh, S.
Wiener, L.
TI When Cure No Longer Seems Possible: Support for Patients, Families and
Health Care Staff
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Zadeh, S.; Wiener, L.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 90
EP 91
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800160
ER
PT J
AU Forsythe, LP
Alfano, CM
Kent, EE
Weaver, KE
Rowland, JH
AF Forsythe, L. P.
Alfano, C. M.
Kent, E. E.
Weaver, K. E.
Rowland, J. H.
TI Social Support in Cancer Survivors: Individual Differences and
Associations With Follow-up Care
SO PSYCHO-ONCOLOGY
LA English
DT Meeting Abstract
C1 [Forsythe, L. P.; Alfano, C. M.; Kent, E. E.; Rowland, J. H.] NCI, Off Canc Survivorship, NIH, DHHS, Bethesda, MD 20892 USA.
[Weaver, K. E.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
SU 1
SI SI
BP 124
EP 125
PG 2
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 885LP
UT WOS:000299780800223
ER
PT J
AU Tai, B
Boyle, M
Ghitza, U
Kaplan, RM
Clark, HW
Gersing, K
AF Tai, Betty
Boyle, Maureen
Ghitza, Udi
Kaplan, Robert M.
Clark, H. Westley
Gersing, Kenneth
TI Meaningful Use of Electronic Behavioral Health Data in Primary Health
Care
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
AB In August 2011, scientists and policy-makers held a conference entitled "Using IT to Improve Community Health: How Health Care Reform Supports Innovation." One of the conference sessions was entitled "Electronic health records: Meaningful use implementation challenges, innovation, and regulations." This meeting report discusses the meaningful use of behavioral health data for the treatment of mental health and substance abuse conditions and optimization of behavioral wellness by primary care physicians.
C1 [Tai, Betty; Ghitza, Udi] Natl Inst Drug Abuse, Ctr Clin Trials Network, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Boyle, Maureen; Kaplan, Robert M.] NIH, Off Behav & Social Sci Res, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Clark, H. Westley] Subst Abuse & Mental Hlth Serv Adm, US Dept Hlth & Human Serv, Rockville, MD 20857 USA.
[Gersing, Kenneth] Duke Univ, Dept Psychiat & Behav Sci, Sch Med, Med Ctr, Durham, NC 27710 USA.
RP Tai, B (reprint author), Natl Inst Drug Abuse, Ctr Clin Trials Network, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM btai@nih.gov
NR 6
TC 3
Z9 3
U1 0
U2 5
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 1
PY 2012
VL 4
IS 119
AR 119mr3
DI 10.1126/scitranslmed.3003324
PG 3
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 891NG
UT WOS:000300223300004
PM 22301552
ER
PT J
AU Gershengorn, MC
AF Gershengorn, Marvin C.
TI History of the Clinical Endocrinology Branch of the National Institute
of Diabetes and Digestive and Kidney Diseases: Impact on Understanding
and Treatment of Diseases of the Thyroid Gland
SO THYROID
LA English
DT Editorial Material
ID RADIOACTIVE IODINE; HORMONE; RECEPTOR; SECRETION; MECHANISM; MICE
C1 NIDDK, Lab Endocrinol & Receptor Biol, NIH, Bethesda, MD 20892 USA.
RP Gershengorn, MC (reprint author), NIDDK, Lab Endocrinol & Receptor Biol, NIH, 50 South Dr,Room 4134, Bethesda, MD 20892 USA.
EM marving@intra.niddk.nih.gov
FU Intramural NIH HHS
NR 18
TC 1
Z9 1
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1050-7256
J9 THYROID
JI Thyroid
PD FEB
PY 2012
VL 22
IS 2
BP 109
EP 111
DI 10.1089/thy.2012.2202.com
PG 3
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 891TY
UT WOS:000300240700001
PM 22257372
ER
PT J
AU Schonfeld, SJ
Neta, G
Sturgis, EM
Pfeiffer, RM
Hutchinson, AA
Xu, L
Wheeler, W
Guenel, P
Rajaraman, P
de Vathaire, F
Ron, E
Tucker, MA
Chanock, SJ
Sigurdson, AJ
Brenner, AV
AF Schonfeld, Sara J.
Neta, Gila
Sturgis, Erich M.
Pfeiffer, Ruth M.
Hutchinson, Amy A.
Xu, Li
Wheeler, William
Guenel, Pascal
Rajaraman, Preetha
de Vathaire, Florent
Ron, Elaine
Tucker, Margaret A.
Chanock, Stephen J.
Sigurdson, Alice J.
Brenner, Alina V.
TI Common Genetic Variants in Sex Hormone Pathway Genes and Papillary
Thyroid Cancer Risk
SO THYROID
LA English
DT Article
ID US RADIOLOGIC TECHNOLOGISTS; POLYMORPHISMS; ASSOCIATION; CARCINOMA;
ESTROGEN; GENDER; AGE
AB Background: Hormonal differences are hypothesized to contribute to the approximately >= 2-fold higher thyroid cancer incidence rates among women compared with men worldwide. Although thyroid cancer cells express estrogen receptors and estrogen has a proliferative effect on papillary thyroid cancer (PTC) cells in vitro, epidemiologic studies have not found clear associations between thyroid cancer and female hormonal factors. We hypothesized that polymorphic variation in hormone pathway genes is associated with the risk of developing papillary thyroid cancer.
Methods: We evaluated the association between PTC and 1151 tag single nucleotide polymorphisms (SNPs) in 58 candidate gene regions involved in sex hormone synthesis and metabolism, gonadotropins, and prolactin in a case-control study of 344 PTC cases and 452 controls, frequency matched on age and sex. Odds ratios and p-values for the linear trend for the association between each SNP genotype and PTC risk were estimated using unconditional logistic regression. SNPs in the same gene region or pathway were aggregated using adaptive rank-truncated product methods to obtain gene region-specific or pathway-specific p-values. To account for multiple comparisons, we applied the false discovery rate method.
Results: Seven SNPs had p-values for linear trend <0.01, including four in the CYP19A1 gene, but none of the SNPs remained significant after correction for multiple comparisons. Results were similar when restricting the dataset to women. p-values for examined gene regions and for all genes combined were >= 0.09.
Conclusions: Based on these results, SNPs in selected hormone pathway genes do not appear to be strongly related to PTC risk. This observation is in accord with the lack of consistent associations between hormonal factors and PTC risk in epidemiologic studies.
C1 [Schonfeld, Sara J.; Neta, Gila; Pfeiffer, Ruth M.; Rajaraman, Preetha; Ron, Elaine; Tucker, Margaret A.; Sigurdson, Alice J.; Brenner, Alina V.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Sturgis, Erich M.; Xu, Li] Univ Texas MD Anderson Canc Ctr, Dept Head & Neck Surg, Houston, TX 77030 USA.
[Sturgis, Erich M.] Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Hutchinson, Amy A.] SAIC Frederick Inc, Core Genotyping Facil, Gaithersburg, MD USA.
[Hutchinson, Amy A.; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, Adv Technol Ctr, Gaithersburg, MD USA.
[Wheeler, William] Informat Management Syst, Rockville, MD USA.
[Guenel, Pascal] Natl Inst Hlth & Med Res, INSERM, CESP, Ctr Res Epidemiol & Populat Hlth, Villejuif, France.
[Guenel, Pascal; de Vathaire, Florent] Univ Paris 11, Villejuif, France.
[de Vathaire, Florent] INSERM, Radiat Epidemiol Grp, Villejuif, France.
[de Vathaire, Florent] Inst Gustave Roussy, Villejuif, France.
RP Schonfeld, SJ (reprint author), NCI, Div Canc Epidemiol & Genet, Executive Plaza S,MSC 7238,6120 Execut Blvd, Bethesda, MD 20892 USA.
EM schonfes@mail.nih.gov
RI Xu, Li/B-9535-2012; Tucker, Margaret/B-4297-2015; de Vathaire,
Florent/L-2983-2016
FU American Registry of Radiologic Technologists; Division of Cancer
Epidemiology and Genetics, National Cancer Institute, National
Institutes of Health; American Thyroid Association; National Cancer
Institute, National Institutes of Health [HHSN261200800001E]
FX The authors are indebted to Elaine Ron's long-term commitment to
understanding causes and prevention of thyroid cancer. Her inspiration,
vision, and leadership were integral to this project. They are grateful
to the radiologic technologists who participated in the USRT Study;
Jerry Reid of the American Registry of Radiologic Technologists for
continued support of this study; Diane Kampa and Allison Iwan of the
University of Minnesota for data collection and study coordination;
Liliana Mugartegui for patient recruitment, data collection, and study
coordination at the University of Texas M. D. Anderson Cancer Center;
and Laura Bowen of Information Management Systems for biomedical
computing statistical support. This research was supported in part by
the Intramural Research Program of the Division of Cancer Epidemiology
and Genetics, National Cancer Institute, National Institutes of Health,
and by a grant from the American Thyroid Association (PI: E.M.S.). This
project has been funded in whole or in part with federal funds from the
National Cancer Institute, National Institutes of Health, under contract
number HHSN261200800001E. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does it mention trade names, commercial
products, or organizations implying endorsement by the U.S. Government.
NR 19
TC 9
Z9 10
U1 0
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1050-7256
J9 THYROID
JI Thyroid
PD FEB
PY 2012
VL 22
IS 2
BP 151
EP 156
DI 10.1089/thy.2011.0309
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 891TY
UT WOS:000300240700009
PM 22224819
ER
PT J
AU Heidebrecht, RW
Mulrooney, C
Austin, CP
Barker, RH
Beaudoin, JA
Cheng, KCC
Comer, E
Dandapani, S
Dick, J
Duvall, JR
Ekland, EH
Fidock, DA
Fitzgerald, ME
Foley, M
Guha, R
Hinkson, P
Kramer, M
Lukens, AK
Masi, D
Marcaurelle, LA
Su, XZ
Thomas, CJ
Weiwer, M
Wiegand, RC
Wirth, D
Xia, MH
Yuan, J
Zhao, JH
Palmer, M
Munoz, B
Schreiber, S
AF Heidebrecht, Richard W., Jr.
Mulrooney, Carol
Austin, Christopher P.
Barker, Robert H., Jr.
Beaudoin, Jennifer A.
Cheng, Ken Chih-Chien
Comer, Eamon
Dandapani, Sivaraman
Dick, Justin
Duvall, Jeremy R.
Ekland, Eric H.
Fidock, David A.
Fitzgerald, Mark E.
Foley, Michael
Guha, Rajarshi
Hinkson, Paul
Kramer, Martin
Lukens, Amanda K.
Masi, Daniela
Marcaurelle, Lisa A.
Su, Xin-Zhuan
Thomas, Craig J.
Weiwer, Michel
Wiegand, Roger C.
Wirth, Dyann
Xia, Menghang
Yuan, Jing
Zhao, Jinghua
Palmer, Michelle
Munoz, Benito
Schreiber, Stuart
TI Diversity-Oriented Synthesis Yields a Novel Lead for the Treatment of
Malaria
SO ACS MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE diversity-oriented synthesis; malaria; macrocycle; high-throughput
screening phenotypic screen; infectious disease; molecular libraries
probe production centers; stereochemical structure-activity
relationships
ID FALCIPARUM DIHYDROOROTATE DEHYDROGENASE; PLASMODIUM-FALCIPARUM;
NATURAL-PRODUCT; DRUG DISCOVERY; INHIBITORS; STRATEGY; IDENTIFICATION;
ANTIMALARIALS; ERADICATION; MOLECULES
AB Here, we describe the discovery of a novel antimalarial agent using phenotypic screening of Plasmodium falciparum asexual blood-stage parasites. Screening a novel compound collection created using diversity-oriented synthesis (DOS) led to the initial hit. Structure activity relationships guided the synthesis of compounds having improved potency and water solubility, yielding a subnanomolar inhibitor of parasite asexual blood-stage growth. Optimized compound 27 has an excellent off-target activity profile in erythrocyte lysis and HepG2 assays and is stable in human plasma. This compound is available via the molecular libraries probe production centers network (MLPCN) and is designated ML238.
C1 [Heidebrecht, Richard W., Jr.; Mulrooney, Carol; Beaudoin, Jennifer A.; Comer, Eamon; Dandapani, Sivaraman; Duvall, Jeremy R.; Fitzgerald, Mark E.; Foley, Michael; Lukens, Amanda K.; Masi, Daniela; Marcaurelle, Lisa A.; Weiwer, Michel; Wiegand, Roger C.; Wirth, Dyann; Palmer, Michelle; Munoz, Benito; Schreiber, Stuart] Broad Inst, Cambridge Ctr 7, Cambridge, MA 02142 USA.
[Austin, Christopher P.; Cheng, Ken Chih-Chien; Guha, Rajarshi; Thomas, Craig J.; Xia, Menghang; Zhao, Jinghua] NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
[Heidebrecht, Richard W., Jr.; Dick, Justin; Lukens, Amanda K.; Wiegand, Roger C.; Wirth, Dyann] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Ekland, Eric H.; Fidock, David A.] Colombia Univ, Dept Microbiol & Immunol, New York, NY 10032 USA.
[Fidock, David A.] Colombia Univ, Dept Med, Div Infect Dis, New York, NY 10032 USA.
[Su, Xin-Zhuan; Yuan, Jing] NIAID, Bethesda, MD 20892 USA.
[Schreiber, Stuart] Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA.
[Barker, Robert H., Jr.; Hinkson, Paul; Kramer, Martin] Genzyme Corp, Waltham, MA 02451 USA.
RP Heidebrecht, RW (reprint author), Broad Inst, Cambridge Ctr 7, Cambridge, MA 02142 USA.
EM richardh@broadinstitute.org
OI Fidock, David/0000-0001-6753-8938; Su, Xinzhuan/0000-0003-3246-3248
FU NIH-MLPCN [1 U54 HG005032-1, 5 U54MH08468-1]; NIGMS (Broad Institute
CMLD) [50 GM069721]; NIH [R01 AI079709]; Genzyme
FX This work was funded by the NIH-MLPCN program (1 U54 HG005032-1 awarded
to S.L.S. and 5 U54MH08468-1 awarded to C.P.A.) and the NIGMS-sponsored
Center of Excellence in Chemical Methodology and Library Development
(Broad Institute CMLD; P50 GM069721). Funding for EHE and DAF was
provided in part by the NIH (R01 AI079709). Funding for specificity
testing was provided by Genzyme.
NR 28
TC 28
Z9 28
U1 5
U2 41
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1948-5875
J9 ACS MED CHEM LETT
JI ACS Med. Chem. Lett.
PD FEB
PY 2012
VL 3
IS 2
BP 112
EP 117
DI 10.1021/ml200244k
PG 6
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 890EA
UT WOS:000300126700007
ER
PT J
AU Kramer, MS
Papageorghiou, A
Culhane, J
Bhutta, Z
Goldenberg, RL
Gravett, M
Iams, JD
Conde-Agudelo, A
Waller, S
Barros, F
Knight, H
Villar, J
AF Kramer, Michael S.
Papageorghiou, Aris
Culhane, Jennifer
Bhutta, Zulfiqar
Goldenberg, Robert L.
Gravett, Michael
Iams, Jay D.
Conde-Agudelo, Agustin
Waller, Sarah
Barros, Fernando
Knight, Hannah
Villar, Jose
TI Challenges in defining and classifying the preterm birth syndrome
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Editorial Material
DE classification; phenotype; preterm birth
ID GESTATIONAL-AGE ESTIMATION; UNITED-STATES; BACTERIAL-VAGINOSIS;
PERINATAL-MORTALITY; RISK-FACTORS; DELIVERY; WEIGHT; PREGNANCY; GROWTH;
TERM
AB In 2009, the Global Alliance to Prevent Prematurity and Stillbirth Conference charged the authors to propose a new comprehensive, consistent, and uniform classification system for preterm birth. This first article reviews issues related to measurement of gestational age, clinical vs etiologic phenotypes, inclusion vs exclusion of multifetal and stillborn infants, and separation vs combination of pathways to preterm birth. The second article proposes answers to the questions raised here, and the third demonstrates how the proposed system might work in practice.
C1 [Iams, Jay D.] Ohio State Univ, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
[Kramer, Michael S.] McGill Univ, Dept Pediat, Fac Med, Montreal, PQ H3A 2T5, Canada.
[Kramer, Michael S.] McGill Univ, Dept Epidemiol Biostat & Occupat Hlth, Fac Med, Montreal, PQ H3A 2T5, Canada.
[Papageorghiou, Aris; Knight, Hannah; Villar, Jose] Univ Oxford, Nuffield Dept Obstet & Gynecol, Oxford, England.
[Papageorghiou, Aris; Knight, Hannah; Villar, Jose] Univ Oxford, Oxford Maternal & Perinatal Hlth Inst, Green Templeton Coll, Oxford, England.
[Culhane, Jennifer] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Bhutta, Zulfiqar] Aga Khan Univ, Div Women & Child Hlth, Karachi, Pakistan.
[Goldenberg, Robert L.] Drexel Univ, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
[Gravett, Michael; Waller, Sarah] Univ Washington, Dept Obstet & Gynecol, Seattle, WA 98195 USA.
[Gravett, Michael] Seattle Childrens Hosp, Seattle, WA USA.
[Conde-Agudelo, Agustin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Conde-Agudelo, Agustin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI USA.
[Barros, Fernando] Univ Catolica Pelotas, Postgrad Course Hlth & Behav, Pelotas, RS, Brazil.
RP Iams, JD (reprint author), Ohio State Univ, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
EM Jay.Iams@osumc.edu
RI Epidemiologicas, Centro de pesquisas /D-4561-2013; Barros,
Fernando/D-4857-2013
NR 61
TC 57
Z9 58
U1 0
U2 14
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 2012
VL 206
IS 2
BP 108
EP 112
DI 10.1016/j.ajog.2011.10.864
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 886FA
UT WOS:000299836800011
PM 22118964
ER
PT J
AU Goldenberg, RL
Gravett, MG
Iams, J
Papageorghiou, AT
Waller, SA
Kramer, M
Culhane, J
Barros, F
Conde-Agudelo, A
Bhutta, ZA
Knight, HE
Villar, J
AF Goldenberg, Robert L.
Gravett, Michael G.
Iams, Jay
Papageorghiou, Aris T.
Waller, Sarah A.
Kramer, Michael
Culhane, Jennifer
Barros, Fernando
Conde-Agudelo, Augustin
Bhutta, Zulfiqar A.
Knight, Hannah E.
Villar, Jose
TI The preterm birth syndrome: issues to consider in creating a
classification system
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Editorial Material
DE classification; phenotype; preterm birth
ID 2ND-TRIMESTER PREGNANCY LOSS; PERINATAL-MORTALITY; BACTERIAL VAGINOSIS;
NEONATAL OUTCOMES; RISK-FACTORS; DELIVERY; TERM; HETEROGENEITY;
STILLBIRTH; SUBTYPES
AB A comprehensive classification system for preterm birth requires expanded gestational boundaries that recognize the early origins of preterm parturition and emphasize fetal maturity over fetal age. Exclusion of stillbirths, pregnancy terminations, and multifetal gestations prevents comprehensive consideration of the potential causes and presentations of preterm birth. Any step in parturition (cervical softening and ripening, decidual-membrane activation, and/or myometrial contractions) may initiate preterm parturition, and should be recorded for every preterm birth, as should the condition of the mother, fetus, newborn, and placenta, before a phenotype is assigned.
C1 [Goldenberg, Robert L.] Drexel Univ, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
[Gravett, Michael G.; Waller, Sarah A.] Univ Washington, Dept Obstet & Gynecol, Seattle, WA 98195 USA.
Seattle Childrens, Global Alliance Prevent Prematur & Stillbirth, Seattle, WA USA.
[Iams, Jay] Ohio State Univ, Dept Obstet & Gynecol, Med Ctr, Div Maternal Fetal Med, Columbus, OH 43210 USA.
[Papageorghiou, Aris T.; Knight, Hannah E.; Villar, Jose] Univ Oxford, Nuffield Dept Obstet & Gynaecol, Oxford, England.
Univ Oxford, Oxford Maternal & Perinatal Hlth Inst, Green Templeton Coll, Oxford, England.
[Kramer, Michael] McGill Univ, Dept Pediat, Fac Med, Montreal, PQ H3A 2T5, Canada.
[Kramer, Michael] McGill Univ, Fac Med, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ H3A 2T5, Canada.
[Culhane, Jennifer] Univ Penn, Dept Pediat, Philadelphia, PA 19104 USA.
[Barros, Fernando] Univ Catolica Pelotas, Postgrad Course Hlth & Behav, Pelotas, RS, Brazil.
[Conde-Agudelo, Augustin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Conde-Agudelo, Augustin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI USA.
[Bhutta, Zulfiqar A.] Aga Khan Univ, Div Women & Child Hlth, Karachi, Pakistan.
RP Goldenberg, RL (reprint author), Drexel Univ, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
RI Epidemiologicas, Centro de pesquisas /D-4561-2013
NR 43
TC 62
Z9 65
U1 1
U2 16
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 2012
VL 206
IS 2
BP 113
EP 118
DI 10.1016/j.ajog.2011.10.865
PG 6
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 886FA
UT WOS:000299836800012
PM 22177186
ER
PT J
AU Villar, J
Papageorghiou, AT
Knight, HE
Gravett, MG
Iams, J
Waller, SA
Kramer, M
Culhane, JF
Barros, FC
Conde-Agudelo, A
Bhutta, ZA
Goldenberg, RL
AF Villar, Jose
Papageorghiou, Aris T.
Knight, Hannah E.
Gravett, Michael G.
Iams, Jay
Waller, Sarah A.
Kramer, Michael
Culhane, Jennifer F.
Barros, Fernando C.
Conde-Agudelo, Agustin
Bhutta, Zulfiqar A.
Goldenberg, Robert L.
TI The preterm birth syndrome: a prototype phenotypic classification
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Editorial Material
DE phenotype; preterm birth
AB Preterm birth is a syndrome with many causes and phenotypes. We propose a classification that is based on clinical phenotypes that are defined by >= 1 characteristics of the mother, the fetus, the placenta, the signs of parturition, and the pathway to delivery. Risk factors and mode of delivery are not included. There are 5 components in a preterm birth phenotype: (1) maternal conditions that are present before presentation for delivery, (2) fetal conditions that are present before presentation for delivery, (3) placental pathologic conditions, (4) signs of the initiation of parturition, and (5) the pathway to delivery. This system does not force any preterm birth into a predefined phenotype and allows all relevant conditions to become part of the phenotype. Needed data can be collected from the medical records to classify every preterm birth. The classification system will improve understanding of the cause and improve surveillance across populations.
C1 [Iams, Jay] Ohio State Univ, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
[Villar, Jose; Papageorghiou, Aris T.; Knight, Hannah E.] Univ Oxford, Nuffield Dept Obstet & Gynaecol, Oxford, England.
[Villar, Jose; Papageorghiou, Aris T.; Knight, Hannah E.] Univ Oxford, Oxford Maternal & Perinatal Hlth Inst, Green Templeton Coll, Oxford, England.
Univ Washington, Dept Obstet & Gynecol, Seattle, WA 98195 USA.
[Gravett, Michael G.; Waller, Sarah A.] Seattle Childrens, Global Alliance Prevent Prematur & Stillbirth, Seattle, WA USA.
[Kramer, Michael] McGill Univ, Dept Pediat, Fac Med, Montreal, PQ H3A 2T5, Canada.
[Kramer, Michael] McGill Univ, Fac Med, Dept Epidemiol Biostat & Occupat Hlth, Montreal, PQ H3A 2T5, Canada.
[Culhane, Jennifer F.] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Barros, Fernando C.] Univ Catolica Pelotas, Postgrad Course Hlth & Behav, Pelotas, RS, Brazil.
[Conde-Agudelo, Agustin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Conde-Agudelo, Agustin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI USA.
[Bhutta, Zulfiqar A.] Aga Khan Univ, Div Women & Child Hlth, Karachi, Pakistan.
[Goldenberg, Robert L.] Drexel Univ, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
RP Iams, J (reprint author), Ohio State Univ, Dept Obstet & Gynecol, Columbus, OH 43210 USA.
EM Jay.Iams@osumc.edu
RI Epidemiologicas, Centro de pesquisas /D-4561-2013; Barros,
Fernando/D-4857-2013
NR 11
TC 63
Z9 65
U1 0
U2 11
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 2012
VL 206
IS 2
BP 119
EP 123
DI 10.1016/j.ajog.2011.10.866
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 886FA
UT WOS:000299836800013
PM 22177191
ER
PT J
AU Esplin, MS
AF Esplin, M. Sean
TI Proteomic identification of serum peptides predicting subsequent
spontaneous preterm birth REPLY
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Letter
C1 Univ Utah, Hlth Sci Ctr, Med Units Network, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Salt Lake City, UT 84132 USA.
RP Esplin, MS (reprint author), Univ Utah, Hlth Sci Ctr, Med Units Network, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Salt Lake City, UT 84132 USA.
EM sean.esplin@imail.org
NR 1
TC 1
Z9 1
U1 1
U2 4
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 2012
VL 206
IS 2
BP E3
EP E4
DI 10.1016/j.ajog.2011.09.011
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 886FA
UT WOS:000299836800003
ER
PT J
AU Romero, R
Nicolaides, K
Conde-Agudelo, A
Tabor, A
O'Brien, JM
Cetingoz, E
Da Fonseca, E
Creasy, GW
Klein, K
Rode, L
Soma-Pillay, P
Fusey, S
Cam, C
Alfirevic, Z
Hassan, SS
AF Romero, Roberto
Nicolaides, Kypros
Conde-Agudelo, Agustin
Tabor, Ann
O'Brien, John M.
Cetingoz, Elcin
Da Fonseca, Eduardo
Creasy, George W.
Klein, Katharina
Rode, Line
Soma-Pillay, Priya
Fusey, Shalini
Cam, Cetin
Alfirevic, Zarko
Hassan, Sonia S.
TI Vaginal progesterone in women with an asymptomatic sonographic short
cervix in the midtrimester decreases preterm delivery and neonatal
morbidity: a systematic review and metaanalysis of individual patient
data
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE admission to neonatal intensive care unit; birthweight < 1500 g;
mechanical ventilation; prematurity; preterm birth; progestin;
respiratory distress syndrome; transvaginal ultrasound; uterine cervix;
17 alpha-hydroxyprogesterone caproate
ID PLACEBO-CONTROLLED TRIAL; RANDOMIZED CONTROLLED-TRIAL; GENE-ENVIRONMENT
INTERACTION; GROWTH-FACTOR-I; DOUBLE-BLIND; UTERINE CERVIX;
17-ALPHA-HYDROXYPROGESTERONE CAPROATE; RECEPTOR-A; HIGH-RISK; MICRONIZED
PROGESTERONE
AB OBJECTIVE: To determine whether the use of vaginal progesterone in asymptomatic women with a sonographic short cervix (<= 25 mm) in the midtrimester reduces the risk of preterm birth and improves neonatal morbidity and mortality.
STUDY DESIGN: Individual patient data metaanalysis of randomized controlled trials.
RESULTS: Five trials of high quality were included with a total of 775 women and 827 infants. Treatment with vaginal progesterone was associated with a significant reduction in the rate of preterm birth <33 weeks (relative risk [RR], 0.58; 95% confidence interval [CI], 0.42-0.80), <35 weeks (RR, 0.69; 95% CI, 0.55-0.88), and <28 weeks (RR, 0.50; 95% CI, 0.30-0.81); respiratory distress syndrome (RR, 0.48; 95% CI, 0.30-0.76); composite neonatal morbidity and mortality (RR, 0.57; 95% CI, 0.40-0.81); birthweight <1500 g (RR, 0.55; 95% CI, 0.38-0.80); admission to neonatal intensive care unit (RR, 0.75; 95% CI, 0.59-0.94); and requirement for mechanical ventilation (RR, 0.66; 95% CI, 0.44-0.98). There were no significant differences between the vaginal progesterone and placebo groups in the rate of adverse maternal events or congenital anomalies.
CONCLUSION: Vaginal progesterone administration to asymptomatic women with a sonographic short cervix reduces the risk of preterm birth and neonatal morbidity and mortality.
C1 [Romero, Roberto; Conde-Agudelo, Agustin; Hassan, Sonia S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Romero, Roberto; Conde-Agudelo, Agustin; Hassan, Sonia S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI USA.
[Nicolaides, Kypros] Kings Coll Hosp London, Dept Obstet & Gynecol, London, England.
[Tabor, Ann; Rode, Line] Rigshosp, Copenhagen Univ Hosp, Dept Fetal Med, DK-2100 Copenhagen, Denmark.
[Tabor, Ann] Univ Copenhagen, Fac Hlth Sci, Copenhagen, Denmark.
[O'Brien, John M.] Univ Kentucky, Perinatal Diagnost Ctr, Cent Baptist Hosp, Lexington, KY USA.
[O'Brien, John M.] Univ Kentucky, Dept Obstet & Gynecol, Lexington, KY USA.
[Cetingoz, Elcin; Cam, Cetin] Zeynep Kamil Women & Children Dis Educ & Res Hosp, Dept Obstet & Gynecol, Istanbul, Turkey.
[Da Fonseca, Eduardo] Univ Sao Paulo, Dept Obstet & Ginecol, Hosp Servidor Publ Estadual Francisco Morato Oliv, Sao Paulo, Brazil.
[Da Fonseca, Eduardo] Univ Sao Paulo, Sch Med, Sao Paulo, Brazil.
[Creasy, George W.] Columbia Labs Inc, Livingston, NJ USA.
[Klein, Katharina] Med Univ Vienna, Dept Obstet & Gynecol, Vienna, Austria.
[Soma-Pillay, Priya] Steve Biko Acad Hosp, Dept Obstet & Gynecol, Pretoria, South Africa.
[Soma-Pillay, Priya] Univ Pretoria, ZA-0002 Pretoria, South Africa.
[Fusey, Shalini] Govt Med Coll & Hosp, Dept Obstet & Gynecol, Nagpur, Maharashtra, India.
[Alfirevic, Zarko] Univ Liverpool, Dept Womens & Childrens Hlth, Liverpool L69 3BX, Merseyside, England.
[Hassan, Sonia S.] Wayne State Univ, Hutzel Hosp, Dept Obstet & Gynecol, Detroit, MI USA.
RP Romero, R (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RI Fonseca, Eduardo/A-2490-2013;
OI Creasy, George/0000-0002-6645-4238
FU Columbia Laboratories Inc; Eunice Kennedy Shriver National Institute of
Child Health and Human Development, National Institutes of Health,
Department of Health and Human Services
FX The majority of the authors report no conflict of interest except as
stated in this paragraph. J.M.O'B. was involved in studies of
progesterone gel treatment for preterm birth prevention sponsored by
Columbia Laboratories Inc, the manufacturer of the preparation used in
the PREGNANT Trial and a previous trial of vaginal progesterone in women
at risk for preterm delivery. J.M.O'B. serves on advisory boards and is
a consultant for Watson Pharmaceuticals, a company with a financial
interest in marketing vaginal progesterone gel for the prevention of
preterm birth. He and others are listed in the patent on the use of all
progesterone compounds to prevent preterm birth (US Patent No.
7,884,093: Progesterone for the Treatment and Prevention of Spontaneous
Preterm Birth). G. W. C. is an employee of Columbia Laboratories Inc.;
This research 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 185
TC 51
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U1 0
U2 7
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 2012
VL 206
IS 2
AR 124.e1
DI 10.1016/j.ajog.2011.12.003
PG 19
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 886FA
UT WOS:000299836800014
PM 22284156
ER
PT J
AU Horvath, B
Mukhopadhyay, P
Hasko, G
Pacher, P
AF Horvath, Bela
Mukhopadhyay, Partha
Hasko, Gyoergy
Pacher, Pal
TI The Endocannabinoid System and Plant-Derived Cannabinoids in Diabetes
and Diabetic Complications
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Review
ID CB1 RECEPTOR ANTAGONIST; OBESE ZUCKER RATS; ENDOPLASMIC-RETICULUM
STRESS; RANDOMIZED CONTROLLED-TRIAL; CORONARY-ARTERY-DISEASE; OXIDATIVE
STRESS; CELL-DEATH; INSULIN-SECRETION; RISK-FACTORS; CARDIOMETABOLIC
RISK
AB Oxidative stress and inflammation play critical roles in the development of diabetes and its complications. Recent studies provided compelling evidence that the newly discovered lipid signaling system (ie, the endocannabinoid system) may significantly influence reactive oxygen species production, inflammation, and subsequent tissue injury, in addition to its well-known metabolic effects and functions. The modulation of the activity of this system holds tremendous therapeutic potential in a wide range of diseases, ranging from cancer, pain, neurodegenerative, and cardiovascular diseases to obesity and metabolic syndrome, diabetes, and diabetic complications. This review focuses on the role of the endocannabinoid system in primary diabetes and its effects on various diabetic complications, such as diabetic cardiovascular dysfunction, nephropathy, retinopathy, and neuropathy, particularly highlighting the mechanisms beyond the metabolic consequences of the activation of the endocannabinoid system. The therapeutic potential of targeting the endocannabinoid system and certain plant-derived cannabinoids, such as cannabidiol and Delta 9-tetra-hydrocannabivarin, which are devoid of psychotropic effects and possess potent anti-inflammatory and/or antioxidant properties, in diabetes and diabetic complications is also discussed. (Am J Pathol 2012, 180:432-442; DOI: 10.1016/j.ajpath.2011.11.003)
C1 [Horvath, Bela; Mukhopadhyay, Partha; Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA.
[Horvath, Bela] Semmelweis Univ, Inst Human Physiol & Clin Expt Res, Budapest, Hungary.
[Hasko, Gyoergy] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Surg, Newark, NJ 07103 USA.
RP Pacher, P (reprint author), NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, 5625 Fishers Lane,MSC-9413, Bethesda, MD 20892 USA.
EM horvathba@mail.nih.gov; pacher@mail.nih.gov
RI Horvath, Bela/A-7368-2009; Pacher, Pal/B-6378-2008; MUKHOPADHYAY,
PARTHA/G-3890-2010
OI Pacher, Pal/0000-0001-7036-8108; MUKHOPADHYAY,
PARTHA/0000-0002-1178-1274
FU National Institute of Alcohol Abuse and Alcoholism, NIH; Hungarian
Scientific Research Fund Fellowship [OTKA-NKTH-EU MB08 80238]
FX Supported by the Intramural Research Program of the National Institute
of Alcohol Abuse and Alcoholism, NIH (P.P.). Dr. Horvath is a recipient
of the Hungarian Scientific Research Fund Fellowship (OTKA-NKTH-EU MB08
80238).
NR 104
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Z9 38
U1 0
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD FEB
PY 2012
VL 180
IS 2
BP 432
EP 442
DI 10.1016/j.ajpath.2011.11.003
PG 11
WC Pathology
SC Pathology
GA 887HZ
UT WOS:000299918800001
PM 22155112
ER
PT J
AU Liu, XF
Ory, V
Chapman, S
Yuan, H
Albanese, C
Kallakury, B
Timofeeva, OA
Nealon, C
Dakic, A
Simic, V
Haddad, BR
Rhim, JS
Dritschilo, A
Riegel, A
McBride, A
Schlegel, R
AF Liu, Xuefeng
Ory, Virginie
Chapman, Sandra
Yuan, Hang
Albanese, Chris
Kallakury, Bhaskar
Timofeeva, Olga A.
Nealon, Caitlin
Dakic, Aleksandra
Simic, Vera
Haddad, Bassem R.
Rhim, Johng S.
Dritschilo, Anatoly
Riegel, Anna
McBride, Alison
Schlegel, Richard
TI ROCK Inhibitor and Feeder Cells Induce the Conditional Reprogramming of
Epithelial Cells
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID PLURIPOTENT STEM-CELLS; HUMAN-PAPILLOMAVIRUS TYPE-16; PRIMARY HUMAN
KERATINOCYTES; TELOMERASE ACTIVITY; HTERT PROMOTER; BREAST-CANCER;
IN-VITRO; IMMORTALIZATION; SURVIVAL; TRANSFORMATION
AB We demonstrate that a Rho kinase inhibitor (Y-27632), in combination with fibroblast feeder cells, induces normal and tumor epithelial cells from many tissues to proliferate indefinitely in vitro, without transduction of exogenous viral or cellular genes. Primary prostate and mammary cells, for example, are reprogrammed toward a basaloid, stem-like phenotype and form well-organized prostaspheres and mammospheres in Matrigel. However, in contrast to the selection of rare stem-like cells, the described growth conditions can generate 2 x 10(6) cells in 5 to 6 days from needle biopsies, and can generate cultures from cryopreserved tissue and from fewer than four viable cells. Continued cell proliferation is dependent on both feeder cells and Y-27632, and the conditionally reprogrammed cells (CRCs) retain a normal karyotype and remain nontumorigenic. This technique also efficiently establishes cell cultures from human and rodent tumors. For example, CRCs established from human prostate adenocarcinoma displayed instability of chromosome 13, proliferated abnormally in Matrigel, and formed tumors in mice with severe combined immunodeficiency. The ability to rapidly generate many tumor cells from small biopsy specimens and frozen tissue provides significant opportunities for cell-based diagnostics and therapeutics (including chemosensitivity testing) and greatly expands the value of biobanking. In addition, the CRC method allows for the genetic manipulation of epithelial cells ex vivo and their subsequent evaluation in vivo in the same host. (Am J Pathol 2012, 180: 599-607; DOI: 10.1016/j.ajpath.2011.10.036)
C1 [Liu, Xuefeng; Yuan, Hang; Albanese, Chris; Kallakury, Bhaskar; Nealon, Caitlin; Dakic, Aleksandra; Simic, Vera; Schlegel, Richard] Georgetown Univ, Sch Med, Lombardi Comprehens Canc Ctr, Dept Pathol, Washington, DC 20057 USA.
[Ory, Virginie; Albanese, Chris; Timofeeva, Olga A.; Haddad, Bassem R.; Dritschilo, Anatoly; Riegel, Anna] Georgetown Univ, Sch Med, Lombardi Comprehens Canc Ctr, Dept Oncol, Washington, DC 20057 USA.
[Chapman, Sandra; McBride, Alison] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
[Rhim, Johng S.] Uniformed Serv Univ Hlth Sci, Dept Surg, Ctr Prostate Dis Res, Bethesda, MD 20814 USA.
RP Schlegel, R (reprint author), Georgetown Univ, Med Ctr, Dept Pathol, 3900 Reservoir Rd NW, Washington, DC 20057 USA.
EM schleger@georgetown.edu
RI Chapman, Sandra/I-8889-2014;
OI Chapman, Sandra/0000-0002-9202-336X; McBride, Alison/0000-0001-5607-5157
FU NIH [R01 CA129003, R01 CA113477, R01 CA106400]; Department of Defense
[W81XWH-10-1-0747]; NCI CCSG [5P30CA051008]; National Institute of
Allergy and Infectious Diseases
FX Supported by NIH grants R01 CA129003 (C.A.), R01 CA113477 (A.R.), and
R01 CA106400 (R.S.); a Department of Defense fellowship
(W81XWH-10-1-0747 to V.O.); and two internal development grants (NCI
CCSG 5P30CA051008 to X.L. and A.R., respectively). This work was funded,
in part, by the Intramural Research Program of the National Institute of
Allergy and Infectious Diseases and the NIH.
NR 54
TC 179
Z9 181
U1 6
U2 38
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD FEB
PY 2012
VL 180
IS 2
BP 599
EP 607
DI 10.1016/j.ajpath.2011.10.036
PG 9
WC Pathology
SC Pathology
GA 887HZ
UT WOS:000299918800016
PM 22189618
ER
PT J
AU Robinson, OJ
Cools, R
Carlisi, CO
Sahakian, BJ
Drevets, WC
AF Robinson, Oliver J.
Cools, Roshan
Carlisi, Christina O.
Sahakian, Barbara J.
Drevets, Wayne C.
TI Ventral Striatum Response During Reward and Punishment Reversal Learning
in Unmedicated Major Depressive Disorder
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID INDUCED DOPAMINE RELEASE; PARKINSONS-DISEASE; BASAL GANGLIA; NEURAL
BASIS; FEEDBACK; MECHANISMS; PREDICTION; DEPLETION; VALENCE; BRAIN
AB Objective: Affective biases may underlie many of the key symptoms of major depressive disorder, from anhedonia to altered cognitive performance. Understanding the cause of these biases is therefore critical in the quest for improved treatments. Depression is associated, for example, with a negative affective bias in reversal learning. However, despite the fact that reversal learning is associated with striatal response in healthy individuals and depressed individuals exhibit attenuated striatal function on multiple tasks, studies to date have not demonstrated striatal involvement in the negative bias in reversal learning in depression. In this study, the authors sought to determine whether this may be because reversal learning tasks conventionally used to study behavior examine reversals only on the basis of unexpected punishment and therefore do not adequately separate reward- and punishment-based behavior.
Method: The authors used functional MRI to compare the hemodynamic response to a reversal learning task with mixed reward- and punishment-based reversal stages between individuals with unmedicated major depressive disorder (N=13) and healthy comparison subjects (N=14).
Results: Impaired reward (but not punishment) reversal accuracy was found alongside attenuated anteroventral striatal response to unexpected reward in depression.
Conclusions: Attenuated neurophysiological response of the anteroventral striatum may reflect dysfunction in circuits involving afferent projections from the orbitofrontal, limbic, and/or mesostriatal dopaminergic pathways, which conceivably may, together with the ventral striatum, underlie anhedonia in depression. Learning to appreciate and enjoy positive life experiences is critical for recovery from depression. This study pinpoints a neural target for such recovery.
C1 [Robinson, Oliver J.] NIMH, Sect Neuroimaging Mood & Anxiety Disorders, Bethesda, MD 20892 USA.
Univ Cambridge, Dept Psychiat, Cambridge, England.
Univ Cambridge, MRC Wellcome Trust Behav & Clin Neurosci Inst, Cambridge, England.
Addenbrookes Hosp, Cambridge, England.
Radboud Univ Nijmegen, Med Ctr, Ctr Cognit Neuroimaging, Donders Inst Brain Cognit & Behav,Dept Psychiat, NL-6525 ED Nijmegen, Netherlands.
Univ Oklahoma, Coll Med, Laureate Inst Brain Res, Tulsa, OK USA.
Univ Oklahoma, Coll Med, Dept Psychiat, Tulsa, OK USA.
RP Robinson, OJ (reprint author), NIMH, Sect Neuroimaging Mood & Anxiety Disorders, Bethesda, MD 20892 USA.
EM oliver.j.robinson@gmail.com
RI Robinson, Oliver/B-3646-2011; Cools, Roshan/D-1905-2010;
OI Robinson, Oliver/0000-0002-3100-1132; Carlisi,
Christina/0000-0002-0942-8586
FU Johnson Johnson; NIMH [04-M-0002]
FX Dr. Sahakian has received grant support from Johnson & Johnson, has
served as a consultant for Boehringer-Ingelheim, Cambridge Cognition,
Eli Lilly, GlaxoSmithKline, Hoffmann-La Roche, Novartis, and Shire, and
receives an honorarium from the Journal of Psychological Medicine, Dr.
Drevets has served as a consultant for Pfizer, Johnson & Johnson, Eisai,
and Rules-Based Medicine. The other authors report no financial
relationships with commercial interests.; Supported by the NIMH
Intramural Research Program (protocol number 04-M-0002).
NR 40
TC 70
Z9 72
U1 1
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 2012
VL 169
IS 2
BP 152
EP 159
DI 10.1176/appi.ajp.2011.11010137
PG 8
WC Psychiatry
SC Psychiatry
GA 890BW
UT WOS:000300121100010
PM 22420038
ER
PT J
AU Vitiello, B
Elliott, GR
Swanson, JM
Arnold, LE
Hechtman, L
Abikoff, H
Molina, BSG
Wells, K
Wigal, T
Jensen, PS
Greenhill, LL
Kaltman, JR
Severe, JB
Odbert, C
Hur, K
Gibbons, R
AF Vitiello, Benedetto
Elliott, Glen R.
Swanson, James M.
Arnold, L. Eugene
Hechtman, Lily
Abikoff, Howard
Molina, Brooke S. G.
Wells, Karen
Wigal, Timothy
Jensen, Peter S.
Greenhill, Laurence L.
Kaltman, Jonathan R.
Severe, Joanne B.
Odbert, Carol
Hur, Kwan
Gibbons, Robert
TI Blood Pressure and Heart Rate Over 10 Years in the Multimodal Treatment
Study of Children With ADHD
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID ATTENTION-DEFICIT/HYPERACTIVITY-DISORDER; SALTS EXTENDED-RELEASE;
SCHOOL-AGED CHILDREN; FOLLOW-UP; SUDDEN-DEATH; VENTRICULAR
TACHYARRHYTHMIAS; OROS METHYLPHENIDATE; TREATMENT STRATEGIES;
NATIONAL-INSTITUTE; SHORT-TERM
AB Objective: It is unknown whether prolonged childhood exposure to stimulant medication for the treatment of attention deficit hyperactivity disorder (ADHD) increases the risk for developing abnormalities in blood pressure or heart rate. The authors examined the association between stimulant medication and blood pressure and heart rate over 10 years.
Method: A total of 579 children, ages 7-9, were randomly assigned to 14 months of medication treatment, behavioral therapy, the combination of the two, or usual community treatment. The controlled trial was followed by naturalistic treatment with periodic assessments. Blood pressure and heart rate data were first analyzed with linear regression models based on an intent-to-treat approach, using raw data and the blood pressure categories of prehypertension and hypertension. Currently medicated patients were then compared with never or previously medicated patients. Associations between cumulative stimulant exposure and blood pressure or heart rate were assessed.
Results: No treatment effect on either systolic or diastolic blood pressure could be detected. Children who were treated with stimulants had a higher heart rate (mean=84.2 bpm [SD=12.4] on medication alone and mean=84.6 bpm [SD=12.2] on medication plus behavioral therapy) than those who were treated with behavioral therapy alone (mean=79.1 bpm [SD=12.0]) or those who received usual community treatment (mean=78.9 bpm [SD=12.9]) at the end of the 14-month controlled trial, but not thereafter. Stimulant medication did not increase the risk for tachycardia, but greater cumulative stimulant exposure was associated with a higher heart rate at years 3 and 8.
Conclusions: Stimulant treatment did not increase the risk for prehypertension or hypertension over the 10-year period of observation. However, stimulants had a persistent adrenergic effect on heart rate during treatment.
C1 [Vitiello, Benedetto] NIMH, Bethesda, MD 20892 USA.
Childrens Hlth Council, Dept Psychiat, Palo Alto, CA USA.
Univ Calif Irvine, Child Dev Ctr, Irvine, CA USA.
Ohio State Univ, Dept Psychiat, Columbus, OH 43210 USA.
McGill Univ, Dept Psychiat, Montreal, PQ, Canada.
NYU, Dept Child & Adolescent Psychiat, New York, NY 10003 USA.
Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA.
Duke Univ, Med Ctr, Family Studies Clin, Durham, NC USA.
REACH Inst, New York, NY USA.
Columbia Univ, Res Unit Pediat Psychopharmacol, New York, NY USA.
New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
NHLBI, Div Cardiovasc Sci, Bethesda, MD 20892 USA.
Univ Illinois, Ctr Hlth Stat, Chicago, IL USA.
Univ Chicago, Ctr Hlth Stat, Chicago, IL 60637 USA.
RP Vitiello, B (reprint author), NIMH, Bethesda, MD 20892 USA.
EM bvitiell@mail.nih.gov
OI Jensen, Peter/0000-0003-2387-0650
FU AstraZeneca; CureMark; Lilly; Neuropharm; Novartis; Organon; Shire;
Targacept; Eli Lilly; GlaxoSmithKline; Ortho-Janssen; Purdue;
Bristol-Myers-Squibb; Celltech; Cephalon; McNeil; Pfizer; Multi-Health
Systems; Addernex; Otsuka; Shionogi; Janssen-Ortho; Johnson Johnson;
Rhodes Pharmaceutical; NIMH [U01MH50461, N01MH12009,
HHSN271200800005-C]; Duke University [U01MH50477, N01MH12012,
HHSN271200800009-C]; University of California, Irvine [U01MH50440, N01
MH12011, HH-SN271200800006-C]; Research Foundation for Mental
Hygiene-New York State Psychiatric Institute/Columbia University
[U01MH50467, N01 MH12007, HHSN271200800007-C]; Long Island Jewish
Medical Center [U01MH50453]; New York University [N01 MH12004,
HHSN271200800004-C]; University of Pittsburgh [U01MH50467, N01 MH12010,
HHSN271200800008-C]; McGill University [N01 MH12008, HHSN271200800003-C]
FX Dr. Elliott has received investigator-initiated research support from
BioMarin Pharmaceuticals. Dr Swanson has received research support from
Alza, Celgene, Cephalon, ICB, McNeil, Novartis, and Shire. Dr. Arnold
has received research funding or consulting, advisory, or speaking fees
from AstraZeneca, CureMark, Lilly, Neuropharm, Novartis, Organon, Shire,
and Targacept. Dr. Hechtman has received research support or advisory or
speaking fees from Eli Lilly, GlaxoSmithKline, Ortho-Janssen, Purdue,
and Shire. Dr. Abikoff has received research funding or consulting or
speaking fees from Bristol-Myers-Squibb, Celltech, Cephalon, Eli Lilly,
McNeil, Novartis, Pfizer, and Shire. Dr. Wells receives royalty income
from Multi-Health Systems and conducts workshop training in psychosocial
treatments for the REACH Institute and the State of New York. Dr. Wigal
has received research support or consulting or speaking fees from
Addernex, Eli Lilly, McNeil, Otsuka, Shionogi, and Shire. Dr. Jensen has
received advisory board or speaking fees from Janssen-Ortho and Shire.
Dr. Greenhill has received research support from Johnson & Johnson,
Rhodes Pharmaceutical, and Shire. The other authors report no financial
relationships with commercial interests.; Supported by cooperative
agreement grants and contracts from NIMH to the University of
California, Berkeley (U01MH50461, N01MH12009, and HHSN271200800005-C),
Duke University (U01MH50477, N01MH12012, and HHSN271200800009-C),
University of California, Irvine (U01MHSO440, N01 MH12011, and
HH-SN271200800006-C), Research Foundation for Mental Hygiene-New York
State Psychiatric Institute/Columbia University (U01MHSO467, N01
MH12007, and HHSN271200800007-C), Long Island Jewish Medical Center
(U01MH50453), New York University (N01 MH12004 and HHSN271200800004-C),
University of Pittsburgh (U01MHSO467, N01 MH12010, and
HHSN271200800008-C), and McGill University (N01 MH12008 and
HHSN271200800003-C). Statistical analysis was funded by a professional
contract to the Center for Health Statistics, University of Illinois at
Chicago.
NR 39
TC 35
Z9 35
U1 2
U2 17
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 2012
VL 169
IS 2
BP 167
EP 177
DI 10.1176/appi.ajp.2011.10111705
PG 11
WC Psychiatry
SC Psychiatry
GA 890BW
UT WOS:000300121100012
PM 21890793
ER
PT J
AU Guyer, AE
Choate, VR
Detloff, A
Benson, B
Nelson, EE
Perez-Edgar, K
Fox, NA
Pine, DS
Ernst, M
AF Guyer, Amanda E.
Choate, Victoria R.
Detloff, Allison
Benson, Brenda
Nelson, Eric E.
Perez-Edgar, Koraly
Fox, Nathan A.
Pine, Daniel S.
Ernst, Monique
TI Striatal Functional Alteration During Incentive Anticipation in
Pediatric Anxiety Disorders
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID MAJOR DEPRESSIVE DISORDER; SOCIAL ANXIETY; BEHAVIORAL-INHIBITION;
FEARFUL FACES; YOUNG-ADULTS; ADOLESCENTS; AMYGDALA; CHILDREN; RISK;
REWARD
AB Objective: Behavioral inhibition is an early childhood temperament recently associated with altered striatal response in adolescence to incentives of increasing magnitudes. Since early childhood behavioral inhibition is also associated with risk for adolescent social phobia, a similar pattern of striatal activation may manifest in social phobia. The present study compares striatal function in healthy adolescents, adolescents with social phobia, and adolescents with generalized anxiety disorder.
Method: Blood-oxygen-level-dependent signal in striatal regions was examined in 58 medication-free adolescents-14 with social phobia, 18 with generalized anxiety disorder but not social phobia, and 26 with no psychiatric disorder matched on sex, age, puberty, IQ, and socioeconomic status. During functional magnetic resonance imaging, participants responded to incentive cues depicting potential monetary gains or losses of varying magnitudes.
Results: While anticipating incentives of increasing magnitude, adolescents with social phobia showed increasingly heightened caudate and putamen activation at a level greater than that seen in the healthy comparison and generalized anxiety disorder groups. The generalized anxiety disorder group showed a unique valence-specific putamen response relative to the healthy comparison or social phobia group. Both patient groups displayed more complex patterns in the nucleus accumbens than in the caudate or putamen.
Conclusions: Caudate and putamen hypersensitivity to incentives of increasing magnitudes characterizes adolescent social phobia, relative to activation in this region in adolescents with generalized anxiety disorder as well as healthy adolescents. Thus, these findings resemble the pattern previously found in adolescents with early childhood behavioral inhibition, thereby implicating similar neural responses to anticipation of incentives in both early childhood behavioral inhibition and adolescent social phobia.
C1 [Guyer, Amanda E.] Univ Calif Davis, Dept Human & Community Dev, Ctr Mind & Brain, Davis, CA 95616 USA.
NIMH, Mood & Anxiety Program, Bethesda, MD 20892 USA.
George Mason Univ, Dept Psychol, Fairfax, VA 22030 USA.
Univ Maryland, Dept Human Dev, College Pk, MD 20742 USA.
RP Guyer, AE (reprint author), Univ Calif Davis, Dept Human & Community Dev, Ctr Mind & Brain, Davis, CA 95616 USA.
EM aeguyer@ucdavis.edu
RI Nelson, Eric/B-8980-2008;
OI Nelson, Eric/0000-0002-3376-2453; Perez-Edgar,
Koraly/0000-0003-4051-9563
FU National Institute of Mental Health; National Institutes of Health
[K99/R00 MH-080076]
FX Supported by the Intramural Research Program of the National Institute
of Mental Health and a National Institutes of Health Career Development
Award (K99/R00 MH-080076) (Dr. Guyer).
NR 40
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Z9 57
U1 4
U2 9
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 2012
VL 169
IS 2
BP 205
EP 212
DI 10.1176/appi.ajp.2011.11010006
PG 8
WC Psychiatry
SC Psychiatry
GA 890BW
UT WOS:000300121100016
PM 22423352
ER
PT J
AU Arrigo, NC
Briese, T
Calisher, CH
Drebot, MA
Fljelle, B
LeDuc, JW
Powers, AM
Repik, PM
Roehrig, JT
Schmaljohn, CS
Tesh, RB
Weaver, SC
AF Arrigo, Nicole C.
Briese, Thomas
Calisher, Charles H.
Drebot, Michael A.
Fljelle, Brian
LeDuc, James W.
Powers, Ann M.
Repik, Patricia M.
Roehrig, John T.
Schmaljohn, Connie S.
Tesh, Robert B.
Weaver, Scott C.
TI Recommendations for Publication of Viral Genetic Data and Sample Access
for Novel Viruses and Strains
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID DEPENDENT DNA POLYMERASE; VIRIONS
C1 [LeDuc, James W.; Tesh, Robert B.; Weaver, Scott C.] Univ Texas Med Branch, Inst Human Infect & Immun, Galveston, TX 77555 USA.
[Arrigo, Nicole C.; Briese, Thomas] Columbia Univ, Ctr Infect & Immun, Mailman Sch Publ Hlth, New York, NY USA.
[Calisher, Charles H.] Colorado State Univ, Arthropod Borne & Infect Dis Lab, Dept Microbiol Immunol & Pathol, Coll Vet Med & Biomed Sci, Ft Collins, CO 80523 USA.
[Drebot, Michael A.] Publ Hlth Agcy Canada, Natl Microbiol Lab, Winnipeg, MB, Canada.
[Fljelle, Brian] Univ New Mexico, Sch Med, Infect Dis & Inflammat Program, Dept Pathol Biol & Mol Genet, Albuquerque, NM 87131 USA.
[Fljelle, Brian] Univ New Mexico, Sch Med, Infect Dis & Inflammat Program, Dept Microbiol, Albuquerque, NM 87131 USA.
[Powers, Ann M.; Roehrig, John T.] Ctr Dis Control & Prevent, Natl Ctr Infect Dis, Div Vector Borne Infect Dis, Ft Collins, CO USA.
[Repik, Patricia M.] NIAID, Virol Branch, Div Microbiol & Infect Dis, NIH, Bethesda, MD 20892 USA.
[Schmaljohn, Connie S.] USA, Med Res Inst Infect Dis, Dept Mol Virol, Div Virol, Frederick, MD USA.
RP Weaver, SC (reprint author), Univ Texas Med Branch, Inst Human Infect & Immun, 301 Univ Blvd, Galveston, TX 77555 USA.
EM ncarrigo@gmail.com; thomas.briese@columbia.edu; calisher@cybersafe.net;
Mike_Drebot@hc-sc.gc.ca; bhjelle@salud.unm.edu; jwleduc@UTMB.EDU;
AKP7@cdc.gov; prepik@niaid.nih.gov; trl@CDC.GOV;
connie.schmaljohn@us.army.mil; rtesh@utmb.edu; sweaver@utmb.edu
RI Weaver, Scott/D-6490-2011;
OI Roehrig, John/0000-0001-7581-0479
NR 5
TC 2
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U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD FEB
PY 2012
VL 86
IS 2
BP 189
EP 191
DI 10.4269/ajtmh.2012.11-0523
PG 3
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 886PQ
UT WOS:000299866700002
PM 22302845
ER
PT J
AU Chaube, R
Kallakunta, VM
Espey, MG
McLarty, R
Faccenda, A
Ananvoranich, S
Mutus, B
AF Chaube, Ruchi
Kallakunta, Vasantha Madhuri
Espey, Michael Graham
McLarty, Ryan
Faccenda, Adam
Ananvoranich, Sirinart
Mutus, Bulent
TI Endoplasmic reticulum stress-mediated inhibition of NSMase2 elevates
plasma membrane cholesterol and attenuates NO production in endothelial
cells
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
LA English
DT Article
DE Neutral sphingomyelinase 2; Nitric oxide synthase; Nitric oxide; ER
stress; Endothelial dysfunction
ID NITRIC-OXIDE SYNTHASE; ELEMENT-BINDING PROTEINS; NECROSIS-FACTOR-ALPHA;
SMOOTH-MUSCLE-CELLS; OXIDATIVE STRESS; NEUTRAL SPHINGOMYELINASE; ENOS
ACTIVITY; ACTIVATION; DYSFUNCTION; APOPTOSIS
AB Chronic exposure of blood vessels to cardiovascular risk factors such as free fatty acids, LDL-cholesterol, homocysteine and hyperglycemia can give rise to endothelial dysfunction, partially due to decreased synthesis and bioavailability of nitric oxide (NO). Many of these same risk factors have been shown to induce endoplasmic reticulum (ER) stress in endothelial cells. The objective of this study was to examine the mechanisms responsible for endothelial dysfunction mediated by ER stress. ER stress elevated both intracellular and plasma membrane (PM) cholesterols in BAEC by similar to 3-fold, indicated by epifluorescence and cholesterol oxidase methods. Increases in cholesterol levels inversely correlated with neutral sphingomyelinase 2 (NSMase2) activity, endothelial nitric oxide synthase (eNOS) phospho-activation and NO-production. To confirm that ER stress-induced effects on PM cholesterol were a direct consequence of decreased NSMase2 activity, enzyme expression was either enhanced or knocked down in BAEC. NSMase2 over-expression did not significantly affect cholesterol levels or NO-production, but increased eNOS phosphorylation by similar to 1.7-fold. Molecular knock down of NSMase2 decreased eNOS phosphorylation and NO-production by 50% and 40%, respectively while increasing PM cholesterol by 1.7-fold and intracellular cholesterol by 2.7-fold. Furthermore, overexpression of NSMase2 in ER-stressed BAEC lowered cholesterol levels to within control levels as well as nearly doubled the NO production, restoring it to similar to 74% and 68% of controls using tunicamycin and palmitate, respectively. This study establishes NSMase2 as a pivotal enzyme in the onset of endothelial ER stress-mediated vascular dysfunction as its inactivation leads to the attenuation of NO production and the elevation of cellular cholesterol. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.
C1 [Chaube, Ruchi; Kallakunta, Vasantha Madhuri; McLarty, Ryan; Faccenda, Adam; Ananvoranich, Sirinart; Mutus, Bulent] Univ Windsor, Dept Chem & Biochem, Windsor, ON N9B 3P4, Canada.
[Espey, Michael Graham] NIDDK, Mol & Clin Nutr Sect, Natl Inst Hlth Bethesda, Bethesda, MD 20892 USA.
RP Mutus, B (reprint author), Univ Windsor, Dept Chem & Biochem, Windsor, ON N9B 3P4, Canada.
EM mutusb@uwindsor.ca
FU Natural Sciences and Engineering Research Council of Canada (NSERC);
University of Windsor
FX This study was supported by a Discovery Grant from the Natural Sciences
and Engineering Research Council of Canada (NSERC) and funds from the
University of Windsor Research Chair Program to BM.
NR 52
TC 7
Z9 7
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1388-1981
J9 BBA-MOL CELL BIOL L
JI Biochim. Biophys. Acta Mol. Cell Biol. Lipids
PD FEB
PY 2012
VL 1821
IS 2
BP 313
EP 323
DI 10.1016/j.bbalip.2011.10.015
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 889KP
UT WOS:000300072900008
PM 22063270
ER
PT J
AU Wu, T
Fallin, MD
Shi, M
Ruczinski, I
Liang, KY
Hetmanski, JB
Wang, H
Ingersoll, RG
Huang, SZ
Ye, XQ
Wu-Chou, YH
Chen, PK
Jabs, EW
Shi, B
Redett, R
Scott, AF
Murray, JC
Marazita, ML
Munger, RG
Beaty, TH
AF Wu, Tao
Fallin, M. Daniele
Shi, Min
Ruczinski, Ingo
Liang, Kung Yee
Hetmanski, Jacqueline B.
Wang, Hong
Ingersoll, Roxann G.
Huang, Shangzhi
Ye, Xiaoqian
Wu-Chou, Yah-Huei
Chen, Philip K.
Jabs, Ethylin Wang
Shi, Bing
Redett, Richard
Scott, Alan F.
Murray, Jeffrey C.
Marazita, Mary L.
Munger, Ronald G.
Beaty, Terri H.
TI Evidence of gene-environment interaction for the RUNX2 gene and
environmental tobacco smoke in controlling the risk of cleft lip
with/without cleft palate
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Article
DE RUNX2; oral clefts; gene-environment interaction; parent-of-origin
effects; imprinting
ID LOG-LINEAR APPROACH; FAMILY-BASED TESTS; PARENT-TRIAD DATA;
CLEIDOCRANIAL DYSPLASIA; LINKAGE DISEQUILIBRIUM; BIRTH-DEFECTS; ORAL
CLEFTS; OROFACIAL CLEFTS; UNIFIED APPROACH; ASSOCIATION
AB This study examined the association between 49 markers in the Runt-related transcription factor 2 (RUNX2) gene and nonsyndromic cleft lip with/without cleft palate (CL/P) among 326 Chinese case-parent trios, while considering gene-environment (GxE) interaction and parent-of-origin effects. Five single-nucleotide polymorphisms (SNPs) showed significant evidence of linkage and association with CL/P and these results were replicated in an independent European sample of 825 case-parent trios. We also report compelling evidence for interaction between markers in RUNX2 and environmental tobacco smoke (ETS). Although most marginal SNP effects (i.e., ignoring maternal exposures) were not statistically significant, eight SNPs were significant when considering possible interaction with ETS when testing for gene (G) and GxE interaction simultaneously or when considering GxE alone. Independent samples from European populations showed consistent evidence of significant GxETS interaction at two SNPs (rs6904353 and rs7748231). Our results suggest genetic variation in RUNX2 may influence susceptibility to CL/P through interacting with ETS. Birth Defects Research (Part A) 2012. (C) 2012 Wiley Periodicals, Inc.
C1 [Wu, Tao; Fallin, M. Daniele; Ruczinski, Ingo; Liang, Kung Yee; Hetmanski, Jacqueline B.; Ingersoll, Roxann G.; Beaty, Terri H.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Wu, Tao; Wang, Hong] Peking Univ, Sch Publ Hlth, Beijing 100871, Peoples R China.
[Shi, Min] NIEHS, Biostat Branch, Res Triangle Pk, NC 27709 USA.
[Ingersoll, Roxann G.; Jabs, Ethylin Wang; Redett, Richard; Scott, Alan F.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Huang, Shangzhi] Peking Union Med Coll, Beijing 100021, Peoples R China.
[Ye, Xiaoqian; Jabs, Ethylin Wang] Mt Sinai Sch Med, New York, NY USA.
[Ye, Xiaoqian] Wuhan Univ, Key Lab Oral Biomed Engn, Minist Educ, Hosp Stomatol, Wuhan 430072, Peoples R China.
[Ye, Xiaoqian] Wuhan Univ, Key Lab Oral Biomed Engn, Minist Educ, Sch Stomatol, Wuhan 430072, Peoples R China.
[Wu-Chou, Yah-Huei; Chen, Philip K.] Chang Gung Mem Hosp, Tao Yuan, Taiwan.
[Shi, Bing] Sichuan Univ, W China Coll Stomatol, Chengdu, Sichuan, Peoples R China.
[Murray, Jeffrey C.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Marazita, Mary L.] Univ Pittsburgh, Sch Dent Med, Pittsburgh, PA USA.
[Munger, Ronald G.] Utah State Univ, Logan, UT 84322 USA.
RP Beaty, TH (reprint author), Johns Hopkins Univ, Dept Epidemiol, Sch Publ Hlth, 615 N Wolfe St, Baltimore, MD 21205 USA.
EM tbeaty@jhsph.edu
OI Jabs, Ethylin/0000-0001-8983-5466
FU National Institute of Dental & Craniofacial Research [R21-DE-013707,
R01-DE-014581]; National Institute for Dental and Craniofacial Research
[U01-DE-004425]; NIH, National Institute of Environmental Health
Sciences
FX We thank all of the families at each recruitment site for participating
in this study, and we gratefully acknowledge the invaluable assistance
of clinical, field, and laboratory staff who contributed to making this
work possible. This research was supported by R21-DE-013707 and
R01-DE-014581 from the National Institute of Dental & Craniofacial
Research. The International Cleft Consortium including genotyping and
analysis was supported by the National Institute for Dental and
Craniofacial Research through U01-DE-004425; "International Consortium
to Identify Genes & Interactions Controlling Oral Clefts", 2007 to 2009;
T. H. Beaty, Principal Investigator. Tao Wu is supported by the
International Collaborative Genetics Research Training Program (ICGRTP),
NIH D43 TW06176. This research was also supported by the Intramural
Research Program of the NIH, National Institute of Environmental Health
Sciences. We thank the Smile Train Foundation for supporting cleft
research in China. We are particularly grateful to Dr. Jae Woong Sull
for his assistance in performing the analyses using LEM.
NR 52
TC 6
Z9 7
U1 0
U2 12
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 2012
VL 94
IS 2
BP 76
EP 83
DI 10.1002/bdra.22885
PG 8
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 888JE
UT WOS:000299999000002
PM 22241686
ER
PT J
AU Jahnke, GD
AF Jahnke, Gloria D.
TI Summary of the public affairs committee symposium at the teratology
society 2011 annual meeting: The thyroid and iodine: Impacts on
pregnancy and child health
SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY
LA English
DT Editorial Material
C1 [Jahnke, Gloria D.] Natl Inst Environm Hlth Serv, Natl Toxicol Program, Res Triangle Pk, NC USA.
RP Jahnke, GD (reprint author), NIEHS MD K2-14,POB 12233,Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM jahnke@niehs.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1542-0752
EI 1542-0760
J9 BIRTH DEFECTS RES A
JI Birth Defects Res. Part A-Clin. Mol. Teratol.
PD FEB
PY 2012
VL 94
IS 2
BP 114
EP 115
DI 10.1002/bdra.22880
PG 2
WC Developmental Biology; Toxicology
SC Developmental Biology; Toxicology
GA 888JE
UT WOS:000299999000007
ER
PT J
AU Loeb, S
Metter, EJ
Kan, DH
Roehl, KA
Catalona, WJ
AF Loeb, Stacy
Metter, E. Jeffrey
Kan, Donghui
Roehl, Kimberly A.
Catalona, William J.
TI Prostate-specific antigen velocity (PSAV) risk count improves the
specificity of screening for clinically significant prostate cancer
SO BJU INTERNATIONAL
LA English
DT Article
DE prostate cancer; PSA velocity; risk count; screening; PSA
ID RADICAL PROSTATECTOMY; UNITED-STATES; MEN; LIFE; CURABILITY; MORTALITY;
THERAPY; WINDOW; CURVE; DEATH
AB OBJECTIVE
To determine whether the prostate-specific antigen velocity (PSAV) risk count (i.e. the number of times PSAV exceeds a specific threshold) could increase the specificity of screening for prostate cancer and potentially life-threatening tumours.
PATIENTS AND METHODS
From 1989 to 2001, we calculated two serial PSAV measurements in 18 214 prostate cancer screening-study participants, of whom 1125 (6.2%) were diagnosed with prostate cancer.
The PSAV risk count was determined as the number of PSAV measurements of > 0.4 ng/mL/year (0, 1, or 2).
We used receiver operating characteristic (ROC) and reclassification analyses to examine the ability of PSAV risk count to predict screen-detected and high-grade prostate cancer.
RESULTS
The PSAV was > 0.4 ng/mL/year twice (risk count 2) in 40% of prostate cancer cases compared with only 4% of those with no cancer (P < 0.001).
After adjusting for age and PSA level, a PSAV risk count of 2 was associated with an 8.2-fold increased risk of prostate cancer (95% confidence interval 7.0-9.6, P < 0.001) and 5.4-fold increased risk of Gleason score 8-10 prostate cancer on biopsy.
Compared with a model with age and PSA level, the addition of the PSAV risk count significantly improved discrimination (area under the ROC curve 0.625 vs 0.725, P = 0.031) and reclassified individuals for the risk of high-grade prostate cancer (net reclassification, P < 0.001).
CONCLUSIONS
Sustained rises in PSA indicate a significantly greater risk of prostate cancer, particularly high-grade disease.
Compared with men with a risk count of = 1, those with two PSAV measurements of > 0.4 ng/mL/year (risk count 2) had an 8-fold increased risk of prostate cancer and 5.4-fold increased risk of Gleason 8-10 disease on biopsy, adjusting for age and PSA level.
Compared to PSA alone, PSAV risk count may be useful in reducing unnecessary biopsies and the diagnosis of low-risk prostate cancer.
C1 [Loeb, Stacy] NYU, Sch Med, Dept Urol, New York, NY 10003 USA.
[Metter, E. Jeffrey] NIA, Baltimore, MD 21224 USA.
[Kan, Donghui; Catalona, William J.] NW Feinberg Sch Med, Dept Urol, Chicago, IL USA.
[Roehl, Kimberly A.] Washington Univ, Sch Med, Dept Obstet & Gynecol, St Louis, MO 63110 USA.
RP Catalona, WJ (reprint author), 675 N St Clair St,Suite 20-150, Chicago, IL 60611 USA.
EM wcatalona@nmff.org
OI Loeb, Stacy/0000-0003-3933-9207
FU Urological Research Foundation; Prostate SPORE [P50 CA90386-05S2];
Robert H. Lurie Comprehensive Cancer Center [P30 CA60553]; National
Institute of Health, National Institute on Aging
FX The research of W.J.C. is supported in part by the Urological Research
Foundation, Prostate SPORE grant (P50 CA90386-05S2) and the Robert H.
Lurie Comprehensive Cancer Center grant (P30 CA60553). E Jeffery Metter
is supported by the Intramural Research Program of the National
Institute of Health, National Institute on Aging.
NR 27
TC 31
Z9 31
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 2012
VL 109
IS 4
BP 508
EP 513
DI 10.1111/j.1464-410X.2011.10900.x
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 887QY
UT WOS:000299945100007
PM 22296334
ER
PT J
AU Vaught, JB
Henderson, MK
Compton, CC
AF Vaught, Jimmie B.
Henderson, Marianne K.
Compton, Carolyn C.
TI Biospecimens and Biorepositories: From Afterthought to Science
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Editorial Material
ID CANCER; GENOME; ART; DNA
AB Biospecimens are recognized as critical components of biomedical research, from basic studies to clinical trials and epidemiologic investigations. Biorepositories have existed in various forms for more than 150 years, from early small collections in pathology laboratories to modern automated facilities managing millions of samples. As collaborative science has developed, it has been recognized that biospecimens must be of consistent quality. Recent years have seen a proliferation of best practices and the recognition of the field of "biospecimen science." The future of this field will depend on the development of more evidence-based practices in both the research and clinical settings. As the field matures, educating a new generation of biospecimen/biobanking scientists will be an important need. Cancer Epidemiol Biomarkers Prey; 21(2); 253-5. (C)2012 AACR.
C1 [Vaught, Jimmie B.; Compton, Carolyn C.] NCI, Off Biorepositories & Biospecimen Res, NIH, Bethesda, MD 20892 USA.
[Henderson, Marianne K.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Vaught, JB (reprint author), NCI, Off Biorepositories & Biospecimen Res, NIH, 11400 Rockville Pike,Rockwall 1,Suite 700, Bethesda, MD 20892 USA.
EM vaughtj@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 27
TC 25
Z9 26
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 2012
VL 21
IS 2
BP 253
EP 255
DI 10.1158/1055-9965.EPI-11-1179
PG 3
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 889KT
UT WOS:000300073300001
PM 22313938
ER
PT J
AU Yassin, R
Weil, C
Lockhart, N
AF Yassin, Rihab
Weil, Carol
Lockhart, Nicole
TI Sharing Individual Research Results with Biospecimen Contributors: Point
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID PARTICIPANTS
C1 [Weil, Carol; Lockhart, Nicole] NCI, Off Biorepositories & Biospecimen Res, NIH, Bethesda, MD 20892 USA.
[Yassin, Rihab] NCI, Div Canc Biol, NIH, Bethesda, MD 20892 USA.
RP Yassin, R (reprint author), NCI, Div Canc Biol, 6130 Execut Blvd,Suite 5000, Rockville, MD 20852 USA.
EM ry38k@nih.gov; Carol.Weil@nih.gov
FU National Cancer Institute
FX This work was supported by general appropriations to the National Cancer
Institute.
NR 13
TC 3
Z9 3
U1 0
U2 0
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 2012
VL 21
IS 2
BP 256
EP 259
DI 10.1158/1055-9965.EPI-11-0853
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 889KT
UT WOS:000300073300002
PM 22313939
ER
PT J
AU Stott-Miller, M
Chen, C
Chuang, SC
Lee, YCA
Boccia, S
Brenner, H
Cadoni, G
Dal Maso, L
La Vecchia, C
Lazarus, P
Levi, F
Matsuo, K
Morgenstern, H
Muller, H
Muscat, J
Olshan, AF
Purdue, MP
Serraino, D
Vaughan, TL
Zhang, ZF
Boffetta, P
Hashibe, M
Schwartz, SM
AF Stott-Miller, Marni
Chen, Chu
Chuang, Shu-Chun
Lee, Yuan-Chin Amy
Boccia, Stefania
Brenner, Hermann
Cadoni, Gabriela
Dal Maso, Luigino
La Vecchia, Carlo
Lazarus, Philip
Levi, Fabio
Matsuo, Keitaro
Morgenstern, Hal
Mueller, Heiko
Muscat, Joshua
Olshan, Andrew F.
Purdue, Mark P.
Serraino, Diego
Vaughan, Thomas L.
Zhang, Zuo-Feng
Boffetta, Paolo
Hashibe, Mia
Schwartz, Stephen M.
TI History of Diabetes and Risk of Head and Neck Cancer: A Pooled Analysis
from the International Head and Neck Cancer Epidemiology Consortium
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; HUMAN-PAPILLOMAVIRUS INFECTION; UPPER
AERODIGESTIVE TRACT; BODY-MASS INDEX; ORAL-CAVITY; MOLECULAR-MECHANISMS;
INHANCE CONSORTIUM; BLOOD-GLUCOSE; MELLITUS; INSULIN
AB Background: A history of diabetes is associated with an increased risk of several types of cancers. Whether diabetes is a risk factor for head and neck cancer (HNC) has received little attention.
Methods: We pooled data from 12 case control studies including 6,448 cases and 13,747 controls, and estimated OR and 95% CI for the associations between diabetes and HNC, adjusted for age, education level, sex, race/ethnicity, study center, cigarette smoking, alcohol use, and body mass index.
Results: We observed a weak association between diabetes and the incidence of HNC overall (OR, 1.09; 95% CI: 0.95-1.24). However, we observed a modest association among never smokers (OR, 1.59; 95% CI: 1.22-2.07), and no association among ever smokers (OR, 0.96; 95% CI: 0.83-1.11); likelihood ratio test for interaction P = 0.001
Conclusion: A history of diabetes was weakly associated with HNC overall, but we observed evidence of effect modification by smoking status, with a positive association among those who never smoked cigarettes.
Impact: This study suggests that glucose metabolism abnormalities may be a HNC risk factor in subgroups of the population. Prospective studies incorporating biomarkers are needed to improve our understanding of the relationship between diabetes and HNC risk, possibly providing new strategies in the prevention of HNC. Cancer Epidemiol Biomarkers Prey; 21(2); 294-304. (C)2011 AACR.
C1 [Stott-Miller, Marni; Chen, Chu; Vaughan, Thomas L.; Schwartz, Stephen M.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98109 USA.
[Stott-Miller, Marni; Chen, Chu; Vaughan, Thomas L.; Schwartz, Stephen M.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Chuang, Shu-Chun] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, London, England.
[Lee, Yuan-Chin Amy; Hashibe, Mia] Univ Utah, Sch Med, Dept Family & Prevent Med, Salt Lake City, UT 84112 USA.
[Boccia, Stefania; Cadoni, Gabriela] Univ Cattolica Sacro Cuore, Inst Hyg, Rome, Italy.
[Brenner, Hermann; Mueller, Heiko] German Canc Res Ctr, D-6900 Heidelberg, Germany.
[Dal Maso, Luigino; Serraino, Diego] Ctr Riferimento Oncol, I-33081 Aviano, PN, Italy.
[La Vecchia, Carlo] Ist Ric Farmacol Mario Negri, Milan, Italy.
[La Vecchia, Carlo] Univ Milan, Milan, Italy.
[Lazarus, Philip; Muscat, Joshua] Penn State Coll Med, Hershey, PA USA.
[Levi, Fabio] Univ Lausanne, Inst Med Sociale & Prevent, Lausanne, Switzerland.
[Matsuo, Keitaro] Aichi Canc Ctr, Res Inst, Nagoya, Aichi 464, Japan.
[Morgenstern, Hal] Univ Michigan, Sch Publ Hlth, Dept Epidemiol & Environm Hlth Sci, Ann Arbor, MI 48109 USA.
[Morgenstern, Hal] Univ Michigan, Ctr Comprehens Canc, Ann Arbor, MI 48109 USA.
[Olshan, Andrew F.] Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC USA.
[Purdue, Mark P.] NCI, Bethesda, MD 20892 USA.
[Zhang, Zuo-Feng] Univ Calif Los Angeles, Sch Publ Hlth, Los Angeles, CA 90024 USA.
[Boffetta, Paolo] Int Prevent Res Inst, Lyon, France.
[Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
RP Schwartz, SM (reprint author), Fred Hutchinson Canc Res Ctr, Mailstop M4-C308,1100 Fairview Ave N, Seattle, WA 98109 USA.
EM sschwart@fhcrc.org
RI Chuang, Shu-Chun/N-3358-2013; Purdue, Mark/C-9228-2016; Brenner,
Hermann/B-4627-2017;
OI Purdue, Mark/0000-0003-1177-3108; Brenner, Hermann/0000-0002-6129-1572;
dal maso, luigino/0000-0001-6163-200X; Serraino,
Diego/0000-0003-0565-8920; La Vecchia, Carlo/0000-0003-1441-897X;
Schwartz, Stephen/0000-0001-7499-8502; Matsuo,
Keitaro/0000-0003-1761-6314
FU INHANCE [NCI R03CA113157]; Italian Association for Research on Cancer
(AIRC); Italian League Against Cancer and Italian Ministry of Research;
Ministry of Science, Research and Arts Baden-Wrttemberg; Japan; Ministry
of Education, Science, Sports, Culture and Technology of Japan
[17015052]; Ministry of Health, Labor and Welfare of Japan [H20-002];
NIH US [P50CA090388, R01DA011386, R03CA077954, T32CA009142, U01CA096134,
R21ES011667, R01CA061188, R01CA030022, R01CA048896, R01DE012609,
P01CA068384, K07CA104231, R01DE013158]; UCLA Jonsson Comprehensive
Cancer Center; National Institute of Environmental Health Sciences
[P30ES010126]; AIRC (Italian Agency for Research on Cancer); Swiss
League against Cancer; Swiss Research against Cancer/Oncosuisse
[KFS-700, OCS-1633]
FX This work was supported by INHANCE Pooled Data Project: NCI R03CA113157;
Avian and Italy Multicentre studies: Italian Association for Research on
Cancer (AIRC), Italian League Against Cancer and Italian Ministry of
Research; Germany-Saarland study: Ministry of Science, Research and Arts
Baden-Wrttemberg; Japan: Scientific Research grant from the Ministry of
Education, Science, Sports, Culture and Technology of Japan (17015052)
and grant for the Third-Term Comprehensive 10-Year Strategy for Cancer
Control from the Ministry of Health, Labor and Welfare of Japan
(H20-002); Los Angeles study: NIH US [P50CA090388, R01DA011386,
R03CA077954, T32CA009142, U01CA096134, R21ES011667] and the Alper
Research Program for Environmental Genomics of the UCLA Jonsson
Comprehensive Cancer Center; Milan study: Italian Association for
Research on Cancer (AIRC); North Carolina study: NIH US [R01CA061188],
and in part by a grant from the National Institute of Environmental
Health Sciences [P30ES010126]; Rome study: AIRC (Italian Agency for
Research on Cancer); Swiss study: Swiss League against Cancer and the
Swiss Research against Cancer/Oncosuisse [KFS-700, OCS-1633];
Seattle-LEO study: (NIH) US [R01CA030022]; Seattle-OralGen study: NIH US
[R01CA048896, R01DE012609]; Tampa study: NIH US [P01CA068384,
K07CA104231, R01DE013158].
NR 60
TC 20
Z9 20
U1 1
U2 10
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 2012
VL 21
IS 2
BP 294
EP 304
DI 10.1158/1055-9965.EPI-11-0590
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 889KT
UT WOS:000300073300008
PM 22144496
ER
PT J
AU Genkinger, JM
Li, RF
Spiegelman, D
Anderson, KE
Albanes, D
Bergkvist, L
Bernstein, L
Black, A
van den Brandt, PA
English, DR
Freudenheim, JL
Fuchs, CS
Giles, GG
Giovannucci, E
Goldbohm, RA
Horn-Ross, PL
Jacobs, EJ
Koushik, A
Mannisto, S
Marshall, JR
Miller, AB
Patel, AV
Robien, K
Rohan, TE
Schairer, C
Stolzenberg-Solomon, R
Wolk, A
Ziegler, RG
Smith-Warner, SA
AF Genkinger, Jeanine M.
Li, Ruifeng
Spiegelman, Donna
Anderson, Kristin E.
Albanes, Demetrius
Bergkvist, Leif
Bernstein, Leslie
Black, Amanda
van den Brandt, Piet A.
English, Dallas R.
Freudenheim, Jo L.
Fuchs, Charles S.
Giles, Graham G.
Giovannucci, Edward
Goldbohm, R. Alexandra
Horn-Ross, Pamela L.
Jacobs, Eric J.
Koushik, Anita
Mannisto, Satu
Marshall, James R.
Miller, Anthony B.
Patel, Alpa V.
Robien, Kim
Rohan, Thomas E.
Schairer, Catherine
Stolzenberg-Solomon, Rachael
Wolk, Alicja
Ziegler, Regina G.
Smith-Warner, Stephanie A.
TI Coffee, Tea, and Sugar-Sweetened Carbonated Soft Drink Intake and
Pancreatic Cancer Risk: A Pooled Analysis of 14 Cohort Studies
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID PAST MEDICAL HISTORY; ALCOHOL-CONSUMPTION; UNITED-STATES;
REGRESSION-MODELS; GLYCEMIC LOAD; LIFE-STYLE; GREEN TEA; BEVERAGE
CONSUMPTION; CALIFORNIA TEACHERS; DIABETES-MELLITUS
AB Background: Coffee has been hypothesized to have pro- and anticarcinogenic properties, whereas tea may contain anticarcinogenic compounds. Studies assessing coffee intake and pancreatic cancer risk have yielded mixed results, whereas findings for tea intake have mostly been null. Sugar-sweetened carbonated soft drink (SSB) intake has been associated with higher circulating levels of insulin, which may promote carcinogenesis. Few prospective studies have examined SSB intake and pancreatic cancer risk; results have been heterogeneous.
Methods: In this pooled analysis from 14 prospective cohort studies, 2,185 incident pancreatic cancer cases were identified among 853,894 individuals during follow-up. Multivariate (MV) study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards models and then pooled using a random-effects model.
Results: No statistically significant associations were observed between pancreatic cancer risk and intake of coffee (MVRR = 1.10; 95% CI, 0.81-1.48 comparing >= 900 to <0 g/d; 237g approximate to 8oz), tea (MVRR = 0.96; 95% CI, 0.78-1.16 comparing >= 400 to 0 g/d; 237g approximate to 8oz), or SSB (MVRR = 1.19; 95% CI, 0.98-1.46 comparing >= 250 to 0 g/d; 355g approximate to 12oz; P value, test for between-studies heterogeneity > 0.05). These associations were consistent across levels of sex, smoking status, and body mass index. When modeled as a continuous variable, a positive association was evident for SSB (MVRR = 1.06; 95% CI, 1.02-1.12).
Conclusion and Impact: Overall, no associations were observed for intakes of coffee or tea during adulthood and pancreatic cancer risk. Although we were only able to examine modest intake of SSB, there was a suggestive, modest positive association for risk of pancreatic cancer for intakes of SSB. Cancer Epidemiol Biomarkers Prev; 21(2); 305-18. (C)2011 AACR.
C1 [Genkinger, Jeanine M.] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10032 USA.
[Li, Ruifeng; Spiegelman, Donna; Giovannucci, Edward; Smith-Warner, Stephanie A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Cambridge, MA 02138 USA.
[Spiegelman, Donna] Harvard Univ, Sch Publ Hlth, Dept Biostat, Cambridge, MA 02138 USA.
[Giovannucci, Edward; Smith-Warner, Stephanie A.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Cambridge, MA 02138 USA.
[Fuchs, Charles S.] Dana Farber Canc Inst, Div Med Oncol, Boston, MA 02115 USA.
[Fuchs, Charles S.; Giovannucci, Edward] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Fuchs, Charles S.; Giovannucci, Edward] Harvard Univ, Sch Med, Boston, MA USA.
[Anderson, Kristin E.; Robien, Kim] Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Anderson, Kristin E.; Robien, Kim] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN USA.
[Albanes, Demetrius; Black, Amanda; Schairer, Catherine; Stolzenberg-Solomon, Rachael; Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Bergkvist, Leif] Cent Hosp Vasteras, Dept Surg, Vasteras, Sweden.
[Bergkvist, Leif] Cent Hosp Vasteras, Clin Res Ctr, Vasteras, Sweden.
[Bernstein, Leslie] City Hope Natl Med Ctr, Beckman Res Inst, Dept Populat Sci, Div Canc Etiol, Duarte, CA 91010 USA.
[van den Brandt, Piet A.] Maastricht Univ, Sch Oncol & Dev Biol GROW, Dept Epidemiol, Maastricht, Netherlands.
[English, Dallas R.; Giles, Graham G.] Univ Melbourne, Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
[English, Dallas R.; Giles, Graham G.] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia.
[Freudenheim, Jo L.; Marshall, James R.] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
[Goldbohm, R. Alexandra] TNO Qual Life, Dept Prevent & Hlth, Leiden, Netherlands.
[Horn-Ross, Pamela L.] No Calif Canc Ctr, Fremont, CA USA.
[Jacobs, Eric J.; Patel, Alpa V.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Koushik, Anita] Univ Montreal, Dept Med Sociale & Prevent, Montreal, PQ, Canada.
[Mannisto, Satu] Natl Publ Hlth Inst, Dept Hlth Promot & Chron Dis Prevent, Helsinki, Finland.
[Miller, Anthony B.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Rohan, Thomas E.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Wolk, Alicja] Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden.
RP Genkinger, JM (reprint author), Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, 722 W 168th St,Rm 803, New York, NY 10032 USA.
EM jg3081@columbia.edu
RI Albanes, Demetrius/B-9749-2015;
OI Mannisto, Satu/0000-0002-8668-3046; Robien, Kim/0000-0002-2120-2280;
Giles, Graham/0000-0003-4946-9099; English, Dallas/0000-0001-7828-8188
FU NIH [CA098566, CA55075, CA139578]
FX This work was supported by NIH grants CA098566, CA55075, and CA139578.
NR 110
TC 26
Z9 30
U1 2
U2 22
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD FEB
PY 2012
VL 21
IS 2
BP 305
EP 318
DI 10.1158/1055-9965.EPI-11-0945-T
PG 14
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 889KT
UT WOS:000300073300009
PM 22194529
ER
PT J
AU Brown, DA
Hance, KW
Rogers, CJ
Sansbury, LB
Albert, PS
Murphy, G
Laiyemo, AO
Wang, ZQ
Cross, AJ
Schatzkin, A
Danta, M
Srasuebkul, P
Amin, J
Law, M
Breit, SN
Lanza, E
AF Brown, David A.
Hance, Kenneth W.
Rogers, Connie J.
Sansbury, Leah B.
Albert, Paul S.
Murphy, Gwen
Laiyemo, Adeyinka O.
Wang, Zhuoqiao
Cross, Amanda J.
Schatzkin, Arthur
Danta, Mark
Srasuebkul, Preeyaporn
Amin, Janaki
Law, Matthew
Breit, Samuel N.
Lanza, Elaine
TI Serum Macrophage Inhibitory Cytokine-1 (MIC-1/GDF15): A Potential
Screening Tool for the Prevention of Colon Cancer?
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID TGF-BETA SUPERFAMILY; ACTIVATED GENE NAG-1; GROWTH-FACTOR-BETA; DIETARY
INTERVENTION; COLORECTAL ADENOMAS; BONE METASTASES; WEIGHT-LOSS;
HIGH-FIBER; LOW-FAT; EXPRESSION
AB Background: Macrophage inhibitory cytokine-1 (MIC-1/GDF15) mediates nonsteroidal anti-inflammatory drug (NSAID) protection from colonic polyps in mice and is linked to the development of colorectal carcinoma in humans. Therefore, changes in serum MIC-1/GDF15 levels could predict the presence of premalignant colonic polyposis and assist in population screening strategies.
Methods: Serum MIC-1/GDF15 levels were measured in subjects in the Polyp Prevention Trial, in which NSAID use and colon cancer risk factors were defined. Subjects had an initial adenoma removed, a repeat colonoscopy removing previously unidentified polyps, and serum MIC-1/GDF15 estimation. Three years later recurrent adenomas were identified and serum MIC-1/GDF15 levels reestimated. The relationship between serum MIC-1/GDF15 levels and adenoma presence or recurrence was examined.
Results: Serum MIC-1/GDF15 levels differed by adenoma status and were significantly related to colon cancer risk factors. In addition, mean serum MIC-1/GDF15 levels rose with increasing numbers of adenomas present and high-risk adenoma recurrence. NSAID users had higher serum MIC-1/GDF15 concentrations, which were related to protection from adenoma recurrence. Furthermore, adjusted serum MIC-1/GDF15 levels at final follow-up were related to adenoma recurrence (highest quartile MIC-1/GDF15; OR = 14.7, 95% CI: 3.0-73).
Conclusions: These data suggest that MIC-1/GDF15 mediates at least some of the protection afforded by NSAIDs against human colonic polyposis. Furthermore, serum MIC-1/GDF15 levels vary with the development of adnenomatous colonic polyps.
Impact: Serum MIC-1/GDF15 determination may hold promise as the first serum screening test to assist the detection of premalignant adenomatous colonic polyposis. Cancer Epidemiol Biomarkers Prev; 21(2); 337-46. (C)2011 AACR.
C1 [Brown, David A.; Breit, Samuel N.] St Vincents Hosp, St Vincents Ctr Appl Med Res, Sydney, NSW 2010, Australia.
[Danta, Mark] St Vincents Hosp, St Vincents Clin Sch, Sydney, NSW 2010, Australia.
[Srasuebkul, Preeyaporn; Amin, Janaki; Law, Matthew] Univ New S Wales, Kirby Inst, Sydney, NSW, Australia.
[Murphy, Gwen; Cross, Amanda J.; Schatzkin, Arthur] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Albert, Paul S.] NICHHD, Biostat & Bioinformat Branch, NIH, Bethesda, MD 20892 USA.
[Laiyemo, Adeyinka O.] Howard Univ, Coll Med, Div Gastroenterol, Washington, DC USA.
[Wang, Zhuoqiao] Informat Management Serv Inc, Silver Spring, MD USA.
RP Brown, DA (reprint author), St Vincents Hosp, St Vincents Ctr Appl Med Res, Victoria St, Sydney, NSW 2010, Australia.
EM D.Brown@amr.org.au
FU NIH; National Cancer Institute; Center for Cancer Research; National
Health and Medical Research Council of Australia; New South Wales Health
Research and Development Infrastructure grant; St Vincent's Clinic
Foundation; NHMRC
FX This research was supported in part by grants from Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research, The National Cancer Institute Cancer Prevention Fellowship
Program, The National Health and Medical Research Council of Australia,
a New South Wales Health Research and Development Infrastructure grant
and St Vincent's Clinic Foundation grant. D.A. Brown is funded by an
NHMRC Career Development Fellowship. The funding sources had no direct
or indirect involvement in the design and conduct of the study; nor the
collection, management, analysis, and interpretation of the data, nor in
the preparation, review, or approval of the manuscript.
NR 43
TC 25
Z9 28
U1 0
U2 4
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 2012
VL 21
IS 2
BP 337
EP 346
DI 10.1158/1055-9965.EPI-11-0786
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 889KT
UT WOS:000300073300012
PM 22144502
ER
PT J
AU McGlynn, KA
London, WT
AF McGlynn, Katherine A.
London, W. Thomas
TI International Liver Cancer Incidence Trends-Letter
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Letter
ID HEPATOCELLULAR-CARCINOMA; HEPATITIS-B; C-VIRUS; MONGOLIA
C1 [McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[London, W. Thomas] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
RP McGlynn, KA (reprint author), NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
NR 10
TC 4
Z9 4
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 2012
VL 21
IS 2
BP 384
EP 385
DI 10.1158/1055-9965.EPI-11-1102
PG 2
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 889KT
UT WOS:000300073300018
PM 22169186
ER
PT J
AU Lu, Y
Liu, PY
Van den Bergh, F
Zellmer, V
James, M
Wen, WD
Grubbs, CJ
Lubet, RA
You, M
AF Lu, Yan
Liu, Pengyuan
Van den Bergh, Francoise
Zellmer, Victoria
James, Michael
Wen, Weidong
Grubbs, Clinton J.
Lubet, Ronald A.
You, Ming
TI Modulation of Gene Expression and Cell-Cycle Signaling Pathways by the
EGFR Inhibitor Gefitinib (Iressa) in Rat Urinary Bladder Cancer
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID LET-7 MICRORNAS; TESTIS ANTIGEN; UP-REGULATION; CARCINOMA; MICE;
CARCINOGENESIS; PROGRESSION; NETWORKS; TUMORS;
N-BUTYL-N-(4-HYDROXYBUTYL)NITROSAMINE
AB The epidermal growth factor receptor inhibitor Iressa has shown strong preventive efficacy in the N-butyl-N-(4-hydroxybutyl)-nitrosamine (OH-BBN) model of bladder cancer in the rat. To explore its antitumor mechanism, we implemented a systems biology approach to characterize gene expression and signaling pathways in rat urinary bladder cancers treated with Iressa. Eleven bladder tumors from control rats, seven tumors from rats treated with Iressa, and seven normal bladder epithelia were profiled by the Affymetrix Rat Exon 1.0 ST Arrays. We identified 713 downregulated and 641 upregulated genes in comparing bladder tumors versus normal bladder epithelia. In addition, 178 genes were downregulated and 96 genes were upregulated when comparing control tumors versus Iressa-treated tumors. Two coexpression modules that were significantly correlated with tumor status and treatment status were identified [r = 0.70, P = 2.80 x 10(-15) (bladder tumor vs. normal bladder epithelium) and r = 0.63, P = 2.00 x 10(-42) (Iressa-treated tumor vs. control tumor), respectively]. Both tumor module and treatment module were enriched for genes involved in cell-cycle processes. Twenty-four and twenty-one highly connected hub genes likely to be key drivers in cell cycle were identified in the tumor module and treatment module, respectively. Analysis of microRNA genes on the array chips showed that tumor module and treatment module were significantly associated with expression levels of let-7c (r = 0.54, P = 3.70 x 10(-8) and r = 0.73, P = 1.50 x 10(-65), respectively). These results suggest that let-7c downregulation and its regulated cell-cycle pathway may play an integral role in governing bladder tumor suppression or collaborative oncogenesis and that Iressa exhibits its preventive efficacy on bladder tumorigenesis by upregulating let-7 and inhibiting the cell cycle. Cell culture study confirmed that the increased expression of let-7c decreases Iressa-treated bladder tumor cell growth. The identified hub genes may also serve as pharmacodynamic or efficacy biomarkers in clinical trials of chemoprevention in human bladder cancer. Cancer Prev Res; 5(2); 248-59. (C) 2011 AACR.
C1 [Van den Bergh, Francoise; Zellmer, Victoria; James, Michael; You, Ming] Med Coll Wisconsin, Dept Pharmacol & Toxicol, Ctr Canc, Milwaukee, WI 53226 USA.
[Lu, Yan; Liu, Pengyuan] Med Coll Wisconsin, Dept Physiol, Ctr Canc, Milwaukee, WI 53226 USA.
[Lu, Yan; Liu, Pengyuan; Wen, Weidong; You, Ming] Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA.
[Lu, Yan; Liu, Pengyuan; Wen, Weidong; You, Ming] Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO 63110 USA.
[Grubbs, Clinton J.] Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
[Lubet, Ronald A.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP You, M (reprint author), Med Coll Wisconsin, Dept Pharmacol & Toxicol, Ctr Canc, Milwaukee, WI 53226 USA.
EM myou@mcw.edu
FU NCI [HHSN-261200433008C (N01-CN43308)]
FX The funding for the studies was provided in part by NCI Contract Number
HHSN-261200433008C (N01-CN43308).
NR 59
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U1 2
U2 6
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 2012
VL 5
IS 2
BP 248
EP 259
DI 10.1158/1940-6207.CAPR-10-0363
PG 12
WC Oncology
SC Oncology
GA 888ZO
UT WOS:000300043500011
PM 21982874
ER
PT J
AU Nguyen, MM
Ahmann, FR
Nagle, RB
Hsu, CH
Tangrea, JA
Pames, HL
Sokoloff, MH
Gretzer, MB
Chow, HHS
AF Nguyen, Mike M.
Ahmann, Frederick R.
Nagle, Raymond B.
Hsu, Chiu-Hsieh
Tangrea, Joseph A.
Pames, Howard L.
Sokoloff, Mitchell H.
Gretzer, Matthew B.
Chow, H-H. Sherry
TI Randomized, Double-Blind, Placebo-Controlled Trial of Polyphenon E in
Prostate Cancer Patients before Prostatectomy: Evaluation of Potential
Chemopreventive Activities
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID GREEN TEA POLYPHENOLS; EPIGALLOCATECHIN GALLATE; GROWTH-FACTOR; TRAMP
MICE; CATECHINS; FINASTERIDE; PREVENTION; MODEL; STAGE
AB Compelling preclinical and pilot clinical data support the role of green tea polyphenols in prostate cancer prevention. We conducted a randomized, double-blind, placebo-controlled trial of polyphenon E (enriched green tea polyphenol extract) in men with prostate cancer scheduled to undergo radical prostatectomy. The study aimed to determine the bioavailability of green tea polyphenols in prostate tissue and to measure its effects on systemic and tissue biomarkers of prostate cancer carcinogenesis. Participants received either polyphenon E (containing 800 mg epigallocatechin gallate) or placebo daily for 3 to 6 weeks before surgery. Following the intervention, green tea polyphenol levels in the prostatectomy tissue were low to undetectable. Polyphenon E intervention resulted in favorable but not statistically significant changes in serum prostate-specific antigen, serum insulin-like growth factor axis, and oxidative DNA damage in blood leukocytes. Tissue biomarkers of cell proliferation, apoptosis, and angiogenesis in the prostatectomy tissue did not differ between the treatment arms. The proportion of subjects who had a decrease in Gleason score between biopsy and surgical specimens was greater in those on polyphenon E but was not statistically significant. The study's findings of low bioavailability and/or bioaccumulation of green tea polyphenols in prostate tissue and statistically insignificant changes in systemic and tissue biomarkers from 3 to 6 weeks of administration suggests that prostate cancer preventive activity of green tea polyphenols, if occurring, may be through indirect means and/or that the activity may need to be evaluated with longer intervention durations, repeated dosing, or in patients at earlier stages of the disease. Cancer Prev Res; 5(2); 290-8. (C) 2011 AACR.
C1 [Nguyen, Mike M.] Univ Arizona, Coll Med, Div Urol, Tucson, AZ 85724 USA.
[Ahmann, Frederick R.; Nagle, Raymond B.; Hsu, Chiu-Hsieh; Chow, H-H. Sherry] Univ Arizona, Arizona Canc Ctr, Tucson, AZ 85724 USA.
[Tangrea, Joseph A.; Pames, Howard L.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Nguyen, MM (reprint author), Univ Arizona, Coll Med, Div Urol, 1501 N Campbell Ave,POB 245077, Tucson, AZ 85724 USA.
EM mnguyen@surgery.arizona.edu
FU National Cancer Institute [N01CN35158]; Arizona Cancer Center [CA023074]
FX This work was supported by a contract (N01CN35158) from the National
Cancer Institute and the Arizona Cancer Center Support Grant (CA023074).
Clinical Trial Registration: clinicaltrials.gov identifier: NCT00459407.
NR 18
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U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD FEB
PY 2012
VL 5
IS 2
BP 290
EP 298
DI 10.1158/1940-6207.CAPR-11-0306
PG 9
WC Oncology
SC Oncology
GA 888ZO
UT WOS:000300043500016
PM 22044694
ER
PT J
AU Nishioka, N
Matsuoka, T
Yashiro, M
Hirakawa, K
Olden, K
Roberts, JD
AF Nishioka, Nobuaki
Matsuoka, Tasuku
Yashiro, Masakazu
Hirakawa, Kosei
Olden, Kenneth
Roberts, John D.
TI Plasminogen activator inhibitor 1 RNAi suppresses gastric cancer
metastasis in vivo
SO CANCER SCIENCE
LA English
DT Article
ID PHASE-II TRIAL; TUMOR-GROWTH; CARCINOMA-CELLS; NUDE-MICE; ANGIOGENESIS;
INVASION; MELANOMA; THERAPY; GENE; 5-FLUOROURACIL
AB Cancer metastasis remains the primary cause of pain, suffering, and death in cancer patients, and even the most current therapeutic strategies have not been highly successful in preventing or inhibiting metastasis. In most patients with scirrhous gastric cancer (one of the most aggressive of diffuse-type gastric cancer), recurrence occurs even after potentially curative resection, most frequently in the form of peritoneal metastasis. Given that the occurrence of diffuse-type gastric cancers has been increasing, the development of new strategies to combat metastasis of this disease is critically important. Plasminogen activator inhibitor-1 (PAI-1) is a critical factor in cancer progression; thus, PAI-1 RNAi may be an effective therapy against cancer metastasis. In the present study, we used an RNAi technique to reduce PAI-1 expression in an in vivo model system for gastric cancer metastasis. Ex vivo plasmid transfection and adenovirus infection were tested as mechanisms to incorporate specific PAI-1 RNAi vectors into human gastric carcinoma cells. Both approaches significantly decreased peritoneal tumor growth and the formation of bloody ascites in the mouse model, suggesting that this approach may provide a new, effective strategy for inhibiting cancer metastasis. (Cancer Sci 2012; 103: 228232)
C1 [Nishioka, Nobuaki; Matsuoka, Tasuku; Olden, Kenneth; Roberts, John D.] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Yashiro, Masakazu; Hirakawa, Kosei] Osaka City Univ, Grad Sch Med, Dept Surg Oncol, Osaka 558, Japan.
RP Matsuoka, T (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
EM matsuoka@med.osaka-cu.ac.jp
FU National Institute of Health (NIH); National Institute of Environmental
Health Sciences (NIEHS)
FX This work was supported by the Intramural Research Program of the
National Institute of Health (NIH) and National Institute of
Environmental Health Sciences (NIEHS). The authors thank Dr Steven K.
Akiyama (Laboratory of Molecular Carcinogenesis, NIEHS, Piedmont, NC,
USA) for helpful discussions.
NR 31
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Z9 14
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1347-9032
J9 CANCER SCI
JI Cancer Sci.
PD FEB
PY 2012
VL 103
IS 2
BP 228
EP 232
DI 10.1111/j.1349-7006.2011.02155.x
PG 5
WC Oncology
SC Oncology
GA 884UJ
UT WOS:000299734000012
PM 22098548
ER
PT J
AU Barry, KH
Koutros, S
Andreotti, G
Sandler, DP
Burdette, LA
Yeager, M
Freeman, LEB
Lubin, JH
Ma, XM
Zheng, TZ
Alavanja, MCR
Berndt, SI
AF Barry, Kathryn Hughes
Koutros, Stella
Andreotti, Gabriella
Sandler, Dale P.
Burdette, Laurie A.
Yeager, Meredith
Freeman, Laura E. Beane
Lubin, Jay H.
Ma, Xiaomei
Zheng, Tongzhang
Alavanja, Michael C. R.
Berndt, Sonja I.
TI Genetic variation in nucleotide excision repair pathway genes, pesticide
exposure and prostate cancer risk
SO CARCINOGENESIS
LA English
DT Article
ID AGRICULTURAL HEALTH; DNA-DAMAGE; CHROMOSOMAL-ABERRATIONS; WORKERS;
ASSOCIATION; CELLS; POLYMORPHISMS; LYMPHOCYTES; APPLICATORS; CARBOFURAN
AB Previous research demonstrates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, human biomonitoring studies indicate increased genetic damage (e.g. chromosomal aberrations) with pesticide exposure. Given that the nucleotide excision repair (NER) pathway repairs a broad range of DNA damage, we evaluated interactions between pesticide exposure and 324 single-nucleotide polymorphisms (SNPs) tagging 27 NER genes among 776 prostate cancer cases and 1444 male controls in a nested case-control study of white Agricultural Health Study pesticide applicators. We determined interaction P values using likelihood ratio tests from logistic regression models and three-level pesticide variables (none/low/high) based on lifetime days of use weighted to an intensity score. We adjusted for multiple comparisons using the false discovery rate (FDR) method. Of the 17 interactions that met FDR < 0.2, 3 displayed a monotonic increase in prostate cancer risk with increasing exposure in one genotype group and no significant association in the other group. Men carrying the variant A allele at ERCC1 rs2298881 exhibited increased prostate cancer risk with high versus no fonofos use [odds ratio (OR) 2.98; 95% confidence interval (CI) 1.65-5.39; P-interact = 3.6 x 10(-4); FDR-adjusted P = 0.11]. Men carrying the homozygous wild-type TT genotype at two correlated CDK7 SNPs, rs11744596 and rs2932778 (r(2) = 1.0), exhibited increased risk with high versus no carbofuran use (OR 2.01; 95% CI 1.31-3.10 for rs11744596; P-interact = 7.2 x 10(-4); FDR-adjusted P = 0.09). In contrast, we did not observe associations among men with other genotypes at these loci. While requiring replication, our findings suggest a role for NER genetic variation in pesticide-associated prostate cancer risk.
C1 [Barry, Kathryn Hughes] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Barry, Kathryn Hughes; Ma, Xiaomei] Yale Univ, Sch Publ Hlth, Div Chron Dis Epidemiol, New Haven, CT 06520 USA.
[Sandler, Dale P.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Burdette, Laurie A.; Yeager, Meredith] NCI, Core Genotyping Facil, Frederick, MD 21702 USA.
[Zheng, Tongzhang] Yale Univ, Div Environm Hlth Sci, Sch Publ Hlth, New Haven, CT 06520 USA.
RP Barry, KH (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,EPS 8111,MSC 7240, Bethesda, MD 20892 USA.
EM barrykh@mail.nih.gov
RI Beane Freeman, Laura/C-4468-2015;
OI Beane Freeman, Laura/0000-0003-1294-4124; Sandler,
Dale/0000-0002-6776-0018
FU National Institutes of Health (National Cancer Institute, Division of
Cancer Epidemiology and Genetics) [Z01CP010119]; National Institutes of
Health (National Institute of Environmental Health Sciences)
[Z01ES049030]; National Institutes of Health (National Cancer Institute)
[T32 CA105666]
FX National Institutes of Health (Intramural Research Program of the
National Cancer Institute, Division of Cancer Epidemiology and Genetics,
Z01CP010119; Intramural Research Program of the National Institute of
Environmental Health Sciences, Z01ES049030 and National Cancer Institute
grant T32 CA105666 to K.H.B.).
NR 49
TC 18
Z9 19
U1 1
U2 19
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD FEB
PY 2012
VL 33
IS 2
BP 331
EP 337
DI 10.1093/carcin/bgr258
PG 7
WC Oncology
SC Oncology
GA 888YF
UT WOS:000300039800013
PM 22102698
ER
PT J
AU Wang, ML
Liu, F
Hsing, AW
Wang, X
Shao, Q
Qi, J
Ye, Y
Wang, Z
Chen, HY
Gao, X
Wang, GZ
Chu, LW
Ding, Q
OuYang, J
Gao, X
Huang, YC
Chen, YB
Gao, YT
Zhang, ZF
Rao, JY
Shi, R
Wu, QJ
Zhang, YY
Jiang, HW
Zheng, J
Hu, YL
Guo, L
Lin, XL
Tao, S
Jin, GF
Sun, JL
Lu, DR
Zheng, SL
Sun, YH
Mo, ZN
Yin, CJ
Zhang, ZD
Xu, JF
AF Wang, Meilin
Liu, Fang
Hsing, Ann W.
Wang, Xiang
Shao, Qiang
Qi, Jun
Ye, Yu
Wang, Zhong
Chen, Hongyan
Gao, Xin
Wang, Guozeng
Chu, Lisa W.
Ding, Qiang
OuYang, Jun
Gao, Xu
Huang, Yichen
Chen, Yanbo
Gao, Yu-Tang
Zhang, Zuo-Feng
Rao, Jiangyu
Shi, Rong
Wu, Qijun
Zhang, Yuanyuan
Jiang, Haowen
Zheng, Jie
Hu, Yanlin
Guo, Ling
Lin, Xiaoling
Tao, Sha
Jin, Guangfu
Sun, Jielin
Lu, Daru
Zheng, S. Lilly
Sun, Yinghao
Mo, Zengnan
Yin, Changjun
Zhang, Zhengdong
Xu, Jianfeng
TI Replication and cumulative effects of GWAS-identified genetic variations
for prostate cancer in Asians: a case-control study in the ChinaPCa
consortium
SO CARCINOGENESIS
LA English
DT Article
ID PROTEIN-COUPLED RECEPTOR; GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI;
RISK; EXPRESSION; VARIANTS; MULTIPLE; CLONING; HUMANS; GPRC6A
AB A recent genome-wide association study has identified five new genetic variants for prostate cancer susceptibility in a Japanese population, but it is unknown whether these newly identified variants are associated with prostate cancer risk in other populations, including Chinese men. We genotyped these five variants in a case-control study of 1524 patients diagnosed with prostate cancer and 2169 control subjects from the Chinese Consortium for Prostate Cancer Genetics (ChinaPCa). We found that three of the five genetic variants were associated with prostate cancer risk (P = 4.33 x 10(-8) for rs12653946 at 5p15, 4.43 x 10(-5) for rs339331 at 6q22 and 8.42 x 10(-4) for rs9600079 at 13q22, respectively). A cumulative effect was observed in a dose-dependent manner with increasing numbers of risk variant alleles (P-trend = 2.58 x 10(-13)), and men with 5-6 risk alleles had a 2-fold higher risk of prostate cancer than men with 0-2 risk alleles (odds ratio = 2.26, 95% confidence interval = 1.78-2.87). Furthermore, rs339331 T allele was significantly associated with RFX6 and GPRC6A higher messenger RNA expression, compared with the C allele. However, none of the variants was associated with clinical stage, Gleason score or family history. These results provide further evidence that the risk loci identified in Japanese men also contribute to prostate cancer susceptibility in Chinese men.
C1 [Wang, Meilin; Zhang, Zhengdong] Nanjing Med Univ, State Key Lab Reprod Med, Nanjing 210029, Jiangsu, Peoples R China.
[Wang, Meilin; Zhang, Zhengdong] Nanjing Med Univ, Dept Mol & Genet Toxicol, Key Lab Modern Toxicol, Minist Educ,Sch Publ Hlth, Nanjing 210029, Jiangsu, Peoples R China.
[Wang, Meilin; Zhang, Zhengdong] Nanjing Med Univ, Dept Occupat Med & Environm Hlth, Jiangsu Key Lab Canc Biomarkers Prevent & Treatme, Ctr Canc, Nanjing 210029, Jiangsu, Peoples R China.
[Liu, Fang; Chen, Hongyan; Lin, Xiaoling; Sun, Jielin; Lu, Daru; Zheng, S. Lilly; Xu, Jianfeng] Fudan Univ, Sch Life Sci, Fudan VARI Ctr Genet Epidemiol, Shanghai 200433, Peoples R China.
[Hsing, Ann W.; Chu, Lisa W.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20894 USA.
[Wang, Xiang; Ding, Qiang; Jiang, Haowen; Zheng, Jie; Xu, Jianfeng] Fudan Univ, Huashan Hosp, Dept Urol, Shanghai 200032, Peoples R China.
[Shao, Qiang] Suzhou Municipal Hosp, Dept Urol, Suzhou 215000, Peoples R China.
[Qi, Jun; Huang, Yichen; Hu, Yanlin] Shanghai Jiao Tong Univ, Dept Urol, Xinhua Hosp, Sch Med, Shanghai 200025, Peoples R China.
[Ye, Yu; Mo, Zengnan] Guangxi Med Univ, Affiliated Hosp 1, Dept Urol, Guangxi 530021, Peoples R China.
[Wang, Zhong; Chen, Yanbo] Shanghai Jiao Tong Univ, Dept Urol, Sch Med, Peoples Hosp 9, Shanghai 200025, Peoples R China.
[Chen, Hongyan; Lu, Daru; Xu, Jianfeng] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Key Lab Contemporary Anthropol, Shanghai 200433, Peoples R China.
[Gao, Xin] Sun Yat Sen Univ, Dept Urol, Affiliated Hosp 3, Guangzhou 510630, Guangdong, Peoples R China.
[Wang, Guozeng] Pudong Gongli Hosp, Dept Urol, Shanghai 200135, Peoples R China.
[OuYang, Jun] Suzhou Univ, Peoples Hosp 1, Dept Urol, Suzhou 215000, Peoples R China.
[Gao, Xu; Sun, Yinghao] Second Mil Med Univ, Dept Urol, Changhai Hosp, Shanghai 200433, Peoples R China.
[Gao, Yu-Tang] Shanghai Canc Inst, Shanghai 200032, Peoples R China.
[Zhang, Zuo-Feng] Univ Calif Los Angeles, Sch Publ Hlth, Dept Epidemiol, Los Angeles, CA 90001 USA.
[Rao, Jiangyu] Univ Calif Los Angeles, David Geffen Sch Med, Dept Pathol & Lab Med, Los Angeles, CA 90001 USA.
[Shi, Rong; Wu, Qijun] Shanghai Jiao Tong Univ, Sch Publ Hlth, Shanghai 200025, Peoples R China.
[Zhang, Yuanyuan] Wake Forest Univ, Bowman Gray Sch Med, Dept Urol, Winston Salem, NC 27106 USA.
[Guo, Ling; Tao, Sha; Xu, Jianfeng] Van Andel Res Inst, Grand Rapids, MI 49503 USA.
[Jin, Guangfu; Sun, Jielin; Zheng, S. Lilly; Xu, Jianfeng] Wake Forest Univ, Bowman Gray Sch Med, Ctr Canc Genom, Winston Salem, NC 27106 USA.
[Yin, Changjun] Nanjing Med Univ, Dept Urol, Affiliated Hosp 1, Nanjing 210029, Jiangsu, Peoples R China.
RP Zhang, ZD (reprint author), Nanjing Med Univ, State Key Lab Reprod Med, 140 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China.
EM drzdzhang@gmail.com; drzdzhang@gmail.com; jxu@wfubmc.edu
RI tao, sha/B-7750-2012
FU National Cancer Institute [1R01CA129684-01]; National Natural Science
Foundation of China [30872084, 30972444, 81102089]; Natural Science
Foundation of Jiangsu Province [BK2010080, BK2011773]; Jiangsu Higher
Education Institutions (Public Health and Preventive Medicine)
FX This study was partly supported by National Cancer Institute
(1R01CA129684-01), National Natural Science Foundation of China
(30872084, 30972444, 81102089), the Key Program of Natural Science
Foundation of Jiangsu Province (BK2010080), Natural Science Foundation
of Jiangsu Province (BK2011773) and the Project Funded by the Priority
Academic Program Development of Jiangsu Higher Education Institutions
(Public Health and Preventive Medicine).
NR 27
TC 28
Z9 28
U1 2
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
EI 1460-2180
J9 CARCINOGENESIS
JI Carcinogenesis
PD FEB
PY 2012
VL 33
IS 2
BP 356
EP 360
DI 10.1093/carcin/bgr279
PG 5
WC Oncology
SC Oncology
GA 888YF
UT WOS:000300039800016
PM 22114074
ER
PT J
AU Chahal, H
McClelland, RL
Tandri, H
Jain, A
Turkbey, EB
Hundley, WG
Barr, RG
Kizer, J
Lima, JAC
Bluemke, DA
Kawut, SM
AF Chahal, Harjit
McClelland, Robyn L.
Tandri, Harikrishna
Jain, Aditya
Turkbey, Evrim B.
Hundley, W. Gregory
Barr, R. Graham
Kizer, Jorge
Lima, Joao A. C.
Bluemke, David A.
Kawut, Steven M.
TI Obesity and Right Ventricular Structure and Function The MESA-Right
Ventricle Study
SO CHEST
LA English
DT Article
ID OBSTRUCTIVE SLEEP-APNEA; CARDIOVASCULAR MAGNETIC-RESONANCE; WEIGHT-LOSS;
ARTERIAL-HYPERTENSION; HEART-FAILURE; MYOCARDIAL PERFORMANCE;
ATHEROSCLEROSIS MESA; CARDIAC STRUCTURE; CARDIOMYOPATHY; ASSOCIATION
AB Background: The relationship between obesity and right ventricular (RV) morphology is not well studied. We aimed to determine the association between obesity and RV structure and function in a large multiethnic population-based cohort.
Methods: The MESA-Right Ventricle Study measured RV mass and volumes by cardiac MRI in participants aged 45 to 84 years without clinical cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis (MESA). Participants were divided into three categories based on BMI: lean (<= 24.9 kg/m(2)), overweight (25-29.9 kg/m(2)), and obese (>= 30 kg/m(2)).
Results: The study sample included 4,127 participants. After adjustment for demographics, height, education, and cardiovascular risk factors, overweight and obese participants had greater RV mass (6% and 9% greater, respectively), larger RV end-diastolic volume (8% and 18% greater, respectively), larger RV stroke volume (7% and 16% greater, respectively), and lower RV ejection fraction ( >= 1% lower) than lean participants (all P < .001). These findings persisted after adjusting for the respective left ventricular (LV) parameters.
Conclusions: Overweight and obesity were independently associated with differences in RV morphology even after adjustment for the respective LV measure. This association could be explained by increased RV afterload, increased blood volume, hormonal effects, or direct obesity-related myocardial effects. CHEST 2012; 141(2):388-395
C1 [Kawut, Steven M.] Univ Penn, Perelman Sch Med, Penn Cardiovasc Inst, Dept Med, Philadelphia, PA 19104 USA.
[Chahal, Harjit; Jain, Aditya] Johns Hopkins Univ, Sch Med, Dept Radiol, Baltimore, MD 21205 USA.
[Tandri, Harikrishna; Lima, Joao A. C.] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA.
[McClelland, Robyn L.] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Turkbey, Evrim B.; Bluemke, David A.] Natl Inst Biomed Imaging & Bioengn, Dept Radiol & Imaging Sci, NIH, Ctr Clin, Bethesda, MD USA.
[Hundley, W. Gregory] Wake Forest Univ, Sch Med, Dept Internal Med, Winston Salem, NC 27109 USA.
[Barr, R. Graham] Columbia Univ, Coll Phys & Surg, Dept Med, New York, NY USA.
[Kizer, Jorge] Weill Cornell Med Coll, Dept Med, New York, NY USA.
[Kawut, Steven M.] Univ Penn, Perelman Sch Med, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
RP Kawut, SM (reprint author), Univ Penn, Perelman Sch Med, Penn Cardiovasc Inst, Dept Med, 718 Blockley Hall,423 Guardian Dr, Philadelphia, PA 19104 USA.
EM kawut@upenn.edu
OI Bluemke, David/0000-0002-8323-8086
FU National Institutes of Health [R01-HL086719, R01-HL077612, N01-HC95159,
N01-HC95169]; US Environmental Protection Agency; Alphal Foundation;
Columbia University
FX This work was supported by National Institutes of Health [Grants
R01-HL086719, R01-HL077612, and N01-HC95159 through N01-HC95169].; The
authors have reported to CHEST the following conflicts of interest: Dr
Barr currently receives grant funding for research support from the
National Institutes of Health, US Environmental Protection Agency,
Alphal Foundation, and Columbia University. Cenesta Health donated a
nutritional supplement for NIT-sponsored trial. Drs Chahal, McClelland,
Tandri, Jain, Turkbey, Hundley, Barr, Kizer, Lima, Bluemke, and Kawut,
have reported that no potential conflicts of interest exist with any
companies/organizations whose products or services may he discussed in
this article.
NR 40
TC 40
Z9 41
U1 0
U2 0
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD FEB
PY 2012
VL 141
IS 2
BP 388
EP 395
DI 10.1378/chest.11-0172
PG 8
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 887HQ
UT WOS:000299917900016
PM 21868467
ER
PT J
AU Eberlein, M
Permutt, S
Chahla, MF
Bolukbas, S
Nathan, SD
Shlobin, OA
Shelhamer, JH
Reed, RM
Pearse, DB
Orens, JB
Brower, RG
AF Eberlein, Michael
Permutt, Solbert
Chahla, Mayy F.
Bolukbas, Servet
Nathan, Steven D.
Shlobin, Oksana A.
Shelhamer, James H.
Reed, Robert M.
Pearse, David B.
Orens, Jonathan B.
Brower, Roy G.
TI Lung Size Mismatch in Bilateral Lung Transplantation is Associated With
Allograft Function and Bronchiolitis Obliterans Syndrome
SO CHEST
LA English
DT Article
ID MAXIMAL EXPIRATORY FLOW; PULMONARY SURFACTANT ACTIVITY; HEART-LUNG;
RESIDUAL VOLUME; RECOIL PRESSURE; VITAL CAPACITY; CANINE LUNG; DONOR;
RESTRICTION; MECHANICS
AB Background: Size mismatch between donor lungs and a recipient thorax could affect the major determinants of maximal expiratory airflow: airway resistance, propensity of airways to collapse, and lung elastic recoil.
Methods: A retrospective review of 159 adults who received bilateral lung transplants was performed. The predicted total lung capacity (pTLC) for donors and recipients was calculated based on sex and height. Size matching was represented using the following formula: pTLC ratio = donor pTLC/recipient pTLC. Patients were grouped according to those with a pTLC ratio > 1.0 (oversized) or those with a pTLC ratio 1.0 (undersized). Allograft function was analyzed in relation to the pTLC ratio and to recipient and donor predicted function.
Results: The 96 patients in the oversized cohort had a mean pTLC ratio of 1.16 +/- 0.13 vs 0.89 +/- 0.09 in the 63 patients of the undersized group. At 1 to 6 months posttransplant, the patients in the oversized cohort had higher FEV1/FVC ratios (0.895 +/- 0.13 vs 0.821 +/- 0.13, P < .01) and lower time constant estimates of lung emptying (0.38 +/- 0.2 vs 0.64 +/- 0.4, P < .01) than patients in the undersized cohort. Although the FVCs expressed as % predicted for the recipient were not different between cohorts, the FVCs expressed as % predicted for the donor organ were lower in the oversized cohort compared with the undersized cohort (at 1-6 months, 52.4% +/- 17.1% vs 65.3% 18.3%, P < .001). Kaplan-Meier estimates for the occurrence of bronchiolitis obliterans syndrome (BOS) showed that patients in the oversized cohort had a lower probability of BOS (P < .001).
Conclusions: A pTLC ratio > 1.0, suggestive of an oversized allograft, is associated with higher expiratory airflow capacity and a less frequent occurrence of BOS. CHEST 2012; 141(2):451-460
C1 [Eberlein, Michael; Permutt, Solbert; Pearse, David B.; Orens, Jonathan B.; Brower, Roy G.] Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD USA.
[Chahla, Mayy F.] Johns Hopkins Univ, Sch Med, Div Hosp Med, Baltimore, MD USA.
[Reed, Robert M.] Univ Maryland, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD 21201 USA.
[Eberlein, Michael; Shelhamer, James H.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Bolukbas, Servet] Horst Schmidt Klin, Dept Thorac Surg, Wiesbaden, Germany.
[Nathan, Steven D.; Shlobin, Oksana A.] Inova Fairfax Hosp, Adv Lung Dis Program, Falls Church, VA USA.
RP Eberlein, M (reprint author), Univ Iowa, Div Pulm Crit Care & Occupat Med, Carver Coll Med, 200 Hawkins Dr, Iowa City, IA 52242 USA.
EM michael-eberlein@uiowa.edu
NR 37
TC 33
Z9 33
U1 1
U2 2
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD FEB
PY 2012
VL 141
IS 2
BP 451
EP 460
DI 10.1378/chest.11-0767
PG 10
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 887HQ
UT WOS:000299917900024
PM 21799025
ER
PT J
AU Lauer, MS
AF Lauer, Michael S.
TI Advancing Cardiovascular Research
SO CHEST
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; TYPE-2 DIABETES-MELLITUS;
MYOCARDIAL-INFARCTION; UNITED-STATES; HEART-DISEASE; CLINICAL-PRACTICE;
OUTCOMES; RISK; THERAPY; 9P21
AB Over the past 50 years, we have seen dramatic changes in cardiovascular science and clinical care, accompanied by marked declines in the morbidity and mortality. Nonetheless, cardiovascular disease remains the leading cause of death and disability in the world, and its nature is changing as Americans become older, fatter, and ethnically more diverse. Instead of young or middle-aged men with ST-segment elevation myocardial infarction, the "typical" cardiac patient now presents with acute coronary syndrome or with complications related to chronic hypertension or ischemic heart disease, including heart failure, sudden death, and atrial fibrillation. Analogously, structural heart disease is now dominated by degenerative valve or congenital disease, far more common than rheumatic disease. The changing clinical scene presents cardiovascular scientists with a number of opportunities and challenges, including taking advantage of high-throughput technologies to elucidate complex disease mechanisms, accelerating development and implementation of evidence-based strategies, assessing evolving technologies of unclear value, addressing a global epidemic of cardiovascular disease, and maintaining high levels of innovation in a time of budgetary constraint and economic turmoil. CHEST 2012; 141(2):500-505
C1 NHLBI, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
RP Lauer, MS (reprint author), NHLBI, Div Cardiovasc Sci, NIH, 6701 Rockledge Dr,Rm 8128, Bethesda, MD 20892 USA.
EM lauerm@nhlbi.nih.gov
RI Lauer, Michael/L-9656-2013
OI Lauer, Michael/0000-0002-9217-8177
NR 58
TC 9
Z9 9
U1 0
U2 2
PU AMER COLL CHEST PHYSICIANS
PI NORTHBROOK
PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 USA
SN 0012-3692
J9 CHEST
JI Chest
PD FEB
PY 2012
VL 141
IS 2
BP 500
EP 505
DI 10.1378/chest.11-2521
PG 6
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 887HQ
UT WOS:000299917900030
PM 22315116
ER
PT J
AU Bellanti, JA
Lin, FYC
Chu, C
Shiloach, J
Leppla, SH
Benavides, GA
Karpas, A
Moayeri, M
Guo, C
Robbins, JB
Schneerson, R
AF Bellanti, Joseph A.
Lin, Feng-Ying C.
Chu, Chiayung
Shiloach, Joseph
Leppla, Stephen H.
Benavides, German A.
Karpas, Arthur
Moayeri, Mahtab
Guo, Chunyan
Robbins, John B.
Schneerson, Rachel
TI Phase 1 Study of a Recombinant Mutant Protective Antigen of Bacillus
anthracis
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Article
ID VACCINE ADSORBED AVA; INHALATION ANTHRAX; ANTIBODY-RESPONSE; LETHAL
FACTOR; EDEMA FACTOR; TOXIN GENES; IMMUNOGENICITY; CEREUS; INFECTION;
CORRELATE
AB A phase 1 study of a recombinant mutant protective antigen (rPA) vaccine was conducted in 186 healthy adults aged 18 to 45 years. Volunteers were randomized to receive one of three formulations of rPA (formalin treated, alum adsorbed, or both), in 10- or 20-mu g dosages each, or the licensed vaccine, AVA. Three injections were given at 2-month intervals and a 4th 1 year after the 3rd. Vaccinees were examined at the clinic once following each injection, at 48 to 72 h postinjection. Adverse reactions were recorded in diaries for 7 days. Sera were collected before each injection and 1 week after the 1st, 2 weeks after the 3rd and 4th, and 1 year after the 4th. Serum anti-PA IgG was assayed by enzyme-linked immunosorbent assay (ELISA) and toxin neutralization assay (TNA). All formulations at both dosages were safe and immunogenic, inducing booster responses, with the highest antibody levels following the 4th injection (354 to 732 mu g/ml). The lowest levels were induced by the formalin-only-treated rPA; there was no statistical difference between levels induced by alum-adsorbed and formalin-treated/alum-adsorbed rPA or by the two dosages. The antibody levels declined in all groups during the 1-year intervals after the 3rd and 4th injections but less so during the 2nd year, after the 4th injection (fold decreases were 10 to 25 versus 3.4 to 7.0, P < 0.001). There were too few AVA recipients for statistical comparisons, but their antibody levels followed those of rPA. Anti-rPA measured by ELISA correlated with TNA titers (r = 0.97). These data support studying alum-adsorbed rPA in children.
C1 [Lin, Feng-Ying C.; Chu, Chiayung; Karpas, Arthur; Guo, Chunyan; Robbins, John B.; Schneerson, Rachel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev & Mol Immun, NIH, Bethesda, MD USA.
[Bellanti, Joseph A.; Benavides, German A.] Georgetown Univ, Med Ctr, Int Ctr Interdisciplinary Studies Immunol, Washington, DC 20007 USA.
[Bellanti, Joseph A.; Benavides, German A.] Georgetown Univ, Sch Med, Washington, DC USA.
[Shiloach, Joseph] NIDDK, Biotechnol Unit, Lab Cellular & Dev Biol, NIH, Bethesda, MD USA.
[Leppla, Stephen H.; Moayeri, Mahtab] NIAID, Bacterial Toxins & Therapeut Sect, NIH, Bethesda, MD 20892 USA.
RP Schneerson, R (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev & Mol Immun, NIH, Bethesda, MD USA.
EM schneerr@mail.nih.gov
OI Bellanti, Joseph/0000-0002-5038-7202
FU Division of Intramural Research, NICHD, National Institutes of Health;
Division of Intramural Research, NIAID, National Institutes of Health
FX This research was supported by the Divisions of Intramural Research,
NICHD and NIAID, National Institutes of Health.
NR 28
TC 7
Z9 7
U1 0
U2 5
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 2012
VL 19
IS 2
BP 140
EP 145
DI 10.1128/CVI.05556-11
PG 6
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 889AB
UT WOS:000300044800004
PM 22190398
ER
PT J
AU Smith, WM
Lange, JM
Sturm, AC
Tanner, SM
Mauger, TF
AF Smith, Wendy M.
Lange, Julie M.
Sturm, Amy C.
Tanner, Stephan M.
Mauger, Thomas F.
TI Familial Peripheral Keratopathy Without PAX6 Mutation
SO CORNEA
LA English
DT Article
DE stem cell; aniridia; corectopia; PAX6
ID AUTOSOMAL-DOMINANT KERATITIS; ANIRIDIA; SPECTRUM
AB Purpose: To describe the clinical features of a familial abnormality of the corneal stem cells and to investigate the role of PAX6 mutations in the affected family members.
Methods: A family with multiple generations of peripheral keratopathy was evaluated. Because of the corneal phenotypic similarity to aniridia-related keratopathy, it was hypothesized that the affected patients might have a dominantly inherited mutation of PAX6 on chromosome 11. Commercial sequencing of germline DNA from 1 affected family member did not identify any PAX6 mutations in the exons or intron-exon boundary regions. Because the commercial analysis is not designed to identify PAX6 deletions, germline DNA was collected from 5 unaffected and 2 additional affected family members. DNA repeat markers in the region of PAX6 were analyzed to determine whether this chromosomal region segregates with the disease phenotype.
Results: Affected family members with this autosomal dominant peripheral corneal abnormality showed evidence of progressive corneal stem cell dysfunction. Several individuals demonstrated corectopia, and 1 individual had ectropion uvea but no other iris or ocular abnormalities associated with aniridia. Genotyping data of affected and unaffected family members demonstrated that the PAX6 region does not segregate with the disease phenotype.
Conclusions: The features of this autosomal dominant abnormality show some similarity to aniridia, although the classic characteristics of severe iris hypoplasia and macular hypoplasia are absent. Mutational screening and genotyping could not conclusively clarify a role for PAX6 in this disease phenotype, suggesting that it is a distinct clinical and genetic disease entity, not a variant of aniridia.
C1 [Smith, Wendy M.; Lange, Julie M.; Mauger, Thomas F.] Ohio State Univ, Dept Ophthalmol, Havener Eye Inst, Columbus, OH 43212 USA.
[Smith, Wendy M.] NEI, NIH, Bethesda, MD 20892 USA.
[Sturm, Amy C.] Ohio State Univ, Coll Med, Div Human Genet, Columbus, OH 43212 USA.
[Tanner, Stephan M.] Ohio State Univ, Ctr Comprehens Canc, Human Canc Genet Program, Columbus, OH 43212 USA.
RP Mauger, TF (reprint author), Ohio State Univ, Dept Ophthalmol, Havener Eye Inst, 915 Olentangy River Rd, Columbus, OH 43212 USA.
EM thomas.mauger@osumc.edu
RI Sturm, Amy/E-4162-2011
NR 9
TC 2
Z9 2
U1 1
U2 1
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 2012
VL 31
IS 2
BP 130
EP 133
DI 10.1097/ICO.0b013e3182222779
PG 4
WC Ophthalmology
SC Ophthalmology
GA 889FQ
UT WOS:000300059400006
PM 22146551
ER
PT J
AU Yau, JWY
Xie, J
Lamoureux, E
Klein, R
Klein, BEK
Cotch, MF
Bertoni, AG
Shea, S
Wong, TY
AF Yau, Joanne Wen Yee
Xie, Jing
Lamoureux, Ecosse
Klein, Ronald
Klein, Barbara E. K.
Cotch, Mary Frances
Bertoni, Alain G.
Shea, Steven
Wong, Tien Y.
TI Retinal microvascular calibre and risk of incident diabetes: The
multi-ethnic study of atherosclerosis
SO DIABETES RESEARCH AND CLINICAL PRACTICE
LA English
DT Article
DE Retinal microvascular calibre; Retinopathy; Diabetes; Impaired fasting
glucose
ID LIFE-STYLE AUSDIAB; IMPAIRED FASTING GLUCOSE; BLUE MOUNTAINS EYE;
VASCULAR CALIBER; VESSEL DIAMETERS; SUBSEQUENT RISK; RETINOPATHY;
MELLITUS; OBESITY; ABNORMALITIES
AB Aim: To prospectively examine the association of retinal microvascular signs with incident diabetes and impaired fasting glucose (IFG) in a multi-ethnic population-based cohort.
Methods: The multi-ethnic study of atherosclerosis comprised Caucasians, African-Americans, Hispanics and Chinese aged 45-84 years. Retinal vascular calibre and retinopathy were quantified from baseline retinal photographs. Incident diabetes and IFG were ascertained prospectively.
Results: After a median follow-up of 3 years, 243 (4.9%) people developed diabetes and 565 (15.0%) developed IFG. After adjusting for known risk factors, participants with wider retinal arteriolar calibre had a higher risk of developing diabetes [HR: 1.60; 95% CI: 1.12-2.29, p = 0.011 comparing highest with lowest arteriolar calibre tertile]. In ethnic subgroup analysis, the association between wider retinal arteriolar calibre and incident diabetes was stronger and statistically significant only in Caucasians [HR: 2.78; 95% CI: 1.37-5.62, p = 0.005]. Retinal venular calibre and retinopathy signs were not related to risk of diabetes or IFG.
Conclusion: Wider retinal arteriolar calibre is independently associated with an increased risk of diabetes, supporting a possible role for early arteriolar changes in diabetes development. This effect was largely seen in Caucasians, and not in other ethnic groups, and may reflect ethnic differences in susceptibility to diabetes from microvascular pathways. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Yau, Joanne Wen Yee; Xie, Jing; Lamoureux, Ecosse; Wong, Tien Y.] Univ Melbourne, Ctr Eye Res Australia, Royal Victorian Eye & Ear Hosp, Melbourne, Vic 3002, Australia.
[Lamoureux, Ecosse; Wong, Tien Y.] Singapore Natl Eye Ctr, Singapore Eye Res Inst, Singapore, Singapore.
[Klein, Ronald; Klein, Barbara E. K.] Univ Wisconsin, Dept Ophthalmol & Visual Sci, Madison, WI 53706 USA.
[Cotch, Mary Frances] NEI, Div Epidemiol & Clin Applicat, NIH, Bethesda, MD 20892 USA.
[Bertoni, Alain G.] Wake Forest Univ, Bowman Gray Sch Med, Dept Epidemiol & Prevent, Winston Salem, NC USA.
[Shea, Steven] Columbia Univ, Dept Med, New York, NY USA.
[Shea, Steven] Columbia Univ, Dept Epidemiol, New York, NY USA.
RP Yau, JWY (reprint author), Univ Melbourne, Ctr Eye Res Australia, 32 Gisborne St, Melbourne, Vic 3002, Australia.
EM jwyau@unimelb.edu.au
OI Cotch, Mary Frances/0000-0002-2046-4350; Klein,
Ronald/0000-0002-4428-6237
FU National Heart, Lung, and Blood Institute [N01-HC-95159, N01-HC-95165,
N01-HC-95169]; NIH from the National Eye Institute [Z01EY000403];
National Institutes of Health [HL69979-03]; National Health and Medical
Research Council (NHMRC), Australia [52993]
FX This research was supported by contracts N01-HC-95159 through
N01-HC-95165 and N01-HC-95169 from the National Heart, Lung, and Blood
Institute and NIH Intramural Research award Z01EY000403 from the
National Eye Institute (MFC). Additional support was provided by
National Institutes of Health grants HL69979-03 (Klein R. and Wong T.Y.)
and the National Health and Medical Research Council (NHMRC), 52993,
Australia (Wong T.Y.).
NR 28
TC 8
Z9 8
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0168-8227
J9 DIABETES RES CLIN PR
JI Diabetes Res. Clin. Pract.
PD FEB
PY 2012
VL 95
IS 2
BP 265
EP 274
DI 10.1016/j.diabres.2011.10.027
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 887TS
UT WOS:000299953900019
PM 22088792
ER
PT J
AU Morens, DM
Taubenberger, JK
AF Morens, David M.
Taubenberger, Jeffery K.
TI 1918 Influenza, a Puzzle with Missing Pieces
SO EMERGING INFECTIOUS DISEASES
LA English
DT Editorial Material
ID PNEUMONIA; DEATH
C1 [Morens, David M.; Taubenberger, Jeffery K.] NIAID, NIH, Bethesda, MD 20892 USA.
RP Morens, DM (reprint author), NIAID, NIH, Bldg 31,Rm 7A03, Bethesda, MD 20892 USA.
EM dmorens@niaid.nih.gov
NR 8
TC 11
Z9 11
U1 0
U2 7
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 2012
VL 18
IS 2
BP 332
EP 335
DI 10.3201/eid1802.111409
PG 4
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 889MU
UT WOS:000300078600026
PM 22304897
ER
PT J
AU Matsuura, K
Fujimoto, K
Fu, LZ
Shi, YB
AF Matsuura, Kazuo
Fujimoto, Kenta
Fu, Liezhen
Shi, Yun-Bo
TI Liganded Thyroid Hormone Receptor Induces Nucleosome Removal and Histone
Modifications to Activate Transcription during Larval Intestinal Cell
Death and Adult Stem Cell Development
SO ENDOCRINOLOGY
LA English
DT Article
ID XENOPUS-LAEVIS METAMORPHOSIS; AMPHIBIAN METAMORPHOSIS; POSTEMBRYONIC
DEVELOPMENT; CHROMATIN MODIFICATIONS; VERTEBRATE DEVELOPMENT; FROG
METAMORPHOSIS; GENE-EXPRESSION; HUMAN GENOME; COMPLEXES; METHYLATION
AB Thyroid hormone (T-3) plays an important role in regulating multiple cellular and metabolic processes, including cell proliferation, cell death, and energy metabolism, in vertebrates. Dysregulation of T-3 signaling results in developmental abnormalities, metabolic defects, and even cancer. We used T-3-dependent Xenopus metamorphosis as a model to study how T-3 regulates transcription during vertebrate development. T-3 exerts its metamorphic effects through T-3 receptors (TR). TR recruits, in a T-3-dependent manner, cofactor complexes that can carry out chromatin remodeling/histone modifications. Whether and how histone modifications change upon gene regulation by TR during vertebrate development is largely unknown. Here we analyzed histone modifications at T-3 target genes during intestinal metamorphosis, a process that involves essentially total apoptotic degeneration of the simple larval epithelium and de novo development of the adult epithelial stem cells, followed by their proliferation and differentiation into the complex adult epithelium. We demonstrated for the first time in vivo during vertebrate development that TR induces the removal of core histones at the promoter region and the recruitment of RNA polymerase. Furthermore, a number of histone activation and repression marks have been defined based on correlations with mRNA levels in cell cultures. Most but not all correlate with gene expression induced by liganded TR during development, suggesting that tissue and developmental context influences the roles of histone modifications in gene regulation. Our findings provide important mechanistic insights on how chromatin remodeling affects developmental gene regulation in vivo. (Endocrinology 153: 961-972, 2012)
C1 [Matsuura, Kazuo; Fujimoto, Kenta; Fu, Liezhen; Shi, Yun-Bo] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Morphogenesis, Lab Gene Regulat & Dev, Program Cellular Regulat & Metab,NIH, Bethesda, MD 20892 USA.
RP Shi, YB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Morphogenesis, Lab Gene Regulat & Dev, Program Cellular Regulat & Metab,NIH, Bldg 18T,Room 106,18 Lib Dr,MSC 5431, Bethesda, MD 20892 USA.
EM shi@helix.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health
FX This work was supported by the Intramural Research Program of the Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health.
NR 68
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U1 0
U2 11
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 2012
VL 153
IS 2
BP 961
EP 972
DI 10.1210/en.2011-1736
PG 12
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 887LF
UT WOS:000299928200043
PM 22147009
ER
PT J
AU Su, D
Cha, YM
West, AE
AF Su, Dan
Cha, Young May
West, Anne E.
TI Mutation of MeCP2 alters transcriptional regulation of select
immediate-early genes
SO EPIGENETICS
LA English
DT Article
DE MeCP2; immediate-early genes; chromatin regulation; RNA polymerase II;
transcriptional initiation and elongation; Junb; Arc; cocaine;
striatumform
ID CPG-BINDING PROTEIN-2; RNA-POLYMERASE-II; RETT-SYNDROME; MOUSE MODEL;
NUCLEUS-ACCUMBENS; DNA METHYLATION; HISTONE DEACETYLASE; CHROMATIN
STATE; NEURONAL MECP2; MUTANT MICE
AB Loss-of-function mutations in the methyl-DNA binding protein MeCP2 are associated with neurological dysfunction and impaired neural plasticity. However, the transcriptional changes that underlie these deficits remain poorly understood. Here, we show that mice bearing a C-terminal truncating mutation in Mecp2 (Mecp2(308)) are hypersensitive to the locomotor stimulating effects of cocaine. Furthermore, these mice have gene-specific alterations in striatal immediate-early gene (IEG) induction following cocaine administration. MeCP2 mutant mice show normal levels of baseline and cocaine-induced striatal Fos expression compared with their wild-type littermates. However, the mutant mice have enhanced cocaine-induced transcription of Junb and Arc. At the chromatin level, we find increased histone H3 acetylation at gene promoters in the Mecp2 mutant mice compared with their wild-type littermates, whereas two sites of repressive histone methylation are unchanged. Interestingly, we find that MeCP2 mutant mice show increased steady-state association of elongation-competent RNA Polymerase II (RNAP II) with the Junb and Arc promoters, whereas levels of RNAP II association at the Fos promoter are unchanged. These data reveal a gene-specific effect of MeCP2 on the recruitment of RNAP II to gene promoters that may modulate the inducibility of IEGs. In addition, our findings raise the possibility that aberrant regulation of IEGs including Junb and Arc may contribute to altered cocaine-induced neuronal and behavioral plasticity in Mecp2 mutant mice.
C1 [Su, Dan; Cha, Young May; West, Anne E.] Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA.
NIEHS, Environm Genom Grp, Res Triangle Pk, NC 27709 USA.
RP West, AE (reprint author), Duke Univ, Med Ctr, Dept Neurobiol, Durham, NC 27710 USA.
EM west@neuro.duke.edu
FU NIH [R01-DA022202]
FX We thank A.N. Hutchinson, J.V. Deng and W.C. Wetsel for assistance with
the animal experiments. This work was supported by NIH grant
R01-DA022202 to A.E.W.
NR 55
TC 7
Z9 7
U1 0
U2 5
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1559-2294
J9 EPIGENETICS-US
JI Epigenetics
PD FEB
PY 2012
VL 7
IS 2
BP 146
EP 154
DI 10.4161/epi.7.2.18907
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 890OR
UT WOS:000300154600006
PM 22395464
ER
PT J
AU Shiao, YH
Anderson, LM
AF Shiao, Yih-Horng
Anderson, Lucy M.
TI Structural genomic changes during mammalian ontogeny: a new dimension
SO EPIGENOMICS
LA English
DT Editorial Material
DE DNA methylation; epigenetic; genome structure instability; LINE-1
elements; mammalian development; mosaicism; ontogeny; rDNA; tissue
specificity
ID RIBOSOMAL-RNA GENES; DNA TOPOISOMERASE-I; COMPLEX; CANCER; CELLS;
EXPRESSION; NUCLEOLUS; TARGET; BRAIN
C1 [Shiao, Yih-Horng; Anderson, Lucy M.] NCI, Comparat Carcinogenesis Lab, Frederick, MD 21702 USA.
RP Anderson, LM (reprint author), NCI, Comparat Carcinogenesis Lab, Bldg 538,Room 205A,POB B, Frederick, MD 21702 USA.
EM lmandersonphd@gmail.com
FU Intramural NIH HHS
NR 29
TC 0
Z9 0
U1 0
U2 1
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
1QB, ENGLAND
SN 1750-1911
J9 EPIGENOMICS-UK
JI Epigenomics
PD FEB
PY 2012
VL 4
IS 1
BP 1
EP 4
DI 10.2217/EPI.11.100
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 890FG
UT WOS:000300129900001
PM 22332651
ER
PT J
AU Qi, QB
Workalemahu, T
Zhang, CL
Hu, FB
Qi, L
AF Qi, Qibin
Workalemahu, Tsegaselassie
Zhang, Cuilin
Hu, Frank B.
Qi, Lu
TI Genetic variants, plasma lipoprotein(a) levels, and risk of
cardiovascular morbidity and mortality among two prospective cohorts of
type 2 diabetes
SO EUROPEAN HEART JOURNAL
LA English
DT Article
DE Cardiovascular disease; Genome-wide association; Lipoprotein(a); Type 2
diabetes
ID CORONARY-HEART-DISEASE; MIDDLE-AGED PATIENTS; ARTERY-DISEASE;
ASSOCIATION ANALYSIS; LDL CHOLESTEROL; FOLLOW-UP; MELLITUS; WOMEN;
INSULIN; STROKE
AB Aims To examine the relations between genetic loci, plasma lipoprotein(a) [Lp(a)] levels, and cardiovascular disease (CVD) risk among diabetic patients and compare with the observations in the general population.
Methods and results In two prospective cohorts of patients with type 2 diabetes (n = 2308) from the Nurses' Health Study and the Health Professional Follow-Up Study, we performed (i) genome-wide association (GWA) scans for plasma Lp(a); (ii) prospective analysis of plasma Lp(a) for CVD risk and mortality; and (iii) genetic association analysis for CVD risk and mortality. Meta-analysis of the two GWA scans yielded 71 single-nucleotide polymorphisms (SNPs) on chromosome 6q associated with plasma Lp(a) levels at a genome-wide significance level (P < 5 x 10(-8)). The SNP rs10455872 in LPA was most strongly associated with Lp(a) (P = 4.60 x 10(-39)). Forward-selection analysis indicated that rs10455872 and other five SNPs in a region encompassing LPA, PLG, SLC22A3, and LPAL2 genes were independently associated with Lp(a) levels and jointly explained similar to 20% of variation in diabetic patients. In prospective analysis, we did not find any significant association between plasma levels and CVD incidence; the relative risk for coronary heart disease (CHD), CVD, and CVD death was 1.05 [95% confidence interval (CI): 0.95-1.15], 1.05 (0.96-1.15), and 1.21 (0.99-1.47) per 1-SD higher log-transformed Lp(a) levels, respectively. Consistently, none of the Lp(a) SNPs were associated with CVD risk or mortality (all P > 0.09). For the best SNP rs10455872 for plasma Lp(a) levels, the OR for CHD, CVD, and CVD death was 0.94 (95% CI: 0.69-1.28), 0.97 (0.72-1.29), and 1.23 (0.79-1.92), respectively. The genetic effect on CHD risk showed a significant heterogeneity between the diabetic and the general populations (P = 0.006).
Conclusion Our data indicate that the effect of Lp(a) on CVD risk among diabetic patients might be different from that in the general population. Diabetes status may attenuate the relation between Lp(a) and cardiovascular risk.
C1 [Qi, Qibin; Workalemahu, Tsegaselassie; Hu, Frank B.; Qi, Lu] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD USA.
[Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Hu, Frank B.; Qi, Lu] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Hu, Frank B.; Qi, Lu] Harvard Univ, Sch Med, Boston, MA 02115 USA.
RP Qi, L (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA.
EM nhlqi@channing.harvard.edu
RI Qi, Qibin/H-9055-2012
FU National Institutes of Health [HL71981]; Boston Obesity Nutrition
Research Center [DK46200]; American Heart Association [0730094N]; Eunice
Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health
FX This study was supported by grant HL71981 from the National Institutes
of Health, DK46200, from the Boston Obesity Nutrition Research Center.
L.Q. was a recipient of the American Heart Association Scientist
Development Award (0730094N). C.Z. was supported by the Intramural
Research Program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development, National Institutes of Health.
NR 46
TC 36
Z9 37
U1 0
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0195-668X
J9 EUR HEART J
JI Eur. Heart J.
PD FEB
PY 2012
VL 33
IS 3
BP 325
EP 334
DI 10.1093/eurheartj/ehr350
PG 10
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 889AO
UT WOS:000300046100013
PM 21900290
ER
PT J
AU Steward, O
Popovich, PG
Dietrich, WD
Kleitman, N
AF Steward, Oswald
Popovich, Phillip G.
Dietrich, W. Dalton
Kleitman, Naomi
TI Replication and reproducibility in spinal cord injury research
SO EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE Replication; Regeneration
ID NOGO-66 RECEPTOR ANTAGONIST; FUNCTIONAL RECOVERY; DELAYED
TRANSPLANTATION; NEUROPROTECTIVE AGENT; REGENERATIVE GROWTH;
CORTICOSPINAL TRACT; LOCOMOTOR RECOVERY; PROMOTES RECOVERY; AXON
REGENERATION; IMPROVES RECOVERY
AB This special issue of Experimental Neurology compiles a series of papers that either explicitly replicate published studies or retest phenomena reported in previous publications. The explicit replications were carried out as part of the "Facilities of Research Excellence-Spinal Cord Injury" (FORE-SCI) program launched by the National Institute of Neurological Disorders and Stroke (NINDS) in 2003. Here, we review the FORE-SCI replication experiments published prior to those in this special issue. We then discuss emerging issues regarding replication and reproducibility in spinal cord injury research, especially in terms of potential translation to clinical trials. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Steward, Oswald] Univ Calif Irvine, Reeve Irvine Res Ctr, Gillespie Neurosci Res Facil 1105, Sch Med, Irvine, CA 92697 USA.
[Steward, Oswald] Univ Calif Irvine, Sch Med, Dept Anat & Neurobiol, Irvine, CA 92697 USA.
[Steward, Oswald] Univ Calif Irvine, Sch Med, Dept Neurobiol & Behav, Irvine, CA 92697 USA.
[Steward, Oswald] Univ Calif Irvine, Sch Med, Dept Neurosurg, Irvine, CA 92697 USA.
[Popovich, Phillip G.] Ohio State Univ, Coll Med, Ctr Brain & Spinal Cord Repair, Columbus, OH USA.
[Popovich, Phillip G.] Ohio State Univ, Coll Med, Dept Neurosci, Columbus, OH 43210 USA.
[Dietrich, W. Dalton] Univ Miami, Leonard M Miller Sch Med, Miami Project Cure Paralysis, Miami, FL 33136 USA.
[Dietrich, W. Dalton] Univ Miami, Leonard M Miller Sch Med, Dept Neurol Surg, Miami, FL 33136 USA.
[Kleitman, Naomi] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD 20892 USA.
RP Steward, O (reprint author), Univ Calif Irvine, Reeve Irvine Res Ctr, Gillespie Neurosci Res Facil 1105, Sch Med, Irvine, CA 92697 USA.
EM osteward@uci.edu
OI Kleitman, Naomi/0000-0003-1089-0257; Steward, Oswald/0000-0001-7069-8756
FU [N01-NS-3-2353]; [HHSN271200800039C]; [HHSN271200800040C];
[N01-NS-3-2352]
FX Supported by N01-NS-3-2353 and HHSN271200800039C (O.S.),
HHSN271200800040C (P.G.P.), and N01-NS-3-2352 (W.D.D.). The authors
gratefully acknowledge Ms. Laurie Leonard, who serves as Contracting
Officer for the FORE-SCI contracts and Dr. Arlene Chiu, who initiated
the NINDS FORE-SCI program.
NR 48
TC 68
Z9 68
U1 2
U2 8
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4886
J9 EXP NEUROL
JI Exp. Neurol.
PD FEB
PY 2012
VL 233
IS 2
SI SI
BP 597
EP 605
DI 10.1016/j.expneurol.2011.06.017
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 890CV
UT WOS:000300123600001
PM 22078756
ER
PT J
AU Huang, Y
Ko, H
Cheung, ZH
Yung, KKL
Yao, T
Wang, JJ
Morozov, A
Ke, Y
Ip, NY
Yung, WH
AF Huang, Ying
Ko, Ho
Cheung, Zelda H.
Yung, Ken K. L.
Yao, Tai
Wang, Jian-Jun
Morozov, Alexei
Ke, Ya
Ip, Nancy Y.
Yung, Wing-Ho
TI Dual actions of brain-derived neurotrophic factor on GABAergic
transmission in cerebellar Purkinje neurons
SO EXPERIMENTAL NEUROLOGY
LA English
DT Article
DE BDNF; GABA(A); KCC2; Cdk5; Purkinje neurons
ID CL-COTRANSPORTER KCC2; RAT VISUAL-CORTEX; SYNAPTIC-TRANSMISSION;
DOWN-REGULATION; MESSENGER-RNAS; DORSAL-HORN; FACTOR BDNF; EXPRESSION;
RECEPTORS; MODULATION
AB The ability to regulate inhibitory synapses is a critical feature of the nervous system and a growing body of evidence indicates that brain-derived neurotrophic factor (BDNF) acutely modulates the efficacy of GABA synaptic transmission. Although the neuronal potassium-chloride cotransporter 2 (KCC2) has been implied in this BDNF-induced ionic plasticity, the reports about actions of BDNF on GABA signaling remain conflicting. Here we show dual effects of BDNF on GABAergic synaptic transmission in Purkinje neurons in rat cerebellar slices. BDNF decreased the amplitude of evoked outward IPSCs postsynaptically. It induced a depolarizing shift in the reversal potential (E-IPSC), which reduced the driving force for outward IPSCs. However, in the absence of KCC2 activity, BDNF directly potentiated rather than inhibited GABA(A) receptor, which was reflected by an increase in the amplitude of outward IPSCs. This action of BDNF coincided with its effect in increasing the amplitude of inward IPSCs. Furthermore, an interaction between GABA(A) receptor and KCC2 was revealed by co-immunoprecipitation. The effects of BDNF on both GABA(A) receptor and KCC2 were dependent on TrkB and also activation of cyclin-dependent kinase 5 (Cdk5). However, only the effect of BDNF on KCC2 activity was dependent on a rise of intracellular calcium. Taken together, these data highlight distinct actions of BDNF on KCC2 and GABA(A) receptor in the regulation of GABAergic synaptic transmission. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Huang, Ying; Yao, Tai] Fudan Univ, Dept Physiol & Pathophysiol, Shanghai Med Coll, Shanghai, Peoples R China.
[Huang, Ying; Ko, Ho; Ke, Ya; Yung, Wing-Ho] Chinese Univ Hong Kong, Fac Med, Sch Biomed Sci, Shatin, Hong Kong, Peoples R China.
[Cheung, Zelda H.; Ip, Nancy Y.] Hong Kong Univ Sci & Technol, Dept Biochem, Biotechnol Res Inst, Hong Kong, Hong Kong, Peoples R China.
[Cheung, Zelda H.; Ip, Nancy Y.] Hong Kong Univ Sci & Technol, Mol Neurosci Ctr, Hong Kong, Hong Kong, Peoples R China.
[Yung, Ken K. L.] Hong Kong Baptist Univ, Dept Biol, Kowloon Tong, Hong Kong, Peoples R China.
[Wang, Jian-Jun] Nanjing Univ, Sch Life Sci, Dept Biol Sci & Technol, Nanjing, Jiangsu, Peoples R China.
[Huang, Ying; Morozov, Alexei] NIMH, Unit Behav Genet, Mol Pathophysiol Lab, NIH, Bethesda, MD 20892 USA.
RP Huang, Y (reprint author), Fudan Univ, Dept Physiol & Pathophysiol, Shanghai Med Coll, Shanghai, Peoples R China.
EM yinghuang@shmu.edu.cn; whyung@cuhk.edu.hk
RI Ko, Ho/I-7513-2016;
OI Ko, Ho/0000-0002-0254-3274; Yung, Ken KL/0000-0002-9588-2573
FU Research Grants Council of Hong Kong [2900336]; NSFC/RGC from National
Natural Science Foundation of China [30931160433]
FX We thank Mr. Kenny Ho and Mr. Alan S.L. Wong for expert technical
assistance. This work was supported by the Research Grants Council of
Hong Kong (2900336) and the NSFC/RGC Joint Research Scheme 30931160433
from the National Natural Science Foundation of China.
NR 47
TC 12
Z9 13
U1 0
U2 9
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4886
J9 EXP NEUROL
JI Exp. Neurol.
PD FEB
PY 2012
VL 233
IS 2
SI SI
BP 791
EP 798
DI 10.1016/j.expneurol.2011.11.043
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 890CV
UT WOS:000300123600027
PM 22178325
ER
PT J
AU Rausch, M
Lorch, S
Chung, K
Frederick, M
Zhang, J
Barnhart, K
AF Rausch, Mary
Lorch, Scott
Chung, Karine
Frederick, Margaret
Zhang, Jun
Barnhart, Kurt
TI A cost-effectiveness analysis of surgical versus medical management of
early pregnancy loss
SO FERTILITY AND STERILITY
LA English
DT Article
DE Cost-effectiveness analysis; early pregnancy loss; electric vacuum
aspiration; manual vacuum aspiration; miscarriage; misoprostol
ID RANDOMIZED CONTROLLED-TRIAL; MANUAL VACUUM ASPIRATION; QUALITY-OF-LIFE;
1ST-TRIMESTER MISCARRIAGE; INCOMPLETE MISCARRIAGE; EXPECTANT MANAGEMENT;
SPONTANEOUS-ABORTION; ECONOMIC-EVALUATION; CLINICAL-TRIAL; MIST TRIAL
AB Objective: To determine the cost-effectiveness of medical and surgical management of early pregnancy loss.
Design: Analyses of cost, effectiveness, and incremental cost-effectiveness ratios and utilities of a multicenter trial with 652 women with first-trimester pregnancy failure randomized to medical or surgical management.
Setting: Analysis of data from a multicenter trial.
Patient(s): Secondary analysis of a multicenter trial.
Intervention(s): Cost-effectiveness analysis.
Main Outcome Measure(s): Cost and effectiveness of competing treatment strategies.
Result(s): Cost analysis of treatment demonstrates an increased cost of US$336 for 13% increased efficacy of surgical management. This analysis was sensitive to the probability of an extra office visit, the cost of the visit, and the probability of success. When the surgical arm is divided into outpatient manual vacuum aspiration (MVA) versus inpatient electric vacuum aspiration (EVA), there is an increased cost of $745 for EVA but a decreased cost of $202 for MVA compared with medical management. In general, MVA was found to be more cost-effective than medical management. For treatment of incomplete or inevitable abortion, medical management was found to be less costly and more efficacious. Utilities studies demonstrated that a patient would need to prefer surgery 14% less than medication for its treatment efficacy to be outweighed by the desire to avoid surgery.
Conclusion(s): Surgical or medical management of early pregnancy failure can be cost effective, depending on the circumstances. Surgery is cost effective and more efficacious when performed in an outpatient setting. For incomplete or inevitable abortion, medical management is cost effective and more efficacious. (Fertil Steril (R) 2012;97:355-60. (C)2012 by American Society for Reproductive Medicine.)
C1 [Barnhart, Kurt] Univ Penn, Med Ctr, Philadelphia, PA 19104 USA.
[Rausch, Mary] N Shore Univ Hosp, Manhasset, NY USA.
[Lorch, Scott] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Chung, Karine] Univ So Calif, Los Angeles, CA USA.
[Frederick, Margaret] Clinical Trials & Surveys Corp, Owings Mills, MD USA.
[Zhang, Jun] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Barnhart, K (reprint author), Univ Penn, Med Ctr, 3701 Market St,Suite 800, Philadelphia, PA 19104 USA.
EM kbarnhart@obgyn.upenn.edu
FU National Institute of Child Health and Human Development, National
Institutes of Health, Department of Health and Human Services
[N01-HD-1-3321, N01-HD-1-3322, N01-HD-1-3323, N01-HD-1-3324,
N01-HD-1-3325, R01-HD036455, K24HD060687, T32-HD007440]
FX Funded by the National Institute of Child Health and Human Development,
National Institutes of Health, Department of Health and Human Services
under Contract Numbers: N01-HD-1-3321 through 3325 with additional
support from R01-HD036455 (K.B.), K24HD060687 (K.B.), and T32-HD007440
(M.R.).
NR 22
TC 23
Z9 23
U1 2
U2 8
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 2012
VL 97
IS 2
BP 355
EP U379
DI 10.1016/j.fertnstert.2011.11.044
PG 7
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 887WG
UT WOS:000299961800021
PM 22192348
ER
PT J
AU Schaefer, GO
Sinaii, N
Grady, C
AF Schaefer, Gerald Owen
Sinaii, Ninet
Grady, Christine
TI Informing egg donors of the potential for embryonic research: a survey
of consent forms from US in vitro fertilization clinics
SO FERTILITY AND STERILITY
LA English
DT Article
DE Informed consent; oocyte donors; research
ID STEM-CELL RESEARCH
AB Objective: To understand whether and to what extent U.S. IVF clinics inform egg donors that resultant embryos initially intended to be implanted for reproductive purposes may in fact be used for research instead.
Design: Four hundred seventy U. S. IVF clinics were asked to respond to a questionnaire and provide a copy of the egg donor consent form(s) used at the clinic.
Setting: Four hundred seventy U. S. IVF clinics listed in a Centers for Disease Control and Prevention database; only forms from clinics that both accepted donor eggs and provided excess embryos for research were analyzed for content.
Patient(s): Not applicable.
Intervention(s): Not applicable.
Main Outcome Measure(s): Responses to the questionnaire, demographic data from a Centers for Disease Control and Prevention database, and the content of egg donor consent forms.
Result(s): Of 222 U. S. IVF clinics that responded to our query, 100 clinics both accepted donor eggs and provided some excess embryos for research. We received 66 consent forms from these 100 clinics, which showed that although most egg donor consent forms inform donors that they will not have control over embryos resulting from their eggs, 30% inform them that some embryos may be used for research, and even fewer mention stem cell research.
Conclusion(s): Egg donors in the United States, including some who may have a moral objection to research and stem cell research, are not being informed that embryos created with their donated eggs may in fact be used for these purposes. This can be corrected with the inclusion of succinct, nontechnical language in egg donor consent forms. (Fertil Steril(R) 2012;97:427-33. (C) 2012 by American Society for Reproductive Medicine.)
C1 [Schaefer, Gerald Owen; Grady, Christine] Natl Inst Hlth Clin Ctr, Dept Bioeth, Bethesda, MD 20892 USA.
[Schaefer, Gerald Owen] Univ Oxford, St Cross Coll, Fac Philosophy, Oxford, England.
[Sinaii, Ninet] Natl Inst Hlth Clin Ctr, Biostat & Clin Epidemiol Serv, Bethesda, MD USA.
RP Grady, C (reprint author), Natl Inst Hlth Clin Ctr, Dept Bioeth, Bldg 10-1C118, Bethesda, MD 20892 USA.
EM cgrady@nih.gov
OI Schaefer, Gerald Owen/0000-0002-6915-6148
FU National Institutes of Health Clinical Center
FX Funding and support for design and conduct of the study; collection,
management, analysis, and interpretation of the data; and preparation,
review, or approval of the manuscript were provided by the National
Institutes of Health Clinical Center.
NR 13
TC 5
Z9 5
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 2012
VL 97
IS 2
BP 427
EP 433
DI 10.1016/j.fertnstert.2011.11.035
PG 7
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA 887WG
UT WOS:000299961800033
PM 22196714
ER
PT J
AU Rothenberg, KH
Bush, LW
AF Rothenberg, Karen H.
Bush, Lynn W.
TI Genes and plays: bringing ELSI issues to life
SO GENETICS IN MEDICINE
LA English
DT Article
DE ELSI; genetics; genomic research; plays; vignettes
ID MEDICAL-EDUCATION; CLINICAL-PRACTICE; PERFORMANCE; STUDENTS; ETHICS;
DRAMA; TIME; WIT
AB Ethical complexities surround the promise of genomic technology and the power of genetic information as they alter conceptions of identity and dynamics within personal and professional relationships. Creative approaches such as dramatic vignettes offer a unique analytical stage for imagining the bioethical past and future. Dramatic narratives can bring to life images of differing perspectives and values when experiencing innovations in medicine. Although the scientific landscape shifts, concerns expressed in theatre from 50 years ago parallel many contemporary ELSI (ethical, legal, and social implications) issues, highlighting the ongoing struggle to appreciate the impact of emerging genetic technologies on relationships. To illuminate these enduring concerns, we explore how perceptions and relationships have influenced and been influenced by genetics as portrayed through dramatic vignettes. We build on the legacy of using case vignettes as a clinical teaching modality, and believe similar value exists within the research ethics domain. The selection of dialogue discussed encompasses abbreviated excerpts from two existing and one original vignette that we staged at the ELSI 2011 Congress and various academic and health institutions. Genet Med 2012:14(2):274-277
C1 [Rothenberg, Karen H.] Univ Maryland Francis King Carey Sch Law, Baltimore, MD USA.
[Rothenberg, Karen H.] NHGRI, Dept Bioeth, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Bush, Lynn W.] Columbia Univ, Dept Clin Genet, New York, NY USA.
RP Rothenberg, KH (reprint author), Univ Maryland Francis King Carey Sch Law, Baltimore, MD USA.
EM krothenberg@law.umaryland.edu
NR 34
TC 0
Z9 1
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD FEB
PY 2012
VL 14
IS 2
BP 274
EP 277
DI 10.1038/gim.2011.47
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 890BI
UT WOS:000300119700014
PM 22241098
ER
PT J
AU Heidari, S
Mofenson, LM
Hobbs, CV
Cotton, MF
Marlink, R
Katabira, E
AF Heidari, Shirin
Mofenson, Lynne M.
Hobbs, Charlotte V.
Cotton, Mark F.
Marlink, Richard
Katabira, Elly
TI Unresolved Antiretroviral Treatment Management Issues in HIV-Infected
Children
SO JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
LA English
DT Review
DE antiretroviral; childhood growth and development; drug complications;
HIV-infected infants; malaria; malnutrition; tuberculosis
ID RECONSTITUTION INFLAMMATORY SYNDROME; PLASMODIUM-FALCIPARUM MALARIA;
BONE-MINERAL DENSITY; IMMUNODEFICIENCY-VIRUS-INFECTION; TENOFOVIR
DISOPROXIL FUMARATE; OPTIMIZED BACKGROUND REGIMEN; SOUTH-AFRICAN
CHILDREN; SUB-SAHARAN AFRICA; UNINFECTED CHILDREN; COTRIMOXAZOLE
PROPHYLAXIS
AB Antiretroviral therapy in children has expanded dramatically in low-income and middle-income countries. The World Health Organization revised its pediatric HIV guidelines to recommend initiation of antiretroviral therapy in all HIV-infected children younger than 2 years, regardless of CD4 count or clinical stage. The number of children starting life-long antiretroviral therapy should therefore expand dramatically over time. The early initiation of antiretroviral therapy has indisputable benefits for children, but there is a paucity of definitive information on the potential adverse effects. In this review, a comprehensive literature search was conducted to provide an overview of our knowledge about the complications of treating pediatric HIV.
Antiretroviral therapy in children, as in adults, is associated with enhanced survival, reduction in opportunistic infections, improved growth and neurocognitive function, and better quality of life. Despite antiretroviral therapy, HIV-infected children may continue to lag behind their uninfected peers in growth and development. In addition, epidemic concurrent conditions, such as tuberculosis, malaria, and malnutrition, can combine with HIV to yield more rapid disease progression and poor treatment outcomes.
Additional studies are required to evaluate the long-term effects of antiretroviral therapy in HIV-infected infants, children, and adolescents, particularly in resource-limited countries where concomitant infections and conditions may enhance the risk of adverse effects. There is an urgent need to evaluate drug-drug interactions in children to determine optimal treatment regimens for both HIV and coinfections.
C1 [Heidari, Shirin] Int AIDS Soc, Dept Res Promot, CH-1216 Geneva, Switzerland.
[Mofenson, Lynne M.] NIH, Pediat Adolescent & Maternal AIDS Branch, Bethesda, MD 20892 USA.
[Hobbs, Charlotte V.] NIAID, Lab Malaria Immunol & Vaccinol, NIH, Rockville, MD USA.
[Cotton, Mark F.] Univ Stellenbosch, Dept Pediat & Child Hlth, ZA-7600 Stellenbosch, South Africa.
[Cotton, Mark F.] Tygerberg Childrens Hosp, Tygerberg, South Africa.
[Marlink, Richard] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Marlink, Richard] Elizabeth Glaser Pediat AIDS Fdn, Los Angeles, CA USA.
[Katabira, Elly] Makerere Univ, Coll Hlth Sci, Kampala, Uganda.
RP Heidari, S (reprint author), Int AIDS Soc, Dept Res Promot, 71 Ave Louis Casai, CH-1216 Geneva, Switzerland.
EM shirin.heidar-i@iasociety.org
OI Mofenson, Lynne/0000-0002-2818-9808
FU Abbott; Boehringer Ingelheim; Gilead; Merck; Pfizer; Tibotec; ViiV
Healthcare; International AIDS Society
FX The mapping exercise was financially supported by unrestricted
educational grants from Abbott, Boehringer Ingelheim, Gilead, Merck,
Pfizer, Tibotec and ViiV Healthcare, and the International AIDS
Society.; The authors S. H. is an employee of the International AIDS
Society, and her salary is provided partly by unrestricted educational
grants from the following pharmaceutical companies: Abbott, Boehringer
Ingelheim, Gilead, Merck, Pfizer, Tibotec and ViiV Healthcare. M. F. C.
is an investigator on GSK and Boehringer Ingelheim trials and has
received honoraria from Abbott and GSK within the past 6 months. R. M.
has served as an advisor to the BMS Foundation and the Merck Company
Foundation. L. M. M., C. V. H., and E. K. have no competing interests.
NR 101
TC 16
Z9 16
U1 1
U2 7
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 2012
VL 59
IS 2
BP 161
EP 169
DI 10.1097/QAI.0b013e3182427029
PG 9
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 885OX
UT WOS:000299789600014
PM 22138766
ER
PT J
AU Hirano, Y
Suzuki, T
Matsumoto, T
Ishihara, Y
Takaki, Y
Kono, M
Dohmae, N
Tsuji, S
AF Hirano, Yuichi
Suzuki, Takehiro
Matsumoto, Takumi
Ishihara, Yoshimi
Takaki, Yoshie
Kono, Mari
Dohmae, Naoshi
Tsuji, Shuichi
TI Disulphide linkage in mouse ST6Gal-I: determination of linkage positions
and mutant analysis
SO JOURNAL OF BIOCHEMISTRY
LA English
DT Article
ID POLYMERASE-CHAIN-REACTION; CLONING; SIALYLTRANSFERASES; PROTEINS;
LOCALIZATION; EXPRESSION; MECHANISM; RESIDUES; DONOR
AB All cloned sialyltransferases from vertebrates are classified into four subfamilies and are characterized as having type II transmembrane topology. The catalytic domain has highly conserved motifs known as sialylmotifs. Besides sialylmotifs, each family has several unique conserved cysteine (Cys) residues mainly in the catalytic domain. The number and loci of conserved amino acids, however, differ with each subfamily, suggesting that the conserved Cys-residues and/or disulphide linkages they make may contribute to linkage specificity. Using Matrix Assisted Laser Desorption/Ionization-Time of Flight Mass Spectrometry (MALDI-TOF)-mass spectrometry, the present study performed disulphide linkage analysis on soluble mouse ST6Gal-I, which has six Cys-residues. Results confirmed that there were no free Cys-residues, and all six residues contributed to disulphide linkage formation, C-139-C-403, C-181-C-332 and C-350-C-361. Study of single amino acid-substituted mutants revealed that the disulphide linkage C-181-C-332 was necessary for molecular expression of the enzyme, and that the disulphide linkage C-350-C-361 was necessary for enzyme activity. The remaining disulphide linkage C-139-C-403 was not necessary for enzyme expression or for activity, including substrate specificity. Crystallographic study of pig ST3Gal I has recently been reported. Interestingly, the loci of disulphide linkages in ST6Gal-I differ from those in ST3Gal I, suggesting that the linkage specificity of sialyltransferase may results from significant structural differences, including the loci of disulphide linkages.
C1 [Hirano, Yuichi; Matsumoto, Takumi; Takaki, Yoshie; Tsuji, Shuichi] Tokai Univ, Inst Glycosci, Hiratsuka, Kanagawa 2591292, Japan.
[Hirano, Yuichi; Ishihara, Yoshimi] RIKEN Adv Sci Inst, Biomol Characterizat Team, Wako, Saitama 3510198, Japan.
[Suzuki, Takehiro; Dohmae, Naoshi] Tokai Univ, Dept Chem, Sch Sci, Hiratsuka, Kanagawa 2591292, Japan.
[Kono, Mari] NIH, Genet Dev & Dis Branch, Bethesda, MD 20892 USA.
RP Tsuji, S (reprint author), Tokai Univ, Inst Glycosci, 4-1-1 Kitakaname, Hiratsuka, Kanagawa 2591292, Japan.
EM stsuji@tokai-u.jp
RI Dohmae, Naoshi/C-2040-2011
NR 17
TC 5
Z9 6
U1 1
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0021-924X
J9 J BIOCHEM
JI J. Biochem.
PD FEB
PY 2012
VL 151
IS 2
BP 197
EP 203
DI 10.1093/jb/mvr133
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 885NZ
UT WOS:000299787000010
PM 22039275
ER
PT J
AU Reinholdt-Dunne, ML
Mogg, K
Benson, V
Bradley, BP
Hardin, MG
Liversedge, SP
Pine, DS
Ernsts, M
AF Reinholdt-Dunne, M. L.
Mogg, K.
Benson, V.
Bradley, B. P.
Hardin, M. G.
Liversedge, S. P.
Pine, D. S.
Ernsts, M.
TI Anxiety and selective attention to angry faces: An antisaccade study
SO JOURNAL OF COGNITIVE PSYCHOLOGY
LA English
DT Article
DE Angry faces; Antisaccade; Anxiety; Selective attention
ID COGNITIVE CONTROL; DEPRESSED ADOLESCENTS; TASK; PSYCHOPATHOLOGY;
PROSACCADES; PERFORMANCE; INHIBITION; EFFICIENCY; ACCOUNT; SCALES
AB Cognitive models of anxiety propose that anxiety is associated with an attentional bias for threat, which increases vulnerability to emotional distress and is difficult to control. The study aim was to investigate relationships between the effects of threatening information, anxiety, and attention control on eye movements. High and low trait anxious individuals performed antisaccade and prosaccade tasks with angry, fearful, happy, and neutral faces. Results indicated that high-anxious participants showed a greater antisaccade cost for angry than neutral faces (i.e., relatively slower to look away from angry faces), compared with low-anxious individuals. This bias was not found for fearful or happy faces. The bias for angry faces was not related to individual differences in attention control assessed on self-report and behavioural measures. Findings support the view that anxiety is associated with difficulty in using cognitive control resources to inhibit attentional orienting to angry faces, and that attention control is multifaceted.
C1 [Reinholdt-Dunne, M. L.; Mogg, K.; Benson, V.; Bradley, B. P.; Liversedge, S. P.] Univ Southampton, Sch Psychol, Southampton SO17 1BJ, Hants, England.
[Reinholdt-Dunne, M. L.] Univ Copenhagen, Dept Psychol, Copenhagen, Denmark.
[Hardin, M. G.] Univ Maryland, Dept Human Dev, College Pk, MD 20742 USA.
[Pine, D. S.; Ernsts, M.] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
RP Mogg, K (reprint author), Univ Southampton, Sch Psychol, Southampton SO17 1BJ, Hants, England.
EM kmogg@soton.ac.uk
RI Bradley, Brendan/B-9724-2008; Mogg, Karin/C-1181-2008;
OI Mogg, Karin/0000-0002-2738-7378; Bradley, Brendan/0000-0003-2801-4271
NR 34
TC 12
Z9 12
U1 3
U2 22
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND
SN 2044-5911
J9 J COGN PSYCHOL
JI J. Cogn. Psychol.
PD FEB
PY 2012
VL 24
IS 1
SI SI
BP 54
EP 65
DI 10.1080/20445911.2011.560111
PG 12
WC Psychology, Experimental
SC Psychology
GA 887HK
UT WOS:000299917300005
ER
PT J
AU Hingson, RW
Heeren, T
Edwards, EM
Saitz, R
AF Hingson, Ralph W.
Heeren, Timothy
Edwards, Erika M.
Saitz, Richard
TI Young Adults at Risk for Excess Alcohol Consumption Are Often Not Asked
or Counseled About Drinking Alcohol
SO JOURNAL OF GENERAL INTERNAL MEDICINE
LA English
DT Article
DE alcoholism and addictive behavior; communication; patient education;
prevention
ID UNITED-STATES; NATIONAL-SURVEY; IDENTIFICATION; INTERVENTION;
DEPENDENCE; DISEASE
AB Excessive alcohol consumption is most widespread among young adults. Practice guidelines recommend screening and physician advice, which could help address this common cause of injury and premature death.
To assess the proportion of persons ages 18-39 who, in the past year, saw a physician and were asked about their drinking and advised what drinking levels pose health risk, and whether this differed by age or whether respondents exceeded low-risk drinking guidelines [daily (> 4 drinks for men/> 3 for women) or weekly (> 14 for men/> 7 for women)].
Survey of young adults selected from a national internet panel established using random digit dial telephone techniques.
Adults age 18-39 who ever drank alcohol, n = 3,409 from the internet panel and n = 612 non-panel telephone respondents.
Respondents were asked whether they saw a doctor in the past year; those who did see a doctor were asked whether a doctor asked about their drinking, advised about safe drinking levels, or counseled to reduce drinking.
Of respondents, 67% saw a physician in the past year, but only 14% of those exceeding guidelines were asked and advised about risky drinking patterns. Persons 18-25 were the most likely to exceed guidelines (68% vs. 56%, p < 0.001) but were least often asked about drinking (34% vs. 54%, p < 0.001).
Despite practice guidelines, few young adults are asked and advised by physicians about excessive alcohol consumption. Physicians should routinely ask all adults about their drinking and offer advice about levels that pose health risk, particularly to young adults.
C1 [Hingson, Ralph W.] NIAAA, Div Epidemiol & Prevent Res, Bethesda, MD 20892 USA.
[Heeren, Timothy; Edwards, Erika M.; Saitz, Richard] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Saitz, Richard] Boston Med Ctr, Clin Addict Res & Educ CARE Unit, Sect Gen Internal Med, Boston, MA USA.
RP Hingson, RW (reprint author), NIAAA, Div Epidemiol & Prevent Res, 5635 Fishers Lane,Room 2077, Bethesda, MD 20892 USA.
EM rhingson@mail.nih.gov
OI Heeren, Timothy/0000-0001-5643-3559; /0000-0002-2535-1427
FU National Institute on Alcohol Abuse; Alcoholism Center [P60AA13759];
National Institutes of Health (NIH); University of Massachusetts;
Brandeis University
FX This article is dedicated to Helen Marie Witty, who at age 16 was
fatally injured by a young alcohol-impaired driver. Dr. Ralph Hingson
had full access to all of the data in the study and takes responsibility
for the integrity of the data and the accuracy of the data analysis.
This study was supported in part by the National Institute on Alcohol
Abuse and Alcoholism Center Grant P60AA13759.; Drs. Ralph Hingson, Tim
Heeren, and Erika Edwards have no conflicts of interest to report. Dr.
Richard Saitz reports having been a consultant for online
alcohol-related screening and brief intervention education projects
supported by National Institutes of Health (NIH) grants to Medical
Directions and Inflexxion and for NIH grants to the RAND corporation,
Kaiser Permanente, the University of Massachusetts, and Brandeis
University. Dr. Saitz also has been compensated by Beth Israel Deaconess
Hospital and the National Institute on Alcohol Abuse and Alcoholism for
serving on data and safety monitoring boards. He is compensated for
educational work by the Massachusetts Medical Society, the British
Medical Journal Group, and the American Society of Addiction Medicine.
He has developed educational materials for Fusion medical education and
consulted for Saatchi and Saatchi Healthcare on alcohol dependence
treatment. He has or anticipates being compensated as a speaker on
alcohol and drug topics by multiple government agencies, academic
institutions, and professional societies. He has also provided expert
opinion on legal cases involving identification and management of
alcohol and drug related problems.
NR 35
TC 24
Z9 24
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0884-8734
J9 J GEN INTERN MED
JI J. Gen. Intern. Med.
PD FEB
PY 2012
VL 27
IS 2
BP 179
EP 184
DI 10.1007/s11606-011-1851-1
PG 6
WC Health Care Sciences & Services; Medicine, General & Internal
SC Health Care Sciences & Services; General & Internal Medicine
GA 889HS
UT WOS:000300064900012
PM 21935753
ER
PT J
AU Cook, S
Moureau, G
Kitchen, A
Gould, EA
de Lamballerie, X
Holmes, EC
Harbachl, RE
AF Cook, Shelley
Moureau, Gregory
Kitchen, Andrew
Gould, Ernest A.
de Lamballerie, Xavier
Holmes, Edward C.
Harbachl, Ralph E.
TI Molecular evolution of the insect-specific flaviviruses
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Review
ID NATURAL MOSQUITO POPULATION; MULTIPLE SEQUENCE ALIGNMENT;
AEDES-ALBOPICTUS CELLS; FUSING AGENT VIRUS; GENUS FLAVIVIRUS;
PHYLOGENETIC-RELATIONSHIPS; DIPTERA-CULICIDAE; YUCATAN PENINSULA; BORNE
VIRUSES; RNA VIRUSES
AB There has been an explosion in the discovery of 'insect-specific' flaviviruses and/or their related sequences in natural mosquito populations. Herein we review all 'insect-specific' flavivirus sequences currently available and conduct phylogenetic analyses of both the 'insect-specific' flaviviruses and available sequences of the entire genus Flavivirus. We show that there is no statistical support for virus mosquito co-divergence, suggesting that the 'insect-specific' flaviviruses may have undergone multiple introductions with frequent host switching. We discuss potential implications for the evolution of vectoring within the family Flaviviridae. We also provide preliminary evidence for potential recombination events in the history of cell fusing agent virus. Finally, we consider priorities and guidelines for future research on 'insect-specific' flaviviruses, including the vast potential that exists for the study of biodiversity within a range of potential hosts and vectors, and its effect on the emergence and maintenance of the flaviviruses.
C1 [Cook, Shelley; Harbachl, Ralph E.] Nat Hist Museum, London SW7 5BD, England.
[Moureau, Gregory; Gould, Ernest A.; de Lamballerie, Xavier] Univ Aix Marseille 2, Inst Rech Dev, EHESP French Sch Publ Hlth, Unite Virus Emergents UMR190, Marseille, France.
[Kitchen, Andrew; Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Gould, Ernest A.] Ctr Ecol & Hydrol, Wallingford OX10 8BB, Oxon, England.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Cook, S (reprint author), Nat Hist Museum, Cromwell Rd, London SW7 5BD, England.
EM s.cook@nhm.ac.uk
OI Holmes, Edward/0000-0001-9596-3552
FU Wellcome Trust [039833]
FX The work of S. C. is funded by a Sir Henry Wellcome Postdoctoral
Fellowship from the Wellcome Trust (grant 039833).
NR 57
TC 75
Z9 77
U1 3
U2 21
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
EI 1465-2099
J9 J GEN VIROL
JI J. Gen. Virol.
PD FEB
PY 2012
VL 93
BP 223
EP 234
DI 10.1099/vir.0.036525-0
PN 2
PG 12
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 890IY
UT WOS:000300139500001
PM 22012464
ER
PT J
AU Harbison, CE
Weichert, WS
Gurda, BL
Chiorini, JA
Agbandje-McKenna, M
Parrish, CR
AF Harbison, Carole E.
Weichert, Wendy S.
Gurda, Brittney L.
Chiorini, John A.
Agbandje-McKenna, Mavis
Parrish, Colin R.
TI Examining the cross-reactivity and neutralization mechanisms of a panel
of mAbs against adeno-associated virus serotypes 1 and 5
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; GENE-THERAPY VECTOR; MONOCLONAL-ANTIBODIES;
IMMUNE-RESPONSES; MEDIATED NEUTRALIZATION; TRANSGENE EXPRESSION; CANINE
PARVOVIRUS; VIRAL VECTORS; SIALIC-ACID; IN-VITRO
AB Neutralizing antibodies play a central role in the prevention and clearance of viral infections, but can be detrimental to the use of viral capsids for gene delivery. Antibodies present a major hurdle for ongoing clinical trials using adeno-associated viruses (AAVs); however, relatively little is known about the antigenic epitopes of most AAV serotypes or the mechanism(s) of antibody-mediated neutralization. We developed panels of AAV mAbs by repeatedly immunizing mice with AAV serotype 1 (AAV1) capsids, or by sequentially immunizing with AAV1 followed by AAV5 capsids, in order to examine the efficiency and mechanisms of antibody-mediated neutralization. The antibodies were not cross-reactive between heterologous AAV serotypes except for a low level of recognition of AAV1 capsids by the AAV5 antibodies, probably due to the initial immunization with AAV1. The neutralization efficiency of different IgGs varied and Fab fragments derived from these antibodies were generally poorly neutralizing. The antibodies appeared to display various alternative mechanisms of neutralization, which included inhibition of receptor-binding and interference with a post-attachment step.
C1 [Harbison, Carole E.; Weichert, Wendy S.; Parrish, Colin R.] Cornell Univ, Coll Vet Med, Dept Microbiol & Immunol, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
[Gurda, Brittney L.; Agbandje-McKenna, Mavis] Univ Florida, Dept Biochem & Mol Biol, Gainesville, FL 32610 USA.
[Chiorini, John A.] Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, US Natl Inst Hlth NIH, Bethesda, MD 20892 USA.
RP Parrish, CR (reprint author), Cornell Univ, Coll Vet Med, Dept Microbiol & Immunol, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
EM crp3@cornell.edu
OI Gurda, Brittney /0000-0002-0174-9385
FU National Institutes of Allergy and Infectious Diseases [R21AI072341]
FX Supported by National Institutes of Allergy and Infectious Diseases,
grant R21AI072341. The authors would like to thank Sandra Wainer and
Beverly Handleman for excellent technical support.
NR 72
TC 14
Z9 14
U1 0
U2 1
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
J9 J GEN VIROL
JI J. Gen. Virol.
PD FEB
PY 2012
VL 93
BP 347
EP 355
DI 10.1099/vir.0.035113-0
PN 2
PG 9
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 890IY
UT WOS:000300139500014
PM 22071509
ER
PT J
AU Peden, AH
McGuire, LI
Appleford, NEJ
Mallinson, G
Wilham, JM
Orru, CD
Caughey, B
Ironside, JW
Knight, RS
Will, RG
Green, AJE
Head, MW
AF Peden, Alexander H.
McGuire, Lynne I.
Appleford, Nigel E. J.
Mallinson, Gary
Wilham, Jason M.
Orru, Christina D.
Caughey, Byron
Ironside, James W.
Knight, Richard S.
Will, Robert G.
Green, Alison J. E.
Head, Mark W.
TI Sensitive and specific detection of sporadic Creutzfeldt-Jakob disease
brain prion protein using real-time quaking-induced conversion
SO JOURNAL OF GENERAL VIROLOGY
LA English
DT Article
ID IN-VITRO AMPLIFICATION; BLOOD-TRANSFUSION; SEEDED CONVERSION; PRPSC;
TRANSMISSION; CLASSIFICATION; DIAGNOSIS; STRAINS; PATIENT; ASSAY
AB Real-time quaking-induced conversion (RT-QuIC) is an assay in which disease-associated prion protein (PrP) initiates a rapid conformational transition in recombinant PrP (recPrP), resulting in the formation of amyloid that can be monitored in real time using the dye thioflavin T. It therefore has potential advantages over analogous cell-free PrP conversion assays such as protein misfolding cyclic amplification (PMCA). The QuIC assay and the related amyloid seeding assay have been developed largely using rodent-passaged sheep scrapie strains. Given the potential RT-QuIC has for Creutzfeldt-Jakob disease (CJD) research and human prion test development, this study characterized the behaviour of a range of CJD brain specimens with hamster and human recPrP in the RT-QuIC assay. The results showed that RT-QuIC is a rapid, sensitive and specific test for the form of abnormal PrP found in the most commonly occurring forms of sporadic CJD. The assay appeared to be largely independent of species-related sequence differences between human and hamster recPrP and of the methionine/valine polymorphism at codon 129 of the human PrP gene. However, with the same conditions and substrate, the assay was less efficient in detecting the abnormal PrP that characterizes variant CJD brain. Comparison of these QuIC results with those previously obtained using PMCA suggested that these two seemingly similar assays differ in important respects.
C1 [Peden, Alexander H.; McGuire, Lynne I.; Ironside, James W.; Knight, Richard S.; Will, Robert G.; Green, Alison J. E.; Head, Mark W.] Univ Edinburgh, Sch Mol & Clin Med, Natl CJD Res & Surveillance Unit, Edinburgh, Midlothian, Scotland.
[Appleford, Nigel E. J.; Mallinson, Gary] Bristol Inst Transfus Sci, Natl Blood Serv, Bristol, Avon, England.
[Wilham, Jason M.; Orru, Christina D.; Caughey, Byron] NIAID, Persistent Viral Dis Lab, Rocky Mt Labs, Hamilton, MT USA.
RP Head, MW (reprint author), Univ Edinburgh, Sch Mol & Clin Med, Natl CJD Res & Surveillance Unit, Edinburgh, Midlothian, Scotland.
EM m.w.head@ed.ac.uk
OI Head, Mark/0000-0003-2034-8613; Ironside, James/0000-0001-5869-2108
FU Scottish Government Health Directorates Chief Scientist Office
[CZB/4/688]; Alliance BioSecure; National Institute of Allergy and
Infectious Diseases, National Institutes of Health; MRC (UK); NCJDRSU;
Department of Health, UK; Scottish Government
FX This work was funded by grants from the Scottish Government Health
Directorates Chief Scientist Office (CZB/4/688) to M. W. H. and from
Alliance BioSecure to A. J. E. G. This work was also supported in part
by the Intramural Research Program of the National Institute of Allergy
and Infectious Diseases, National Institutes of Health. The National CJD
Surveillance Unit Brain and Tissue Bank is supported by the MRC (UK),
and the NCJDRSU as a whole is funded by the Department of Health, UK,
and the Scottish Government. The views expressed in the publication are
those of the authors and not necessarily those of the Department of
Health, UK. The authors would like to thank the patients and their
relatives for the opportunity to conduct research on tissue specimens.
NR 36
TC 39
Z9 39
U1 1
U2 9
PU SOC GENERAL MICROBIOLOGY
PI READING
PA MARLBOROUGH HOUSE, BASINGSTOKE RD, SPENCERS WOODS, READING RG7 1AG,
BERKS, ENGLAND
SN 0022-1317
J9 J GEN VIROL
JI J. Gen. Virol.
PD FEB
PY 2012
VL 93
BP 438
EP 449
DI 10.1099/vir.0.033365-0
PN 2
PG 12
WC Biotechnology & Applied Microbiology; Virology
SC Biotechnology & Applied Microbiology; Virology
GA 890IY
UT WOS:000300139500024
PM 22031526
ER
PT J
AU Hirvonen, J
Kreisl, WC
Fujita, M
Dustin, I
Khan, O
Appel, S
Zhang, Y
Morse, C
Pike, VW
Innis, RB
Theodore, WH
AF Hirvonen, Jussi
Kreisl, William C.
Fujita, Masahiro
Dustin, Irene
Khan, Omar
Appel, Shmuel
Zhang, Yi
Morse, Cheryl
Pike, Victor W.
Innis, Robert B.
Theodore, William H.
TI Increased In Vivo Expression of an Inflammatory Marker in Temporal Lobe
Epilepsy
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE positron emission tomography; translocator protein 18 kDa; epilepsy;
inflammation
ID PERIPHERAL BENZODIAZEPINE-RECEPTORS; POSITRON-EMISSION-TOMOGRAPHY;
PROTEIN 18 KDA; TRANSLOCATOR PROTEIN; HUMAN BRAIN; HIPPOCAMPAL
SCLEROSIS; PET; ENCEPHALITIS; ASSOCIATION; MICROGLIA
AB Animal studies and clinical observations suggest that epilepsy is associated with inflammation. Translocator protein (TSPO) (18 kDa), a marker of inflammation, is increased in vitro in surgical samples from patients with temporal lobe epilepsy. TSPO can be measured in the living human brain with PET and the novel radioligand C-11-PBR28. In this study, we sought to determine whether in vivo expression of TSPO is increased ipsilateral to the seizure focus in patients with temporal lobe epilepsy. Methods: Sixteen patients with unilateral temporal lobe epilepsy and 30 healthy subjects were studied with C-11-PBR28 PET and MRI. Uptake of radioactivity after injection of C-11-PBR28 was measured from regions of interest drawn bilaterally onto MR images. Brain uptake from ipsilateral and contralateral hemispheres was compared using a paired-samples t test. Results: We found that brain uptake was higher ipsilateral to the seizure focus in the hippocampus, parahippocampal gyrus, amygdala, fusiform gyrus, and choroid plexus but not in other brain regions. This asymmetry was more pronounced in patients with hippocampal sclerosis than in those without. Conclusion: We found increased uptake of radioactivity after injection of C-11-PBR28 ipsilateral to the seizure focus in patients with temporal lobe epilepsy, suggesting increased expression of TSPO. Studies in larger samples are required to confirm this finding and determine the clinical utility of imaging TSPO in temporal lobe epilepsy.
C1 [Hirvonen, Jussi; Kreisl, William C.; Fujita, Masahiro; Zhang, Yi; Morse, Cheryl; Pike, Victor W.; Innis, Robert B.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Dustin, Irene; Khan, Omar; Appel, Shmuel; Theodore, William H.] NINDS, Clin Epilepsy Sect, NIH, Bethesda, MD 20892 USA.
RP Innis, RB (reprint author), NIMH, Mol Imaging Branch, NIH, 10 Ctr Dr,MSC 1026,Bldg 10,Room B1D43, Bethesda, MD 20892 USA.
EM robert.innis@nih.gov
FU National Institute of Mental Health [Z01-MH-002852-04]; National
Institute of Neurological Disorders and Stroke [1Z01-NS002236-34];
Academy of Finland; Finnish Cultural Foundation; Finnish Foundation for
Alcohol Studies; Finnish Medical Foundation; Instrumentarium Foundation;
Jalmari and Rauha Ahokas Foundation; Paulo Foundation; Research
Foundation of Orion Corporation; Yrjo Jahnsson Foundation
FX We thank Desiree Ferraris Araneta and the PET Department in the Clinical
Center for the successful completion of this research. We also thank
Drs. Ruben Kuzniecky and Jacqueline French for referring patients. This
work was supported by the intramural programs of the National Institute
of Mental Health (project Z01-MH-002852-04) and the National Institute
of Neurological Disorders and Stroke (project 1Z01-NS002236-34) and
grants from the Academy of Finland, the Finnish Cultural Foundation, the
Finnish Foundation for Alcohol Studies, the Finnish Medical Foundation,
the Instrumentarium Foundation, the Jalmari and Rauha Ahokas Foundation,
the Paulo Foundation, the Research Foundation of Orion Corporation, and
the Yrjo Jahnsson Foundation. No other potential conflict of interest
relevant to this article was reported.
NR 29
TC 34
Z9 34
U1 0
U2 7
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
J9 J NUCL MED
JI J. Nucl. Med.
PD FEB
PY 2012
VL 53
IS 2
BP 234
EP 240
DI 10.2967/jnumed.111.091694
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 888VN
UT WOS:000300032800014
PM 22238156
ER
PT J
AU Mirabelli, MC
London, SJ
Charles, LE
Pompeii, LA
Wagenknecht, LE
AF Mirabelli, Maria C.
London, Stephanie J.
Charles, Luenda E.
Pompeii, Lisa A.
Wagenknecht, Lynne E.
TI Occupation and the Prevalence of Respiratory Health Symptoms and
Conditions The Atherosclerosis Risk in Communities Study
SO JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE
LA English
DT Article
ID OBSTRUCTIVE PULMONARY-DISEASE; WORK-RELATED ASTHMA; CHRONIC-BRONCHITIS;
CLEANING WORKERS; ONSET ASTHMA; POPULATION; EXPOSURE; BURDEN; ADULTS;
DUST
AB Objectives: To examine associations between occupation and respiratory health in a large, population-based cohort of adults in the United States. Methods: Data from 15,273 participants, aged 45 to 64 years, in the Atherosclerosis Risk in Communities study were used to examine associations of current or most recent job held with the prevalence of self-reported chronic cough, chronic bronchitis, wheezing, asthma, and measures of lung function collected by spirometry. Results: Eleven percent of participants reported wheezing and 9% were classified as having airway obstruction. Compared with individuals in managerial and administrative jobs, increased prevalences of respiratory outcomes were observed among participants in selected occupations, including construction and extractive trades (wheezing, prevalence ratio = 1.92, 95% confidence interval = 1.35, 2.73; airway obstruction, prevalence ratio = 1.31, 95% confidence interval = 1.05, 1.65). Conclusions: Specific occupations are associated with adverse respiratory health.
C1 [Mirabelli, Maria C.] Wake Forest Sch Med, Dept Epidemiol & Prevent, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
[London, Stephanie J.] Natl Inst Environm Hlth Sci, Epidemiol Branch, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA.
[Charles, Luenda E.] NIOSH, Biostat & Epidemiol Branch, Hlth Effects Lab Div, Ctr Dis Control & Prevent,Dept Hlth & Human Serv, Morgantown, WV USA.
[Pompeii, Lisa A.] Univ Texas Sch Publ Hlth, Div Environm & Occupat Hlth Sci, Houston, TX USA.
RP Mirabelli, MC (reprint author), Wake Forest Sch Med, Dept Epidemiol & Prevent, Div Publ Hlth Sci, Winston Salem, NC 27157 USA.
EM mmirabel@wakehealth.edu
OI Mirabelli, Maria/0000-0002-3540-0085; London,
Stephanie/0000-0003-4911-5290
FU National Heart, Lung, and Blood Institute [HHSN268201100005C,
HHSN268201100006C, HHSN268201100007C, HHSN268201100008C,
HHSN268201100009C, HHSN268201100010C, HHSN268201100011C,
HHSN268201100012C]; Division of Intramural Research, National Institute
of Environmental Health Sciences
FX The Atherosclerosis Risk in Communities Study is carried out as a
collaborative study supported by National Heart, Lung, and Blood
Institute contracts (HHSN268201100005C, HHSN268201100006C,
HHSN268201100007C, HHSN268201100008C, HHSN268201100009C,
HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C). Dr. London
is supported by the Division of Intramural Research, National Institute
of Environmental Health Sciences.
NR 41
TC 5
Z9 5
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1076-2752
J9 J OCCUP ENVIRON MED
JI J. Occup. Environ. Med.
PD FEB
PY 2012
VL 54
IS 2
BP 157
EP 165
DI 10.1097/JOM.0b013e31823e3a52
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 891DP
UT WOS:000300197000006
PM 22157701
ER
PT J
AU Raghwani, J
Thomas, XV
Koekkoek, SM
Schinkel, J
Molenkamp, R
van de Laar, TJ
Takebe, Y
Tanaka, Y
Mizokami, M
Rambaut, A
Pybus, OG
AF Raghwani, Jayna
Thomas, Xiomara V.
Koekkoek, Sylvie M.
Schinkel, Janke
Molenkamp, Richard
van de Laar, Thijs J.
Takebe, Yutaka
Tanaka, Yasuhito
Mizokami, Masashi
Rambaut, Andrew
Pybus, Oliver G.
TI Origin and Evolution of the Unique Hepatitis C Virus Circulating
Recombinant Form 2k/1b
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID INTRAVENOUS-DRUG-USERS; MOLECULAR EPIDEMIOLOGY; POPULATION-DYNAMICS; HCV
GENOTYPES; ST-PETERSBURG; INFECTION; SEQUENCES; IDENTIFICATION;
INFERENCE; MODELS
AB Since its initial identification in St. Petersburg, Russia, the recombinant hepatitis C virus (HCV) 2k/1b has been isolated from several countries throughout Eurasia. The 2k/1b strain is the only recombinant HCV to have spread widely, raising questions about the epidemiological background in which it first appeared. In order to further understand the circumstances by which HCV recombinants might be formed and spread, we estimated the date of the recombination event that generated the 2k/1b strain using a Bayesian phylogenetic approach. Our study incorporates newly isolated 2k/1b strains from Amsterdam, The Netherlands, and has employed a hierarchical Bayesian framework to combine information from different genomic regions. We estimate that 2k/1b originated sometime between 1923 and 1956, substantially before the first detection of the strain in 1999. The timescale and the geographic spread of 2k/1b suggest that it originated in the former Soviet Union at about the time that the world's first centralized national blood transfusion and storage service was being established. We also reconstructed the epidemic history of 2k/1b using coalescent theory-based methods, matching patterns previously reported for other epidemic HCV subtypes. This study demonstrates the practicality of jointly estimating dates of recombination from flanking regions of the breakpoint and further illustrates that rare genetic-exchange events can be particularly informative about the underlying epidemiological processes.
C1 [Raghwani, Jayna; Rambaut, Andrew] Univ Edinburgh, Inst Evolutionary Biol, Ashworth Labs, Edinburgh, Midlothian, Scotland.
[Thomas, Xiomara V.; Koekkoek, Sylvie M.; Schinkel, Janke; Molenkamp, Richard] Univ Amsterdam, Acad Med Ctr, Dept Med Microbiol, Sect Clin Virol, NL-1105 AZ Amsterdam, Netherlands.
[van de Laar, Thijs J.] Vrije Univ Amsterdam, Med Ctr, Dept Med Microbiol & Infect Control, Amsterdam, Netherlands.
[Takebe, Yutaka] Natl Inst Infect Dis, AIDS Res Ctr, Tokyo, Japan.
[Tanaka, Yasuhito] Nagoya City Univ, Grad Sch Med Sci, Liver Unit, Nagoya, Aichi, Japan.
[Tanaka, Yasuhito] Nagoya City Univ, Grad Sch Med Sci, Dept Virol, Nagoya, Aichi, Japan.
[Mizokami, Masashi] Natl Ctr Global Hlth & Med, Res Ctr Hepatitis & Immunol, Ichikawa, Japan.
[Rambaut, Andrew] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Pybus, Oliver G.] Univ Oxford, Dept Zool, Oxford OX1 3PS, England.
RP Raghwani, J (reprint author), Univ Edinburgh, Inst Evolutionary Biol, Ashworth Labs, Edinburgh, Midlothian, Scotland.
EM jna.raghwani@gmail.com; oliver.pybus@zoo.ox.ac.uk
RI pybus, oliver/B-2640-2012; Schinkel, Janke/I-3099-2012;
OI Schinkel, Janke/0000-0002-1112-0644; Pybus, Oliver/0000-0002-8797-2667;
Raghwani, Jayna/0000-0001-8538-4995; Rambaut, Andrew/0000-0003-4337-3707
FU Wellcome Trust [095831]
NR 72
TC 19
Z9 22
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 2012
VL 86
IS 4
BP 2212
EP 2220
DI 10.1128/JVI.06184-11
PG 9
WC Virology
SC Virology
GA 886OA
UT WOS:000299862500029
PM 22114341
ER
PT J
AU Qureshi, H
Ma, ZM
Huang, Y
Hodge, G
Thomas, MA
DiPasquale, J
DeSilva, V
Fritts, L
Bett, AJ
Casimiro, DR
Shiver, JW
Robert-Guroff, M
Robertson, MN
McChesney, MB
Gilbert, PB
Miller, CJ
AF Qureshi, Huma
Ma, Zhong-Min
Huang, Ying
Hodge, Gregory
Thomas, Michael A.
DiPasquale, Janet
DeSilva, Veronique
Fritts, Linda
Bett, Andrew J.
Casimiro, Danilo R.
Shiver, John W.
Robert-Guroff, Marjorie
Robertson, Michael N.
McChesney, Michael B.
Gilbert, Peter B.
Miller, Christopher J.
TI Low-Dose Penile SIVmac251 Exposure of Rhesus Macaques Infected with
Adenovirus Type 5 (Ad5) and Then Immunized with a Replication-Defective
Ad5-Based SIV gag/pol/nef Vaccine Recapitulates the Results of the Phase
IIb Step Trial of a Similar HIV-1 Vaccine
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID SIMIAN IMMUNODEFICIENCY VIRUS; CD4(+) T-CELLS;
MAMU-B-ASTERISK-08-POSITIVE MACAQUES; CHALLENGE EXPERIMENTS; VIRAL
REPLICATION; MEDIATED-IMMUNITY; VAGINAL CHALLENGE; MONKEYS; RESPONSES;
EFFICACY
AB The Step Trial showed that the MRKAd5 HIV-1 subtype B Gag/Pol/Nef vaccine did not protect men from HIV infection or reduce setpoint plasma viral RNA (vRNA) levels but, unexpectedly, it did modestly enhance susceptibility to HIV infection in adenovirus types (Ad5)-seropositive, uncircumcised men. As part of the process to understand the results of the Step Trial, we designed a study to determine whether rhesus macaques chronically infected with a host-range mutant Ad5 (Ad5hr) and then immunized with a replication defective Ad5 SIVmac239 Gag/Pol/Nef vaccine were more resistant or susceptible to SIV infection than unimmunized rhesus macaques challenged with a series of escalating dose penile exposures to SIVmac 251. The Ad5 SLY vaccine induced CD8(+) T cell responses in 70% of the monkeys, which is similar to the proportion of humans that responded to the vaccine in the Step Trial. However, the vaccine did not protect vaccinated animals from penile SIV challenge. At the lowest SIV exposure dose (10(3) 50% tissue culture infective doses), 2 of 9 Ad5-seropositive animals immunized with the Ad5 SIV vaccine became infected compared to 0 of 34 animals infected in the other animal groups (naive animals, Ad5-seropositive animals immunized with the empty Ad5 vector, Ad5-seronegative animals immunized with the Ad5 SIV vaccine, and Ad5-seronegative animals immunized with the empty Ad5 vector). Penile exposure to more concentrated virus inocula produced similar rates of infection in all animal groups. Although setpoint viral loads were unaffected in Step vaccinees, the Ad5 SLY-immunized animals had significantly lower acute-phase plasma vRNA levels compared to unimmunized animals. Thus, the results of the nonhuman primate (NHP) study described here recapitulate the lack of protection against HIV acquisition seen in the Step Trial and suggest a greater risk of infection in the Ad5-seropositive animals immunized with the Ad5 SLY vaccine. Further studies are necessary to confirm the enhancement of virus acquisition and to discern associated mechanisms.
C1 [Qureshi, Huma; Ma, Zhong-Min; DeSilva, Veronique; Fritts, Linda; Miller, Christopher J.] Univ Calif Davis, Ctr Comparat Med, Davis, CA 95616 USA.
[Qureshi, Huma; Ma, Zhong-Min; Hodge, Gregory; DeSilva, Veronique; Fritts, Linda; McChesney, Michael B.; Miller, Christopher J.] Univ Calif Davis, Calif Natl Primate Res Ctr, Davis, CA 95616 USA.
[Huang, Ying; Gilbert, Peter B.] Fred Hutchinson Canc Res Ctr, SCHARP, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
[Thomas, Michael A.; DiPasquale, Janet; Robert-Guroff, Marjorie] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Bett, Andrew J.; Casimiro, Danilo R.; Shiver, John W.; Robertson, Michael N.] Merck Res Labs, West Point, PA USA.
RP Miller, CJ (reprint author), Univ Calif Davis, Ctr Comparat Med, Davis, CA 95616 USA.
EM cjmiller@ucdavis.edu
FU Public Health Service from the National Center for Research Resources
[P51RR00169]; National Institute of Allergy and Infectious Diseases [P01
AI8227, R37 AI054165]; NIH, National Cancer Institute
FX This study was supported by Public Health Service grants P51RR00169 from
the National Center for Research Resources, P01 AI8227 (to C.J.M.) and
R37 AI054165 (to P.B.G.) from the National Institute of Allergy and
Infectious Diseases and in part by the Intramural Research Program of
the NIH, National Cancer Institute.
NR 47
TC 52
Z9 54
U1 0
U2 1
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 2012
VL 86
IS 4
BP 2239
EP 2250
DI 10.1128/JVI.06175-11
PG 12
WC Virology
SC Virology
GA 886OA
UT WOS:000299862500032
PM 22156519
ER
PT J
AU Jewell, CM
Scoltock, AB
Hamel, BL
Yudt, MR
Cidlowski, JA
AF Jewell, Christine M.
Scoltock, Alyson B.
Hamel, Brant L.
Yudt, Matthew R.
Cidlowski, John A.
TI Complex Human Glucocorticoid Receptor dim Mutations Define
Glucocorticoid Induced Apoptotic Resistance in Bone Cells
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID DNA-BINDING DOMAIN; NF-KAPPA-B; GENE-EXPRESSION; NUCLEAR RECEPTORS;
TARGET GENES; MECHANISMS; TRANSCRIPTION; REPRESSION; PROTEIN; ANTAGONISM
AB A mutation in the D-loop of the second zinc finger of the DNA-binding domain of the human glucocorticoid receptor (hGR), A458T (GR(dim)), has been suggested to be essential for dimerization and DNA binding of the GR, and genetically altered GR(dim) mice survive, whereas murine GR knockout mice die. Interestingly, thymocytes isolated from the GR(dim) mice were reported to be resistant to glucocorticoid-induced apoptosis. To further evaluate the dim mutations in glucocorticoid-induced apoptosis, we stably expressed either the hGR(dim) (A458T) or the hGR(dim4) (A458T, R460D, D462C, and N454D) mutant receptors in human osteosarcoma (U-2 OS) cells that are devoid of hGR and unresponsive to glucocorticoids. We analyzed these cell lines by comparison with a stable expression hGR alpha U-2 OS cell line, which undergoes apoptosis after glucocorticoid treatment. Transient reporter gene assays with glucocorticoid response element-driven vectors revealed that the hGR(dim) mutation had diminished steroid responsiveness and cells carrying the hGR(dim4) mutation were unresponsive to steroid, whereas glucocorticoid-induced nuclear factor kappa B repression was unaffected by either mutation. Interestingly, both the hGR(dim) and hGR(dim4) receptors readily formed dimers as measured by immunoprecipitation. Examination of GR-mediated apoptosis showed that hGR(dim) cells were only partially resistant to apoptosis, whereas hGR(dim4) cells were completely resistant to glucocorticoid-induced cell death despite remaining sensitive to other apoptotic stimuli. Global gene expression analysis revealed that hGR(dim4) cells widely regulated gene expression but differentially regulated apoptotic mRNA when compared with cells expressing wild-type hGR alpha. These studies challenge conclusions drawn from previous studies of GR dim mutants. (Molecular Endocrinology 26: 244-256, 2012)
C1 [Jewell, Christine M.; Scoltock, Alyson B.; Hamel, Brant L.; Yudt, Matthew R.; Cidlowski, John A.] NIEHS, NIH, Lab Signal Transduct, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Jewell, CM (reprint author), NIEHS, NIH, Lab Signal Transduct, Dept Hlth & Human Serv, 111 TW Alexander Dr,Bldg 101,MD F3-07, Res Triangle Pk, NC 27709 USA.
EM jewell@niehs.nih.gov
FU National Institutes of Health, National Institute of Environmental
Health Sciences
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences.
NR 44
TC 25
Z9 25
U1 0
U2 3
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD FEB
PY 2012
VL 26
IS 2
BP 244
EP 256
DI 10.1210/me.2011-1116
PG 13
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 888LJ
UT WOS:000300004700004
PM 22174376
ER
PT J
AU Anderson, KA
Lin, FM
Ribar, TJ
Stevens, RD
Muehlbauer, MJ
Newgard, CB
Means, AR
AF Anderson, Kristin A.
Lin, Fumin
Ribar, Thomas J.
Stevens, Robert D.
Muehlbauer, Michael J.
Newgard, Christopher B.
Means, Anthony R.
TI Deletion of CaMKK2 from the Liver Lowers Blood Glucose and Improves
Whole-Body Glucose Tolerance in the Mouse
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; FATTY-ACID OXIDATION; INSULIN-RESISTANCE;
HEPATIC GLUCONEOGENESIS; HISTONE DEACETYLASES; MUSCLE; TRANSCRIPTION;
HOMEOSTASIS; BETA; PHOSPHORYLATION
AB Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a member of the Ca2+/CaM-dependent protein kinase family that is expressed abundantly in brain. Previous work has revealed that CaMKK2 knockout (CaMKK2 KO) mice eat less due to a central nervous system -signaling defect and are protected from diet-induced obesity, glucose intolerance, and insulin resistance. However, here we show that pair feeding of wild-type mice to match food consumption of CAMKK2 mice slows weight gain but fails to protect from diet-induced glucose intolerance, suggesting that other alterations in CaMKK2 KO mice are responsible for their improved glucose metabolism. CaMKK2 is shown to be expressed in liver and acute, specific reduction of the kinase in the liver of high-fat diet-fed CaMKK2(floxed) mice results in lowered blood glucose and improved glucose tolerance. Primary hepatocytes isolated from CaMKK2 KO mice produce less glucose and have decreased mRNA encoding peroxisome proliferator-activated receptor gamma coactivator 1-alpha and the gluconeogenic enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase, and these mRNA fail to respond specifically to the stimulatory effect of catecholamine in a cell-autonomous manner. The mechanism responsible for suppressed gene induction in CaMKK2 KO hepatocytes may involve diminished phosphorylation of histone deacetylase 5, an event necessary in some contexts for derepression of the peroxisome proliferator-activated receptor gamma coactivator 1-alpha promoter. Hepatocytes from CaMKK2 KO mice also show increased rates of de novo lipogenesis and fat oxidation. The changes in fat metabolism observed correlate with steatotic liver and altered acyl carnitine metabolomic profiles in CaMKK2 KO mice. Collectively, these results are consistent with suppressed catecholamine-induced induction of gluconeogenic gene expression in CaMKK2 KO mice that leads to improved whole-body glucose homeostasis despite the presence of increased hepatic fat content. (Molecular Endocrinology 26: 281-291, 2012)
C1 [Anderson, Kristin A.] Duke Univ, Sch Med, Dept Pharmacol & Canc Biol, Sarah W Stedman Nutr & Metab Ctr, Durham, NC 27710 USA.
[Stevens, Robert D.; Muehlbauer, Michael J.] Duke Univ, Sch Med, Dept Med Endocrinol & Metab, Sarah W Stedman Nutr & Metab Ctr, Durham, NC 27710 USA.
[Lin, Fumin] NIEHS, Res Triangle Pk, NC USA.
RP Anderson, KA (reprint author), Duke Univ, Sch Med, Dept Pharmacol & Canc Biol, Sarah W Stedman Nutr & Metab Ctr, Durham, NC 27710 USA.
RI LIN, Fumin/D-5709-2015
OI LIN, Fumin/0000-0003-1229-0685
FU NIH [GM033976, P01DK58398]
FX This work was supported by NIH Grants to A. R. M. (GM033976) and to
C.B.N. (P01DK58398).
NR 46
TC 10
Z9 10
U1 0
U2 4
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD FEB
PY 2012
VL 26
IS 2
BP 281
EP 291
DI 10.1210/me.2011-1299
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 888LJ
UT WOS:000300004700007
PM 22240810
ER
PT J
AU Bear, AS
Morgan, RA
Cornetta, K
June, CH
Binder-Scholl, G
Dudley, ME
Feldman, SA
Rosenberg, SA
Shurtleff, SA
Rooney, CM
Heslop, HE
Dotti, G
AF Bear, Adham S.
Morgan, Richard A.
Cornetta, Kenneth
June, Carl H.
Binder-Scholl, Gwendolyn
Dudley, Mark E.
Feldman, Steven A.
Rosenberg, Steven A.
Shurtleff, Sheila A.
Rooney, Cliona M.
Heslop, Helen E.
Dotti, Gianpietro
TI Replication-Competent Retroviruses in Gene-Modified T Cells Used in
Clinical Trials: Is It Time to Revise the Testing Requirements?
SO MOLECULAR THERAPY
LA English
DT Editorial Material
ID APE LEUKEMIA-VIRUS; PACKAGING CELLS; LYMPHOCYTES; VECTORS; THERAPY;
RECEPTORS
C1 [Bear, Adham S.; Rooney, Cliona M.; Heslop, Helen E.; Dotti, Gianpietro] Methodist Hosp, Houston, TX 77030 USA.
[Morgan, Richard A.; Dudley, Mark E.; Feldman, Steven A.; Rosenberg, Steven A.] NCI, Surg Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Cornetta, Kenneth] Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN USA.
[June, Carl H.; Binder-Scholl, Gwendolyn] Univ Penn, Sch Med, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Shurtleff, Sheila A.] St Jude Childrens Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Rooney, Cliona M.; Heslop, Helen E.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
[Rooney, Cliona M.; Dotti, Gianpietro] Baylor Coll Med, Dept Immunol, Houston, TX 77030 USA.
[Heslop, Helen E.; Dotti, Gianpietro] Baylor Coll Med, Dept Med, Houston, TX 77030 USA.
[Bear, Adham S.; Rooney, Cliona M.; Heslop, Helen E.; Dotti, Gianpietro] Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, Houston, TX 77030 USA.
RP Dotti, G (reprint author), Texas Childrens Hosp, Baylor Coll Med, Ctr Cell & Gene Therapy, 6621 Fannin St,MC 3-3320, Houston, TX 77030 USA.
EM gdotti@bcm.edu
FU NCI NIH HHS [P01 CA094237, 3P50CA126752, P01 CA094237-10, P01CA094237,
P50 CA126752, P50 CA126752-05]; NCRR NIH HHS [P40 RR024928, P40
RR024928-03]; NHLBI NIH HHS [5U54HL081007, P40 HL116242, T32 HL092332,
U54 HL081007, U54 HL081007-05]
NR 15
TC 18
Z9 18
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1525-0016
J9 MOL THER
JI Mol. Ther.
PD FEB
PY 2012
VL 20
IS 2
BP 246
EP 249
DI 10.1038/mt.2011.288
PG 4
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA 888CM
UT WOS:000299981400002
PM 22297819
ER
PT J
AU Prescott, J
Wentzensen, IM
Savage, SA
De Vivo, I
AF Prescott, Jennifer
Wentzensen, Ingrid M.
Savage, Sharon A.
De Vivo, Immaculata
TI Epidemiologic evidence for a role of telomere dysfunction in cancer
etiology
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Review
DE Telomere length; Cancer; Epidemiology
ID INCIDENT COLORECTAL-CARCINOMA; BREAST-CANCER; CELLULAR SENESCENCE;
CIGARETTE-SMOKING; BLOOD-CELLS; PREDISPOSITION FACTOR; OXIDATIVE STRESS;
QUANTITATIVE PCR; BLADDER-CANCER; CHROMOSOME 17P
AB Telomeres, the dynamic nucleoprotein structures at the ends of linear chromosomes, maintain the genomic integrity of a cell. Telomere length shortens with age due to the incomplete replication of DNA ends with each cell division as well as damage incurred by oxidative stress. Patterns of telomere shortening, genomic instability, and telomerase expression in many cancer tissues compared to adjacent normal tissue implicate telomere crisis as a common crucial event in malignant transformation. In order to understand the role of telomere length in cancer etiology, most epidemiologic studies have measured average telomere length of peripheral blood or buccal cell DNA as a surrogate tissue biomarker of telomere dysfunction and cancer risk. In this review, we present the results from epidemiologic investigations conducted of telomere length and cancer risk. We note differences in reported associations based on study design, which may be due to biases intrinsic to retrospective studies. Finally, we conclude with study design considerations as future investigations are needed to elucidate the relationship between telomere length and a number of cancer sites. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Prescott, Jennifer; De Vivo, Immaculata] Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab,Dept Med, Boston, MA 02115 USA.
[Prescott, Jennifer; De Vivo, Immaculata] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Prescott, Jennifer; De Vivo, Immaculata] Harvard Univ, Sch Publ Hlth, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Wentzensen, Ingrid M.; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP De Vivo, I (reprint author), Harvard Univ, Brigham & Womens Hosp, Sch Med, Channing Lab,Dept Med, 181 Longwood Ave, Boston, MA 02115 USA.
EM nhjxp@channing.harvard.edu; wentzeni@mail.nih.gov;
savagesh@mail.nih.gov; devivo@channing.harvard.edu
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
FU National Institute of Health [CA65725, CA134958, CA082838]; Division of
Cancer Epidemiology and Genetics, National Cancer Institute, National
Institutes of Health
FX JP and IDV are supported by the National Institute of Health (grants:
CA65725, CA134958, CA082838). This work was supported, in part, by the
intramural research program of the Division of Cancer Epidemiology and
Genetics, National Cancer Institute, National Institutes of Health.
NR 76
TC 39
Z9 39
U1 1
U2 15
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0027-5107
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD FEB 1
PY 2012
VL 730
IS 1-2
SI SI
BP 75
EP 84
DI 10.1016/j.mrfmmm.2011.06.009
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 889MW
UT WOS:000300078800011
PM 21756922
ER
PT J
AU Blank, M
Tang, Y
Yamashita, M
Burkett, SS
Cheng, SY
Zhang, YE
AF Blank, Michael
Tang, Yi
Yamashita, Motozo
Burkett, Sandra S.
Cheng, Steven Y.
Zhang, Ying E.
TI A tumor suppressor function of Smurf2 associated with controlling
chromatin landscape and genome stability through RNF20
SO NATURE MEDICINE
LA English
DT Article
ID UBIQUITIN LIGASE SMURF2; BREAST-CANCER CELLS; HISTONE H2B; DEPENDENT
DEGRADATION; H3 METHYLATION; UBIQUITYLATION; DNA; MONOUBIQUITINATION;
ELONGATION; EXPRESSION
AB In addition to allelic mutations, cancers are known to harbor alterations in their chromatin landscape. Here we show that genomic ablation of Smad ubiquitin regulatory factor 2 (Smurf2), a HECT-domain E3 ubiquitin ligase, results in dysregulation of both the DNA damage response and genomic stability, culminating in increased susceptibility to various types of cancers in aged mice. We show that Smurf2 regulates the monoubiquitination of histone H2B as well as the trimethylation of histone H3 at Lys4 and Lys79 by targeting ring finger protein 20 (RNF20) for proteasomal degradation in both mouse and human cells. We also show that Smurf2 and RNF20 are colocalized at the gamma-H2AX foci of double-stranded DNA breaks in the nucleus. Thus, Smurf2 has a tumor suppression function that normally maintains genomic stability by controlling the epigenetic landscape of histone modifications through RNF20.
C1 [Blank, Michael; Tang, Yi; Yamashita, Motozo; Zhang, Ying E.] NCI, Cellular & Mol Biol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Burkett, Sandra S.] NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA.
[Cheng, Steven Y.] Nanjing Med Univ, Dept Dev Genet, Sch Basic Med Sci, Nanjing, Jiangsu, Peoples R China.
RP Zhang, YE (reprint author), NCI, Cellular & Mol Biol Lab, Ctr Canc Res, Bldg 37, Bethesda, MD 20892 USA.
EM zhangyin@mail.nih.gov
RI Zhang, Ying/G-3657-2015
OI Zhang, Ying/0000-0003-2753-7601
FU US National Cancer Institute, US National Institutes of Health, Center
for Cancer Research; Japan Society for the Promotion of Science
[21689053]
FX We thank M. Anver for pathology services, V. Barr for assistance with
microscope, X. Wu for assistance with the microarray experiments, N.
Morris for the animal husbandry and N. Teja for assistance with cell
culture. We also thank K. Sixt for comments on the manuscript. This
research is supported by the Intramural Research Program of the US
National Cancer Institute, US National Institutes of Health, Center for
Cancer Research. M.Y. was partially supported by the Japan Society for
the Promotion of Science grant 21689053.
NR 38
TC 53
Z9 55
U1 0
U2 14
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD FEB
PY 2012
VL 18
IS 2
BP 227
EP 234
PG 8
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 890JG
UT WOS:000300140300036
PM 22231558
ER
PT J
AU Chen, F
Liu, ZG
Wu, WH
Rozo, C
Bowdridge, S
Millman, A
Van Rooijen, N
Urban, JF
Wynn, TA
Gause, WC
AF Chen, Fei
Liu, Zhugong
Wu, Wenhui
Rozo, Cristina
Bowdridge, Scott
Millman, Ariel
Van Rooijen, Nico
Urban, Joseph F., Jr.
Wynn, Thomas A.
Gause, William C.
TI An essential role for T(H)2-type responses in limiting acute tissue
damage during experimental helminth infection
SO NATURE MEDICINE
LA English
DT Article
ID ALTERNATIVELY ACTIVATED MACROPHAGES; INDUCED PULMONARY INFLAMMATION;
INDUCED LUNG INJURY; NEMATODE PARASITES; T-CELLS; ACUTE SCHISTOSOMIASIS;
ALVEOLAR MACROPHAGES; IMMUNE-RESPONSES; GENE-EXPRESSION; TYPE-2 IMMUNITY
AB Helminths induce potent T helper 2 (T(H)2)-type immune responses that can mediate worm expulsion, but the role of this response in controlling the acute tissue damage caused by migrating multicellular parasites through vital tissues remains uncertain. We used a helminth infection model in which parasitic nematode larvae migrate transiently through the lung, resulting in hemorrhage and inflammation. We found that IL-17 initially contributed to inflammation and lung damage, whereas subsequent IL-4 receptor (IL-4R) signaling reduced elevations in IL-17 mRNA levels, enhanced the expression of insulin-like growth factor 1 (IGF-1) and IL-10 and stimulated the development of M2 macrophages, all of which contributed to the rapid resolution of tissue damage. These studies indicate an essential role for T(H)2-type immune responses in mediating acute wound healing during helminth infection.
C1 [Chen, Fei; Liu, Zhugong; Wu, Wenhui; Rozo, Cristina; Bowdridge, Scott; Millman, Ariel; Gause, William C.] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Med, Newark, NJ 07103 USA.
[Chen, Fei; Liu, Zhugong; Wu, Wenhui; Rozo, Cristina; Bowdridge, Scott; Millman, Ariel; Gause, William C.] Univ Med & Dent New Jersey, New Jersey Med Sch, Ctr Immun & Inflammat, Newark, NJ 07103 USA.
[Van Rooijen, Nico] Vrije Univ Amsterdam, Med Ctr, Dept Mol Cell Biol, Amsterdam, Netherlands.
[Urban, Joseph F., Jr.] ARS, USDA, Beltsville Human Nutr Res Ctr, Diet Genom & Immunol Lab, Beltsville, MD USA.
[Wynn, Thomas A.] NIAID, Parasit Dis Lab, US Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Gause, WC (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Med, Newark, NJ 07103 USA.
EM gausewc@umdnj.edu
RI Wynn, Thomas/C-2797-2011;
OI Urban, Joseph/0000-0002-1590-8869
FU US National Institutes of Health [AI031678]
FX This work was supported by US National Institutes of Health grants
AI031678.
NR 56
TC 150
Z9 152
U1 4
U2 28
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
J9 NAT MED
JI Nat. Med.
PD FEB
PY 2012
VL 18
IS 2
BP 260
EP 266
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 890JG
UT WOS:000300140300040
PM 22245779
ER
PT J
AU Cox, S
Rosten, E
Monypenny, J
Jovanovic-Talisman, T
Burnette, DT
Lippincott-Schwartz, J
Jones, GE
Heintzmann, R
AF Cox, Susan
Rosten, Edward
Monypenny, James
Jovanovic-Talisman, Tijana
Burnette, Dylan T.
Lippincott-Schwartz, Jennifer
Jones, Gareth E.
Heintzmann, Rainer
TI Bayesian localization microscopy reveals nanoscale podosome dynamics
SO NATURE METHODS
LA English
DT Article
ID HIDDEN MARKOV-MODELS; FLUORESCENCE MICROSCOPY; LIVE CELLS;
SUPERRESOLUTION; STORM; LIMIT
AB We describe a localization microscopy analysis method that is able to extract results in live cells using standard fluorescent proteins and xenon arc lamp illumination. Our Bayesian analysis of the blinking and bleaching (38 analysis) method models the entire dataset simultaneously as being generated by a number of fluorophores that may or may not be emitting light at any given time. The resulting technique allows many overlapping fluorophores in each frame and unifies the analysis of the Localization from blinking and bleaching events. By modeling the entire dataset, we were able to use each reappearance of a fluorophore to improve the localization accuracy. The high performance of this technique allowed us to reveal the nanoscale dynamics of podosome formation and dissociation throughout an entire cell with a resolution of 50 nm on a 4-s timescale.
C1 [Cox, Susan; Monypenny, James; Jones, Gareth E.; Heintzmann, Rainer] Kings Coll London, Randall Div, London WC2R 2LS, England.
[Rosten, Edward] Univ Cambridge, Dept Engn, Cambridge CB2 1PZ, England.
[Rosten, Edward] Comp Vis Consulting Ltd, Woking, Surrey, England.
[Jovanovic-Talisman, Tijana; Burnette, Dylan T.; Lippincott-Schwartz, Jennifer] NIH, Cell Biol & Metab Branch, Bethesda, MD 20892 USA.
[Heintzmann, Rainer] Univ Jena, Inst Phys Chem, D-6900 Jena, Germany.
[Heintzmann, Rainer] Inst Photon Technol, Jena, Germany.
RP Cox, S (reprint author), Kings Coll London, Randall Div, Guys Campus, London WC2R 2LS, England.
EM susan.cox@kcl.ac.uk
RI Heintzmann, Rainer/I-5667-2012; Jones, Gareth/H-2282-2012;
OI Jones, Gareth/0000-0001-5879-3048; Jovanovic-Talisman,
Tijana/0000-0003-1928-4763
FU EU [GA 215597, ITN 237946 T3Ne]; Wellcome Trust; Medical Research
Council (UK); Royal Society
FX We acknowledge helpful discussions with A. Fraser, F. Viola, P.
Fox-Roberts, O. Mandula and J. Sleep. We thank M. Kielhorn for
assistance in aligning the optical system and K. Glocer for critical
reading of the manuscript. We thank M. Parsons (King's College London)
for providing the template pLasmid. We acknowledge support from the EU
Seventh Framework Programme (FP7 Project GA 215597 (S.C. and R.H.), EU.
FP7 Project ITN 237946 T3Net (G.E.J.)), the Wellcome Trust (S.C., J.M.
and G.E.J.), the Medical Research Council (UK) (G.E.J.) and the Royal
Society (S.C.).
NR 25
TC 135
Z9 140
U1 4
U2 52
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1548-7091
J9 NAT METHODS
JI Nat. Methods
PD FEB
PY 2012
VL 9
IS 2
BP 195
EP 200
DI 10.1038/NMETH.1812
PG 6
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 888UH
UT WOS:000300029600033
ER
PT J
AU Sheng, ZH
Cai, Q
AF Sheng, Zu-Hang
Cai, Qian
TI Mitochondrial transport in neurons: impact on synaptic homeostasis and
neurodegeneration
SO NATURE REVIEWS NEUROSCIENCE
LA English
DT Review
ID AMYOTROPHIC-LATERAL-SCLEROSIS; DYNAMIN-RELATED PROTEIN-1; FAST
AXONAL-TRANSPORT; AUTOPHAGY-LYSOSOMAL FUNCTION; KINESIN HEAVY-CHAIN;
NERVE GROWTH-FACTOR; CYTOPLASMIC DYNEIN; IN-VIVO; HIPPOCAMPAL-NEURONS;
LIGHT-CHAIN
AB Mitochondria have a number of essential roles in neuronal function. Their complex mobility patterns within neurons are characterized by frequent changes in direction. Mobile mitochondria can become stationary or pause in regions that have a high metabolic demand and can move again rapidly in response to physiological changes. Defects in mitochondrial transport are implicated in the pathogenesis of several major neurological disorders. Research into the mechanisms that regulate mitochondrial transport is thus an important emerging frontier.
C1 [Sheng, Zu-Hang; Cai, Qian] NINDS, Synapt Funct Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
[Cai, Qian] Rutgers State Univ, Dept Cell Biol & Neurosci, Piscataway, NJ 08854 USA.
RP Sheng, ZH (reprint author), NINDS, Synapt Funct Sect, Porter Neurosci Res Ctr, NIH, Room 28-215,35 Convent Dr, Bethesda, MD 20892 USA.
EM shengz@ninds.nih.gov
FU US National Institute of Neurological Disorder and Stroke (NINDS); US
National Institutes of Health (NIH); NIH [K99]
FX The authors thank M. Davis for editing and other members of the Sheng
laboratory for their assistance and discussion. This work was supported
by the Intramural Research Program of the US National Institute of
Neurological Disorder and Stroke (NINDS), US National Institutes of
Health (NIH) (Z.-H.S.) and the NIH Pathway to Independence Award K99
(Q.C.).
NR 179
TC 201
Z9 208
U1 9
U2 59
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-003X
EI 1471-0048
J9 NAT REV NEUROSCI
JI Nat. Rev. Neurosci.
PD FEB
PY 2012
VL 13
IS 2
BP 77
EP 93
DI 10.1038/nrn3156
PG 17
WC Neurosciences
SC Neurosciences & Neurology
GA 888AN
UT WOS:000299976300007
PM 22218207
ER
PT J
AU Kales, SC
Ryan, PE
Lipkowitz, S
AF Kales, Stephen C.
Ryan, Philip E.
Lipkowitz, Stanley
TI Cbl exposes its RING finger
SO NATURE STRUCTURAL & MOLECULAR BIOLOGY
LA English
DT Editorial Material
ID INDUCED CONFORMATIONAL-CHANGE; UBIQUITIN-CONJUGATING ENZYME;
GROWTH-FACTOR RECEPTOR; T-CELLS; LIGASE ACTIVITY; C-CBL; PROTEIN LIGASE;
DOMAIN; KINASE; ACTIVATION
AB The Cbl family of RING finger ubiquitin ligases regulates signaling in many systems. Two new studies provide a structural basis for how phosphorylation of a specific tyrosine in the Cbl proteins enhances their ubiquitin ligase activity, giving insight into how ubiquitination by Cbl proteins is restricted to specific substrates.
C1 [Kales, Stephen C.; Ryan, Philip E.; Lipkowitz, Stanley] NCI, Cellular & Mol Biol Lab, Ctr Canc Res, US Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Kales, SC (reprint author), NCI, Cellular & Mol Biol Lab, Ctr Canc Res, US Natl Inst Hlth, Bldg 37, Bethesda, MD 20892 USA.
EM lipkowis@mail.nih.gov
NR 29
TC 11
Z9 11
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1545-9993
J9 NAT STRUCT MOL BIOL
JI Nat. Struct. Mol. Biol.
PD FEB
PY 2012
VL 19
IS 2
BP 131
EP 133
PG 3
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 888UF
UT WOS:000300029400002
PM 22301873
ER
PT J
AU Martiniova, L
Cleary, S
Lai, EW
Kiesewetter, DO
Seidel, J
Dawson, LF
Phillips, JK
Thomasson, D
Chen, XY
Eisenhofer, G
Powers, JF
Kvetnansky, R
Pacak, K
AF Martiniova, Lucia
Cleary, Susannah
Lai, Edwin W.
Kiesewetter, Dale O.
Seidel, Jurgen
Dawson, Linda F.
Phillips, Jacqueline K.
Thomasson, David
Chen, Xiaoyuan
Eisenhofer, Graeme
Powers, James F.
Kvetnansky, Richard
Pacak, Karel
TI Usefulness of [F-18]-DA and [F-18]-DOPA for PET imaging in a mouse model
of pheochromocytoma
SO NUCLEAR MEDICINE AND BIOLOGY
LA English
DT Article
DE Pheochromocytoma; PET; MicroCT; MRI; Metastatic mice model;
Fluorodopamine; Fluorodopa; Norepinephrine transporter; Vesicular
monoamine transporter
ID POSITRON-EMISSION-TOMOGRAPHY; VESICULAR MONOAMINE TRANSPORTER;
METASTATIC PHEOCHROMOCYTOMA; NORADRENALINE TRANSPORTER; CONTRAST
ENHANCEMENT; ENDOCRINE-CELLS; EXPRESSION; LOCALIZATION; TUMORS; PLASMA
AB Purpose: To evaluate the usefulness of [F-18]-6-fluorodopamine ([F-18]-DA) and [F-18]-L-6-fluoro-3,4-dihydroxyphenylalanine ([F-18-DOPA) positron emission tomography (PET) in the detection of subcutaneous (s.c.) and metastatic pheochromocytoma in mice; to assess the expression of the norepinephrine transporter (NET) and vesicular monoamine transporters I and 2 (VMAT1 and VMAT2), all important for [F-18]-DA and [F-18]-DOPA uptake. Furthermore, to compare tumor detection by micro-computed tomography (microCT) to magnetic resonance imaging (MRI) in individual mouse.
Methods: SUVmax values were calculated from [F-18]-DA and [F-18]-DOPA PET, tumor-to-liver ratios (TLR) were obtained and expression of NET, VMAT1 and VMAT2 was evaluated.
Results: [F-18]-DA detected less metastatic lesions compared to [F-18]-DOPA. TLR values for liver metastases were 2.26-2.71 for [F-18]-DOPA and 1.83-2.83 for [F-18]-DA. A limited uptake of [F-18]-DA was found in s.c. tumors (TLR=0.22-0.27) compared to [F-18]-DOPA (TLR=1.56-2.24). Overall, NET and VMAT2 were expressed in all organ and s.c. tumors. However, s.c. tumors lacked expression of VMAT1. We confirmed [F-18]-DA's high affinity for the NET for its uptake and VMAT1 and VMAT2 for its storage and retention in pheochromocytoma cell vesicles. In contrast, [F-18]-DOPA was found to utilize only VMAT2.
Conclusion: MRI was superior in the detection of all organ tumors compared to microCT and PET. [F-18]-DOPA had overall better sensitivity than [F-18]-DA for the detection of metastases. Subcutaneous tumors were localized only with [F-18]-DOPA, a finding that may reflect differences in expression of VMAT1 and VMAT2, perhaps similar to some patients with pheochromocytoma where [F-18]-DOPA provides better visualization of lesions than [F-18]-DA. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Martiniova, Lucia; Lai, Edwin W.; Pacak, Karel] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20892 USA.
[Cleary, Susannah] Natl Inst Neurol Disorders & Stroke, Clin Neurocardiol Sect, NIH, Bethesda, MD 20892 USA.
[Kiesewetter, Dale O.; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
[Seidel, Jurgen] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Dawson, Linda F.; Phillips, Jacqueline K.] Murdoch Univ, Fac Hlth Sci, Perth, WA 6150, Australia.
[Phillips, Jacqueline K.] Macquarie Univ, Australian Sch Adv Med, Sydney, NSW 2109, Australia.
[Thomasson, David] NIH, Lab Diagnost Radiol, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Eisenhofer, Graeme] Univ Dresden, Dept Med, D-01307 Dresden, Germany.
[Eisenhofer, Graeme] Univ Dresden, Inst Clin Chem & Lab Med, D-01307 Dresden, Germany.
[Powers, James F.] Tufts Med Ctr, Dept Pathol, Boston, MA 02111 USA.
[Martiniova, Lucia; Kvetnansky, Richard] Slovak Acad Sci, Inst Expt Endocrinol, SK-83306 Bratislava, Slovakia.
RP Pacak, K (reprint author), NICHD, NIH, 10 Ctr Dr,MSC-1109, Bethesda, MD 20892 USA.
EM karel@mail.nih.gov
OI Phillips, Jacqueline/0000-0002-4917-7734
FU Eunice Kennedy Shriver National Institutes of Child Health and Human
Development; Warren Grant Magnuson Clinical Center; National Institute
of Neurological Disorders and Stroke; National Institute of Biomedical
Imaging and Bioengineering, National Cancer Institute; PheoPara
Alliance; [APVV-0148-06]
FX We would like to acknowledge the valuable assistance of the colleagues
in our group; we thank Mr. Stephen Uyeno and Mr. Eli Thompson for their
assistance with animals. This research was supported (in part) by the
Intramural Research Program of the Eunice Kennedy Shriver National
Institutes of Child Health and Human Development, Warren Grant Magnuson
Clinical Center, National Institute of Neurological Disorders and
Stroke, National Institute of Biomedical Imaging and Bioengineering,
National Cancer Institute, by the grant from the PheoPara Alliance (to
J.P.) and APVV-0148-06 (to R.K.). The authors have no conflict of
interest to disclose.
NR 44
TC 7
Z9 7
U1 1
U2 8
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0969-8051
J9 NUCL MED BIOL
JI Nucl. Med. Biol.
PD FEB
PY 2012
VL 39
IS 2
BP 215
EP 226
DI 10.1016/j.nucmedbio.2011.07.007
PG 12
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 890BY
UT WOS:000300121300006
PM 21958851
ER
PT J
AU Machado-Vieira, R
Ibrahim, L
Henter, LD
Zarate, CA
AF Machado-Vieira, Rodrigo
Ibrahim, Lobna
Henter, Loline D.
Zarate, Carlos A., Jr.
TI Novel glutamatergic agents for major depressive disorder and bipolar
disorder
SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
LA English
DT Review
DE Bipolar disorder; Depression; Glutamate; Mood disorders; Novel
treatments; Pathophysiology
ID MAGNETIC-RESONANCE-SPECTROSCOPY; D-ASPARTATE ANTAGONIST; OPEN-LABEL
TRIAL; STAR-ASTERISK-D; SEROTONIN REUPTAKE INHIBITORS;
OBSESSIVE-COMPULSIVE DISORDER; RAPID ANTIDEPRESSANT RESPONSE; ANTERIOR
CINGULATE ACTIVITY; MGLU5 RECEPTOR ANTAGONIST; GAMMA-AMINOBUTYRIC-ACID
AB Mood disorders such as major depressive disorder (MDD) and bipolar disorder (BPD) are common, chronic, recurrent mental illnesses that affect the lives and functioning of millions of individuals worldwide. Growing evidence suggests that the glutamatergic system is central to the neurobiology and treatment of these disorders. Here, we review data supporting the involvement of the glutamatergic system in the pathophysiology of mood disorders as well as the efficacy of glutamatergic agents as novel therapeutics. Published by Elsevier Inc.
C1 [Ibrahim, Lobna; Zarate, Carlos A., Jr.] NIMH, Expt Therapeut & Pathophysiol Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Machado-Vieira, Rodrigo] Univ Sao Paulo, Sch Med, L1M 27, Inst & Dept Psychiat,USP, Sao Paulo, Brazil.
[Henter, Loline D.] NIMH, Mol Imaging Branch, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Zarate, CA (reprint author), 10 Ctr Dr,CRC,7 Southeast Unit,Rm 7-3465, Bethesda, MD 20892 USA.
EM zaratec@intra.nimh.nih.gov
RI MACHADO-VIEIRA, RODRIGO/D-8293-2012
OI MACHADO-VIEIRA, RODRIGO/0000-0002-4830-1190
FU National Institute of Mental Heath, National Institutes of Health
(NIMH-NIH)
FX The authors gratefully acknowledge the support of the Intramural
Research Program of the National Institute of Mental Heath, National
Institutes of Health (IRP-NIMH-NIH). Dr. Zarate is listed among the
inventors on a patent application submitted for the use of ketamine in
depression. He has assigned his rights on the patent to the US
government. The authors have no conflict of interest to disclose,
financial or otherwise.
NR 178
TC 39
Z9 40
U1 3
U2 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0091-3057
J9 PHARMACOL BIOCHEM BE
JI Pharmacol. Biochem. Behav.
PD FEB
PY 2012
VL 100
IS 4
SI SI
BP 678
EP 687
DI 10.1016/j.pbb.2011.09.010
PG 10
WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy
SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy
GA 888UE
UT WOS:000300029300004
PM 21971560
ER
PT J
AU Bentolila, S
Stefanov, S
AF Bentolila, Stephane
Stefanov, Stefan
TI A Reevaluation of Rice Mitochondrial Evolution Based on the Complete
Sequence of Male-Fertile and Male-Sterile Mitochondrial Genomes
SO PLANT PHYSIOLOGY
LA English
DT Article
ID CYTOPLASMIC MALE-STERILITY; ARABIDOPSIS-THALIANA; DNA-MOLECULES; MAIZE;
GENE; PLANTS; RECOMBINATION; RESTORER; MUTANT; ORYZA
AB Plant mitochondrial genomes have features that distinguish them radically from their animal counterparts: a high rate of rearrangement, of uptake and loss of DNA sequences, and an extremely low point mutation rate. Perhaps the most unique structural feature of plant mitochondrial DNAs is the presence of large repeated sequences involved in intramolecular and intermolecular recombination. In addition, rare recombination events can occur across shorter repeats, creating rearrangements that result in aberrant phenotypes, including pollen abortion, which is known as cytoplasmic male sterility (CMS). Using next-generation sequencing, we pyrosequenced two rice (Oryza sativa) mitochondrial genomes that belong to the indica subspecies. One genome is normal, while the other carries the wild abortive-CMS. We find that numerous rearrangements in the rice mitochondrial genome occur even between close cytotypes during rice evolution. Unlike maize (Zea mays), a closely related species also belonging to the grass family, integration of plastid sequences did not play a role in the sequence divergence between rice cytotypes. This study also uncovered an excellent candidate for the wild abortive-CMS-encoding gene; like most of the CMS-associated open reading frames that are known in other species, this candidate was created via a rearrangement, is chimeric in structure, possesses predicted transmembrane domains, and coopted the promoter of a genuine mitochondrial gene. Our data give new insights into rice mitochondrial evolution, correcting previous reports.
C1 [Bentolila, Stephane] Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA.
[Stefanov, Stefan] Natl Lib Med, Bethesda, MD 20892 USA.
RP Bentolila, S (reprint author), Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA.
EM sb46@cornell.edu
RI Bentolila, Stephane/P-2361-2015
OI Bentolila, Stephane/0000-0003-2805-7298
FU U.S. Department of Agriculture National Research Initiative
[2006-35301-16889]
FX This work was supported by the U.S. Department of Agriculture National
Research Initiative (grant no. 2006-35301-16889 to S.B.).
NR 54
TC 34
Z9 38
U1 0
U2 16
PU AMER SOC PLANT BIOLOGISTS
PI ROCKVILLE
PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 USA
SN 0032-0889
J9 PLANT PHYSIOL
JI Plant Physiol.
PD FEB
PY 2012
VL 158
IS 2
BP 996
EP 1017
DI 10.1104/pp.111.190231
PG 22
WC Plant Sciences
SC Plant Sciences
GA 889DS
UT WOS:000300054300037
PM 22128137
ER
PT J
AU Averbeck, BB
Bobin, T
Evans, S
Shergill, SS
AF Averbeck, B. B.
Bobin, T.
Evans, S.
Shergill, S. S.
TI Emotion recognition and oxytocin in patients with schizophrenia
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Emotion; faces; oxytocin; schizophrenia; social
ID MICROTUS-OCHROGASTER; MATERNAL-BEHAVIOR; HUMANS; FACES; VASOPRESSIN;
IDENTITY; VALENCE; MEMORY; BRAIN; RATS
AB Background. Studies have suggested that patients with schizophrenia are impaired at recognizing emotions. Recently, it has been shown that the neuropeptide oxytocin can have beneficial effects on social behaviors.
Method. To examine emotion recognition deficits in patients and see whether oxytocin could improve these deficits, we carried out two experiments. In the first experiment we recruited 30 patients with schizophrenia and 29 age-and IQ-matched control subjects, and gave them an emotion recognition task. Following this, we carried out a second experiment in which we recruited 21 patients with schizophrenia for a double-blind, placebo-controlled cross-over study of the effects of oxytocin on the same emotion recognition task.
Results. In the first experiment we found that patients with schizophrenia had a deficit relative to controls in recognizing emotions. In the second experiment we found that administration of oxytocin improved the ability of patients to recognize emotions. The improvement was consistent and occurred for most emotions, and was present whether patients were identifying morphed or non-morphed faces.
Conclusions. These data add to a growing literature showing beneficial effects of oxytocin on social-behavioral tasks, as well as clinical symptoms. Received 10 May 2011; Revised 5 July 2011; Accepted 6 July 2011; First published online 11 August 2011
C1 [Averbeck, B. B.] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
[Bobin, T.; Shergill, S. S.] Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
[Bobin, T.; Shergill, S. S.] Kings Coll London, Imaging Lab, Dept Psychosis Studies, London WC2R 2LS, England.
[Evans, S.] UCL, Sobell Dept Motor Neurosci & Movement Disorders, Inst Neurol, London, England.
RP Averbeck, BB (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 9, Bethesda, MD 20892 USA.
EM averbeckbb@mail.nih.gov
FU Medical Research Council (MRC); National Institutes of Health (NIH),
National Institute of Mental Health; GlaxoSmith-Kline
FX The authors wish to thank all the volunteers who participated in this
study. This work was supported by a Medical Research Council (MRC)
project grant to S.S.S. and this work was also supported in part by the
Intramural Program of the National Institutes of Health (NIH), National
Institute of Mental Health.; S.S.S. has received compensation from
GlaxoSmith-Kline over the past 3 years.
NR 42
TC 33
Z9 35
U1 1
U2 21
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD FEB
PY 2012
VL 42
IS 2
BP 259
EP 266
DI 10.1017/S0033291711001413
PG 8
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 886XL
UT WOS:000299887700004
PM 21835090
ER
PT J
AU Young, KD
Erickson, K
Nugent, AC
Fromm, SJ
Mallinger, AG
Furey, ML
Drevets, WC
AF Young, K. D.
Erickson, K.
Nugent, A. C.
Fromm, S. J.
Mallinger, A. G.
Furey, M. L.
Drevets, W. C.
TI Functional anatomy of autobiographical memory recall deficits in
depression
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Anterior insula; autobiographical memory; depression; fMRI; hippocampus
ID MAJOR DEPRESSION; BIPOLAR DISORDER; CINGULATE CORTEX; PERSONAL EVENTS;
MOOD CHALLENGE; RETRIEVAL; BRAIN; FMRI; NEUROANATOMY; HIPPOCAMPUS
AB Background. Major depressive disorder (MDD) is associated with deficits in recalling specific autobiographical memories (AMs). Extensive research has examined the functional anatomical correlates of AM in healthy humans, but no studies have examined the neurophysiological underpinnings of AM deficits in MDD. The goal of the present study was to examine the differences in the hemodynamic response between patients with MDD and controls while they engage in AM recall.
Method. Participants (12 unmedicated MDD patients; 14 controls) underwent functional magnetic resonance imaging (fMRI) scanning while recalling AMs in response to positive, negative and neutral cue words. The hemodynamic response during memory recall versus performing subtraction problems was compared between MDD patients and controls. Additionally, a parametric linear analysis examined which regions correlated with increasing arousal ratings.
Results. Behavioral results showed that relative to controls, the patients with MDD had fewer specific (p = 0.013), positive (p = 0.030), highly arousing (p = 0.036) and recent (p = 0.020) AMs, and more categorical (p < 0.001) AMs. The blood oxygen level-dependent (BOLD) response in the parahippocampus and hippocampus was higher for memory recall versus subtraction in controls and lower in those with MDD. Activity in the anterior insula was lower for specific AM recall versus subtraction, with the magnitude of the decrement greater in MDD patients. Activity in the anterior cingulate cortex was positively correlated with arousal ratings in controls but not in patients with MDD.
Conclusions. We replicated previous findings of fewer specific and more categorical AMs in patients with MDD versus controls. We found differential activity in medial temporal and prefrontal lobe structures involved in AM retrieval between MDD patients and controls as they engaged in AM recall. These neurophysiological deficits may underlie AM recall impairments seen in MDD. Received 6 January 2011; Revised 13 June 2011; Accepted 23 June 2011; First published online 29 July 2011
C1 [Young, K. D.; Drevets, W. C.] Laureate Inst Brain Res, Tulsa, OK 74136 USA.
[Young, K. D.; Erickson, K.; Nugent, A. C.; Fromm, S. J.; Mallinger, A. G.; Furey, M. L.; Drevets, W. C.] NIMH, NIH, Sect Neuroimaging Mood & Anxiety Disorders, Bethesda, MD 20892 USA.
[Drevets, W. C.] Univ Oklahoma, Coll Med, Dept Psychiat, Tulsa, OK USA.
RP Young, KD (reprint author), Laureate Inst Brain Res, 6655 S Yale Ave, Tulsa, OK 74136 USA.
EM kyoung@laureateinstitute.org
RI Furey, Maura/H-5273-2013;
OI Nugent, Allison/0000-0003-2569-2480; Young, Kymberly/0000-0001-5133-2142
FU National Institutes of Health, National Institute of Mental Health
(NIMH) [Z01-MH002792]; NIMH
FX Grant support for the work was provided by the National Institutes of
Health, National Institute of Mental Health (NIMH), via grant no.
Z01-MH002792. The NIMH Division of Intramural Research Programs (DIRP)
arranged peer review of the study design, provided IRB oversight of the
data collection, management and analysis, and approved submission of the
manuscript for publication. However, this sponsor did not influence
directly the interpretation of the results or preparation of the
manuscript.; We thank Dr Harvey Iwamoto for programming the AM task,
Joan Williams and Michele Drevets for assistance with recruitment and
clinical assessment of the participants, and Jeanette Black and Renee
Hill for MRI technologist support. We also acknowledge the support of
the NIMH Intramural Research Program.
NR 59
TC 29
Z9 30
U1 5
U2 17
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD FEB
PY 2012
VL 42
IS 2
BP 345
EP 357
DI 10.1017/S0033291711001371
PG 13
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 886XL
UT WOS:000299887700012
PM 21798113
ER
PT J
AU Magnusson, A
Lundholm, C
Goransson, M
Copeland, W
Heilig, M
Pedersen, NL
AF Magnusson, A.
Lundholm, C.
Goransson, M.
Copeland, W.
Heilig, M.
Pedersen, N. L.
TI Familial influence and childhood trauma in female alcoholism
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Alcohol dependence; childhood trauma; early onset; female twins;
heritability
ID CROSS-FOSTERING ANALYSIS; SUBSTANCE USE DISORDERS; SEXUAL-ABUSE; TWIN
SAMPLE; WOMEN; ASSOCIATION; DEPENDENCE; ONSET; RISK; REPLICATION
AB Background. To assess the role of genetic and environmental factors in female alcoholism using a large population-based twin sample, taking into account possible differences between early and late onset disease subtype.
Method. Twins aged 20-47 years from the Swedish Twin Registry (n = 24 119) answered questions to establish lifetime alcohol use disorders. Subjects with alcoholism were classified for subtype. Structural equation modeling was used to quantify the proportion of phenotypic variance due to genetic and environmental factors and test whether heritability in women differed from that in men. The association between childhood trauma and alcoholism was then examined in females, controlling for background familial factors.
Results. Lifetime prevalence of alcohol dependence was 4.9% in women and 8.6% in men. Overall, heritability for alcohol dependence was 55%, and did not differ significantly between men and women, although women had a significantly greater heritability for late onset (type I). Childhood physical trauma and sexual abuse had a stronger association with early onset compared to late onset alcoholism [odds ratio (OR) 2.54, 95% confidence interval (CI) 1.53-3.88 and OR 2.29, 95% CI 1.38-3.79 respectively]. Co-twin analysis indicated that familial factors largely accounted for the influence of physical trauma whereas the association with childhood sexual abuse reflected both familial and specific effects.
Conclusions. Heritability of alcoholism in women is similar to that in men. Early onset alcoholism is strongly association with childhood trauma, which seems to be both a marker of familial background factors and a specific individual risk factor per se. Received 17 September 2010; Revised 20 June 2011; Accepted 25 June 2011; First published online 29 July 2011
C1 [Magnusson, A.; Goransson, M.; Heilig, M.] Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden.
[Lundholm, C.; Pedersen, N. L.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Copeland, W.] Duke Univ, Ctr Dev Epidemiol, Durham, NC USA.
[Heilig, M.] NIAAA, Lab Clin & Translat Studies, Bethesda, MD USA.
RP Magnusson, A (reprint author), Karolinska Univ Sjukhuset, BCS Ctr Dependence Disorders Stockholm I 66, S-14186 Stockholm, Sweden.
EM asa.magnusson@sll.se
RI copeland, william/N-5413-2014;
OI Lundholm, Cecilia/0000-0002-6546-3650
FU Swedish Department of Higher Education; Swedish Research Council;
AstraZeneca; County of Stockholm; National Institute on Alcohol Abuse
and Alcoholism
FX The Swedish Twin Registry is supported by grants from the Swedish
Department of Higher Education and the Swedish Research Council, and an
unrestricted research grant from AstraZeneca. This work was also
supported by funding from the County of Stockholm and the National
Institute on Alcohol Abuse and Alcoholism intramural research funds.
NR 40
TC 10
Z9 10
U1 6
U2 13
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD FEB
PY 2012
VL 42
IS 2
BP 381
EP 389
DI 10.1017/S0033291711001310
PG 9
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 886XL
UT WOS:000299887700015
PM 21798111
ER
PT J
AU Dettmer, AM
Novak, MA
Suomi, SJ
Meyer, JS
AF Dettmer, Amanda M.
Novak, Melinda A.
Suomi, Stephen J.
Meyer, Jerrold S.
TI Physiological and behavioral adaptation to relocation stress in
differentially reared rhesus monkeys: Hair cortisol as a biomarker for
anxiety-related responses
SO PSYCHONEUROENDOCRINOLOGY
LA English
DT Article
DE Hair; Cortisol; Infant; Early experience; Anxiety; Development
ID CORTICOTROPIN-RELEASING-FACTOR; CSF MONOAMINE METABOLITE;
CEREBROSPINAL-FLUID; NONHUMAN-PRIMATES; PLASMA-CORTISOL; MACACA-MULATTA;
EMOTIONAL REACTIVITY; REARING EXPERIENCES; SEPARATION; NEUROENDOCRINE
AB Increased hair cortisol concentrations have been associated with stress exposure in both human and nonhuman primates, and hair cortisol is now gaining attention as a biomarker for stress-related health problems. The present study examined the behavioral and physiological reactions of rhesus monkey (Macoca mulatto) infants reared in three different rearing environments to the major stressor of relocation. Infant monkeys (n = 61) were studied from birth through 2 years of age. For the first 8 months of life, infants were either with their mothers and peers (MPR, n = 21) or reared in a nursery using either peer-rearing (PR, n = 20) or surrogate-peer-rearing (SPR, n = 20). At approximately 8 months of age, infants were removed from their rearing group, simultaneously placed into a large social environment consisting of infants from all three rearing conditions, and observed for the next 16 months. Behavior was recorded twice per week from 1 to 24 months, and composite anxiety scores were calculated for each monkey. Monkeys were initially shaved at the nape of the neck on day 14 to remove any prenatal effects on hair cortisol deposition. Hair samples were then collected by re-shaving at 6, 12, 18 and 24 months and analyzed for cortisol content. MPR monkeys were the least affected by the stressor, showing smaller increases in anxious behavior than the other groups and more rapid physiological adaptation as assessed using hair cortisol. PR monkeys showed heightened and prolonged anxious behavior, had the highest cortisol levels prior to relocation, and their cortisol levels did not decline until more than a year later. SPR monkeys exhibited more rapid behavioral adaptation than PR monkeys, showing heightened but not prolonged anxious behavior. However, the SPR group showed a marked increase in cortisol in response to the relocation, and like the PR group, their physiological adaptation was slower than that of the MPR group as indicated by elevated cortisol levels at 18 months. By 24 months of age (16 months after relocation), all rearing groups were indistinguishable from one another physiologically and behaviorally. Spearman rank correlation revealed that hair cortisol taken at month 6 was not correlated with composite anxiety scores from months 6 to 8 (just before the relocation), but was positively correlated with composite anxiety scores between months 8 and 12 (immediately after relocation) for PR infants only (r(s) = 0.75, p < 0.001). Month 6-hair cortisol tended to positively correlate with composite anxiety scores for the following 6 months (months 12-18) for PR monkeys only (r(s), = 0.47, p = 0.037), which exhibited more anxious behavior than MPR and SPR infants during this period (ANOVA: F-(2,F-60) = 14.761, p < 0.001) This is the first study to show that elevated hair cortisol early in life is a biomarker for the later development of anxious behavior in response to a major life stressor, particularly for infant monkeys exposed to early life adversity in the form of peer-rearing. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Dettmer, Amanda M.] Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15213 USA.
[Novak, Melinda A.; Meyer, Jerrold S.] Univ Massachusetts, Dept Psychol, Amherst, MA 01003 USA.
[Suomi, Stephen J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, NIH, Bethesda, MD USA.
RP Dettmer, AM (reprint author), Univ Pittsburgh, Dept Psychiat, 3811 Ohara St, Pittsburgh, PA 15213 USA.
EM ame48@pitt.edu
OI Meyer, Jerrold/0000-0002-8382-7075
FU Division of Intramural Research, National Institute of Child Health Et
Human Development, NIH; NIH [RR11122]
FX This research was supported by funds from the Division of Intramural
Research, National Institute of Child Health Et Human Development, NIH,
and by NIH Grant RR11122 to M.A.N. Neither the NIH nor the NICHD had any
further role in study design; in the collection, analysis and
interpretation of data; in the writing of the report; and in the
decision to submit the paper for publication.
NR 47
TC 44
Z9 45
U1 3
U2 27
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4530
J9 PSYCHONEUROENDOCRINO
JI Psychoneuroendocrinology
PD FEB
PY 2012
VL 37
IS 2
BP 191
EP 199
DI 10.1016/j.psyneuen.2011.06.003
PG 9
WC Endocrinology & Metabolism; Neurosciences; Psychiatry
SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry
GA 888BW
UT WOS:000299979800003
PM 21715101
ER
PT J
AU Weber, R
Weimar, C
Wanke, I
Moller-Hartmann, C
Gizewski, ER
Blatchford, J
Hermansson, K
Demchuk, AM
Forsting, M
Sacco, RL
Saver, JL
Warach, S
Diener, HC
Diehl, A
AF Weber, Ralph
Weimar, Christian
Wanke, Isabel
Moeller-Hartmann, Claudia
Gizewski, Elke R.
Blatchford, Jon
Hermansson, Karin
Demchuk, Andrew M.
Forsting, Michael
Sacco, Ralph L.
Saver, Jeffrey L.
Warach, Steven
Diener, Hans Christoph
Diehl, Anke
CA PRoFESS Imaging Substudy Grp
TI Risk of Recurrent Stroke in Patients With Silent Brain Infarction in the
Prevention Regimen for Effectively Avoiding Second Strokes (PRoFESS)
Imaging Substudy
SO STROKE
LA English
DT Article
DE cerebral infarction; ischemic stroke; magnetic resonance imaging;
mortality; silent brain infarction
ID EXTENDED-RELEASE DIPYRIDAMOLE; ISCHEMIC-STROKE; TELMISARTAN;
CLOPIDOGREL; POPULATION; PREVALENCE; MORTALITY; EVENTS; MRI
AB Background and Purpose-Silent brain infarctions are associated with an increased risk of stroke in healthy individuals. Risk of recurrent stroke in patients with both symptomatic and silent brain infarction (SBI) has only been investigated in patients with cardioembolic stroke in the European Atrial Fibrillation Trial. We assessed whether patients with recent noncardioembolic stroke and SBI detected on MRI are at increased risk for recurrent stroke, other cardiovascular events, and mortality.
Methods-The prevalence of SBI detected on MRI was assessed in 1014 patients enrolled in the imaging substudy of the Prevention Regimen for Effectively Avoiding Second Strokes (PRoFESS) trial. The primary outcome was first recurrence of stroke in patients with both symptomatic stroke and SBI in comparison with age- and sex-matched patients with stroke without SBI. Secondary outcomes were a combined vascular end point, other vascular events, and mortality. The 2 groups were compared using conditional logistic regression.
Results-Silent brain infarction was detected in 207 (20.4%) of the 1014 patients. Twenty-seven (13.0%) patients with SBI and 19 (9.2%) without SBI had a recurrent stroke (OR, 1.42; 95% CI, 0.79-2.56; P=0.24) during a mean follow-up of 2.5 years. Similarly, there was no statistically significant difference for all secondary outcome parameters between patients with SBI and matched patients without SBI.
Conclusions-The presence of SBI in patients with recent mild noncardioembolic ischemic stroke could not be shown to be an independent risk factor for recurrent stroke, other vascular events, or a higher mortality rate. Clinical Trial Registration URL: http://clinicaltrials.gov. Unique identifier: NCT00153062. (Stroke. 2012;43:350-355.)
C1 [Weber, Ralph; Weimar, Christian; Diener, Hans Christoph] Univ Duisburg Essen, Dept Neurol, D-45122 Essen, Germany.
[Blatchford, Jon] Boehringer Ingelhelm Ltd, Bracknell, Berks, England.
[Hermansson, Karin] Boehringer Ingelheim AB, Stockholm, Sweden.
[Demchuk, Andrew M.] Univ Calgary, Dept Clin Neurosci, Hotchkiss Brain Inst, Calgary, AB, Canada.
[Sacco, Ralph L.] Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA.
[Saver, Jeffrey L.] Univ Calif Los Angeles, Stroke Ctr, Los Angeles, CA USA.
[Saver, Jeffrey L.] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90024 USA.
[Warach, Steven] NINDS, Stroke Diagnost & Therapeut Sect, NIH, Bethesda, MD 20892 USA.
RP Diener, HC (reprint author), Univ Duisburg Essen, Dept Neurol, Hufelandstr 55, D-45122 Essen, Germany.
EM hans.diener@uni-duisburg-essen.de
RI bladin, chris/B-9136-2013; Forsting, Michael/C-6925-2013; Demchuk,
Andrew/E-1103-2012;
OI Demchuk, Andrew/0000-0002-4930-7789; Ringleb, Peter/0000-0002-5473-8671;
Blatchford, Jon/0000-0001-9354-9657; Saver, Jeffrey/0000-0001-9141-2251
FU National Institute of Neurological Disorders and Stroke; Astra/Zeneca;
GSK; Boehringer Ingelheim; Novartis; Janssen-Cilag; Sanofi-Aventis
FX C.W. received honoraria for participation in clinical trials and
contribution to advisory boards or oral presentations from Boehringer
Ingelheim, Bristol-Myers Squib, Daiichi Asubio, Novartis, NovoNordisk,
and Sanofi-Aventis. J.B. and K.H. are employees of Boehringer Ingelheim.
A.M.D. received honoraria for contribution to advisory boards or oral
presentations from Boehringer Ingelheim and Merck. R.L.S. received
grants from the National Institute of Neurological Disorders and Stroke
for the Northern Manhattan Study. He served as a consultant to
Boehringer Ingelheim during the conduct of the PRoFESS trial. J.L.S. is
an employee of the University of California, which received payments
based on clinical trial contracts for the number of subjects enrolled
from Boehringer Ingelheim and AGA Medical and received payments for
faculty participation on scientific advisory boards from AGA Medical.
H.C.D. received honoraria for participation in clinical trials and
contribution to advisory boards or oral presentations from Abbott,
AstraZeneca, Bayer Vital, BMS, Boehringer Ingelheim, CoAxia, D-Pharm,
Fresenius, GlaxoSmithKline, Janssen-Cilag, MSD, MindFrame, Novartis,
Novo-Nordisk, Paion, Parke-Davis, Pfizer, Sanofi-Aventis, Sankyo,
Servier, Solvay, Thrombogenics, Wyeth, and Yamaguchi. He also received
financial support for research projects provided by Astra/Zeneca, GSK,
Boehringer Ingelheim, Novartis, Janssen-Cilag, and Sanofi-Aventis. A.D.
received honoraria for contribution to advisory boards or oral
presentations from Boehringer Ingelheim and Bristol-Myers-Squibb.
NR 21
TC 8
Z9 10
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD FEB
PY 2012
VL 43
IS 2
BP 350
EP 355
DI 10.1161/STROKEAHA.111.631739
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 885RK
UT WOS:000299798300016
PM 22267825
ER
PT J
AU Nogueira, RG
Ferreira, R
Grant, PE
Maier, SE
Koroshetz, WJ
Gonzalez, RG
Sheth, KN
AF Nogueira, Raul G.
Ferreira, Rafael
Grant, P. Ellen
Maier, Stephan E.
Koroshetz, Walter J.
Gonzalez, Ramon G.
Sheth, Kevin N.
TI Restricted Diffusion in Spinal Cord Infarction Demonstrated by Magnetic
Resonance Line Scan Diffusion Imaging
SO STROKE
LA English
DT Article
DE spinal cord infarct; MRI; diffusion
ID MRI; ISCHEMIA; DWI
AB Background and Purpose-We report on the use of line scan diffusion magnetic resonance imaging in the evaluation of spinal cord infarctions.
Methods-Data on 19 patients with clinical findings consistent with spinal cord infarctions and abnormal findings on line scan diffusion imaging were reviewed. The Apparent Diffusion Coefficient (ADC) measurements for the normal spinal cord and for the areas of abnormality were calculated from trace ADC maps.
Results-Restricted diffusion was found in all 19 patients. Absolute ADC values in the ischemic area ranged between 395.4 and 575.8X10(-6) mm(2)/s, with ADC ratios ranging between 39.4% and 57.4%.
Conclusions-Line scan diffusion imaging is technically feasible and appears to be a reliable method to diagnose spinal cord infarction in the acute setting. (Stroke. 2012;43:532-535.)
C1 [Nogueira, Raul G.; Ferreira, Rafael; Grant, P. Ellen; Gonzalez, Ramon G.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neuroradiol, Boston, MA USA.
[Nogueira, Raul G.] Emory Univ, Sch Med, Dept Neurol, Marcus Stroke & Neurosci Ctr,Grady Mem Hosp, Atlanta, GA 30322 USA.
[Nogueira, Raul G.] Emory Univ, Sch Med, Dept Neurosurg, Marcus Stroke & Neurosci Ctr,Grady Mem Hosp, Atlanta, GA USA.
[Nogueira, Raul G.] Emory Univ, Sch Med, Dept Radiol, Marcus Stroke & Neurosci Ctr,Grady Mem Hosp, Atlanta, GA 30322 USA.
[Maier, Stephan E.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Dept Radiol, Boston, MA 02115 USA.
[Koroshetz, Walter J.] NIH, Washington, DC USA.
[Sheth, Kevin N.] Univ Maryland, Sch Med, Shock Trauma & Anesthesiol Res Ctr, Dept Neurol Emergency Med & Neurosurg, Baltimore, MD 21201 USA.
[Grant, P. Ellen] Childrens Hosp, Dept Med, Ctr Fetal Neonatal Neuroimaging & Dev Sci, Boston, MA 02115 USA.
[Grant, P. Ellen] Childrens Hosp, Dept Radiol, Ctr Fetal Neonatal Neuroimaging & Dev Sci, Boston, MA 02115 USA.
RP Nogueira, RG (reprint author), Emory Fac Off Bldg,80 Jesse Hill Dr SE,Room 398, Atlanta, GA 30303 USA.
EM rnoguei@emory.edu
FU American Heart Association; National Institutes of Health; [NIH R01
EB006867]
FX R.G.N., Consultant/Scientific Advisory Board Concentric Medical, ev3
Neurovascular, CoAxia, and Rapid Medical; S.E.M., Research Grant-NIH R01
EB006867; R.G.G., Research Grant from the National Institutes of Health;
K.N.S., Research Grant from the American Heart Association.
NR 14
TC 4
Z9 4
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD FEB
PY 2012
VL 43
IS 2
BP 532
EP 535
DI 10.1161/STROKEAHA.111.624023
PG 4
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 885RK
UT WOS:000299798300042
PM 22033988
ER
PT J
AU Hallenbeck, JM
AF Hallenbeck, John M.
TI Tracks of a Non-Main Path Traveler 2011 Thomas Willis Lecture
SO STROKE
LA English
DT Editorial Material
DE animal models; basic science; brain infarction; endothelium; immunology;
inflammation; risk factors
ID CENTRAL-NERVOUS-SYSTEM; ISCHEMIC-STROKE; DECOMPRESSION-SICKNESS;
MAMMALIAN HIBERNATION; CEREBRAL-ISCHEMIA; BLOOD-FLOW; BRAIN;
NEUROPROTECTION; REPERFUSION; ACTIVATION
AB After an unconventional beginning in stroke research, I veered off the main path repeatedly to view problems from a different perspective. In this lecture summary, I would like to return to several points along the byways that led to research with some continuity. (Stroke. 2012;43:585-590.)
C1 NINDS, Stroke Branch, NIH, Bethesda, MD 20892 USA.
RP Hallenbeck, JM (reprint author), NINDS, Stroke Branch, NIH, 10 Ctr Dr,MSC 1401,Bldg 10,Room 5B02, Bethesda, MD 20892 USA.
EM hallenbj@ninds.nih.gov
FU Intramural NIH HHS [ZIA NS002924-16]
NR 47
TC 0
Z9 0
U1 1
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0039-2499
J9 STROKE
JI Stroke
PD FEB
PY 2012
VL 43
IS 2
BP 585
EP 590
DI 10.1161/STROKEAHA.111.643668
PG 6
WC Clinical Neurology; Peripheral Vascular Disease
SC Neurosciences & Neurology; Cardiovascular System & Cardiology
GA 885RK
UT WOS:000299798300056
PM 22246691
ER
PT J
AU Hu, G
Luo, J
AF Hu, Guang
Luo, Ji
TI A primer on using pooled shRNA libraries for functional genomic screens
SO ACTA BIOCHIMICA ET BIOPHYSICA SINICA
LA English
DT Review
DE shRNA library; pooled screen; RNAi
ID LENTIVIRAL RNAI LIBRARY; BREAST-CANCER; TUMOR SUPPRESSORS;
MAMMALIAN-CELLS; GENETIC SCREEN; GROWTH ARREST; RAS ONCOGENE; IN-VIVO;
INTERFERENCE; REGULATORS
AB The discovery of RNA interference (RNAi) has revolutionized genetic analysis in mammalian cells. Loss-of-function RNAi screens enable rapid, functional annotation of the genome. Of the various RNAi approaches, pooled shRNA libraries have received considerable attention because of their versatility. A number of genome-wide shRNA libraries have been constructed against the human and mouse genomes, and these libraries can be readily applied to a variety of screens to interrogate the function of human and mouse genes in an unbiased fashion. We provide an introduction to the technical aspects of using pooled shRNA libraries for genetic screens.
C1 [Hu, Guang] NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
[Luo, Ji] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Luo, J (reprint author), NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
EM hug4@niehs.nih.gov; ji.luo@nih.gov
RI Hu, Guang/E-7474-2016
OI Hu, Guang/0000-0003-0437-4723
FU National Institutes of Health of USA [Z01ES102745]; NCI-CCR at the US
National Cancer Institute
FX This work was supported by the grants from the National Institutes of
Health Intramural Research Program of USA (Z01ES102745) (to G. H.) and
the NCI-CCR intramural research program at the US National Cancer
Institute (to J.L.).
NR 45
TC 13
Z9 14
U1 2
U2 12
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1672-9145
J9 ACTA BIOCH BIOPH SIN
JI Acta Biochim. Biophys. Sin.
PD FEB
PY 2012
VL 44
IS 2
BP 103
EP 112
DI 10.1093/abbs/gmr116
PG 10
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 884YE
UT WOS:000299744000001
PM 22271906
ER
PT J
AU Brzezinski, K
Dauter, Z
Jaskolski, M
AF Brzezinski, Krzysztof
Dauter, Zbigniew
Jaskolski, Mariusz
TI Structures of NodZ a1,6-fucosyltransferase in complex with GDP and
GDP-fucose
SO ACTA CRYSTALLOGRAPHICA SECTION D-BIOLOGICAL CRYSTALLOGRAPHY
LA English
DT Article
DE glycosyltransferases; fucosyltransferases; family GT-23
glycosyltransferases; chitooligosaccharide fucosylation; Nod-factor
biosynthesis; nodulation; Nod factors; legume-rhizobium symbiosis;
nitrogen fixation
ID CRYSTAL-STRUCTURE; MAMMALIAN ALPHA-1,6-FUCOSYL-TRANSFERASE;
RHIZOBIUM-LEGUMINOSARUM; ACETYL TRANSFERASE; NODULATION SIGNAL; ROOT
NODULATION; GLYCOSYLTRANSFERASES; BIOSYNTHESIS; MECHANISM; PROTEIN
AB Rhizobial NodZ a1,6-fucosyltransferase (a1,6-FucT) catalyzes the transfer of the fucose (Fuc) moiety from guanosine 5'-diphosphate-beta-l-fucose to the reducing end of the chitin oligosaccharide core during Nod-factor (NF) biosynthesis. NF is a key signalling molecule required for successful symbiosis with a legume host for atmospheric nitrogen fixation. To date, only two a1,6-FucT structures have been determined, both without any donor or acceptor molecule that could similar to highlight the structural background of the catalytic mechanism. Here, the first crystal structures of a1,6-FucT in complex with its substrate GDP-Fuc and with GDP, which is similar to a similar to byproduct of the enzymatic reaction, are presented. The crystal of the complex with GDP-Fuc was obtained through soaking of native NodZ crystals with the ligand and its structure has been determined at 2.35 angstrom resolution. The fucose residue is exposed to solvent and is disordered. The enzymeproduct complex crystal was obtained by cocrystallization with GDP and an acceptor molecule, penta-N-acetyl-l-glucosamine (penta-NAG). The structure has been determined at 1.98 angstrom resolution, showing that only the GDP molecule is present in the complex. In both structures the ligands are located in a cleft formed between the two domains of NodZ and extend towards the C-terminal domain, but their conformations differ significantly. The structures revealed that residues in three regions of the C-terminal domain, which are conserved among a1,2-, a1,6- and protein O-fucosyltransferases, are involved in interactions with the sugar-donor molecule. There is also an interaction with the side chain of Tyr45 in the N-terminal domain, which is very unusual for a GT-B-type glycosyltransferase. Only minor conformational changes of the protein backbone are observed upon ligand binding. The only exception is a movement of the loop located between strand beta C2 and helix aC3. In addition, there is a shift of the aC3 helix itself upon GDP-Fuc binding.
C1 [Brzezinski, Krzysztof; Jaskolski, Mariusz] Polish Acad Sci, Inst Bioorgan Chem, Ctr Biocrystallog Res, PL-61704 Poznan, Poland.
[Brzezinski, Krzysztof; Dauter, Zbigniew] Argonne Natl Lab, Synchrotron Radiat Res Sect, MCL, NCI, Argonne, IL 60439 USA.
[Jaskolski, Mariusz] Adam Mickiewicz Univ, Dept Crystallog, Fac Chem, PL-60780 Poznan, Poland.
RP Jaskolski, M (reprint author), Polish Acad Sci, Inst Bioorgan Chem, Ctr Biocrystallog Res, PL-61704 Poznan, Poland.
EM mariuszj@amu.edu.pl
FU Polish Ministry of Science and Higher Education [N N302 4305 34]; NIH,
National Cancer Institute, Center for Cancer Research; National Cancer
Institute, National Institutes of Health [HHSN2612008000001E]; National
Center for Research Resources at the National Institutes of Health
[RR-15301]; US Department of Energy, Office of Basic Energy Sciences
[W-31-109-Eng-38]
FX This work was supported in part by a grant from the Polish Ministry of
Science and Higher Education (No. N N302 4305 34), by the Intramural
Research Program of NIH, National Cancer Institute, Center for Cancer
Research and by Federal funds from the National Cancer Institute,
National Institutes of Health under Contract HHSN2612008000001E. The
content of this publication does not necessarily reflect the views or
policies of the Department of Health and Human Services, nor does the
mention of trade names, commercial products, or organizations imply
endorsement by the US Government. Use of the SER-CAT beamline was
supported by award RR-15301 from the National Center for Research
Resources at the National Institutes of Health and the use of the
Advanced Photon Source was supported by the US Department of Energy,
Office of Basic Energy Sciences under Contract No. W-31-109-Eng-38.
NR 48
TC 5
Z9 6
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0907-4449
J9 ACTA CRYSTALLOGR D
JI Acta Crystallogr. Sect. D-Biol. Crystallogr.
PD FEB
PY 2012
VL 68
BP 160
EP 168
DI 10.1107/S0907444911053157
PN 2
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Crystallography
SC Biochemistry & Molecular Biology; Biophysics; Crystallography
GA 881FX
UT WOS:000299469100009
PM 22281745
ER
PT J
AU Babitz, S
AF Babitz, Shuly
TI In Memory of Morris E. Chafetz, MD, 1924-2011
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Biographical-Item
C1 NIAAA, Bethesda, MD 20892 USA.
RP Babitz, S (reprint author), NIAAA, 5635 Fishers Lane, Bethesda, MD 20892 USA.
EM shuly.babitz@nih.gov
NR 1
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
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 2012
VL 36
IS 2
BP 191
EP 192
DI 10.1111/j.1530-0277.2011.01733.x
PG 2
WC Substance Abuse
SC Substance Abuse
GA 883DS
UT WOS:000299614700001
ER
PT J
AU Vatsalya, V
Issa, JE
Hommer, DW
Ramchandani, VA
AF Vatsalya, Vatsalya
Issa, Julnar E.
Hommer, Daniel W.
Ramchandani, Vijay A.
TI Pharmacodynamic Effects of Intravenous Alcohol on Hepatic and Gonadal
Hormones: Influence of Age and Sex
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Age; Alcohol; Estradiol; Growth Hormone; IGF-1; Sex; Testosterone
ID GROWTH-FACTOR-I; PREMENOPAUSAL WOMEN; LUTEINIZING-HORMONE;
GENE-EXPRESSION; CHRONIC ETHANOL; TESTOSTERONE; SECRETION; MEN; PLASMA;
ELIMINATION
AB Background: Growth hormone (GH)insulin-like growth factor-1 (IGF-1) axis and gonadal hormones demonstrate extensively associated regulation; however, little is known about the effects of acute alcohol exposure on these hormones. This study examined the effects of intravenous alcohol on the GHIGF-1 axis and gonadal hormone concentrations, and the influence of age and sex on their regulation.
Methods: Forty-eight healthy volunteers (24 men and 24 women each in the 21 to 25 and 55 to 65 year age groups) underwent a 2-session single-blinded study. Subjects received in randomized counter-balanced order, alcohol infusions, individually computed based on a physiologically based pharmacokinetic model, to maintain a steady-state ("clamped") exposure of 50 mg% or saline for 3 hours in separate sessions. Blood samples collected at baseline and postinfusion in each session were assayed for levels of GH, IGF-1, free testosterone, and estradiol.
Results: Acute alcohol administration resulted in changes in gonadal hormones that differed by sex. Change in free testosterone showed a significant treatment x baseline interaction (p < 0.001), indicating that alcohol-induced suppression of testosterone occurred predominantly in men. On the other hand, change in estradiol showed a significant treatment x sex interaction (p = 0.028), indicating that alcohol-induced increases in estradiol occurred predominantly in women. There was a trend for alcohol-induced decreases in IGF-1 levels. Change in GH showed a significant main effect of baseline (p < 0.001) and a trend for treatment by baseline interaction, suggesting an alcohol-induced decrease in individuals with high baseline GH values. There was also a significant main effect of sex (p = 0.046) indicating that men had greater changes in GH across treatment compared with women.
Conclusions: Alcohol induced a complex pattern of hormonal responses that varied between younger and older men and women. Some of the observed sex-based differences may help improve our understanding of the greater susceptibility to alcohol-related hepatic damage seen in women.
C1 [Vatsalya, Vatsalya; Issa, Julnar E.; Ramchandani, Vijay A.] NIAAA, Sect Human Psychopharmacol, Lab Clin & Translat Studies, Bethesda, MD 20892 USA.
[Hommer, Daniel W.] NIAAA, Lab Clin & Translat Studies, Sect Brain Electrophysiol & Imaging, Bethesda, MD 20892 USA.
RP Vatsalya, V (reprint author), NIAAA, Sect Human Psychopharmacol, Lab Clin & Translat Studies, 10 Ctr Dr,Room 2-2352, Bethesda, MD 20892 USA.
EM vijayr@mail.nih.gov
FU Intramural NIH HHS [ZIA AA000466-06, ZIA AA000466-07]
NR 37
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Z9 11
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD FEB
PY 2012
VL 36
IS 2
BP 207
EP 213
DI 10.1111/j.1530-0277.2011.01600.x
PG 7
WC Substance Abuse
SC Substance Abuse
GA 883DS
UT WOS:000299614700004
PM 21797891
ER
PT J
AU Tetrault, JM
Tate, JP
McGinnis, KA
Goulet, JL
Sullivan, LE
Bryant, K
Justice, AC
Fiellin, DA
AF Tetrault, Jeanette M.
Tate, Janet P.
McGinnis, Kathleen A.
Goulet, Joseph L.
Sullivan, Lynn E.
Bryant, Kendall
Justice, Amy C.
Fiellin, David A.
CA Vet Aging Cohort Study Team
TI Hepatic Safety and Antiretroviral Effectiveness in HIV-Infected Patients
Receiving Naltrexone
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE HIV; Naltrexone; Alcoholism; Opioid-Related Disorders
ID HUMAN-IMMUNODEFICIENCY-VIRUS; RANDOMIZED CONTROLLED-TRIAL; HIGH-DOSE
NALTREXONE; ILLICIT DRUG-USE; ALCOHOL DEPENDENCE; MEDICATION ADHERENCE;
RELEASE NALTREXONE; OPIOID DEPENDENCE; THERAPY; DRINKING
AB Background: We sought to determine the impact of naltrexone on hepatic enzymes and HIV biomarkers in HIV-infected patients.
Methods: We used data from the Veterans Aging Cohort Study-Virtual Cohort, an electronic database of administrative, pharmacy, and laboratory data. We restricted our sample to HIV-infected patients who received an initial oral naltrexone prescription of at least 7 days duration. We examined aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and HIV biomarker (CD4 and HIV RNA) values for the 365 days prior to, during, and for the 365 days post-naltrexone prescription. We also examined cases of liver enzyme elevation (LEE; defined as > 5 times baseline ALT or AST or > 3.5 times baseline if baseline ALT or AST was > 40 IU/l).
Results: Of 114 HIV-infected individuals, 97% were men, 45% white, 57% Hepatitis C co-infected; median age was 49 years; 89% of the sample had a history of alcohol dependence and 32% had opioid dependence. Median duration of naltrexone prescription was 49 (interquartile range 30 to 83) days, representing 9,525 person-days of naltrexone use. Mean ALT and AST levels remained below the upper limit of normal. Two cases of LEE occurred. Mean CD4 count remained stable and mean HIV RNA decreased after naltrexone prescription.
Conclusions: In HIV-infected patients, oral naltrexone is rarely associated with clinically significant ALT or AST changes and does not have a negative impact on biologic parameters. Therefore, HIV-infected patients with alcohol or opioid dependence can be treated with naltrexone.
C1 [Tetrault, Jeanette M.; Goulet, Joseph L.; Sullivan, Lynn E.; Justice, Amy C.; Fiellin, David A.] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06510 USA.
[Tate, Janet P.; McGinnis, Kathleen A.; Goulet, Joseph L.; Justice, Amy C.; Fiellin, David A.] Vet Aging Cohort Study, West Haven, CT USA.
[Tate, Janet P.; Goulet, Joseph L.; Justice, Amy C.] VA Connecticut Healthcare Syst, West Haven, CT USA.
[McGinnis, Kathleen A.] VA Pittsburgh Healthcare Syst, Ctr Hlth Equ Res & Promot, Pittsburgh, PA USA.
[Bryant, Kendall] NIAAA, Rockville, MD 20852 USA.
RP Tetrault, JM (reprint author), 367 Cedar St,4th Floor, New Haven, CT 06510 USA.
EM jeanette.tetrault@yale.edu
OI Fiellin, David/0000-0002-4006-010X; Goulet, Joseph/0000-0002-0842-804X
FU National Institute on Alcohol Abuse and Alcoholism [U10 AA 13566]; VHA
Public Health Strategic Health Core Group; National Institute on Alcohol
and Alcohol Abuse [U01 AA 13566]; National Institute on Drug Abuse
(NIDA) [R01 DA019511-03, R01 DA025991, R01 DA020576-01A1, K23
DA024050-02]
FX The Veterans Aging Cohort Study is funded by the National Institute on
Alcohol Abuse and Alcoholism (U10 AA 13566) and the VHA Public Health
Strategic Health Core Group. The material presented in this study is
based upon work supported in part by funding from the National Institute
on Alcohol and Alcohol Abuse (U01 AA 13566) and the National Institute
on Drug Abuse (NIDA R01 DA019511-03, R01 DA025991, R01 DA020576-01A1,
K23 DA024050-02).
NR 46
TC 10
Z9 10
U1 2
U2 3
PU WILEY-BLACKWELL
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 2012
VL 36
IS 2
BP 318
EP 324
DI 10.1111/j.1530-0277.2011.01601.x
PG 7
WC Substance Abuse
SC Substance Abuse
GA 883DS
UT WOS:000299614700018
PM 21797892
ER
PT J
AU Snell, LD
Ramchandani, VA
Saba, L
Herion, D
Heilig, M
George, DT
Pridzun, L
Helander, A
Schwandt, ML
Phillips, MJ
Hoffman, PL
Tabakoff, B
AF Snell, Lawrence D.
Ramchandani, Vijay A.
Saba, Laura
Herion, David
Heilig, Markus
George, David T.
Pridzun, Lutz
Helander, Anders
Schwandt, Melanie L.
Phillips, Monte J.
Hoffman, Paula L.
Tabakoff, Boris
CA WHO ISBRA Study State Trait
TI The Biometric Measurement of Alcohol Consumption
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcohol Consumption; Biomarkers; MAO Protein; Platelets
ID PLATELET MONOAMINE-OXIDASE; CARBOHYDRATE-DEFICIENT TRANSFERRIN; TRAIT
MARKERS; SMOKING; DEPENDENCE; DRINKING; PERSONALITY; INHIBITION;
DISORDERS; WHO/ISBRA
AB Background: Proper ascertainment of the history of alcohol consumption by an individual is an important component of medical diagnosis of disease and influences the implementation of appropriate treatment strategies that include prescription of medication, as well as intervention for the negative physical and social consequences of hazardous/harmful levels of alcohol consumption. Biological (biometric) diagnostic tests that provide information on current and past quantity and frequency of alcohol consumption by an individual, prior to onset of organ damage, continue to be sought.
Methods: Platelet monoamine oxidase B (MAO-B) protein was quantitated in 2 populations of subjects who had histories of different levels of alcohol consumption. Levels were assayed by immunoblotting or by ELISA. The development and evaluation of the new ELISA-based measure of platelet MAO-B protein levels is described.
Results: One subject population constituted a nontreatment-seeking, cross-sectional subject sample, and the other population was a longitudinally followed, hospitalized group of subjects. An algorithm combining measures of platelet MAO-B protein with the plasma levels of carbohydrate-deficient transferrin (CDT) and with liver enzymes (aspartate aminotransferase or gamma-glutamyltransferase [GGT]) can detect hazardous/harmful alcohol use (HHAU) with the highest sensitivity and specificity in the cross-sectional nontreatment-seeking population. In the treatment-seeking population, low MAO-B protein levels at admission are associated with heavy drinking prior to admission, and these protein levels increase over a period of abstinence from alcohol.
Conclusions: The platelet MAO-B protein measurement is particularly effective for male alcohol consumers. The combined use of MAO-B protein measures together with measures of CDT and GGT does, however, improve the diagnostic utility of both markers for ascertaining HHAU in women. Furthermore, measurement of changes in platelet MAO-B protein levels during treatment for alcohol dependence may help monitor the success of the treatment program.
C1 [Saba, Laura; Hoffman, Paula L.; Tabakoff, Boris] Univ Colorado, Sch Med, Dept Pharmacol, Aurora, CO 80045 USA.
[Snell, Lawrence D.; Tabakoff, Boris] Lohocla Res Corp, Aurora, CO USA.
[Ramchandani, Vijay A.; Herion, David; Heilig, Markus; George, David T.; Schwandt, Melanie L.; Phillips, Monte J.] NIAAA, Lab Clin & Translat Studies, Bethesda, MD USA.
[Pridzun, Lutz] Mediagnost GmbH, Reutlingen, Germany.
[Helander, Anders] Karolinska Inst, Dept Lab Med, Stockholm, Sweden.
RP Tabakoff, B (reprint author), Univ Colorado, Sch Med, Dept Pharmacol, MS 8303,POB 6511,12800 E,19th Ave, Aurora, CO 80045 USA.
EM boris.tabakoff@ucdenver.edu
RI Schwandt, Melanie/L-9866-2016;
OI Heilig, Markus/0000-0003-2706-2482; Saba, Laura/0000-0001-9649-1294
FU Lohocla Research Corporation [R44AA014531, R43AA017374]; Banbury Fund;
WHO/ISBRA
FX Funding for Lohocla Research Corporation: SBIR grants R44AA014531 and
R43AA017374 and the Banbury Fund. Mediagnost thanks Nadine Wachendorfer
for her excellent technical assistance. This work is in part a result of
the work of WHO/ISBRA Investigators: K.M. Conigrave, M. Dongier, H.
Edenberg, C.J.P. Eriksson, M.L.O.S. Formigoni, B.F. Grant, A. Helander,
P.L. Hoffman, K. Kiianmaa, T. Koyama, L. Legault, T.-K. Li, T. Mathuen,
M.G. Monteiro, T. Saito, M. Salaspuro, J.B. Saunders, B. Tabakoff, S.
Tufik, J.B. Whitfield, and F.M. Wurst.
NR 32
TC 5
Z9 5
U1 0
U2 4
PU WILEY-BLACKWELL
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 2012
VL 36
IS 2
BP 332
EP 341
DI 10.1111/j.1530-0277.2011.01605.x
PG 10
WC Substance Abuse
SC Substance Abuse
GA 883DS
UT WOS:000299614700020
PM 21895709
ER
PT J
AU Mukherjee, B
Ahn, J
Gruber, SB
Chatterjee, N
AF Mukherjee, Bhramar
Ahn, Jaeil
Gruber, Stephen B.
Chatterjee, Nilanjan
TI Testing Gene-Environment Interaction in Large-Scale Case-Control
Association Studies: Possible Choices and Comparisons
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE case-control studies; efficiency; familywise error rate; genome-wide
association study; profile likelihood; robustness; shrinkage
ID GENOME-WIDE ASSOCIATION; BREAST-CANCER RISK; MAXIMUM-LIKELIHOOD;
INDEPENDENCE; MODELS; GENOTYPE; EXPOSURE; DESIGNS; POWER; BIAS
AB Several methods for screening gene-environment interaction have recently been proposed that address the issue of using gene-environment independence in a data-adaptive way. In this report, the authors present a comparative simulation study of power and type I error properties of 3 classes of procedures: 1) the standard 1-step case-control method; 2) the case-only method that requires an assumption of gene-environment independence for the underlying population; and 3) a variety of hybrid methods, including empirical-Bayes, 2-step, and model averaging, that aim at gaining power by exploiting the assumption of gene-environment independence and yet can protect against false positives when the independence assumption is violated. These studies suggest that, although the case-only method generally has maximum power, it has the potential to create substantial false positives in large-scale studies even when a small fraction of markers are associated with the exposure under study in the underlying population. All the hybrid methods perform well in protecting against such false positives and yet can retain substantial power advantages over standard case-control tests. The authors conclude that, for future genome-wide scans for gene-environment interactions, major power gain is possible by using alternatives to standard case-control analysis. Whether a case-only type scan or one of the hybrid methods should be used depends on the strength and direction of gene-environment interaction and association, the level of tolerance for false positives, and the nature of replication strategies.
C1 [Chatterjee, Nilanjan] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Mukherjee, Bhramar; Ahn, Jaeil] Univ Michigan, Sch Publ Hlth, Dept Biostat, Ann Arbor, MI 48109 USA.
[Gruber, Stephen B.] Univ Michigan, Dept Internal Med Human Genet & Epidemiol, Ann Arbor, MI 48109 USA.
RP Chatterjee, N (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd, Rockville, MD 20852 USA.
EM chattern@mail.nih.gov
FU National Institutes of Health [CA-156608, U19 NCI-895700]; National
Science Foundation [DMS-1007494]; National Cancer Institute
FX This research was partially supported by National Institutes of Health
grant CA-156608 and National Science Foundation grant DMS-1007494 to B.
M., National Institutes of Health grant U19 NCI-895700 to S. B. G. and
B. M., and the Intramural Research Program of the National Cancer
Institute to N. C.
NR 32
TC 50
Z9 50
U1 1
U2 11
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 2012
VL 175
IS 3
BP 177
EP 190
DI 10.1093/aje/kwr367
PG 14
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 882XC
UT WOS:000299596200003
PM 22199027
ER
PT J
AU Cornelis, MC
Tchetgen, EJT
Liang, LM
Qi, L
Chatterjee, N
Hu, FB
Kraft, P
AF Cornelis, Marilyn C.
Tchetgen, Eric J. Tchetgen
Liang, Liming
Qi, Lu
Chatterjee, Nilanjan
Hu, Frank B.
Kraft, Peter
TI Gene-Environment Interactions in Genome-Wide Association Studies: A
Comparative Study of Tests Applied to Empirical Studies of Type 2
Diabetes
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE case-control studies; case study; diabetes mellitus; type 2;
epidemiologic methods; genome-wide association study;
genotype-environment interaction
ID RANDOM FORESTS; DESIGNS; SUSCEPTIBILITY; INDEPENDENCE; DEFINITIONS;
INFERENCE; VARIANTS; DISEASES; MODELS; POWER
AB The question of which statistical approach is the most effective for investigating gene-environment (G-E) interactions in the context of genome-wide association studies (GWAS) remains unresolved. By using 2 case-control GWAS (the Nurses' Health Study, 1976-2006, and the Health Professionals Follow-up Study, 1986-2006) of type 2 diabetes, the authors compared 5 tests for interactions: standard logistic regression-based case-control; case-only; semiparametric maximum-likelihood estimation of an empirical-Bayes shrinkage estimator; and 2-stage tests. The authors also compared 2 joint tests of genetic main effects and G-E interaction. Elevated body mass index was the exposure of interest and was modeled as a binary trait to avoid an inflated type I error rate that the authors observed when the main effect of continuous body mass index was misspecified. Although both the case-only and the semiparametric maximum-likelihood estimation approaches assume that the tested markers are independent of exposure in the general population, the authors did not observe any evidence of inflated type I error for these tests in their studies with 2,199 cases and 3,044 controls. Both joint tests detected markers with known marginal effects. Loci with the most significant G-E interactions using the standard, empirical-Bayes, and 2-stage tests were strongly correlated with the exposure among controls. Study findings suggest that methods exploiting G-E independence can be efficient and valid options for investigating G-E interactions in GWAS.
C1 [Cornelis, Marilyn C.; Qi, Lu; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Tchetgen, Eric J. Tchetgen; Liang, Liming; Hu, Frank B.; Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Tchetgen, Eric J. Tchetgen; Liang, Liming; Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Qi, Lu; Hu, Frank B.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA.
[Qi, Lu; Hu, Frank B.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Chatterjee, Nilanjan] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
RP Cornelis, MC (reprint author), Harvard Univ, Sch Publ Hlth, Dept Nutr, 665 Huntington Ave, Boston, MA 02115 USA.
EM mcomeli@hsph.harvard.edu
FU National Institutes of Health (NIH) Genes, Environment, and Health
Initiative (GEI) [U01HG-004738, U01HG004422, U01HG004402, U01HG004729,
U01HG004726, U01HG004735, U01HG004415, U01HG-004436, U01HG004423,
U01HG004728, RFAHG006033]; NIH (National Institute of Dental and
Craniofacial Research) [U01DE018993, U01DE018903]; NIH (National
Institute on Alcohol Abuse and Alcoholism) [U10AA008401]; NIH (National
Institute on Drug Abuse) [P01CA089392, R01DA013423]; NIH (National
Cancer Institute) [CA63464, CA54281, CA 136792, Z01CP010200]; NIH GEI
[U01HG04424, U01HG004438]; Johns Hopkins University Center for Inherited
Disease Research; NIH [HHSN-268200782096C, 1R21 ES019712-01]; National
Cancer Institute [P01CA087969, P01CA055075]; National Institute of
Diabetes and Digestive and Kidney Diseases [R01DK058845]; Canadian
Institutes of Health Research
FX The Nurses' Health Study/Health Professionals Follow-up Study Type 2
Diabetes GWAS (U01HG004399) is a component of a collaborative project
that includes 13 other GWAS funded as part of the Gene-Environment
Association Studies (GENEVA) under the National Institutes of Health
(NIH) Genes, Environment, and Health Initiative (GEI) (U01HG-004738,
U01HG004422, U01HG004402, U01HG004729, U01HG004726, U01HG004735,
U01HG004415, U01HG-004436, U01HG004423, U01HG004728, RFAHG006033), with
additional support from individual institutes of the NIH (National
Institute of Dental and Craniofacial Research: U01DE018993, U01DE018903;
National Institute on Alcohol Abuse and Alcoholism: U10AA008401;
National Institute on Drug Abuse: P01CA089392, R01DA013423; and National
Cancer Institute: CA63464, CA54281, CA 136792, Z01CP010200). Assistance
with phenotype harmonization and genotype cleaning, as well as with
general study coordination, was provided by the Coordinating Center of
the Gene-Environment Association Studies (U01HG004446). Assistance with
data cleaning was provided by the National Center for Biotechnology
Information. Genotyping was performed at the Broad Institute of the
Massachusetts Institute of Technology and Harvard, with funding support
from the NIH GEI (U01HG04424), and Johns Hopkins University Center for
Inherited Disease Research, with support from the NIH GEI (U01HG004438)
and an NIH contract (HHSN-268200782096C). Additional funding for the
current research was provided by the NIH (1R21 ES019712-01), the
National Cancer Institute (P01CA087969, P01CA055075), and the National
Institute of Diabetes and Digestive and Kidney Diseases (R01DK058845).
M. C. C. is a recipient of a Canadian Institutes of Health Research
Fellowship.
NR 40
TC 45
Z9 45
U1 1
U2 5
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 2012
VL 175
IS 3
BP 191
EP 202
DI 10.1093/aje/kwr368
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 882XC
UT WOS:000299596200004
PM 22199026
ER
PT J
AU Mukherjee, B
Ahn, J
Gruber, SB
Chatterjee, N
AF Mukherjee, Bhramar
Ahn, Jaeil
Gruber, Stephen B.
Chatterjee, Nilanjan
TI Mukherjee et al. Respond to "GE-Whiz! Ratcheting Up Gene-Environment
Studies"
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Editorial Material
C1 [Chatterjee, Nilanjan] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD 20852 USA.
[Mukherjee, Bhramar; Ahn, Jaeil] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Gruber, Stephen B.] Univ Michigan, Dept Internal Med Human Genet & Biostat, Ann Arbor, MI 48109 USA.
RP Chatterjee, N (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, 6120 Execut Blvd, Rockville, MD 20852 USA.
EM chattern@mail.nih.gov
NR 6
TC 4
Z9 4
U1 0
U2 0
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 2012
VL 175
IS 3
BP 208
EP 209
DI 10.1093/aje/kwr366
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 882XC
UT WOS:000299596200006
ER
PT J
AU Hall, KL
Stokols, D
Stipelman, BA
Vogel, AL
Feng, A
Masimore, B
Morgan, G
Moser, RP
Marcus, SE
Berrigan, D
AF Hall, Kara L.
Stokols, Daniel
Stipelman, Brooke A.
Vogel, Amanda L.
Feng, Annie
Masimore, Beth
Morgan, Glen
Moser, Richard P.
Marcus, Stephen E.
Berrigan, David
TI Assessing the Value of Team Science A Study Comparing Center- and
Investigator-Initiated Grants
SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE
LA English
DT Article
ID TRANSDISCIPLINARY RESEARCH; HEALTH; COLLABORATION; READINESS; OUTCOMES;
ADDRESS
AB Background: Large cross-disciplinary scientific teams are becoming increasingly prominent in the conduct of research.
Purpose: This paper reports on a quasi-experimental longitudinal study conducted to compare bibliometric indicators of scientific collaboration, productivity, and impact of center-based transdisciplinary team science initiatives and traditional investigator-initiated grants in the same field.
Methods: All grants began between 1994 and 2004 and up to 10 years of publication data were collected for each grant. Publication information was compiled and analyzed during the spring and summer of 2010.
Results: Following an initial lag period, the transdisciplinary research center grants had higher overall publication rates than the investigator-initiated R01 (NIH Research Project Grant Program) grants. There were relatively uniform publication rates across the research center grants compared to dramatically dispersed publication rates among the R01 grants. On average, publications produced by the research center grants had greater numbers of coauthors but similar journal impact factors compared with publications produced by the R01 grants.
Conclusions: The lag in productivity among the transdisciplinary center grants was offset by their overall higher publication rates and average number of coauthors per publication, relative to investigator-initiated grants, over the 10-year comparison period. The findings suggest that transdisciplinary center grants create benefits for both scientific productivity and collaboration. (Am J Prev Med 2012; 42(2): 157-163) Published by Elsevier Inc. on behalf of American Journal of Preventive Medicine
C1 [Hall, Kara L.; Stipelman, Brooke A.; Morgan, Glen; Moser, Richard P.; Berrigan, David] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Marcus, Stephen E.] Natl Inst Gen Med Sci, Ctr Bioinformat & Computat Biol, NIH, Bethesda, MD USA.
[Vogel, Amanda L.] SAIC Frederick Inc, NCI Frederick, Clin Res Directorate CMRP, Frederick, MD USA.
[Masimore, Beth] Discovery Log, Rockville, MD USA.
[Stokols, Daniel] Univ Calif Irvine, Sch Social Ecol, Irvine, CA USA.
[Feng, Annie] Feng Consulting, Livingston, NJ USA.
RP Hall, KL (reprint author), NCI, Div Canc Control & Populat Sci, 6130 Execut Blvd,MSC 7338,Execut Plaza N,Room 407, Bethesda, MD 20892 USA.
EM hallka@mail.nih.gov
FU National Cancer Institute, NIH [HHSN261200800001E];
[HHSN-276-2007-00235U]
FX We thank James Corrigan (NCI), Lawrence Solomon (NCI), Joshua Schnell
(Discovery Logic Inc.), and Laurel Haak (Discovery Logic Inc.) for their
assistance and helpful comments in the preparation of this manuscript.
This work was supported by contract number HHSN-276-2007-00235U. This
project was funded, in whole or in part, with federal funds from the
National Cancer Institute, NIH, under contract no. HHSN261200800001E.
The content of this publication does not necessarily reflect the views
or policies of the DHHS, nor does mention of trade names, commercial
products, or organizations imply endorsement by the U. S. Government.
NR 38
TC 40
Z9 43
U1 1
U2 27
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0749-3797
J9 AM J PREV MED
JI Am. J. Prev. Med.
PD FEB
PY 2012
VL 42
IS 2
BP 157
EP 163
DI 10.1016/j.amepre.2011.10.011
PG 7
WC Public, Environmental & Occupational Health; Medicine, General &
Internal
SC Public, Environmental & Occupational Health; General & Internal Medicine
GA 879DQ
UT WOS:000299310300007
PM 22261212
ER
PT J
AU Hyvonen, MT
Keinanen, TA
Khomutov, M
Simonian, A
Vepsalainen, J
Park, JH
Khomutov, AR
Alhonen, L
Park, MH
AF Hyvonen, Mervi T.
Keinanen, Tuomo A.
Khomutov, Maxim
Simonian, Alina
Vepsalainen, Jouko
Park, Jong Hwan
Khomutov, Alex R.
Alhonen, Leena
Park, Myung Hee
TI Effects of novel C-methylated spermidine analogs on cell growth via
hypusination of eukaryotic translation initiation factor 5A
SO AMINO ACIDS
LA English
DT Article
DE Polyamine; Methylated spermidine; Cell growth; Deoxyhypusine synthase;
Hypusine; eIF5A
ID YEAST SACCHAROMYCES-CEREVISIAE; DEOXYHYPUSINE SYNTHASE ACTIVITY;
POLYAMINE METABOLISM; POSTTRANSLATIONAL SYNTHESIS; AMINO-ACID; PROTEIN;
INHIBITION; CYTOSTASIS; VIABILITY; DEPLETION
AB The polyamines, putrescine, spermidine, and spermine, are ubiquitous multifunctional cations essential for cellular proliferation. One specific function of spermidine in cell growth is its role as a butylamine donor for hypusine synthesis in the eukaryotic initiation factor 5A (eIF5A). Here, we report the ability of novel mono-methylated spermidine analogs (alpha-MeSpd, beta-MeSpd, gamma-MeSpd, and omega-MeSpd) to function in the hypusination of eIF5A and in supporting the growth of DFMO-treated DU145 cells. We also tested them as substrates and inhibitors for deoxyhypusine synthase (DHS) in vitro. Of these compounds, alpha-MeSpd, beta-MeSpd, and gamma-MeSpd (but not omega-MeSpd) were substrates for DHS in vitro, while they all inhibited the enzyme reaction. As racemic mixtures, only alpha-MeSpd and beta-MeSpd supported long-term growth (9-18 days) of spermidine-depleted DU145 cells, whereas gamma-MeSpd and omega-MeSpd did not. The S-enantiomer of alpha-MeSpd, which supported long-term growth, was a good substrate for DHS in vitro, whereas the R-isomer was not. The long-term growth of DFMO-treated cells correlated with the hypusine modification of eIF5A by intracellular methylated spermidine analogs. These results underscore the critical requirement for hypusine modification in mammalian cell proliferation and provide new insights into the specificity of the deoxyhypusine synthase reaction.
C1 [Hyvonen, Mervi T.; Alhonen, Leena] Univ Eastern Finland, Bioctr Kuopio, AI Virtanen Inst Mol Sci, Kuopio 70210, Finland.
[Keinanen, Tuomo A.; Vepsalainen, Jouko] Univ Eastern Finland, Bioctr Kuopio, Chem Lab, Dept Biosci, Kuopio 70210, Finland.
[Khomutov, Maxim; Simonian, Alina; Khomutov, Alex R.] Russian Acad Sci, Engelhardt Inst Mol Biol, Moscow 119991, Russia.
[Park, Jong Hwan; Park, Myung Hee] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Hyvonen, MT (reprint author), Univ Eastern Finland, Bioctr Kuopio, AI Virtanen Inst Mol Sci, Yliopistonranta 1E, Kuopio 70210, Finland.
EM mervi.hyvonen@uef.fi; mhpark@nih.gov
RI khomutov, maxim/G-2234-2015;
OI Keinanen, Tuomo/0000-0002-0659-5573
FU National Institute of Dental and Craniofacial Research (NIDCR), NIH;
Academy of Finland; Russian Foundation for Basic Research [09-04-01272];
Presidium of the Russian Academy of Sciences; Finnish Cultural
Foundation; University of Eastern Finland
FX The research was supported in part by the Intramural Research Program of
National Institute of Dental and Craniofacial Research (NIDCR), NIH and
by grants from the Academy of Finland, the Russian Foundation for Basic
Research [grant number 09-04-01272], the program Molecular and Cell
Biology of the Presidium of the Russian Academy of Sciences, the North
Savo Regional Fund of the Finnish Cultural Foundation and by the
University of Eastern Finland (Novel Materials, Technologies and Drug
Molecules Based on Phosphorus and/or Nitrogen Compounds; JV/TAK). The
authors thank Ms. Sisko Juutinen, Ms. Anne Karppinen, Ms Arja Korhonen,
and Ms. Tuula Reponen for skillful technical assistance and Dr. Edith C.
Wolff (NIDCR, NIH) for critical reading of the manuscript and helpful
suggestions.
NR 40
TC 9
Z9 10
U1 0
U2 8
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0939-4451
J9 AMINO ACIDS
JI Amino Acids
PD FEB
PY 2012
VL 42
IS 2-3
BP 685
EP 695
DI 10.1007/s00726-011-0984-1
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 881RT
UT WOS:000299506000026
PM 21861168
ER
PT J
AU Dias, CAO
Gregio, APB
Rossi, D
Galvao, FC
Watanabe, TF
Park, MH
Valentini, SR
Zanelli, CF
AF Dias, Camila A. O.
Borges Gregio, Ana Paula
Rossi, Danuza
Galvao, Fabio Carrilho
Watanabe, Tatiana F.
Park, Myung Hee
Valentini, Sandro R.
Zanelli, Cleslei F.
TI eIF5A interacts functionally with eEF2
SO AMINO ACIDS
LA English
DT Article
DE eIF5A; Hypusine; eEF2; Translation elongation
ID INITIATION-FACTOR 5A; PROMOTES TRANSLATION ELONGATION;
SACCHAROMYCES-CEREVISIAE; PROTEIN-SYNTHESIS; HYPUSINE MODIFICATION;
YEAST; GROWTH; PROLIFERATION; REVEAL; MUTANT
AB eIF5A is highly conserved from archaea to mammals, essential for cell viability and the only protein known to contain the essential amino acid residue hypusine, generated by a unique posttranslational modification. eIF5A was originally identified as a translation initiation factor due to its ability to stimulate the formation of the first peptide bond. However, recent studies have shown that depletion of eIF5A causes a significant decrease in polysome run-off and an increase in the ribosome transit time, suggesting that eIF5A is actually involved in the elongation step of protein synthesis. We have previously shown that the depletion mutant tif51A-3 (eIF5A(C39Y/G118D)) shows a sicker phenotype when combined with the dominant negative mutant eft2 (H699K) of the elongation factor eEF2. In this study, we used the eIF5A(K56A) mutant to further investigate the relationship between eIF5A and eEF2. The eIF5A(K56A) mutant is temperature sensitive and has a defect in protein synthesis, but instead of causing depletion of the eIF5A protein, this mutant has a defect in hypusine modification. Like the mutant tif51A-3, the eIF5A(K56A) mutant is synthetic sick with the mutant eft2 (H699K) of eEF2. High-copy eEF2 not only improves cell growth of the eIF5A(K56A) mutant, but also corrects its increased cell size defect. Moreover, eEF2 suppression of the eIF5A(K56A) mutant is correlated with the improvement of total protein synthesis and with the increased resistance to the protein synthesis inhibitor hygromycin B. Finally, the polysome profile defect of the eIF5A(K56A) mutant is largely corrected by high-copy eEF2. Therefore, these results demonstrate that eIF5A is closely related to eEF2 function during translation elongation.
C1 [Dias, Camila A. O.; Borges Gregio, Ana Paula; Rossi, Danuza; Galvao, Fabio Carrilho; Watanabe, Tatiana F.; Valentini, Sandro R.; Zanelli, Cleslei F.] UNESP Univ Estadual Paulista, Sch Pharmaceut Sci, Dept Biol Sci, Araraquara, SP, Brazil.
[Park, Myung Hee] Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD USA.
RP Zanelli, CF (reprint author), UNESP Univ Estadual Paulista, Sch Pharmaceut Sci, Dept Biol Sci, Araraquara, SP, Brazil.
EM zanellicf@fcfar.unesp.br
RI Valentini, Sandro/C-4353-2012; Dias, Camila/G-3494-2012; zanelli,
cleslei/C-1916-2013; Inov Farmaceutica, Inct/K-2313-2013
FU Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP); Conselho
Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq); PADC from
Faculdade de Ciencias Farmaceuticas, UNESP; CAPES
FX This work was supported by grants to S.R.V. from Fundacao de Amparo a
Pesquisa do Estado de Sao Paulo (FAPESP), Conselho Nacional de
Desenvolvimento Cientifico e Tecnologico (CNPq) and PADC from Faculdade
de Ciencias Farmaceuticas, UNESP. We also thank FAPESP, CNPq and CAPES
for fellowships awarded to most of the authors (C. A. O. D.; A. P. B.
G.; D. R.; F. C. G. and T. F. W.).
NR 28
TC 13
Z9 17
U1 0
U2 5
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 2012
VL 42
IS 2-3
BP 697
EP 702
DI 10.1007/s00726-011-0985-0
PG 6
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 881RT
UT WOS:000299506000027
PM 21822730
ER
PT J
AU Nishimura, K
Lee, SB
Park, JH
Park, MH
AF Nishimura, Kazuhiro
Lee, Seung Bum
Park, Jong Hwan
Park, Myung Hee
TI Essential role of eIF5A-1 and deoxyhypusine synthase in mouse embryonic
development
SO AMINO ACIDS
LA English
DT Article
DE eIF5A; Hypusine; Polyamine; Spermidine; Deoxyhypusine synthase; Gene
knockout
ID INITIATION-FACTOR 5A; TRANSLATION INITIATION; HYPUSINE MODIFICATION;
AMINO-ACID; POSTTRANSLATIONAL SYNTHESIS; CELL-CYCLE; PROTEIN; YEAST;
INHIBITION; EXPRESSION
AB The eukaryotic initiation factor 5A (eIF5A) contains a polyamine-derived amino acid, hypusine [N-epsilon-(4-amino-2-hydroxybutyl)lysine]. Hypusine is formed post-translationally by the addition of the 4-aminobutyl moiety from the polyamine spermidine to a specific lysine residue, catalyzed by deoxyhypusine synthase (DHPS), and subsequent hydroxylation by deoxyhypusine hydroxylase (DOHH). The eIF5A precursor protein and both of its modifying enzymes are highly conserved, suggesting a vital cellular function for eIF5A and its hypusine modification. To address the functions of eIF5A and the first modification enzyme, DHPS, in mammalian development, we knocked out the Eif5a or the Dhps gene in mice. Eif5a heterozygous knockout mice and Dhps heterozygous knockout mice were viable and fertile. However, homozygous Eif5a1 (gt/gt) embryos and Dhps (gt/gt) embryos died early in embryonic development, between E3.5 and E7.5. Upon transfer to in vitro culture, homozygous Eif5a (gt/gt) or Dhps (gt/gt) blastocysts at E3.5 showed growth defects when compared to heterozygous or wild type blastocysts. Thus, the knockout of either the eIF5A-1 gene (Eif5a) or of the deoxyhypusine synthase gene (Dhps) caused early embryonic lethality in mice, indicating the essential nature of both eIF5A-1 and deoxyhypusine synthase in mammalian development.
C1 [Nishimura, Kazuhiro; Lee, Seung Bum; Park, Jong Hwan; Park, Myung Hee] NIDCR, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Park, MH (reprint author), NIDCR, Oral & Pharyngeal Canc Branch, NIH, Bldg 30,Room 211, Bethesda, MD 20892 USA.
EM mhpark@nih.gov
FU National Institute of Dental and Craniofacial Research (NIDCR) NIH;
KANAE Foundation for the Promotion of Medical Science (Japan)
FX The research was supported in part by the Intramural Research Program of
National Institute of Dental and Craniofacial Research (NIDCR) NIH and
KANAE Foundation for the Promotion of Medical Science (Japan). We thank
Dr. Edith C. Wolff (NIDCR, NIH) for critical reading of the manuscript
and helpful suggestions.
NR 37
TC 33
Z9 33
U1 0
U2 7
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 2012
VL 42
IS 2-3
BP 703
EP 710
DI 10.1007/s00726-011-0986-z
PG 8
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 881RT
UT WOS:000299506000028
PM 21850436
ER
PT J
AU Chen, CZ
Sobczak, K
Hoskins, J
Southall, N
Marugan, JJ
Zheng, W
Thornton, CA
Austin, CP
AF Chen, Catherine Z.
Sobczak, Krzysztof
Hoskins, Jason
Southall, Noel
Marugan, Juan J.
Zheng, Wei
Thornton, Charles A.
Austin, Christopher P.
TI Two high-throughput screening assays for aberrant RNA-protein
interactions in myotonic dystrophy type 1
SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY
LA English
DT Article
DE Myotonic dystrophy type 1; DM1; Muscleblind-like 1; MBNL1
ID TRINUCLEOTIDE REPEATS; SKELETAL-MUSCLE; RATIONAL DESIGN; CTG REPEAT;
MBNL; BINDING; TRANSCRIPTS; MOLECULES; DISCOVERY; EXPANSION
AB Myotonic dystrophy type 1 (DM1), the most prevalent form of adult muscular dystrophy, is caused by expansion of a CTG repeat in the 3' untranslated region of the DM protein kinase (DMPK) gene. The pathogenic effects of the CTG expansion arise from the deleterious effects of the mutant transcript. RNA with expanded CUG tracts alters the activities of several RNA binding proteins, including muscleblind-like 1 (MBNL1). MBNL1 becomes sequestered in nuclear foci in complex with the expanded CUG-repeat RNA. The resulting loss of MBNL1 activity causes misregulated alternative splicing of multiple genes, leading to symptoms of DM1. The binding interaction between MBNL1 and mutant RNA could be a key step in the pathogenesis of DM1 and serves as a potential target for therapeutic intervention. We have developed two high-throughput screens suitable assays using both homogenous time-resolved fluorescence energy transfer and AlphaScreen technologies to detect the binding of a C-terminally His-tagged MBNL1 and a biotinylated (CUG)(12) RNA. These assays are homogenous and successfully miniaturized to 1,536-well plate format. Both assays were validated and show robust signal-to-basal ratios and Z' factors.
C1 [Chen, Catherine Z.; Southall, Noel; Marugan, Juan J.; Zheng, Wei; Austin, Christopher P.] NHGRI, NIH Chem Genom Ctr, NIH, Bethesda, MD 20892 USA.
[Sobczak, Krzysztof; Hoskins, Jason; Thornton, Charles A.] Univ Rochester, Dept Neurol, Sch Med & Dent, Rochester, NY 14642 USA.
[Sobczak, Krzysztof] Adam Mickiewicz Univ Poznan, Dept Gene Express, Inst Mol Biol & Biotechnol, PL-61251 Poznan, Poland.
RP Zheng, W (reprint author), NHGRI, NIH Chem Genom Ctr, NIH, 9800 Med Ctr Dr, Bethesda, MD 20892 USA.
EM wzheng@mail.nih.gov; cthorn@mail.neurology.rochester.edu
RI Hoskins, Jason/F-5672-2012; Southall, Noel/H-8991-2012; Zheng,
Wei/J-8889-2014
OI Hoskins, Jason/0000-0001-6944-1996; Southall, Noel/0000-0003-4500-880X;
Zheng, Wei/0000-0003-1034-0757
FU Molecular Libraries Initiative of the NIH Roadmap for Medical Research,
National Institutes of Health; Marigold Foundation; Polish Ministry of
Science and Higher Education [N302 260938]; [MH087421]; [AR049077];
[NS48843]
FX This research was supported by the Molecular Libraries Initiative of the
NIH Roadmap for Medical Research, National Institutes of Health, the
Marigold Foundation research fellowship, the US grants MH087421,
AR049077, and NS48843, and the Polish Ministry of Science and Higher
Education grant N302 260938.
NR 32
TC 11
Z9 11
U1 1
U2 8
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1618-2642
J9 ANAL BIOANAL CHEM
JI Anal. Bioanal. Chem.
PD FEB
PY 2012
VL 402
IS 5
BP 1889
EP 1898
DI 10.1007/s00216-011-5604-0
PG 10
WC Biochemical Research Methods; Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 886GA
UT WOS:000299840700015
PM 22218462
ER
PT J
AU Lucenteforte, E
La Vecchia, C
Silverman, D
Petersen, GM
Bracci, PM
Ji, BT
Bosetti, C
Li, D
Gallinger, S
Miller, AB
Bueno-de-Mesquita, HB
Talamini, R
Polesel, J
Ghadirian, P
Baghurst, PA
Zatonski, W
Fontham, E
Bamlet, WR
Holly, EA
Gao, YT
Negri, E
Hassan, M
Cotterchio, M
Su, J
Maisonneuve, P
Boffetta, P
Duell, EJ
AF Lucenteforte, E.
La Vecchia, C.
Silverman, D.
Petersen, G. M.
Bracci, P. M.
Ji, B. T.
Bosetti, C.
Li, D.
Gallinger, S.
Miller, A. B.
Bueno-de-Mesquita, H. B.
Talamini, R.
Polesel, J.
Ghadirian, P.
Baghurst, P. A.
Zatonski, W.
Fontham, E.
Bamlet, W. R.
Holly, E. A.
Gao, Y. T.
Negri, E.
Hassan, M.
Cotterchio, M.
Su, J.
Maisonneuve, P.
Boffetta, P.
Duell, E. J.
TI Alcohol consumption and pancreatic cancer: a pooled analysis in the
International Pancreatic Cancer Case-Control Consortium (PanC4)
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE alcohol drinking; case-control studies; ethanol; pancreatic cancer;
pooled analysis; risk factors
ID RISK-FACTORS; CIGARETTE-SMOKING; BEVERAGE CONSUMPTION; COFFEE
CONSUMPTION; LIFE-STYLE; DIABETES-MELLITUS; EXOCRINE PANCREAS; MEDICAL
HISTORY; TOBACCO; COHORT
AB Background: Heavy alcohol drinking has been related to pancreatic cancer, but the issue is still unsolved.
Methods: To evaluate the role of alcohol consumption in relation to pancreatic cancer, we conducted a pooled analysis of 10 case-control studies (5585 cases and 11 827 controls) participating in the International Pancreatic Cancer Case-Control Consortium. We computed pooled odds ratios (ORs) by estimating study-specific ORs adjusted for selected covariates and pooling them using random effects models.
Results: Compared with abstainers and occasional drinkers (<1 drink per day), we observed no association for light-to-moderate alcohol consumption (<= 4 drinks per day) and pancreatic cancer risk; however, associations were above unity for higher consumption levels (OR = 1.6, 95% confidence interval 1.2-2.2 for subjects drinking >= 9 drinks per day). Results did not change substantially when we evaluated associations by tobacco smoking status, or when we excluded participants who reported a history of pancreatitis, or participants whose data were based upon proxy responses. Further, no notable differences in pooled risk estimates emerged across strata of sex, age, race, study type, and study area.
Conclusion: This collaborative-pooled analysis provides additional evidence for a positive association between heavy alcohol consumption and the risk of pancreatic cancer.
C1 [Boffetta, P.] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY 10029 USA.
[Lucenteforte, E.; La Vecchia, C.; Bosetti, C.; Negri, E.] Ist Ric Farmacol Mario Negri, Dept Epidemiol, Milan, Italy.
[Lucenteforte, E.; La Vecchia, C.] Univ Milan, Dept Occupat Hlth, Milan, Italy.
[Silverman, D.; Ji, B. T.; Su, J.] NCI, Bethesda, MD 20892 USA.
[Petersen, G. M.; Bamlet, W. R.] Mayo Clin, Rochester, MN USA.
[Bracci, P. M.; Holly, E. A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Li, D.; Hassan, M.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Gallinger, S.] Toronto Gen Hosp, Toronto, ON, Canada.
[Miller, A. B.; Cotterchio, M.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[Bueno-de-Mesquita, H. B.] Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands.
[Bueno-de-Mesquita, H. B.] Univ Med Ctr Utrecht UMCU, Dept Gastroenterol & Hepatol, Utrecht, Netherlands.
[Talamini, R.; Polesel, J.] Ctr Riferimento Oncol CRO Natl Canc Inst, Aviano, PN, Italy.
[Ghadirian, P.] Univ Montreal Hosp Ctr CRCHUM, Epidemiol Res Unit, Res Ctr, Montreal, PQ, Canada.
[Baghurst, P. A.] Womens & Childrens Hosp, Adelaide, SA, Australia.
[Zatonski, W.] Ctr Canc, Warsaw, Poland.
[Zatonski, W.] Inst Oncol, Warsaw, Poland.
[Fontham, E.] Louisiana State Univ, New Orleans, LA USA.
[Gao, Y. T.] Shanghai Canc Inst, Shanghai, Peoples R China.
[Cotterchio, M.] Canc Care Ontario, Populat Studies & Surveillance, Toronto, ON, Canada.
[Maisonneuve, P.] European Inst Oncol, Milan, Italy.
[Boffetta, P.] Int Prevent Res Inst, Lyon, France.
[Duell, E. J.] Int Agcy Res Canc, F-69372 Lyon, France.
[Duell, E. J.] Catalan Inst Oncol ICO IDIBELL, Barcelona, Spain.
RP Boffetta, P (reprint author), Mt Sinai Sch Med, Tisch Canc Inst, 1 Gustave L Levy Pl, New York, NY 10029 USA.
EM paolo.boffetta@exchange.mssm.edu
RI Negri, Eva/B-7244-2013; Gallinger, Steven/E-4575-2013;
OI Negri, Eva/0000-0001-9712-8526; Polesel, Jerry/0000-0001-9381-1520;
Duell, Eric J/0000-0001-5256-0163; La Vecchia,
Carlo/0000-0003-1441-897X; Lucenteforte, Ersilia/0000-0001-5608-5902;
Maisonneuve, Patrick/0000-0002-5309-4704
FU Italian Association for Cancer Research; Louisiana Board of Regents
Millennium Trust; National Institute of Health, National Cancer
Institute, Division of Cancer Epidemiology and Genetics [N01-CP-51090,
N01-CP-51089, N01-CP-51092, N01-CP-05225, N01-CP-31022, N01-CP-05227];
Cancer Research Society; National Cancer Institute of Canada; Dutch
Ministry of Public Health, Welfare and Sports; National Cancer Institute
[CA098889, CA59706, CA108370, CA109767, CA89726, N01-PC-35136]; Rombauer
Pancreatic Cancer Research Fund; California Department of Public Health;
Environmental Cancer Risk, Nutrition and Individual Susceptibility;
Province of Milan; ISCIII of the Spanish Ministry of Health [RETICC
DR06/0020]
FX The Italian and Milan studies were supported by the Italian Association
for Cancer Research. The Louisiana State University study was supported
by the Louisiana Board of Regents Millennium Trust Health Excellence
Fund [Project 5: HEF (2000-05, Genetics Studies in the Acadian
Population)]. The NCI study was supported by the Intramural Research
Program of the National Institute of Health, National Cancer Institute,
Division of Cancer Epidemiology and Genetics (N01-CP-51090,
N01-CP-51089, N01-CP-51092, N01-CP-05225, N01-CP-31022, N01-CP-05227).
The Montreal investigation in the SEARCH study was supported by the
Cancer Research Society, the Toronto contribution was supported by the
National Cancer Institute of Canada, and the Netherlands investigation
was supported by the Dutch Ministry of Public Health, Welfare and Sports
(formerly Welfare, Health, and Culture). The University of
California-San Francisco (UCSF) study work was supported in part by
National Cancer Institute grants (CA098889 to E.J.D., CA59706, CA108370,
CA109767, CA89726 to E.A.H.), and by the Rombauer Pancreatic Cancer
Research Fund. Cancer incidence data collection in the UCSF study was
supported by the California Department of Public Health, the National
Cancer Institute's Surveillance, Epidemiology and End Results Program
contract N01-PC-35136 awarded to the Northern California Cancer Center.
E.L. was supported by Environmental Cancer Risk, Nutrition and
Individual Susceptibility [European Union, Sixth Framework Program (FP6)
Network of Excellence] and the Province of Milan. At Catalan Institute
of Oncology, E.J.D. was supported by ISCIII of the Spanish Ministry of
Health (RETICC DR06/0020).
NR 79
TC 62
Z9 65
U1 0
U2 19
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 2012
VL 23
IS 2
BP 374
EP U353
DI 10.1093/annonc/mdr120
PG 9
WC Oncology
SC Oncology
GA 884YI
UT WOS:000299744400015
PM 21536662
ER
PT J
AU Coudert, B
Ciuleanu, T
Park, K
Wu, YL
Giaccone, G
Brugger, W
Gopalakrishna, P
Cappuzzo, F
AF Coudert, B.
Ciuleanu, T.
Park, K.
Wu, Y. -L.
Giaccone, G.
Brugger, W.
Gopalakrishna, P.
Cappuzzo, F.
CA SATURN Investigators
TI Survival benefit with erlotinib maintenance therapy in patients with
advanced non-small-cell lung cancer (NSCLC) according to response to
first-line chemotherapy
SO ANNALS OF ONCOLOGY
LA English
DT Article
DE erlotinib; maintenance; NSCLC; phase III; SATURN; stable disease
ID GROWTH-FACTOR RECEPTOR; PHASE-III TRIAL; CISPLATIN PLUS GEMCITABINE;
ENHANCED SENSITIVITY; CARBOPLATIN; PACLITAXEL; BEVACIZUMAB; DOCETAXEL;
INSTITUTE; SELECTION
AB Background: In the placebo-controlled phase III SATURN study, maintenance erlotinib after first-line chemotherapy demonstrated significantly prolonged progression-free survival (PFS) and overall survival (OS) in the overall study population of patients with advanced non-small-cell lung cancer (NSCLC).
Methods: After four cycles of platinum-based doublet chemotherapy, patients without progressive disease (PD) were randomised to erlotinib (150 mg/day) or placebo until PD or unacceptable toxicity. In this pre-planned analysis, data are assessed according to response to first-line chemotherapy (complete/partial response [CR/PR] or stable disease [SD]).
Results: Following first-line chemotherapy, 889 non-PD patients were included in the intention-to-treat population (55% SD; 44% CR/PR; < 1% unknown response). Erlotinib maintenance therapy significantly prolonged PFS in both the SD (hazard ratio [HR] = 0.68; P < 0.0001) and CR/PR (HR = 0.74; P = 0.0059) groups, while OS was significantly prolonged in the SD group only (HR = 0.72; P = 0.0019). The erlotinib-related OS benefit in the SD group remained significant across subgroups, irrespective of tumour histology and/or EGFR mutation status. The incidence of adverse events was similar in the SD group and the overall population, and erlotinib treatment did not negatively impact quality of life.
Conclusions: Patients with advanced NSCLC and SD following first-line platinum-based doublet chemotherapy derive a significant OS benefit from maintenance erlotinib therapy.
C1 [Coudert, B.] Ctr Georges Francois Leclerc, Dept Med Oncol, Off Clin & Therapeut Studies, F-21000 Dijon, France.
[Ciuleanu, T.] Inst Oncol Ion Chiricuta, Cluj Napoca, Romania.
[Park, K.] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Med, Seoul, South Korea.
[Wu, Y. -L.] Guangdong Gen Hosp, Guangdong Lung Canc Inst, Guangzhou, Guangdong, Peoples R China.
[Giaccone, G.] NIH, Med Oncol Branch, Bethesda, MD 20892 USA.
[Brugger, W.] Univ Freiburg, Dept Hematol Oncol, Schwarzwald Baar Clin, Teaching Hosp, Villingen Schwenningen, Germany.
[Gopalakrishna, P.] Roche Prod Ltd, Dept Pharma Dev, Welwyn Garden City AL7 3AY, Herts, England.
[Cappuzzo, F.] Osped Civile Livorno, Dept Hematol Oncol, Livorno, Italy.
RP Coudert, B (reprint author), Ctr Georges Francois Leclerc, Dept Med Oncol, Off Clin & Therapeut Studies, 1 Rue Pr Marion, F-21000 Dijon, France.
EM BCoudert@cgfl.fr
RI Giaccone, Giuseppe/E-8297-2017;
OI Giaccone, Giuseppe/0000-0002-5023-7562; Wu, Yi-Long/0000-0002-3611-0258;
Cappuzzo, Federico/0000-0002-6295-6767
FU F. Hoffmann-La Roche Ltd.
FX funding; This work was supported by F. Hoffmann-La Roche Ltd.
NR 28
TC 49
Z9 53
U1 1
U2 8
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 2012
VL 23
IS 2
BP 388
EP 394
DI 10.1093/annonc/mdr125
PG 7
WC Oncology
SC Oncology
GA 884YI
UT WOS:000299744400017
PM 21610154
ER
PT J
AU Le, K
Li, RF
Xu, SW
Wu, XQ
Huang, HQ
Bao, YX
Cai, Y
Lan, T
Moss, J
Li, CX
Zou, J
Shen, XY
Liu, PQ
AF Le, Kang
Li, Ruifang
Xu, Suowen
Wu, Xiaoqian
Huang, Heqing
Bao, Yingxia
Cai, Yi
Lan, Tian
Moss, Joel
Li, Cuixian
Zou, Jian
Shen, Xiaoyan
Liu, Peiqing
TI PPAR alpha activation inhibits endothelin-1-induced cardiomyocyte
hypertrophy by prevention of NFATc4 binding to GATA-4
SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Article
DE NFATc4; PPAR alpha; Cardiac hypertrophy; GATA-4; Fenofibrate
ID CONGESTIVE-HEART-FAILURE; CARDIAC GENE-EXPRESSION; RECEPTOR-ALPHA;
SIGNALING PATHWAYS; NUCLEAR-FACTOR; TRANSCRIPTION FACTORS; CELL
HYPERTROPHY; NEONATAL-RAT; IN-VITRO; T-CELLS
AB Peroxisome proliferator-activated receptor alpha (PPAR alpha) has been implicated in the pathogenesis of cardiac hypertrophy, although its mechanism of action remains largely unknown. To determine the effect of PPARa activation on endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy and explore its molecular mechanisms, we evaluated the interaction of PPAR alpha with nuclear factor of activated T-cells c4 (NFATc4) in nuclei of cardiomyocytes from neonatal rats in primary culture. In ET-1-stimulated cardiomyocytes, data from electrophoretic mobility-shift assays (EMSA) and co-immunoprecipitation (co-IP) revealed that fenofibrate (Fen), a PPAR alpha activator, in a concentration-dependent manner, enhanced the association of NFATc4 with PPAR alpha and decreased its interaction with GATA-4, in promoter complexes involved in activation of the rat brain natriuretic peptide (rBNP) gene. Effects of PPAR alpha overexpression were similar to those of its activation by Fen. PPAR alpha depletion by small interfering RNA abolished inhibitory effects of Fen on NFATc4 binding to GATA-4 and the rBNP DNA. Quantitative RT-PCR and confocal microscopy confirmed inhibitory effects of PPAR alpha activation on elevation of rBNP mRNA levels and ET-1-induced cardiomyocyte hypertrophy. Our results suggest that activated PPAR alpha can compete with GATA-4 binding to NFATc4, thereby decreasing transactivation of NFATc4, and interfering with ET-1 induced cardiomyocyte hypertrophy. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Shen, Xiaoyan] Sun Yat Sen Univ, Dept Pharmacol & Toxicol, Sch Pharmaceut Sci, Higher Educ Mega Ctr, Guangzhou 510006, Guangdong, Peoples R China.
[Li, Ruifang] Henan Univ Sci & Technol, Dept Pharmacol, Luoyang, Peoples R China.
[Wu, Xiaoqian] Guangzhou Med Univ, Dept Pharmacol, Guangzhou, Guangdong, Peoples R China.
[Le, Kang; Xu, Suowen; Moss, Joel] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
RP Shen, XY (reprint author), Sun Yat Sen Univ, Dept Pharmacol & Toxicol, Sch Pharmaceut Sci, Higher Educ Mega Ctr, 132 E Wai Huan Rd, Guangzhou 510006, Guangdong, Peoples R China.
EM xyshen08@gmail.com; liupq@mail.sysu.edu.cn
RI Le, Kang/D-1630-2016
FU National Natural Science Foundation of China [81072641]; NSFC-CIHR
China-Canada Joint Health Research Initiative Proposal [30811120434];
National Science and Technology Major Project of China "Key New Drug
Creation and Manufacturing Program" [2009ZX09102-152, 2011ZX09401-307];
Major Project of Guangdong Province [2008A030201013]; Major Project of
Guangzhou City [2008Z1-E571]; National Institutes of Health, NHLBI
FX This work was supported by grants from the National Natural Science
Foundation of China (No. 81072641); NSFC-CIHR China-Canada Joint Health
Research Initiative Proposal (No. 30811120434); the National Science and
Technology Major Project of China "Key New Drug Creation and
Manufacturing Program" (No. 2009ZX09102-152, 2011ZX09401-307); Major
Project of Guangdong Province (2008A030201013) Major Project of
Guangzhou City (2008Z1-E571), and Intramural Research Program, National
Institutes of Health, NHLBI (J.M.). We thank Dr. Martha Vaughan
(Cardiovascular and Pulmonary Branch, NHLBI, National Institutes of
Health) for valuable discussions and manuscript review. We extend our
gratitude to all members of the Department of Pharmacology and
Toxicology for technical assistance.
NR 49
TC 15
Z9 17
U1 1
U2 10
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-9861
J9 ARCH BIOCHEM BIOPHYS
JI Arch. Biochem. Biophys.
PD FEB 1
PY 2012
VL 518
IS 1
BP 71
EP 78
DI 10.1016/j.abb.2011.11.024
PG 8
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 885TM
UT WOS:000299803700010
PM 22198280
ER
PT J
AU Smith, SB
Maixner, DW
Fillingim, RB
Slade, G
Gracely, RH
Ambrose, K
Zaykin, DV
Hyde, C
John, S
Tan, K
Maixner, W
Diatchenko, L
AF Smith, Shad B.
Maixner, Dylan W.
Fillingim, Roger B.
Slade, Gary
Gracely, Richard H.
Ambrose, Kirsten
Zaykin, Dmitri V.
Hyde, Craig
John, Sally
Tan, Keith
Maixner, William
Diatchenko, Luda
TI Large candidate gene association study reveals genetic risk factors and
therapeutic targets for fibromyalgia
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID O-METHYLTRANSFERASE GENE; IRRITABLE-BOWEL-SYNDROME; RGS PROTEINS; PAIN;
POLYMORPHISM; RECEPTOR; TRANSPORTER; EXPRESSION; RAT; THRESHOLDS
AB Objective Fibromyalgia (FM) represents a complex disorder that is characterized by widespread pain and tenderness and is frequently accompanied by additional somatic and cognitive/affective symptoms. Genetic risk factors are known to contribute to the etiology of the syndrome. The aim of this study was to examine >350 genes for association with FM, using a large-scale candidate gene approach.
Methods. The study group comprised 496 patients with FM (cases) and 348 individuals with no chronic pain (controls). Genotyping was performed using a dedicated gene array chip, the Pain Research Panel, which assays variants characterizing >350 genes known to be involved in the biologic pathways relevant to nociception, inflammation, and mood. Association testing was performed using logistic regression.
Results. Significant differences in allele frequencies between cases and controls were observed for 3 genes: GABRB3 (rs4906902; P = 3.65 x 10(-6)), TAAR1 (rs8192619; P = 1.11 x 10(-5)), and GBP1 (rs7911; P = 1.06 x 10(-4)). These 3 genes and 7 other genes with suggestive evidence for association were examined in a second, independent cohort of patients with FM and control subjects who were genotyped using the Perlegen 600K platform. Evidence of association in the replication cohort was observed for TAAR1, RGS4, CNR1, and GRIA4.
Conclusion. Variation in these 4 replicated genes may serve as a basis for development of new diagnostic approaches, and the products of these genes may contribute to the pathophysiology of FM and represent potential targets for therapeutic action.
C1 [Smith, Shad B.; Fillingim, Roger B.; Slade, Gary; Gracely, Richard H.; Ambrose, Kirsten; Maixner, William; Diatchenko, Luda] Algynomics, Chapel Hill, NC 27514 USA.
[Smith, Shad B.; Maixner, Dylan W.; Slade, Gary; Gracely, Richard H.; Maixner, William; Diatchenko, Luda] Univ N Carolina, Chapel Hill, NC USA.
[Fillingim, Roger B.] Univ Florida, Gainesville, FL USA.
[Zaykin, Dmitri V.] Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC USA.
[Hyde, Craig; John, Sally] Pfizer Global Res & Dev, Groton, CT USA.
[Tan, Keith] Pfizer Global Res & Dev, Sandwich, Kent, England.
RP Diatchenko, L (reprint author), Algynomics, 208 N Columbia St, Chapel Hill, NC 27514 USA.
EM ldiatchenko@algynomics.com
FU Pfizer; Algynomics; NIH (National Institute of Environmental Health
Sciences); NIH [R01-DE-16558]; Cytogel; Codman; Eli Lilly; Jazz
Pharmaceuticals
FX Supported by Pfizer and Algynomics. Dr. Zaykin's work was supported by
the NIH Intramural Research Program (National Institute of Environmental
Health Sciences). An NIH grant (National Institute of Dental and
Craniofacial Research grant R01-DE-16558 to Drs. Maixner and Diatchenko)
supported the collection of a portion of the study data.; Dr. Fillingim
has received consulting fees, speaking fees, and/or honoraria from
Cytogel and Codman (less than $10,000 each). Dr. Gracely has received
consulting fees, speaking fees, and/or honoraria from Eli Lilly and Jazz
Pharmaceuticals (less than $10,000 each). Mr. Maixner has received
consulting fees, speaking fees, and/or honoraria from Algynomics (less
than $10,000). Dr. Diatchenko has received consulting fees, speaking
fees, and/or honoraria from Algynomics (more than $10,000) and has
provided paid consultation with investment analysts on behalf of
Algynomics. Mr. Maixner and Dr. Diatchenko are coinventors on the patent
for the Pain Research Panel, a dedicated gene array chip used for
genotyping; the patent is owned by the University of North Carolina and
licensed to Algynomics. Drs. Smith, Fillingim, Slade, Gracely, and
Diatchenko, and Mr. Maixner and Ms Ambrose own stock or stock options in
Algynomics; Mr. Maixner is an equity holder in Algynomics. Drs. Hyde,
John, and Tan own stock or stock options in Pfizer.
NR 51
TC 28
Z9 30
U1 0
U2 11
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 2012
VL 64
IS 2
BP 584
EP 593
DI 10.1002/art.33338
PG 10
WC Rheumatology
SC Rheumatology
GA 883HU
UT WOS:000299625700034
PM 21905019
ER
PT J
AU Abidi, MH
Agarwal, R
Tageja, N
Ayash, L
Ventimiglia, M
Deol, A
Al-Kadhimi, Z
Lum, L
Ratanatharathorn, V
Abrams, J
Uberti, JP
AF Abidi, M. H.
Agarwal, R.
Tageja, N.
Ayash, L.
Ventimiglia, M.
Deol, A.
Al-Kadhimi, Z.
Lum, L.
Ratanatharathorn, V
Abrams, J.
Uberti, J. P.
TI MELPHALAN 180mg/m(2) CAN BE SAFELY ADMINISTERED AS CONDITIONING REGIMEN
PRIOR TO AN AUTOLOGOUS STEM CELL TRANSPLANTATION IN MULTIPLE MYELOMA
PATIENTS WITH CREATININE CLEARANCE <= 60ml/min/1.73 m(2) WITH USE OF
PALIFERMIN FOR CYTO-PROTECTION: RESULTS OF A PHASE I TRIAL
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Abidi, M. H.; Ayash, L.; Deol, A.; Al-Kadhimi, Z.; Lum, L.; Ratanatharathorn, V; Abrams, J.; Uberti, J. P.] Wayne State Univ, Detroit, MI USA.
[Abidi, M. H.; Ayash, L.; Ventimiglia, M.; Deol, A.; Al-Kadhimi, Z.; Lum, L.; Ratanatharathorn, V; Abrams, J.; Uberti, J. P.] Karmanos Canc Ctr, Detroit, MI USA.
[Agarwal, R.] Cent Michigan Univ, Saginaw, MI USA.
[Tageja, N.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 130
BP S252
EP S253
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600131
ER
PT J
AU Baird, K
Booher, S
Comis, LE
Joe, GO
Steinberg, SM
Spencer, SD
Figg, WD
Takebe, N
Pavletic, SZ
Cowen, EW
AF Baird, K.
Booher, S.
Comis, L. E.
Joe, G. O.
Steinberg, S. M.
Spencer, S. D.
Figg, W. D.
Takebe, N.
Pavletic, S. Z.
Cowen, E. W.
TI PHASE II PILOT STUDY OF IMATINIB MESYLATE FOR THE TREATMENT OF SEVERE
SCLEROTIC SKIN CHRONIC GRAFT VERSUS HOST DISEASE (ScGVHD)
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Baird, K.; Booher, S.; Comis, L. E.; Joe, G. O.; Steinberg, S. M.; Spencer, S. D.; Figg, W. D.; Takebe, N.; Pavletic, S. Z.; Cowen, E. W.] NIH, Bethesda, MD 20892 USA.
RI Figg Sr, William/M-2411-2016
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 2012
VL 18
IS 2
SU 2
MA 16
BP S208
EP S208
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600017
ER
PT J
AU Battiwalla, M
Fakhrejahani, F
Klotz, J
Pophali, P
Draper, D
Haggerty, J
McIver, Z
Chawla, K
Ito, S
Barrett, J
AF Battiwalla, M.
Fakhrejahani, F.
Klotz, J.
Pophali, P.
Draper, D.
Haggerty, J.
McIver, Z.
Chawla, K.
Ito, S.
Barrett, J.
TI RADIATION EXPOSURE FROM DIAGNOSTIC PROCEDURES IN ALLOGENEIC STEM CELL
TRANSPLANTATION DOES NOT SIGNIFICANTLY IMPACT OVERALL SURVIVAL OR
NON-RELAPSE MORTALITY
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Battiwalla, M.; Fakhrejahani, F.; Klotz, J.; Pophali, P.; Draper, D.; Haggerty, J.; McIver, Z.; Chawla, K.; Ito, S.; Barrett, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Pophali, Priyanka/P-8646-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 370
BP S341
EP S341
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600369
ER
PT J
AU Battiwalla, M
McIver, Z
Klotz, J
Draper, D
Haggerty, J
Chawla, K
Superata, J
Stroncek, D
Khuu, H
Citrin, D
Sabatino, M
Leitman, S
Ito, S
Barrett, J
AF Battiwalla, M.
McIver, Z.
Klotz, J.
Draper, D.
Haggerty, J.
Chawla, K.
Superata, J.
Stroncek, D.
Khuu, H.
Citrin, D.
Sabatino, M.
Leitman, S.
Ito, S.
Barrett, J.
TI OUTCOMES AFTER CD34+SELECTION WITH OR WITHOUT THE ADDITION OF
PHOTO-ALLODEPLETED T LYMPHOCYTES IN MYELOABLATIVE HLA-MATCHED SIBLING
TRANSPLANTATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Battiwalla, M.; McIver, Z.; Klotz, J.; Draper, D.; Haggerty, J.; Chawla, K.; Superata, J.; Ito, S.; Barrett, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Stroncek, D.; Khuu, H.; Sabatino, M.; Leitman, S.] NIH, CC, Bethesda, MD 20892 USA.
[Citrin, D.] NCI, CCR, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
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 2012
VL 18
IS 2
SU 2
MA 151
BP S260
EP S260
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600152
ER
PT J
AU Boyiadzis, M
Klein, JP
Arora, M
Weisdorf, DJ
Hassebroek, A
Lee, SJ
Flowers, ME
Cutler, CS
Urbano-Ispizua, A
Antin, JH
Bolwell, BJ
Cahn, JY
Cairo, MS
Gale, RP
Herzig, RH
Isola, LM
Jacobsohn, DA
Jagasia, MH
Klumpp, TR
Petersdorf, EW
Wingard, JR
Horowitz, MM
Pavletic, SZ
AF Boyiadzis, M.
Klein, J. P.
Arora, M.
Weisdorf, D. J.
Hassebroek, A.
Lee, S. J.
Flowers, M. E.
Cutler, C. S.
Urbano-Ispizua, A.
Antin, J. H.
Bolwell, B. J.
Cahn, J-Y
Cairo, M. S.
Gale, R. P.
Herzig, R. H.
Isola, L. M.
Jacobsohn, D. A.
Jagasia, M. H.
Klumpp, T. R.
Petersdorf, E. W.
Wingard, J. R.
Horowitz, M. M.
Pavletic, S. Z.
TI IMPACT OF CHRONIC GVHD ON LATE RELAPSE, TREATMENT RELATED MORTALITY AND
SURVIVAL AFTER ALLOGENEIC HEMATOPOIETIC CELL TRANSPLANTATION FOR
HEMATOLOGICAL MALIGNANCIES
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Boyiadzis, M.] UPMC Canc Ctr, Pittsburgh, PA USA.
[Klein, J. P.; Horowitz, M. M.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Arora, M.; Weisdorf, D. J.] Univ Minnesota Med Ctr, Minneapolis, MN USA.
[Hassebroek, A.] Ctr Int Blood & Marrow Transplant Res, Minneapolis, MN USA.
[Lee, S. J.; Flowers, M. E.; Petersdorf, E. W.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Cutler, C. S.; Antin, J. H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Urbano-Ispizua, A.] Hosp Clin Barcelona, Barcelona, Spain.
[Bolwell, B. J.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Cahn, J-Y] CHU Grenoble, Hosp A Michallon, F-38043 Grenoble, France.
[Cairo, M. S.] Morgan Stanley Childrens Hosp New York Presbyteri, New York, NY USA.
[Gale, R. P.] Celgene Corp, Los Angeles, CA USA.
[Herzig, R. H.] James Brown Canc Ctr, Louisville, KY USA.
[Isola, L. M.] Mt Sinai Sch Med, New York, NY USA.
[Jacobsohn, D. A.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Jagasia, M. H.] Vanderbilt Univ Sch Med, Nashville, TN USA.
[Klumpp, T. R.] Temple Univ Bone Marrow Transplant Program, Philadelphia, PA USA.
[Wingard, J. R.] Univ Florida, Gainesville, FL USA.
[Wingard, J. R.] Shands HealthCare, Gainesville, FL USA.
[Pavletic, S. Z.] NCI, Bethesda, MD 20892 USA.
RI Cahn, Jean-Yves/M-6493-2014
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 2012
VL 18
IS 2
SU 2
MA 19
BP S209
EP S210
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600020
ER
PT J
AU Buxbaum, NP
Williams, KM
Amarnath, S
Treadwell, S
Eckhaus, M
Gress, RE
AF Buxbaum, N. P.
Williams, K. M.
Amarnath, S.
Treadwell, S.
Eckhaus, M.
Gress, R. E.
TI SEVERE CHRONIC GRAFT-VERSUS-HOST DISEASE IS ASSOCIATED WITH IMPAIRED
THYMOPOIESIS AND PERIPHERAL LYMPHOCYTE EXPANSION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Buxbaum, N. P.; Williams, K. M.; Amarnath, S.; Treadwell, S.; Eckhaus, M.; Gress, R. E.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 435
BP S364
EP S365
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600434
ER
PT J
AU Carpenter, PA
Chai, X
Kurland, BF
Palmer, JM
Inamoto, Y
Martin, PJ
Johnston, L
Arora, M
Cutler, C
Arai, S
Flowers, ME
Jacobsohn, D
Pavletic, S
Lee, SJ
AF Carpenter, P. A.
Chai, X.
Kurland, B. F.
Palmer, J. M.
Inamoto, Y.
Martin, P. J.
Johnston, L.
Arora, M.
Cutler, C.
Arai, S.
Flowers, M. E.
Jacobsohn, D.
Pavletic, S.
Lee, S. J.
TI RECOMMENDED MEASURES FOR JOINT CHRONIC GVHD: RESULTS FROM THE CHRONIC
GVHD CONSORTIUM
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Carpenter, P. A.; Chai, X.; Kurland, B. F.; Inamoto, Y.; Martin, P. J.; Flowers, M. E.; Lee, S. J.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Palmer, J. M.] Med Coll Wisconsin, Milwaulkee, WI USA.
[Johnston, L.; Arai, S.] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Cutler, C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Jacobsohn, D.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Pavletic, S.] NCI, Bethesda, MD 20892 USA.
[Arora, M.] Univ Minnesota, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 414
BP S357
EP S357
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600413
ER
PT J
AU Cruz, CRY
Micklethwaite, KP
Savoldo, B
Ku, S
Krance, RA
Diouf, O
Kamble, R
Kennedy-Nasser, A
Barrett, AJ
Shpall, EJ
Heslop, HE
Rooney, CM
Brenner, MK
Bollard, CM
Dotti, G
AF Cruz, C. R. Y.
Micklethwaite, K. P.
Savoldo, B.
Ku, S.
Krance, R. A.
Diouf, O.
Kamble, R.
Kennedy-Nasser, A.
Barrett, A. J.
Shpall, E. J.
Heslop, H. E.
Rooney, C. M.
Brenner, M. K.
Bollard, C. M.
Dotti, G.
TI SAFETY AND PERSISTENCE OF INFUSED CD19-CAR-MODIFIED MULTIVIRUS SPECIFIC
CTLS IN B CELL MALIGNANCIES POST ALLOGENEIC HEMATOPOIETIC STEM CELL
TRANSPLANTATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Cruz, C. R. Y.; Micklethwaite, K. P.; Savoldo, B.; Ku, S.; Krance, R. A.; Diouf, O.; Kamble, R.; Kennedy-Nasser, A.; Heslop, H. E.; Rooney, C. M.; Brenner, M. K.; Bollard, C. M.; Dotti, G.] Texas Childrens Hosp, Baylor Coll Med, Methodist Hosp, Houston, TX 77030 USA.
[Barrett, A. J.] NIH, Bethesda, MD 20892 USA.
[Shpall, E. J.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 1
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 2012
VL 18
IS 2
SU 2
MA 191
BP S274
EP S274
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600192
ER
PT J
AU Kennedy-Nasser, AA
Ku, S
Melenhorst, J
Barrett, J
Hazrat, Y
Durett, AG
Foster, A
Savoldo, B
Yvon, E
Heslop, HE
Carrum, G
Kamble, RT
Brenner, MK
Krance, RA
Bollard, CM
AF Kennedy-Nasser, A. A.
Ku, S.
Melenhorst, J.
Barrett, J.
Hazrat, Y.
Durett, A. G.
Foster, A.
Savoldo, B.
Yvon, E.
Heslop, H. E.
Carrum, G.
Kamble, R. T.
Brenner, M. K.
Krance, R. A.
Bollard, C. M.
TI ULTRA LOW-DOSE IL-2 MEDIATED EXPANSION OF REGULATORY T CELLS AS GVHD
PROPHYLAXIS FOR RECIPIENTS OF ALLOGENEIC HEMATOPOIETIC STEM CELLS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Kennedy-Nasser, A. A.; Ku, S.; Hazrat, Y.; Durett, A. G.; Foster, A.; Savoldo, B.; Yvon, E.; Heslop, H. E.; Carrum, G.; Kamble, R. T.; Brenner, M. K.; Krance, R. A.; Bollard, C. M.] Baylor Coll Med, Houston, TX 77030 USA.
[Melenhorst, J.; Barrett, J.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 416
BP S358
EP S358
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600415
ER
PT J
AU Pidala, J
Vogelsang, G
Martin, P
Chai, X
Storer, B
Pavletic, S
Weisdorf, D
Jagasia, M
Cutler, C
Palmer, J
Jacobsohn, D
Arai, S
Lee, SJ
AF Pidala, J.
Vogelsang, G.
Martin, P.
Chai, X.
Storer, B.
Pavletic, S.
Weisdorf, D.
Jagasia, M.
Cutler, C.
Palmer, J.
Jacobsohn, D.
Arai, S.
Lee, S. J.
TI OVERLAP SUBTYPE OF CHRONIC GVHD IS ASSOCIATED WITH ADVERSE PROGNOSIS,
FUNCTIONAL IMPAIRMENT, AND INFERIOR PATIENT REPORTED OUTCOMES: A CHRONIC
GVHD CONSORTIUM STUDY
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Pidala, J.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Martin, P.; Chai, X.; Storer, B.; Lee, S. J.] Fred Hutchinson Canc Res Ctr, Seattle, WA USA.
[Pavletic, S.] NCI, Bethesda, MD 20892 USA.
[Weisdorf, D.] Univ Minnesota, Minneapolis, MN 55455 USA.
[Jagasia, M.] Vanderbilt Univ, Nashville, TN 37235 USA.
[Cutler, C.] Dana Farber Canc Inst, Boston, MA USA.
[Palmer, J.] Med Coll Wisconsin, Milwaukee, WI USA.
[Arai, S.] Stanford Univ, Stanford, CA 94305 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 6
BP S204
EP S204
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600007
ER
PT J
AU Pophali, PA
Klotz, J
Chawla, K
Koklanaris, E
Ito, S
Le, RQ
Savani, BN
Barrett, J
Battiwalla, M
AF Pophali, P. A.
Klotz, J.
Chawla, K.
Koklanaris, E.
Ito, S.
Le, R. Q.
Savani, B. N.
Barrett, J.
Battiwalla, M.
TI MAGNITUDE OF DYSLIPIDEMIAS AND CARDIOVASCULAR RISK IN SURVIVORS OF
ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION (SCT) UP TO THE
SECOND DECADE POST-TRANSPLANT
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Pophali, P. A.; Klotz, J.; Chawla, K.; Koklanaris, E.; Ito, S.; Le, R. Q.; Barrett, J.; Battiwalla, M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Savani, B. N.] Vanderbilt Univ, Nashville, TN USA.
RI Pophali, Priyanka/P-8646-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 222
BP S286
EP S286
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600223
ER
PT J
AU Pophali, PA
Klotz, J
Koklanaris, E
Savani, BN
Chawla, K
Le, RQ
Wu, C
Barrett, J
Battiwalla, M
AF Pophali, P. A.
Klotz, J.
Koklanaris, E.
Savani, B. N.
Chawla, K.
Le, R. Q.
Wu, C.
Barrett, J.
Battiwalla, M.
TI CHRONIC GVHD AND AGE ARE NOT ASSOCIATED WITH BONE MINERAL DENSITY LOSS
IN THE SECOND DECADE POST-ALLOGENEIC STEM CELL TRANSPLANTATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Pophali, P. A.; Klotz, J.; Koklanaris, E.; Chawla, K.; Le, R. Q.; Wu, C.; Barrett, J.; Battiwalla, M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Savani, B. N.] Vanderbilt Univ, Nashville, TN USA.
RI Pophali, Priyanka/P-8646-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 200
BP S277
EP S277
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600201
ER
PT J
AU Shah, NN
Loeb, D
Khuu, H
Stroncek, D
Raffeld, M
Delbrook, C
Richards, K
Baird, K
Levine, J
Leitman, S
Mackall, CL
Fry, TJ
Wayne, AS
AF Shah, N. N.
Loeb, D.
Khuu, H.
Stroncek, D.
Raffeld, M.
Delbrook, C.
Richards, K.
Baird, K.
Levine, J.
Leitman, S.
Mackall, C. L.
Fry, T. J.
Wayne, A. S.
TI A PILOT TRIAL OF WTI PEPTIDE-LOADED ALLOGENEIC DENDRITIC CELL (DC)
VACCINATION AND DONOR LYMPHOCYTE INFUSION (DLI) FOR WTI-EXPRESSING
HEMATOLOGIC MALIGNANCIES AND POST-TRANSPLANT RELAPSE
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Shah, N. N.; Khuu, H.; Stroncek, D.; Raffeld, M.; Delbrook, C.; Richards, K.; Baird, K.; Levine, J.; Leitman, S.; Mackall, C. L.; Fry, T. J.; Wayne, A. S.] NIH, Bethesda, MD 20892 USA.
[Loeb, D.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 150
BP S259
EP S260
PG 2
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600151
ER
PT J
AU Shah, NN
Bhojwani, D
Silverman, LB
Whitlock, JA
Richards, K
Stetler-Stevenson, M
Buzoianu, M
Ibrahim, R
Pastan, I
Wayne, AS
AF Shah, N. N.
Bhojwani, D.
Silverman, L. B.
Whitlock, J. A.
Richards, K.
Stetler-Stevenson, M.
Buzoianu, M.
Ibrahim, R.
Pastan, I
Wayne, A. S.
TI A NOVEL ANTI-CD22 IMMUNOTOXIN, MOXETUMOMAB PASUDOTOX (HA22, CAT-8015):
ACTIVITY IN PEDIATRIC PATIENTS WITH RELAPSED ACUTE LYMPHOBLASTIC
LEUKEMIA (ALL) AFTER ALLOGENEIC HEMATOPOIETIC STEM CELL TRANSPLANTATION
(SCT)
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Shah, N. N.; Richards, K.; Stetler-Stevenson, M.; Pastan, I; Wayne, A. S.] NIH, Bethesda, MD 20892 USA.
[Bhojwani, D.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Silverman, L. B.] Childrens Hosp, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Whitlock, J. A.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Buzoianu, M.; Ibrahim, R.] MedImmune LLC, Gaithersburg, MD USA.
NR 0
TC 2
Z9 3
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 2012
VL 18
IS 2
SU 2
MA 84
BP S234
EP S234
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600085
ER
PT J
AU Shand, JC
Capitini, CM
Qin, H
Fry, TJ
AF Shand, J. C.
Capitini, C. M.
Qin, H.
Fry, T. J.
TI BROAD EXPRESSION OF A MINOR HISTOCOMPATIBILITY ANTIGEN RESULTS IN
IMPAIRED ANTITUMOR IMMUNITY THAT CANNOT BE OVERCOME WITH DENDRITIC CELL
VACCINATION
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Shand, J. C.] Johns Hopkins Univ, Natl Canc Inst Combined Fellowship, Baltimore, MD USA.
[Capitini, C. M.; Qin, H.; Fry, T. J.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 334
BP S328
EP S328
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600333
ER
PT J
AU Shanis, DL
Pophali, P
Koklanaris, E
Battiwalla, M
Barrett, J
Stratton, P
AF Shanis, D. L.
Pophali, P.
Koklanaris, E.
Battiwalla, M.
Barrett, J.
Stratton, P.
TI CERVICAL CYTOLOGY SCREENING IN LONG-TERM SURVIVORS OF ALLOGENEIC STEM
CELL TRANSPLANTATION WITH GENITAL GRAFT VERSUS HOST DISEASE
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Shanis, D. L.; Stratton, P.] Eunice Kennedy Shriver NICHD, NIH, Bethesda, MD USA.
[Pophali, P.; Koklanaris, E.; Battiwalla, M.; Barrett, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Pophali, Priyanka/P-8646-2016
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 2012
VL 18
IS 2
SU 2
MA 214
BP S282
EP S282
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600215
ER
PT J
AU Shanis, DL
Pophali, P
Koklanaris, E
Savani, BN
Battiwalla, M
Barrett, J
Stratton, P
AF Shanis, D. L.
Pophali, P.
Koklanaris, E.
Savani, B. N.
Battiwalla, M.
Barrett, J.
Stratton, P.
TI HIGH RATES OF GENITAL TRACT DYSPLASIA IN LONG-TERM SURVIVORS OF
ALLOGENEIC STEM CELL TRANSPLANTATION AND ASSOCIATED RISK FACTORS
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Shanis, D. L.; Stratton, P.] Eunice Kennedy Shriver NICHD, NIH, Bethesda, MD USA.
[Pophali, P.; Koklanaris, E.; Battiwalla, M.; Barrett, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Savani, B. N.] Vanderbilt Univ, Med Ctr, Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
RI Pophali, Priyanka/P-8646-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 212
BP S282
EP S282
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600213
ER
PT J
AU Tomblyn, M
Trifilio, S
Chen, M
Klein, J
Boeckh, M
Gea-Banacloche, J
Szabolcs, P
Bennett, C
AF Tomblyn, M.
Trifilio, S.
Chen, M.
Klein, J.
Boeckh, M.
Gea-Banacloche, J.
Szabolcs, P.
Bennett, C.
TI RISK FACTORS AND OUTCOMES IN PATIENTS WITH ATYPICAL MOLD INFECTION (AMI)
FOLLOWING ALLOGENEIC HEMATOPOIETIC CELL TRANSPLANTATION (HCT): A CIBMTR
ANALYSIS FROM THE INFECTION AND IMMUNE RECONSTITUTION WORKING COMMITTEE
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Tomblyn, M.] Univ S Florida, H Lee Moffitt Canc Ctr, Tampa, FL 33682 USA.
[Trifilio, S.] Northwestern Univ, Chicago, IL 60611 USA.
[Chen, M.; Klein, J.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Boeckh, M.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Gea-Banacloche, J.] NIH, Bethesda, MD 20892 USA.
[Szabolcs, P.] Univ Pittsburgh, Pittsburgh, PA USA.
[Bennett, C.] Univ S Carolina, Columbia, SC 29208 USA.
NR 0
TC 0
Z9 0
U1 1
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 2012
VL 18
IS 2
SU 2
MA 96
BP S238
EP S238
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600097
ER
PT J
AU Treister, N
Lee, S
Chai, X
Kurland, B
Pidala, J
Palmer, J
Flowers, M
Jagasia, M
Pavletic, S
Cutler, C
AF Treister, N.
Lee, S.
Chai, X.
Kurland, B.
Pidala, J.
Palmer, J.
Flowers, M.
Jagasia, M.
Pavletic, S.
Cutler, C.
TI MEASUREMENT OF ORAL CHRONIC GRAFT-VERSUS-HOST DISEASE
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Treister, N.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Lee, S.; Chai, X.; Kurland, B.; Flowers, M.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Pidala, J.] H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL USA.
[Palmer, J.] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Jagasia, M.] Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
[Pavletic, S.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Cutler, C.] Dana Farber Canc Inst, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1083-8791
J9 BIOL BLOOD MARROW TR
JI Biol. Blood Marrow Transplant.
PD FEB
PY 2012
VL 18
IS 2
SU 2
MA 430
BP S363
EP S363
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600429
ER
PT J
AU Williams, KM
Pavletic, SZ
Hakim, FT
Mitchell, SA
Gea-Banacloche, JC
Comis, L
Cowen, EW
Baird, K
Shelhamer, JH
Blacklock-Schuver, BAJ
Avila, D
Carpenter, A
Urban, A
Taylor, T
Zuchlinski, D
Baruffaldi, J
Lee, S
Gress, RE
AF Williams, K. M.
Pavletic, S. Z.
Hakim, F. T.
Mitchell, S. A.
Gea-Banacloche, J. C.
Comis, L.
Cowen, E. W.
Baird, K.
Shelhamer, J. H.
Blacklock-Schuver, B. A. J.
Avila, D.
Carpenter, A.
Urban, A.
Taylor, T.
Zuchlinski, D.
Baruffaldi, J.
Lee, S.
Gress, R. E.
TI PRELIMINARY RESULTS OF A PHASE II TRIAL OF MONTELUKAST FOR THE TREATMENT
OF BRONCHIOLITIS OBLITERANS SYNDROME AFTER HSCT
SO BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
LA English
DT Meeting Abstract
CT BMT Tandem Meeting
CY FEB 01-05, 2012
CL San Diego, CA
C1 [Williams, K. M.; Pavletic, S. Z.; Hakim, F. T.; Mitchell, S. A.; Gea-Banacloche, J. C.; Baird, K.; Blacklock-Schuver, B. A. J.; Avila, D.; Carpenter, A.; Urban, A.; Taylor, T.; Zuchlinski, D.; Baruffaldi, J.; Gress, R. E.] NCI, NIH, Bethesda, MD 20892 USA.
[Lee, S.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 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 2012
VL 18
IS 2
SU 2
MA 428
BP S362
EP S362
PG 1
WC Hematology; Immunology; Transplantation
SC Hematology; Immunology; Transplantation
GA 880HQ
UT WOS:000299398600427
ER
PT J
AU Scott, DW
Lozier, JN
AF Scott, David W.
Lozier, Jay N.
TI Gene therapy for haemophilia: prospects and challenges to prevent or
reverse inhibitor formation
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Review
DE haemophilia; factor VIII (FVIII); factor IX (FIX); gene therapy; immune
tolerance
ID HUMAN-FACTOR-VIII; REGULATORY T-CELLS; HEMATOPOIETIC STEM-CELLS; IMMUNE
TOLERANCE INDUCTION; ANTIGEN-SPECIFIC EFFECTOR; A MICE; FACTOR-IX;
IMMUNOLOGICAL-TOLERANCE; NEPHROTIC SYNDROME; TRANSGENE PRODUCT
AB Monogenic hereditary diseases, such as haemophilia A and B, are ideal targets for gene therapeutic approaches. While these diseases can be treated with protein therapeutics, such as factor VIII (FVIII) or IX (FIX), the notion that permanent transfer of the genes encoding these factors can cure haemophilia is very attractive. An underlying problem with a gene therapy approach, however, is the patients immune response to the therapeutic protein (as well as to the transmission vector), leading to the formation of inhibitory antibodies. Even more daunting is reversing an existing immune response in patients with pre-existing inhibitors. In this review, we will describe the laboratory and clinical progress, and the challenges met thus far, in achieving the goal of gene therapy efficacy, with a focus on the goal of tolerance induction.
C1 [Scott, David W.] Uniformed Serv Univ Hlth Sci, Dept Med, Bethesda, MD 20814 USA.
[Lozier, Jay N.] NIH, Ctr Clin, Dept Lab Med, Bethesda, MD 20892 USA.
RP Scott, DW (reprint author), Uniformed Serv Univ Hlth Sci, Dept Med, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA.
EM david.scott@usuhs.mil
FU USPHS NIH [HL061883, AI035622, DK068343]; Haemophilia Association of New
York
FX The author is indebted to Drs. Federico Mingozzi (Children's Hospital of
Philadelphia) and Roland Herzog (University of Florida) for their
critical review and suggestions, and to Drs. Belinda Jackson and Aihong
Zhang (USUHS), and Keith Hoots (NIH) for reading the manuscript. The
author's work cited herein was supported by grants from the USPHS NIH
(HL061883, AI035622, and DK068343 to DWS), as well as by funds from the
Haemophilia Association of New York. The opinions expressed in this
manuscript are those of the authors and do not constitute US government
policy. This is a US government work and there are no restrictions on
its use. (David W. Scott and Jay N. Lozier wrote the paper.)
NR 87
TC 12
Z9 12
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD FEB
PY 2012
VL 156
IS 3
BP 295
EP 302
DI 10.1111/j.1365-2141.2011.08925.x
PG 8
WC Hematology
SC Hematology
GA 874UQ
UT WOS:000298984000001
PM 22055221
ER
PT J
AU Mast, AE
Lee, TH
Schlumpf, KS
Wright, DJ
Johnson, B
Carrick, DM
Cable, RG
Kiss, JE
Glynn, SA
Steele, WR
Murphy, EL
Sacher, R
Busch, MP
AF Mast, Alan E.
Lee, Tzong-Hae
Schlumpf, Karen S.
Wright, David J.
Johnson, Bryce
Carrick, Danielle M.
Cable, Ritchard G.
Kiss, Joseph E.
Glynn, Simone A.
Steele, Whitney R.
Murphy, Edward L.
Sacher, Ronald
Busch, Michael P.
CA NHLBI Retrovirus Epidemiol Donor
TI The impact of HFE mutations on haemoglobin and iron status in
individuals experiencing repeated iron loss through blood donation
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE HFE; blood donor; iron deficiency; haemoglobin; ferritin
ID GENOME-WIDE ASSOCIATION; DONORS; DEFICIENCY; OVERLOAD; HEMOCHROMATOSIS;
HEPCIDIN; TMPRSS6; GENE; METABOLISM; VARIANTS
AB Frequent blood donors become iron deficient. HFE mutations are present in over 30% of donors. A 24-month study of 888 first time/reactivated donors and 1537 frequent donors measured haemoglobin and iron status to assess how HFE mutations impact the development of iron deficiency erythropoiesis. Donors with two HFE mutations had increased baseline haemoglobin and iron stores as did those with one mutation, albeit to a lesser extent. Over multiple donations haemoglobin and iron status of donors with HFE mutations paralleled those lacking mutations. The prevalence of HFE mutations was not increased in higher intensity donors. Thus, in general, HFE mutations do not temper donation-induced changes in haemoglobin and iron status. However, in Black donors there was an increase of H63D carriers at baseline, from 3.7% in first time/reactivated donors to 15.8% in frequent donors, suggesting that the relative effects of HFE mutations on iron absorption may vary between racial/ethnic groups. In secondary analyses, venous haemoglobin decreased more slowly in donors with ferritin =12 mu g/l; and haemoglobin recovery time was shorter in donors with reticulocyte haemoglobin (CHr) =32.6 pg, indicating that these biochemical measures are better indicators of a donors response to phlebotomy than their HFE mutation status.
C1 [Mast, Alan E.] Blood Ctr Wisconsin, Blood Res Inst, Milwaukee, WI 53201 USA.
[Mast, Alan E.] Med Coll Wisconsin, Dept Cell Biol Neurobiol & Anat, Milwaukee, WI 53226 USA.
[Lee, Tzong-Hae; Busch, Michael P.] Blood Syst Res Inst, San Francisco, CA USA.
[Schlumpf, Karen S.; Wright, David J.; Johnson, Bryce; Carrick, Danielle M.; Steele, Whitney R.] Westat Corp, Rockville, MD USA.
[Cable, Ritchard G.] Amer Red Cross Blood Serv, Farmington, CT USA.
[Kiss, Joseph E.] Inst Transfus Med, Pittsburgh, PA USA.
[Glynn, Simone A.] NHLBI, Bethesda, MD 20892 USA.
[Murphy, Edward L.] Univ Calif San Francisco, San Francisco & Blood Syst Res Inst, San Francisco, CA 94143 USA.
[Sacher, Ronald] Univ Cincinnati, Acad Hlth Ctr, Hoxworth Blood Ctr, Cincinnati, OH USA.
RP Mast, AE (reprint author), Blood Ctr Wisconsin, Blood Res Inst, 8727 Watertown Plank Rd,POB 2178, Milwaukee, WI 53201 USA.
EM alan.mast@bcw.edu
FU NHLBI [N01-HB-47168, -47169, -47170, -47171, -47172, -47174, -47175,
-57181]
FX This work was supported by NHLBI contracts N01-HB-47168, -47169, -47170,
-47171, -47172, -47174, -47175, and -57181.
NR 23
TC 10
Z9 10
U1 1
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD FEB
PY 2012
VL 156
IS 3
BP 388
EP 401
DI 10.1111/j.1365-2141.2011.08952.x
PG 14
WC Hematology
SC Hematology
GA 874UQ
UT WOS:000298984000012
PM 22118647
ER
PT J
AU Speranza, G
Gutierrez, ME
Kummar, S
Strong, JM
Parker, RJ
Collins, J
Yu, YK
Cao, L
Murgo, AJ
Doroshow, JH
Chen, A
AF Speranza, Giovanna
Gutierrez, Martin E.
Kummar, Shivaani
Strong, John M.
Parker, Robert J.
Collins, Jerry
Yu, Yunkai
Cao, Liang
Murgo, Anthony J.
Doroshow, James H.
Chen, Alice
TI Phase I study of the synthetic triterpenoid, 2-cyano-3, 12-dioxoolean-1,
9-dien-28-oic acid (CDDO), in advanced solid tumors
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE Triterpenoid; CDDO; Adverse event; Thromboembolism
ID ACTIVATED RECEPTOR-GAMMA; ACUTE MYELOGENOUS LEUKEMIA; VENOUS THROMBOSIS;
CANCER CELLS; APOPTOSIS; PATHWAY; GROWTH; AGGREGATION; TRAIL; FLIP
AB The triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic Acid (CDDO, previously RTA 401) is a multifunctional molecule that controls cellular growth and differentiation. While CDDO is capable of activating the transcription factor peroxisome proliferator activator receptor-gamma (PPAR gamma), its apoptotic effects in malignant cells have been shown to occur independently of PPAR gamma. A phase I dose-escalation study was conducted to determine the toxicity, the maximum tolerated dose, and the pharmacokinetics and pharmacodynamics of CDDO, administered as a 5-day continuous infusion every 28 days in patients with advanced cancers.
An accelerated titration design was followed, with one patient per cohort entered, and doses ranging from 0.6 to 38.4 mg/m(2)/h. Pharmacokinetics of CDDO was assessed and cleaved poly (ADP-ribose) polymerase (c-PARP), as a marker of apoptosis, was measured in peripheral blood mononuclear cells to assess drug effect.
Seven patients, one patient per dose level up to dose level 7 (38.4 mg/m(2)/h), were enrolled and received a total of 11 courses of treatment. Cmax increased proportionally with dose. Preclinically determined efficacious blood level (1 mu M) of drug was attained at the highest dose level. One patient, at dose level 6, experienced grade 2 mucositis, nausea, vomiting, and anorexia. Four patients developed thromboembolic events subsequently considered as dose-limiting toxicity. No antitumor activity was noted.
A causal relationship of observed thromboembolic events to CDDO was considered possible but could not be established.
C1 [Speranza, Giovanna; Kummar, Shivaani; Collins, Jerry; Murgo, Anthony J.; Doroshow, James H.; Chen, Alice] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Gutierrez, Martin E.; Kummar, Shivaani; Yu, Yunkai; Cao, Liang; Doroshow, James H.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Strong, John M.; Parker, Robert J.] Food & Drug Adm, Ctr Drug Evaluat & Res, Lab Clin Pharmacol, Silver Spring, MD USA.
RP Chen, A (reprint author), 6301 Execut Blvd,Suite 7130, Rockville, MD 20852 USA.
EM chenali@mail.nih.gov
FU NCI NIH HHS [HHSN261200800001E]
NR 33
TC 9
Z9 9
U1 0
U2 1
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 2012
VL 69
IS 2
BP 431
EP 438
DI 10.1007/s00280-011-1712-y
PG 8
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 881UW
UT WOS:000299516700016
PM 21805353
ER
PT J
AU Nikanjam, M
Chadwick, EG
Robbins, B
Alvero, C
Palumbo, P
Yogev, R
Pinto, J
Hazra, R
Hughes, ML
Heckman, BE
Capparelli, EV
AF Nikanjam, M.
Chadwick, E. G.
Robbins, B.
Alvero, C.
Palumbo, P.
Yogev, R.
Pinto, J.
Hazra, R.
Hughes, M. L.
Heckman, B. E.
Capparelli, E. V.
CA IMPAACT P1030 Team
TI Assessment of Lopinavir Pharmacokinetics With Respect to Developmental
Changes in Infants and the Impact on Weight Band-Based Dosing
SO CLINICAL PHARMACOLOGY & THERAPEUTICS
LA English
DT Article
ID VIRUS-INFECTED CHILDREN; POPULATION PHARMACOKINETICS; HIV-1-INFECTED
PATIENTS; PROTEASE INHIBITOR; RITONAVIR; HIV-1; AGE;
LOPINAVIR/RITONAVIR; COMBINATION; NELFINAVIR
AB Improved antiretroviral therapies are needed for the treatment of HIV-infected infants, given the rapid progression of the disease and drug resistance resulting from perinatal exposure to antiretrovirals. We examined longitudinal pharmacokinetics (PK) data from a clinical trial of lopinavir/ritonavir (LPV/r) in HIV-infected infants in whom therapy was initiated at less than 6 months of age. A population PK analysis was performed using NONMEM to characterize changes in lopinavir (LPV) PK relating to maturational changes in infants, and to assess dosing requirements in this population. We also investigated the relationship between LPV PK and viral dynamic response. Age and ritonavir concentrations were the only covariates found to be significant. Population PK of LPV was characterized by high apparent clearance (CL/F) in young infants, which decreased with increasing age. Although younger infants had lower LPV concentrations, the viral dynamics did not correlate with initial LPV exposure. Monte Carlo simulations demonstrated that WHO weight band based dosing recommendations predicted therapeutic LPV concentrations and provided drug exposure levels comparable to those resulting from US Food and Drug Administration (FDA)-suggested dosing regimens.
C1 [Nikanjam, M.; Capparelli, E. V.] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Chadwick, E. G.; Yogev, R.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Robbins, B.] Univ Nebraska, Med Ctr, Omaha, NE USA.
[Alvero, C.; Hughes, M. L.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Palumbo, P.] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Hanover, NH 03756 USA.
[Pinto, J.] Univ Fed Minas Gerais, Belo Horizonte, MG, Brazil.
[Hazra, R.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Heckman, B. E.] Frontier Sci & Technol Res Fdn Inc, Amherst, NY USA.
RP Capparelli, EV (reprint author), Univ Calif San Diego, La Jolla, CA 92093 USA.
EM ecapparelli@ucsd.edu
FU National Institute of Allergy and Infectious Diseases (NIAID) [U01
AI068632]; Eunice Kennedy Shriver National Institute of Child Health and
Human Development (NICHD); National Institute of Mental Health (NIMH)
[AI068632]; Statistical and Data Analysis Center at the Harvard School
of Public Health under NIAID [5 U01 AI41110, 1 U01 AI068616]; NIAID;
NICHD [N01-DK-9-001/HHSN267200800001C]; Roche; Abbott Labs; Boehringer
Ingelheim; Bristol-Meyers Squibb; Chiron; Medicines Development; Pfizer;
Tibotec; Vironyx
FX The study team thanks John Rodman for his contributions to the design
and performance of the study, Donald Barkauskas for his assistance with
the model cross-validation, Abbott Laboratories for donating the study
drug, and the patients and families who participated in this study.
Overall support for the International Maternal-Pediatric-Adolescent AIDS
Clinical Trials Group (IMPAACT) was provided by the National Institute
of Allergy and Infectious Diseases (NIAID) (U01 AI068632), the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
(NICHD), and the National Institute of Mental Health (NIMH) (AI068632).
The content of this paper is solely the responsibility of the authors
and does not necessarily represent the official views of the National
Institutes of Health. This work was supported by the Statistical and
Data Analysis Center at the Harvard School of Public Health, under NIAID
cooperative agreement 5 U01 AI41110 with the Pediatric AIDS Clinical
Trials Group and 1 U01 AI068616 with the IMPAACT Group. Support at the
study sites was provided by NIAID and the NICHD International and
Domestic Pediatric and Maternal HIV Clinical Trials Network funded by
NICHD (contract N01-DK-9-001/HHSN267200800001C).; E.V.C. has served as a
consultant to GlaxoSmithKline, Bristol-Meyers Squibb, and Johnson &
Johnson. E.G.C. has had consultancies with Pfizer and Bristol-Meyers
Squibb and has owned stock+/-stock options in Abbott Labs,
GlaxoSmithKline, Merck Inc., Bristol-Meyers Squibb, and Schering Plough.
M.D.H. received grant support from Roche, and honoraria/consultancy fees
from Abbott Labs, Boehringer Ingelheim, Bristol-Meyers Squibb, Chiron,
Medicines Development, Roche, Pfizer, Tibotec, and Vironyx. R.Y. has
served on speaker's bureaus for Merck Inc. and GlaxoSmithKline. The
other authors declared no conflict of interest
NR 29
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Z9 5
U1 0
U2 0
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 2012
VL 91
IS 2
BP 243
EP 249
DI 10.1038/clpt.2011.218
PG 7
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 883SC
UT WOS:000299654000023
PM 22190064
ER
PT J
AU Kaplan, RM
AF Kaplan, Robert M.
TI Short, Simple, but Still of Uncertain Value
SO COPD-JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE
LA English
DT Editorial Material
ID QUALITY-OF-LIFE; EMPHYSEMA
C1 [Kaplan, Robert M.] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD USA.
RP Kaplan, RM (reprint author), Off Behav & Social Sci Res, 31 Ctr Dr,Room B1C19, Bethesda, MD 20892 USA.
EM Robert.kaplan@nih.gov
NR 9
TC 0
Z9 0
U1 0
U2 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1541-2555
J9 COPD
JI COPD-J. Chronic Obstr. Pulm. Dis.
PD FEB
PY 2012
VL 9
IS 1
BP 1
EP 2
DI 10.3109/15412555.2012.651935
PG 2
WC Respiratory System
SC Respiratory System
GA 884XY
UT WOS:000299743400001
PM 22292591
ER
PT J
AU Byrnes, C
Lee, YT
Donahue, RE
Miller, JL
AF Byrnes, Colleen
Lee, Y. Terry
Donahue, Robert E.
Miller, Jeffery L.
TI Identification of a cross-reacting, monoclonal anti-human CD233 antibody
for identification and sorting of rhesus macaque erythrocytes
SO CYTOMETRY PART A
LA English
DT Article
DE CD233; rhesus macaque; erythrocyte; malaria
ID EMBRYONIC STEM-CELLS; MALARIA VACCINE; BAND-3 PROTEIN; MONKEYS;
IMMUNOGENICITY; PARAMETERS; EPITOPES; INVASION; RECEPTOR; DOMAIN
AB Erythroid biology research involving rhesus macaques has been applied to several topics including malaria, hemoglobinopathy and gene therapy research. However, analyses of the rhesus red blood cells are limited by the inability to identify and sort those cells in research blood samples using flow cytometry. Here it is reported that the BRIC 6 hybridoma clone raised to the human erythroid surface molecule (referred to as CD233, Band 3, AE1, or SLC4A1) produces cross-reactive and erythroid-specific antibodies for flow cytometric detection and sorting of rhesus macaque erythrocytes. (C) 2011 International Society for Advancement of Cytometry
C1 [Byrnes, Colleen; Lee, Y. Terry; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
[Donahue, Robert E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Miller, JL (reprint author), NIDDK, Mol Med Branch, NIH, 10 Ctr Dr,Bldg 10,Room 9N311, Bethesda, MD 20892 USA.
EM jm7f@nih.gov
FU National Institutes of Health; National Institute of Diabetes and
Digestive and Kidney Diseases; National Heart Lung and Blood Institute
FX The authors thank the NIH Intramural primate research community for
helpful conversations and related reagents. This U.S. government
research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Diabetes and
Digestive and Kidney Diseases and National Heart Lung and Blood
Institute.
NR 22
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U1 0
U2 1
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 2012
VL 81A
IS 2
BP 165
EP 168
DI 10.1002/cyto.a.22005
PG 4
WC Biochemical Research Methods; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 880AQ
UT WOS:000299376900011
PM 22170815
ER
PT J
AU Delahanty, LM
Pan, Q
Jablonski, IA
Watson, KE
McCaffery, JM
Shuldiner, A
Kahn, SE
Knowler, WC
Florez, JC
Franks, PW
AF Delahanty, Linda M.
Pan, Qing
Jablonski, Icatiileen A.
Watson, Karol E.
McCaffery, Jeanne M.
Shuldiner, Alan
Kahn, Steven E.
Knowler, William C.
Florez, Jose C.
Franks, Paul W.
CA Diabet Prevention Program Res Grp
TI Genetic Predictors of Weight Loss and Weight Regain After Intensive
Lifestyle Modification, Metformin Treatment, or Standard Care in the
Diabetes Prevention Program
SO DIABETES CARE
LA English
DT Article
ID POLYMORPHISMS; INTERVENTION; RECEPTOR
AB OBJECTIVE-We tested genetic associations with weight loss and weight regain in the Diabetes Prevention Program, a randomized controlled trial of weight-loss inducing interventions (lifestyle and metformin) versus placebo.
RESEARCH DESIGN AND METHODS-Sixteen obesity-predisposing single nucleotide polymorphisms (SNPs) were tested for association with short-term (baseline to 6 months) and long-term (baseline to 2 years) weight loss and weight regain (6 months to study end).
RESULTS-Irrespective of treatment, the Ala12 allele at PPARG associated with short- and long-term weight loss (-0.63 and -0.93 kg/allele, P <= 0.005, respectively). Gene-treatment interactions were observed for short-term (LYPLAL1 rs2605100, P-lifestyle*SNP = 0.032; GNPDA2 rs10938397, P-lifestyle*SNP = 0.016; MTCH2 rs10838738, P-lifestyle*SNP = 0.022) and long-term (NEGR1 rs2815752, P-metformin*SNP = 0.028; FTO rs9939609, P-lifestyle*SNP = 0.044) weight loss. Three of 16 SNPs were associated with weight regain (NEGR1 rs2815752, BDNF rs6265, PPARG rs1801282), irrespective of treatment. TMEM18 rs6548238 and KTCD15 rs29941 showed treatment-specific effects (P-lifestyle*SNP < 0.05).
CONCLUSIONS-Genetic information may help identify people who require additional support to maintain reduced weight after clinical intervention.
C1 [Franks, Paul W.] Lund Univ, Skane Univ Hosp, Ctr Diabet, Dept Clin Sci,Genet & Mol Epidemiol Unit, Malmo, Sweden.
[Delahanty, Linda M.; Florez, Jose C.] Massachusetts Gen Hosp, Diabet Res Ctr, Boston, MA 02114 USA.
[Delahanty, Linda M.; Florez, Jose C.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Pan, Qing; Jablonski, Icatiileen A.] George Washington Univ, Ctr Biostat, Rockville, MD USA.
[Watson, Karol E.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[McCaffery, Jeanne M.] Miriam Hosp, Weight Control & Diabet Res Ctr, Providence, RI 02906 USA.
[McCaffery, Jeanne M.] Brown Med Sch, Providence, RI USA.
[Shuldiner, Alan] Univ Maryland, Sch Med, Dept Med, Div Endocrinol Diabet & Nutr, Baltimore, MD 21201 USA.
[Shuldiner, Alan] Univ Maryland, Sch Med, Program Genet & Genom Med, Baltimore, MD 21201 USA.
[Kahn, Steven E.] VA Puget Sound Hlth Care Syst, Dept Med, Div Metab Endocrinol & Nutr, Seattle, WA USA.
[Kahn, Steven E.] Univ Washington, Seattle, WA 98195 USA.
[Knowler, William C.] NIDDK, Phoenix, AZ USA.
[Florez, Jose C.] Massachusetts Gen Hosp, Dept Med, Ctr Human Genet Res, Boston, MA 02114 USA.
[Florez, Jose C.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Franks, Paul W.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
RP Franks, PW (reprint author), Lund Univ, Skane Univ Hosp, Ctr Diabet, Dept Clin Sci,Genet & Mol Epidemiol Unit, Malmo, Sweden.
EM paul.franks@med.lu.se
RI de Bakker, Paul/B-8730-2009; Uwaifo, Gabriel/M-2361-2016;
OI de Bakker, Paul/0000-0001-7735-7858; Uwaifo,
Gabriel/0000-0002-6962-9304; Franks, Paul/0000-0002-0520-7604; Kahn,
Steven/0000-0001-7307-9002
FU Novo Nordisk; Swedish Research Council; Swedish Heart-Lung Foundation;
Swedish Diabetes Association; Department of Veterans Affairs; Doris Duke
Charitable Foundation; National Institute of Diabetes and Digestive and
Kidney Diseases (NIDDK) of the National Institutes of Health; NIDDK;
Indian Health Service; National Center for Research Resources; Office of
Research on Minority Health; National Institute of Child Health and
Human Development; National Institute on Aging; Centers for Disease
Control and Prevention; Office of Research on Women's Health; American
Diabetes Association; Henry M. Jackson Foundation; McKesson BioServices
Corporation; Matthews Media Group; [R01 DK-072041-02]
FX This work was funded by R01 DK-072041-02 to J.C.F., K.A.J., and A.S.
(P.W.F. and W.C.K. are coinvestigators). P.W.F. was supported by grants
from Novo Nordisk, the Swedish Research Council, the Swedish Heart-Lung
Foundation, and the Swedish Diabetes Association. S.E.K. is supported in
part by the Department of Veterans Affairs. J.C.F. is supported by a
Doris Duke Charitable Foundation Clinical Scientist Development Award.
The National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK) of the National Institutes of Health funded the clinical centers
and the Coordinating Center for the design and conduct of the study and
the collection, management, analysis, and interpretation of the data.
The Southwestern American Indian Centers were supported directly by the
NIDDK and the Indian Health Service. The General Clinical Research
Center Program, National Center for Research Resources, supported data
collection at many of the clinical centers. The Office of Research on
Minority Health, the National Institute of Child Health and Human
Development, the National Institute on Aging, the Centers for Disease
Control and Prevention, Office of Research on Women's Health, the
Department of Veterans Affairs, and the American Diabetes Association
funded data collection and provided participant support. This research
was also supported, in part, by the intramural research program of the
NIDDK. The Henry M. Jackson Foundation provided support services under
subcontract with the Coordinating Center.; LifeScan, Health O Meter,
Hoechst Marion Roussel, Merck-Medco Managed Care, Merck and Co., Nike
Sports Marketing, Slim Fast Foods Co., and Quaker Oats Co. donated
materials, equipment, or medicines for concomitant conditions.
Bristol-Myers Squibb and Parke-Davis provided medication. McKesson
BioServices Corporation and Matthews Media Group provided support
services under subcontract with the Coordinating Center. No other
potential conflicts of interest relevant to this article were reported.
NR 12
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U1 0
U2 3
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 2012
VL 35
IS 2
BP 363
EP 366
DI 10.2337/dc11-1328
PG 4
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 886LN
UT WOS:000299856000030
PM 22179955
ER
PT J
AU Seaquist, ER
Miller, ME
Bonds, DE
Feinglos, M
Goff, DC
Peterson, K
Senior, P
AF Seaquist, Elizabeth R.
Miller, Michael E.
Bonds, Denise E.
Feinglos, Mark
Goff, David C., Jr.
Peterson, Kevin
Senior, Peter
CA ACCORD Investigators
TI The Impact of Frequent and Unrecognized Hypoglycemia on Mortality in the
ACCORD Study
SO DIABETES CARE
LA English
DT Article
AB OBJECTIVE-The aim of this study was to examine the relationship between frequent and unrecognized hypoglycemia and mortality in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study cohort.
RESEARCH DESIGN AND METHODS-A total of 10,096 ACCORD study participants with follow-up for both hypoglycemia and mortality were included. Hazard ratios (95% CIs) relating the risk of death to the updated annualized number of hypoglycemic episodes and the updated annualized number of intervals with unrecognized hypoglycemia were obtained using Cox proportional hazards regression models, allowing for these hypoglycemia variables as time-dependent covariates and controlling for the baseline covariates.
RESULTS-Participants in the intensive group reported a mean of 1.06 hypoglycemic episodes (self-monitored blood glucose <70 mg/dL or <3.9 mmol/L) in the 7 days preceding their regular 4-month visit, whereas participants in the standard group reported an average of 0.29 episodes. Unrecognized hypoglycemia was reported, on average, at 5.8% of the intensive group 4-month visits and 2.6% of the standard group visits. Hazard ratios for mortality in models including frequency of hypoglycemic episodes were 0.93 (95% CI 0.9-0.97; P < 0.001) for participants in the intensive group and 0.98 (0.91-1.06; P = 0.615) for participants in the standard group. The hazard ratios for mortality in models, including unrecognized hypoglycemia, were not statistically significant for either group.
CONCLUSIONS-Recognized and unrecognized hypoglycemia was more common in the intensive group than in the standard group. In the intensive group of the ACCORD study, a small but statistically significant inverse relationship of uncertain clinical importance was identified between the number of hypoglycemic episodes and the risk of death among participants.
C1 [Seaquist, Elizabeth R.] Univ Minnesota, Dept Med, Minneapolis, MN 55455 USA.
[Miller, Michael E.] Wake Forest Sch Med, Div Publ Hlth Sci, Dept Biostat Sci, Winston Salem, NC USA.
[Bonds, Denise E.] NHLBI, Bethesda, MD 20892 USA.
[Feinglos, Mark] Duke Univ, Med Ctr, Div Endocrinol Metab & Nutr, Durham, NC USA.
[Goff, David C., Jr.] Wake Forest Univ, Bowman Gray Sch Med, Dept Internal Med, Winston Salem, NC 27103 USA.
[Peterson, Kevin] Univ Minnesota, Dept Family Med, Minneapolis, MN 55455 USA.
[Senior, Peter] Univ Alberta, Dept Med, Sch Med, Div Endocrinol, Edmonton, AB, Canada.
RP Seaquist, ER (reprint author), Univ Minnesota, Dept Med, Box 736 UMHC, Minneapolis, MN 55455 USA.
EM seaqu001@umn.edu
RI Senior, Peter/E-3031-2013;
OI Senior, Peter/0000-0003-1033-8673; Peterson, Kevin/0000-0002-6914-8586
FU National Heart, Lung, and Blood Institute [N01-HC-95178, N01-HC-95179,
N01-HC-95180, N01-HC-95181, N01-HC-95182, N01-HC-95183, N01-HC-95184,
IAA-Y1-HC-9035, IAA-Y1-HC-1010]; National Institutes of Health; National
Institute of Diabetes and Digestive and Kidney Diseases; National
Institute on Aging; National Eye Institute; Centers for Disease Control
and Prevention; general clinical research centers
FX This work was supported by grants (N01-HC-95178, N01-HC-95179,
N01-HC-95180, N01-HC-95181, N01-HC-95182, N01-HC-95183, N01-HC-95184,
IAA-Y1-HC-9035, and IAA-Y1-HC-1010) from the National Heart, Lung, and
Blood Institute and by other branches of the National Institutes of
Health, including the National Institute of Diabetes and Digestive and
Kidney Diseases, the National Institute on Aging, and the National Eye
Institute; by the Centers for Disease Control and Prevention; and by
general clinical research centers.
NR 10
TC 54
Z9 57
U1 1
U2 3
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 2012
VL 35
IS 2
BP 409
EP 414
DI 10.2337/dc11-0996
PG 6
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 886LN
UT WOS:000299856000037
PM 22179956
ER
PT J
AU Kizer, JR
Arnold, AM
Benkeser, D
Ix, JH
Djousse, L
Zieman, SJ
Barzilay, JI
Tracy, RP
Mantzoros, CS
Siscovick, DS
Mukamal, KJ
AF Kizer, Jorge R.
Arnold, Alice M.
Benkeser, David
Ix, Joachim H.
Djousse, Luc
Zieman, Susan J.
Barzilay, Joshua I.
Tracy, Russell P.
Mantzoros, Christos S.
Siscovick, David S.
Mukamal, Kenneth J.
TI Total and High-Molecular-Weight Adiponectin and Risk of Incident
Diabetes in Older People
SO DIABETES CARE
LA English
DT Article
ID CORONARY-HEART-DISEASE; BETA-CELL FUNCTION; CARDIOVASCULAR HEALTH;
INSULIN-RESISTANCE; WOMEN; MEN; POPULATION; ADIPOSITY; MELLITUS; GLUCOSE
AB OBJECTIVE-To delineate the associations of total adiponectin, high-molecular-weight (HMW) adiponectin, and the HMW-to-total adiponectin ratio with diabetes in older adults.
RESEARCH DESIGN AND METHODS-Total and HMW adiponectin were measured in a population-based study of older adults. The relations of total adiponectin, HMW adiponectin, and their ratio with incident diabetes (n = 309) were assessed in 3,802 individuals.
RESULTS-Total and HMW adiponectin were highly correlated (r = 0.94). Analysis using cubic splines revealed that the associations between total and HMW adiponectin and new-onset diabetes were not linear. Specifically, after adjustment for confounders, there were similar inverse relationships for total (hazard ratio per SD 0.49 [95% CI 0.39-0.63]) and HMW adiponectin (0.42 [0.32-0.56]) with diabetes up to values of 20 and 10 mg/L, respectively, above which the associations plateaued. These associations persisted after adjustment for potential mediators (blood pressure, lipids, C-reactive protein, and homeostasis model assessment of insulin resistance [HOMA-IR]). There was, however, evidence of interaction by HOMA-IR in the lower range of adiponectin, with stronger inverse associations among insulin-sensitive than insulin-resistant participants. HMW-to-total adiponectin ratio showed a linear adjusted association with outcome, but this was abolished by inclusion of mediating variables.
CONCLUSIONS-In this older cohort, increasing concentrations of total and HMW adiponectin were associated with comparably lower risks of diabetes, but these associations leveled off with further increases above concentrations of 20 and 10 mg/L, respectively. The more pronounced risk decreases at the lower range among participants without insulin resistance support a role for adiponectin that is independent of baseline hyperinsulinemia, but this will require further investigation.
C1 [Kizer, Jorge R.] Weill Cornell Med Coll, Dept Med, New York, NY USA.
[Kizer, Jorge R.] Weill Cornell Med Coll, Dept Publ Hlth, New York, NY USA.
[Arnold, Alice M.; Benkeser, David] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Ix, Joachim H.] Vet Affairs San Diego Healthcare Syst, Nephrol Sect, San Diego, CA USA.
[Ix, Joachim H.] Univ Calif San Diego, Dept Med, Div Nephrol, San Diego, CA 92103 USA.
[Djousse, Luc] Brigham & Womens Hosp, Dept Med, Div Aging, Boston, MA 02115 USA.
[Djousse, Luc; Mantzoros, Christos S.; Mukamal, Kenneth J.] Harvard Univ, Sch Med, Boston, MA USA.
[Zieman, Susan J.] NIA, Div Geriatr & Clin Gerontol, Bethesda, MD 20892 USA.
[Barzilay, Joshua I.] Emory Univ, Sch Med, Div Endocrinol, Atlanta, GA USA.
[Tracy, Russell P.] Univ Vermont, Dept Pathol, Colchester, VT USA.
[Tracy, Russell P.] Univ Vermont, Dept Biochem, Colchester, VT USA.
[Mantzoros, Christos S.] Beth Israel Deaconess Med Ctr, Div Endocrinol Diabet & Metab, Boston, MA 02215 USA.
[Mantzoros, Christos S.] Boston VA Healthcare Syst, Endocrinol Sect, Boston, MA USA.
[Siscovick, David S.] Univ Washington, Dept Med, Cardiovasc Hlth Res Unit, Seattle, WA USA.
[Siscovick, David S.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Mukamal, Kenneth J.] Beth Israel Deaconess Med Ctr, Div Gen Med & Primary Care, Boston, MA 02215 USA.
RP Kizer, JR (reprint author), Weill Cornell Med Coll, Dept Med, New York, NY USA.
EM jok2007@med.cornell.edu
RI Djousse, Luc/F-5033-2017
OI Djousse, Luc/0000-0002-9902-3047
FU National Heart, Lung, and Blood Institute (NHLBI) [R01-HL-094555,
N01-HC-85239, N01-HC-85079, N01-HC-85086, N01-HC-35129, N01-HC-15103,
N01-HC-55222, N01-HC-75150, N01-HC-45133, HL-080295]; National Institute
of Neurological Disorders and Stroke; National Institute on Aging
[AG-023629, AG-15928, AG-20098, AG-027058]
FX This work was supported by R01-HL-094555 from the National Heart, Lung,
and Blood Institute (NHLBI). The CHS was supported by NHLBI contracts
N01-HC-85239, N01-HC-85079 through N01-HC-85086, N01-HC-35129,
N01-HC-15103, N01-HC-55222, N01-HC-75150, N01-HC-45133, and NHLBI Grant
HL-080295, with additional contribution from the National Institute of
Neurological Disorders and Stroke. Additional support was provided
through AG-023629, AG-15928, AG-20098, and AG-027058 from the National
Institute on Aging. See also http://www.chs-nhlbi.org/pi.htm.
NR 30
TC 22
Z9 25
U1 1
U2 1
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 2012
VL 35
IS 2
BP 415
EP 423
DI 10.2337/dc11-1519
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 886LN
UT WOS:000299856000038
PM 22148099
ER
PT J
AU Houdayer, E
Beck, S
Karabanov, A
Poston, B
Hallett, M
AF Houdayer, Elise
Beck, Sandra
Karabanov, Anke
Poston, Brach
Hallett, Mark
TI The differential modulation of the ventral premotor-motor interaction
during movement initiation is deficient in patients with focal hand
dystonia
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE motor cortex; movement disorders; surround inhibition; transcranial
magnetic stimulation; ventral premotor cortex
ID TRANSCRANIAL MAGNETIC STIMULATION; WRITERS CRAMP; SURROUND INHIBITION;
FRONTAL-LOBE; CORTICOSPINAL PROJECTIONS; SENSORIMOTOR INTEGRATION;
TORSION DYSTONIA; LATERAL SURFACE; CORTEX OUTPUTS; BASAL GANGLIA
AB A major feature of focal hand dystonia (FHD) pathophysiology is the loss of inhibition. One inhibitory process, surround inhibition, for which the cortical mechanisms are still unknown, is abnormal in FHD. As the ventral premotor cortex (PMv) plays a key role in the sensorimotor processing involved in shaping finger movements and has many projections onto the primary motor cortex (M1), we hypothesized that the PMvM1 connections might play a role in surround inhibition. A paired-pulse transcranial magnetic stimulation paradigm was used in order to evaluate and compare the PMvM1 interactions during different phases (rest, preparation and execution) of an index finger movement in patients with FHD and controls. A sub-threshold conditioning pulse (80% resting motor threshold) was applied to the PMv at 6 ms before M1 stimulation. The right abductor pollicis brevis, a surround muscle, was the target muscle. In healthy controls, the results showed that PMv stimulation induced an ipsilateral ventral premotormotor inhibition at rest. This cortico-cortical interaction changed into an early facilitation (100 ms before movement onset) and turned back to inhibition 50 ms later. In patients with FHD, this PMvM1 interaction and its modulation were absent. Our results show that, although the ipsilateral ventral premotormotor inhibition does not play a key role in the genesis of surround inhibition, PMv has a dynamic influence on M1 excitability during the early steps of motor execution. The impaired cortico-cortical interactions observed in patients with FHD might contribute, at least in part, to the abnormal motor command.
C1 [Houdayer, Elise; Beck, Sandra; Karabanov, Anke; Poston, Brach; Hallett, Mark] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Beck, Sandra] Univ Freiburg, Dept Neurol & Clin Neurophysiol, D-79106 Freiburg, Germany.
RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, 10 Ctr Dr,MSC 1428,Bldg 10,Room 7D37, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
OI Karabanov, Anke Ninija/0000-0003-1874-393X
FU National Institute of Neurological Disorders and Stroke; Fyssen
Foundation
FX This work was supported by the National Institute of Neurological
Disorders and Stroke Intramural Research Program. E. H. was funded by
the Fyssen Foundation.
NR 50
TC 11
Z9 11
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD FEB
PY 2012
VL 35
IS 3
BP 478
EP 485
DI 10.1111/j.1460-9568.2011.07960.x
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 884GL
UT WOS:000299692800014
PM 22288483
ER
PT J
AU Kleykamp, BA
Griffiths, RR
McCann, UD
Smith, MT
Mintzer, MZ
AF Kleykamp, Bethea A.
Griffiths, Roland R.
McCann, Una D.
Smith, Michael T.
Mintzer, Miriam Z.
TI Acute Effects of Zolpidem Extended-Release on Cognitive Performance and
Sleep in Healthy Males After Repeated Nightly Use
SO EXPERIMENTAL AND CLINICAL PSYCHOPHARMACOLOGY
LA English
DT Article
DE zolpidem; Ambien; psychomotor; cognition; tolerance; memory
ID TERM BENZODIAZEPINE USE; MEMORY FUNCTIONS; PSYCHOMOTOR PERFORMANCE;
RETROGRADE FACILITATION; ATTENTIONAL PROCESSES; ADMINISTRATION 5; ABUSE
LIABILITY; SEMANTIC MEMORY; TRIAZOLAM; LORAZEPAM
AB The extended-release formulation of zolpidem (Ambien CR) is approved for the treatment of insomnia without a treatment duration limit. Acutely zolpidem impairs performance, and no research to date has examined whether tolerance develops to these performance impairments during nighttime awakening. The present double-blind, placebo-controlled study examined whether tolerance develops to zolpidem-induced acute performance impairment after repeated (22-30 days) nightly use. Effects of bedtime administration of zolpidem extended-release (ZOL; 12.5 mg) were tested on a battery of performance measures assessed during a forced nighttime awakening in 15 healthy male volunteers who completed overnight polysomnographic recording sessions in our laboratory at baseline and after approximately a month of at-home ZOL. As expected, bedtime ZOL administration was associated with changes in sleep architecture and impairments across all performance domains during nighttime testing (psychomotor function, attention, working memory, episodic memory, metacognition) with no residual next morning impairment. Tolerance did not develop to the observed ZOL-related impairments on any outcome. Possible evidence of acute abstinence effects after discontinuation of ZOL was observed on some performance and sleep outcomes. Overall, these findings suggest that performance is significantly impaired during nighttime awakening even after a month of nightly ZOL administration, and these impairments could significantly impact safety should nighttime awakening require unimpaired functioning (e.g., driving; combat-related activities in the military).
C1 [Kleykamp, Bethea A.] NIDA, IRTA, Nicotine Psychopharmacol Sect, Clin Pharmacol & Therapeut Branch,Intramural Res, Baltimore, MD 21224 USA.
[Griffiths, Roland R.; McCann, Una D.; Smith, Michael T.; Mintzer, Miriam Z.] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21218 USA.
RP Kleykamp, BA (reprint author), NIDA, IRTA, Nicotine Psychopharmacol Sect, Clin Pharmacol & Therapeut Branch,Intramural Res, 251 Bayview Blvd,Room 01A941, Baltimore, MD 21224 USA.
EM annie.kleykamp@nih.gov
FU National Institute on Drug Abuse [DA-11936, DA-07209]; National
Institute of Arthritis and Musculoskeletal and Skin Diseases
[AR-054871]; National Center of Research Resources, National Institutes
of Health [M01RR-02719]
FX We thank Crystal Barnhouser, Jared Saletin, and Jenna Cohen for protocol
management and technical assistance, John Yingling for computer
programming assistance and technical support, and Paul Nuzzo for
assistance with the data analysis. Portions of these data were presented
at the 72nd annual meeting of the College on Problems of Drug
Dependence. This project was supported by National Institute on Drug
Abuse Grants DA-11936 and DA-07209, National Institute of Arthritis and
Musculoskeletal and Skin Diseases Grant AR-054871, and Grant M01RR-02719
from the Clinical Research Unit Program of the National Center of
Research Resources, National Institutes of Health.
NR 51
TC 6
Z9 6
U1 7
U2 15
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 2012
VL 20
IS 1
BP 28
EP 39
DI 10.1037/a0025237
PG 12
WC Psychology, Biological; Psychology, Clinical; Pharmacology & Pharmacy;
Psychiatry
SC Psychology; Pharmacology & Pharmacy; Psychiatry
GA 886OR
UT WOS:000299864200004
PM 21928913
ER
PT J
AU Amiri-Kordestani, L
Tan, AR
Swain, SM
AF Amiri-Kordestani, Laleh
Tan, Antoinette R.
Swain, Sandra M.
TI Pazopanib for the treatment of breast cancer
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Editorial Material
DE breast cancer; pazopanib; PDGFR; tyrosine kinase inhibitor; VEGF; VEGFR
ID ENDOTHELIAL GROWTH-FACTOR; RENAL-CELL CARCINOMA; TYROSINE KINASE
INHIBITOR; ADVANCED SOLID TUMORS; BETA-RECEPTOR EXPRESSION; PHASE-II;
FACTOR PDGF; PROGNOSTIC-SIGNIFICANCE; ANGIOGENIC FACTORS; SUNITINIB
MALATE
AB Introduction: Several clinical trials have shown clinical benefit of angiogenesis inhibitors in the treatment of solid tumors. Pazopanib is a multitargeted tyrosine kinase inhibitor that is currently approved for the treatment of patients with advanced renal cell carcinoma (RCC).
Areas covered: In this article, the clinical development of pazopanib as it relates to breast cancer is reviewed including its evaluation in clinical trials and side effect profile. Preclinical data show the anti-tumor activity of pazopanib in animal models. Several trials of pazopanib monotherapy and combination therapy in breast cancer have been completed or are underway.
Expert opinion: The development of biomarkers predictive of response and toxicity to angiogenesis inhibitors remains a challenging endeavor and is necessary to help guide treatment decision.
C1 [Swain, Sandra M.] Washington Hosp Ctr, Washington Canc Inst, MedStar Hlth, Washington, DC 20010 USA.
[Amiri-Kordestani, Laleh] NCI, Bethesda, MD 20892 USA.
[Tan, Antoinette R.] Canc Inst New Jersey,Med Oncol, New Brunswick, NJ USA.
RP Swain, SM (reprint author), Washington Hosp Ctr, Washington Canc Inst, MedStar Hlth, Washington, DC 20010 USA.
EM sandra.m.swain@medstar.net
OI Swain, Sandra/0000-0002-1320-3830
NR 67
TC 7
Z9 7
U1 0
U2 3
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1354-3784
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD FEB
PY 2012
VL 21
IS 2
BP 217
EP 225
DI 10.1517/13543784.2012.652304
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 875UD
UT WOS:000299059800009
PM 22233389
ER
PT J
AU Trotter, JF
Everhart, JE
AF Trotter, James F.
Everhart, James E.
TI Outcomes Among Living Liver Donors
SO GASTROENTEROLOGY
LA English
DT Editorial Material
ID HEPATIC LOBE DONORS; QUALITY-OF-LIFE; UNITED-STATES; TRANSPLANTATION;
DONATION
C1 [Trotter, James F.] Baylor Univ, Med Ctr, Dallas, TX 75246 USA.
[Everhart, James E.] NIDDK, Bethesda, MD USA.
RP Trotter, JF (reprint author), Baylor Univ, Med Ctr, 3410 Worth St,Suite 860, Dallas, TX 75246 USA.
EM james.trotter@baylorhealth.edu
NR 16
TC 0
Z9 1
U1 0
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 2012
VL 142
IS 2
BP 207
EP 210
DI 10.1053/j.gastro.2011.12.018
PG 5
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 882CV
UT WOS:000299540000022
PM 22198246
ER
PT J
AU Catalan, MA
Flores, CA
Gonzalez-Begne, M
Zhang, Y
Sepulveda, FV
Melvin, JE
AF Catalan, Marcelo A.
Flores, Carlos A.
Gonzalez-Begne, Mireya
Zhang, Yan
Sepulveda, Francisco V.
Melvin, James E.
TI Severe Defects in Absorptive Ion Transport in Distal Colons of Mice That
Lack ClC-2 Channels
SO GASTROENTEROLOGY
LA English
DT Article
DE NaCl Absorption; KCl Absorption; Fluid Secretory Defects; Intestinal
Epithelial Cells
ID TRANSMEMBRANE CONDUCTANCE REGULATOR; CYSTIC-FIBROSIS; CHLORIDE CHANNEL;
ELECTROLYTE TRANSPORT; SMALL-INTESTINE; ACINAR-CELLS; SECRETION; RAT;
EPITHELIUM; ACTIVATION
AB BACKGROUND & AIMS: The fluid secretion model predicts that intestinal obstruction disorders can be alleviated by promoting epithelial Cl- secretion. The adenosine 3',5'-cyclic monophosphate (cAMP)-activated anion channel CFTR mediates Cl- -dependent fluid secretion in the intestine. Although the role of the ClC-2 channel has not been determined in the intestine, this voltage-gated Cl- channel might compensate for the secretory defects observed in patients with cystic fibrosis and other chronic constipation disorders. We investigated whether mice that lack ClC-2 channels (Clcn2(-/-)) have defects in intestinal ion transport. METHODS: Immunolocalization and immunoblot analyses were used to determine the cellular localization and the amount of ClC-2 expressed in mouse early distal colon (EDC) and late distal colon (LDC). Colon sheets from wild-type and Clcn2(-/-) littermates were mounted in Ussing chambers to determine transepithelial bioelectrical parameters and Na+, K+, and Cl- fluxes. RESULTS: Expression of ClC-2 was higher in the basolateral membrane of surface cells in the EDC compared with the LDC, with little expression in crypts. Neither cAMP nor Ca2+-induced secretion of Cl- was affected in the EDC or LDC of Clcn2(-/-) mice, whereas the amiloride-sensitive short-circuit current was increased approximately 3-fold in Clcn2(-/-) EDC compared with control littermates. Conversely, electroneutral Na+, K+, and Cl- absorption was dramatically reduced in colons of Clcn2(-/-) mice. CONCLUSIONS: Basolateral ClC-2 channels are required for colonic electroneutral absorption of NaCl and KCl. The increase in the amiloride-sensitive short-circuit current in Clcn2(-/-) mice revealed a compensatory mechanism that is activated in the colons of mice that lack the ClC-2 channel.
C1 [Catalan, Marcelo A.; Zhang, Yan; Melvin, James E.] Natl Inst Dent & Craniofacial Res, Secretory Mech & Dysfunct Sect, NIH, Bethesda, MD 20892 USA.
[Flores, Carlos A.; Sepulveda, Francisco V.] Ctr Estudios Cient, Valdivia, Chile.
[Gonzalez-Begne, Mireya] Univ Rochester, Med Ctr, Ctr Oral Biol, Rochester, NY 14642 USA.
RP Melvin, JE (reprint author), Natl Inst Dent & Craniofacial Res, Secretory Mech & Dysfunct Sect, NIH, 10 Ctr Dr,Bldg 10,Room 5-2531, Bethesda, MD 20892 USA.
EM james.melvin@nih.gov
OI Catalan, Marcelo/0000-0003-3544-2821
FU National Institutes of Health [DE09621]; Takeda Pharmaceuticals North
America, Inc; Fondecyt [11100408]; Conicyt-PFB; Gobierno Regional de Los
Rios
FX Supported in part by the National Institutes of Health Intramural
Research Program and research grants from the National Institutes of
Health (DE09621) and Takeda Pharmaceuticals North America, Inc (to
J.E.M.) and Fondecyt (11100408) (to C. A. F.). Centro de Estudios
Cientificos is funded by Conicyt-PFB and Gobierno Regional de Los Rios.
NR 45
TC 11
Z9 11
U1 2
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 2012
VL 142
IS 2
BP 346
EP 354
DI 10.1053/j.gastro.2011.10.037
PG 9
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 882CV
UT WOS:000299540000041
PM 22079595
ER
PT J
AU Nakamoto, N
Ebinuma, H
Kanai, T
Chu, PS
Ono, Y
Mikami, Y
Ojiro, K
Lipp, M
Love, PE
Saito, H
Hibi, T
AF Nakamoto, Nobuhiro
Ebinuma, Hirotoshi
Kanai, Takanori
Chu, Po-Sung
Ono, Yuichi
Mikami, Yohei
Ojiro, Keisuke
Lipp, Martin
Love, Paul E.
Saito, Hidetsugu
Hibi, Toshifumi
TI CCR9(+) Macrophages Are Required for Acute Liver Inflammation in Mouse
Models of Hepatitis
SO GASTROENTEROLOGY
LA English
DT Article
DE Immune Regulation; Hepatic Disease; Chemokine Receptor; T-Cell
Activation
ID PLASMACYTOID DENDRITIC CELLS; T-CELLS; CROHNS-DISEASE; CONCANAVALIN-A;
SIGLEC-H; RECEPTOR; PRECURSORS; TOLERANCE; LYMPHOCYTES; CCL25/CCR9
AB BACKGROUND & AIMS: Antigen-presenting cells (APCs) are involved in the induction of liver inflammation. We investigated the roles of specific APCs in the pathogenesis of acute liver injury in mice. METHODS: We used concanavalin A (con A) or carbon tetrachloride to induce acute liver inflammation in mice and studied the roles of macrophages that express CCR9. RESULTS: After injection of con A, we detected CCR9(+)CD11b(+)CD11c(-)macrophages that express tumor necrosis factor (TNF)-alpha in livers of mice, whereas CCR9(+) Siglec-H(+)CD11b(-)CD11c(low) plasmacytoid DCs (pDCs), which are abundant in normal livers, disappeared. The CCR9(+) macrophages were also detected in the livers of RAG-2(-/-) mice, which lack lymphocytes and natural killer T cells, after injection of con A. Under inflammatory conditions, CCR9(+) macrophages induced naive CD4(+) T cells to become interferon gamma-producing Th1 cells in vivo and in vitro. CCR9 (/) mice injected with con A did not develop hepatitis unless they also received CCR9(+) macrophages from mice that received con A; more CCR9(+) macrophages accumulated in their inflamed livers than CCR9(+) pDCs, CCR9(-)pDCs, or CCR9(-)macrophages isolated from mice that had received injections of con A. Levels of CCL25 messenger RNA increased in livers after injection of con A; neutralizing antibodies against CCL25 reduced the induction of hepatitis by con A by blocking the migration of CCR9(+) macrophages and their production of TNF-alpha. Peripheral blood samples from patients with acute hepatitis had greater numbers of TNF-alpha-producing CCR9(+)CD14(+) CD16(high) monocytes than controls. CONCLUSIONS: CCR9(+)macrophages contribute to the induction of acute liver inflammation in mouse models of hepatitis.
C1 [Nakamoto, Nobuhiro; Ebinuma, Hirotoshi; Kanai, Takanori; Chu, Po-Sung; Ono, Yuichi; Mikami, Yohei; Ojiro, Keisuke; Saito, Hidetsugu; Hibi, Toshifumi] Keio Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, Tokyo 1808582, Japan.
[Lipp, Martin] Max Delbruck Ctr Mol Med, Dept Tumor Genet & Immunogenet, Berlin, Germany.
[Love, Paul E.] NICHHD, Lab Mammalian Genes & Dev, NIH, Bethesda, MD 20892 USA.
RP Kanai, T (reprint author), Keio Univ, Sch Med, Dept Internal Med, Div Gastroenterol & Hepatol, Tokyo 1808582, Japan.
EM takagast@sc.itc.keio.ac.jp; thibi@sc.itc.keio.ac.jp
FU Japanese Ministry of Education, Culture, Sports, Science and Technology;
Japanese Ministry of Health, Labour and Welfare; Japan Medical
Association; Foundation for Advancement of International Science; Keio
University
FX Supported part by grants-in-aid for Scientific Research, Scientific
Research on Priority Areas, Exploratory Research and Creative Scientific
Research from the Japanese Ministry of Education, Culture, Sports,
Science and Technology; the Japanese Ministry of Health, Labour and
Welfare; the Japan Medical Association; Foundation for Advancement of
International Science; and Keio University Medical Fund.; Writing
assistance was provided by Dr Peter Hawkes (Kansai Language College) and
Edanz Group Ltd and funded by grants-in-aid for Scientific Research,
Scientific Research on Priority Areas, Exploratory Research.
NR 30
TC 25
Z9 25
U1 1
U2 8
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 2012
VL 142
IS 2
BP 366
EP 376
DI 10.1053/j.gastro.2011.10.039
PG 11
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 882CV
UT WOS:000299540000043
PM 22079594
ER
PT J
AU Vahabzadeh, B
Seetharam, AB
Cook, MB
Wani, S
Rastogi, A
Bansal, A
Early, DS
Sharma, P
AF Vahabzadeh, Babac
Seetharam, Anil B.
Cook, Michael B.
Wani, Sachin
Rastogi, Amit
Bansal, Ajay
Early, Dayna S.
Sharma, Prateek
TI Validation of the Prague C & M criteria for the endoscopic grading of
Barrett's esophagus by gastroenterology trainees: a multicenter study
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
ID GASTROESOPHAGEAL-REFLUX; EARLY NEOPLASIA; RISK-FACTORS; ADENOCARCINOMA;
LENGTH; RELIABILITY; DYSPLASIA; PROGRESSION; DIAGNOSIS; SIZE
AB Background: The Prague C & M criteria, developed for the endoscopic grading of Barrett's esophagus (BE), (C = circumferential length, M = maximal length) were previously validated among a panel of 29 expert encloscopists with a special interest in BE. Its performance among gastroenterology trainees is unknown.
Objective: To test interobserver agreement among gastroenterology trainees for the Prague C & M criteria, identification of the gastroesophageal junction (GEJ) and the diaphragmatic hiatus.
Design: A prospective study.
Setting: Two tertiary referral centers.
Patients and Interventions: Standardized endoscopic videos were used.
Main Outcome Measurements: Interobserver agreement.
Results: Eighteen high-quality videos (normal esophagus, short and long lengths of BE, equally distributed) were independently evaluated by 18 gastroenterology trainees (year 1, n = 5; year 2, n = 6; year 3, n = 7) after administration of a formal teaching module by an expert endoscopist. Overall intraclass correlation coefficients for assessment of the C and M extent of the endoscopic BE segment above the GEJ were 0.94 (95% CI, 0.89-0.98) and 0.96 (95% CI, 0.94-0.98), respectively. The overall intraclass correlation coefficients for GEJ and diaphragmatic hiatus location recognition were 0.92 (0.86-0.96) and 0.90 (0.82-0.95), respectively. The year of training did not affect interobserver agreement.
Limitations: The use of videos for encloscopic evaluation.
Conclusion: After standardized teaching, the Prague C & M criteria have high overall validity among gastroenterology trainees irrespective of the level of training for endoscopic evaluation of visualized BE lengths as well as key endoscopic landmarks. (Gastrointest Endosc 2012;75:236-41.)
C1 [Vahabzadeh, Babac; Rastogi, Amit; Bansal, Ajay; Sharma, Prateek] Vet Affairs Med Ctr, Kansas City, MO USA.
[Vahabzadeh, Babac; Rastogi, Amit; Bansal, Ajay; Sharma, Prateek] Univ Kansas, Med Ctr, Kansas City, KS 66103 USA.
[Seetharam, Anil B.; Wani, Sachin; Early, Dayna S.] Washington Univ, Sch Med, St Louis, MO USA.
[Cook, Michael B.] NCI, Bethesda, MD 20892 USA.
RP Sharma, P (reprint author), Univ Kansas, Sch Med, Dept Vet Affairs Med Ctr, 4801 E Linwood Blvd, Kansas City, MO 64128 USA.
RI Cook, Michael/A-5641-2009
OI Cook, Michael/0000-0002-0533-7302
FU Intramural VA [VA999999]
NR 24
TC 23
Z9 23
U1 1
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD FEB
PY 2012
VL 75
IS 2
BP 236
EP 241
DI 10.1016/j.gie.2011.09.017
PG 6
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 885BF
UT WOS:000299752800002
PM 22248595
ER
PT J
AU Zhu, JJ
Nguyen, MT
Nakamura, E
Yang, JM
Mackem, S
AF Zhu, Jianjian
Minh-Thanh Nguyen
Nakamura, Eiichiro
Yang, Junming
Mackem, Susan
TI Cre-mediated recombination can induce apoptosis in vivo by activating
the p53 DNA damage-induced pathway
SO GENESIS
LA English
DT Article
DE transgenic mice; loxP sites; Cre recombinase; apoptosis
ID SITE-SPECIFIC RECOMBINATION; SONIC-HEDGEHOG; LIMB BUD; INVERTED REPEATS;
MAMMALIAN-CELLS; TRANSGENIC MICE; LATERAL PLATE; EXPRESSION; MOUSE; GENE
AB Cre-mediated apoptosis has been observed in many contexts in mice expressing Cre-recombinase and can confound the analysis of genetically engineered conditional mutant or transgenic alleles. Several mechanisms have been proposed to explain this phenomenon. We find that the degree of apoptosis induced correlates roughly with the copy number of loxP sites present in the genome and that some level of increased apoptosis accompanies the presence of even only a few loxP sites, as occurs in conditional floxed alleles. Cre-induced apoptosis in this context is completely p53-dependent, suggesting that the apoptosis is stimulated by p53 activation in response to DNA damage incurred during the process of Cre-mediated recombination. genesis 50:102111, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Zhu, Jianjian; Minh-Thanh Nguyen; Nakamura, Eiichiro; Yang, Junming; Mackem, Susan] NCI, Ctr Canc Res, Canc & Dev Biol Lab, Ft Detrick, MD 21702 USA.
[Minh-Thanh Nguyen] Univ Cincinnati, Dept Ophthalmol, Cincinnati, OH 45221 USA.
[Nakamura, Eiichiro] Univ Occupat & Environm Hlth, Dept Orthoped Surg, Kitakyushu Fukuoka 8078555, Japan.
RP Mackem, S (reprint author), NCI, Ctr Canc Res, Canc & Dev Biol Lab, 1050 Boyles St,Bldg 539,Room 121A, Ft Detrick, MD 21702 USA.
EM smack@helix.nih.gov
FU Center for Cancer Research, National Cancer Institute, NIH
FX Contract grant sponsor: Center for Cancer Research, National Cancer
Institute, NIH
NR 41
TC 8
Z9 8
U1 1
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1526-954X
J9 GENESIS
JI Genesis
PD FEB
PY 2012
VL 50
IS 2
BP 102
EP 111
DI 10.1002/dvg.20799
PG 10
WC Developmental Biology; Genetics & Heredity
SC Developmental Biology; Genetics & Heredity
GA 886EQ
UT WOS:000299835500003
PM 21913308
ER
PT J
AU Berquam-Vrieze, KE
Swing, DA
Tessarollo, L
Dupuy, AJ
AF Berquam-Vrieze, Katherine E.
Swing, Deborah A.
Tessarollo, Lino
Dupuy, Adam J.
TI Characterization of transgenic mice expressing cancer-associated
variants of human NOTCH1
SO GENESIS
LA English
DT Article
DE mouse models of cancer; BAC recombineering; BAC transgenesis
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ACTIVATED NOTCH1; PROGRESSION; MUTATIONS;
APOPTOSIS; BINDING; GENES; CELLS; CD4
AB The Notch1 receptor plays a critical role in cell fate decisions during development. Activation of Notch signaling has been implicated in several types of cancer, particularly T-cell acute lymphoblastic leukemia (T-ALL). Consequently, several transgenic mouse strains have been made to study the role of Notch1 in T-ALL. However, the existing Notch1 transgenic lines mimic a translocation event found in only similar to 1% of T-ALL cases. Here we describe three novel NOTCH1 transgenic mouse strains that have Cre-inducible expression of the entire human NOTCH1 locus, each possessing a common mutation found in T-ALL. Unlike existing Notch1 transgenic strains, these NOTCH1 transgenic strains express full-length receptors from anendogenous human promoter that should be susceptible to a number of Notch antagonists that have recently been developed. These strains will allow researchers to modulate Notch signaling to study bothnormal development and cancer biology. genesis 50:112118, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Berquam-Vrieze, Katherine E.; Dupuy, Adam J.] Univ Iowa, Carver Coll Med, Dept Anat & Cell Biol, Iowa City, IA 52242 USA.
[Swing, Deborah A.; Tessarollo, Lino] NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA.
RP Dupuy, AJ (reprint author), Univ Iowa, Coll Med, Dept Anat & Cell Biol, Iowa City, IA 52242 USA.
EM adam-dupuy@uiowa.edu
FU NCI NIH HHS [R01 CA130867, R01 CA130867-04]
NR 29
TC 3
Z9 3
U1 0
U2 0
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1526-954X
J9 GENESIS
JI Genesis
PD FEB
PY 2012
VL 50
IS 2
BP 112
EP 118
DI 10.1002/dvg.20798
PG 7
WC Developmental Biology; Genetics & Heredity
SC Developmental Biology; Genetics & Heredity
GA 886EQ
UT WOS:000299835500004
PM 21898766
ER
PT J
AU Hendrickson, AEW
Oberg, AL
Glaser, G
Camoriano, JK
Peethambaram, PP
Colon-Otero, G
Erlichman, C
Ivy, SP
Kaufmann, SH
Karnitz, LM
Haluska, P
AF Hendrickson, Andrea E. Wahner
Oberg, Ann L.
Glaser, Gretchen
Camoriano, John K.
Peethambaram, Prema P.
Colon-Otero, Gerardo
Erlichman, Charles
Ivy, S. Percy
Kaufmann, Scott H.
Karnitz, Larry M.
Haluska, Paul
TI A phase II study of gemcitabine in combination with tanespimycin in
advanced epithelial ovarian and primary peritoneal carcinoma
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Phase I/II trials; Tanespimycin; Gemcitabine; Ovarian cancer; Peritoneal
cancer; Heat shock protein 90
ID REFRACTORY ADVANCED CANCERS; LEUKEMIA-CELLS; IN-VIVO; HSP90;
17-ALLYLAMINO-17-DEMETHOXYGELDANAMYCIN; INHIBITION; TRIAL; GELDANAMYCIN;
HEAT-SHOCK-PROTEIN-90; ACTIVATION
AB Objective. To evaluate the efficacy and biological effects of the gemcitabine/tanespimycin combination in patients with advanced ovarian and peritoneal cancer. To assess the effect of tanespimycin on tumor cells, levels of the chaperone proteins HSP90 and HSP70 were examined in peripheral blood mononuclear cells (PBMC) and paired tumor biopsy lysates.
Methods. Two-cohort phase II clinical trial. Patients were grouped according to prior gemcitabine therapy. All participants received tanespimycin 154 mg/m(2) on days 1 and 9 of cycle 1 and days 2 and 9 of subsequent cycles. Patients also received gemcitabine 750 mg/m(2) on day 8 of the first treatment cycle and days 1 and 8 of subsequent cycles.
Results. The tanespimycin/gemcitabine combination induced a partial response in 1 gemcitabine naive patient and no partial responses in gemcitabine resistant patients. Stable disease was seen in 6 patients (2 gemcitabine naive and 4 gemcitabine resistant). The most common toxicities were hematologic (anemia and neutropenia) as well as nausea and vomiting. Immunoblotting demonstrated limited upregulation of HSP70 but little or no change in levels of most client proteins in PBMC and paired tumor samples.
Conclusions. Although well tolerated, the tanespimycin/gemcitabine combination exhibited limited anticancer activity in patients with advanced epithelial ovarian and primary peritoneal carcinoma, perhaps because of failure to significantly downregulate the client proteins at clinically achievable exposures. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Hendrickson, Andrea E. Wahner; Peethambaram, Prema P.; Erlichman, Charles; Haluska, Paul] Mayo Clin, Div Med Oncol, Rochester, MN 55905 USA.
[Oberg, Ann L.] Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN 55905 USA.
[Glaser, Gretchen] Mayo Clin, Div Gynecol Oncol, Rochester, MN 55905 USA.
[Colon-Otero, Gerardo] Mayo Clin, Div Hematol Oncol, Jacksonville, FL 32224 USA.
[Camoriano, John K.] Mayo Clin, Div Hematol Oncol, Scottsdale, AZ 85054 USA.
[Ivy, S. Percy] NCI, Rockville, MD 20852 USA.
[Kaufmann, Scott H.; Karnitz, Larry M.] Mayo Clin, Div Oncol Res, Rochester, MN 55905 USA.
[Kaufmann, Scott H.; Karnitz, Larry M.] Mayo Clin, Dept Mol Pharmacol & Expt Therapeut, Rochester, MN 55905 USA.
RP Haluska, P (reprint author), Mayo Clin, Div Med Oncol, Gonda 10,200 1st St SW, Rochester, MN 55905 USA.
EM haluska.paul@mayo.edu
OI Kaufmann, Scott/0000-0002-4900-7145
FU Mayo Phase 2 [N01-CM 62205, K12 CA090628, R01 CA104378]
FX Supported by The Mayo Phase 2 contract N01-CM 62205 (C.E.), K12 CA090628
(P. H.) and R01 CA104378 (L.M.K.).
NR 31
TC 13
Z9 14
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 0090-8258
J9 GYNECOL ONCOL
JI Gynecol. Oncol.
PD FEB
PY 2012
VL 124
IS 2
BP 210
EP 215
DI 10.1016/j.ygyno.2011.10.002
PG 6
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 885UE
UT WOS:000299805500007
PM 22047770
ER
PT J
AU Francis, JH
Kleinerman, RA
Seddon, JM
Abramson, DH
AF Francis, Jasmine H.
Kleinerman, Ruth A.
Seddon, Johanna M.
Abramson, David H.
TI Increased risk of secondary uterine leiomyosarcoma in hereditary
retinoblastoma
SO GYNECOLOGIC ONCOLOGY
LA English
DT Article
DE Retinoblastoma; Uterine leiomyosarcoma; Secondary cancers
ID SOFT-TISSUE SARCOMAS; ALTERED PATTERNS; TUMOR-SUPPRESSOR; CANCER
INCIDENCE; URINARY-BLADDER; FOLLOW-UP; SURVIVORS; CHILDHOOD; MUTATIONS;
UTERUS
AB Objective. In the US, second non-ocular malignancies are the primary cause of death in retinoblastoma survivors with the germline RB1 mutation. Soft tissue sarcomas are one of the most likely malignancies to pose a risk to these patients, with leiomyosarcoma (LMS) being the most common subtype. As our cohort is followed for a longer period, we discover new second malignancy risks for these patients.
Methods. We estimated the risk for uterine leiomyosarcoma (ULMS) in a cohort of 1854 patients with retinoblastoma who were diagnosed at two US institutions from 1914 through 1996. The standardized incidence ratio and excess absolute risk were calculated by comparison with population data from the Connecticut Tumor Registry or from National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) database. The cumulative risk at 50 years of age was also calculated.
Results. Seven of 525 female hereditary retinoblastoma patients developed ULMS. Five of these patients were used in the risk analysis, resulting in an excess risk of 3.87 per 10,000 women. Among hereditary patients who developed ULMS the excess risk increases dramatically with age: to 20/10,000 for female hereditary retinoblastoma patients aged between 30 and 39 years, and to 27/10,000 for patients aged 40+ years.
Conclusion. There is a substantial excess risk of ULMS in female hereditary retinoblastoma patients. As more patients survive into their thirties, this number is likely to increase. These findings raise the question of early childbearing, screening and prophylactic measures in hereditary retinoblastoma patients: all issues that would benefit from confirmation from other retinoblastoma cohorts, to allow for better guided counsel of these patients. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Francis, Jasmine H.; Abramson, David H.] Mem Sloan Kettering Canc Ctr, Ophthalm Oncol Serv, New York, NY 10021 USA.
[Francis, Jasmine H.] New York Eye & Ear Infirm, New York, NY 10003 USA.
[Kleinerman, Ruth A.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Seddon, Johanna M.] Tufts Univ New England Med Ctr, Ophthalm Epidemiol & Genet Serv, Boston, MA USA.
RP Abramson, DH (reprint author), Mem Sloan Kettering Canc Ctr, Ophthalm Oncol Serv, 70 E 66th St, New York, NY 10021 USA.
EM abramsod@mskcc.org
OI Kleinerman, Ruth/0000-0001-7415-2478
FU National Institutes of Health; National Cancer Institute, Division of
Cancer Epidemiology and Genetics; Fund for Ophthalmic Knowledge
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, the National Cancer Institute,
Division of Cancer Epidemiology and Genetics and by The Fund for
Ophthalmic Knowledge.
NR 55
TC 11
Z9 12
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 2012
VL 124
IS 2
BP 254
EP 259
DI 10.1016/j.ygyno.2011.10.019
PG 6
WC Oncology; Obstetrics & Gynecology
SC Oncology; Obstetrics & Gynecology
GA 885UE
UT WOS:000299805500015
PM 22027510
ER
PT J
AU Simons-Morton, B
Abraido-Lanza, AF
Bernhardt, JM
Schoenthaler, A
Schnitzer, A
Allegrante, JP
AF Simons-Morton, Bruce
Abraido-Lanza, Ana F.
Bernhardt, Jay M.
Schoenthaler, Antoinette
Schnitzer, Amanda
Allegrante, John P.
TI Demystifying Peer Review
SO HEALTH EDUCATION & BEHAVIOR
LA English
DT Editorial Material
C1 [Allegrante, John P.] Columbia Univ, Teachers Coll, Dept Hlth & Behav Studies, New York, NY 10027 USA.
[Simons-Morton, Bruce; Allegrante, John P.] NIH, Bethesda, MD 20892 USA.
[Bernhardt, Jay M.] Univ Florida, Gainesville, FL USA.
[Schoenthaler, Antoinette] NYU, New York, NY USA.
[Schnitzer, Amanda] Soc Publ Hlth Educ, Washington, DC USA.
RP Allegrante, JP (reprint author), Columbia Univ, Teachers Coll, Dept Hlth & Behav Studies, 525 W 120th St, New York, NY 10027 USA.
EM jpa1@columbia.edu
OI Bernhardt, Jay/0000-0002-2045-4005; Schoenthaler,
Antoinette/0000-0003-4905-5136; Simons-Morton, Bruce/0000-0003-1099-6617
FU Intramural NIH HHS; NCI NIH HHS [R21CA134247]; NIGMS NIH HHS
[R25GM62454]
NR 5
TC 3
Z9 3
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1090-1981
J9 HEALTH EDUC BEHAV
JI Health Educ. Behav.
PD FEB
PY 2012
VL 39
IS 1
BP 3
EP 7
DI 10.1177/1090198111433309
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 885LN
UT WOS:000299780600001
PM 22301900
ER
PT J
AU Kaphingst, KA
Goodman, M
Pyke, O
Stafford, J
Lachance, C
AF Kaphingst, Kimberly A.
Goodman, Melody
Pyke, Owen
Stafford, Jewel
Lachance, Christina
TI Relationship Between Self-Reported Racial Composition of High School and
Health Literacy Among Community Health Center Patients
SO HEALTH EDUCATION & BEHAVIOR
LA English
DT Article
DE community health centers; health disparities; health literacy;
residential segregation
ID NEWEST VITAL SIGN; ADULT LITERACY; RESIDENTIAL SEGREGATION;
AFRICAN-AMERICAN; PRIMARY-CARE; DISPARITIES; SKILLS; POPULATION;
BEHAVIOR
AB Intervention and policy approaches targeting the societal factors that affect health literacy (e.g., educational systems) could have promise to improve health outcomes, but little research has investigated these factors. This study examined the associations between self-reported racial composition of prior educational and neighborhood contexts and health literacy among 1,061 English- and Spanish-speaking adult community health center patients. The authors found that self-reported racial composition of high school was a significant predictor of health literacy among those who received schooling in the United States, controlling for race/ethnicity, education, age, country of birth, and survey language. Black and Hispanic patients had significantly lower health literacy than White patients within educational strata among those schooled in the United States. The findings revealed substantial disparities in health literacy. Self-reported racial composition of school context was a significant predictor of health literacy. Transdisciplinary, multilevel intervention approaches are likely to be needed to address the health literacy needs of this population.
C1 [Kaphingst, Kimberly A.] Washington Univ, Sch Med, Dept Surg, Div Publ Hlth Sci, St Louis, MO 63110 USA.
[Goodman, Melody; Pyke, Owen; Stafford, Jewel] SUNY Stony Brook, Stony Brook, NY 11794 USA.
[Lachance, Christina] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Kaphingst, KA (reprint author), Washington Univ, Sch Med, Dept Surg, Div Publ Hlth Sci, Campus Box 8100, St Louis, MO 63110 USA.
EM kkaphingst@gwbmail.wustl.edu
RI Goodman, Melody/F-6768-2011
OI Goodman, Melody/0000-0001-8932-624X
FU Intramural NIH HHS [Z01 HG200321-04]
NR 39
TC 4
Z9 4
U1 2
U2 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1090-1981
EI 1552-6127
J9 HEALTH EDUC BEHAV
JI Health Educ. Behav.
PD FEB
PY 2012
VL 39
IS 1
BP 35
EP 44
DI 10.1177/1090198111406538
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 885LN
UT WOS:000299780600005
PM 21636703
ER
PT J
AU de Heer, HD
Balcazar, HG
Castro, F
Schulz, L
AF de Heer, Hendrik Dirk
Balcazar, Hector G.
Castro, Felipe
Schulz, Leslie
TI A Path Analysis of a Randomized Promotora de Salud Cardiovascular
Disease-Prevention Trial Among At-Risk Hispanic Adults
SO HEALTH EDUCATION & BEHAVIOR
LA English
DT Article
DE cardiovascular disease; community; education; Hispanic; nutrition;
promotoras de salud; structural equation model
ID STRUCTURAL EQUATION MODELS; UNITED-STATES; BEHAVIORAL-THEORY;
MEXICAN-AMERICANS; HEALTH; ACCULTURATION; LATINO; MORTALITY; COHESION;
CONTEXT
AB This study assessed effectiveness of an educational community intervention taught by promotoras de salud in reducing cardiovascular disease (CVD) risk among Hispanics using a structural equation modeling (SEM) approach. Model development was guided by a social ecological framework proposing CVD risk reduction through improvement of protective health behaviors, health beliefs, contextual and social factors. Participants were 328 Hispanic adults with at least one CVD risk factor. SEM analyses assessed direct and indirect effects of intervention participation on CVD risk (Framingham score) and latent variables nutrition intake and health beliefs. The model fit was adequate (root mean square error of approximation = .056 [90% confidence interval = .040, .072], comparative fit index = .967, normed fit index = .938, nonnormed fit index = .947). Intervention participation was associated with improved nutritional consumption, but not lower CVD risk. Stronger health beliefs predicted healthier nutritional habits. This project provided evidence for the adequacy of a conceptual framework that can be used to elicit new pathways toward CVD risk reduction among at-risk Hispanic populations.
C1 [Balcazar, Hector G.] Univ Texas El Paso, Sch Publ Hlth, El Paso, TX 79902 USA.
[de Heer, Hendrik Dirk] NHGRI, Bethesda, MD 20892 USA.
[Castro, Felipe] Arizona State Univ, Tempe, AZ USA.
[Schulz, Leslie] No Arizona Univ, Flagstaff, AZ 86011 USA.
RP Balcazar, HG (reprint author), Univ Texas El Paso, Sch Publ Hlth, El Paso Reg Campus,1100 N Stanton, El Paso, TX 79902 USA.
EM hector.g.balcazar@uth.tmc.edu
RI de Heer, Hendrik/D-3192-2013
OI de Heer, Hendrik/0000-0002-9241-5021
FU NIMHD NIH HHS [R24 MD0001785-01, R24 MD001785]
NR 40
TC 6
Z9 6
U1 0
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1090-1981
J9 HEALTH EDUC BEHAV
JI Health Educ. Behav.
PD FEB
PY 2012
VL 39
IS 1
BP 77
EP 86
DI 10.1177/1090198111408720
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 885LN
UT WOS:000299780600009
PM 21680806
ER
PT J
AU Ruhl, CE
Everhart, JE
AF Ruhl, Constance E.
Everhart, James E.
TI Upper limits of normal for alanine aminotransferase activity in the
United States population
SO HEPATOLOGY
LA English
DT Article
ID TRANSAMINASE-ACTIVITY; REFERENCE INTERVALS; HEALTHY RANGES;
BLOOD-DONORS; HEPATITIS-C; SERUM; ALT; PREVALENCE; VALUES
AB Alanine aminotransferase (ALT) is an important test for liver disease, yet there is no generally accepted upper limit of normal (ULN) in the United States. Furthermore, the ability of ALT to differentiate persons with and without liver disease is uncertain. We examined cut-offs for ALT for their ability to discriminate between persons with positive hepatitis C virus (HCV) RNA and those at low risk for liver injury in the U.S. population. Among adult participants in the 1999-2008 U.S. National Health and Nutrition Examination Survey, 259 were positive for serum HCV RNA and 3,747 were at low risk for liver injury (i.e., negative HCV RNA and hepatitis B surface antigen, low alcohol consumption, no evidence of diabetes, and normal body mass index and waist circumference). Serum ALT activity was measured centrally. Maximum correct classification was achieved at ALT = 29 IU/L for men (88% sensitivity, 83% specificity) and 22 IU/L (89% sensitivity, 82% specificity) for women. The cut-off for 95% sensitivity was an ALT = 24 IU/L (70% specificity) for men and 18 IU/L (63% specificity) for women. The cut-off for 95% specificity was ALT = 44 IU/L (64% sensitivity) for men and 32 IU/L (59% sensitivity) for women. The area under the curve was 0.929 for men and 0.915 for women. If the cut-offs with the best correct classification were applied to the entire population, 36.4% of men and 28.3% of women would have had abnormal ALT. Conclusion: ALT discriminates persons infected with HCV from those at low risk of liver disease, but would be considered elevated in a large proportion of the U.S. population. (HEPATOLOGY 2012)
C1 [Ruhl, Constance E.] Social & Sci Syst Inc, Silver Spring, MD 20910 USA.
[Everhart, James E.] NIDDKD, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 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).
NR 25
TC 33
Z9 34
U1 4
U2 9
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD FEB
PY 2012
VL 55
IS 2
BP 447
EP 454
DI 10.1002/hep.24725
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 883KM
UT WOS:000299632900013
PM 21987480
ER
PT J
AU Altekruse, SF
McGlynn, KA
Dickie, LA
Kleiner, DE
AF Altekruse, Sean F.
McGlynn, Katherine A.
Dickie, Lois A.
Kleiner, David E.
TI Hepatocellular Carcinoma Confirmation, Treatment, and Survival in
Surveillance, Epidemiology, and End Results Registries, 1992-2008
SO HEPATOLOGY
LA English
DT Article
ID UNITED-STATES; DIAGNOSIS; TRENDS; RATES
AB Approaches to the diagnosis and management of hepatocellular carcinoma (HCC) are improving survival. In the Surveillance, Epidemiology, and End Results-13 registries, HCC stage, histological confirmation, and first-course surgery were examined. Among 21,390 HCC cases diagnosed with follow-up of vital status during 1998-2008, there were 4,727 (22%) with reported first-course invasive liver surgery, local tumor destruction, or both. The proportion with reported liver surgery or ablation was 39% among localized stage cases and only 4% among distant/unstaged cases. Though 70% of cases had histologically confirmed diagnoses, the proportion with confirmed diagnoses was higher among cases with reported invasive surgery (99%), compared to cases receiving ablation (81%) or no reported therapy (65%). Incidence rates of histologically unconfirmed HCC increased faster than those of confirmed HCC from 1992 to 2008 (8% versus 3% per year). Two encouraging findings were that incidence rates of localized-stage HCC increased faster than rates of regional- and distant-stage HCC combined (8% versus 4% per year), and that incidence rates of reported first-course surgery or tumor destruction increased faster than incidence rates of HCC without such therapy (11% versus 7%). Between 1975-1977 and 1998-2007, 5-year cause-specific HCC survival increased from just 3% to 18%. Survival was 84% among transplant recipients, 53% among cases receiving radiofrequency ablation at early stage, 47% among cases undergoing resection, and 35% among cases receiving local tumor destruction. Asian or Pacific Islander cases had significantly better 5-year survival (23%) than white (18%), Hispanic (15%), or black cases (12%). Conclusion: HCC survival is improving, because more cases are diagnosed and treated at early stages. Additional progress may be possible with continued use of clinical surveillance to follow individuals at risk for HCC, enabling early intervention. (HEPATOLOGY 2012;)
C1 [Altekruse, Sean F.; Dickie, Lois A.] NCI, Div Canc Control & Populat Sci, Rockville, MD 20852 USA.
[McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Kleiner, David E.] NCI, Div Basic Sci, Pathol Lab, Rockville, MD 20852 USA.
RP Altekruse, SF (reprint author), NCI, Div Canc Control & Populat Sci, 6116 Execut Blvd,Room 5003, Rockville, MD 20852 USA.
EM altekrusesf@mail.nih.gov
OI Kleiner, David/0000-0003-3442-4453
FU National Cancer Institute (NCI), Division of Cancer Control and
Population Sciences; NIH, National Cancer Institute
FX This study was supported by the National Cancer Institute (NCI),
Division of Cancer Control and Population Sciences, Surveillance
Research Program contracts with SEER Registries and Information
Management Services and by the Intramural Research Program of the NIH,
National Cancer Institute.
NR 25
TC 76
Z9 83
U1 1
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0270-9139
J9 HEPATOLOGY
JI Hepatology
PD FEB
PY 2012
VL 55
IS 2
BP 476
EP 482
DI 10.1002/hep.24710
PG 7
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 883KM
UT WOS:000299632900016
PM 21953588
ER
PT J
AU Sastalla, I
Tang, SX
Crown, D
Liu, SH
Eckhaus, MA
Hewlett, IK
Leppla, SH
Moayeri, M
AF Sastalla, Inka
Tang, Shixing
Crown, Devorah
Liu, Shihui
Eckhaus, Michael A.
Hewlett, Indira K.
Leppla, Stephen H.
Moayeri, Mahtab
TI Anthrax Edema Toxin Impairs Clearance in Mice
SO INFECTION AND IMMUNITY
LA English
DT Article
ID BACILLUS-ANTHRACIS; DIPHTHERIA-TOXIN; PROTECTIVE ANTIGEN; WATER CHANNEL;
LETHAL TOXIN; ADENYLATE-CYCLASE; CELL CHEMOTAXIS; AQUAPORIN-2; RECEPTOR;
PHOSPHORYLATION
AB The anthrax edema toxin (ET) of Bacillus anthracis is composed of the receptor-binding component protective antigen (PA) and of the adenylyl cyclase catalytic moiety, edema factor (EF). Uptake of ET into cells raises intracellular concentrations of the secondary messenger cyclic AMP, thereby impairing or activating host cell functions. We report here on a new consequence of ET action in vivo. We show that in mouse models of toxemia and infection, serum PA concentrations were significantly higher in the presence of enzymatically active EF. These higher concentrations were not caused by ET-induced inhibition of PA endocytosis; on the contrary, ET induced increased PA binding and uptake of the PA oligomer in vitro and in vivo through upregulation of the PA receptors TEM8 and CMG2 in both myeloid and nonmyeloid cells. ET effects on protein clearance from circulation appeared to be global and were not limited to PA. ET also impaired the clearance of ovalbumin, green fluorescent protein, and EF itself, as well as the small molecule biotin when these molecules were coinjected with the toxin. Effects on injected protein levels were not a result of general increase in protein concentrations due to fluid loss. Functional markers for liver and kidney were altered in response to ET. Concomitantly, ET caused phosphorylation and activation of the aquaporin-2 water channel present in the principal cells of the collecting ducts of the kidneys that are responsible for fluid homeostasis. Our data suggest that in vivo, ET alters circulatory protein and small molecule pharmacokinetics by an as-yet-undefined mechanism, thereby potentially allowing a prolonged circulation of anthrax virulence factors such as EF during infection.
C1 [Sastalla, Inka; Crown, Devorah; Liu, Shihui; Leppla, Stephen H.; Moayeri, Mahtab] NIAID, Bacterial Toxins & Therapeut Sect, NIH, Bethesda, MD 20892 USA.
[Tang, Shixing; Hewlett, Indira K.] US FDA, Mol Virol Lab, Ctr Biol Evaluat & Res, Bethesda, MD 20014 USA.
[Eckhaus, Michael A.] NIH, Diagnost & Res Serv Branch, Div Vet Resources, Off Res Serv, Bethesda, MD 20892 USA.
RP Moayeri, M (reprint author), NIAID, Bacterial Toxins & Therapeut Sect, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM mmoayeri@niaid.nih.gov
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases; Biodefense Advanced Research and Development
Agency, U.S. Department of Health and Human Services
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Allergy and
Infectious Diseases and Biodefense Advanced Research and Development
Agency, U.S. Department of Health and Human Services.
NR 54
TC 4
Z9 4
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 2012
VL 80
IS 2
BP 529
EP 538
DI 10.1128/IAI.05947-11
PG 10
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA 883UU
UT WOS:000299661200006
PM 22104108
ER
PT J
AU Ali, M
Bath, P
Brady, M
Davis, S
Diener, HC
Donnan, G
Fisher, M
Hacke, W
Hanley, DF
Luby, M
Tsivgoulis, G
Wahlgren, N
Warach, S
Lees, KR
AF Ali, Myzoon
Bath, Philip
Brady, Marian
Davis, Stephen
Diener, Hans-Christoph
Donnan, Geoffrey
Fisher, Marc
Hacke, Werner
Hanley, Daniel F.
Luby, Marie
Tsivgoulis, G.
Wahlgren, Nils
Warach, Steven
Lees, Kennedy R.
CA VISTA Steering Comm
TI Development, expansion, and use of a stroke clinical trials resource for
novel exploratory analyses
SO INTERNATIONAL JOURNAL OF STROKE
LA English
DT Article
DE database; secondary analysis; stroke; trial design
ID RANDOMIZED CONTROLLED-TRIAL; ACUTE ISCHEMIC-STROKE; ARCHIVE VISTA;
ASPIRIN; THROMBOLYSIS; CLOPIDOGREL; DIPYRIDAMOLE; PREVENTION; OUTCOMES;
REGISTRY
AB Introduction Analysis of reliable registry data can direct future research to influence clinical care. Data from the Virtual International Stroke Trials Archive have been used to test hypotheses and inform trial design. We sought to expand Virtual International Stroke Trials Archive into a broader stroke resource with new opportunities for research and international collaboration.
Methods Using procedures initially developed for an acute stroke trial archive, we invited trialists to lodge data on rehabilitation, secondary prevention, intracerebral haemorrhage, imaging, and observational stroke studies.
Results We have extended Virtual International Stroke Trials Archive into six subsections: Virtual International Stroke Trials Archive-Acute (n = 28 190 patients' data), Virtual International Stroke Trials Archive-Rehab (n = 10 194), Virtual International Stroke Trials Archive-intracerebral haemorrhage (n = 1829), Virtual International Stroke Trials Archive-Prevention, Virtual International Stroke Trials Archive-Imaging (n = 1300), and Virtual International Stroke Trials Archive-Plus (n = 6573). Enrollment continues, with commitments for the contribution of six further trials to Virtual International Stroke Trials Archive-Prevention, 13 trials to Virtual International Stroke Trials Archive-Rehab, and one registry to Virtual International Stroke Trials Archive-Plus. Data on age, type of stroke, medical history, outcomes by modified Rankin scale and Barthel Index (BI), mortality, and adverse events are available for analyses. The Virtual International Stroke Trials Archive network encourages the development of young investigators and provides opportunities for international peer review and collaboration.
Conclusions Application of the original Virtual International Stroke Trials Archive concepts beyond acute stroke trials can extend the value of clinical research at low cost, without threatening commercial or intellectual property interests. This delivers valuable research output to inform the efficiency of future stroke research. We invite stroke researchers to participate actively in Virtual International Stroke Trials Archive and encourage the extension of Virtual International Stroke Trials Archive principles to other disease areas.
C1 [Ali, Myzoon; Brady, Marian] Glasgow Caledonian Univ, NMAHP Res Unit, Glasgow G4 0BA, Lanark, Scotland.
[Bath, Philip] Univ Nottingham, Inst Neurosci, Nottingham NG7 2RD, England.
[Davis, Stephen] Univ Melbourne, Royal Melbourne Hosp, Dept Neurol, Melbourne, Vic 3050, Australia.
[Diener, Hans-Christoph] Univ Duisburg Essen, Dept Neurol, Essen, Germany.
[Fisher, Marc] Univ Massachusetts, Sch Med, Dept Neurol, Worcester, MA USA.
[Hacke, Werner] Heidelberg Univ, Dept Neurol, Heidelberg, Germany.
[Hanley, Daniel F.] Johns Hopkins Med Inst, Div Brain Injury Outcomes, Baltimore, MD 21205 USA.
[Luby, Marie; Warach, Steven] NINDS, Stroke Diagnost & Therapeut Sect, Bethesda, MD 20892 USA.
[Tsivgoulis, G.] Democritus Univ Thrace, Dept Neurol, Alexandroupolis, Greece.
[Wahlgren, Nils] Karolinska Hosp, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
[Ali, Myzoon; Lees, Kennedy R.] Univ Glasgow, Western Infirm, Inst Cardiovasc Med Sci, Glasgow G11 6NT, Lanark, Scotland.
RP Ali, M (reprint author), Glasgow Caledonian Univ, NMAHP Res Unit, Cowcaddens Rd, Glasgow G4 0BA, Lanark, Scotland.
EM vista.collaboration@glasgow.ac.uk
RI Davis, Stephen/L-5260-2013; Tyson, Sarah/J-3874-2014;
OI Davis, Stephen/0000-0003-0962-2300; Tyson, Sarah/0000-0001-6301-8791;
Bowen, Audrey/0000-0003-4075-1215; Stibrant Sunnerhagen,
Katharina/0000-0002-5940-4400; Drummond, Avril/0000-0003-1220-8354;
Bath, Philip/0000-0003-2734-5132; Gregson, Barbara/0000-0003-4868-9137;
Donnan, Geoffrey/0000-0001-6324-3403; Pollock, Alex/0000-0003-4941-7985;
Logan, Philippa/0000-0002-6657-2381; Kaste, Markku/0000-0001-6557-6412
FU Chief Scientist Office (CSO) Scottish Government's Health Directorate,
Scotland
FX Funding: VISTA is a not-for-profit collaboration of researchers from
academia and commercial organizations. The VISTA Steering Committee
members have each contributed to the organization of contributing
trials, and where these have involved industry support, they have
acknowledged that within the original publications. No author has any
additional conflict of interest to declare in relation to this work,
which was not externally supported. MA, MB, and the Nursing, Midwifery
and Allied Health Professions Research Unit are funded by the Chief
Scientist Office (CSO) Scottish Government's Health Directorate,
Scotland.
NR 20
TC 37
Z9 37
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1747-4930
EI 1747-4949
J9 INT J STROKE
JI Int. J. Stroke
PD FEB
PY 2012
VL 7
IS 2
BP 133
EP 138
DI 10.1111/j.1747-4949.2011.00735.x
PG 6
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 879MS
UT WOS:000299334600006
PM 22264365
ER
PT J
AU Yin, J
Yan, XD
Yao, X
Zhang, YL
Shan, Y
Mao, N
Yang, YL
Pan, LY
AF Yin, Jie
Yan, Xuedong
Yao, Xin
Zhang, Yongli
Shan, Ying
Mao, Ning
Yang, Yili
Pan, Lingya
TI Secretion of annexin A3 from ovarian cancer cells and its association
with platinum resistance in ovarian cancer patients
SO JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
LA English
DT Article
DE annexin A3; ovarian cancer; platinum; drug resistance; biomarker
ID BRUSH-BORDER MEMBRANE; ELECTRON-MICROSCOPY; EXPRESSION; CISPLATIN;
CARCINOMA; PROTEIN; IV
AB Early detection of resistance to platinum-based therapy is critical for improving the treatment of ovarian cancers. We have previously found that increased expression of annexin A3 is a mechanism for platinum resistance in ovarian cancer cells. Here we demonstrate that annexin A3 can be detected in the culture medium of ovarian cancer cells, particularly these cells that express high levels of annexin A3. Levels of annexin A3 were then determined in sera from ovarian cancer patients using an enzyme-linked immunosorbent assay. Compared with those from normal donors, sera from ovarian cancer patients contain significantly higher levels of annexin A3. Furthermore, serum levels of annexin A3 were significantly higher in platinum-resistant patients than in platinum-sensitive patients. To gain insight into the mechanism of secretion, the ovarian cancer cell lines were examined using both transmission electron microscopy and immunoelectron microscopy. Compared with parent cells, there are significantly more vesicles in the cytoplasm of ovarian cancer cells that express high levels of annexin A3, and at least some vesicles are annexin A3-positive. Moreover, some vesicles appear to be fused with the cell membrane, suggesting that annexin A3 secretion may be associated with exocytosis and the release of exosomes. This is supported by our observation that ovarian cancer cells expressing higher levels of annexin A3 released increased numbers of exosomes. Furthermore, annexin A3 can be detected in exosomes released from cisplatin-resistant cells (SKOV3/Cis) by immunoblotting and immunoelectron microscopy.
C1 [Yin, Jie; Yan, Xuedong; Yao, Xin; Zhang, Yongli; Shan, Ying; Pan, Lingya] Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Obstet & Gynecol, Beijing 100730, Peoples R China.
[Yin, Jie; Yan, Xuedong; Yao, Xin; Zhang, Yongli; Shan, Ying; Pan, Lingya] Peking Union Med Coll, Beijing 100730, Peoples R China.
[Mao, Ning] Chinese Acad Med Sci, Inst Basic Med Sci, Dept Cell Biol, Beijing 100730, Peoples R China.
[Yang, Yili] NCI, Canc & Dev Biol Lab, Frederick, MD 21701 USA.
RP Pan, LY (reprint author), Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Obstet & Gynecol, 1 Shuai Fu Yuan,Wang Fu Jing St, Beijing 100730, Peoples R China.
EM lingyapan@hotmail.com
FU Key Foundation of PUMC Hospital [200203]; Department of Cell Biology,
Institute of Basic Medical Sciences
FX This work was supported by the Key Foundation of PUMC Hospital (Grant
200203). We thank Dr. Joel D. Ernst (University of California, San
Francisco, USA) for anti-annexin A3 antibody, Professor Wei Dai
(Electron Microscopy Center, Peking Union Medical College, Beijing,
China) for technical assistance in electron microscopy. We are also
grateful to our colleagues in the Department of Cell Biology, Institute
of Basic Medical Sciences, for their support and technical assistance,
and to Dr. Alan O. Perantoni for his editing of the paper.
NR 37
TC 26
Z9 30
U1 2
U2 13
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 2012
VL 16
IS 2
BP 337
EP 348
DI 10.1111/j.1582-4934.2011.01316.x
PG 12
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 883KU
UT WOS:000299633700013
PM 21435174
ER
PT J
AU Ehler, M
AF Ehler, M.
TI Random Tight Frames
SO JOURNAL OF FOURIER ANALYSIS AND APPLICATIONS
LA English
DT Article
DE Frames; Probability; Optimal configurations
ID BI-FRAMES; EXPANSIONS; ERASURES
AB We introduce probabilistic frames to study finite frames whose elements are chosen at random. While finite tight frames generalize orthonormal bases by allowing redundancy, independent, uniformly distributed points on the sphere approximately form a finite unit norm tight frame (FUNTF). In the present paper, we develop probabilistic versions of tight frames and FUNTFs to significantly weaken the requirements on the random choice of points to obtain an approximate finite tight frame. Namely, points can be chosen from any probabilistic tight frame, they do not have to be identically distributed, nor have unit norm. We also observe that classes of random matrices used in compressed sensing are induced by probabilistic tight frames.
C1 [Ehler, M.] NICHHD, Sect Med Biophys, NIH, Bethesda, MD 20892 USA.
[Ehler, M.] Univ Maryland, Norbert Wiener Ctr, Dept Math, College Pk, MD 20742 USA.
RP Ehler, M (reprint author), NICHHD, Sect Med Biophys, NIH, Bethesda, MD 20892 USA.
EM ehlermar@mail.nih.gov
FU National Institute of Child Health and Human Development; NIH/DFG [EH
405/1-1/575910]
FX The author was supported by the Intramural Research Program of the
National Institute of Child Health and Human Development and by NIH/DFG
Research Career Transition Awards Program (EH 405/1-1/575910). The
author would also like to thank the anonymous referees for detailed
comments and suggestions.
NR 27
TC 8
Z9 8
U1 2
U2 10
PU BIRKHAUSER BOSTON INC
PI CAMBRIDGE
PA 675 MASSACHUSETTS AVE, CAMBRIDGE, MA 02139 USA
SN 1069-5869
J9 J FOURIER ANAL APPL
JI J. Fourier Anal. Appl.
PD FEB
PY 2012
VL 18
IS 1
BP 1
EP 20
DI 10.1007/s00041-011-9182-5
PG 20
WC Mathematics, Applied
SC Mathematics
GA 881XL
UT WOS:000299525200001
ER
PT J
AU Goswami, R
Jabeen, R
Yagi, R
Pham, D
Zhu, JF
Goenka, S
Kaplan, MH
AF Goswami, Ritobrata
Jabeen, Rukhsana
Yagi, Ryoji
Duy Pham
Zhu, Jinfang
Goenka, Shreevrat
Kaplan, Mark H.
TI STAT6-Dependent Regulation of Th9 Development
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID TRANSCRIPTION FACTOR GATA-3; CD4(+) T-CELLS; C-MAF; SIGNAL TRANSDUCER;
GENE-EXPRESSION; HELPER-CELLS; TGF-BETA; DIFFERENTIATION; STAT6; IL-4
AB Th cell effector subsets develop in response to specific cytokine environments. The development of a particular cytokine-secreting pattern requires an integration of signals that may promote the development of opposing pathways. A recent example of this paradigm is the IL-9-secreting Th9 cell that develops in response to TGF-beta and IL-4, cytokines that, in isolation, promote the development of inducible regulatory T cells and Th2 cells, respectively. To determine how the balance of these factors results in priming for IL-9 secretion, we examined the effects of each pathway on transcription factors that regulate Th cell differentiation. We demonstrated that TGF-beta induces the PU.1-encoding Sfpi1 locus and that this is independent of IL-4-induced STAT6 activation. IL-4-activated STAT6 is required for repressing the expression of T-bet and Foxp3 in Th9 cells, transcription factors that inhibit IL-9 production, and STAT6 is required for the induction of IRF4, which promotes Th9 development. These data established a transcription factor network that regulates IL-9 and demonstrated how combinations of cytokine signals generate cytokine-secreting potential by altering the expression of a panel of transcription factors. The Journal of Immunology, 2012, 188: 968-975.
C1 [Goswami, Ritobrata; Jabeen, Rukhsana; Duy Pham; Goenka, Shreevrat; Kaplan, Mark H.] Indiana Univ Sch Med, Herman B Wells Ctr Pediat Res, Dept Pediat, Indianapolis, IN 46202 USA.
[Goswami, Ritobrata; Duy Pham; Goenka, Shreevrat; Kaplan, Mark H.] Indiana Univ Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA.
[Yagi, Ryoji; Zhu, Jinfang] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA.
RP Kaplan, MH (reprint author), Indiana Univ Sch Med, Herman B Wells Ctr Pediat Res, Dept Pediat, 1044 W Walnut St,Room 202, Indianapolis, IN 46202 USA.
EM mkaplan2@iupui.edu
RI Zhu, Jinfang/B-7574-2012;
OI Kaplan, Mark/0000-0002-2923-8245
FU Public Health Service [AI057459, HL093105]; Division of Intramural
Research of the National Institute of Allergy and Infectious Diseases,
the National Institutes of Health
FX This work was supported by Public Health Service Grants AI057459 (to M.
H. K.) and HL093105 (to S. G.). Y.R. and J.Z. were supported by the
Division of Intramural Research of the National Institute of Allergy and
Infectious Diseases, the National Institutes of Health.
NR 39
TC 78
Z9 85
U1 0
U2 17
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 2012
VL 188
IS 3
BP 968
EP 975
DI 10.4049/jimmunol.1102840
PG 8
WC Immunology
SC Immunology
GA 884FL
UT WOS:000299690200009
PM 22180613
ER
PT J
AU Janbazian, L
Price, DA
Canderan, G
Filali-Mouhim, A
Asher, TE
Ambrozak, DR
Scheinberg, P
Boulassel, MR
Routy, JP
Koup, RA
Douek, DC
Sekaly, RP
Trautmann, L
AF Janbazian, Loury
Price, David A.
Canderan, Glenda
Filali-Mouhim, Abdelali
Asher, Tedi E.
Ambrozak, David R.
Scheinberg, Phillip
Boulassel, Mohamad Rachid
Routy, Jean-Pierre
Koup, Richard A.
Douek, Daniel C.
Sekaly, Rafick-Pierre
Trautmann, Lydie
TI Clonotype and Repertoire Changes Drive the Functional Improvement of
HIV-Specific CD8 T Cell Populations under Conditions of Limited
Antigenic Stimulation
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS-INFECTION; ANTIRETROVIRAL THERAPY;
IMMUNE-RESPONSES; PD-1 EXPRESSION; HIGH-AVIDITY; IN-VIVO; HUMAN
CYTOMEGALOVIRUS; VIRAL PERSISTENCE; LYMPHOCYTE ESCAPE; TYPE-1 INFECTION
AB Persistent exposure to cognate Ag leads to the functional impairment and exhaustion of HIV-specific CD8 T cells. Ag withdrawal, attributable either to antiretroviral treatment or the emergence of epitope escape mutations, causes HIV-specific CD8 T cell responses to wane over time. However, this process does not continue to extinction, and residual CD8 T cells likely play an important role in the control of HIV replication. In this study, we conducted a longitudinal analysis of clonality, phenotype, and function to define the characteristics of HIV-specific CD8 T cell populations that persist under conditions of limited antigenic stimulation. Ag decay was associated with dynamic changes in the TCR repertoire, increased expression of CD45RA and CD127, decreased expression of programmed death-1, and the emergence of polyfunctional HIV-specific CD8 T cells. High-definition analysis of individual clonotypes revealed that the Ag loss-induced gain of function within HIV-specific CD8 T cell populations could be attributed to two nonexclusive mechanisms: 1) functional improvement of persisting clonotypes; and 2) recruitment of particular clonotypes endowed with superior functional capabilities. The Journal of Immunology, 2012, 188: 1156-1167.
C1 [Canderan, Glenda; Sekaly, Rafick-Pierre; Trautmann, Lydie] Vaccine & Gene Therapy Inst Florida, Port St Lucie, FL 34987 USA.
[Janbazian, Loury; Filali-Mouhim, Abdelali; Sekaly, Rafick-Pierre] Univ Montreal, Dept Microbiol & Immunol, Immunol Lab, Montreal, PQ H2X 1P1, Canada.
[Price, David A.; Asher, Tedi E.; Ambrozak, David R.; Scheinberg, Phillip; Koup, Richard A.; Douek, Daniel C.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Sekaly, Rafick-Pierre; Trautmann, Lydie] Cardiff Univ, Sch Med, Inst Infect & Immun, Cardiff CF14 4XN, S Glam, Wales.
[Boulassel, Mohamad Rachid; Routy, Jean-Pierre] McGill Univ, Ctr Hlth, Royal Victoria Hosp, Div Hematol, Montreal, PQ H3A 1A1, Canada.
[Sekaly, Rafick-Pierre] McGill Univ, Dept Microbiol & Immunol, Fac Med, Montreal, PQ H3A 2B4, Canada.
[Sekaly, Rafick-Pierre; Trautmann, Lydie] Univ Miami, Miller Sch Med, Dept Microbiol & Immunol, Miami, FL 33101 USA.
RP Trautmann, L (reprint author), Vaccine & Gene Therapy Inst Florida, 11350 SW Village Pkwy, Port St Lucie, FL 34987 USA.
EM ltrautmann@vgtifl.org
RI Price, David/C-7876-2013;
OI Price, David/0000-0001-9416-2737; Scheinberg,
Phillip/0000-0002-9047-4538
FU Canadian Institutes for Health Research; Fonds de la Recherche en Sante
du Quebec Reseau Sida et Maladies Infectieuses; National Institutes of
Health [IDPIDA028871-01]; Office of Tourism, Trade, and Economic
Development of Florida
FX This work was supported by funds from the Canadian Institutes for Health
Research, the Fonds de la Recherche en Sante du Quebec Reseau Sida et
Maladies Infectieuses, the National Institutes of Health (Grant
IDPIDA028871-01), and the Office of Tourism, Trade, and Economic
Development of Florida. D.A.P. is a Medical Research Council (U.K.)
Senior Clinical Fellow.
NR 65
TC 19
Z9 19
U1 0
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 2012
VL 188
IS 3
BP 1156
EP 1167
DI 10.4049/jimmunol.1102610
PG 12
WC Immunology
SC Immunology
GA 884FL
UT WOS:000299690200030
PM 22210916
ER
PT J
AU Baranova, IN
Vishnyakova, TG
Bocharov, AV
Leelahavanichkul, A
Kurlander, R
Chen, ZG
Souza, ACP
Yuen, PST
Star, RA
Csako, G
Patterson, AP
Eggerman, TL
AF Baranova, Irina N.
Vishnyakova, Tatyana G.
Bocharov, Alexander V.
Leelahavanichkul, Asada
Kurlander, Roger
Chen, Zhigang
Souza, Ana C. P.
Yuen, Peter S. T.
Star, Robert A.
Csako, Gyorgy
Patterson, Amy P.
Eggerman, Thomas L.
TI Class B Scavenger Receptor Types I and II and CD36 Mediate Bacterial
Recognition and Proinflammatory Signaling Induced by Escherichia coli,
Lipopolysaccharide, and Cytosolic Chaperonin 60
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID HIGH-DENSITY-LIPOPROTEIN; ATHEROSCLEROTIC LESION DEVELOPMENT; HEAT-SHOCK
PROTEINS; SMOOTH-MUSCLE-CELLS; INNATE IMMUNE CELLS; ENDOTHELIAL-CELLS;
DENDRITIC CELLS; HUMAN MONOCYTES; GLUCOCORTICOID PRODUCTION;
INFLAMMATORY RESPONSES
AB Class B scavenger receptors (SR-B) are lipoprotein receptors that also mediate pathogen recognition, phagocytosis, and clearance as well as pathogen-induced signaling. In this study we report that three members of the SR-B family, namely, CLA-1, CLA-2, and CD36, mediate recognition of bacteria not only through interaction with cell wall LPS but also with cytosolic chaperonin 60. HeLa cells stably transfected with any of these SR-Bs demonstrated markedly (3- to 5-fold) increased binding and endocytosis of Escherichia coli, LPS, and chaperonin 60 (GroEL) as revealed by both FACS analysis and confocal microscopy imaging. Increased pathogen (E. coli, LPS, and GroEL) binding to SR-Bs was also associated with the dose-dependent stimulation of cytokine secretion in the order of CD36 > CLA-2 > CLA-1 in HEK293 cells. Pathogen-induced IL-6-secretion was reduced in macrophages from CD36- and SR-BI/II-null mice by 40-50 and 30-40%, respectively. Intravenous GroEL administration increased plasma IL-6 and CXCL1 levels in mice. The cytokine responses were 40-60% lower in CD36(-/-) relative to wild-type mice, whereas increased cytokine responses were found in SR-BI/II-/- mice. While investigating the discrepancy of in vitro versus in vivo data in SR-BI/II deficiency, SR-BI/II-/- mice were found to respond to GroEL administration without increases in either plasma corticosterone or aldosterone as normally seen in wild-type mice. SR-BI/II-/- mice with mineralocorticoid replacement demonstrated an similar to 40-50% reduction in CXCL1 and IL-6 responses. These results demonstrate that, by recognizing and mediating inflammatory signaling of both bacterial cell wall LPS and cytosolic GroEL, all three SR-B family members play important roles in innate immunity and host defense. The Journal of Immunology, 2012, 188: 1371-1380.
C1 [Eggerman, Thomas L.] NIDDKD, Div Diabet Endocrinol & Metab Dis, NIH, Bethesda, MD 20892 USA.
[Baranova, Irina N.; Vishnyakova, Tatyana G.; Bocharov, Alexander V.; Kurlander, Roger; Chen, Zhigang; Csako, Gyorgy; Patterson, Amy P.; Eggerman, Thomas L.] NIDDKD, Dept Lab Med, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Leelahavanichkul, Asada; Souza, Ana C. P.; Yuen, Peter S. T.; Star, Robert A.] NIDDKD, Renal Diagnost & Therapeut Unit, NIH, Bethesda, MD 20892 USA.
[Leelahavanichkul, Asada] Chulalongkorn Univ, Fac Med, Dept Microbiol, Bangkok 10330, Thailand.
[Patterson, Amy P.] NIH, Off Biotechnol Activ, Off Director, Bethesda, MD 20892 USA.
RP Eggerman, TL (reprint author), NIDDKD, Div Diabet Endocrinol & Metab Dis, NIH, 6707 Democracy Blvd,Room 697,MSC 5460, Bethesda, MD 20892 USA.
EM abocharov@cc.nih.gov; Eggermant@niddk.nih.gov
RI Yuen, Peter/B-1954-2008
OI Yuen, Peter/0000-0001-9557-3909
FU Clinical Center, National Institute of Diabetes and Digestive and Kidney
Diseases; National Institute of Allergy and Infectious Diseases,
National Institutes of Health
FX This work was supported by the Intramural Research Program of the
Clinical Center, National Institute of Diabetes and Digestive and Kidney
Diseases, and by the National Institute of Allergy and Infectious
Diseases, National Institutes of Health.
NR 70
TC 36
Z9 39
U1 0
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 2012
VL 188
IS 3
BP 1371
EP 1380
DI 10.4049/jimmunol.1100350
PG 10
WC Immunology
SC Immunology
GA 884FL
UT WOS:000299690200052
PM 22205027
ER
PT J
AU Crampton, SP
Deane, JA
Feigenbaum, L
Bolland, S
AF Crampton, Steve P.
Deane, Jonathan A.
Feigenbaum, Lionel
Bolland, Silvia
TI Ifih1 Gene Dose Effect Reveals MDA5-Mediated Chronic Type I IFN Gene
Signature, Viral Resistance, and Accelerated Autoimmunity
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; BLOOD MONONUCLEAR-CELLS; CHRONIC DISEASE;
IMMUNE-SYSTEM; INTERFERON; EXPRESSION; MICE; RESPONSES; RECEPTOR; ANEMIA
AB Type I IFNs (IFN-I) are normally produced during antiviral responses, yet high levels of chronic IFN-I expression correlate with autoimmune disease. A variety of viral sensors generate IFN-I in their response, but other than TLRs, it is not fully known which pathways are directly involved in the development of spontaneous immune pathologies. To further explore the link between IFN-I induced by viral pathways and autoimmunity, we generated a new transgenic mouse line containing multiple copies of Ifih1, a gene encoding the cytoplasmic dsRNA sensor MDA5 with proven linkage to diabetes and lupus. We show that MDA5 overexpression led to a chronic IFN-I state characterized by resistance to a lethal viral infection through rapid clearance of virus in the absence of a CD8(+) or Ab response. Spontaneous MDA5 activation was not sufficient to initiate autoimmune or inflammatory pathology by itself, even though every immune cell population had signs of IFN activation. When combined with the lupus-susceptible background of the Fc gamma R2B deficiency, MDA5 overexpression did accelerate the production of switched autoantibodies, the incidence of glomerulonephritis, and early lethality. Thus, MDA5 transgenic mice provide evidence that chronic elevated levels of IFN-I are not sufficient to initiate autoimmunity or inflammation although they might exacerbate an ongoing autoimmune pathology. The Journal of Immunology, 2012, 188: 1451-1459.
C1 [Crampton, Steve P.; Bolland, Silvia] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Deane, Jonathan A.] Novartis Res Fdn, Genom Inst, San Diego, CA 92121 USA.
[Feigenbaum, Lionel] NCI, NIH, Frederick, MD 21702 USA.
RP Bolland, S (reprint author), NIAID, Immunogenet Lab, NIH, Twinbrook 2,12441 Parklawn Dr,Room 217,MSC 8180, Rockville, MD 20852 USA.
EM sbolland@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health
FX This work was supported in part by the Intramural Research Program of
the National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 45
TC 35
Z9 36
U1 3
U2 6
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 2012
VL 188
IS 3
BP 1451
EP 1459
DI 10.4049/jimmunol.1102705
PG 9
WC Immunology
SC Immunology
GA 884FL
UT WOS:000299690200060
PM 22205024
ER
PT J
AU Calamusa, G
Valenti, RM
Vitale, F
Mammina, C
Romano, N
Goedert, JJ
Gori-Savellini, G
Cusi, MG
Amodio, E
AF Calamusa, Giuseppe
Valenti, Rosalia Maria
Vitale, Francesco
Mammina, Caterina
Romano, Nino
Goedert, James Jerome
Gori-Savellini, Gianni
Cusi, Maria Grazia
Amodio, Emanuele
TI Seroprevalence of and risk factors for Toscana and Sicilian virus
infection in a sample population of Sicily (Italy)
SO JOURNAL OF INFECTION
LA English
DT Article
DE Toscana virus; Sicilian virus; Re-emergence; Italy
ID ACUTE MENINGITIS; PHLEBOVIRUS; PREVALENCE
AB Objective: The present study aimed to assess seroprevalence of and risk factors for Toscana (TOSV) and Sicilian (SFSV) virus infections in a sample of Sicilian subjects.
Methods: A cross-sectional seroepidemiological study was conducted on 271 individuals. Each participant completed a self-administrated questionnaire and provided a serum sample which was analyzed for the presence of IgG specific anti-TOSV and anti-SFSV viruses.
Results: Overall, 90 subjects (33.2%) were positive for TOSV IgG, 25 (9.2%) were positive for SFSV IgG and 11 (4%) were positive for both the viruses. A higher risk for TOSV seropositivity was found in participants who were older (adjOR = 1.02 per year; 95% CI=1.01-1.03), having a pet living outdoors (adjOR = 2.62; 95% CI = 1.42-4.83) and being obese (adjOR = 2.37; 95% CI = 1.06-5.30).
Conclusions: TOSV seroprevalence appears to be relatively high in Sicilian general population, especially in older adults, representing a potential public health concern. The observations that seropositivity for TOSV was not significantly associated with SFSV seropositivity, and none of the risk factors associated with TOSV were associated with SFSV seem to suggest that these two phleboviruses may have different ecology and transmission pathways. (C) 2011 The British Infection Association. Published by Elsevier Ltd. All rights reserved.
C1 [Calamusa, Giuseppe; Valenti, Rosalia Maria; Vitale, Francesco; Mammina, Caterina; Romano, Nino; Amodio, Emanuele] Univ Palermo, Dept Sci Hlth Promot G DAlessandro, I-90127 Cap, Italy.
[Goedert, James Jerome] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Gori-Savellini, Gianni; Cusi, Maria Grazia] Univ Siena, Dept Mol Biol, Microbiol Sect, I-53100 Siena, Italy.
RP Amodio, E (reprint author), Univ Palermo, Dept Sci Hlth Promot G DAlessandro, Via Vespro 133, I-90127 Cap, Italy.
EM emanuele.amodio@unipa.it
RI Mammina, Caterina/M-9339-2013;
OI Gori Savellini, Gianni/0000-0003-2287-9258; Mammina,
Caterina/0000-0003-2881-8018
FU Intramural NIH HHS [ZIA CP010214-01]
NR 25
TC 5
Z9 5
U1 0
U2 1
PU W B SAUNDERS CO LTD
PI LONDON
PA 32 JAMESTOWN RD, LONDON NW1 7BY, ENGLAND
SN 0163-4453
J9 J INFECTION
JI J. Infect.
PD FEB
PY 2012
VL 64
IS 2
BP 212
EP 217
DI 10.1016/j.jinf.2011.11.012
PG 6
WC Infectious Diseases
SC Infectious Diseases
GA 879EP
UT WOS:000299312800011
PM 22120113
ER
PT J
AU Patel, GK
Yee, CL
Yuspa, SH
Vogel, JC
AF Patel, Girish K.
Yee, Carole L.
Yuspa, Stuart H.
Vogel, Jonathan C.
TI A Humanized Stromal Bed Is Required for Engraftment of Isolated Human
Primary Squamous Cell Carcinoma Cells in Immunocompromised Mice
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Article
ID NONMELANOMA SKIN-CANCER; SCID MICE; KAPPA-B; MOUSE; INFLAMMATION;
PROGRESSION; POPULATION; TISSUE; P53
AB Epithelial cancers are the most common malignancies and the greatest cause of cancer mortality worldwide. The incidence of keratinocyte-derived (non-melanoma) skin cancers is increasing rapidly. Despite access to abundant tumor tissue and ease of observation, acceptance of non-melanoma skin cancers as model carcinomas has been hindered by the lack of a reliable xenograft model. Herein we describe conditions that allow routine xeno-engraftment of primary human squamous cell carcinoma (SCCa) cells. Tumor development required creation of an appropriate stromal bed before xenografting tumor tissue onto the backs of athymic nude mice. We also demonstrate that the stromal bed must be "humanized" if primary human SCCa is to be propagated from cell suspensions. SCCa xenografts recapitulated the histological grade and phenotype of the original tumors with considerable fidelity, even after serial passage, irrespective of the histological grade of the primary human SCCa. This model, which to our knowledge is previously unreported, can be used for drug testing, as well as for studies that are relevant to the biology of primary human SCCa and other epithelial cancers.
C1 [Patel, Girish K.; Yee, Carole L.; Vogel, Jonathan C.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Yuspa, Stuart H.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Patel, GK (reprint author), Cardiff Univ, Sch Med, Dept Dermatol & Wound Healing, Heath Pk, Cardiff CF14 4XN, S Glam, Wales.
EM patelgk@cardiff.ac.uk
RI Patel, Girish/N-7075-2013
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX We thank all the members of the Dermatology Branch (National Cancer
Institute, NIH, Bethesda, Maryland), including Dr Mark Udey for many
helpful discussions and comments and, in particular, Vogel laboratory
members for their helpful comments. We thank Drs Andrew Montemarano
(Rockledge Skin Cancer Clinic, Bethesda, Maryland), Kurt Maggio (Walter
Reed Army Medical Center Dermatology Service, Washington, DC), and
Martin Braun (Braun & Braun MDs, Washington, DC) for providing tumor
tissue samples. It is with great sadness that we also inform you of the
recent and untimely death of Dr Jonathan C Vogel, the lead principal
investigator of this paper. This research was supported by the
Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research.
NR 30
TC 12
Z9 12
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD FEB
PY 2012
VL 132
IS 2
BP 284
EP 290
DI 10.1038/jid.2011.284
PG 7
WC Dermatology
SC Dermatology
GA 877XH
UT WOS:000299215500007
PM 21975825
ER
PT J
AU Patel, GK
Yee, CL
Terunuma, A
Telford, WG
Voong, N
Yuspa, SH
Vogel, JC
AF Patel, Girish K.
Yee, Carole L.
Terunuma, Atsushi
Telford, William G.
Voong, Nga
Yuspa, Stuart H.
Vogel, Jonathan C.
TI Identification and Characterization of Tumor-Initiating Cells in Human
Primary Cutaneous Squamous Cell Carcinoma
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Article
ID CANCER STEM-CELLS; SKIN-CANCER; INVOLUCRIN EXPRESSION; CD133;
PROGRESSION; POPULATION; MARKER; P53
AB Primary human squamous cell carcinomas (SCCas) are heterogeneous invasive tumors with proliferating outer layers and inner differentiating cell masses. To determine if tumor-initiating cells (TICs) are present in SCCas, we utilized newly developed reliable in vitro and in vivo xenograft assays that propagate human SCCas, and demonstrated that a small subset of SCCa cells (similar to 1%) expressing Prominin-1 (CD133) in the outer layers of SCCas were highly enriched for TICs (similar to 1/400) compared with unsorted SCCa cells (TICs similar to 1/10(6)). Xenografts of CD133+ SCCas recreated the original SCCa tumor histology and organizational hierarchy, whereas CD133- cells did not, and only CD133+ cells demonstrated the capacity for self-renewal in serial transplantation studies. We present a model of human SCCas in which tumor projections expand with outer leading edges that contain CD133+ TICs. Successful cancer treatment will likely require that the TICs identified in cancers be targeted therapeutically. The demonstration that TICs are present in SCCas and are enriched in a CD133- expressing subpopulation has not been, to our knowledge, previously reported.
C1 [Patel, Girish K.; Yee, Carole L.; Terunuma, Atsushi; Vogel, Jonathan C.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Telford, William G.; Voong, Nga] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Yuspa, Stuart H.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Patel, GK (reprint author), Cardiff Univ, Sch Med, Dept Dermatol & Wound Healing, Heath Pk, Cardiff CF14 4XN, S Glam, Wales.
EM patelgk@cardiff.ac.uk
RI Patel, Girish/N-7075-2013
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX We thank all members of the Dermatology Branch (National Cancer
Institute, NIH, Bethesda, Maryland), including Dr Mark Udey, for many
helpful discussions and comments, and in particular Vogel laboratory
members for their helpful comments. We thank Ms Rachelle Graham for
undertaking immunohistochemical characterization of SCCas. Also, we
thank Drs Andrew Montemarano (Rockledge Skin Cancer Clinic, Bethesda,
Maryland), Kurt Maggio (Walter Reed Army Medical Center Dermatology
Service, Washington, DC), and Martin Braun (Braun & Braun MDs,
Washington, DC) for providing tumor tissue samples. This research was
supported by the Intramural Research Program of the National Institutes
of Health, National Cancer Institute, Center for Cancer Research.
NR 26
TC 22
Z9 22
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD FEB
PY 2012
VL 132
IS 2
BP 401
EP 409
DI 10.1038/jid.2011.317
PG 9
WC Dermatology
SC Dermatology
GA 877XH
UT WOS:000299215500021
PM 22011906
ER
PT J
AU Law, MH
Montgomery, GW
Brown, KM
Martin, NG
Mann, GJ
Hayward, NK
MacGregor, S
AF Law, Matthew H.
Montgomery, Grant W.
Brown, Kevin M.
Martin, Nicholas G.
Mann, Graham J.
Hayward, Nicholas K.
MacGregor, Stuart
CA Q-MEGA & AMFS Investigators
TI Meta-Analysis Combining New and Existing Data Sets Confirms that the
TERT-CLPTM1L Locus Influences Melanoma Risk
SO JOURNAL OF INVESTIGATIVE DERMATOLOGY
LA English
DT Letter
ID GENOME-WIDE ASSOCIATION; TELOMERE LENGTH; CANCER-RISK; SUSCEPTIBILITY;
VARIANTS; SEQUENCE; DESIGN; CELLS; TERT; LINE
C1 [Law, Matthew H.; Montgomery, Grant W.; Martin, Nicholas G.; Hayward, Nicholas K.; MacGregor, Stuart] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Brown, Kevin M.] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Mann, Graham J.] Univ Sydney, Westmead Inst Canc Res, Millennium Inst, Westmead, NSW 2145, Australia.
[Mann, Graham J.] Melanoma Inst Australia, Westmead, NSW, Australia.
RP Law, MH (reprint author), Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
EM matthew.law@qimr.edu.au
RI Macgregor, Stuart/C-6442-2009; Stark, Mitchell/E-3542-2010; Mann,
Graham/G-4758-2014; hayward, nicholas/C-1367-2015; Montgomery,
Grant/B-7148-2008; Duffy, David/B-7392-2013
OI Gruis, Nelleke/0000-0002-5210-9150; Macgregor,
Stuart/0000-0001-6731-8142; Stark, Mitchell/0000-0002-4510-2161; Puig,
Susana/0000-0003-1337-9745; Martin, Nicholas/0000-0003-4069-8020; Mann,
Graham/0000-0003-1301-405X; hayward, nicholas/0000-0003-4760-1033;
Montgomery, Grant/0000-0002-4140-8139; Duffy, David/0000-0001-7227-632X
FU NCI NIH HHS [R01 CA122838-03, P01 CA055075, P01 CA055075-17, P01
CA087969, P01 CA087969-12, R01 CA049449, R01 CA049449-14, R01 CA083115,
R01 CA083115-10, R01 CA088363, R01 CA088363-10, R01 CA100264, R01
CA100264-05, R01 CA122838, R01 CA133996, R01 CA133996-03, U01 CA049449,
U19 CA148127]
NR 17
TC 26
Z9 26
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0022-202X
J9 J INVEST DERMATOL
JI J. Invest. Dermatol.
PD FEB
PY 2012
VL 132
IS 2
BP 485
EP 487
DI 10.1038/jid.2011.322
PG 4
WC Dermatology
SC Dermatology
GA 877XH
UT WOS:000299215500036
PM 21993562
ER
PT J
AU Mehta, GU
Lonser, RR
Oldfield, EH
AF Mehta, Gautam U.
Lonser, Russell R.
Oldfield, Edward H.
TI The history of pituitary surgery for Cushing disease
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE Cushing disease; Harvey Cushing; history; pituitary adenoma;
transsphenoidal surgery
ID TRANSSPHENOIDAL REMOVAL; BASOPHILISM; HYPOPHYSIS; HYPOTHALAMUS;
MICROADENOMA; ADENOMA; TUMORS; GLAND
AB Although he never performed a pituitary operation for the disease, Harvey Cushing was the first to describe and treat patients with Cushing disease (CD). Other surgeons at the time were reluctant to operate on the pituitary due to the normal sella on skull radiographs in CD and the unclear etiology of the disorder. To better define and understand factors influencing the history of pituitary surgery for CD, the authors analyzed historical texts related to CD biology, diagnosis, and treatment. Cushing's monograph on basophilic pituitary adenomas and cortisol excess appeared in 1932. One year later in 1933, Alfred Pattison performed the first successful pituitary operation for CD by implanting radon seeds in the sella. Resection of a pituitary adenoma for CD was attempted 1 month later in 1933 by Howard Naffziger, resulting in only transient improvement that corresponded to the lack of tumor in the resected tissue. Soon thereafter, Susman in 1935 and Costello in 1936 described pituitary basophilic adenomas at autopsy in patients without premorbid endocrinopathy. They concluded that the adrenal gland was the cause of CD, which resulted in a 3-decade abandonment of pituitary surgery for CD. Jules Hardy in 1963 used the operating microscope to perform the first selective removal of an adrenocorticotropic hormone (ACTH) secreting microadenoma, which established a pituitary cause and defined the modern treatment of CD. Subsequent reports by Hardy. Laws, and Wilson resulted in widespread acceptance of pituitary surgery for CD. Initial reluctance to operate on the pituitary for CD was multifaceted and included general uncertainty surrounding the etiology of Cushing syndrome as well as a lack of early surgical success, both due to the small size of ACTH-secreting adenomas. Selective removal of ACTH-secreting adenomas identified the source of CD and ended the delay in acceptance of pituitary surgery for CD. (DOI: 10.3171/2011.8.JNS102005)
C1 [Mehta, Gautam U.; Oldfield, Edward H.] Univ Virginia, Dept Neurosurg, Univ Virginia Hlth Syst, Charlottesville, VA 22901 USA.
[Mehta, Gautam U.; Lonser, Russell R.; Oldfield, Edward H.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Oldfield, EH (reprint author), Univ Virginia, Dept Neurosurg, Univ Virginia Hlth Syst, Charlottesville, VA 22901 USA.
EM eho4u@hscmail.mcc.virginia.edu
OI Mehta, Gautam/0000-0002-8009-6430
NR 43
TC 7
Z9 8
U1 0
U2 2
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD FEB
PY 2012
VL 116
IS 2
BP 261
EP 268
DI 10.3171/2011.8.JNS102005
PG 8
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 882SB
UT WOS:000299583100001
PM 21962161
ER
PT J
AU Lonser, RR
Oldfield, EH
AF Lonser, Russell R.
Oldfield, Edward H.
TI Invasion of the corticotrophs Response
SO JOURNAL OF NEUROSURGERY
LA English
DT Editorial Material
ID PITUITARY-ADENOMAS; DURAL INVASION; PSEUDOCAPSULE; SURGERY
C1 [Lonser, Russell R.; Oldfield, Edward H.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Oldfield, Edward H.] Univ Virginia Hlth Syst, Dept Neurol Surg, Charlottesville, VA USA.
RP Lonser, RR (reprint author), NINDS, Surg Neurol Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD FEB
PY 2012
VL 116
IS 2
BP 270
EP 271
PG 2
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 882SB
UT WOS:000299583100003
ER
PT J
AU Lonser, RR
Ksendzovsky, A
Wind, JJ
Vortmeyer, AO
Oldfield, EH
AF Lonser, Russell R.
Ksendzovsky, Alexander
Wind, Joshua J.
Vortmeyer, Alexander O.
Oldfield, Edward H.
TI Prospective evaluation of the characteristics and incidence of
adenoma-associated dural invasion in Cushing disease
SO JOURNAL OF NEUROSURGERY
LA English
DT Article
DE adenoma; cavernous sinus; Cushing disease; dura; invasion; pituitary
surgery
ID PITUITARY-ADENOMAS; SURGERY; TUMORS; CLASSIFICATION; PERSISTENT;
DIAGNOSIS; CHILDREN
AB Object. Dural invasion by adrenocorticotropic hormone (ACTH)-secreting adenomas is a significant risk factor for incomplete resection and recurrence in Cushing disease (CD). Since ACTH-producing adenomas are often the smallest of the various types of pituitary tumors at the time of resection, examining their invasion provides the best opportunity to identify the precise sites of early dural invasion by pituitary adenomas. To characterize the incidence and anatomical distribution of dural invasion by ACTH-secreting adenomas, the authors prospectively and systematically analyzed features of dural invasion in patients with CD.
Methods. The authors prospectively studied consecutive patients with CD undergoing the systematic removal of ACTH-secreting adenoma and histological analysis of the anterior sella dura as well as other sites of dural invasion that were evident at surgery. Clinical, imaging, histological, and operative findings were analyzed.
Results. Eighty-seven patients with CD (58 females and 29 males) were included in the study. Overall, dural invasion by an ACTH-positive adenoma was histologically confirmed in 30 patients (34%). Eighteen patients (60% of dural invasion cases, 21% of all patients) had evidence of cavernous sinus wall invasion (4 of these patients also had other contiguous sites of invasion), and 12 patients (40% of dural invasion cases) had invasion of the sella dura excluding the cavernous sinus wall. Eleven patients (13% all patients) had invasion of the routinely procured anterior sella dura specimen. Preoperative MR imaging revealed an adenoma in 64 patients (74%) but accurately predicted dural invasion in only 4 patients (22%) with cavernous sinus invasion and none of the patients with non cavernous sinus invasion. Adenomas associated with dural invasion (mean SD, 10.9 +/- 7.8 mm, range 2-37 mm) were significantly larger than those not associated with dural invasion (5.7 +/- 2.1 mm, range 2.5-12 mm; p = 0.0006, Mann-Whitney test).
Conclusions. Dural invasion by ACTH-producing adenomas preferentially occurs laterally into the wall of the cavernous sinus. Preoperative MR imaging infrequently detects dural invasion, including cavernous sinus invasion. Invasion is directly associated with tumor size. To provide a biochemical cure and avoid recurrence after resection, identification and removal of invaded sella dura, including the medial cavernous sinus wall, are necessary. (DOI: 10.3171/2011.8.JNS11456)
C1 [Lonser, Russell R.; Ksendzovsky, Alexander; Wind, Joshua J.; Vortmeyer, Alexander O.; Oldfield, Edward H.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Oldfield, Edward H.] Univ Virginia, Dept Neurol Surg, Univ Virginia Hlth Syst, Charlottesville, VA USA.
RP Lonser, RR (reprint author), NINDS, Surg Neurol Branch, NIH, Bldg 10,Rm 3D20, Bethesda, MD 20892 USA.
EM lonserr@ninds.nih.gov
RI Wind, Joshua/D-5480-2013
OI Wind, Joshua/0000-0003-3443-8476
FU National Institute of Neurologic Disorders and Stroke at the National
Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Neurologic Disorders and Stroke at the National
Institutes of Health.
NR 23
TC 14
Z9 16
U1 0
U2 1
PU AMER ASSOC NEUROLOGICAL SURGEONS
PI ROLLING MEADOWS
PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA
SN 0022-3085
J9 J NEUROSURG
JI J. Neurosurg.
PD FEB
PY 2012
VL 116
IS 2
BP 272
EP 279
DI 10.3171/2011.8.JNS11456
PG 8
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 882SB
UT WOS:000299583100004
PM 21923247
ER
PT J
AU Cao, XL
Yang, CL
Pei, HR
Li, XH
Xu, XB
Ito, Y
AF Cao, Xueli
Yang, Chunlei
Pei, Hairun
Li, Xinghong
Xu, Xiaobai
Ito, Yoichiro
TI Application of counter-current chromatography as a new pretreatment
method for the determination of polycyclic aromatic hydrocarbons in
environmental water
SO JOURNAL OF SEPARATION SCIENCE
LA English
DT Article
DE Counter-current chromatography (CCC); Enrichment and cleanup;
Environmental water; Polycyclic aromatic hydrocarbons (PAHs);
Pretreatment
ID LIQUID-LIQUID-EXTRACTION; SOLID-PHASE EXTRACTION; SAMPLES; PESTICIDES;
SEPARATION
AB Counter-current chromatography (CCC) was investigated as a new sample pretreatment method for the determination of trace polycyclic aromatic hydrocarbons (PAHs) in water environmental samples. The experiment was performed with a non-aqueous binary two-phase solvent system composed of n-heptane and acetonitrile. The CCC column was first filled with the upper stationary phase, and then a large volume of water sample was pumped into the column while the CCC column was rotated at 1600?rpm. Finally, the trace amounts of PAHs extracted and enriched in the stationary phase were eluted out by the lower mobile phase and determined by gas chromatographyflame ionization detector (GC-FID) or gas chromatographymass spectrometry (GC-MS). The enrichment and cleanup of PAHs can be fulfilled online by this method with high recoveries (84.1103.2%) and good reproducibility (RSDs: 4.912.2%) for 16 EPA PAHs under the optimized CCC pretreatment conditions. This method has been successfully applied to determine PAHs in lake water where 8 PAHs were detected in the concentration of 40.989.9?ng/L. The present method is extremely suitable for the preparation of large volume of environmental water sample for the determination of trace amounts of organic pollutants including PAHs as studied in this paper.
C1 [Cao, Xueli; Yang, Chunlei; Pei, Hairun] Beijing Technol & Business Univ, Sch Food & Chimer Engn, Beijing 100048, Peoples R China.
[Li, Xinghong; Xu, Xiaobai] Chinese Acad Sci, Ecoenvironm Sci Res Ctr, State Key Lab Environm Chem & Ecotoxicol, Beijing, Peoples R China.
[Ito, Yoichiro] NHLBI, Bioseparat Technol Lab, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Cao, XL (reprint author), Beijing Technol & Business Univ, Sch Food & Chimer Engn, 33 Fucheng Rd, Beijing 100048, Peoples R China.
EM caoxl@th.btbu.edu.cn
RI Li, Hong/M-3851-2013
FU National Natural Science Foundation of China [20877005]; National High
Technology Research and Development Program ("863" Program)
[2007AA061601]
FX The authors acknowledge the financial support of this work by the
National Natural Science Foundation of China (No. 20877005) the National
High Technology Research and Development Program ("863" Program No.
2007AA061601).
NR 17
TC 3
Z9 4
U1 1
U2 32
PU WILEY PERIODICALS, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN STREET, MALDEN, MA 02148-529 USA
SN 1615-9306
J9 J SEP SCI
JI J. Sep. Sci.
PD FEB
PY 2012
VL 35
IS 4
BP 596
EP 601
DI 10.1002/jssc.201100852
PG 6
WC Chemistry, Analytical
SC Chemistry
GA 882FL
UT WOS:000299548100016
PM 22282420
ER
PT J
AU Fox, NA
Pine, DS
AF Fox, Nathan A.
Pine, Daniel S.
TI Temperament and the Emergence of Anxiety Disorders
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID BEHAVIORAL-INHIBITION; FRAMEWORK
C1 [Fox, Nathan A.] Univ Maryland, College Pk, MD 20742 USA.
[Pine, Daniel S.] NIMH, Bethesda, MD 20892 USA.
RP Fox, NA (reprint author), Univ Maryland, 3304 Benjamin, College Pk, MD 20742 USA.
EM fox@umd.edu
FU NICHD NIH HHS [R01 HD017899, R37 HD017899, R37HD17899]; NIMH NIH HHS
[U01MH093349, R01 MH074454, U01 MH074454, U01 MH093349]
NR 12
TC 23
Z9 23
U1 0
U2 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD FEB
PY 2012
VL 51
IS 2
BP 125
EP 128
DI 10.1016/j.jaac.2011.10.006
PG 4
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 882YD
UT WOS:000299598900001
PM 22265356
ER
PT J
AU Scahill, L
McDougle, CJ
Aman, MG
Johnson, C
Handen, B
Bearss, K
Dziura, J
Butter, E
Swiezy, NG
Arnold, LE
Stigler, KA
Sukhodolsky, DD
Lecavalier, L
Pozdol, SL
Nikolov, R
Hollway, JA
Korzekwa, P
Gavaletz, A
Kohn, AE
Koenig, K
Grinnon, S
Mulick, JA
Yu, S
Vitiello, B
AF Scahill, Lawrence
McDougle, Christopher J.
Aman, Michael G.
Johnson, Cynthia
Handen, Benjamin
Bearss, Karen
Dziura, James
Butter, Eric
Swiezy, Naomi G.
Arnold, L. Eugene
Stigler, Kimberly A.
Sukhodolsky, Denis D.
Lecavalier, Luc
Pozdol, Stacie L.
Nikolov, Roumen
Hollway, Jill A.
Korzekwa, Patricia
Gavaletz, Allison
Kohn, Arlene E.
Koenig, Kathleen
Grinnon, Stacie
Mulick, James A.
Yu, Sunkyung
Vitiello, Benedetto
CA Pediat Psychopharmacology Autism
TI Effects of Risperidone and Parent Training on Adaptive Functioning in
Children With Pervasive Developmental Disorders and Serious Behavioral
Problems
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE risperidone; parent training; pervasive developmental disorders;
children; adaptive behavior
ID AUTISM-SPECTRUM DISORDERS; PSYCHOSOCIAL INTERVENTIONS; YOUNG-PEOPLE;
MEDICATION; INDIVIDUALS; PREVALENCE; COMMUNITY; CHECKLIST; VERSION;
TRIAL
AB Objective: Children with Pervasive Developmental Disorders (PDDs) have social interaction deficits, delayed communication, and repetitive behaviors as well as impairments in adaptive functioning. Many children actually show a decline in adaptive skills compared with age mates over time. Method: This 24-week, three-site, controlled clinical trial randomized 124 children (4 through 13 years of age) with PDDs and serious behavioral problems to medication alone (MED; n = 49; risperidone 0.5 to 3.5 mg/day; if ineffective, switch to aripiprazole was permitted) or a combination of medication plus parent training (PT) (COMB; n = 75). Parents of children in COMB received an average of 11.4 PT sessions. Standard scores and Age-Equivalent scores on Vineland Adaptive Behavior Scales were the outcome measures of primary interest. Results: Seventeen subjects did not have a post-randomization Vineland assessment. Thus, we used a mixed model with outcome conditioned on the baseline Vineland scores. Both groups showed improvement over the 24-week trial on all Vineland domains. Compared with MED. Vineland Socialization and Adaptive Composite Standard scores showed greater improvement in the COMB group (p = .01 and .05, and effect sizes = 0.35 and 0.22, respectively). On Age Equivalent scores, Socialization and Communication domains showed greater improvement in COMB versus MED (p = .03 and 0.05, and effect sizes = 0.33 and 0.14, respectively). Using logistic regression, children in the COMB group were twice as likely to make at least 6 months' gain (equal to the passage of time) in the Vineland Communication Age Equivalent score compared with MED (p = .02). After controlling for IQ this difference was no longer significant. Conclusion: Reduction of serious maladaptive behavior promotes improvement in adaptive behavior. Medication plus PT shows modest additional benefit over medication alone. Clinical trial registration information-RUPP PI PDD: Drug and Behavioral Therapy for Children With Pervasive Developmental Disorders; http://www.clinicaltrials.gov; NCT00080145. J. Am. Acad. Child Adolesc. Psychiatry, 2012;51(2):136-146.
C1 [Scahill, Lawrence] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
[McDougle, Christopher J.; Swiezy, Naomi G.; Stigler, Kimberly A.; Pozdol, Stacie L.; Korzekwa, Patricia; Kohn, Arlene E.] Indiana Univ, Bloomington, IN 47405 USA.
[Aman, Michael G.; Butter, Eric; Arnold, L. Eugene; Lecavalier, Luc; Hollway, Jill A.; Mulick, James A.] Ohio State Univ, Columbus, OH 43210 USA.
[Johnson, Cynthia; Handen, Benjamin] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Vitiello, Benedetto] NIMH, Bethesda, MD 20892 USA.
RP Scahill, L (reprint author), Yale Univ, Ctr Child Study, POB 207900, New Haven, CT 06520 USA.
EM Lawrence.scahill@yale.edu
OI Sukhodolsky, Denis/0000-0002-5401-792X; Scahill,
Lawrence/0000-0001-5073-1707
FU National Institute of Mental Health (NIMH) by Research Units on
Pediatric Psychopharmacology (RUPP) [U10MH66764, U10MH66766,
U10MH66768]; Yale Clinical and Translational Science Award (CTSA) [UL1
RR024139]; Indiana University CTSA [UL1 RR025761]; Ohio State University
CTSA from the National Center for Research Resources (NCRR) [UL1
RR025755]; NIMH; Shire; Seaside; Bristol-Myers Squibb; Johnson and
Johnson; Eli Lilly and Co.; Autism Speaks; Neuropharm; Targacept;
Janssen; Pediamed
FX This work was funded by the National Institute of Mental Health (NIMH)
by the following Research Units on Pediatric Psychopharmacology (RUPP)
grants: U10MH66764 (Yale); U10MH66766 (Indiana University); U10MH66768
(Ohio State University). NIMH staff participated in the design and
implementation, analysis of data, and authorship of the manuscript.
Johnson and Johnson Pharmaceutical Research and Development provided
active risperidone for the study, but had no role in the design and
implementation, analysis of the data, or authorship of the manuscript.
This publication was also supported by the Yale Clinical and
Translational Science Award (CTSA) UL1 RR024139, Indiana University CTSA
UL1 RR025761, and Ohio State University CTSA UL1 RR025755 from the
National Center for Research Resources (NCRR). Drs. Scahill, McDougle,
Amon, Johnson, Handen, Bearss, Dziura, Butter, Swiezy, Arnold, Stigler,
Sukhodolsky, Lecavalier, Mulick, Pozdol, Nikolov, Korzekwa, and
Vitiello, and Ms. Ritz, Ms. Holloway, Ms. Gavaletz, Ms. Kohn, Ms,
Koenig, Ms. Grinnon, and Ms. Yu received salary support from NIMH in
support of the study.; Dr. Scahill serves as a consultant for BioMarin,
BoehringerIngelheim, Hoffman, NeuroSearch, and Pfizer. He has received
research support from Shire and Seaside. Dr. Aman has sewed as a
consultant to Bristol-Myers Squibb, BioMarin, Forest, Hoffman, Pfizer,
and Supernus. He has received research support from Bristol-Myers Squibb
and Johnson and Johnson. Dr. Arnold has served as a consultant to
Abbott, BioMarin, Novartis, Naves, Organon, Shire, and Targacept. He has
received research support from Eli Lilly and Co., Autism Speaks,
Neuropharm, the National Institute of Mental Health (NIMH), Shire, and
Targacept. Dr. McDougle has served as a consultant to Bristol-Myers
Squibb and Forest. He has received research support from and served on
the speakers' bureau for Bristol-Myers Squibb. Dr. Stigler has received
research support from Bristol-Myers Squibb, Eli Lilly and Co., and
Janssen. Dr. Handen has received research support from Bristol-Myers
Squibb, Neuropharm, and Pediamed. He has served as a consultant to
Forest and Eisai. Drs. Beams, Sukhodolsky, Nikolov, Dziura, Butter,
Lecavalier, Mulick, Swiezy, Johnson, and Vitiello, and Ms. Koenig, Ms.
Gavaletz, Ms. Yu, Ms. Holloway, Ms. Kohn, Ms. Pozdol, Ms. Korzekwa, and
Ms. Grinnon report no biomedical financial interests or potential
conflicts of interest.
NR 32
TC 25
Z9 26
U1 2
U2 14
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD FEB
PY 2012
VL 51
IS 2
BP 136
EP 146
DI 10.1016/j.jaac.2011.11.010
PG 11
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 882YD
UT WOS:000299598900005
PM 22265360
ER
PT J
AU Le Couteur, DG
McLachlan, AJ
de Cabo, R
AF Le Couteur, David G.
McLachlan, Andrew J.
de Cabo, Rafael
TI Aging, Drugs, and Drug Metabolism
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Editorial Material
ID CLINICAL-PHARMACOLOGY; LIFE-SPAN; LIVER; MICE
C1 [Le Couteur, David G.; McLachlan, Andrew J.] Univ Sydney, Ctr Educ & Res Ageing, Concord Hosp, Concord, NSW 2139, Australia.
[Le Couteur, David G.] Univ Sydney, ANZAC Res Inst, Concord Hosp, Concord, NSW 2139, Australia.
[McLachlan, Andrew J.] Univ Sydney, Fac Pharm, Concord, NSW 2139, Australia.
[de Cabo, Rafael] NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
RP Le Couteur, DG (reprint author), Univ Sydney, Ctr Educ & Res Ageing, Concord RG Hosp, Hosp Rd, Concord, NSW 2139, Australia.
EM david.lecouteur@sydney.edu.au
RI de Cabo, Rafael/J-5230-2016;
OI de Cabo, Rafael/0000-0002-3354-2442; , rafael/0000-0003-2830-5693;
McLachlan, Andrew/0000-0003-4674-0242
NR 16
TC 4
Z9 4
U1 1
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD FEB
PY 2012
VL 67
IS 2
BP 137
EP 139
DI 10.1093/gerona/glr084
PG 3
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 885RT
UT WOS:000299799200004
PM 21768500
ER
PT J
AU Le Couteur, DG
McLachlan, AJ
Quinn, RJ
Simpson, SJ
de Cabo, R
AF Le Couteur, David G.
McLachlan, Andrew J.
Quinn, Ronald J.
Simpson, Stephen J.
de Cabo, Rafael
TI Aging Biology and Novel Targets for Drug Discovery
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
ID GENETICALLY HETEROGENEOUS MICE; CALORIE RESTRICTION MIMETICS;
SMALL-MOLECULE ACTIVATORS; EXTENDING LIFE-SPAN; GROWTH-HORMONE;
OXIDATIVE STRESS; SACCHAROMYCES-CEREVISIAE; CLINICAL-PHARMACOLOGY;
DIETARY RESTRICTION; RETARDED GROWTH
AB Despite remarkable technological advances in genetics and drug screening, the discovery of new pharmacotherapies has slowed and new approaches to drug development are needed. Research into the biology of aging is generating many novel targets for drug development that may delay all age-related diseases and be used long term by the entire population. Drugs that successfully delay the aging process will clearly become "blockbusters." To date, the most promising leads have come from studies of the cellular pathways mediating the longevity effects of caloric restriction (CR), particularly target of rapamycin and the sirtuins. Similar research into pathways governing other hormetic responses that influence aging is likely to yield even more targets. As aging becomes a more attractive target for drug development, there will be increasing demand to develop biomarkers of aging as surrogate outcomes for the testing of the effects of new agents on the aging process.
C1 [Le Couteur, David G.; McLachlan, Andrew J.] Univ Sydney, Ctr Educ & Res Ageing, Concord Hosp, Sydney, NSW 2006, Australia.
[Le Couteur, David G.] Univ Sydney, ANZAC Res Inst, Concord Hosp, Sydney, NSW 2006, Australia.
[McLachlan, Andrew J.] Univ Sydney, Fac Pharm, Sydney, NSW 2006, Australia.
[Quinn, Ronald J.] Griffith Univ, Eskitis Inst, Brisbane, Qld 4111, Australia.
[Simpson, Stephen J.] Univ Sydney, Sch Biol Sci, Sydney, NSW 2006, Australia.
[de Cabo, Rafael] NIA, Lab Expt Gerontol, Baltimore, MD 21224 USA.
RP Le Couteur, DG (reprint author), Concord RG Hosp, Ctr Educ & Res Ageing, Hosp Rd, Concord, NSW 2139, Australia.
EM dlecouteur@med.usyd.edu.au
RI Quinn, Ronald/A-7931-2008; de Cabo, Rafael/J-5230-2016;
OI Quinn, Ronald/0000-0002-4022-2623; de Cabo, Rafael/0000-0002-3354-2442;
Simpson, Stephen J./0000-0003-0256-7687; , rafael/0000-0003-2830-5693;
McLachlan, Andrew/0000-0003-4674-0242
FU Australian National Health and Medical Research Council [570937,
571328]; Medical Foundation of the University of Sydney; Ageing and
Alzheimer's Research Foundation
FX This study was funded by the Australian National Health and Medical
Research Council (grant 570937, 571328), the Medical Foundation of the
University of Sydney, and the Ageing and Alzheimer's Research
Foundation.
NR 96
TC 24
Z9 24
U1 0
U2 14
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD FEB
PY 2012
VL 67
IS 2
BP 168
EP 174
DI 10.1093/gerona/glr095
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 885RT
UT WOS:000299799200008
PM 21693687
ER
PT J
AU Katzman, W
Cawthon, P
Hicks, GE
Vittinghoff, E
Shepherd, J
Cauley, JA
Harris, T
Simonsick, EM
Strotmeyer, E
Womack, C
Kado, DM
AF Katzman, Wendy
Cawthon, Peggy
Hicks, Gregory E.
Vittinghoff, Eric
Shepherd, John
Cauley, Jane A.
Harris, Tamara
Simonsick, Eleanor M.
Strotmeyer, Elsa
Womack, Catherine
Kado, Deborah M.
TI Association of Spinal Muscle Composition and Prevalence of Hyperkyphosis
in Healthy Community-Dwelling Older Men and Women
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Kyphosis; Hyperkyphosis; Prevalence; Spinal muscle; Fat infiltration
ID FLEXION-RELAXATION PHENOMENON; LOWER-EXTREMITY PERFORMANCE;
BODY-COMPOSITION; RANCHO-BERNARDO; OSTEOPOROTIC FRACTURES; VERTEBRAL
FRACTURES; PHYSICAL FUNCTION; FLEXED POSTURE; BACK-PAIN; SKELETAL-MUSCLE
AB Background. Older adults with hyperkyphosis are at increased risk of falls, fractures, and functional decline. Modifiable risk factors for hyperkyphosis have not been well studied. Our objective was to determine whether spinal muscle area and density are associated with hyperkyphosis, independent of age, race, sex, bone mineral density, and trunk fat.
Methods. Using data from the Pittsburgh site of the Health, Aging, and Body Composition study, we performed a baseline cross-sectional analysis. Participants were black and white men and women 70-79 years old (N = 1172), independent in activities of daily living and able to walk 1/4 mile and up 10 steps without resting. We measured Cobb's angle of kyphosis from supine lateral scout computed tomography scans, and categorized hyperkyphosis as Cobb's angle >40 degrees. Axial images from lateral scout computed tomography scans assessed spinal extensor muscle cross-sectional area and density (proxy for fat infiltration).
Results. In our sample, 21% had hyperkyphosis. Prevalence in black men was 11%; in white men, 17%; in black women, 26%; and in white women, 30%. In multivariate analysis, each standard deviation increase in muscle density was associated with a 29% reduction in the odds of hyperkyphosis, independent of covariates. Muscle area was not significantly associated with hyperkyphosis.
Conclusions. Lower spinal muscle density is associated with hyperkyphosis in healthy community-dwelling older adults. This potentially modifiable risk factor could be targeted in exercise interventions. Randomized trials are needed to determine whether an exercise program targeting spinal muscle density reduces hyperkyphosis and in turn improves health outcomes.
C1 [Katzman, Wendy] Univ Calif San Francisco, Dept Phys Therapy & Rehabil Sci, San Francisco, CA 94143 USA.
[Cawthon, Peggy] Calif Pacific Med Ctr, Res Inst, San Francisco, CA USA.
[Hicks, Gregory E.] Univ Delaware, Dept Phys Therapy, Newark, DE 19716 USA.
[Vittinghoff, Eric] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Shepherd, John] Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94143 USA.
[Cauley, Jane A.; Strotmeyer, Elsa] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
[Harris, Tamara] NIA, Intramural Res Program, Bethesda, MD 20892 USA.
[Simonsick, Eleanor M.] NIA, Dept Epidemiol, Clin Res Branch, Baltimore, MD 21224 USA.
[Womack, Catherine] Univ Tennessee, Ctr Hlth Sci, Memphis, TN 38163 USA.
[Kado, Deborah M.] Univ Calif Los Angeles, Dept Orthopaed Surg, Los Angeles, CA 90024 USA.
[Kado, Deborah M.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
RP Katzman, W (reprint author), Univ Calif San Francisco, Dept Phys Therapy & Rehabil Sci, 1500 Owens,Suite 400, San Francisco, CA 94143 USA.
EM wendy.katzman@ucsfmedctr.org
RI Strotmeyer, Elsa/F-3015-2014;
OI Strotmeyer, Elsa/0000-0002-4093-6036; Cauley, Jane A/0000-0003-0752-4408
FU UCSF; National Institute of Child Health and Human Development; Office
of Research on Women's Health [5 K12 HD052163]; National Institutes of
Health (NIH) [2R56AG024246]; National Institute on Aging (NIA)
[N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106, R01-AG028050]; NINR
[R01-NR012459]; NIH, NIA
FX This research was supported in part by the UCSF-Kaiser Building
Interdisciplinary Research Careers in Women's Health and cofunded by the
National Institute of Child Health and Human Development and the Office
of Research on Women's Health 5 K12 HD052163; National Institutes of
Health (NIH) Director's Bridge Award 2R56AG024246; National Institute on
Aging (NIA) Contracts N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106,
NIA grant R01-AG028050, and NINR grant R01-NR012459; Intramural Research
Program of the NIH, NIA, and the UCSF Mount Zion Health Fund.
NR 38
TC 21
Z9 22
U1 2
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD FEB
PY 2012
VL 67
IS 2
BP 191
EP 195
DI 10.1093/gerona/glr160
PG 5
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA 885RT
UT WOS:000299799200011
PM 21878482
ER
PT J
AU Pei, Y
Lan, Z
Wang, KR
Garcia-Gonzalez, M
He, N
Dicks, E
Parfrey, P
Germino, G
Watnick, T
AF Pei, York
Lan, Zheng
Wang, Kairong
Garcia-Gonzalez, Miguel
He, Ning
Dicks, Elizabeth
Parfrey, Patrick
Germino, Gregory
Watnick, Terry
TI A missense mutation in PKD1 attenuates the severity of renal disease
SO KIDNEY INTERNATIONAL
LA English
DT Article
DE ADPKD; functional assay; hypomorphic allele; missense variant; mutation
analysis
ID POLYCYSTIC KIDNEY-DISEASE; MOLECULAR DIAGNOSTICS; GENE; EXPRESSION;
ALLELES; PATHOGENESIS; ADPKD
AB Mutations of PKD1 and PKD2 account for most cases of autosomal dominant polycystic kidney disease (ADPKD). Compared with PKD2, patients with PKD1 typically have more severe renal disease. Here, we report a follow-up study of a unique multigeneration family with bilineal ADPKD (NFL10) in which a PKD1 disease haplotype and a PKD2 (L736X) mutation co-segregated with 18 and 14 affected individuals, respectively. In our updated genotype-phenotype analysis of the family, we found that PKD1-affected individuals had uniformly mild renal disease similar to the PKD2-affected individuals. By sequencing all the exons and splice junctions of PKD1, we identified two missense mutations (Y528C and R1942H) from a PKD1-affected individual. Although both variants were predicted to be damaging to the mutant protein, only Y528C co-segregated with all of the PKD1-affected individuals in NFL10. Studies in MDCK cells stably expressing wild-type and mutant forms of PKD found that cell lines expressing the Y528C variant formed cysts in culture and displayed increased rates of growth and apoptosis. Thus, Y528C functions as a hypomorphic PKD1 allele. These findings have important implications for pathogenic mechanisms and molecular diagnostics of ADPKD. Kidney International (2012) 81, 412-417; doi:10.1038/ki.2011.370; published online 26 October 2011
C1 [Pei, York; Wang, Kairong; He, Ning] Univ Toronto, Div Nephrol, Toronto, ON, Canada.
[Lan, Zheng; Garcia-Gonzalez, Miguel; Germino, Gregory; Watnick, Terry] Johns Hopkins Sch Med, Div Nephrol, Baltimore, MD 21205 USA.
[Garcia-Gonzalez, Miguel] Complexo Hosp Univ Santiago, Lab Invest Nefrol, Santiago De Compostela, Spain.
[Dicks, Elizabeth; Parfrey, Patrick] Mem Univ Newfoundland, Div Nephrol, St John, NF, Canada.
[Germino, Gregory] NIDDK, NIH, Bethesda, MD USA.
RP Pei, Y (reprint author), Univ Hlth Network, Div Nephrol, 8N838,585 Univ Ave, Toronto, ON M5G 2N2, Canada.
EM york.pei@uhn.on.ca; twatnick@jhmi.edu
RI Garcia-Gonzalez, Miguel/G-6920-2011;
OI Germino, Gregory/0000-0002-3609-5588
FU Canadian Institutes of Health Research (CIHR) [MOP77806]; National
Institutes of Health [RO1DK0617, RO1GM73704]; NIDDK [P30 DK090868];
[DK48006]
FX We are indebted to all the participating members of the NFL10 family.
This work was supported by grants from the Canadian Institutes of Health
Research (CIHR; MOP77806) to YP, from the National Institutes of Health
(RO1DK0617 and RO1GM73704) to TW and (DK48006 and NIDDK Intramural
Research Program) to GG, and by the CIHR Distinguished Scientist Award
to PP. These studies utilized Resources provided by the NIDDK-sponsored
Johns Hopkins PKD Research and Clinical Core Center (P30 DK090868).
NR 28
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U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0085-2538
J9 KIDNEY INT
JI Kidney Int.
PD FEB
PY 2012
VL 81
IS 4
BP 412
EP 417
DI 10.1038/ki.2011.370
PG 6
WC Urology & Nephrology
SC Urology & Nephrology
GA 886JJ
UT WOS:000299850400012
PM 22031115
ER
PT J
AU Masood, MA
Rao, RP
Acharya, JK
Blonder, J
Veenstra, TD
AF Masood, M. Athar
Rao, Raghavendra P.
Acharya, Jairaj K.
Blonder, Josip
Veenstra, Timothy D.
TI Quantitation of Multiple Sphingolipid Classes Using Normal and
Reversed-Phase LC-ESI-MS/MS: Comparative Profiling of Two Cell Lines
SO LIPIDS
LA English
DT Article
DE Ceramides; Hexosylceramides; Sphingomyelins; Normal-phase and
reversed-phase LC-MS/MS; Quantitation; Mouse embryonic fibroblast; Human
embryonic kidney cells
ID TANDEM MASS-SPECTROMETRY; CORONARY-HEART-DISEASE; FATTY-ACIDS;
SPHINGOSINE 1-PHOSPHATE; BIOLOGICAL SAMPLES; LIFE-SPAN; LIPIDOMICS;
CANCER; RISK; DEGENERATION
AB Sphingolipids are an important class of compounds that regulate signal transduction and other vital cellular processes. Herein, we report sensitive normal and reversed phase LC-MS/MS methods for quantitation of multiple sphingolipid classes. In the normal-phase ESI/MS/MS method, a high content of organic solvents was utilized, which, although it included hexane, ethyl acetate, acetonitrile containing 2% methanol, 1-2% acetic acid, and 5 mM ammonium acetate, resulted in a very efficient electrospray ionization of the ceramides (Cers) and hexosylceramides (MHCers). Three normal-phase LC-MS/MS methods using segmented phases were developed to specifically target Cers, MHCers, or sphingomyelins (SMs). This segmentation scheme increases the number of data points acquired for a given analyte and enhances the sensitivity and specificity of the measurements. Nine separate reversed phase chromatography methods were developed for the three classes of compounds. These assays were used for comparing the levels of Cers, SMs, and MHCers from mouse embryonic fibroblast (pMEF) and human embryonic kidney (HEK293) cells. These findings were then compared with the reported data from RAW264.7 mouse macrophage cells, BHK21 hamster cells, and human plasma and serum samples. The analysis of cell lines, using both normal and reversed phase chromatography, revealed discrimination based on the type of chromatography chosen, while sphingolipid assays of samples containing different amounts of protein showed different results, even after normalizing for protein content. Also, LC/MS/MS profiles were provided for the classes and individual compounds so that they could be used as "molecular profiles" for class or individual sample analysis.
C1 [Masood, M. Athar; Blonder, Josip; Veenstra, Timothy D.] SAIC Frederick Inc, Lab Prote & Analyt Technol, NCI, Frederick, MD 21702 USA.
[Rao, Raghavendra P.; Acharya, Jairaj K.] NCI, Lab Cell & Dev Signaling, Frederick, MD 21702 USA.
RP Masood, MA (reprint author), SAIC Frederick Inc, Lab Prote & Analyt Technol, NCI, Frederick, MD 21702 USA.
EM masoodaa@mail.nih.gov
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute, National Institutes of Health, under
contract HHSN261200800001E. The content of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial
products, or organizations imply endorsement by the US Government.
NR 48
TC 5
Z9 5
U1 0
U2 41
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0024-4201
J9 LIPIDS
JI Lipids
PD FEB
PY 2012
VL 47
IS 2
BP 209
EP 226
DI 10.1007/s11745-011-3633-2
PG 18
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA 882AI
UT WOS:000299533100010
PM 22124806
ER
PT J
AU Bandettini, PA
Bowtell, R
Jezzard, P
Turner, R
AF Bandettini, Peter A.
Bowtell, Richard
Jezzard, Peter
Turner, Robert
TI Ultrahigh field systems and applications at 7 T and beyond: Progress,
pitfalls, and potential
SO MAGNETIC RESONANCE IN MEDICINE
LA English
DT Article
DE high field; fMRI; MRI; DTI; susceptibility
ID BRAIN-TISSUE; MRI; ORIENTATION; SUSCEPTIBILITY; SENSITIVITY; FREQUENCY;
MULTIPLE; IMAGE; MAP
AB About 150 researchers around the world convened at the Chateau Lake Louise on February 2023, 2011 to present and discuss the latest research in human and animal imaging and spectroscopy at field strengths of 7 T or above (termed ultrahigh field) at the third ISMRM-sponsored high field workshop. The clear overall message from the workshop presentations and discussion is that ultrahigh field imaging is gaining momentum with regard to new clinically relevant findings, anatomic and functional MRI results, susceptibility contrast advancements, solutions to high field-related image quality challenges, and to generally push the limits of resolution and speed of high field imaging. This meeting report is organized in a manner reflecting the meeting organization itself, covering the seven sessions that were approximately titled: (1) high field overview from head to body to spectroscopy; (2) susceptibility imaging; (3) proffered session on susceptibility, ultrafast imaging, unique contrast at 7 T, and angiography; (4) neuroscience applications; (5) proffered session on coils, shimming, parallel imaging, diffusion tensor imaging, and MRI-PET fusion; (6) high field animal imaging and spectroscopy, as well as a vendor overview, and (7) Cutting edge technology at 7 T. Magn Reson Med, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Bandettini, Peter A.] NIMH, Sect Funct Imaging Methods, Bethesda, MD 20882 USA.
[Bandettini, Peter A.] NIMH, Funct MRI Core Facil, Bethesda, MD 20882 USA.
[Bowtell, Richard] Univ Nottingham, Sir Peter Mansfield Magnet Resonance Ctr, Nottingham NG7 2RD, England.
[Jezzard, Peter] Univ Oxford, Nuffield Dept Clin Neurosci, FMRIB Ctr, Oxford, England.
[Turner, Robert] Max Planck Inst Human Cognit & Brain Sci, Leipzig, Germany.
RP Bandettini, PA (reprint author), NIMH, Sect Funct Imaging Methods, Bldg 10,Room 1D80,10 Ctr Dr,MSC 1148, Bethesda, MD 20882 USA.
EM Bandettini@nih.gov
OI Bowtell, Richard/0000-0001-8656-412X; Turner,
Robert/0000-0001-5055-9644; Jezzard, Peter/0000-0001-7912-2251
FU Intramural NIH HHS [ZIA MH002783-09, Z99 MH999999]; Medical Research
Council [G0700399, G0901321]
NR 27
TC 16
Z9 16
U1 0
U2 11
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0740-3194
J9 MAGN RESON MED
JI Magn. Reson. Med.
PD FEB
PY 2012
VL 67
IS 2
BP 317
EP 321
DI 10.1002/mrm.23151
PG 5
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 880AM
UT WOS:000299376500005
PM 22083719
ER
PT J
AU Grewal, J
Carmichael, SL
Yang, W
Shaw, GM
AF Grewal, Jagteshwar
Carmichael, Suzan L.
Yang, Wei
Shaw, Gary M.
TI Paternal Age and Congenital Malformations in Offspring in California,
1989-2002
SO MATERNAL AND CHILD HEALTH JOURNAL
LA English
DT Article
DE Congenital malformations; Paternal age; Birth defects
ID BIRTH-DEFECTS; DELAYED CHILDBEARING; MATERNAL AGE; RISK; ASSOCIATION;
POPULATION; PREGNANCY; NORWAY; OLDER
AB This study examined the association between paternal age and a wide range of structural birth defects. Data were drawn from The California Birth Defects Monitoring Program, a population-based active surveillance system for collecting information on infants and fetuses with defects born between 1989 and 2002. The analysis included 46,114 cases with defects, plus a random sample of 36,838 non-malformed births. After adjustment for maternal age, risks of anomalies of the nervous system for 38 and 42 year-old fathers, as compared to 29 year-old fathers, were 1.05-fold [1.00, 1.11] and 1.10-fold [1.02, 1.18] higher, respectively. Similar results were observed for anomalies of the limbs, where 38 and 42 year-old fathers had a 1.06-fold [1.02, 1.11] and 1.11-fold [1.05, 1.18] higher risk, respectively. Risks of anomalies of the integument were 1.05-fold [1.00, 1.09] and 1.10-fold [1.03, 1.16] higher for 38 and 42 year olds, respectively. Young paternal age, i.e., less than 29 years, was associated with an increased risk of amniotic bands (OR: 0.87 [0.78, 0.97]), pyloric stenosis (OR: 0.93 [0.90, 0.96]) and anomalies of the great veins (OR: 0.93 [0.87, 1.00]). In sum, both advanced and young paternal age was associated with select birth defects in California between 1989 and 2002.
C1 [Carmichael, Suzan L.; Yang, Wei; Shaw, Gary M.] Stanford Univ, Palo Alto, CA 94304 USA.
[Grewal, Jagteshwar] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, NIH, Bethesda, MD USA.
RP Carmichael, SL (reprint author), Stanford Univ, Palo Alto, CA 94304 USA.
EM scarmichael@stanford.edu
OI Grewal, Jagteshwar/0000-0002-0141-4876
NR 29
TC 7
Z9 7
U1 0
U2 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1092-7875
EI 1573-6628
J9 MATERN CHILD HLTH J
JI Matern. Child Health J.
PD FEB
PY 2012
VL 16
IS 2
BP 385
EP 392
DI 10.1007/s10995-011-0759-z
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 879YJ
UT WOS:000299370400013
PM 21344170
ER
PT J
AU Abrames, E
Folio, L
AF Abrames, Erik
Folio, Les
TI CT Severity Spectrum of Penetrating Eye Injuries From Blasts
SO MILITARY MEDICINE
LA English
DT Article
ID IRAQI FREEDOM; ORBIT
AB Penetrating eye trauma from blasts can result in a vast spectrum of ocular injuries. Several cases of orbital trauma are reviewed, all of which occurred during combat operations and treated M an Air Force Theater Hospital. Computed tomography was used as the primary imaging modality and proved crucial in determining the extent of ocular injury. This report focuses on factors we believe affect globe salvageability, reviews imaging modalities in theater, and briefly discusses management in theater and aeromedical evacuation after initial injury.
C1 [Abrames, Erik] Yokota Air Base Hosp, Med Grp 374th, Yokota Air Base, Japan.
[Folio, Les] NIH, Bethesda, MD 20892 USA.
RP Abrames, E (reprint author), Yokota Air Base Hosp, Med Grp 374th, Bldg 4412,McGuire Ave, Yokota Air Base, Japan.
NR 10
TC 1
Z9 1
U1 0
U2 2
PU ASSOC MILITARY SURG US
PI BETHESDA
PA 9320 OLD GEORGETOWN RD, BETHESDA, MD 20814 USA
SN 0026-4075
J9 MIL MED
JI Milit. Med.
PD FEB
PY 2012
VL 177
IS 2
BP 169
EP 173
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 886KC
UT WOS:000299852300010
PM 22360062
ER
PT J
AU Jeong, JH
Kim, HJ
Kim, KH
Shin, M
Hong, Y
Rhee, JH
Schneider, TD
Choy, HE
AF Jeong, Jae-Ho
Kim, Hyun-Ju
Kim, Kun-Hee
Shin, Minsang
Hong, Yeongjin
Rhee, Joon Haeng
Schneider, Thomas D.
Choy, Hyon E.
TI An unusual feature associated with LEE1 P1 promoters in enteropathogenic
Escherichia coli (EPEC)
SO MOLECULAR MICROBIOLOGY
LA English
DT Article
ID ENTEROCYTE EFFACEMENT GENES; START SITE SELECTION; RNA-POLYMERASE;
REITERATIVE TRANSCRIPTION; H-NS; REGULATORY REGION; GALP2 PROMOTER;
SEQUENCE LOGOS; LOCUS; DNA
AB Transcription start points in bacteria are influenced by the nature of the RNA polymerase.promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing sigma 70, it is presumed that specific sequence in one or more of the -10, extended -10 and -35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the LEE1 operon in enteropathogenic E. coli and found two promoters separated by 10 bp, LEE1 P1A (+1) and LEE1 P1B (+10) using various in vitro biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighbouring As at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under in vivo conditions, dominant P1B, but not P1A, was subject to regulation by IHF.
C1 [Jeong, Jae-Ho; Kim, Hyun-Ju; Kim, Kun-Hee; Shin, Minsang; Hong, Yeongjin; Choy, Hyon E.] Chonnam Natl Univ, Sch Med, Ctr Host Def Enteropathogen Bacteria Infect, Kwangju 501746, South Korea.
[Jeong, Jae-Ho; Kim, Hyun-Ju; Kim, Kun-Hee; Shin, Minsang; Hong, Yeongjin; Rhee, Joon Haeng; Choy, Hyon E.] Chonnam Natl Univ, Sch Med, Dept Microbiol, Kwangju 501746, South Korea.
[Schneider, Thomas D.] NCI, NIH, Gene Regulat & Chromosome Biol Lab, Nci Frederick, MD USA.
RP Choy, HE (reprint author), Chonnam Natl Univ, Sch Med, Ctr Host Def Enteropathogen Bacteria Infect, Kwangju 501746, South Korea.
EM hyonchoy@jnu.ac.kr
OI Schneider, Thomas/0000-0002-9841-1531
FU Korea Science and Engineering Foundation; MOST [2007-04213]; Ministry of
Knowledge Economy (MKE) [RTI05-01-01]; NIH, National Cancer Institute,
Center for Cancer Research
FX This work was supported by the Korea Science and Engineering Foundation
grant that was funded by MOST (No. 2007-04213). J.H.R. was supported by
Grant No. RTI05-01-01 from the Regional Technology Innovation Program of
the Ministry of Knowledge Economy (MKE). T.S. was supported by the
Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 53
TC 5
Z9 5
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0950-382X
J9 MOL MICROBIOL
JI Mol. Microbiol.
PD FEB
PY 2012
VL 83
IS 3
BP 612
EP 622
DI 10.1111/j.1365-2958.2011.07956.x
PG 11
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA 878JE
UT WOS:000299251900012
PM 22229878
ER
PT J
AU Crockett, MJ
Clark, L
Roiser, JP
Robinson, OJ
Cools, R
Chase, HW
den Ouden, H
Apergis-Schoute, A
Campbell-Meikeljohn, D
Seymour, B
Sahakian, BJ
Rogers, RD
Robbins, TW
AF Crockett, M. J.
Clark, L.
Roiser, J. P.
Robinson, O. J.
Cools, R.
Chase, H. W.
den Ouden, H.
Apergis-Schoute, A.
Campbell-Meikeljohn, D.
Seymour, B.
Sahakian, B. J.
Rogers, R. D.
Robbins, T. W.
TI Converging evidence for central 5-HT effects in acute tryptophan
depletion
SO MOLECULAR PSYCHIATRY
LA English
DT Letter
ID SEROTONIN; RELEASE; MEMORY; RATS
C1 [Crockett, M. J.; Apergis-Schoute, A.; Sahakian, B. J.; Robbins, T. W.] Behav & Clin Neurosci Inst, Cambridge, England.
[Crockett, M. J.; Clark, L.; Apergis-Schoute, A.; Robbins, T. W.] Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England.
[Roiser, J. P.] UCL, Inst Cognit Neurosci, London, England.
[Robinson, O. J.] NIMH, Mood & Anxiety Disorders Program, Bethesda, MD 20892 USA.
[Cools, R.; den Ouden, H.] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Ctr Cognit Neuroimaging, NL-6525 ED Nijmegen, Netherlands.
[Cools, R.; den Ouden, H.] Dept Psychiat, Nijmegen, Netherlands.
[Chase, H. W.] Univ Pittsburgh, Sch Med, Dept Psychiat, Western Psychiat Inst & Clin, Pittsburgh, PA USA.
[Campbell-Meikeljohn, D.] Aarhus Univ, CFIN, Aarhus, Denmark.
[Seymour, B.] UCL, Wellome Trust Ctr Neuroimaging, London, England.
[Sahakian, B. J.] Univ Cambridge, Dept Psychiat, Cambridge, England.
[Rogers, R. D.] Univ Oxford, Dept Psychiat, Oxford, England.
[Rogers, R. D.] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England.
RP Crockett, MJ (reprint author), Behav & Clin Neurosci Inst, Cambridge, England.
EM mollycrockett@gmail.com
RI Roiser, Jonathan/A-1791-2010; den Ouden, Hanneke/D-3019-2009; Robinson,
Oliver/B-3646-2011; Cools, Roshan/D-1905-2010; Crockett,
Molly/F-8217-2014;
OI den Ouden, Hanneke/0000-0001-7039-5130; Robinson,
Oliver/0000-0002-3100-1132; Crockett, Molly/0000-0001-8800-410X;
Seymour, Ben/0000-0003-1724-5832; Campbell-Meiklejohn,
Daniel/0000-0002-8916-265X
NR 12
TC 26
Z9 26
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD FEB
PY 2012
VL 17
IS 2
BP 121
EP 123
DI 10.1038/mp.2011.106
PG 3
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 885SZ
UT WOS:000299802400004
PM 21876544
ER
PT J
AU Stark, MS
Woods, SL
Gartside, MG
Bonazzi, VF
Dutton-Regester, K
Aoude, LG
Chow, D
Sereduk, C
Niemi, NM
Tang, NY
Ellis, JJ
Reid, J
Zismann, V
Tyagi, S
Muzny, D
Newsham, I
Wu, YQ
Palmer, JM
Pollak, T
Youngkin, D
Brooks, BR
Lanagan, C
Schmidt, CW
Kobe, B
MacKeigan, JP
Yin, HW
Brown, KM
Gibbs, R
Trent, J
Hayward, NK
AF Stark, Mitchell S.
Woods, Susan L.
Gartside, Michael G.
Bonazzi, Vanessa F.
Dutton-Regester, Ken
Aoude, Lauren G.
Chow, Donald
Sereduk, Chris
Niemi, Natalie M.
Tang, Nanyun
Ellis, Jonathan J.
Reid, Jeffrey
Zismann, Victoria
Tyagi, Sonika
Muzny, Donna
Newsham, Irene
Wu, YuanQing
Palmer, Jane M.
Pollak, Thomas
Youngkin, David
Brooks, Bradford R.
Lanagan, Catherine
Schmidt, Christopher W.
Kobe, Bostjan
MacKeigan, Jeffrey P.
Yin, Hongwei
Brown, Kevin M.
Gibbs, Richard
Trent, Jeffrey
Hayward, Nicholas K.
TI Frequent somatic mutations in MAP3K5 and MAP3K9 in metastatic melanoma
identified by exome sequencing
SO NATURE GENETICS
LA English
DT Article
ID MALIGNANT-MELANOMA; HUMAN CANCER; APOPTOSIS; KINASE-1; TEMOZOLOMIDE;
INHIBITION; ACTIVATION; GENES; BRAF
AB We sequenced eight melanoma exomes to identify new somatic mutations in metastatic melanoma. Focusing on the mitogen-activated protein (MAP) kinase kinase kinase (MAP3K) family, we found that 24% of melanoma cell lines have mutations in the protein-coding regions of either MAP3K5 or MAP3K9. Structural modeling predicted that mutations in the kinase domain may affect the activity and regulation of these protein kinases. The position of the mutations and the loss of heterozygosity of MAP3K5 and MAP3K9 in 85% and 67% of melanoma samples, respectively, together suggest that the mutations are likely to be inactivating. In in vitro kinase assays, MAP3K5 1780F and MAP3K9 W333* variants had reduced kinase activity. Overexpression of MAP3K5 or MAP3K9 mutants in HEK293T cells reduced the phosphorylation of downstream MAP kinases. Attenuation of MAP3K9 function in melanoma cells using siRNA led to increased cell viability after temozolomide treatment, suggesting that decreased MAP3K pathway activity can lead to chemoresistance in melanoma.
C1 [Stark, Mitchell S.; Woods, Susan L.; Gartside, Michael G.; Bonazzi, Vanessa F.; Dutton-Regester, Ken; Aoude, Lauren G.; Tyagi, Sonika; Palmer, Jane M.; Pollak, Thomas; Lanagan, Catherine; Schmidt, Christopher W.; Hayward, Nicholas K.] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Dutton-Regester, Ken] Queensland Univ Technol, Brisbane, Qld 4001, Australia.
[Aoude, Lauren G.] Univ Queensland, Sch Med, Brisbane, Qld, Australia.
[Chow, Donald; Sereduk, Chris; Ellis, Jonathan J.; Zismann, Victoria; Youngkin, David; Yin, Hongwei; Brown, Kevin M.; Trent, Jeffrey] Translat Genom Res Inst, Phoenix, AZ USA.
[Niemi, Natalie M.; Brooks, Bradford R.; MacKeigan, Jeffrey P.; Trent, Jeffrey] Van Andel Res Inst, Grand Rapids, MI USA.
[Ellis, Jonathan J.; Kobe, Bostjan] Univ Queensland, Sch Chem & Mol Biosci, Inst Mol Biosci, Brisbane, Qld, Australia.
[Ellis, Jonathan J.; Kobe, Bostjan] Univ Queensland, Ctr Infect Dis Res, Brisbane, Qld, Australia.
[Reid, Jeffrey; Muzny, Donna; Newsham, Irene; Wu, YuanQing; Gibbs, Richard] Baylor Coll Med, Human Genome Sequencing Ctr, Houston, TX 77030 USA.
[Brown, Kevin M.] NCI, Adv Technol Ctr, Gaithersburg, MD USA.
RP Hayward, NK (reprint author), Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
EM nick.hayward@qimr.edu.au
RI Kobe, Bostjan/D-1292-2009; Ellis, Jonathan/F-2920-2010; Stark,
Mitchell/E-3542-2010; Aoude, Lauren/C-7484-2014; hayward,
nicholas/C-1367-2015;
OI Kobe, Bostjan/0000-0001-9413-9166; Ellis, Jonathan/0000-0003-0410-5064;
Stark, Mitchell/0000-0002-4510-2161; Aoude, Lauren/0000-0003-1448-3923;
hayward, nicholas/0000-0003-4760-1033; Woods, Susan/0000-0002-8955-2017;
Bonazzi, Vanessa/0000-0002-2574-0334
FU National Health and Medical Research Council of Australia; Australian
Centre for Vaccine Development; US National Cancer Institute
[5U01CA129447]; US National Cancer Institute, Division of Cancer
Epidemiology and Genetics
FX The authors would like to acknowledge M. Aziz for data processing, M.
Kassner for technical support and J.-C. Deza for graphics support. This
work was funded through grants from the National Health and Medical
Research Council of Australia, the Australian Centre for Vaccine
Development, the US National Cancer Institute (5U01CA129447 to J.T.),
the US National Cancer Institute, Division of Cancer Epidemiology and
Genetics (to K.M.B.), and a charitable donation by Francis Najafi (to
K.M.B. and IT.).
NR 24
TC 95
Z9 96
U1 0
U2 7
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD FEB
PY 2012
VL 44
IS 2
BP 165
EP 169
DI 10.1038/ng.1041
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 883WA
UT WOS:000299664400013
PM 22197930
ER
PT J
AU O'Seaghdha, CM
Fox, CS
AF O'Seaghdha, Conall M.
Fox, Caroline S.
TI Genome-wide association studies of chronic kidney disease: what have we
learned?
SO NATURE REVIEWS NEPHROLOGY
LA English
DT Review
ID STAGE RENAL-DISEASE; MANGANESE SUPEROXIDE-DISMUTASE; TYPE-2
DIABETIC-PATIENTS; CARNOSINASE GENE CNDP1; AFRICAN-AMERICANS; IGA
NEPHROPATHY; PROSPECTIVE COHORT; NATURAL-SELECTION; JAPANESE PATIENTS;
SERUM CREATININE
AB The past 3 years have witnessed a dramatic expansion in our knowledge of the genetic determinants of estimated glomerular filtration rate (eGFR) and chronic kidney disease (CKD). However, heritability estimates of eGFR indicate that we have only identified a small proportion of the total heritable contribution to the phenotypic variation. The majority of associations reported from genome-wide association studies identify genomic regions of interest and further work will be required to identify the causal variants responsible for a specific phenotype. Progress in this area is likely to stem from the identification of novel risk genotypes, which will offer insight into the pathogenesis of disease and potential novel therapeutic targets. Follow-up studies stimulated by findings from genome-wide association studies of kidney disease are already yielding promising results, such as the identification of an association between urinary uromodulin levels and incident CKD. Although this work is at an early stage, prospects for progress in our understanding of CKD and its treatment look more promising now than at any point in the past.
C1 [O'Seaghdha, Conall M.; Fox, Caroline S.] Natl Heart Lung & Blood Inst, Framingham Heart Study & Ctr Populat Studies, Framingham, MA 01702 USA.
RP Fox, CS (reprint author), Natl Heart Lung & Blood Inst, Framingham Heart Study & Ctr Populat Studies, 73 Mt Wayte Ave,Suite 2, Framingham, MA 01702 USA.
EM foxca@nhlbi.nih.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 107
TC 23
Z9 23
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-5061
J9 NAT REV NEPHROL
JI Nat. Rev. Nephrol.
PD FEB
PY 2012
VL 8
IS 2
BP 89
EP 99
DI 10.1038/nrneph.2011.189
PG 11
WC Urology & Nephrology
SC Urology & Nephrology
GA 888AK
UT WOS:000299976000008
PM 22143329
ER
PT J
AU Geocadin, RG
Bleck, TP
Koroshetz, WJ
Robertson, CS
Zaidat, OO
LeRoux, PD
Wijman, CAC
Suarez, JI
AF Geocadin, R. G.
Bleck, T. P.
Koroshetz, W. J.
Robertson, C. S.
Zaidat, O. O.
LeRoux, P. D.
Wijman, C. A. C.
Suarez, J. I.
TI Research Priorities in Neurocritical Care
SO NEUROCRITICAL CARE
LA English
DT Review
DE Neurocritical care; Critical care; Clinical trials; Research network;
Consortium
ID TRAUMATIC BRAIN-INJURY; VENOUS THROMBOEMBOLISM; CRITICALLY-ILL;
INTENSIVE-CARE; HEAD-INJURY; TRANSFUSION; PROPHYLAXIS; MORTALITY;
RECOMMENDATIONS; MULTICENTER
AB This summary of the last session of the First Neurocritical Care Research Conference reviews the discussions about research priorities in neurocritical care. The first presentation reviewed current projects funded by the National Institute of Neurological Disorders and Stroke at the National Institutes of Health and potential models to follow including an independent Neurocritical Care Network or the creation of such a network with the goal of collaborating with already existing ones. Experienced neurointensivists then presented their views on the most common and important research questions that need to be answered and investigated in the field. Finally, utility of clinical registries was discussed emphasizing their importance as hypothesis generators. During the group discussion, interests in comparative effectiveness research, the use of physiological endpoints from monitoring and alternate trial design were expressed.
C1 [Geocadin, R. G.] Johns Hopkins Univ, Dept Neurol, Sch Med, Johns Hopkins Hosp, Baltimore, MD 21287 USA.
[Geocadin, R. G.] Johns Hopkins Univ, Dept Anesthesiol Crit Care Med, Sch Med, Johns Hopkins Hosp, Baltimore, MD 21287 USA.
[Geocadin, R. G.] Johns Hopkins Univ, Dept Neurosurg, Sch Med, Johns Hopkins Hosp, Baltimore, MD 21287 USA.
[Bleck, T. P.] Rush Univ, Dept Neurol Sci, Chicago, IL 60612 USA.
[Bleck, T. P.] Rush Univ, Dept Neurosurg, Chicago, IL 60612 USA.
[Bleck, T. P.] Rush Univ, Dept Med, Chicago, IL 60612 USA.
[Bleck, T. P.] Rush Univ, Dept Anesthesiol, Chicago, IL 60612 USA.
[Koroshetz, W. J.] NINDS, NIH, Bethesda, MD 20892 USA.
[Robertson, C. S.] Baylor Coll Med, Dept Neurol Surg, Houston, TX 77030 USA.
[Zaidat, O. O.] Med Coll Wisconsin, Dept Neurol & Neurosurg, Milwaukee, WI 53226 USA.
[LeRoux, P. D.] Univ Penn, Dept Neurosurg, Philadelphia, PA 19104 USA.
[Wijman, C. A. C.] Stanford Univ, Dept Neurol, Palo Alto, CA 94304 USA.
[Suarez, J. I.] Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA.
RP Geocadin, RG (reprint author), Johns Hopkins Univ, Dept Neurol, Sch Med, Johns Hopkins Hosp, 600 N Wolfe St,Meyer 8-140, Baltimore, MD 21287 USA.
EM rgeocad1@jhmi.edu
OI Bleck, Thomas/0000-0002-8267-9787
FU National Institute of Neurological Disorders and Stroke [R13NS065494];
Integra Foundation; Neuroscience Center of the St Luke's Episcopal
Hospital in Houston, TX
FX The First Neurocritical Care Research Conference was funded by award
R13NS065494 from the National Institute of Neurological Disorders and
Stroke (P. I.: JI Suarez), the Integra Foundation, and the Neuroscience
Center of the St Luke's Episcopal Hospital in Houston, TX, and endorsed
by the Neurocritical Care Society.
NR 26
TC 1
Z9 1
U1 0
U2 4
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1541-6933
J9 NEUROCRIT CARE
JI Neurocrit. Care
PD FEB
PY 2012
VL 16
IS 1
BP 35
EP 41
DI 10.1007/s12028-011-9611-y
PG 7
WC Critical Care Medicine; Clinical Neurology
SC General & Internal Medicine; Neurosciences & Neurology
GA 881QW
UT WOS:000299502500006
PM 21792752
ER
PT J
AU Liu, ZM
de Zwart, JA
van Gelderen, P
Kuo, LW
Duyn, JH
AF Liu, Zhongming
de Zwart, Jacco A.
van Gelderen, Peter
Kuo, Li-Wei
Duyn, Jeff H.
TI Statistical feature extraction for artifact removal from concurrent
fMRI-EEG recordings
SO NEUROIMAGE
LA English
DT Article
DE Gradient artifact; Ballistocardiogram; Singular value decomposition;
Independent component analysis; Mutual information
ID INDEPENDENT COMPONENT ANALYSIS; BALLISTOCARDIOGRAM ARTIFACT; FUNCTIONAL
MRI; SIMULTANEOUS EEG/FMRI; IMAGING-ARTIFACT; PULSE ARTIFACT; REDUCTION;
SCANNER; ELECTROENCEPHALOGRAM; IDENTIFICATION
AB We propose a set of algorithms for sequentially removing artifacts related to MRI gradient switching and cardiac pulsations from electroencephalography (EEG) data recorded during functional magnetic resonance imaging (fMRI). Special emphasis is directed upon the use of statistical metrics and methods for the extraction and selection of features that characterize gradient and pulse artifacts. To remove gradient artifacts, we use channel-wise filtering based on singular value decomposition (SVD). To remove pulse artifacts, we first decompose data into temporally independent components and then select a compact cluster of components that possess sustained high mutual information with the electrocardiogram (ECG). After the removal of these components, the time courses of remaining components are filtered by SVD to remove the temporal patterns phase-locked to the cardiac timing markers derived from the ECG. The filtered component time courses are then inversely transformed into multi-channel EEG time series free of pulse artifacts. Evaluation based on a large set of simultaneous EEG-fMRI data obtained during a variety of behavioral tasks, sensory stimulations and resting conditions showed excellent data quality and robust performance attainable with the proposed methods. These algorithms have been implemented as a Matlab-based toolbox made freely available for public access and research use. Published by Elsevier Inc.
C1 [Liu, Zhongming; de Zwart, Jacco A.; van Gelderen, Peter; Kuo, Li-Wei; Duyn, Jeff H.] NINDS, Adv MRI Sect, LFMI, NIH, Bethesda, MD 20982 USA.
RP Liu, ZM (reprint author), NINDS, Adv MRI Sect, LFMI, NIH, Bldg 10,Room B1D-723,9000 Rockville Pike,MSC 1065, Bethesda, MD 20982 USA.
EM liuz5@mail.nih.gov
RI Kuo, Li-Wei/G-4007-2011
FU National Institute of Neurological Disorders and Stroke, National
Institutes of Health
FX The authors appreciate Dr. Hanchuan Peng for kindly sharing his C
program for computing entropy and mutual information, Dr. Masaki
Fukunaga and Susan Guttman for their assistance in data collection and
Drs. Qi Duan and Hendrik Mandelkow for useful discussions and carefully
reading this manuscript. This research was supported by the Intramural
Research Program of the National Institute of Neurological Disorders and
Stroke, National Institutes of Health.
NR 46
TC 26
Z9 27
U1 3
U2 18
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD FEB 1
PY 2012
VL 59
IS 3
BP 2073
EP 2087
DI 10.1016/j.neuroimage.2011.10.042
PG 15
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 881NS
UT WOS:000299494000011
PM 22036675
ER
PT J
AU Kimura, Y
Simeon, FG
Zoghbi, SS
Zhang, Y
Hatazawa, J
Pike, VW
Innis, RB
Fujita, M
AF Kimura, Yasuyuki
Simeon, Fabrice G.
Zoghbi, Sami S.
Zhang, Yi
Hatazawa, Jun
Pike, Victor W.
Innis, Robert B.
Fujita, Masahiro
TI Quantification of metabotropic glutamate subtype 5 receptors in the
brain by an equilibrium method using F-18-SP203
SO NEUROIMAGE
LA English
DT Article
DE F-18-SP203; Bolus plus constant infusion; Equilibrium method;
Metabotropic glutamate subtype 5 receptor (mGluR5); Positron emission
tomography (PET)
ID POSITRON-EMISSION-TOMOGRAPHY; CONSTANT INFUSION; QUANTITATION; BOLUS;
PET
AB A new PET ligand, 3-fluoro-5-(2-(2-F-18-(fluoromethyl)-thiazol-4-yl)ethynyl)benzonitrile (F-18-SP203) can quantify metabotropic glutamate subtype 5 receptors (mGluR5) in human brain by a bolus injection and kinetic modeling. As an alternative approach to a bolus injection, binding can simply be measured as a ratio of tissue to metabolite-corrected plasma at a single time point under equilibrium conditions achieved by administering the radioligand with a bolus injection followed by a constant infusion. The purpose of this study was to validate the equilibrium method as an alternative to the standard kinetic method for measuring F-18-SP203 binding in the brain. Nine healthy subjects were injected with F-18-SP203 using a bolus plus constant infusion for 300 min. A single ratio of bolus-to-constant infusion (the activity of bolus equaled to that of infusion over 219 min) was applied to all subjects to achieve equilibrium in approximately 120 min. Ass measure of ligand binding, we compared total distribution volume (V-T) calculated by the equilibrium and kinetic methods in each scan. The equilibrium method calculated V-T by the ratio of radioactivity in the brain to the concentration of F-18-SP203 in arterial plasma at 120 min, and the kinetic method calculated V-T by a two-tissue compartment model using brain and plasma dynamic data from 0 to 120 min. V-T obtained via the equilibrium method was highly correlated with V-T obtained via kinetic modeling. Inter-subject variability of V-T obtained via the equilibrium method was slightly smaller than V-T obtained via the kinetic method. V-T obtained via the equilibrium method was -10% higher than V-T obtained via the kinetic method, indicating a small difference between the measurements. Taken together, the results of this study show that using the equilibrium method is an acceptable alternative to the standard kinetic method when using F-18-SP203 to measure mGluR5. Although small differences in the measurements obtained via the equilibrium and kinetic methods exist, both methods consistently measured mGluR5 as indicated by the highly correlated V-T values; the equilibrium method was slightly more precise, as indirectly measured by the smaller coefficient of variability across subjects. In addition, when using F-18-SP203, the equilibrium method is more efficient because it requires much less data. (C) 2011 Published by Elsevier Inc.
C1 [Kimura, Yasuyuki; Simeon, Fabrice G.; Zoghbi, Sami S.; Zhang, Yi; Pike, Victor W.; Innis, Robert B.; Fujita, Masahiro] NIMH, Mol Imaging Branch, Bethesda, MD 20892 USA.
[Hatazawa, Jun] Osaka Univ, Grad Sch Med, Dept Nucl Med & Tracer Kinet, Suita, Osaka 5650871, Japan.
[Kimura, Yasuyuki] Natl Inst Radiol Sci, Mol Imaging Ctr, Chiba 2638555, Japan.
RP Fujita, M (reprint author), NIMH, Mol Imaging Branch, 10 Ctr Dr,MSC 1026,Bldg 10,Rm B1D43, Bethesda, MD 20892 USA.
EM y-kimura@nirs.go.jp; simeonf@mail.nih.gov; zoghbis@mail.nih.gov;
yizhang@mail.nih.gov; hatazawa@tracer.med.osaka-u.ac.jp;
pikev@mail.nih.gov; innisr@mail.nih.gov; fujitam@mail.nih.gov
RI Kimura, Yasuyuki/D-4459-2016
OI Kimura, Yasuyuki/0000-0002-7927-9483
FU National Institute of Mental Health [Z01-MH-002795-07, Z01-MH-002852-04]
FX This research was supported by the Intramural Program of the National
Institute of Mental Health (projects Z01-MH-002795-07 and
Z01-MH-002852-04). We thank Kacey Anderson, Leah P. Dickstein, Maria D.
Ferraris Araneta, Gerald L Hodges, Kimberly Jenko, Nobuyo Kimura,
William C. Kreisl, Barbara A. Scepura, Cheryl L. Wallisch, JeihSan Liow,
Robert L Gladding, and the staff of the PET Department for successful
completion of the studies, George J. Grimes, Judith M. Starling and
Christine Y. Hon for their comments on adsorption of the ligand, David
Luckenbaugh for his comments on the statistics, loline Henter for
editorial assistance, and PMOD Technologies (Zurich, Switzerland) for
providing its image analysis and modeling software.
NR 13
TC 7
Z9 7
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 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD FEB 1
PY 2012
VL 59
IS 3
BP 2124
EP 2130
DI 10.1016/j.neuroimage.2011.10.028
PG 7
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 881NS
UT WOS:000299494000015
PM 22032949
ER
PT J
AU Chen, R
Resnick, SM
Davatzikos, C
Herskovits, EH
AF Chen, Rong
Resnick, Susan M.
Davatzikos, Christos
Herskovits, Edward H.
TI Dynamic Bayesian network modeling for longitudinal brain morphometry
SO NEUROIMAGE
LA English
DT Article
DE Dynamic Bayesian network; Longitudinal morphometry
ID MILD COGNITIVE IMPAIRMENT; VOXEL-BASED MORPHOMETRY; MCI; MRI;
CONVERSION; ATROPHY; IMAGES; VOLUME; MAPS
AB Identifying interactions among brain regions from structural magnetic-resonance images presents one of the major challenges in computational neuroanatomy. We propose a Bayesian data-mining approach to the detection of longitudinal morphological changes in the human brain. Our method uses a dynamic Bayesian network to represent evolving inter-regional dependencies. The major advantage of dynamic Bayesian network modeling is that it can represent complicated interactions among temporal processes. We validated our approach by analyzing a simulated atrophy study, and found that this approach requires only a small number of samples to detect the ground-truth temporal model. We further applied dynamic Bayesian network modeling to a longitudinal study of normal aging and mild cognitive impairment - the Baltimore Longitudinal Study of Aging. We found that interactions among regional volume-change rates for the mild cognitive impairment group are different from those for the normal-aging group. (C) 2011 Elsevier Inc. All rights reserved.
C1 [Chen, Rong; Davatzikos, Christos; Herskovits, Edward H.] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
[Resnick, Susan M.] NIA, NIH, Baltimore, MD 21224 USA.
RP Chen, R (reprint author), Univ Penn, Dept Radiol, 3400 Spruce St, Philadelphia, PA 19104 USA.
EM rong.chen@uphs.upenn.edu
RI Chen, Robert/B-3899-2009
OI Chen, Robert/0000-0002-8371-8629
FU National Institutes of Health [R01 AG13743, R03 EB-009310]; National
Institute of Aging; National Institute of Mental Health; American
Recovery and Reinvestment Act; [N01-AG-3-2124]
FX This work was supported by National Institutes of Health grant R01
AG13743, which is funded by the National Institute of Aging, and the
National Institute of Mental Health; this work was also supported by the
American Recovery and Reinvestment Act. This work was supported by
National Institutes of Health grant R03 EB-009310. This research was
supported in part by the Intramural Research Program, National Institute
on Aging. NIH and by research and development contract N01-AG-3-2124.
NR 33
TC 15
Z9 15
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD FEB 1
PY 2012
VL 59
IS 3
BP 2330
EP 2338
DI 10.1016/j.neuroimage.2011.09.023
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 881NS
UT WOS:000299494000035
PM 21963916
ER
PT J
AU Zhang, J
Laughon, SK
Branch, DW
AF Zhang, Jun
Laughon, S. Katherine
Branch, D. Ware
TI Oxytocin Regimen for Labor Augmentation, Labor Progression, and
Perinatal Outcomes Reply
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Letter
C1 [Zhang, Jun] Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, MOE Shanghai Key Lab Childrens Environm Hlth, Shanghai 200030, Peoples R China.
[Laughon, S. Katherine] NICHHD, Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
[Branch, D. Ware] Intermt Healthcare, Dept Obstet & Gynecol, Salt Lake City, UT USA.
[Branch, D. Ware] Univ Utah, Salt Lake City, UT USA.
RP Zhang, J (reprint author), Shanghai Jiao Tong Univ, Sch Med, Xinhua Hosp, MOE Shanghai Key Lab Childrens Environm Hlth, Shanghai 200030, Peoples R China.
NR 2
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD FEB
PY 2012
VL 119
IS 2
BP 381
EP 382
PN 1
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 883AF
UT WOS:000299604300030
ER
PT J
AU Leventhal, AM
David, SP
Brightman, M
Strong, D
McGeary, JE
Brown, RA
Lloyd-Richardson, EE
Munafo, M
Uhl, GR
Niaura, R
AF Leventhal, A. M.
David, S. P.
Brightman, M.
Strong, D.
McGeary, J. E.
Brown, R. A.
Lloyd-Richardson, E. E.
Munafo, M.
Uhl, G. R.
Niaura, R.
TI Dopamine D4 receptor gene variation moderates the efficacy of bupropion
for smoking cessation
SO PHARMACOGENOMICS JOURNAL
LA English
DT Article
DE DRD4; VNTR; smoking cessation; bupropion
ID DRD4 VNTR POLYMORPHISM; EXON-III POLYMORPHISM; TOBACCO DEPENDENCE;
CIGARETTE-SMOKING; CLINICAL-TRIAL; D-4 RECEPTORS; ALCOHOL; ASSOCIATION;
CUES; VARIANTS
AB Smokers (>= 10 cigarettes per day, N = 331) of European ancestry taking part in a double-blind placebo-controlled randomized trial of 12 weeks of treatment with bupropion along with counseling for smoking cessation were genotyped for a variable number of tandem repeats polymorphism in exon III of the dopamine D4 receptor gene. Generalized estimating equations predicting point-prevalence abstinence at end of treatment and 2, 6 and 12 months after the end of treatment indicated that bupropion (vs placebo) predicted increased odds of abstinence. The main effect of Genotype was not significant. A Genotype x Treatment interaction (P = 0.005) showed that bupropion predicted increased odds of abstinence in long-allele carriers (odds ratios (OR) = 1.31, P < 0.0001), whereas bupropion was not associated with abstinence among short-allele homozygotes (OR = 1.06, P = 0.23). The Genotype x Treatment interaction remained when controlling for demographic and clinical covariates (P = 0.01) and in analyses predicting continuous abstinence (P's <= 0.054). Bupropion may be more efficacious for smokers who carry the long allele, which is relevant to personalized pharmacogenetic treatment approaches. The Pharmacogenomics Journal (2012) 12, 86-92; doi:10.1038/tpj.2010.64; published online 27 July 2010
C1 [Leventhal, A. M.; Brightman, M.] Univ So Calif, Dept Prevent Med, Keck Sch Med, Los Angeles, CA 90033 USA.
[David, S. P.] Stanford Univ, Sch Med, Dept Family & Community Med, Palo Alto, CA 94304 USA.
[Strong, D.; McGeary, J. E.; Brown, R. A.] Brown Univ, Dept Psychiat & Human Behav, Alpert Med Sch, Providence, RI 02912 USA.
[Lloyd-Richardson, E. E.] Univ Massachusetts, Dept Psychol, Dartmouth, MA USA.
[Munafo, M.] Univ Bristol, Dept Expt Psychol, Bristol, Avon, England.
[Uhl, G. R.] Natl Inst Drug Abuse, Mol Neurobiol Res Branch, Intramural Res Program, Baltimore, MD USA.
[Niaura, R.] Amer Legacy Fdn, Schroder Inst, Washington, DC USA.
RP Leventhal, AM (reprint author), Univ So Calif, Dept Prevent Med, Keck Sch Med, 2250 Alcazar St,CSC 240, Los Angeles, CA 90033 USA.
EM adam.leventhal@usc.edu
OI David, Sean/0000-0002-4922-2603; Munafo, Marcus/0000-0002-4049-993X
FU NIH [DA025041, HL32318, CA84719, DA08511, DA14276, DA27331]; NIDA-IRP
FX This research was supported by NIH grants DA025041 (AML), HL32318 and
CA84719 (RN), DA08511 (RAB), DA14276 and DA27331 (SPD) and NIDA-IRP.
NR 43
TC 15
Z9 15
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1470-269X
J9 PHARMACOGENOMICS J
JI Pharmacogenomics J.
PD FEB
PY 2012
VL 12
IS 1
BP 86
EP 92
DI 10.1038/tpj.2010.64
PG 7
WC Genetics & Heredity; Pharmacology & Pharmacy
SC Genetics & Heredity; Pharmacology & Pharmacy
GA 884PE
UT WOS:000299719200010
PM 20661272
ER
PT J
AU Miller, CM
Rindflesch, TC
Fiszman, M
Hristovski, D
Shin, D
Rosemblat, G
Zhang, H
Strohl, KP
AF Miller, Christopher M.
Rindflesch, Thomas C.
Fiszman, Marcelo
Hristovski, Dimitar
Shin, Dongwook
Rosemblat, Graciela
Zhang, Han
Strohl, Kingman P.
TI A Closed Literature-Based Discovery Technique Finds a Mechanistic Link
Between Hypogonadism and Diminished Sleep Quality in Aging Men
SO SLEEP
LA English
DT Article
DE Information technology; literature-based discovery; testosterone;
cortisol; sleep; men
ID PITUITARY-ADRENAL AXIS; OLDER MEN; TESTOSTERONE LEVELS; HEALTHY-MEN;
PLASMA TESTOSTERONE; CORTISOL SECRETION; CIRCADIAN-RHYTHM; SEX; HORMONE;
ASSOCIATION
AB Study Objectives: Sleep quality commonly diminishes with age, and, further, aging men often exhibit a wider range of sleep pathologies than women. We used a freely available, web-based discovery technique (Semantic MEDLINE) supported by semantic relationships to automatically extract information from MEDLINE titles and abstracts.
Design: We assumed that testosterone is associated with sleep (the A-C relationship in the paradigm) and looked for a mechanism to explain this association (B explanatory link) as a potential or partial mechanism underpinning the etiology of eroded sleep quality in aging men.
Measurements and Results: Review of full-text papers in critical nodes discovered in this manner resulted in the proposal that testosterone enhances sleep by inhibiting cortisol. Using this discovery method, we posit, and could confirm as a novel hypothesis, cortisol as part of a mechanistic link elucidating the observed correlation between decreased testosterone in aging men and diminished sleep quality.
Conclusions: This approach is publically available and useful not only in this manner but also to generate from the literature alternative explanatory models for observed experimental results.
C1 [Miller, Christopher M.] NIH, Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Cognit Sci Branch, Bethesda, MD 20894 USA.
[Strohl, Kingman P.] Louis Stokes Cleveland DVA Med Ctr, Case Sch Med, Div Pulm Crit Care & Sleep Med, Cleveland, OH USA.
[Strohl, Kingman P.] Univ Ljubljana Fac Med, Inst Biomed Informat, Ljubljana, Slovenia.
[Zhang, Han] China Med Univ, Dept Med Informat, Shenyang, Peoples R China.
RP Miller, CM (reprint author), NIH, Natl Lib Med, Lister Hill Natl Ctr Biomed Commun, Cognit Sci Branch, Bldg 38A,Rm B1N-28C,MSC 3841, Bethesda, MD 20894 USA.
EM millercm@mail.nih.gov
OI Hristovski, Dimitar/0000-0001-6908-0246
FU National Institutes of Health, National Library of Medicine
FX This study was supported in part by the Intramural Research Program of
the National Institutes of Health, National Library of Medicine. The
seventh author was supported by an appointment to the National Library
of Medicine Research Participation Program administered by the Oak Ridge
Institute for Science and Education through an inter-agency agreement
between the U. S. Department of Energy and the National Library of
Medicine. For access to Semantic MEDLINE, send email to
trindflesch@mail.nih.gov. Research carried out at National Institutes of
Health, National Library of Medicine, Lister Hill National Center for
Biomedical Communications, Bethesda, MD 20894.
NR 60
TC 16
Z9 17
U1 0
U2 2
PU AMER ACAD SLEEP MEDICINE
PI WESTCHESTER
PA ONE WESTBROOK CORPORATE CTR, STE 920, WESTCHESTER, IL 60154 USA
SN 0161-8105
J9 SLEEP
JI Sleep
PD FEB 1
PY 2012
VL 35
IS 2
BP 279
EP 285
DI 10.5665/sleep.1640
PG 7
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 885LF
UT WOS:000299779800016
PM 22294819
ER
PT J
AU Matthews, CE
George, SM
Moore, SC
Bowles, HR
Blair, A
Park, Y
Troiano, RP
Hollenbeck, A
Schatzkin, A
AF Matthews, Charles E.
George, Stephanie M.
Moore, Steven C.
Bowles, Heather R.
Blair, Aaron
Park, Yikyung
Troiano, Richard P.
Hollenbeck, Albert
Schatzkin, Arthur
TI Amount of time spent in sedentary behaviors and cause-specific mortality
in US adults
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID TELEVISION VIEWING TIME; CARDIOVASCULAR-DISEASE MORTALITY;
PHYSICAL-ACTIVITY; PLASMA-GLUCOSE; UNITED-STATES; LEISURE-TIME;
SITTING-TIME; OLDER-ADULTS; ALL-CAUSE; WOMEN
AB Background: Sedentary behaviors predominate modern life, yet we do not fully understand the adverse effects of these behaviors on mortality after considering the benefits of moderate-vigorous physical activity (MVPA).
Objective: We tested the hypotheses that higher amounts of overall sitting time and television viewing are positively associated with mortality and described the independent and combined effects of these sedentary behaviors and MVPA on mortality.
Design: In the NIH-AARP Diet and Health Study, we examined 240,819 adults (aged 50-71 y) who did not report any cancer, cardiovascular disease, or respiratory disease at baseline. Mortality was ascertained over 8.5 y.
Results: Sedentary behaviors were positively associated with mortality after adjustment for age, sex, education, smoking, diet, race, and MVPA. Participants who reported the most television viewing (>= 7 h compared with <1 h/d) were at greater risk of all-cause (HR: 1.61; 95% CI: 1.47, 1.76), cardiovascular (HR: 1.85; 95% CI: 1.56, 2.20), and cancer (HR: 1.22; 95% CI: 1.06, 1.40) mortality after adjustment for MVPA. Overall sitting was associated with all-cause mortality. Even among adults reporting high levels of MVPA (>7 h/wk), high amounts of television viewing (>= 7 h/d) remained associated with increased risk of all-cause (HR: 1.47; 95% CI: 1.20, 1.79) and cardiovascular (HR: 2.00; 95% CI: 1.33, 3.00) mortality compared with those reporting the least television viewing (<1 h/d).
Conclusions: Time spent in sedentary behaviors was positively associated with mortality, and participation in high levels of MVPA did not fully mitigate health risks associated with prolonged time watching television. Adults should be encouraged to reduce time spent in sedentary behaviors, when possible, and to participate in MVPA at recommended levels. The NIH-AARP Diet and Health Study was registered at clinicaltrials.gov as NCT00340015. Ant J Clin Nutr 2012;95:437-45.
C1 [Matthews, Charles E.; George, Stephanie M.; Moore, Steven C.; Park, Yikyung; Schatzkin, Arthur] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Blair, Aaron] NCI, Occupat Epidemiol Branch, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Bowles, Heather R.; Troiano, Richard P.] NCI, Risk Factor Monitoring & Methods Branch, Div Canc Control & Populat Sci, Rockville, MD USA.
[Hollenbeck, Albert] AARP, Washington, DC USA.
RP Matthews, CE (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 3028, Bethesda, MD 20892 USA.
EM charles.matthews2@nih.gov
RI matthews, Charles/E-8073-2015; Moore, Steven/D-8760-2016;
OI matthews, Charles/0000-0001-8037-3103; Moore,
Steven/0000-0002-8169-1661; Troiano, Richard/0000-0002-6807-989X; Park,
Yikyung/0000-0002-6281-489X
FU NIH, National Cancer Institute
FX Supported in part by the Intramural Research Program of the NIH,
National Cancer Institute.
NR 37
TC 212
Z9 216
U1 3
U2 55
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD FEB
PY 2012
VL 95
IS 2
BP 437
EP 445
DI 10.3945/ajcn.111.019620
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 883QC
UT WOS:000299647800023
PM 22218159
ER
PT J
AU Bowers, K
Tobias, DK
Yeung, E
Hu, FB
Zhang, CL
AF Bowers, Katherine
Tobias, Deirdre K.
Yeung, Edwina
Hu, Frank B.
Zhang, Cuilin
TI A prospective study of prepregnancy dietary fat intake and risk of
gestational diabetes
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID GLUCOSE-TOLERANCE; CHOLESTEROL INTAKE; BETA-CELL; MELLITUS; WOMEN;
PREGNANCY; HYPERGLYCEMIA
AB Background: Fatty acids play a vital role in glucose homeostasis; however, studies on habitual dietary fat intakes and gestational diabetes mellitus (GDM) risk are limited and provide conflicting findings.
Objective: We determined whether the total amount and the type and source of prepregnancy dietary fats are related to risk of GDM.
Design: A prospective study was conducted in 13,475 women who reported a singleton pregnancy between 1991 and 2001 in the Nurses' Health Study II. In these women, 860 incident GDM cases were reported. The adjusted RR of GDM was estimated for quintiles of total fat, specific fat, and the source of fat intakes by pooled logistic regression.
Results: Higher animal fat and cholesterol intakes were significantly associated with increased GDM risk. Across increasing quintiles of animal fat, RRs (95% CIs) for GDM were 1.00 (reference), 1.55 (1.20, 1.98), 1.43 (1.09, 1.88), 1.40 (1.04, 1.89), and 1.88 (1.36, 2.60) (P-trend = 0.05). Corresponding RRs (95% CIs) for dietary cholesterol were 1.00 (reference), 1.08 (0.84, 1.32), 1.02 (0.78, 1.29), 1.20 (0.93, 1.55), and 1.45 (1.11, 1.89) (P-trend = 0.04). The substitution of 5% of energy from animal fat for an equal percentage of energy from carbohydrates was associated with significantly increased risk of GDM [RR (95% CI): 1.13 (1.08, 1.18); P < 0.0001]. No significant associations were observed between dietary polyunsaturated fat, monounsaturated fat, or trans fat intakes and GDM risk.
Conclusion: Higher prepregnancy intakes of animal fat and cholesterol were associated with elevated GDM risk. Am J Clin Nutr 2012;95:446-53.
C1 [Bowers, Katherine; Yeung, Edwina; Zhang, Cuilin] Eunice Kennedy Shrive Natl Inst Child Hlth & Huma, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD USA.
[Tobias, Deirdre K.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Tobias, Deirdre K.; Hu, Frank B.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hu, Frank B.] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.
[Hu, Frank B.] Harvard Univ, Sch Med, Boston, MA USA.
RP Zhang, CL (reprint author), Eunice Kennedy Shrive Natl Inst Child Hlth & Huma, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, 6100 Execut Blvd,Room 7B03, Rockville, MD 20852 USA.
EM bowerska2@mail.nih.gov; zhangcu@mail.nih.gov
RI Yeung, Edwina/F-5992-2015; Bowers, Katherine/N-5226-2015
OI Yeung, Edwina/0000-0002-3851-2613;
FU NIH [CA50385, DK58845]; Eunice Kennedy Shriver National Institute of
Child Health and Human Development, NIH
FX Supported by research grants CA50385 and DK58845 from the NIH and the
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, NIH (KB, CZ, and EY).
NR 34
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Z9 30
U1 0
U2 8
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD FEB
PY 2012
VL 95
IS 2
BP 446
EP 453
DI 10.3945/ajcn.111.026294
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 883QC
UT WOS:000299647800024
PM 22218158
ER
PT J
AU Schliep, KC
Schisterman, EF
Mumford, SL
Pollack, AZ
Zhang, CL
Ye, AJ
Stanford, JB
Hammoud, AO
Porucznik, CA
Wactawski-Wende, J
AF Schliep, Karen C.
Schisterman, Enrique F.
Mumford, Sunni L.
Pollack, Anna Z.
Zhang, Cuilin
Ye, Aijun
Stanford, Joseph B.
Hammoud, Ahmad O.
Porucznik, Christina A.
Wactawski-Wende, Jean
TI Caffeinated beverage intake and reproductive hormones among
premenopausal women in the BioCycle Study
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID FOOD FREQUENCY QUESTIONNAIRE; MARGINAL STRUCTURAL MODELS; EPITHELIAL
OVARIAN-CANCER; MENSTRUAL-CYCLE; GENETIC POLYMORPHISMS; PERIMENOPAUSAL
WOMEN; BINDING GLOBULIN; CYP1A2 GENOTYPE; ESTROGEN-LEVELS; BREAST-CANCER
AB Background: Caffeinated beverages are widely consumed among women of reproductive age, but their association with reproductive hormones, and whether race modifies any such associations, is not well understood.
Objective: We assessed the relation between caffeine and caffeinated beverage intake and reproductive hormones in healthy premenopausal women and evaluated the potential effect modification by race.
Design: Participants (n = 259) were followed for up to 2 menstrual cycles and provided fasting blood specimens for hormonal assessment at up to 8 visits per cycle and four 24-h dietary recalls per cycle. Weighted linear mixed models and nonlinear mixed models with harmonic terms were used to estimate associations between caffeine and hormone concentrations, adjusted for age, adiposity, physical activity, energy and alcohol intakes, and perceived stress. On the basis of a priori assumptions, an interaction between race and caffeine was tested, and stratified results are presented.
Results: Caffeine intake >= 200 mg/d was inversely associated with free estradiol concentrations among white women (beta = -0.15; 95% CI: -0.26, -0.05) and positively associated among Asian women (beta = 0.61; 95% CI: 0.31, 0.92). Caffeinated soda intake and green tea intake >= 1 cup/d (1 cup = 240 mL) were positively associated with free estradiol concentrations among all races: beta = 0.14 (95% CI: 0.06, 0.22) and beta = 0.26 (95% CI: 0.07, 0.45), respectively.
Conclusions: Moderate consumption of caffeine was associated with reduced estradiol concentrations among white women, whereas caffeinated soda and green tea intakes were associated with increased estradiol concentrations among all races. Further research is warranted on the association between caffeine and caffeinated beverages and reproductive hormones and whether these relations differ by race. Am J Clin Nutr 2012;95:488-97.
C1 [Schisterman, Enrique F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, Rockville, MD 20852 USA.
[Schliep, Karen C.; Stanford, Joseph B.; Porucznik, Christina A.] Univ Utah, Dept Family & Prevent Med, Salt Lake City, UT USA.
[Hammoud, Ahmad O.] Univ Utah, Dept Obstet & Gynecol, Salt Lake City, UT USA.
[Wactawski-Wende, Jean] SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA.
RP Schisterman, EF (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Epidemiol Branch, Div Epidemiol Stat & Prevent Res, 6100 Execut Blvd,7B03M, Rockville, MD 20852 USA.
EM schistee@mail.nih.gov
OI Pollack, Anna/0000-0002-4313-3298; Schisterman,
Enrique/0000-0003-3757-641X
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, NIH
FX Supported by the Intramural Research Program of the Eunice Kennedy
Shriver National Institute of Child Health and Human Development, NIH.
NR 59
TC 15
Z9 15
U1 1
U2 11
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 2012
VL 95
IS 2
BP 488
EP 497
DI 10.3945/ajcn.111.021287
PG 10
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 883QC
UT WOS:000299647800029
PM 22237060
ER
PT J
AU Tembhare, P
Yuan, CM
Morris, JC
Janik, JE
Filie, AC
Stetler-Stevenson, M
AF Tembhare, Prashant
Yuan, Constance M.
Morris, John C.
Janik, John E.
Filie, Armando C.
Stetler-Stevenson, Maryalice
TI Flow Cytometric Immunophenotypic Assessment of T-Cell Clonality by
V-beta Repertoire Analysis in Fine-Needle Aspirates and Cerebrospinal
Fluid
SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY
LA English
DT Article
DE T-cell clonality; Flow cytometry; V-beta repertoire; Cerebrospinal
fluid; Fine-needle aspirate
ID LEPTOMENINGEAL DISEASE; RECURRENT LYMPHOMA; DIAGNOSIS;
LEUKEMIA/LYMPHOMA; CYTOMORPHOLOGY; CLASSIFICATION; INVOLVEMENT;
NEOPLASMS; SPECIMENS; THERAPY
AB Flow cytometric T-cell receptor V-beta repertoire analysis (TCR-V-beta-R) is a sensitive method to detect T-cell clonality; however, its implementation in low-cellularity specimens has not been established. We developed a strategy to use TCR-V-beta-R in cerebrospinal fluid (CSF) and fine-needle aspirate (FNA) specimens. Initially, full TCR-V-beta-R was evaluated in diagnostic/screening specimens from 8 patients with T-cell neoplasia to determine tumor-specific TCR-V-beta protein expression. Subsequently, an abbreviated, patient-specific TCR-V-beta-R evaluation was performed in 17 paucicellular specimens from the patients (8 CSF, 9 FNA) for staging and monitoring of minimal residual disease (MRD). A single cocktail containing 3 anti-V-beta antibodies (1 tumor-specific and 2 negative controls) in combination with other antibodies chosen to help gate on atypical T cells is highly sensitive and specific for detecting low-level neoplastic T-cell involvement in paucicellular specimens. This TCR-V-beta-R strategy is valuable in staging and evaluating MRD in patients with T-cell non-Hodgkin lymphoma.
C1 [Tembhare, Prashant; Yuan, Constance M.; Stetler-Stevenson, Maryalice] NCI, Flow Cytometry Unit, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Filie, Armando C.] NCI, Cytopathol Sect, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Morris, John C.; Janik, John E.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Stetler-Stevenson, M (reprint author), NCI, Flow Cytometry Unit, Pathol Lab, NIH, Bldg 10,Room 2A-33,Mail Stop 1500, Bethesda, MD 20892 USA.
FU National Cancer Institute, National Institutes of Health, Bethesda, MD
FX Supported by the Intramural Research Program of the National Cancer
Institute, National Institutes of Health, Bethesda, MD.
NR 25
TC 11
Z9 11
U1 0
U2 0
PU AMER SOC CLINICAL PATHOLOGY
PI CHICAGO
PA 2100 W HARRISON ST, CHICAGO, IL 60612 USA
SN 0002-9173
J9 AM J CLIN PATHOL
JI Am. J. Clin. Pathol.
PD FEB
PY 2012
VL 137
IS 2
BP 220
EP 226
DI 10.1309/AJCPPT93VZMAREHK
PG 7
WC Pathology
SC Pathology
GA 881KZ
UT WOS:000299484900008
PM 22261447
ER
PT J
AU Boghossian, NS
Horbar, JD
Murray, JC
Carpenter, JH
AF Boghossian, Nansi S.
Horbar, Jeffrey D.
Murray, Jeffrey C.
Carpenter, Joseph H.
CA Vermont Oxford Network
TI Anthropometric charts for infants with trisomies 21, 18, or 13 born
between 22 weeks gestation and term: The VON charts
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE trisomy 21; trisomy 18; trisomy 13; Down syndrome; Edward syndrome;
Patau syndrome; autosomal trisomies; growth curves; neonatal
anthropometric charts; intrauterine growth; weight for gestational age;
head circumference for gestational age
ID BIRTH-WEIGHT; DOWNS-SYNDROME; INTRAUTERINE GROWTH; HEAD CIRCUMFERENCE;
AGE; CHILDREN; MORTALITY; FETUSES; PREVALENCE; CURVES
AB Data on birth weight for gestational age (GA) are not well described for infants with trisomy 21 (T21), trisomy 18 (T18), or trisomy 13 (T13). We report on anthropometric charts of infants with these conditions using data from the Vermont Oxford Network (VON). Data from a total of 5,147 infants with T21 aged 2241 weeks, 1,053 infants with T18 aged 2241 weeks, and 613 infants with T13 aged 2240 weeks were used to create birth weight for GA charts. Head circumference for GA charts were created for infants with T21 only. Combined-sex charts were generated for infants with T18 or T13 while sex-specific charts were generated for infants with T21. Smoothed centiles were created using LmsChartMaker Pro 2.3. Among the three examined groups, infants with T18 were the most likely to be growth restricted while infants with T21 were the least likely to be growth restricted. The new charts for infants with T21 were also compared to the Lubchenco and Fenton charts and both show frequent misclassification of infants with T21 as small or large for GA. The new charts should prove to be useful, especially for infants with T21, to assist in medical management and guide nutrition care decisions. (C) 2012 Wiley Periodicals, Inc.
C1 [Boghossian, Nansi S.; Murray, Jeffrey C.] Univ Iowa, Dept Pediat, Iowa City, IA 52242 USA.
[Horbar, Jeffrey D.; Carpenter, Joseph H.; Vermont Oxford Network] Vermont Oxford Network, Burlington, VT USA.
[Horbar, Jeffrey D.] Univ Vermont, Dept Pediat, Burlington, VT USA.
RP Boghossian, NS (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Div Epidemiol Stat & Prevent Res, Epidemiol Branch, 6100 Execut Blvd,Room 7B03C, Bethesda, MD 20892 USA.
EM nansi.boghossian@nih.gov
FU Vermont Oxford Network
FX Conflict of interest: Dr. Horbar is the Chief Executive and Scientific
Officer of the Vermont Oxford Network. Mr. Carpenter is the Director of
Operations and Statistics at the Vermont Oxford Network. Both receive
salary from the Vermont Oxford Network. None of the authors have
disclosures to report.
NR 31
TC 8
Z9 8
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD FEB
PY 2012
VL 158A
IS 2
BP 322
EP 332
DI 10.1002/ajmg.a.34423
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 879LY
UT WOS:000299331900008
PM 22246859
ER
PT J
AU Friedman, A
Robbins, E
Wendler, D
AF Friedman, Alexander
Robbins, Emily
Wendler, David
TI WHICH BENEFITS OF RESEARCH PARTICIPATION COUNT AS 'DIRECT'?
SO BIOETHICS
LA English
DT Article
DE direct benefits; fallacy of the package deal; informed consent;
vulnerable subjects
AB It is widely held that individuals who are unable to provide informed consent should be enrolled in clinical research only when the risks are low, or the research offers them the prospect of direct benefit. There is now a rich literature on when the risks of clinical research are low enough to enroll individuals who cannot consent. Much less attention has focused on which benefits of research participation count as direct, and the few existing accounts disagree over how this crucial concept should be defined. This disagreement raises concern over whether those who cannot consent, including children and adults with severe dementia, are being adequately protected. The present paper attempts to address this concern by considering first what additional protections are needed for these vulnerable individuals. This analysis suggests that the extant definitions of direct benefits either provide insufficient protection for research subjects or pose excessive obstacles to appropriate research. This analysis also points to a modified definition of direct benefits with the potential to avoid these two extremes, protecting individuals who cannot consent without blocking appropriate research.
C1 [Wendler, David] NIH, Ctr Clin, Dept Bioeth, Bethesda, MD 20892 USA.
RP Wendler, D (reprint author), NIH, Ctr Clin, Dept Bioeth, Bldg 10,Room 1C118, Bethesda, MD 20892 USA.
EM dwendler@nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 20
TC 9
Z9 9
U1 2
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0269-9702
J9 BIOETHICS
JI Bioethics
PD FEB
PY 2012
VL 26
IS 2
BP 60
EP 67
DI 10.1111/j.1467-8519.2010.01825.x
PG 8
WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical
SC Social Sciences - Other Topics; Medical Ethics; Social Issues;
Biomedical Social Sciences
GA 878JG
UT WOS:000299252300002
PM 20497168
ER
PT J
AU Sun, W
Liu, KL
Ryu, H
Kang, DW
Kim, YS
Kim, MS
Cho, Y
Bhondwe, RS
Thorat, SA
Kim, HS
Pearce, LV
Pavlyukovets, VA
Tran, R
Morgan, MA
Lazar, J
Ryder, CB
Toth, A
Blumberg, PM
Lee, J
AF Sun, Wei
Liu, Keliang
Ryu, HyungChul
Kang, Dong Wook
Kim, Yong Soo
Kim, Myeong Seop
Cho, Yongsung
Bhondwe, Rahul S.
Thorat, Shivaji A.
Kim, Ho Shin
Pearce, Larry V.
Pavlyukovets, Vladimir A.
Tran, Richard
Morgan, Matthew A.
Lazar, Jozsef
Ryder, Christopher B.
Toth, Attila
Blumberg, Peter M.
Lee, Jeewoo
TI 2-(4-Methylsulfonylaminophenyl) propanamide TRPV1 antagonists:
Structure-activity relationships in the B and C-regions
SO BIOORGANIC & MEDICINAL CHEMISTRY
LA English
DT Article
DE TRPV1 antagonists; Analgesic; Capsaicin; Resiniferatoxin
ID VANILLOID RECEPTOR; CAPSAICIN RECEPTORS; ANALOGS; POTENT; AGONISTS;
CHANNEL
AB On the basis of the previous lead N-4-t-butylbenzyl 2-(3-fluoro-4-methylsulfonylaminophenyl) propanamide (3) as a potent TRPV1 antagonist, structure-activity relationships for the B (propanamide part) and C-region (4-t-butylbenzyl part) have been investigated for rTRPV1 in CHO cells. The B-region was modified with dimethyl, cyclopropyl and reverse amides and then the C-region was replaced with 4-substituted phenyl, aryl alkyl and diaryl alkyl derivatives. Among them, compound 50 showed high binding affinity with K-i = 21.5 nM, which was twofold more potent than 3 and compound 54 exhibited potent antagonism with K-i(ant) = 8.0 nM comparable to 3. (C) 2011 Elsevier Ltd. All rights reserved.
C1 [Ryu, HyungChul; Kang, Dong Wook; Kim, Yong Soo; Kim, Myeong Seop; Cho, Yongsung; Bhondwe, Rahul S.; Thorat, Shivaji A.; Kim, Ho Shin; Lee, Jeewoo] Seoul Natl Univ, Med Chem Lab, Pharmaceut Sci Res Inst, Coll Pharm, Seoul 151742, South Korea.
[Sun, Wei; Liu, Keliang] Shenyang Pharmaceut Univ, Shenyang 110016, Liaoning, Peoples R China.
[Pearce, Larry V.; Pavlyukovets, Vladimir A.; Tran, Richard; Morgan, Matthew A.; Lazar, Jozsef; Ryder, Christopher B.; Toth, Attila; Blumberg, Peter M.] NCI, Lab Canc Biol & Genet, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Lee, J (reprint author), Seoul Natl Univ, Med Chem Lab, Pharmaceut Sci Res Inst, Coll Pharm, Seoul 151742, South Korea.
EM jeewoo@snu.ac.kr
RI Toth, Attila/F-4859-2010
OI Toth, Attila/0000-0001-6503-3653
FU National Research Foundation of Korea (NRF) [R11-2007-107-02001-0];
National Institutes of Health, Center for Cancer Research, National
Cancer Institute [Z1A BC 005270]
FX This research was supported by Research Funding from Digital-biotech,
Grants R11-2007-107-02001-0 from the National Research Foundation of
Korea (NRF), and the Intramural Research Program of the National
Institutes of Health, Center for Cancer Research, National Cancer
Institute (Z1A BC 005270). We thank multiple additional fellows for
technical assistance.
NR 21
TC 2
Z9 2
U1 0
U2 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0968-0896
J9 BIOORGAN MED CHEM
JI Bioorg. Med. Chem.
PD FEB 1
PY 2012
VL 20
IS 3
BP 1310
EP 1318
DI 10.1016/j.bmc.2011.12.014
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Chemistry,
Organic
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry
GA 882BE
UT WOS:000299535400017
PM 22227463
ER
PT J
AU Enewold, L
Zhou, J
McGlynn, KA
Anderson, WF
Shriver, CD
Potter, JF
Zahm, SH
Zhu, KM
AF Enewold, Lindsey
Zhou, Jing
McGlynn, Katherine A.
Anderson, William F.
Shriver, Craig D.
Potter, John F.
Zahm, Shelia H.
Zhu, Kangmin
TI Racial variation in breast cancer treatment among Department of Defense
beneficiaries
SO CANCER
LA English
DT Article
ID AFRICAN-AMERICAN PATIENTS; BLACK-AND-WHITE; DISPARITIES; CARE; WOMEN;
CARCINOMA; MORTALITY; OPPORTUNITIES; CHEMOTHERAPY; POPULATION
AB BACKGROUND: Although the overall age-adjusted incidence rates for female breast cancer are higher among whites than blacks, mortality rates are higher among blacks. Many attribute this discrepancy to disparities in health care access and to blacks presenting with later stage disease. Within the Department of Defense (DoD) Military Health System, all beneficiaries have equal access to health care. The aim of this study was to determine whether female breast cancer treatment varied between white and black patients in the DoD system. METHODS: The study data were drawn from the DoD cancer registry and medical claims databases. Study subjects included 2308 white and 391 black women diagnosed with breast cancer between 1998 and 2000. Multivariate logistic regression analyses that controlled for demographic factors, tumor characteristics, and comorbidities were used to assess racial differences in the receipt of surgery, chemotherapy, and hormonal therapy. RESULTS: There was no significant difference in surgery type, particularly when mastectomy was compared with breast-conserving surgery plus radiation (blacks vs whites: odds ratio [OR], 1.1; 95% confidence interval [CI], 0.8-1.5). Among those with local stage tumors, blacks were as likely as whites to receive chemotherapy (OR, 1.2; 95% CI, 0.9-1.7) and hormonal therapy (OR, 1.0; 95% CI, 0.6-1.4). Among those with regional stage tumors, blacks were significantly less likely than whites to receive chemotherapy (OR, 0.4; 95% CI, 0.2-0.7) and hormonal therapy (OR, 0.5; 95% CI, 0.3-0.8). CONCLUSIONS: Even within an equal access health care system, stage-related racial variations in breast cancer treatment are evident. Studies that identify driving factors behind these within-stage racial disparities are warranted. Cancer 2012; 118: 812-20. (C) 2011 American Cancer Society.
C1 [Enewold, Lindsey; Zhou, Jing; Shriver, Craig D.; Potter, John F.; Zhu, Kangmin] Walter Reed Army Med Ctr, US Mil Canc Inst, Washington, DC 20307 USA.
[McGlynn, Katherine A.; Anderson, William F.; Zahm, Shelia H.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Shriver, Craig D.] Walter Reed Army Med Ctr, Dept Surg, Div Surg Oncol, Washington, DC 20307 USA.
[Potter, John F.; Zhu, Kangmin] Uniformed Serv Univ Hlth Sci, Bethesda, MD USA.
RP Enewold, L (reprint author), Walter Reed Army Med Ctr, US Mil Canc Inst, Bldg 1,Suite E-111,6900 Georgia Ave, Washington, DC 20307 USA.
EM Lindsey.Enewold@us.army.mil
RI Zahm, Shelia/B-5025-2015
FU United States Military Cancer Institute (USMCI) via the Uniformed
Services University of the Health Sciences under the auspices of the
Henry M. Jackson Foundation for the Advancement of Military Medicine;
Walter Reed Army Medical Center; Division of Cancer Epidemiology and
Genetics (DCEG), National Cancer Institute, National Institutes of
Health
FX Supported by the United States Military Cancer Institute (USMCI) via the
Uniformed Services University of the Health Sciences under the auspices
of the Henry M. Jackson Foundation for the Advancement of Military
Medicine; the Clinical Breast Care Project, Walter Reed Army Medical
Center; and the Intramural Research Program of the Division of Cancer
Epidemiology and Genetics (DCEG), National Cancer Institute, National
Institutes of Health. The original data linkage was supported by the
USMCI and DCEG.
NR 29
TC 12
Z9 12
U1 0
U2 1
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 2012
VL 118
IS 3
BP 812
EP 820
DI 10.1002/cncr.26346
PG 9
WC Oncology
SC Oncology
GA 879NB
UT WOS:000299335500027
PM 21766298
ER
PT J
AU Zhao, XZ
Maddali, K
Metifiot, M
Smith, SJ
Vu, BC
Marchand, C
Hughes, SH
Pommier, Y
Burke, TR
AF Zhao, Xue Zhi
Maddali, Kasthuraiah
Metifiot, Mathieu
Smith, Steven J.
Vu, B. Christie
Marchand, Christophe
Hughes, Stephen H.
Pommier, Yves
Burke, Terrence R., Jr.
TI Bicyclic Hydroxy-1H-pyrrolopyridine-trione Containing HIV-1 Integrase
Inhibitors
SO CHEMICAL BIOLOGY & DRUG DESIGN
LA English
DT Article
DE drug discovery; mechanism-based drug design; nonpeptide
ID DEPROTONATION-CYCLOADDITION CASCADE; RALTEGRAVIR; RESISTANCE; DISCOVERY;
INFECTION; POTENT; IMIDOSULFOXIDES; ELVITEGRAVIR
AB HIV-1 integrase (IN) is a validated therapeutic target for the treatment of AIDS. However, the emergence of resistance to raltegravir, the sole marketed FDA-approved IN inhibitor, emphasizes the need to develop second-generation inhibitors that retain efficacy against clinically relevant IN mutants. We report herein bicyclic hydroxy-1H-pyrrolopyridine-triones as a new family of HIV-1 integrase inhibitors that were efficiently prepared using a key Pummerer cyclization deprotonation cycloaddition cascade of imidosulfoxides. In in vitro HIV-1 integrase assays, the analogs showed low micromolar inhibitory potencies with selectivity for strand transfer reactions as compared with 3'-processing inhibition. A representative inhibitor (5e) retained most of its inhibitory potency against the three major raltegravir-resistant IN mutant enzymes, G140S/Q148H, Y143R, and N155H. In antiviral assays employing viral vectors coding these IN mutants, compound 5e was approximately 200- and 20-fold less affected than raltegravir against the G140S/Q148H and Y143R mutations, respectively. Against the N155H mutation, 5e was approximately 10-fold less affected than raltegravir. Thus, our new compounds represent a novel structural class that may be further developed to overcome resistance to raltegravir, particularly in the case of the G140S/Q148H mutations.
C1 [Zhao, Xue Zhi; Burke, Terrence R., Jr.] NCI, Chem Biol Lab, Mol Discovery Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
[Maddali, Kasthuraiah; Metifiot, Mathieu; Marchand, Christophe; Pommier, Yves] NCI, Lab Mol Pharmacol, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
[Smith, Steven J.; Vu, B. Christie; Hughes, Stephen H.] NCI, HIV Drug Resistance Program, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Zhao, XZ (reprint author), NCI, Chem Biol Lab, Mol Discovery Program, Ctr Canc Res,NIH, Frederick, MD 21702 USA.
EM xuezhi.zhao@nih.gov; tburke@helix.nih.gov
RI Zhao, Xue Zhi/N-9594-2014; Burke, Terrence/N-2601-2014
OI Zhao, Xue Zhi/0000-0003-1006-6364;
FU NIH, Center for Cancer Research, NCI-Frederick; National Cancer
Institute, National Institutes of Health; Joint Science and Technology
Office of the Department of Defense
FX This work was supported in part by the Intramural Research Program of
the NIH, Center for Cancer Research, NCI-Frederick and the National
Cancer Institute, National Institutes of Health and the Joint Science
and Technology Office of the Department of Defense. 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 26
TC 10
Z9 11
U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1747-0277
J9 CHEM BIOL DRUG DES
JI Chem. Biol. Drug Des.
PD FEB
PY 2012
VL 79
IS 2
BP 157
EP 165
DI 10.1111/j.1747-0285.2011.01270.x
PG 9
WC Biochemistry & Molecular Biology; Chemistry, Medicinal
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 872WP
UT WOS:000298841400002
PM 22107736
ER
PT J
AU Vandenberg, LN
Chahoud, I
Heindel, JJ
Padmanabhan, V
Paumgartten, FJR
Schoenfelder, G
AF Vandenberg, Laura N.
Chahoud, Ibrahim
Heindel, Jerrold J.
Padmanabhan, Vasantha
Paumgartten, Francisco J. R.
Schoenfelder, Gilbert
TI Urinary, Circulating, and Tissue Biomonitoring Studies Indicate
Widespread Exposure to Bisphenol A
SO CIENCIA & SAUDE COLETIVA
LA English
DT Review
DE Endocrine disruptor; Human exposure; PBPK/PBTK model; Pregnancy; Risk
assessment; Toxicokinetics
ID PERFORMANCE LIQUID-CHROMATOGRAPHY; SOLID-PHASE EXTRACTION; TANDEM
MASS-SPECTROMETRY; HPLC-MS/MS METHOD; ENVIRONMENTAL PHENOLS;
ESTROGEN-RECEPTOR; ADIPOSE-TISSUE; HUMAN SERUM; FLUORESCENCE DETECTION;
DISRUPTING CHEMICALS
AB Bisphenol A (BPA) is one of the highest-volume chemicals produced worldwide, and human exposure to BPA is thought to be ubiquitous. Thus, there are concerns that the amount of BPA to which humans are exposed may cause adverse health effects. We examined many possibilities for why biomonitoring and toxicokinetic studies could come to seemingly conflicting conclusions. More than 80 published human biomonitoring studies that measured BPA concentrations in human tissues, urine, blood, and other fluids, along with two toxicokinetic studies of human BPA metabolism were examined. Unconjugated BPA was routinely detected in blood (in the nanograms per milliliter range), and conjugated BPA was routinely detected in the vast majority of urine samples (also in the nanograms per milliliter range). In stark contrast, toxicokinetic studies proposed that humans are not internally exposed to BPA. Available data from biomonitoring studies clearly indicate that the general population is exposed to BPA and is at risk from internal exposure to unconjugated BPA. The two toxicokinetic studies that suggested human BPA exposure is negligible have significant deficiencies, are directly contradicted by hypothesis-driven studies, and are therefore not reliable for risk assessment purposes.
C1 [Vandenberg, Laura N.] Tufts Univ, Dept Biol, Tufts Ctr Regenerat & Dev Biol, Medford, MA 02155 USA.
[Chahoud, Ibrahim] Charite, Inst Klin Pharmakol & Toxikol, D-13353 Berlin, Germany.
[Heindel, Jerrold J.] Natl Inst Environm Hlth Sci, Div Extramural Res & Training, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC USA.
[Padmanabhan, Vasantha] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA.
[Paumgartten, Francisco J. R.] Fundacao Oswaldo Cruz, Natl Sch Publ Hlth, Lab Environm Toxicol, Rio De Janeiro, Brazil.
[Schoenfelder, Gilbert] Univ Wurzburg, Inst Pharmacol & Toxicol, Wurzburg, Germany.
RP Vandenberg, LN (reprint author), Tufts Univ, Dept Biol, Tufts Ctr Regenerat & Dev Biol, 200 Boston Ave,Suite 4600, Medford, MA 02155 USA.
EM laura.vandenberg@tufts.edu
RI Padmanabhan, Vasantha/C-8558-2017;
OI Padmanabhan, Vasantha/0000-0002-8443-7212; Schonfelder,
Gilbert/0000-0001-6134-1990
NR 128
TC 57
Z9 58
U1 3
U2 56
PU ABRASCO
PI RIO DE JANEIRO
PA RUA HESPERIA, 16-PARTE MANGUINHOS, RIO DE JANEIRO, 21050-040, BRAZIL
SN 1413-8123
J9 CIENC SAUDE COLETIVA
JI Cienc. Saude Coletiva
PD FEB
PY 2012
VL 17
IS 2
BP 407
EP 434
PG 28
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 880CX
UT WOS:000299383400016
PM 22267036
ER
PT J
AU Wynn, JL
Tan, S
Gantz, MG
Das, A
Goldberg, RN
Adams-Chapman, I
Stoll, BJ
Shankaran, S
Walsh, MC
Auten, KJ
Miller, NA
Sanchez, PJ
Higgins, RD
Cotten, CM
Smith, PB
Benjamin, DK
AF Wynn, James L.
Tan, Sylvia
Gantz, Marie G.
Das, Abhik
Goldberg, Ronald N.
Adams-Chapman, Ira
Stoll, Barbara J.
Shankaran, Seetha
Walsh, Michele C.
Auten, Kathy J.
Miller, Nancy A.
Sanchez, Pablo J.
Higgins, Rosemary D.
Cotten, C. Michael
Smith, P. Brian
Benjamin, Daniel K., Jr.
CA NICHD Neonatal Res Network
TI Outcomes Following Candiduria in Extremely Low Birth Weight Infants
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID NEONATAL RESEARCH NETWORK; URINARY-TRACT-INFECTION; INTENSIVE-CARE-UNIT;
FUNGAL-INFECTION; PRETERM INFANTS; RISK-FACTORS; CANDIDIASIS; SEPSIS
AB Background. Candidiasis carries a significant risk of death or neurodevelopmental impairment (NDI) in extremely low birth weight infants (ELBW; < 1000 g). We sought to determine the impact of candiduria in ELBW preterm infants.
Methods. Our study was a secondary analysis of the Neonatal Research Network study Early Diagnosis of Nosocomial Candidiasis. Follow-up assessments included Bayley Scales of Infant Development examinations at 18-22 months of corrected age. Risk factors were compared between groups using exact tests and general linear modeling. Death, NDI, and death or NDI were compared using generalized linear mixed modeling.
Results. Of 1515 infants enrolled, 34 (2.2%) had candiduria only. Candida was isolated from blood only (69 of 1515 [4.6%]), cerebrospinal fluid (CSF) only (2 of 1515 [0.1%]), other sterile site only (not urine, blood, or CSF; 4 of 1515 [0.3%]), or multiple sources (28 of 1515 [2%]). Eleven infants had the same Candida species isolated in blood and urine within 3 days; 3 (27%) had a positive urine culture result first. Most urine isolates were Candida albicans (21 of 34 [62%]) or Candida parapsilosis (7 of 34 [29%]). Rate of death or NDI was greater among those with candiduria (50%) than among those with suspected but not proven infection (32%; odds ratio, 2.5 [95% confidence interval, 1.2-5.3]) after adjustment. No difference in death and death or NDI was noted between infants with candiduria and those with candidemia.
Conclusions. These findings provide compelling evidence that ELBW infants with candiduria are at substantial risk of death or NDI. Candiduria in ELBW preterm infants should prompt a systemic evaluation (blood, CSF, and abdominal ultrasound) for disseminated Candida infection and warrants treatment.
C1 [Benjamin, Daniel K., Jr.] Duke Univ, Dept Pediat, Duke Clin Res Inst, Durham, NC 27715 USA.
[Tan, Sylvia; Gantz, Marie G.] RTI Int, Stat & Epidemiol Unit, Res Triangle Pk, NC USA.
[Das, Abhik] RTI Int, Stat & Epidemiol Unit, Rockville, MD USA.
[Adams-Chapman, Ira; Stoll, Barbara J.] Emory Univ, Dept Pediat, Atlanta, GA 30322 USA.
[Shankaran, Seetha] Wayne State Univ, Dept Pediat, Detroit, MI 48202 USA.
[Walsh, Michele C.] Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Dept Pediat, Cleveland, OH 44106 USA.
[Miller, Nancy A.; Sanchez, Pablo J.] Univ Texas SW Med Ctr Dallas, Dept Pediat, Dallas, TX 75390 USA.
[Higgins, Rosemary D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Benjamin, DK (reprint author), Duke Univ, Dept Pediat, Duke Clin Res Inst, 2400 Pratt St, Durham, NC 27715 USA.
EM danny.benjamin@duke.edu
RI Smith, Phillip/I-5565-2014
FU ASPE HHS [1R18AE000028-01]; NCATS NIH HHS [UL1 TR000454]; NCRR NIH HHS
[M01 RR007122, M01 RR008084, UL1 RR024139, UL1 RR024160, UL1 RR025008];
NICHD NIH HHS [U10 HD021364, 1K23HD060040-01, HD-044799-03, K23
HD044799, K23 HD060040, K24 HD058735, U10 HD021373, U10 HD021385, U10
HD021397, U10 HD027851, U10 HD027853, U10 HD027856, U10 HD027871, U10
HD027880, U10 HD027904, U10 HD034216, U10 HD036790, U10 HD040461, U10
HD040492, U10 HD040498, U10 HD040521, U10 HD040689, U10 HD053089, U10
HD053109, U10 HD053119, U10 HD40492]
NR 21
TC 14
Z9 14
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD FEB 1
PY 2012
VL 54
IS 3
BP 331
EP 339
DI 10.1093/cid/cir800
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 876SM
UT WOS:000299128000010
PM 22144537
ER
PT J
AU Besson, GJ
McMahon, D
Maldarelli, F
Mellors, JW
AF Besson, Guillaume J.
McMahon, Deborah
Maldarelli, Frank
Mellors, John W.
TI Short-Course Raltegravir Intensification Does Not Increase 2 Long
Terminal Repeat Episomal HIV-1 DNA in Patients on Effective
Antiretroviral Therapy
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Letter
ID VIREMIA
C1 [Besson, Guillaume J.; McMahon, Deborah; Mellors, John W.] Univ Pittsburgh, Div Infect Dis, Sch Med, Pittsburgh, PA 15261 USA.
[Maldarelli, Frank] NCI, Frederick, MD 21701 USA.
RP Mellors, JW (reprint author), Univ Pittsburgh, Div Infect Dis, Sch Med, 818 Scaife Hall,3550 Terrace St, Pittsburgh, PA 15261 USA.
EM jwm1@pitt.edu
FU PHS HHS [25XS119]
NR 7
TC 22
Z9 22
U1 1
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 1
PY 2012
VL 54
IS 3
BP 451
EP 453
DI 10.1093/cid/cir721
PG 3
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 876SM
UT WOS:000299128000032
PM 22016501
ER
PT J
AU Seam, N
Meduri, GU
Wang, HH
Nylen, ES
Sun, JF
Schultz, MJ
Tropea, M
Suffredini, AF
AF Seam, Nitin
Meduri, G. Umberto
Wang, Honghui
Nylen, Eric S.
Sun, Junfeng
Schultz, Marcus J.
Tropea, Margaret
Suffredini, Anthony F.
TI Effects of methylprednisolone infusion on markers of inflammation,
coagulation, and angiogenesis in early acute respiratory distress
syndrome
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE ARDS; coagulation; corticosteroids; inflammation; proadrenomedullin;
protein C
ID ACUTE LUNG INJURY; ACTIVATED PROTEIN-C; PERSISTENT ELEVATION;
CLINICAL-TRIAL; ARDS; SEPSIS; CORTICOSTEROIDS; BIOMARKERS; CYTOKINES;
PULMONARY
AB Objective: Evaluate the effects of methylprednisolone on markers of inflammation, coagulation, and angiogenesis during early acute respiratory distress syndrome.
Design: Retrospective analysis. Setting: Four intensive care units.
Subjects: Seventy-nine of 91 patients with available samples enrolled in a randomized, blinded controlled trial.
Interventions: Early methylprednisolone infusion (n = 55) compared with placebo (n = 24).
Measurements and Main Results: Interleukin-6, tumor necrosis factor alpha, vascular endothelial growth factor, protein C, procalcitonin, and proadrenomedullin were measured in archived plasma. Changes from baseline to day 3 and day 7 were compared between groups and in subgroups based on the precipitating cause of acute respiratory distress syndrome. Methylprednisolone therapy was associated with greater improvement in Lung Injury Score (p = .003), shorter duration of mechanical ventilation (p = .005), and lower intensive care unit mortality (p = .05) than control subjects. On days 3 and 7, methylprednisolone decreased interleukin-6 and increased protein C levels (all p < .0001) compared with control subjects. Proadrenomedullin levels were lower by day 3 with methylprednisolone treatment (p < .004). Methylprednisolone decreased interleukin-6 by days 3 and 7 in patients with pulmonary causes of acute respiratory distress syndrome but only at day 3 in those with extrapulmonary causes of acute respiratory distress syndrome. Protein C levels were increased with methylprednisolone on days 3 and 7 in patients with infectious and/or pulmonary causes of acute respiratory distress syndrome (all p < .0001) but not in patients with noninfectious or extrapulmonary causes of acute respiratory distress syndrome. Proadrenomedullin levels were decreased with methylprednisolone on day 3 in patients with infectious or extrapulmonary causes of acute respiratory distress syndrome (both p < .008) but not in noninfectious or pulmonary acute respiratory distress syndrome. Tumor necrosis factor, vascular endothelial growth factor, and procalcitonin were elevated but not differentially affected by methylprednisolone therapy.
Conclusions: In early acute respiratory distress syndrome, administration of methylprednisolone was associated with improvement in important biomarkers of inflammation and coagulation and clinical outcomes. Biomarker changes varied with the precipitating cause of acute respiratory distress syndrome, suggesting that the underlying mechanisms and response to anti-inflammatory therapy may vary with the cause of acute respiratory distress syndrome. (Crit Care Med 2012; 40: 495-501)
C1 [Seam, Nitin] Vet Affairs Med Ctr, Pulm Sect, Washington, DC 20422 USA.
[Meduri, G. Umberto] Univ Tennessee, Hlth Sci Ctr, Div Pulm Crit Care Med, Memphis, TN USA.
Memphis Vet Affairs Med Ctr, Memphis, TN USA.
[Seam, Nitin; Wang, Honghui; Sun, Junfeng; Tropea, Margaret; Suffredini, Anthony F.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Nylen, Eric S.] Vet Affairs Med Ctr, Endocrinol Sect, Washington, DC 20422 USA.
[Schultz, Marcus J.] Univ Amsterdam, Acad Med Ctr, Dept Intens Care Med, NL-1105 AZ Amsterdam, Netherlands.
RP Seam, N (reprint author), Vet Affairs Med Ctr, Pulm Sect, 50 Irving St NW, Washington, DC 20422 USA.
EM nitin.seam@va.gov
RI Schultz, Marcus/K-6147-2012
FU Critical Care Medicine Department of the National Institutes of Health;
National Institutes of Health
FX This research was supported by the Intramural Research Program of the
Critical Care Medicine Department of the National Institutes of Health.;
Dr. Seam, Mr. Wang, Mr. Sun, and Dr. Suffredini received funding from
the National Institutes of Health. The remaining authors have not
disclosed any potential conflicts of interest.
NR 37
TC 24
Z9 28
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD FEB
PY 2012
VL 40
IS 2
BP 495
EP 501
DI 10.1097/CCM.0b013e318232da5e
PG 7
WC Critical Care Medicine
SC General & Internal Medicine
GA 879EW
UT WOS:000299313500019
PM 21983371
ER
PT J
AU Needham, DM
Davidson, J
Cohen, H
Hopkins, RO
Weinert, C
Wunsch, H
Zawistowski, C
Bemis-Dougherty, A
Berney, SC
Bienvenu, OJ
Brady, SL
Brodsky, MB
Denehy, L
Elliott, D
Flatley, C
Harabin, AL
Jones, C
Louis, D
Meltzer, W
Muldoon, SR
Palmer, JB
Perme, C
Robinson, M
Schmidt, DM
Scruth, E
Spill, GR
Storey, CP
Render, M
Votto, J
Harvey, MA
AF Needham, Dale M.
Davidson, Judy
Cohen, Henry
Hopkins, Ramona O.
Weinert, Craig
Wunsch, Hannah
Zawistowski, Christine
Bemis-Dougherty, Anita
Berney, Susan C.
Bienvenu, O. Joseph
Brady, Susan L.
Brodsky, Martin B.
Denehy, Linda
Elliott, Doug
Flatley, Carl
Harabin, Andrea L.
Jones, Christina
Louis, Deborah
Meltzer, Wendy
Muldoon, Sean R.
Palmer, Jeffrey B.
Perme, Christiane
Robinson, Marla
Schmidt, David M.
Scruth, Elizabeth
Spill, Gayle R.
Storey, C. Porter
Render, Marta
Votto, John
Harvey, Maurene A.
TI Improving long-term outcomes after discharge from intensive care unit:
Report from a stakeholders' conference
SO CRITICAL CARE MEDICINE
LA English
DT Article
DE aftercare; caregivers; continuity of patient care; critical care;
follow-up studies; intensive care units; outcome assessment; patient
care planning; patient care team; postintensive care syndrome; stress
disorders, post-traumatic; survivors
ID RESPIRATORY-DISTRESS-SYNDROME; QUALITY-OF-LIFE;
POSTTRAUMATIC-STRESS-DISORDER; RANDOMIZED CONTROLLED-TRIAL; CRITICAL
ILLNESS; REHABILITATION PROGRAM; FUNCTIONAL DISABILITY; COGNITIVE
IMPAIRMENT; MOBILIZING PATIENTS; CRITICALLY-ILL
AB Background: Millions of patients are discharged from intensive care units annually. These intensive care survivors and their families frequently report a wide range of impairments in their health status which may last for months and years after hospital discharge.
Objectives: To report on a 2-day Society of Critical Care Medicine conference aimed at improving the long-term outcomes after critical illness for patients and their families.
Participants: Thirty-one invited stakeholders participated in the conference. Stakeholders represented key professional organizations and groups, predominantly from North America, which are involved in the care of intensive care survivors after hospital discharge.
Design: Invited experts and Society of Critical Care Medicine members presented a summary of existing data regarding the potential long-term physical, cognitive and mental health problems after intensive care and the results from studies of postintensive care unit interventions to address these problems. Stakeholders provided reactions, perspectives, concerns and strategies aimed at improving care and mitigating these long-term health problems.
Measurements and Main Results: Three major themes emerged from the conference regarding: (1) raising awareness and education, (2) understanding and addressing barriers to practice, and (3) identifying research gaps and resources. Postintensive care syndrome was agreed upon as the recommended term to describe new or worsening problems in physical, cognitive, or mental health status arising after a critical illness and persisting beyond acute care hospitalization. The term could be applied to either a survivor or family member.
Conclusions: Improving care for intensive care survivors and their families requires collaboration between practitioners and researchers in both the inpatient and outpatient settings. Strategies were developed to address the major themes arising from the conference to improve outcomes for survivors and families. (Crit Care Med 2012; 40: 502-509)
C1 [Needham, Dale M.] Johns Hopkins Univ, OACIS Grp, Baltimore, MD 21218 USA.
[Davidson, Judy] Scripps Mercy Hosp, San Diego, CA USA.
[Cohen, Henry] Kingsbrook Jewish Med Ctr, Woodmere, NY USA.
[Hopkins, Ramona O.] Brigham Young Univ, Intermt Med Ctr, Salt Lake City, UT USA.
Brigham Young Univ, Psychol & Neurosci Ctr, Salt Lake City, UT USA.
[Weinert, Craig] Univ Minnesota, Clin Outcomes Res Ctr, Minneapolis, MN USA.
[Wunsch, Hannah] Columbia Univ, New York, NY USA.
[Zawistowski, Christine] Mt Sinai Kravis Childrens Hosp, Brooklyn, NY USA.
[Bemis-Dougherty, Anita] Amer Phys Therapy Assoc, Dept Practice, Alexandria, VA USA.
[Berney, Susan C.] Austin Heath, Physiotherapy Dept, Melbourne, Vic, Australia.
[Brady, Susan L.] Marianjoy Rehabil Hosp, Roselle, IL USA.
[Denehy, Linda] Univ Melbourne, Melbourne Sch Hlth Sci, Melbourne, Vic, Australia.
[Elliott, Doug] Univ Technol Sydney, Fac Nursing, Sydney, NSW 2007, Australia.
[Flatley, Carl] Sepsis Alliance, Tampa, FL USA.
[Harabin, Andrea L.] NHLBI, Div Lung Dis, Bethesda, MD 20892 USA.
[Jones, Christina] Whiston Hosp, Prescot, England.
[Louis, Deborah] Kaiser Sunnyside Med Ctr, Clackamus, OR USA.
[Muldoon, Sean R.] Kindred Healthcare, Hosp Div, Louisville, KY USA.
[Meltzer, Wendy] Illinois Citizens Better Care, Chicago, IL USA.
[Perme, Christiane] Methodist Hosp, Houston, TX 77030 USA.
[Robinson, Marla] Univ Chicago, Med Ctr, Chicago, IL 60637 USA.
[Schmidt, David M.] Kaiser Sunnyside Med Ctr, Clackamus, OR USA.
[Scruth, Elizabeth] Kaiser Permanente, No Calif Qual Dept, San Jose, CA USA.
[Spill, Gayle R.] Rehabil Inst Chicago, Canc Rehabil Program, Chicago, IL 60611 USA.
[Storey, C. Porter] Amer Acad Hosp & Palliat Med, Boulder, CO USA.
Univ Cincinnati, Coll Med, Cincinnati, OH USA.
[Render, Marta] Vet Affairs Med Ctr, Inpatient Evaluat Ctr, Cincinnati, OH 45267 USA.
[Votto, John] Hosp Special Care, New Britain, CT USA.
[Harvey, Maurene A.] Soc Crit Care Med, Lake Tahoe, NV USA.
RP Needham, DM (reprint author), Johns Hopkins Univ, OACIS Grp, Baltimore, MD 21218 USA.
EM Dale.needham@jhmi.edu
OI Denehy, Linda/0000-0002-2926-8436; Elliott, Doug/0000-0002-6081-5442
FU National Institutes of Health
FX Dr. Needham has received grant support from the National Institutes of
Health. Dr. Bienvenu has received funding from the National Institutes
of Health. Ms. Louis is employed by Kaiser Permanente. Dr. Muldoon is
employed by and has stock ownership in Kindred Healthcare. The remaining
authors have not disclosed any potential conflicts of interest.
NR 76
TC 238
Z9 242
U1 2
U2 34
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD FEB
PY 2012
VL 40
IS 2
BP 502
EP 509
DI 10.1097/CCM.0b013e318232da75
PG 8
WC Critical Care Medicine
SC General & Internal Medicine
GA 879EW
UT WOS:000299313500020
PM 21946660
ER
PT J
AU O'Grady, NP
AF O'Grady, Naomi P.
TI Zero risk for central line-associated bloodstream infections ... is this
realistic?
SO CRITICAL CARE MEDICINE
LA English
DT Editorial Material
DE central venous catheters; elimination; prevention; risk
ID CRITICALLY-ILL PATIENTS; INTENSIVE-CARE; INTERVENTION; OUTCOMES
C1 NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
RP O'Grady, NP (reprint author), NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z99 CL999999]
NR 11
TC 5
Z9 5
U1 0
U2 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD FEB
PY 2012
VL 40
IS 2
BP 657
EP 658
DI 10.1097/CCM.0b013e3182372ba6
PG 2
WC Critical Care Medicine
SC General & Internal Medicine
GA 879EW
UT WOS:000299313500042
PM 22249034
ER
PT J
AU Souza, ACP
Yuen, PST
AF Souza, Ana C. P.
Yuen, Peter S. T.
TI How can antibiotics worsen acute kidney injury but improve survival in
experimental sepsis?
SO CRITICAL CARE MEDICINE
LA English
DT Editorial Material
ID SEPTIC SHOCK; ANTIMICROBIAL THERAPY; HYPOTENSION; INITIATION; DURATION;
OUTCOMES
C1 [Souza, Ana C. P.; Yuen, Peter S. T.] NIDDK, Renal Diagnost & Therapeut Unit, NIH, Bethesda, MD 20892 USA.
RP Souza, ACP (reprint author), NIDDK, Renal Diagnost & Therapeut Unit, NIH, Bethesda, MD 20892 USA.
RI Yuen, Peter/B-1954-2008
OI Yuen, Peter/0000-0001-9557-3909
FU Intramural NIH HHS [Z99 DK999999, ZIA DK043403-11]
NR 15
TC 2
Z9 2
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
J9 CRIT CARE MED
JI Crit. Care Med.
PD FEB
PY 2012
VL 40
IS 2
BP 685
EP 686
DI 10.1097/CCM.0b013e318236e162
PG 3
WC Critical Care Medicine
SC General & Internal Medicine
GA 879EW
UT WOS:000299313500061
PM 22249053
ER
PT J
AU Williams, M
Burdsal, C
Periasamy, A
Lewandoski, M
Sutherland, A
AF Williams, Margot
Burdsal, Carol
Periasamy, Ammasi
Lewandoski, Mark
Sutherland, Ann
TI Mouse primitive streak forms in situ by initiation of epithelial to
mesenchymal transition without migration of a cell population
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE primitive streak; epithelial to mesenchymal transition; gastrulation;
mouse embryo; morphogenesis
ID GASTRULATING RABBIT EMBRYO; ANTERIOR VISCERAL ENDODERM; NEURAL-TUBE
DEFECTS; EPIBLAST CELLS; MESODERM DIFFERENTIATION; CADHERIN EXPRESSION;
AVIAN GASTRULATION; MOVEMENT PATTERNS; PROGENITOR CELLS; CLONAL ANALYSIS
AB Background: During gastrulation, an embryo acquires the three primordial germ layers that will give rise to all of the tissues in the body. In amniote embryos, this process occurs via an epithelial to mesenchymal transition (EMT) of epiblast cells at the primitive streak. Although the primitive streak is vital to development, many aspects of how it forms and functions remain poorly understood. Results: Using live, 4 dimensional imaging and immunohistochemistry, we have shown that the posterior epiblast of the pre-streak murine embryo does not display convergence and extension behavior or large scale migration or rearrangement of a cell population. Instead, the primitive streak develops in situ and elongates by progressive initiation EMT in the posterior epiblast. Loss of basal lamina (BL) is the first step of this EMT, and is strictly correlated with ingression of nascent mesoderm. Once the BL is lost in a given region, cells leave the epiblast by apical constriction in order to enter the primitive streak. Conclusions: This is the first description of dynamic cell behavior during primitive streak formation in the mouse embryo, and reveals mechanisms that are quite distinct from those observed in other amniote model systems. Unlike chick and rabbit, the murine primitive streak arises in situ by progressive initiation of EMT beginning in the posterior epiblast, without large-scale movement or convergence and extension of epiblast cells. Developmental Dynamics 241:270283, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Williams, Margot; Sutherland, Ann] Univ Virginia, Dept Cell Biol, Charlottesville, VA 22908 USA.
[Burdsal, Carol] Tulane Univ, Sch Sci & Engn, Dept Cell & Mol Biol, New Orleans, LA 70118 USA.
[Periasamy, Ammasi] Univ Virginia, Keck Ctr Cellular Imaging, Charlottesville, VA 22908 USA.
[Periasamy, Ammasi] Univ Virginia, Dept Biol, Charlottesville, VA 22908 USA.
[Lewandoski, Mark] NCI, Ctr Canc Res, Frederick, MD 21701 USA.
RP Sutherland, A (reprint author), Univ Virginia, Dept Cell Biol, POB 800732, Charlottesville, VA 22908 USA.
EM as9n@virginia.edu
OI Sutherland, Ann/0000-0003-1925-2825
FU National Science Foundation [IOS-1051294]; National Institute for Child
Health and Human Development; National Institutes of Health [RO1
HD034807, T32 GM008136]
FX We thank Dr. Ray Keller for critical reading of the manuscript and
advice on data analysis, and the faculty and staff of the W. M. Keck
Center for Cellular Imaging for advice and assistance with imaging. A.
E. S. was funded by the National Science Foundation and the National
Institute for Child Health and Human Development, as well as private
donations from Drs. Tom and Jean Sutherland. M. W. was supported by a
training grant from the National Institutes of Health.; Grant sponsor:
NIH; Grant numbers: RO1 HD034807, T32 GM008136; Grant sponsor: NSF;
Grant number: IOS-1051294.
NR 59
TC 24
Z9 24
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1058-8388
J9 DEV DYNAM
JI Dev. Dyn.
PD FEB
PY 2012
VL 241
IS 2
BP 270
EP 283
DI 10.1002/dvdy.23711
PG 14
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 880MZ
UT WOS:000299412500005
PM 22170865
ER
PT J
AU Hasebe, T
Kajita, M
Fu, LZ
Shi, YB
Ishizuya-Oka, A
AF Hasebe, Takashi
Kajita, Mitsuko
Fu, Liezhen
Shi, Yun-Bo
Ishizuya-Oka, Atsuko
TI Thyroid hormone-induced sonic hedgehog signal up-regulates its own
pathway in a paracrine manner in the Xenopus laevis intestine during
metamorphosis
SO DEVELOPMENTAL DYNAMICS
LA English
DT Article
DE Patched (Ptc); Smoothened (Smo); Sonic hedgehog (Shh); Gli transcription
factor; Xenopus laevis; metamorphosis; intestinal remodeling
ID ADULT EPITHELIAL DEVELOPMENT; GASTROINTESTINAL-TRACT; EXPRESSION
PROFILES; GENE-EXPRESSION; BINDING-SITE; GLI PROTEINS; FLOOR PLATE;
IN-VITRO; ACTIVATION; SHH
AB Background: During Xenopus laevis metamorphosis, Sonic hedgehog (Shh) is directly induced by thyroid hormone (TH) at the transcription level as one of the earliest events in intestinal remodeling. However, the regulation of other components of this signaling pathway remains to be analyzed. Here, we analyzed the spatiotemporal expression of Patched (Ptc)-1, Smoothened (Smo), Gli1, Gli2, and Gli3 during natural and TH-induced intestinal remodeling. Results: We show that all of the genes examined are transiently up-regulated in the mesenchymal tissues during intestinal metamorphosis. Conclusions: Interestingly, in the presence of protein synthesis inhibitors, Gli2 but not the others was induced by TH, suggesting that Gli2 is a direct TH response gene, while the others are likely indirect ones. Furthermore, we demonstrate by the organ culture experiment that overexpression of Shh enhances the expression of Ptc-1, Smo, and Glis even in the absence of TH, indicating that Shh regulates its own pathway components during intestinal remodeling. Developmental Dynamics 241:403414, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Hasebe, Takashi; Ishizuya-Oka, Atsuko] Nippon Med Sch, Dept Biol, Nakahara Ku, Kawasaki, Kanagawa 2110063, Japan.
[Kajita, Mitsuko; Ishizuya-Oka, Atsuko] Nippon Med Sch, Dept Mol Biol, Inst Dev & Aging Sci, Nakahara Ku, Kawasaki, Kanagawa 2110063, Japan.
[Fu, Liezhen; Shi, Yun-Bo] NICHHD, Lab Gene Regulat & Dev, NIH, Bethesda, MD 20892 USA.
RP Hasebe, T (reprint author), Nippon Med Sch, Dept Biol, Nakahara Ku, 2-297-2 Kosugi Cho, Kawasaki, Kanagawa 2110063, Japan.
EM hasebet@nms.ac.jp
FU JSPS [20570060]; NICHD, NIH
FX We thank Drs. Masakazu Fujiwara (Nippon Medical School), Itaru Hasunuma
(Toho University), Kosuke Kawamura (Waseda University) for providing us
technical information; Dr. Kazuhito Takeshima (Nagoya University) for
helpful discussions about Gli genes; Dr. Yoshinori Abe (Nippon Medical
School) for helpful discussions about Shh signaling; and Dr. Ariel Ruiz
i Altaba (University of Geneva) for kind gifts of Gli plasmids. This
work was supported in part by JSPS Grants-in-Aid for Scientific Research
(C) to A. I.-O., and in part by the Intramural Research Program of
NICHD, NIH to Y.-B.S.; Grant sponsor: JSPS Grants-in-Aid for Scientific
Research (C); Grant number: 20570060; Grant sponsor: Intramural Research
Program of NICHD; NIH.
NR 57
TC 7
Z9 7
U1 0
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1058-8388
J9 DEV DYNAM
JI Dev. Dyn.
PD FEB
PY 2012
VL 241
IS 2
BP 403
EP 414
DI 10.1002/dvdy.23723
PG 12
WC Anatomy & Morphology; Developmental Biology
SC Anatomy & Morphology; Developmental Biology
GA 880MZ
UT WOS:000299412500017
PM 22190352
ER
PT J
AU Lord, CC
Betters, JL
Ivanova, PT
Milne, SB
Myers, DS
Madenspacher, J
Thomas, G
Chung, S
Liu, MX
Davis, MA
Lee, RG
Crooke, RM
Graham, MJ
Parks, JS
Brasaemle, DL
Fessler, MB
Brown, HA
Brown, JM
AF Lord, Caleb C.
Betters, Jenna L.
Ivanova, Pavlina T.
Milne, Stephen B.
Myers, David S.
Madenspacher, Jennifer
Thomas, Gwynneth
Chung, Soonkyu
Liu, Mingxia
Davis, Matthew A.
Lee, Richard G.
Crooke, Rosanne M.
Graham, Mark J.
Parks, John S.
Brasaemle, Dawn L.
Fessler, Michael B.
Brown, H. Alex
Brown, J. Mark
TI CGI-58/ABHD5-Derived Signaling Lipids Regulate Systemic Inflammation and
Insulin Action
SO DIABETES
LA English
DT Article
ID CHANARIN-DORFMAN-SYNDROME; IONIZATION MASS-SPECTROMETRY; DIET-INDUCED
OBESITY; PHOSPHATIDIC-ACID; STORAGE DISEASE; HEPATIC STEATOSIS;
CYTOPLASMIC TRIACYLGLYCEROLS; LYSOPHOSPHATIDIC ACID; HUMAN FIBROBLASTS;
MESANGIAL CELLS
AB Mutations of comparative gene identification 58 (CGI-58) in humans cause Chanarin-Dorfman syndrome, a rare autosomal recessive disease in which excess triacylglycerol (TAG) accumulates in multiple tissues. CGI-58 recently has been ascribed two distinct biochemical activities, including coactivation of adipose triglyceride lipase and acylation of lysophosphatidic acid (LPA). It is noteworthy that both the substrate (LPA) and the product (phosphatidic acid) of the LPA acyltransferase reaction are well-known signaling lipids. Therefore, we hypothesized that CGI-58 is involved in generating lipid mediators that regulate TAG metabolism and insulin sensitivity. Here, we show that CGI-58 is required for the generation of signaling lipids in response to inflammatory stimuli and that lipid second messengers generated by CGI-58 play a critical role in maintaining the balance between inflammation and insulin action. Furthermore, we show that CGI-58 is necessary for maximal T(H)1 cytokine signaling in the liver. This novel role for CGI-58 in cytokine signaling may explain why diminished CGI-58 expression causes severe hepatic lipid accumulation yet paradoxically improves hepatic insulin action. Collectively, these findings establish that CGI-58 provides a novel source of signaling lipids. These findings contribute insight into the basic mechanisms linking TH1 cytokine signaling to nutrient metabolism. Diabetes 61:355-363, 2012
C1 [Lord, Caleb C.; Betters, Jenna L.; Thomas, Gwynneth; Chung, Soonkyu; Liu, Mingxia; Davis, Matthew A.; Parks, John S.; Brown, J. Mark] Wake Forest Univ, Dept Pathol, Sect Lipid Sci, Sch Med, Winston Salem, NC 27109 USA.
[Ivanova, Pavlina T.; Milne, Stephen B.; Myers, David S.; Brown, H. Alex] Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37212 USA.
[Madenspacher, Jennifer; Fessler, Michael B.] NIEHS, Lab Resp Biol, Res Triangle Pk, NC 27709 USA.
[Lee, Richard G.; Crooke, Rosanne M.; Graham, Mark J.] ISIS Pharmaceut, Antisense Drug Discovery, Cardiovasc Grp, Carlsbad, CA 92008 USA.
[Brasaemle, Dawn L.] Rutgers State Univ, Dept Nutr Sci, New Brunswick, NJ 08903 USA.
RP Brown, JM (reprint author), Wake Forest Univ, Dept Pathol, Sect Lipid Sci, Sch Med, Winston Salem, NC 27109 USA.
EM mabrown@wakehealth.edu
RI Ivanova, Pavlina/K-8307-2012;
OI Brasaemle, Dawn/0000-0002-8553-8285
FU Department of Pathology at Wake Forest University from the American
Heart Association [11BGIA7840072]; National Heart, Lung, and Blood
Institute [1-K99-HL-096166, 5-T32-HL-091796, 5-P01-HL-049373]; National
Institute of Diabetes and Digestive and Kidney Diseases
[1-F32-DK-084582, 1-R01-054797]; National Institute of General Medical
Sciences LIPID MAPS [U54-GM-069338]; National Institute of Environmental
Health Sciences [NIEHS Z01-ES-102005]
FX This work was supported by the Department of Pathology at Wake Forest
University and by grants from the American Heart Association (grant
11BGIA7840072 to J.M.B.); the National Heart, Lung, and Blood Institute
(grants 1-K99-HL-096166 to J.M.B., 5-T32-HL-091796 to C.C.L., and
5-P01-HL-049373 to J.S.P.); the National Institute of Diabetes and
Digestive and Kidney Diseases (grants 1-F32-DK-084582 to J.L.B. and
1-R01-054797 to D.L.B.); the National Institute of General Medical
Sciences LIPID MAPS (grant U54-GM-069338 to H.A.B.); and the Intramural
Research Program of the National Institute of Environmental Health
Sciences (grant NIEHS Z01-ES-102005 to M.B.F.).
NR 50
TC 23
Z9 23
U1 1
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 2012
VL 61
IS 2
BP 355
EP 363
DI 10.2337/db11-0994
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 885RI
UT WOS:000299798100013
PM 22228714
ER
PT J
AU Hiekkalinna, T
Goring, HHH
Lambert, B
Weiss, KM
Norrgrann, P
Schaffer, AA
Terwilliger, JD
AF Hiekkalinna, Tero
Goering, Harald H. H.
Lambert, Brian
Weiss, Kenneth M.
Norrgrann, Petri
Schaeffer, Alejandro A.
Terwilliger, Joseph D.
TI On the statistical properties of family-based association tests in
datasets containing both pedigrees and unrelated case-control samples
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE power; type-I error; genetic linkage analysis; linkage disequilibrium;
family-based association; genome-wide association studies
ID LINKAGE DISEQUILIBRIUM ANALYSIS; GENOME-WIDE SEARCH; SUSCEPTIBILITY
LOCUS; NUCLEAR FAMILIES; GENETIC-ANALYSIS; UNIFIED APPROACH; POPULATION;
ASSIGNMENT; DISEASE; IDENTIFICATION
AB A common approach to genetic mapping of loci for complex diseases is to perform a genome-wide association study (GWAS) by analyzing a vast number of SNP markers in cohorts of unrelated cases and controls. A direct motivation for the case-control design is that unrelated, affected individuals can be easier to collect than large families with multiple affected persons in the Western world. Despite its higher potential power, investigators have not actively pursued family ascertainment in part because of a dearth of methods for analyzing such correlated data on a large scale. We examine the statistical properties of several commonly used family-based association tests, as to their performance using real-life mixtures of families and singletons taken from our own migraine and schizophrenia studies, as well as population-based data for a complex trait simulated with the evolutionary phenogenetic simulator, ForSim. In virtually every situation, the full likelihood-based methods in the PSEUDOMARKER program outperformed those implemented in FBAT, GENEHUNTER TDT, PLINK (family-based options), HRR/HHRR, QTDT, TRANSMIT, UNPHASED, MENDEL, and LAMP. We further show that GWAS is much more powerful when family samples are used rather than unrelateds, on a genotype-by-genotype basis. European Journal of Human Genetics (2012) 20, 217-223; doi:10.1038/ejhg.2011.173; published online 21 September 2011
C1 [Hiekkalinna, Tero; Norrgrann, Petri; Terwilliger, Joseph D.] Univ Helsinki, Inst Mol Med Finland, Helsinki, Finland.
[Goering, Harald H. H.] Texas Biomed Res Inst, Dept Genet, San Antonio, TX USA.
[Lambert, Brian; Weiss, Kenneth M.] Penn State Univ, Dept Anthropol, State Coll, PA USA.
[Schaeffer, Alejandro A.] NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, US Dept HHS, Bethesda, MD 20892 USA.
[Terwilliger, Joseph D.] Columbia Univ, Dept Psychiat, New York, NY USA.
[Terwilliger, Joseph D.] Columbia Univ, Dept Genet & Dev, New York, NY USA.
[Terwilliger, Joseph D.] Columbia Univ, Columbia Genome Ctr, New York, NY USA.
[Terwilliger, Joseph D.] New York State Psychiat Inst & Hosp, Div Med Genet, New York, NY 10032 USA.
[Hiekkalinna, Tero; Norrgrann, Petri; Terwilliger, Joseph D.] Natl Inst Hlth & Welf, Unit Publ Hlth Genom, Helsinki, Finland.
RP Hiekkalinna, T (reprint author), Biomedicum Helsinki, Publ Hlth Genom Unit, Natl Inst Hlth & Welf THL, POB 104, FIN-00251 Helsinki, Finland.
EM tero.hiekkalinna@helsinki.fi
RI Schaffer, Alejandro/F-2902-2012
FU Academy of Finland from the National Institutes of Health [MH84995,
MH59490, RR017515]; Helsingin Sanomat Centennial Foundation; Biomedicum
Helsinki Foundation; Emil Aaltonen Foundation; Otto A. Malm Foundation;
Jenny and Antti Wihuri Foundation; Finnish Cultural Society; SBC
Foundation; NIH, NLM
FX This research work was funded by the FiDiPro program of the Academy of
Finland, Grants MH84995, MH59490 and RR017515 from the National
Institutes of Health, the Helsingin Sanomat Centennial Foundation,
Biomedicum Helsinki Foundation, Emil Aaltonen Foundation, Otto A. Malm
Foundation, Jenny and Antti Wihuri Foundation, Finnish Cultural Society,
and the SBC Foundation are gratefully acknowledged. This research was
supported in part by the Intramural Research Program of the NIH, NLM
(AAS). Maija Wessman, Verneri Anttila, Mari Kaunisto, and Tiina Paunio
are acknowledged for providing Finnish migraine and schizophrenia
pedigree structures for simulation studies. Markus Perola and Leena
Peltonen-Palotie are greatly acknowledged for their guidance and support
over the years. The great majority of simulations were executed on the
Linux-based supercomputers of the Finnish IT Center for Science (CSC).
CSC is greatly acknowledged. Thanks to three reviewers for numerous
helpful suggestions to improve the manuscript.
NR 52
TC 6
Z9 7
U1 1
U2 7
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 2012
VL 20
IS 2
BP 217
EP 223
DI 10.1038/ejhg.2011.173
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 879IN
UT WOS:000299323000023
PM 21934707
ER
PT J
AU Greub, G
Gikas, A
Heinzen, RA
Dumler, JS
AF Greub, Gilbert
Gikas, Achilles
Heinzen, Robert A.
Dumler, J. Stephen
TI Rickettsia and other intracellular bacteria: recent outbreaks, novel
pathogens, emerging diseases, new tools, and outstanding discoveries
SO FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY
LA English
DT Editorial Material
C1 [Greub, Gilbert] Univ Lausanne, Inst Microbiol, CH-1011 Lausanne, Switzerland.
[Gikas, Achilles] Univ Hosp Heraklion, Dept Internal Med & Infect Dis, Iraklion, NE, Greece.
[Heinzen, Robert A.] NIAID, Intracellular Parasites Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Dumler, J. Stephen] Johns Hopkins Univ, Sch Med, Div Med Microbiol, Dept Pathol, Baltimore, MD 21205 USA.
RP Greub, G (reprint author), Univ Lausanne, Inst Microbiol, Rue Bugnon 48, CH-1011 Lausanne, Switzerland.
EM gilbert.greub@chuv.ch; gikas@med.uoc.gr; rheinzen@niaid.nih.gov;
sdumler@jhmi.edu
OI Gikas, Achilleas/0000-0002-8455-9631
NR 3
TC 1
Z9 1
U1 0
U2 4
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0928-8244
J9 FEMS IMMUNOL MED MIC
JI FEMS Immunol. Med. Microbiol.
PD FEB
PY 2012
VL 64
IS 1
SI SI
BP 1
EP 2
DI 10.1111/j.1574-695X.2011.00915.x
PG 2
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 874LA
UT WOS:000298957500001
PM 22118608
ER
PT J
AU Chaves, LF
Morrison, AC
Kitron, UD
Scott, TW
AF Chaves, Luis F.
Morrison, Amy C.
Kitron, Uriel D.
Scott, Thomas W.
TI Nonlinear impacts of climatic variability on the density-dependent
regulation of an insect vector of disease
SO GLOBAL CHANGE BIOLOGY
LA English
DT Article
DE Aedes aegypti; climate change; exogenous forcing; kurtosis; modeling;
mosquito; population regulation; Schmalhausen's law
ID AEDES-AEGYPTI DIPTERA; ECOLOGICAL TIME-SERIES; YELLOW-FEVER MOSQUITO;
POPULATION-DYNAMICS; INTRASPECIFIC COMPETITION; MALARIA; CULICIDAE;
PATTERNS; TEMPERATURE; EVOLUTION
AB Aedes aegypti is one of the most common urban tropical mosquito species and an important vector of dengue, chikungunya, and yellow fever viruses. It is also an organism with a complex life history where larval stages are aquatic and adults are terrestrial. This ontogenetic niche shift could shape the density-dependent regulation of this and other mosquito species, because events that occur during the larval stages impact adult densities. Herein, we present results from simple density-dependent mathematical models fitted using maximum likelihood methods to weekly time series data from Puerto Rico and Thailand. Density-dependent regulation was strong in both populations. Analysis of climatic forcing indicated that populations were more sensitive to climatic variables with low kurtosis, i.e., climatic factors highly variable around the median, rainfall in Puerto Rico, and temperature in Thailand. Changes in environmental variability appear to drive sharp changes in the abundance of mosquitoes. The identification of density-independent (i.e., exogenous) variables forcing sharp changes in disease vector populations using the exogenous factors statistical properties, such as kurtosis, could be useful to assess the impacts of changing climate patterns on the transmission of vector-borne diseases.
C1 [Chaves, Luis F.] Hokkaido Univ, Grad Sch Environm Sci, Sapporo, Hokkaido 0600810, Japan.
[Chaves, Luis F.] Hokkaido Univ, Excellence Program Integrated Field Environm Sci, Global Ctr, Sapporo, Hokkaido 0600810, Japan.
[Chaves, Luis F.] Univ Nacl, Programa Invest Enfermedades Trop, Escuela Med Vet, Heredia, Costa Rica.
[Morrison, Amy C.; Scott, Thomas W.] Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
[Kitron, Uriel D.] Emory Univ, Dept Environm Studies, Atlanta, GA 30322 USA.
[Kitron, Uriel D.; Scott, Thomas W.] Fogarty Int Ctr, NIH, Bethesda, MD 20892 USA.
RP Chaves, LF (reprint author), Hokkaido Univ, Grad Sch Environm Sci, Sapporo, Hokkaido 0600810, Japan.
EM lchaves@ees.hokudai.ac.jp
RI Chaves, Luis Fernando/F-3448-2010
OI Chaves, Luis Fernando/0000-0002-5301-2764
FU American Society of Tropical Medicine and Hygiene (ASTMH); Japan Society
for the Promotion of Science (JSPS); Emory University; Research and
Policy for Infectious Disease Dynamics (RAPIDD) of the Science and
Technology Directorate; Fogarty International Center, National
Institutes of Health
FX Valuable comments were provided by Prof Chepina Hernandez, Prof N.
Minakawa, Prof T. Takada, Dr A. Ponlawat, and Dr T. Revilla. LFC was
supported by a Gorgas Memorial Research Award from the American Society
of Tropical Medicine and Hygiene (ASTMH), and by a Grant in Aid for
Research of Japan Society for the Promotion of Science (JSPS). UDK was
supported by Emory University. UDK and TWS were supported by Research
and Policy for Infectious Disease Dynamics (RAPIDD) mosquito-borne
disease program of the Science and Technology Directorate and the
Fogarty International Center, National Institutes of Health.
NR 62
TC 34
Z9 35
U1 4
U2 56
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1354-1013
J9 GLOBAL CHANGE BIOL
JI Glob. Change Biol.
PD FEB
PY 2012
VL 18
IS 2
BP 457
EP 468
DI 10.1111/j.1365-2486.2011.02522.x
PG 12
WC Biodiversity Conservation; Ecology; Environmental Sciences
SC Biodiversity & Conservation; Environmental Sciences & Ecology
GA 875PB
UT WOS:000299042500006
ER
PT J
AU Maltsev, VA
Lakatta, EG
AF Maltsev, Victor A.
Lakatta, Edward G.
TI The funny current in the context of the coupled-clock pacemaker cell
system
SO HEART RHYTHM
LA English
DT Editorial Material
DE Intracellular Ca2+; Cardiac pacemaker cells
ID PIG SINOATRIAL NODE; CA2+ RELEASES
C1 [Maltsev, Victor A.; Lakatta, Edward G.] NIA, Cardiovasc Sci Lab, IRP, NIH, Baltimore, MD 21224 USA.
RP Lakatta, EG (reprint author), NIA, Cardiovasc Sci Lab, IRP, NIH, 5600 Nathan Shock Dr, Baltimore, MD 21224 USA.
EM LakattaE@grc.nia.nih.gov
FU Intramural NIH HHS [Z01 AG000863-02]
NR 13
TC 19
Z9 19
U1 1
U2 11
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 2012
VL 9
IS 2
BP 302
EP 307
DI 10.1016/j.hrthm.2011.09.022
PG 6
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 882DL
UT WOS:000299541600033
PM 21925132
ER
PT J
AU Mirabello, L
Yeager, M
Chowdhury, S
Qi, L
Deng, X
Wang, Z
Hutchinson, A
Savage, SA
AF Mirabello, L.
Yeager, M.
Chowdhury, S.
Qi, L.
Deng, X.
Wang, Z.
Hutchinson, A.
Savage, S. A.
TI Worldwide genetic structure in 37 genes important in telomere biology
SO HEREDITY
LA English
DT Article
DE telomere; selection; single-nucleotide polymorphism; HGDP; HapMap
ID MULTILOCUS GENOTYPE DATA; GENOME-WIDE ASSOCIATION; BASAL-CELL CARCINOMA;
HUMAN-POPULATIONS; NATURAL-SELECTION; LINKAGE DISEQUILIBRIUM;
SUSCEPTIBILITY LOCI; STATISTICAL-METHOD; COMMON VARIANTS; HAPLOTYPE MAP
AB Telomeres form the ends of eukaryotic chromosomes and are vital in maintaining genetic integrity. Telomere dysfunction is associated with cancer and several chronic diseases. Patterns of genetic variation across individuals can provide keys to further understanding the evolutionary history of genes. We investigated patterns of differentiation and population structure of 37 telomere maintenance genes among 53 worldwide populations. Data from 898 unrelated individuals were obtained from the genome-wide scan of the Human Genome Diversity Panel (HGDP) and from 270 unrelated individuals from the International HapMap Project at 716 single-nucleotide polymorphism (SNP) loci. We additionally compared this gene set to HGDP data at 1396 SNPs in 174 innate immunity genes. The majority of the telomere biology genes had low to moderate haplotype diversity (45-85%), high ancestral allele frequencies (> 60%) and low differentiation (F(ST) <0.10). Heterozygosity and differentiation were significantly lower in telomere biology genes compared with the innate immunity genes. There was evidence of evolutionary selection in ACD, TERF21P, NOLA2, POT1 and TNKS in this data set, which was consistent in HapMap 3. TERT had higher than expected levels of haplotype diversity, likely attributable to a lack of linkage disequilibrium, and a potential cancer-associated SNP in this gene, rs2736100, varied substantially in genotype frequency across major continental regions. It is possible that the genes under selection could influence telomere biology diseases. As a group, there appears to be less diversity and differentiation in telomere biology genes than in genes with different functions, possibly due to their critical role in telomere maintenance and chromosomal stability. Heredity (2012) 108, 124-133; doi:10.1038/hdy.2011.55; published online 6 July 2011
C1 [Mirabello, L.; Savage, S. A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Yeager, M.; Chowdhury, S.; Qi, L.; Deng, X.; Wang, Z.; Hutchinson, A.] NCI, Core Genotyping Facil, Div Canc Epidemiol & Genet, SAIC Frederick Inc, Frederick, MD 21701 USA.
RP Savage, SA (reprint author), NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, NIH 6120 Execut Blvd,EPS-7018, Bethesda, MD 20892 USA.
EM savagesh@mail.nih.gov
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
FU Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health; National Cancer Institute, National
Institutes of Health [HHSN261200800001E]
FX This project has been funded by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health, and with federal funds from the National
Cancer Institute, National Institutes of Health, under contract number
HHSN261200800001E. The cc:intent of this publication does not
necessarily reflect the views or policies of the Department of Health
and Human Services, nor does mention of trade names, commercial products
or organizations imply endorsement by the U.S. Government. We thank the
staff of the NCI core genotyping facility, Dr Stephen Chanock, NCI and
Elliott Richards, NCI, for valuable assistance and helpful discussions.
NR 71
TC 4
Z9 4
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0018-067X
J9 HEREDITY
JI Heredity
PD FEB
PY 2012
VL 108
IS 2
BP 124
EP 133
DI 10.1038/hdy.2011.55
PG 10
WC Ecology; Evolutionary Biology; Genetics & Heredity
SC Environmental Sciences & Ecology; Evolutionary Biology; Genetics &
Heredity
GA 882UR
UT WOS:000299589900005
PM 21731055
ER
PT J
AU Peters, U
Hutter, CM
Hsu, L
Schumacher, FR
Conti, DV
Carlson, CS
Edlund, CK
Haile, RW
Gallinger, S
Zanke, BW
Lemire, M
Rangrej, J
Vijayaraghavan, R
Chan, AT
Hazra, A
Hunter, DJ
Ma, J
Fuchs, CS
Giovannucci, EL
Kraft, P
Liu, Y
Chen, L
Jiao, S
Makar, KW
Taverna, D
Gruber, SB
Rennert, G
Moreno, V
Ulrich, CM
Woods, MO
Green, RC
Parfrey, PS
Prentice, RL
Kooperberg, C
Jackson, RD
LaCroix, AZ
Caan, BJ
Hayes, RB
Berndt, SI
Chanock, SJ
Schoen, RE
Chang-Claude, J
Hoffmeister, M
Brenner, H
Frank, B
Bezieau, S
Kury, S
Slattery, ML
Hopper, JL
Jenkins, MA
Le Marchand, L
Lindor, NM
Newcomb, PA
Seminara, D
Hudson, TJ
Duggan, DJ
Potter, JD
Casey, G
AF Peters, Ulrike
Hutter, Carolyn M.
Hsu, Li
Schumacher, Fredrick R.
Conti, David V.
Carlson, Christopher S.
Edlund, Christopher K.
Haile, Robert W.
Gallinger, Steven
Zanke, Brent W.
Lemire, Mathieu
Rangrej, Jagadish
Vijayaraghavan, Raakhee
Chan, Andrew T.
Hazra, Aditi
Hunter, David J.
Ma, Jing
Fuchs, Charles S.
Giovannucci, Edward L.
Kraft, Peter
Liu, Yan
Chen, Lin
Jiao, Shuo
Makar, Karen W.
Taverna, Darin
Gruber, Stephen B.
Rennert, Gad
Moreno, Victor
Ulrich, Cornelia M.
Woods, Michael O.
Green, Roger C.
Parfrey, Patrick S.
Prentice, Ross L.
Kooperberg, Charles
Jackson, Rebecca D.
LaCroix, Andrea Z.
Caan, Bette J.
Hayes, Richard B.
Berndt, Sonja I.
Chanock, Stephen J.
Schoen, Robert E.
Chang-Claude, Jenny
Hoffmeister, Michael
Brenner, Hermann
Frank, Bernd
Bezieau, Stephane
Kuery, Sebastien
Slattery, Martha L.
Hopper, John L.
Jenkins, Mark A.
Le Marchand, Loic
Lindor, Noralane M.
Newcomb, Polly A.
Seminara, Daniela
Hudson, Thomas J.
Duggan, David J.
Potter, John D.
Casey, Graham
TI Meta-analysis of new genome-wide association studies of colorectal
cancer risk
SO HUMAN GENETICS
LA English
DT Article
ID MULTILOCUS GENOTYPE DATA; SUSCEPTIBILITY LOCI; COMMON VARIANTS; RARE
VARIANTS; 8Q24; SCAN; INFERENCE; DISEASES; 5P15.33; GENE
AB Colorectal cancer is the second leading cause of cancer death in developed countries. Genome-wide association studies (GWAS) have successfully identified novel susceptibility loci for colorectal cancer. To follow up on these findings, and try to identify novel colorectal cancer susceptibility loci, we present results for GWAS of colorectal cancer (2,906 cases, 3,416 controls) that have not previously published main associations. Specifically, we calculated odds ratios and 95% confidence intervals using log-additive models for each study. In order to improve our power to detect novel colorectal cancer susceptibility loci, we performed a meta-analysis combining the results across studies. We selected the most statistically significant single nucleotide polymorphisms (SNPs) for replication using ten independent studies (8,161 cases and 9,101 controls). We again used a meta-analysis to summarize results for the replication studies alone, and for a combined analysis of GWAS and replication studies. We measured ten SNPs previously identified in colorectal cancer susceptibility loci and found eight to be associated with colorectal cancer (p value range 0.02 to 1.8 x 10(-8)). When we excluded studies that have previously published on these SNPs, five SNPs remained significant at p < 0.05 in the combined analysis. No novel susceptibility loci were significant in the replication study after adjustment for multiple testing, and none reached genome-wide significance from a combined analysis of GWAS and replication. We observed marginally significant evidence for a second independent SNP in the BMP2 region at chromosomal location 20p12 (rs4813802; replication p value 0.03; combined p value 7.3 x 10(-5)). In a region on 5p33.15, which includes the coding regions of the TERT-CLPTM1L genes and has been identified in GWAS to be associated with susceptibility to at least seven other cancers, we observed a marginally significant association with rs2853668 (replication p value 0.03; combined p value 1.9 x 10(-4)). Our study suggests a complex nature of the contribution of common genetic variants to risk for colorectal cancer.
C1 [Peters, Ulrike; Hutter, Carolyn M.; Carlson, Christopher S.; Jiao, Shuo; Makar, Karen W.; Ulrich, Cornelia M.; LaCroix, Andrea Z.; Newcomb, Polly A.] Fred Hutchinson Canc Res Ctr, Canc Prevent Program, Seattle, WA 98104 USA.
[Peters, Ulrike; Ulrich, Cornelia M.; Potter, John D.] Univ Washington, Dept Epidemiol, Sch Publ Hlth, Seattle, WA 98195 USA.
[Hsu, Li] Fred Hutchinson Canc Res Ctr, Biostat & Biomath Program, Seattle, WA 98104 USA.
[Schumacher, Fredrick R.; Conti, David V.; Haile, Robert W.; Casey, Graham] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Gallinger, Steven] Toronto Gen Hosp, Univ Hlth Network, Dept Surg, Toronto, ON, Canada.
[Zanke, Brent W.] Ottawa Hosp Res Inst, Clin Epidemiol Program, Ottawa, ON, Canada.
[Lemire, Mathieu; Rangrej, Jagadish; Hudson, Thomas J.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Vijayaraghavan, Raakhee; Taverna, Darin; Duggan, David J.] Translat Genom Res Inst, Phoenix, AZ USA.
[Chan, Andrew T.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Gastroenterol, Boston, MA USA.
[Chan, Andrew T.; Hazra, Aditi; Ma, Jing; Fuchs, Charles S.; Giovannucci, Edward L.] Harvard Univ, Sch Med, Boston, MA USA.
[Chan, Andrew T.; Hazra, Aditi; Ma, Jing; Fuchs, Charles S.; Giovannucci, Edward L.] Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA.
[Hazra, Aditi; Hunter, David J.; Kraft, Peter] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Program Mol & Genet Epidemiol, Boston, MA 02115 USA.
[Fuchs, Charles S.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
[Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Liu, Yan] Stephens & Associates, Dallas Res Ctr, Dallas, TX USA.
[Chen, Lin] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
[Gruber, Stephen B.] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Rennert, Gad] Carmel Hosp, Dept Community Med & Epidemiol, Haifa, Israel.
[Rennert, Gad] Technion Fac Med, Haifa, Israel.
[Moreno, Victor] Catalan Inst Oncol IDIBELL, Biostat & Bioinformat Unit, Barcelona, Spain.
[Ulrich, Cornelia M.] German Canc Res Ctr, Div Prevent Oncol, D-6900 Heidelberg, Germany.
[Woods, Michael O.; Green, Roger C.] Mem Univ Newfoundland, Fac Med, Discipline Genet, St John, NF, Canada.
[Parfrey, Patrick S.] Mem Univ Newfoundland, Fac Med, Discipline Med, St John, NF, Canada.
[Prentice, Ross L.; Kooperberg, Charles; Potter, John D.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Jackson, Rebecca D.] Ohio State Univ, Div Endocrinol Diabet & Metab, Columbus, OH 43210 USA.
[Caan, Bette J.] Kaiser Permanente Med Care Program, Div Res, Oakland, CA USA.
[Hayes, Richard B.] NYU, Dept Environm Med, Sch Med, Div Epidemiol, New York, NY 10016 USA.
[Berndt, Sonja I.; Chanock, Stephen J.] NCI, Div Canc Epidemiol & Genet, US Dept HHS, NIH, Bethesda, MD 20892 USA.
[Schoen, Robert E.] Univ Pittsburgh, Dept Epidemiol, Med Ctr, Pittsburgh, PA 15261 USA.
[Chang-Claude, Jenny] German Canc Res Ctr, Div Canc Epidemiol, D-6900 Heidelberg, Germany.
[Hoffmeister, Michael; Brenner, Hermann; Frank, Bernd] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-6900 Heidelberg, Germany.
[Bezieau, Stephane; Kuery, Sebastien] Ctr Hosp Univ CHU Nantes, Serv Genet Med, Nantes, France.
[Slattery, Martha L.] Univ Utah, Dept Internal Med, Hlth Sci Ctr, Salt Lake City, UT 84112 USA.
[Hopper, John L.; Jenkins, Mark A.] Univ Melbourne, Ctr Mol Environm Genet & Analyt Epidemiol, Melbourne, Vic, Australia.
[Le Marchand, Loic] Univ Hawaii Manoa, Program Epidemiol, Canc Res Ctr Hawaii, Honolulu, HI 96822 USA.
[Lindor, Noralane M.] Mayo Clin, Dept Med Genet, Rochester, MN USA.
[Seminara, Daniela] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Hudson, Thomas J.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Hudson, Thomas J.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
RP Peters, U (reprint author), Fred Hutchinson Canc Res Ctr, Canc Prevent Program, 1124 Columbia St, Seattle, WA 98104 USA.
EM upeters@fhcrc.org; gcasey@usc.edu
RI Hoffmeister, Michael/B-5745-2012; Gallinger, Steven/E-4575-2013; KURY,
Sebastien/G-5971-2015; Bezieau, stephane/G-5621-2015; Jenkins,
Mark/P-7803-2015; Brenner, Hermann/B-4627-2017;
OI Hoffmeister, Michael/0000-0002-8307-3197; Moreno,
Victor/0000-0002-2818-5487; KURY, Sebastien/0000-0001-5497-0465;
Bezieau, stephane/0000-0003-0095-1319; Jenkins,
Mark/0000-0002-8964-6160; Brenner, Hermann/0000-0002-6129-1572; Hayes,
Richard/0000-0002-0918-661X; Potter, John/0000-0001-5439-1500
FU Canadian Cancer Society Research Institute; Ontario Institute for Cancer
Research; National Cancer Institute, National Institutes of Health
[CA-95-011, U01 CA122839]; Australasian Colorectal Cancer Family
Registry [U01 CA097735]; Familial Colorectal Neoplasia Collaborative
Group [U01 CA074799]; Mayo Clinic Cooperative Family Registry for Colon
Cancer Studies [U01 CA074800]; Ontario Registry for Studies of Familial
Colorectal Cancer [U01 CA074783]; Seattle Colorectal Cancer Family
Registry [U01 CA074794]; University of Hawaii Colorectal Cancer Family
Registry [U01 CA074806]; German Research Council (Deutsche
Forschungsgemeinschaft [BR 1704/6-1, BR 1704/6-3, BR 1704/6-4, CH
117/1-1]; German Federal Ministry of Education and Research [01KH0404,
01ER0814]; National Cancer Institute, National Institutes of Health,
U.S. Department of Health and Human Services [R01 CA48998]; National
Cancer Institute, Institutes of Health, U.S. Department of Health and
Human Services [R01 CA059045, R25 CA094880, U01 CA137088]; regional
Hospital Clinical Research Program (PHRC); Regional Council of Pays de
la Loire; Groupement des Entreprises Francaises dans la LUtte contre le
Cancer (GEFLUC); Association Anne de Bretagne Genetique and the Ligue
Regionale Contre le Cancer (LRCC); National Institutes of Health [P01 CA
055075, R01 137178, P50 CA 127003, P01 CA 087969]; National Institutes
of Health, U.S. Department of Health and Human Services [R01 CA81488,
U01 CA74783]; Interdisciplinary Health Research Team from the Canadian
Institutes of Health Research [CRT 43821]; National Cancer Institute of
Canada [18223, 18226]; Division of Cancer Epidemiology and Genetics;
Division of Cancer Prevention, National Cancer Institute, National
Institutes of Health, U.S. Department of Health and Human Services;
National Cancer Institute; National Institutes of Health, Genes,
Environment and Health Initiative [NIH GEI] [Z01 CP 010200, U01 HG
004438]; National Heart, Lung, and Blood Institute, National Institutes
of Health, U.S. Department of Health and Human Services [N01WH22110,
24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122,
42107-26, 42129-32, 44221, 268200764316C]
FX ARCTIC: This work was supported by the Cancer Risk Evaluation (CaRE)
Program grant from the Canadian Cancer Society Research Institute. TJH
and BWZ are recipients of Senior Investigator Awards from the Ontario
Institute for Cancer Research, through generous support from the Ontario
Ministry of Research.; CCFR: This work was supported by the National
Cancer Institute, National Institutes of Health under RFA # CA-95-011
and through cooperative agreements with members of the Colon Cancer
Family Registry and P.I.s. This genome-wide scan was supported by the
National Cancer Institute, National Institutes of Health by U01
CA122839. The content of this manuscript does not necessarily reflect
the views or policies of the National Cancer Institute or any of the
collaborating centers in the CFRs, nor does mention of trade names,
commercial products, or organizations imply endorsement by the US
Government or the CFR. The following Colon CFR centers contributed data
to this manuscript and were supported by the following sources:
Australasian Colorectal Cancer Family Registry (U01 CA097735), Familial
Colorectal Neoplasia Collaborative Group (U01 CA074799), Mayo Clinic
Cooperative Family Registry for Colon Cancer Studies (U01 CA074800),
Ontario Registry for Studies of Familial Colorectal Cancer (U01
CA074783), Seattle Colorectal Cancer Family Registry (U01 CA074794),
University of Hawaii Colorectal Cancer Family Registry (U01 CA074806).;
DACHS: This work was supported by grants from the German Research
Council (Deutsche Forschungsgemeinschaft, BR 1704/6-1, BR 1704/6-3, BR
1704/6-4 and CH 117/1-1), and the German Federal Ministry of Education
and Research (01KH0404 and 01ER0814). We thank all participants and
cooperating clinicians, and Ute Handte-Daub, Belinda-Su Kaspereit and
Ursula Eilber for excellent technical assistance.; DALS: This work was
supported by the National Cancer Institute, National Institutes of
Health, U.S. Department of Health and Human Services (R01 CA48998 to
MLS).; DALS, PLCO and WHI GWAS: Funding for the genome-wide scan of
DALS, PLCO, and DALS was provided by the National Cancer Institute,
Institutes of Health, U.S. Department of Health and Human Services (R01
CA059045 to UP). CMH was supported by a training grant from the National
Cancer Institute, Institutes of Health, U.S. Department of Health and
Human Services (R25 CA094880).; FRENCH: This work was funded by a
regional Hospital Clinical Research Program (PHRC) and supported by the
Regional Council of Pays de la Loire, the Groupement des Entreprises
Francaises dans la LUtte contre le Cancer (GEFLUC), the Association Anne
de Bretagne Genetique and the Ligue Regionale Contre le Cancer (LRCC).;
GECCO: Funding for GECCO infrastructure is supported by National Cancer
Institute, Institutes of Health, U.S. Department of Health and Human
Services (U01 CA137088 to UP).; HPFS: This work was supported by the
National Institutes of Health (P01 CA 055075 to C. S. F., R01 137178 to
A. T. C., and P50 CA 127003 to C. S. F.). We acknowledge Patrice Soule
and Hardeep Ranu for genotyping at the Dana-Farber Harvard Cancer Center
High Throughput Polymorphism Core under the supervision of David J.
Hunter, and Carolyn Guo for programming assistance.; MECC: This work was
supported by the National Institutes of Health, U.S. Department of
Health and Human Services (R01 CA81488 to SBG and GR).; NFCCR: This work
was supported by an Interdisciplinary Health Research Team award from
the Canadian Institutes of Health Research (CRT 43821); the National
Institutes of Health, U.S. Department of Health and Human Services (U01
CA74783); and National Cancer Institute of Canada grants (18223 and
18226). The authors wish to acknowledge the contribution of Alexandre
Belisle and the genotyping team of the McGill University and Genome
Quebec Innovation Centre, Montreal, Canada, for genotyping the Sequenom
panel in the NFCCR samples.; NHS: This work was supported by the
National Institutes of Health (P01 CA 087969 to ELG, R01 137178 to ATC,
and P50 CA 127003 to CSF). We acknowledge Patrice Soule and Hardeep Ranu
for genotyping at the Dana-Farber Harvard Cancer Center High Throughput
Polymorphism Core under the supervision of David J. Hunter, and Carolyn
Guo for programming assistance.; PLCO: This research was supported by
the Intramural Research Program of the Division of Cancer Epidemiology
and Genetics and supported by contracts from the Division of Cancer
Prevention, National Cancer Institute, National Institutes of Health,
U.S. Department of Health and Human Services. The authors thank Drs.
Christine Berg and Philip Prorok at the Division of Cancer Prevention at
the National Cancer Institute, and investigators and staff from the
screening centers of the Prostate, Lung, Colorectal, and Ovarian (PLCO)
Cancer Screening Trial, Mr. Thomas Riley and staff at Information
Management Services, Inc., Ms. Barbara O'Brien and staff at Westat,
Inc., and Mr. Tim Sheehy and staff at SAIC-Frederick. Most importantly,
we acknowledge the study participants for their contributions to making
this study possible.; Control samples were genotyped as part of the
Cancer Genetic Markers of Susceptibility (CGEMS) prostate cancer scan
were supported by the Intramural Research Program of the National Cancer
Institute. The datasets used in this analysis were accessed with
appropriate approval through the dbGaP online resource
(http://cgems.cancer.gov/data_access.html) through dbGaP accession
number 000207v.1p1.c1 (National Cancer Institute 2009; Yeager et al.
2007). Control samples were also genotyped as part of the GWAS of Lung
Cancer and Smoking. Funding for this work was provided through the
National Institutes of Health, Genes, Environment and Health Initiative
[NIH GEI] (Z01 CP 010200). The human subjects participating in the GWAS
are derived from the Prostate, Lung, Colon and Ovarian Screening Trial
and the study is supported by intramural resources of the National
Cancer Institute. Assistance with genotype cleaning, as well as with
general study coordination, was provided by the Gene Environment
Association Studies, GENEVA Coordinating Center (U01 HG004446).
Assistance with data cleaning was provided by the National Center for
Biotechnology Information. Funding support for genotyping, which was
performed at the Johns Hopkins University Center for Inherited Disease
Research, was provided by the NHI GEI (U01 HG 004438). The datasets used
for the analyses described in this manuscript were obtained from dbGaP
at http://www.ncbi.nlm.nih.gov/gap through dbGaP accession number
ph000093.v2.p2.c1.; WHI: The WHI program is funded by the National
Heart, Lung, and Blood Institute, National Institutes of Health, U.S.
Department of Health and Human Services through contracts N01WH22110,
24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-32119, 32122,
42107-26, 42129-32, 44221, and 268200764316C.
NR 70
TC 102
Z9 103
U1 0
U2 16
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 2012
VL 131
IS 2
BP 217
EP 234
DI 10.1007/s00439-011-1055-0
PG 18
WC Genetics & Heredity
SC Genetics & Heredity
GA 876QQ
UT WOS:000299123000006
PM 21761138
ER
PT J
AU Pineda-Alvarez, DE
Roessler, E
Hu, P
Srivastava, K
Solomon, BD
Siple, CE
Fan, CM
Muenke, M
AF Pineda-Alvarez, Daniel E.
Roessler, Erich
Hu, Ping
Srivastava, Kshitij
Solomon, Benjamin D.
Siple, C. Evan
Fan, Chen-Ming
Muenke, Maximilian
TI Missense substitutions in the GAS1 protein present in holoprosencephaly
patients reduce the affinity for its ligand, SHH
SO HUMAN GENETICS
LA English
DT Article
ID SONIC-HEDGEHOG GENE; LOSS-OF-FUNCTION; HUMAN SIX3 GENE;
EMBRYONIC-DEVELOPMENT; MUTATIONS; PHENOTYPE; SPECTRUM; DISEASE; BINDING;
ZIC2
AB Holprosencephaly (HPE) is the most common disorder of the developing forebrain in humans, and is characterized by varying degrees of abnormal union of the cerebral hemispheres. These defects are typically co-associated with midline craniofacial anomalies. The combination of forebrain and craniofacial defects that comprise HPE can present along a broad and variable phenotypic spectrum. Both the SHH and NODAL signaling pathways play important roles in the pathogenesis of this disorder. Disruption of these pathways by chromosomal rearrangements, mutations in pathway-related genes and/or biochemical alterations are proposed to contribute to HPE in a large number of patients. Additional factors that are not yet fully delineated are also very likely to be involved in the pathogenesis and phenotypic heterogeneity of the disorder. Genetic loss of GAS1, a cell membrane receptor and positive regulator of SHH, has been demonstrated to contribute to the HPE phenotypic spectrum in animal models. We have evaluated the coding and flanking sequence of GAS1 in 394 patients who have clinical findings within the HPE phenotypic spectrum, and now report five novel missense sequence variants among five unrelated HPE probands. Finally, we tested the effect of these variants (as well as previously reported GAS1 variants) on the ability of GAS1 to bind to SHH. Here, we demonstrate that sequence variants in GAS1 can impair its physical interaction with SHH, suggesting a decrease in the SHH downstream signaling cascade as a pathogenic mechanism of disease.
C1 [Pineda-Alvarez, Daniel E.; Roessler, Erich; Hu, Ping; Srivastava, Kshitij; Solomon, Benjamin D.; Muenke, Maximilian] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Siple, C. Evan; Fan, Chen-Ming] Carnegie Inst Sci, Dept Embryol, Baltimore, MD 21218 USA.
RP Muenke, M (reprint author), NHGRI, Med Genet Branch, NIH, 35 Convent Dr,Bldg 35,Room 1B403, Bethesda, MD 20892 USA.
EM mamuenke@mail.nih.gov
FU Division of Intramural Research (DIR) of the National Human Genome
Research Institute [RO1 DK084963]
FX We thank the families who participated in these research studies, and
the National Institute of Neurological Disorders and Stroke's (NINDS)
DNA Sequencing Facility for their technical support with DNA sequencing.
This work was supported in part by the Division of Intramural Research
(DIR) of the National Human Genome Research Institute (MM) and RO1
DK084963 (C-M F).
NR 40
TC 23
Z9 23
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 2012
VL 131
IS 2
BP 301
EP 310
DI 10.1007/s00439-011-1078-6
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 876QQ
UT WOS:000299123000012
PM 21842183
ER
PT J
AU Raza, MH
Amjad, R
Riazuddin, S
Drayna, D
AF Raza, Muhammad Hashim
Amjad, Rana
Riazuddin, Sheikh
Drayna, Dennis
TI Studies in a consanguineous family reveal a novel locus for stuttering
on chromosome 16q
SO HUMAN GENETICS
LA English
DT Article
ID LINKAGE ANALYSIS
C1 [Raza, Muhammad Hashim; Drayna, Dennis] Natl Inst Deafness & Other Commun Disorders NIDCD, NIH, Bethesda, MD USA.
[Amjad, Rana; Riazuddin, Sheikh] Univ Punjab, Allama Iqbal Med Res Ctr, Lahore, Pakistan.
[Amjad, Rana; Riazuddin, Sheikh] Univ Punjab, Ctr Excellence Mol Biol, Lahore, Pakistan.
RP Drayna, D (reprint author), Natl Inst Deafness & Other Commun Disorders NIDCD, NIH, Bethesda, MD USA.
EM drayna@nidcd.nih.gov
FU Higher Education Commission; Ministry of Science and Technology,
Islamabad, Pakistan; National Institute on Deafness and Other
Communication Disorders/National Institutes of Health [Z01-000046-11]
FX We thank Ms. Bushra Raza for assistance with stuttering diagnosis, and
A. Schaffer, T. Friedman, and R. Morell for helpful comments on the
manuscript. We particularly thank the family members who participated in
this research study. This work was supported by the Higher Education
Commission and the Ministry of Science and Technology, Islamabad,
Pakistan and by the National Institute on Deafness and Other
Communication Disorders/National Institutes of Health Intramural Grant #
Z01-000046-11.
NR 6
TC 8
Z9 9
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 2012
VL 131
IS 2
BP 311
EP 313
DI 10.1007/s00439-011-1134-2
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA 876QQ
UT WOS:000299123000013
PM 22205390
ER
PT J
AU Bornstein, MH
Mash, C
Arterberry, ME
Manian, N
AF Bornstein, Marc H.
Mash, Clay
Arterberry, Martha E.
Manian, Nanmathi
TI Object perception in 5-month-old infants of clinically depressed and
nondepressed mothers
SO INFANT BEHAVIOR & DEVELOPMENT
LA English
DT Article
DE Object perception; Maternal depression
ID POSTNATAL DEPRESSION; MATERNAL DEPRESSION; POSTPARTUM DEPRESSION;
COGNITIVE-DEVELOPMENT; ORIENTATION DISCRIMINATION; FAMILIARIZATION TIME;
PARENTING BEHAVIOR; CHILDREN; IMPACT; PREFERENCES
AB Five-month-old infants of clinically depressed and nondepressed mothers were familiarized to a wholly novel object and afterward tested for their discrimination of the same object presented in the familiar and in a novel perspective. Infants in both groups were adequately familiarized, but infants of clinically depressed mothers failed to discriminate between novel and familiar views of the object, whereas infants of nondepressed mothers successfully discriminated. The difference in discrimination between infants of depressed and nondepressed mothers is discussed in light of infants' differential object processing and maternal sociodemographics, mind-mindedness, depression, stress, and interaction styles that may moderate opportunities for infants to learn about their world or influence the development of their perceptuocognitive capacities. Published by Elsevier Inc.
C1 [Bornstein, Marc H.; Mash, Clay] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, 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, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
FU Intramural NIH HHS [Z01 HD001119-20]
NR 63
TC 1
Z9 1
U1 3
U2 9
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 2012
VL 35
IS 1
BP 150
EP 157
DI 10.1016/j.infbeh.2011.07.008
PG 8
WC Psychology, Developmental
SC Psychology
GA 881NE
UT WOS:000299492600014
PM 21903275
ER
PT J
AU Burstein, M
Georgiades, K
Lamers, F
Swanson, SA
Cui, LH
He, JP
Avenevoli, S
Merikangas, KR
AF Burstein, Marcy
Georgiades, Katholiki
Lamers, Femke
Swanson, Sonja A.
Cui, Lihong
He, Jian-Ping
Avenevoli, Shelli
Merikangas, Kathleen R.
TI Empirically Derived Subtypes of Lifetime Anxiety Disorders:
Developmental and Clinical Correlates in US Adolescents
SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY
LA English
DT Article
DE anxiety disorders; lifetime comorbidity; epidemiology; adolescents;
National Coinorbidity Survey Replication-Adolescent Supplement (NCS-A)
ID COMORBIDITY SURVEY REPLICATION; LATENT CLASS ANALYSIS; SUPPLEMENT NCS-A;
BEHAVIORAL GROUP-THERAPY; COMMON MENTAL-DISORDERS; DSM-IV ANXIETY;
SOCIAL PHOBIA; YOUNG-ADULTS; CHILD PSYCHOPATHOLOGY; DEPRESSIVE SYMPTOMS
AB Objective: The current study examined the sex- and age-specific structure and comorbidity of lifetime anxiety disorders among U.S. adolescents. Method: The sample consisted of 2,539 adolescents (1,505 females and 1,034 males) from the National Comorbidity Survey Adolescent Supplement who met criteria for Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev. [DSM-IV-TR]) lifetime anxiety disorders (American Psychiatric Association, 2000). Adolescents ranged in age from 13 to 18 years (M = 15.2 years, SE = 0.08 years) and were 39% non-White. Multiple-group latent class analysis was conducted by adolescent sex and age to identify subgroups of adolescents with similar anxiety disorder profiles. Developmental and clinical correlates of empirically derived classes were also examined to assess the nomological validity of identified subgroups. Results: A 7-class solution provided the best tit to the data, with classes defined primarily by one rather than multiple anxiety disorders. Results also indicated that classes displayed similar diagnostic profiles across age, but varied by sex. Classes characterized by multiple anxiety disorders were consistently associated with a greater degree of persistence, clinical severity, impairment, and comorbidity with other DSM-IV-TR psychiatric disorders. Conclusions: The presentation of lifetime anxiety disorders among adolescents and the observation of unique correlates of specific classes provide initial evidence for the utility of individual DSM-IV-TR anxiety disorder categories. Although findings of the present study should be considered preliminary, results emphasize the potential value of early intervention and gender-specific conceptualization and treatment of anxiety disorders.
C1 [Burstein, Marcy; Lamers, Femke; Cui, Lihong; He, Jian-Ping; Merikangas, Kathleen R.] NIMH, Genet Epidemiol Res Branch, Bethesda, MD 20892 USA.
[Georgiades, Katholiki] McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada.
[Swanson, Sonja A.] Harvard Univ, Dept Epidemiol, Sch Publ Hlth, Cambridge, MA 02138 USA.
[Avenevoli, Shelli] NIMH, Div Dev Translat Res, Bethesda, MD 20892 USA.
RP Burstein, M (reprint author), NIMH, Genet Epidemiol Res Branch, Bldg 35,Room 1A104,35 Convent Dr,MSC 3720, Bethesda, MD 20892 USA.
EM marcy.burstein@nih.gov
RI Lamers, Femke/G-5161-2012
FU Intramural NIH HHS; NIDA NIH HHS [R01 DA016558, R01 DA016558-01]; NIMH
NIH HHS [U01 MH060220, U01 MH060220-01, U01-MH60220]
NR 92
TC 11
Z9 11
U1 3
U2 11
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0022-006X
J9 J CONSULT CLIN PSYCH
JI J. Consult. Clin. Psychol.
PD FEB
PY 2012
VL 80
IS 1
BP 102
EP 115
DI 10.1037/a0026069
PG 14
WC Psychology, Clinical
SC Psychology
GA 882SX
UT WOS:000299585300010
PM 22081863
ER
PT J
AU Hsu, JC
Di Pasquale, G
Harunaga, JS
Onodera, T
Hoffman, MP
Chiorini, JA
Yamada, KM
AF Hsu, J. C.
Di Pasquale, G.
Harunaga, J. S.
Onodera, T.
Hoffman, M. P.
Chiorini, J. A.
Yamada, K. M.
TI Viral Gene Transfer to Developing Mouse Salivary Glands
SO JOURNAL OF DENTAL RESEARCH
LA English
DT Article
DE AAV; embryonic; gene transfer; organogenesis; salivary glands;
transduction
ID VIRUS TYPE-2 INFECTION; GROWTH-FACTOR RECEPTOR; BRANCHING MORPHOGENESIS;
SUBMANDIBULAR-GLAND; SYSTEMS-ANALYSIS; EXPRESSION; CELL; CORECEPTOR;
DYNAMICS; DNA
AB Branching morphogenesis is essential for the formation of salivary glands, kidneys, lungs, and many other organs during development, but the mechanisms underlying this process are not adequately understood. Microarray and other gene expression methods have been powerful approaches for identifying candidate genes that potentially regulate branching morphogenesis. However, functional validation of the proposed roles for these genes has been severely hampered by the absence of efficient techniques to genetically manipulate cells within embryonic organs. Using ex vivo cultured embryonic mouse submandibular glands (SMGs) as models to study branching morphogenesis, we have identified new vectors for viral gene transfer with high efficiency and cell-type specificity to developing SMGs. We screened adenovirus, lentivirus, and 11 types of adeno-associated viruses (AAV) for their ability to transduce embryonic day 12 or 13 SMGs. We identified two AAV types, AAV2 and bovine AAV (BAAV), that are selective in targeting expression differentially to SMG epithelial and mesenchymal cell populations, respectively. Transduction of SMG epithelia with self-complementary (sc) AAV2 expressing fibroblast growth factor 7 (Fgf7) supported gland survival and enhanced SMG branching morphogenesis. Our findings represent, to our knowledge, the first successful selective gene targeting to epithelial vs. mesenchymal cells in an organ undergoing branching morphogenesis.
C1 [Hsu, J. C.; Harunaga, J. S.; Onodera, T.; Hoffman, M. P.; Yamada, K. M.] Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, NIH, Bethesda, MD 20892 USA.
[Di Pasquale, G.; Chiorini, J. A.] Natl Inst Dent & Craniofacial Res, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
RP Yamada, KM (reprint author), Natl Inst Dent & Craniofacial Res, Lab Cell & Dev Biol, NIH, Bldg 30,Room 426,30 Convent Dr,MSC 4370, Bethesda, MD 20892 USA.
EM kenneth.yamada@nih.gov
RI Onodera, Tomohiro/G-1686-2012;
OI Yamada, Kenneth/0000-0003-1512-6805
FU Division of Intramural Research, National Institute of Dental and
Craniofacial Research, National Institutes of Health [ZIA DE000525]
FX The authors thank Shelagh Johnson for excellent editing. This work was
supported by the Division of Intramural Research, National Institute of
Dental and Craniofacial Research, National Institutes of Health, Grant
no. ZIA DE000525. The authors declare no potential conflicts of interest
with respect to the authorship and/or publication of this article.
NR 30
TC 4
Z9 4
U1 0
U2 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0345
J9 J DENT RES
JI J. Dent. Res.
PD FEB
PY 2012
VL 91
IS 2
BP 197
EP 202
DI 10.1177/0022034511429346
PG 6
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 878QT
UT WOS:000299272300015
PM 22095070
ER
PT J
AU Bachmann-Gagescu, R
Ishak, GE
Dempsey, JC
Adkins, J
O'Day, D
Phelps, IG
Gunay-Aygun, M
Kline, AD
Szczaluba, K
Martorell, L
Alswaid, A
Alrasheed, S
Pai, S
Izatt, L
Ronan, A
Parisi, MA
Mefford, H
Glass, I
Doherty, D
AF Bachmann-Gagescu, Ruxandra
Ishak, Gisele E.
Dempsey, Jennifer C.
Adkins, Jonathan
O'Day, Diana
Phelps, Ian G.
Gunay-Aygun, Meral
Kline, Antonie D.
Szczaluba, Krzysztof
Martorell, Loreto
Alswaid, Abdulrahman
Alrasheed, Shatha
Pai, Shashidhar
Izatt, Louise
Ronan, Anne
Parisi, Melissa A.
Mefford, Heather
Glass, Ian
Doherty, Dan
TI Genotype-phenotype correlation in CC2D2A-related Joubert syndrome
reveals an association with ventriculomegaly and seizures
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
ID BARDET-BIEDL-SYNDROME; MECKEL-GRUBER-SYNDROME; OUTER SEGMENT
DEVELOPMENT; RETINAL DEGENERATION; VESICLE TRAFFICKING; SYNDROME GENE;
MUTATIONS; PROTEIN; CC2D2A; CILIOPATHIES
AB Background Joubert syndrome (JS) is a ciliopathy characterised by a distinctive brain malformation (the 'molar tooth sign'), developmental delay, abnormal eye movements and abnormal breathing pattern. Retinal dystrophy, cystic kidney disease, liver fibrosis and polydactyly are variably present, resulting in significant phenotypic heterogeneity and overlap with other ciliopathies. JS is also genetically heterogeneous, resulting from mutations in 13 genes. These factors render clinical/molecular diagnosis and management challenging. CC2D2A mutations are a relatively common cause of JS and also cause Meckel syndrome. The clinical consequences of CC2D2A mutations in patients with JS have been incompletely reported.
Methods Subjects with JS from 209 families were evaluated to identify mutations in CC2D2A. Clinical and imaging features in subjects with CC2D2A mutations were compared with those in subjects without CC2D2A mutations and reports in the literature.
Results 10 novel CC2D2A mutations in 20 subjects were identified; a summary is provided of all published CC2D2A mutations. Subjects with CC2D2A-related JS were more likely to have ventriculomegaly (p<0.0001) and seizures (p=0.024) than subjects without CC2D2A mutations. No mutation-specific genotype-phenotype correlations could be identified, but the findings confirm the observation that mutations that cause CC2D2A-related JS are predicted to be less deleterious than mutations that cause CC2D2A-related Meckel syndrome. Missense variants in the coiled-coil and C2 domains, as well as the C-terminal region, identify these regions as important for the biological mechanisms underlying JS.
Conclusions CC2D2A testing should be prioritised in patients with JS and ventriculomegaly and/or seizures. Patients with CC2D2A-related JS should be monitored for hydrocephalus and seizures.
C1 [Bachmann-Gagescu, Ruxandra; Dempsey, Jennifer C.; Adkins, Jonathan; O'Day, Diana; Phelps, Ian G.; Mefford, Heather; Glass, Ian; Doherty, Dan] Univ Washington, Div Med Genet, Dept Pediat, Seattle, WA 98195 USA.
[Ishak, Gisele E.] Univ Washington, Dept Radiol, Seattle Childrens Hosp, Seattle, WA 98195 USA.
[Gunay-Aygun, Meral] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Kline, Antonie D.] Greater Baltimore Med Ctr, Harvey Inst Human Genet, Baltimore, MD USA.
[Szczaluba, Krzysztof] Inst Mother & Child Hlth, Dept Med Genet, Warsaw, Poland.
[Martorell, Loreto] Hosp St Joan de Deu, Mol Genet Sect, Barcelona, Spain.
[Alswaid, Abdulrahman; Alrasheed, Shatha] King Abdul Aziz Med City, Dept Pediat, Riyadh, Saudi Arabia.
[Pai, Shashidhar] Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA.
[Izatt, Louise] Guys & St Thomas NHS Fdn Trust, Dept Clin Genet, London, England.
[Ronan, Anne] Hunter Genet Unit, Waratah, NSW, Australia.
[Parisi, Melissa A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Doherty, Dan] Univ Washington, Div Dev Med, Dept Pediat, Seattle, WA 98195 USA.
RP Doherty, D (reprint author), Univ Washington, Div Med Genet, Dept Pediat, Box 356320,RR-249,1959 NE Pacific St, Seattle, WA 98195 USA.
EM ddoher@uw.edu
RI Bachmann-Gagescu, Ruxandra/A-8444-2016
OI Bachmann-Gagescu, Ruxandra/0000-0002-3571-5271
FU National Institute of Health [5KL2RR025015, R01NS064077, K12HD043376];
March of Dimes Foundation [5-FY09-13]; Arc of Washington Trust; Lung GO
Sequencing Project [HL-102923]; WHI [HL-102924]; Broad GO Sequencing
Project [HL-102925]; Seattle GO Sequencing Project [HL-102926]; Heart GO
Sequencing Project [HL-103010]
FX This work was supported by National Institute of Health grants
5KL2RR025015 and R01NS064077 to DD, and K12HD043376 to RB-G, by Basil
O'Connor Start Scholar Research Grant No 5-FY09-13 from the March of
Dimes Foundation to DD, and by an Arc of Washington Trust Fund grant to
DD. We would also like to thank the NHLBI GO Exome Sequencing Project
and its ongoing studies which produced and provided exome variant calls
for comparison: the Lung GO Sequencing Project (HL-102923), the WHI
Sequencing Project (HL-102924), the Broad GO Sequencing Project
(HL-102925), the Seattle GO Sequencing Project (HL-102926) and the Heart
GO Sequencing Project (HL-103010).
NR 48
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U1 3
U2 3
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
J9 J MED GENET
JI J. Med. Genet.
PD FEB
PY 2012
VL 49
IS 2
BP 126
EP 137
DI 10.1136/jmedgenet-2011-100552
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 879DC
UT WOS:000299308900010
PM 22241855
ER
PT J
AU Warren, KE
Gururangan, S
Geyer, JR
McLendon, RE
Poussaint, TY
Wallace, D
Balis, FM
Berg, SL
Packer, RJ
Goldman, S
Minturn, JE
Pollack, IF
Boyett, JM
Kun, LE
AF Warren, Katherine E.
Gururangan, Sri
Geyer, J. Russell
McLendon, Roger E.
Poussaint, Tina Young
Wallace, Dana
Balis, Frank M.
Berg, Stacey L.
Packer, Roger J.
Goldman, Stewart
Minturn, Jane E.
Pollack, Ian F.
Boyett, James M.
Kun, Larry E.
TI A phase II study of O6-benzylguanine and temozolomide in pediatric
patients with recurrent or progressive high-grade gliomas and brainstem
gliomas: a Pediatric Brain Tumor Consortium study
SO JOURNAL OF NEURO-ONCOLOGY
LA English
DT Article
DE Glioma; Pediatric; Resistance; Alkylating agent; Brainstem glioma; AGT;
MGMT
ID NERVOUS-SYSTEM TUMORS; MGMT PROMOTER METHYLATION; CHILDRENS ONCOLOGY
GROUP; MALIGNANT GLIOMA; O-6-ALKYLGUANINE-DNA ALKYLTRANSFERASE;
ANTITUMOR IMIDAZOTETRAZINES; GLIOBLASTOMA-MULTIFORME; PLUS
O-6-BENZYLGUANINE; DRUG TEMOZOLOMIDE; MISMATCH REPAIR
AB To estimate the sustained (a parts per thousand yen8 weeks) objective response rate in pediatric patients with recurrent or progressive high-grade gliomas (HGG, Stratum A) or brainstem gliomas (BSG, Stratum B) treated with the combination of O6-benzylguanine (O6BG) and temozolomide(A (R)) (TMZ). Patients received O6BG 120 mg/m(2)/d IV followed by TMZ 75 mg/m(2)/d orally daily for 5 consecutive days of each 28-day course. The target objective response rate to consider the combination active was 17%. A two-stage design was employed. Forty-three patients were enrolled; 41 were evaluable for response, including 25 patients with HGG and 16 patients with BSG. The combination of O6BG and TMZ was tolerable, and the primary toxicities were myelosuppression and gastrointestinal symptoms. One sustained (a parts per thousand yen8 weeks) partial response was observed in the HGG cohort; no sustained objective responses were observed in the BSG cohort. Long-term (a parts per thousand yen6 courses) stable disease (SD) was observed in 4 patients in Stratum A and 1 patient in Stratum B. Of the 5 patients with objective response or long-term SD, 3 underwent central review with 2 reclassified as low-grade gliomas. The combination of O6BG and TMZ did not achieve the target response rate for activity in pediatric patients with recurrent or progressive HGG and BSG.
C1 [Warren, Katherine E.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Gururangan, Sri; McLendon, Roger E.] Duke Univ, Med Ctr, Durham, NC 27706 USA.
[Geyer, J. Russell] Seattle Childrens Hosp, Seattle, WA USA.
[Poussaint, Tina Young] Childrens Hosp, Boston, MA 02115 USA.
[Wallace, Dana; Boyett, James M.] Operat & Biostat Ctr Pediat Brain Tumor Consortiu, Memphis, TN USA.
[Balis, Frank M.; Minturn, Jane E.] Childrens Hosp, Philadelphia, PA 19104 USA.
[Berg, Stacey L.] Texas Childrens Canc Ctr, Houston, TX USA.
[Packer, Roger J.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Goldman, Stewart] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Pollack, Ian F.] Childrens Hosp Pittsburgh, Pittsburgh, PA 15213 USA.
[Kun, Larry E.] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
RP Warren, KE (reprint author), NCI, Pediat Oncol Branch, Bldg 10 CRC,Room 1-5750, Bethesda, MD 20892 USA.
EM warrenk@mail.nih.gov
FU NIH [U01 CA81457, 5M01RR000188]; American Lebanese Syrian Associated
Charities
FX This work was supported in part by NIH grant U01 CA81457 for the
Pediatric Brain Tumor Consortium, NIH grant 5M01RR000188, and the
American Lebanese Syrian Associated Charities, and the intramural
program of the NIH. The authors and the PBTC acknowledge the protocol
management of Mr. Christopher Smith, the central pathology review
participation of Dr. Adesina Adekunle and Dr. Veena Rajaram and the
statistical support of Mr. Shawn Lesh.
NR 38
TC 15
Z9 16
U1 2
U2 9
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-594X
J9 J NEURO-ONCOL
JI J. Neuro-Oncol.
PD FEB
PY 2012
VL 106
IS 3
BP 643
EP 649
DI 10.1007/s11060-011-0709-z
PG 7
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA 879LX
UT WOS:000299331800022
PM 21968943
ER
PT J
AU Emaminia, A
Corcoran, PC
Siegenthaler, MP
Means, M
Rasmussen, S
Krause, L
LaPar, DJ
Horvath, KA
AF Emaminia, Abbas
Corcoran, Phillip C.
Siegenthaler, Michael P.
Means, Melissa
Rasmussen, Sarah
Krause, Linda
LaPar, Damien J.
Horvath, Keith A.
TI The universal bed model for patient care improves outcome and lowers
cost in cardiac surgery
SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
LA English
DT Article; Proceedings Paper
CT 37th Annual Meeting of the Western-Thoracic-Surgical-Association
CY JUN 22-25, 2011
CL Colorado Springs, CO
SP Western Thorac Surg Assoc
ID ROOMS
AB Objective: With the escalating demands to increase the efficiency and decrease the cost, innovations in postoperative cardiac surgical patient care are needed. The universal bed model is an innovative care delivery system that allows patient care to be managed in one setting from postoperation to discharge. We hypothesized that the universal bed model in the context of cardiac surgery would improve outcomes and efficacy.
Methods: A total of 610 consecutive patients were admitted to the universal bed unit and prospectively entered into the Society of Thoracic Surgeons National Cardiac Database. Intensive care unit level of care was determined by acuity and staffing needs. Telemetry was employed from admission to discharge, and multidisciplinary rounds were conducted twice daily. Postoperative outcomes were recorded during hospital stay, and comparisons were made with the Society of Thoracic Surgeons National Cardiac Database using identical variables over the same period of time.
Results: Decreased ventilation time, intensive care unit and hospital stay, and reduction in the incidence of atrial fibrillation and infectious complications yielded a financial benefit in the universal bed group compared with the traditional model of admission. Stroke rate and in-hospital mortality were the same compared with regional and national centers. Compared with regional centers, there was an average cost savings between $6200 and $9500 per patient depending on the operation. Patient care satisfaction by independent survey was in the 99th percentile.
Conclusions: The universal bed patient care model allows for expedient and efficacious care as measured by decreased length of intensive care unit and hospital stay, improved postoperative outcomes, patient satisfaction, and cost savings. (J Thorac Cardiovasc Surg 2012;143:475-81)
C1 [Emaminia, Abbas; Corcoran, Phillip C.; Siegenthaler, Michael P.; Means, Melissa; Rasmussen, Sarah; Krause, Linda; Horvath, Keith A.] Suburban Hosp, Cardiothorac Surg Res Program, NIH, Ctr Heart, Bethesda, MD USA.
[LaPar, Damien J.] Univ Virginia, Dept Surg, Charlottesville, VA USA.
RP Horvath, KA (reprint author), Suburban Hosp, Cardiothorac Surg Res Program, NIH, Ctr Heart, 8600 Old Georgetown Rd, Bethesda, MD USA.
EM horvathka@nhlbi.nih.gov
NR 12
TC 3
Z9 3
U1 2
U2 9
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-5223
J9 J THORAC CARDIOV SUR
JI J. Thorac. Cardiovasc. Surg.
PD FEB
PY 2012
VL 143
IS 2
BP 475
EP 481
DI 10.1016/j.jtcvs.2011.10.001
PG 7
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 879GP
UT WOS:000299318000037
PM 22153858
ER
PT J
AU Wood, BJ
Poon, RT
Locklin, JK
Dreher, MR
Ng, KK
Eugeni, M
Seidel, G
Dromi, S
Neennan, Z
Kolf, M
Black, CDV
Prabhakar, R
Libutti, SK
AF Wood, Bradford J.
Poon, Ronnie T.
Locklin, Julia K.
Dreher, Matthew R.
Ng, K. K.
Eugeni, Michelle
Seidel, Geoffrey
Dromi, Sergio
Neennan, Ziv
Kolf, Michael
Black, Christopher D. V.
Prabhakar, Raj
Libutti, Steven K.
TI Phase I Study of Heat-Deployed Liposomal Doxorubicin during
Radiofrequency Ablation for Hepatic Malignancies
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID TEMPERATURE SENSITIVE LIPOSOMES; COLORECTAL LIVER METASTASES; TUMOR
XENOGRAFT MODEL; THERMAL ABLATION; DRUG-DELIVERY;
HEPATOCELLULAR-CARCINOMA; LOCAL RECURRENCE; COAGULATION; CANCER;
ACCUMULATION
AB Purpose: A phase I dose escalation study was performed with systemically delivered lyso-thermosensitive liposomal doxorubicin (LTLD). The primary objectives were to determine the safe maximum tolerated dose (MTD), pharmacokinetic properties, and dose-limiting toxicity (DLT) of LTLD during this combination therapy.
Materials and Methods: Subjects eligible for percutaneous or surgical radiofrequency (RF) ablation with primary (n = 9) or metastatic (n = 15) tumors of the liver, with four or fewer lesions as large as 7 cm in diameter, were included. RF ablation was initiated 15 minutes after starting a 30-minute intravenous LTLD infusion. Dose levels between 20 mg/m(2) and 60 mg/m(2) were evaluated. Magnetic resonance imaging, positron emission tomography, and computed tomography were performed at predetermined intervals before and after treatment until evidence of recurrence was seen, administration of additional antitumor treatment was performed, or a total of 3 years had elapsed.
Results: DLT criteria were met at 60 mg/m(2), and the MTD was defined as 50 mg/m(2). RF ablation was performed during the peak of the plasma concentration time curve in an effort to yield maximal drug deposition. LTLD produced reversible, dose-dependent neutropenia and leukopenia.
Conclusions: LTLD can be safely administered systemically at the MTD (50 mg/m(2)) in combination with RF ablation, with limited and manageable toxicity. Further evaluation of this agent combined with RF ablation is warranted to determine its role in the management of liver tumors.
C1 [Wood, Bradford J.; Locklin, Julia K.; Dreher, Matthew R.; Dromi, Sergio; Neennan, Ziv] NIH, Ctr Intervent Oncol Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
[Eugeni, Michelle; Seidel, Geoffrey; Kolf, Michael; Libutti, Steven K.] NCI, Surg Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Seidel, Geoffrey] NCI, Clin Monitoring Res Program, Sci Applicat Int Corp Frederick, Frederick, MD 21701 USA.
[Black, Christopher D. V.; Prabhakar, Raj] Celsion, Lawrenceville, NJ USA.
[Poon, Ronnie T.; Ng, K. K.] Univ Hong Kong, Queen Mary Hosp, Dept Surg, Hong Kong, Hong Kong, Peoples R China.
RP Locklin, JK (reprint author), NIH, Ctr Intervent Oncol Radiol & Imaging Sci, Ctr Clin, 9000 Rockville Pk,Bldg 10,Room 1C364,MSC 1182, Bethesda, MD 20892 USA.
EM locklinj@cc.nih.gov
FU National Cancer Institute; National Institutes of Health (NIH)
[HHSN261200800001E]
FX This project has been funded in whole or in part with federal funds from
the National Cancer Institute and the Intramural Research Program of the
National Institutes of Health (NIH), and is also supported by
NIH/Celsion Cooperative Research Development Agreement 01974 and
contract no. HHSN261200800001E.
NR 35
TC 36
Z9 40
U1 2
U2 22
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD FEB
PY 2012
VL 23
IS 2
BP 248
EP 255
DI 10.1016/j.jvir.2011.10.018
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 883TA
UT WOS:000299656600016
PM 22178041
ER
PT J
AU Dreher, MR
Sharma, KV
Woods, DL
Reddy, G
Tang, YQ
Pritchard, WF
Chiesa, OA
Karanian, JW
Esparza, JA
Donahue, D
Levy, EB
Willis, SL
Lewis, AL
Wood, BJ
AF Dreher, Matthew R.
Sharma, Karun V.
Woods, David L.
Reddy, Goutham
Tang, Yiqing
Pritchard, William F.
Chiesa, Oscar A.
Karanian, John W.
Esparza, Juan A.
Donahue, Danielle
Levy, Elliot B.
Willis, Sean L.
Lewis, Andrew L.
Wood, Bradford J.
TI Radiopaque Drug-Eluting Beads for Transcatheter Embolotherapy:
Experimental Study of Drug Penetration and Coverage in Swine
SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY
LA English
DT Article
ID UNRESECTABLE HEPATOCELLULAR-CARCINOMA; RANDOMIZED CONTROLLED TRIAL;
ARTERIAL EMBOLIZATION; TRANSARTERIAL CHEMOEMBOLIZATION; LIVER-TUMORS;
HEPATIC MALIGNANCIES; RABBIT LIVER; IN-VITRO; MICROSPHERES; DOXORUBICIN
AB Purpose: To determine local doxorubicin levels surrounding radiopaque drug-eluting beads (DEBs) in normal swine liver and kidney following transcatheter arterial chemoembolization. The influence of bead size (70-150 mu m or 100-300 mu m) was compared with regard to tissue penetration and spatial distribution of the bead, as well as eventual drug coverage (ie, amount of tissue exposed to drug).
Materials and Methods: Radiopaque DEBs were synthesized by suspension polymerization followed by incorporation of iodized oil and doxorubicin. Chemoembolization of swine liver and kidney was performed under fluoroscopic guidance. Three-dimensional tissue penetration of "imageable" DEBs was investigated ex vivo with micro computed tomography (microCT). Drug penetration from the bead surface and drug coverage was evaluated with epifluorescence microscopy, and cellular localization of doxorubicin was evaluated with confocal microscopy. Necrosis was evaluated with hematoxylin and eosin staining.
Results: MicroCT demonstrated that 70-150-mu m DEBs were present in more distal arteries and located in a more frequent and homogeneous spatial distribution. Tissue penetration of doxorubicin from the bead appeared similar (similar to 300 mu m) for both DEBs, with a maximum tissue drug concentration at 1 hour coinciding with nuclear localization of doxorubicin. The greater spatial frequency of the 70-150-mu m DEBs resulted in approximately twofold improved drug coverage in kidney. Cellular death is predominantly observed around the DEBs beginning at 8 hours, but increased at 24 and 168 hours.
Conclusions: Smaller DEBs penetrated further into targeted tissue (ie, macroscopic) with a higher spatial density, resulting in greater and more uniform drug coverage (ie, microscopic) in swine.
C1 [Dreher, Matthew R.; Sharma, Karun V.; Woods, David L.; Reddy, Goutham; Donahue, Danielle; Levy, Elliot B.; Wood, Bradford J.] NCI, Ctr Intervent Oncol, Ctr Clin, NIH, Bethesda, MD 20892 USA.
[Pritchard, William F.; Chiesa, Oscar A.; Karanian, John W.; Esparza, Juan A.] US FDA, Ctr Devices & Radiol Hlth, Laurel, MD USA.
[Sharma, Karun V.] Georgetown Univ Hosp, Dept Radiol, Washington, DC 20007 USA.
[Tang, Yiqing; Willis, Sean L.; Lewis, Andrew L.] Biocompatibles, Farnham, Surrey, England.
RP Wood, BJ (reprint author), NCI, Ctr Intervent Oncol, Ctr Clin, NIH, 9000 Rockville Pike,Bldg 10,Room 1C341,MSC 1182, Bethesda, MD 20892 USA.
EM bwood@nih.gov
OI Lewis, Andrew/0000-0001-5779-5631
FU Biocompatibles (Farnham, UK); National Institutes of Health (NIH);
Society of Interventional Radiology Foundation; United States Food and
Drug Administration
FX B.J.W. and M.R.D. received research support from Biocompatibles
(Farnham, UK). ALL., S.L.W., and Y.T. are paid employees of
Biocompatibles. None of the other authors have identified a conflict of
interest.; This study was conducted in the Center for Interventional
Oncology and is supported in part by the Intramural Research Program of
the National Institutes of Health (NIH), the Society of Interventional
Radiology Foundation Ring Grant, and an Interagency Agreement between
the NIH and the United States Food and Drug Administration. NIH and
Biocompatibles UK have a Cooperative Research and Development Agreement.
NR 39
TC 26
Z9 27
U1 3
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1051-0443
J9 J VASC INTERV RADIOL
JI J. Vasc. Interv. Radiol.
PD FEB
PY 2012
VL 23
IS 2
BP 257
EP 264
DI 10.1016/j.jvir.2011.10.019
PG 8
WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular
Disease
SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System &
Cardiology
GA 883TA
UT WOS:000299656600017
PM 22178039
ER
PT J
AU Katsounas, A
Trippler, M
Wang, B
Polis, M
Lempicki, RA
Kottilil, S
Gerken, G
Schlaak, JF
AF Katsounas, A.
Trippler, M.
Wang, B.
Polis, M.
Lempicki, R. A.
Kottilil, S.
Gerken, G.
Schlaak, J. F.
TI CCL5 mRNA is a marker for early fibrosis in chronic hepatitis C and is
regulated by interferon-alpha therapy and toll-like receptor 3
signalling
SO JOURNAL OF VIRAL HEPATITIS
LA English
DT Article
DE CCL5; fibrosis; HCV; IFN-a; stellate cells
ID IMMUNE-RESPONSES; STELLATE CELLS; SURFACE EXPRESSION; CCR5 EXPRESSION;
VIRUS-INFECTION; T-LYMPHOCYTES; CHEMOKINE; RANTES; LIVER; IFN
AB . Mechanisms causing liver fibrosis during chronic hepatitis C virus infection (cHCV) are not sufficiently understood. This study was aimed to identify biomarkers for early fibrosis (EF) and to investigate their potential role in cHCV-related fibrogenesis. To this end, peripheral whole blood (PB) samples from 36 patients with cHCV recruited from two independent cohorts were subjected to microarray analysis 12 h before initiation of peginterferon-alpha (Peg-IFN-a) and ribavirin therapy. Liver biopsies were evaluated using the Batts-Ludwig staging (BL-S) classification system for fibrosis. We showed that gene expression profiles (N = 8) distinguished between EF (BL-S: 0,1) and late fibrosis (LF; BL-S: 2,3,4) with 88.9% accuracy. Fibrosis-related functional annotations for chemokine-C-C-motif ligand 5 (CCL5) provided foundation for focused investigation, and qRT-PCR confirmed that CCL5 mRNA levels (PB) reliably discriminate EF from LF (accuracy: 86.7%). Positive correlations (P < 0.05) with CCL5 mRNA levels and EF discovered gene expression profiles (PB) reflecting stable expression of IFN-a receptor 1, negative regulation of the MyD88-dependent toll-like receptor (TLR) pathway and decreased expression of TLR3 in vivo. Remarkably, Peg-IFN-a suppressed CCL5 mRNA levels (PB) in EF in vivo. These findings along with results from parallel in vitro investigation into the effect of IFN-a or poly I:C (TLR3-agonist) on CCL5 gene expression in hepatic stellate cells (HSC) attest to the multi-site involvement of these pathways in regulating fibrogenesis. In conclusion, we identified novel, reliable biomarkers for EF and exposed functional properties of the molecular network regulating CCL5 biosynthesis in peripheral or hepatic cell types with key roles in cHCV-related liver and/or immune pathogenesis.
C1 [Katsounas, A.; Trippler, M.; Wang, B.; Gerken, G.; Schlaak, J. F.] Univ Hosp Essen, Dept Gastroenterol & Hepatol, D-45122 Essen, Germany.
[Katsounas, A.; Lempicki, R. A.] NCI, Lab Immunopathogenesis & Bioinformat, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Polis, M.; Kottilil, S.] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Schlaak, JF (reprint author), Univ Hosp Essen, Dept Gastroenterol & Hepatol, Hufelandstr 55, D-45122 Essen, Germany.
EM joerg.schlaak@uni-due.de
RI Lempicki, Richard/E-1844-2012;
OI Lempicki, Richard/0000-0002-7059-409X; Polis,
Michael/0000-0002-9151-2268; Schlaak, Joerg/0000-0002-9499-1014
FU Association for the Promotion of Scientific Research and Science of the
Clinic for Gastroenterology and Hepatology at the University Hospital
Essen (Essen, NRW, Germany); National Cancer Institute, National
Institutes of Health [HHSN261200800001E]
FX This research was funded in part with funds from the Association for the
Promotion of Scientific Research and Science of the Clinic for
Gastroenterology and Hepatology at the University Hospital Essen (Essen,
NRW, Germany) and in part with federal funds from the National Cancer
Institute, National Institutes of Health, under Contract No.
HHSN261200800001E.
NR 41
TC 4
Z9 4
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1352-0504
J9 J VIRAL HEPATITIS
JI J. Viral Hepatitis
PD FEB
PY 2012
VL 19
IS 2
BP 128
EP 137
DI 10.1111/j.1365-2893.2011.01503.x
PG 10
WC Gastroenterology & Hepatology; Infectious Diseases; Virology
SC Gastroenterology & Hepatology; Infectious Diseases; Virology
GA 876HC
UT WOS:000299097400035
PM 22239502
ER
PT J
AU Johnson, TR
McLellan, JS
Graham, BS
AF Johnson, Teresa R.
McLellan, Jason S.
Graham, Barney S.
TI Respiratory Syncytial Virus Glycoprotein G Interacts with DC-SIGN and
L-SIGN To Activate ERK1 and ERK2
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID HUMAN DENDRITIC CELLS; HEPATITIS-C VIRUS; CD4 T-CELLS; FUSION
GLYCOPROTEIN; CYTOKINE PRODUCTION; IMMUNE-RESPONSES; INFECTION; PROTEIN;
ATTACHMENT; HIV-1
AB Respiratory syncytial virus (RSV) interaction with epithelial and dendritic cells (DCs) is known to require divalent cations, suggesting involvement of C-type lectins. RSV infection and maturation of primary human DCs are reduced in a dose-dependent manner by EDTA. Therefore, we asked whether RSV infection involves DC-SIGN (CD209) or its isoform L-SIGN (CD299) (DC-SIGN/R). Using surface plasmon resonance analysis, we demonstrated that the attachment G glycoprotein of RSV binds both DC-and L-SIGN. However, neutralization of DC-and L-SIGN on primary human DCs did not inhibit RSV infection, demonstrating that interactions between RSV G and DC-or L-SIGN are not required for productive infection. Thus, neither DC-nor L-SIGN represents a functional receptor for RSV. However, inhibition of these interactions increased DC activation, as evidenced by significantly higher levels of alpha interferon (IFN-alpha), MIP-1 alpha, and MIP-1 beta in plasmacytoid DCs (pDCs) exposed to RSV after neutralization of DC-and L-SIGN. To understand the molecular interactions involved, intracellular signaling events triggered by purified RSV G glycoprotein were examined in DC-and L-SIGN-transfected 3T3 cells. RSV G interaction with DC- or L-SIGN was shown to stimulate ERK1 and ERK2 phosphorylation, with statistically significant increases relative to mock-infected cells. Neutralization of DC-and L-SIGN reduced ERK1/2 phosphorylation. With increased DC activation following DC- and L-SIGN neutralization and RSV exposure, these data demonstrate that the signaling events mediated by RSV G interactions with DC/L-SIGN are immunomodulatory and diminish DC activation, which may limit induction of RSV-specific immunity.
C1 [Johnson, Teresa R.; Graham, Barney S.] NIAID, Viral Pathogenesis Lab, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[McLellan, Jason S.] NIAID, Struct Biol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Johnson, TR (reprint author), NIAID, Viral Pathogenesis Lab, Vaccine Res Ctr, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM tjohnson@genvec.com
NR 61
TC 37
Z9 39
U1 1
U2 8
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 2012
VL 86
IS 3
BP 1339
EP 1347
DI 10.1128/JVI.06096-11
PG 9
WC Virology
SC Virology
GA 879CT
UT WOS:000299308000006
PM 22090124
ER
PT J
AU Stucker, KM
Pagan, I
Cifuente, JO
Kaelber, JT
Lillie, TD
Hafenstein, S
Holmes, EC
Parrish, CR
AF Stucker, Karla M.
Pagan, Israel
Cifuente, Javier O.
Kaelber, Jason T.
Lillie, Tyler D.
Hafenstein, Susan
Holmes, Edward C.
Parrish, Colin R.
TI The Role of Evolutionary Intermediates in the Host Adaptation of Canine
Parvovirus
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID FELINE PANLEUKOPENIA VIRUS; MINK ENTERITIS VIRUS; CAPSID STRUCTURE;
MONOCLONAL-ANTIBODIES; TRANSFERRIN RECEPTORS; INFLUENZA-VIRUSES; RANGE;
BINDING; DNA; TYPE-2
AB The adaptation of viruses to new hosts is a poorly understood process likely involving a variety of viral structures and functions that allow efficient replication and spread. Canine parvovirus (CPV) emerged in the late 1970s as a host-range variant of a virus related to feline panleukopenia virus (FPV). Within a few years of its emergence in dogs, there was a worldwide replacement of the initial virus strain (CPV type 2) by a variant (CPV type 2a) characterized by four amino acid differences in the capsid protein. However, the evolutionary processes that underlie the acquisition of these four mutations, as well as their effects on viral fitness, both singly and in combination, are still uncertain. Using a comprehensive experimental analysis of multiple intermediate mutational combinations, we show that these four capsid mutations act in concert to alter antigenicity, cell receptor binding, and relative in vitro growth in feline cells. Hence, host adaptation involved complex interactions among both surface-exposed and buried capsid mutations that together altered cell infection and immune escape properties of the viruses. Notably, most intermediate viral genotypes containing different combinations of the four key amino acids possessed markedly lower fitness than the wild-type viruses.
C1 [Stucker, Karla M.; Kaelber, Jason T.; Lillie, Tyler D.; Parrish, Colin R.] Cornell Univ, Coll Vet Med, Dept Microbiol & Immunol, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
[Pagan, Israel; Holmes, Edward C.] Penn State Univ, Dept Biol, Ctr Infect Dis Dynam, University Pk, PA 16802 USA.
[Cifuente, Javier O.; Hafenstein, Susan] Penn State Univ, Coll Med, Div Infect Dis, Hershey, PA USA.
[Holmes, Edward C.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Parrish, CR (reprint author), Cornell Univ, Coll Vet Med, Dept Microbiol & Immunol, Baker Inst Anim Hlth, Ithaca, NY 14853 USA.
EM crp3@cornell.edu
RI Pagan, Israel/H-1843-2015; Cifuente, Javier/F-3874-2016;
OI Pagan, Israel/0000-0001-8876-1194; Cifuente, Javier/0000-0001-5420-121X;
Kaelber, Jason/0000-0001-9426-1030; Holmes, Edward/0000-0001-9596-3552
FU National Institutes of Health (NIH) [AI28385, AI092571, GM080533,
RR007059]; Marie Curie Fellowship [PIOF-GA-2009-236470]
FX This work was supported by National Institutes of Health (NIH) grants
AI28385 and AI092571 to C. R. P. and GM080533 to E. C. H. K. M. S. was
supported by NIH training grant RR007059 to Douglas D. McGregor, and I.
P. was supported by Marie Curie Fellowship PIOF-GA-2009-236470.
NR 37
TC 17
Z9 18
U1 0
U2 13
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 2012
VL 86
IS 3
BP 1514
EP 1521
DI 10.1128/JVI.06222-11
PG 8
WC Virology
SC Virology
GA 879CT
UT WOS:000299308000021
PM 22114336
ER
PT J
AU Satheshkumar, PS
Moss, B
AF Satheshkumar, P. S.
Moss, Bernard
TI Sequence-Divergent Chordopoxvirus Homologs of the O3 Protein Maintain
Functional Interactions with Components of the Vaccinia Virus
Entry-Fusion Complex
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID CELL-CELL FUSION; SURFACE HEPARAN-SULFATE; MEMBRANE-PROTEIN; POXVIRUS
ENTRY; HOST-CELLS; L1 PROTEIN; GENE; BINDS
AB Composed of 35 amino acids, O3 is the smallest characterized protein encoded by vaccinia virus (VACV) and is an integral component of the entry-fusion complex (EFC). O3 is conserved with 100% identity in all orthopoxviruses except for monkeypox viruses, whose O3 homologs have 2 to 3 amino acid substitutions. Since O3 is part of the EFC, high conservation could suggest an immutable requirement for interaction with multiple proteins. Chordopoxviruses of other genera also encode small proteins with a characteristic predicted N-terminal alpha-helical hydrophobic domain followed by basic amino acids and proline in the same relative genome location as that of VACV O3. However, the statistical significance of their similarity to VACV O3 is low due to the large contribution of the transmembrane domain, their small size, and their sequence diversity. Nevertheless, trans-complementation experiments demonstrated the ability of a representative O3-like protein from each chordopoxvirus genus to rescue the infectivity of a VACV mutant that was unable to express endogenous O3. Moreover, recombinant viruses expressing O3 homologs in place of O3 replicated and formed plaques as well or nearly as well as wild-type VACV. The O3 homologs expressed by the recombinant VACVs were incorporated into the membranes of mature virions and, with one exception, remained stably associated with the detergent-extracted and affinity-purified EFC. The ability of the sequence-divergent O3 homologs to coordinate function with VACV entry proteins suggests the conservation of structural motifs. Analysis of chimeras formed by swapping domains of O3 with those of other proteins indicated that the N-terminal transmembrane segment was responsible for EFC interactions and for the complementation of infectivity.
C1 [Satheshkumar, P. S.; Moss, Bernard] NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Moss, B (reprint author), NIAID, Viral Dis Lab, NIH, Bethesda, MD 20892 USA.
EM BMOSS@niaid.nih.gov
FU Division of Intramural Research, NIAID, NIH
FX This research was supported by the Division of Intramural Research,
NIAID, NIH.
NR 30
TC 6
Z9 6
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 2012
VL 86
IS 3
BP 1696
EP 1705
DI 10.1128/JVI.06069-11
PG 10
WC Virology
SC Virology
GA 879CT
UT WOS:000299308000036
PM 22114343
ER
PT J
AU Mehle, A
Dugan, VG
Taubenberger, JK
Doudna, JA
AF Mehle, Andrew
Dugan, Vivien G.
Taubenberger, Jeffery K.
Doudna, Jennifer A.
TI Reassortment and Mutation of the Avian Influenza Virus Polymerase PA
Subunit Overcome Species Barriers
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID SWINE-ORIGIN H1N1; A VIRUSES; MOLECULAR-BASIS; RNA-POLYMERASE; HIGH
VIRULENCE; PANDEMIC H1N1; AMINO-ACID; HOST-RANGE; GENETIC COMPATIBILITY;
CRYSTAL-STRUCTURE
AB The emergence of new pandemic influenza A viruses requires overcoming barriers to cross-species transmission as viruses move from animal reservoirs into humans. This complicated process is driven by both individual gene mutations and genome reassortments. The viral polymerase complex, composed of the proteins PB1, PB2, and PA, is a major factor controlling host adaptation, and reassortment events involving polymerase gene segments occurred with past pandemic viruses. Here we investigate the ability of polymerase reassortment to restore the activity of an avian influenza virus polymerase that is normally impaired in human cells. Our data show that the substitution of human-origin PA subunits into an avian influenza virus polymerase alleviates restriction in human cells and increases polymerase activity in vitro. Reassortants with 2009 pandemic H1N1 PA proteins were the most active. Mutational analyses demonstrated that the majority of the enhancing activity in human PA results from a threonine-to-serine change at residue 552. Reassortant viruses with avian polymerases and human PA subunits, or simply the T552S mutation, displayed faster replication kinetics in culture and increased pathogenicity in mice compared to those containing a wholly avian polymerase complex. Thus, the acquisition of a human PA subunit, or the signature T552S mutation, is a potential mechanism to overcome the species-specific restriction of avian polymerases and increase virus replication. Our data suggest that the human, avian, swine, and 2009 H1N1-like viruses that are currently cocirculating in pig populations set the stage for PA reassortments with the potential to generate novel viruses that could possess expanded tropism and enhanced pathogenicity.
C1 [Mehle, Andrew; Doudna, Jennifer A.] Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA.
[Doudna, Jennifer A.] Univ Calif Berkeley, Dept Chem, Berkeley, CA 94720 USA.
[Dugan, Vivien G.; Taubenberger, Jeffery K.] NIAID, Viral Pathogenesis & Evolut Sect, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Doudna, Jennifer A.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Phys Biosci Div, Berkeley, CA 94720 USA.
RP Mehle, A (reprint author), Univ Wisconsin, Dept Med Microbiol & Immunol, Madison, WI 53706 USA.
EM amehle@wisc.edu
FU National Institute of General Medical Sciences [K99GM088484]; NIH; NIAID
FX This work was supported in part by National Institute of General Medical
Sciences grant K99GM088484 (to A.M.) and the Intramural Research Program
of the NIH and the NIAID (to J.K.T.).
NR 54
TC 48
Z9 49
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 2012
VL 86
IS 3
BP 1750
EP 1757
DI 10.1128/JVI.06203-11
PG 8
WC Virology
SC Virology
GA 879CT
UT WOS:000299308000041
PM 22090127
ER
PT J
AU Bessen, RA
Wilham, JM
Lowe, D
Watschke, CP
Shearin, H
Martinka, S
Caughey, B
Wiley, JA
AF Bessen, Richard A.
Wilham, Jason M.
Lowe, Diana
Watschke, Christopher P.
Shearin, Harold
Martinka, Scott
Caughey, Byron
Wiley, James A.
TI Accelerated Shedding of Prions following Damage to the Olfactory
Epithelium
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID TRANSMISSIBLE MINK ENCEPHALOPATHY; UPPER RESPIRATORY-TRACT; RECEPTOR
NEURONS; CELL-DEATH; NASAL-MUCOSA; INDUCED APOPTOSIS; NATURAL SCRAPIE;
DOSE-RESPONSE; INFECTION; BULB
AB In this study, we investigated the role of damage to the nasal mucosa in the shedding of prions into nasal samples as a pathway for prion transmission. Here, we demonstrate that prions can replicate to high levels in the olfactory sensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (ORNs) in the OSE resulted in sloughing off of the OSE from nasal turbinates into the lumen of the nasal airway. In the absence of nasotoxic treatment, olfactory marker protein (OMP), which is specific for ORNs, was not detected in nasal lavage samples. However, after nasotoxic treatment that leads to apoptosis of ORNs, both OMP and prion proteins were present in nasal lavage samples. The cellular debris that was released from the OSE into the lumen of the nasal airway was positive for both OMP and the disease-specific isoform of the prion protein, PrPSc. By using the real-time quaking-induced conversion assay to quantify prions, a 100- to 1,000-fold increase in prion seeding activity was observed in nasal lavage samples following nasotoxic treatment. Since neurons replicate prions to higher levels than other cell types and ORNs are the most environmentally exposed neurons, we propose that an increase in ORN apoptosis or damage to the nasal mucosa in a host with a preexisting prion infection of the OSE could lead to a substantial increase in the release of prion infectivity into nasal samples. This mechanism of prion shedding from the olfactory mucosa could contribute to prion transmission.
C1 [Bessen, Richard A.; Lowe, Diana; Watschke, Christopher P.; Shearin, Harold; Martinka, Scott; Wiley, James A.] Montana State Univ, Dept Immunol & Infect Dis, Bozeman, MT 59717 USA.
[Wilham, Jason M.; Caughey, Byron] NIAID, Rocky Mt Labs, Persistent Viral Dis Lab, Hamilton, MT 59840 USA.
RP Bessen, RA (reprint author), Montana State Univ, Dept Immunol & Infect Dis, Bozeman, MT 59717 USA.
EM rbessen@montana.edu
FU National Institutes of Health [R01 AI055043, R21 AI084094, P20
RR020185]; National Research Initiative of the USDA CSREES
[2006-35201-16626]; Murphy Foundation; National Institute for Allergy
and Infectious Diseases, National Institutes of Health
FX This work was supported by Public Health Service grants R01 AI055043,
R21 AI084094, and P20 RR020185 from the National Institutes of Health,
the National Research Initiative of the USDA CSREES grant
2006-35201-16626, and the Murphy Foundation. This work was supported in
part by the Intramural Research Program of the National Institute for
Allergy and Infectious Diseases, National Institutes of Health.
NR 63
TC 13
Z9 13
U1 0
U2 2
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 2012
VL 86
IS 3
BP 1777
EP 1788
DI 10.1128/JVI.06626-11
PG 12
WC Virology
SC Virology
GA 879CT
UT WOS:000299308000044
PM 22130543
ER
PT J
AU San-Juan-Vergara, H
Sampayo-Escobar, V
Reyes, N
Cha, B
Pacheco-Lugo, L
Wong, T
Peeples, ME
Collins, PL
Castano, ME
Mohapatra, SS
AF San-Juan-Vergara, Homero
Sampayo-Escobar, Viviana
Reyes, Niradiz
Cha, Byeong
Pacheco-Lugo, Lisandro
Wong, Terianne
Peeples, Mark E.
Collins, Peter L.
Eugenia Castano, Maria
Mohapatra, Shyam S.
TI Cholesterol-Rich Microdomains as Docking Platforms for Respiratory
Syncytial Virus in Normal Human Bronchial Epithelial Cells
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID SMALL-MOLECULE INHIBITOR; PROTEIN-MEDIATED FUSION; SEMLIKI FOREST VIRUS;
PLASMA-MEMBRANE; FLOW-CYTOMETRY; F-PROTEIN; LIPID MICRODOMAINS;
MAMMALIAN-CELLS; INFECTED-CELLS; CILIATED CELLS
AB Respiratory syncytial virus (RSV) is one of the major causes of respiratory infections in children, and it is the main pathogen causing bronchiolitis in infants. The binding and entry mechanism by which RSV infects respiratory epithelial cells has not yet been determined. In this study, the earliest stages of RSV infection in normal human bronchial epithelial cells were probed by tracking virions with fluorescent lipophilic dyes in their membranes. Virions colocalized with cholesterol-containing plasma membrane microdomains, identified by their ability to bind cholera toxin subunit B. Consistent with an important role for cholesterol in RSV infection, cholesterol depletion profoundly inhibited RSV infection, while cholesterol repletion reversed this inhibition. Merger of the outer leaflets of the viral envelope and the cell membrane appeared to be triggered at these sites. Using small-molecule inhibitors, RSV infection was found to be sensitive to Pak1 inhibition, suggesting the requirement of a subsequent step of cytoskeletal reorganization that could involve plasma membrane rearrangements or endocytosis. It appears that RSV entry depends on its ability to dock to cholesterol-rich microdomains (lipid rafts) in the plasma membrane where hemifusion events begin, assisted by a Pak1-dependent process.
C1 [San-Juan-Vergara, Homero; Sampayo-Escobar, Viviana; Pacheco-Lugo, Lisandro; Eugenia Castano, Maria] Fdn Univ Norte, Dept Med, Barranquilla, Colombia.
[San-Juan-Vergara, Homero; Wong, Terianne; Mohapatra, Shyam S.] Univ S Florida, Dept Internal Med, Div Translat Med, Nanomed Res Ctr, Tampa, FL 33612 USA.
[Reyes, Niradiz] Univ Cartagena, Fac Med, Cartagena, Colombia.
[Cha, Byeong] Univ S Florida, Coll Med, Lisa Muma Weitz Lab Adv Microscopy & Cell Imaging, Tampa, FL USA.
[Pacheco-Lugo, Lisandro] Univ Simon Bolivar, Fac Med, Barranquilla, Colombia.
[Peeples, Mark E.] Nationwide Childrens Hosp, Res Inst, Columbus, OH USA.
[Peeples, Mark E.] Ohio State Univ, Coll Med, Dept Pediat, Columbus, OH 43210 USA.
[Collins, Peter L.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Mohapatra, Shyam S.] James Haley VA Hosp, Tampa, FL USA.
RP San-Juan-Vergara, H (reprint author), Fdn Univ Norte, Dept Med, Barranquilla, Colombia.
EM hsanjuan@uninorte.edu.co
RI Mohapatra, Shyam/C-2500-2012;
OI Pacheco-Lugo, Lisandro/0000-0002-9248-4596
FU National Institutes of Health, National Institute of Allergy and
Infectious Diseases (NIAID) [R01-AI075523]; VA Career Scientist Award;
VA Merit Review Award; Colombian Administrative Department for Science,
Technology and Innovation (COLCIENCIAS) [121540820542, 312-2007,
121549326215, 651-2009]
FX This work was supported by a grant from the National Institutes of
Health, National Institute of Allergy and Infectious Diseases (NIAID;
R01-AI075523) to H.S.-J.-V. and S.S.M., by the VA Career Scientist Award
and the VA Merit Review Award to S.S.M., and by two grants from the
Colombian Administrative Department for Science, Technology and
Innovation (COLCIENCIAS; code 121540820542, contract no. 312-2007; and
code 121549326215, contract no. 651-2009). Neither sponsor had any role
in the study design, data collection and analysis, decision to publish,
or preparation of the manuscript. Peter L. Collins was supported by the
NIAID Intramural Program. The authors declare no conflict of interest
related to this work.
NR 91
TC 23
Z9 24
U1 0
U2 8
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 2012
VL 86
IS 3
BP 1832
EP 1843
DI 10.1128/JVI.06274-11
PG 12
WC Virology
SC Virology
GA 879CT
UT WOS:000299308000049
PM 22090136
ER
PT J
AU Lambrechts, L
Fansiri, T
Pongsiri, A
Thaisomboonsuk, B
Klungthong, C
Richardson, JH
Ponlawat, A
Jarman, RG
Scott, TW
AF Lambrechts, Louis
Fansiri, Thanyalak
Pongsiri, Arissara
Thaisomboonsuk, Butsaya
Klungthong, Chonticha
Richardson, Jason H.
Ponlawat, Alongkot
Jarman, Richard G.
Scott, Thomas W.
TI Dengue-1 Virus Clade Replacement in Thailand Associated with Enhanced
Mosquito Transmission
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID PRIMARY-SCHOOL CHILDREN; LINEAGE REPLACEMENT; KAMPHAENG-PHET;
AEDES-AEGYPTI; PUERTO-RICO; SELECTION; MICROEVOLUTION; EMERGENCE;
EVOLUTION; STRAINS
AB Dengue viruses (DENV) are characterized by extensive genetic diversity and can be organized in multiple, genetically distinct lineages that arise and die out on a regular basis in regions where dengue is endemic. A fundamental question for understanding DENV evolution is the relative extent to which stochastic processes (genetic drift) and natural selection acting on fitness differences among lineages contribute to lineage diversity and turnover. Here, we used a set of recently collected and archived low-passage DENV-1 isolates from Thailand to examine the role of mosquito vector-virus interactions in DENV evolution. By comparing the ability of 23 viruses isolated on different dates between 1985 and 2009 to be transmitted by a present-day Aedes aegypti population from Thailand, we found that a major clade replacement event in the mid-1990s was associated with virus isolates exhibiting increased titers in the vector's hemocoel, which is predicted to result in a higher probability of transmission. This finding is consistent with the hypothesis that selection for enhanced transmission by mosquitoes is a possible mechanism underlying major DENV clade replacement events. There was significant variation in transmission potential among isolates within each clade, indicating that in addition to vector-driven selection, other evolutionary forces act to maintain viral genetic diversity. We conclude that occasional adaptive processes involving the mosquito vector can drive major DENV lineage replacement events.
C1 [Fansiri, Thanyalak; Pongsiri, Arissara; Richardson, Jason H.; Ponlawat, Alongkot] Armed Forces Res Inst Med Sci, Dept Entomol, Bangkok 10400, Thailand.
[Lambrechts, Louis; Fansiri, Thanyalak] Inst Pasteur, Dept Virol, Paris, France.
[Thaisomboonsuk, Butsaya; Klungthong, Chonticha; Jarman, Richard G.] Armed Forces Res Inst Med Sci, Dept Virol, Bangkok 10400, Thailand.
[Scott, Thomas W.] Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA.
[Scott, Thomas W.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Lambrechts, L (reprint author), Armed Forces Res Inst Med Sci, Dept Entomol, Bangkok 10400, Thailand.
EM louis.lambrechts@pasteur.fr
RI Lambrechts, Louis/A-2057-2010; Richardson, Jason/A-9441-2011
OI Lambrechts, Louis/0000-0001-5958-2138;
FU National Institutes of Health [R01 GM-083224]; French Agence Nationale
de la Recherche [ANR-09-RPDOC-007-01]; Science and Technology
Directorate, Department of Homeland Security, and Fogarty International
Center, National Institutes of Health
FX This study was primarily supported by grant R01 GM-083224 from the
National Institutes of Health. L. L. was supported by grant
ANR-09-RPDOC-007-01 from the French Agence Nationale de la Recherche. T.
W. S. received support from the Research and Policy for Infectious
Disease Dynamics Program of the Science and Technology Directorate,
Department of Homeland Security, and Fogarty International Center,
National Institutes of Health.
NR 48
TC 42
Z9 43
U1 0
U2 14
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 2012
VL 86
IS 3
BP 1853
EP 1861
DI 10.1128/JVI.06458-11
PG 9
WC Virology
SC Virology
GA 879CT
UT WOS:000299308000051
PM 22130539
ER
PT J
AU Liu, R
Sui, XM
Laditka, JN
Church, TS
Colabianchi, N
Hussey, J
Blair, SN
AF Liu, Rui
Sui, Xuemei
Laditka, James N.
Church, Timothy S.
Colabianchi, Natalie
Hussey, Jim
Blair, Steven N.
TI Cardiorespiratory Fitness as a Predictor of Dementia Mortality in Men
and Women
SO MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
LA English
DT Article
DE PHYSICAL FITNESS; COGNITIVE FUNCTION; ALZHEIMER DISEASE; VASCULAR
DEMENTIA; METS
ID PHYSICAL-ACTIVITY; OLDER-ADULTS; LATE-LIFE; COGNITIVE FUNCTION;
ALZHEIMER-DISEASE; APOLIPOPROTEIN-E; BLOOD-PRESSURE; EXERCISE TEST;
BRAIN; RISK
AB LIU, R., X. SUI, J. N. LADITKA, T. S. CHURCH, N. COLABIANCHI, J. HUSSEY, and S. N. BLAIR. Cardiorespiratory Fitness as a Predictor of Dementia Mortality in Men and Women. Med. Sci. Sports Exerc., Vol. 44, No. 2, pp. 253-259, 2012. There is evidence that physical activity may reduce the risk of developing Alzheimer disease and dementia. However, few reports have examined the physical activity-dementia association with objective measures of physical activity. Cardiorespiratory fitness (hereafter called fitness) is an objective reproducible measure of recent physical activity habits. Purpose: We sought to determine whether fitness is associated with lower risk for dementia mortality in women and men. Methods: We followed 14,811 women and 45,078 men, age 20-88 yr at baseline, for an average of 17 yr. All participants completed a preventive health examination at the Cooper Clinic in Dallas, TX, during 1970-2001. Fitness was measured with a maximal treadmill exercise test, with results expressed in maximal METs. The National Death Index identified deaths through 2003. Cox proportional hazards models were used to examine the association between baseline fitness and dementia mortality, adjusting for age, sex, examination year, body mass index, smoking, alcohol use, abnormal ECGs, and health status. Results: There were 164 deaths with dementia listed as the cause during 1,012,125 person-years of exposure. Each 1-MET increase in fitness was associated with a 14% lower adjusted risk of dementia mortality (95% confidence interval (CI) - 6%-22%). With fitness expressed in tertiles, adjusted hazard ratios (HRs) for those in the middle-and high-fitness groups suggest their risk of dementia mortality was less than half that of those in the lowest fitness group (HR = 0.44, CI = 0.26-0.74 and HR = 0.49, CI = 0.26-0.90, respectively). Conclusions: Greater fitness was associated with lower risk of mortality from dementia in a large cohort of men and women.
C1 [Liu, Rui] Natl Inst Environm Hlth Sci, Epidemiol Branch, Res Triangle Pk, NC 27709 USA.
[Sui, Xuemei; Blair, Steven N.] Univ S Carolina, Dept Exercise Sci, Arnold Sch Publ Hlth, Columbia, SC 29208 USA.
[Laditka, James N.] Univ N Carolina, Dept Publ Hlth Sci, Charlotte, NC 28223 USA.
[Church, Timothy S.] Pennington Biomed Res Ctr, Lab Prevent Med, Baton Rouge, LA USA.
[Colabianchi, Natalie; Hussey, Jim; Blair, Steven N.] Univ S Carolina, Dept Epidemiol & Biostat, Arnold Sch Publ Hlth, Columbia, SC 29208 USA.
RP Liu, R (reprint author), Natl Inst Environm Hlth Sci, Epidemiol Branch, 111 TW Alexan Dr,POB 12233,Mail Drop A3-05, Res Triangle Pk, NC 27709 USA.
EM liur2@niehs.nih.gov
FU National Institutes of Health [AG06945, HL62508, R21DK088195]
FX The study was supported by National Institutes of Health grants AG06945,
HL62508, and R21DK088195.
NR 32
TC 28
Z9 28
U1 2
U2 20
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0195-9131
J9 MED SCI SPORT EXER
JI Med. Sci. Sports Exerc.
PD FEB
PY 2012
VL 44
IS 2
BP 253
EP 259
DI 10.1249/MSS.0b013e31822cf717
PG 7
WC Sport Sciences
SC Sport Sciences
GA 879FY
UT WOS:000299316300009
PM 21796048
ER
PT J
AU Butler, NS
Moebius, J
Pewe, LL
Traore, B
Doumbo, OK
Tygrett, LT
Waldschmidt, TJ
Crompton, PD
Harty, JT
AF Butler, Noah S.
Moebius, Jacqueline
Pewe, Lecia L.
Traore, Boubacar
Doumbo, Ogobara K.
Tygrett, Lorraine T.
Waldschmidt, Thomas J.
Crompton, Peter D.
Harty, John T.
TI Therapeutic blockade of PD-L1 and LAG-3 rapidly clears established
blood-stage Plasmodium infection
SO NATURE IMMUNOLOGY
LA English
DT Article
ID CD4 T-CELLS; CHRONIC VIRAL-INFECTION; FALCIPARUM-MALARIA;
CHABAUDI-CHABAUDI; IMMUNE-RESPONSES; ENDEMIC AREA; B-CELLS; YOELII;
PERSISTENCE; EXHAUSTION
AB Infection of erythrocytes with Plasmodium species induces clinical malaria. Parasite-specific CD4(+) T cells correlate with lower parasite burdens and severity of human malaria and are needed to control blood-stage infection in mice. However, the characteristics of CD4(+) T cells that determine protection or parasite persistence remain unknown. Here we show that infection of humans with Plasmodium falciparum resulted in higher expression of the inhibitory receptor PD-1 associated with T cell dysfunction. In vivo blockade of the PD-1 ligand PD-L1 and the inhibitory receptor LAG-3 restored CD4(+) T cell function, amplified the number of follicular helper T cells and germinal-center B cells and plasmablasts, enhanced protective antibodies and rapidly cleared blood-stage malaria in mice. Thus, chronic malaria drives specific T cell dysfunction, and proper function can be restored by inhibitory therapies to enhance parasite control.
C1 [Moebius, Jacqueline; Crompton, Peter D.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Butler, Noah S.; Pewe, Lecia L.; Harty, John T.] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA.
[Traore, Boubacar; Doumbo, Ogobara K.] Univ Bamako, Malaria Res & Training Ctr, Dept Epidemiol Parasit Dis, Fac Med Pharm & Odontostomatol, Bamako, Mali.
[Tygrett, Lorraine T.; Waldschmidt, Thomas J.; Harty, John T.] Univ Iowa, Dept Pathol, Iowa City, IA 52242 USA.
[Waldschmidt, Thomas J.; Harty, John T.] Univ Iowa, Interdisciplinary Grad Program Immunol, Iowa City, IA 52242 USA.
RP Crompton, PD (reprint author), NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
EM pcrompton@niaid.nih.gov; john-harty@uiowa.edu
RI Crompton, Peter/N-1130-2016
FU Division of Intramural Research of the National Institute of Allergy and
Infectious Diseases; US National Institutes of Health [AI085515,
AI42767]; Department of Microbiology, University of Iowa
FX We thank the residents of Kambila, Mali, for their participation; F.
Lund (University of Rochester) for C57BL/6 Aicda-/- mice
lacking the immunoglobulin heavy-chain mu-chain secretory domain; D. A.
A. Vignali (St. Jude Children's Research Hospital) for hybridoma clone
C9B7W; and S. Perlman, N. Schmidt and V. Badovinac for comments.
Supported by the Division of Intramural Research of the National
Institute of Allergy and Infectious Diseases, the US National Institutes
of Health (for work in Mali; and AI085515 and AI42767 for work in the
J.T.H. laboratory) and the Department of Microbiology, University of
Iowa (for work in the J.T.H. laboratory).
NR 50
TC 139
Z9 144
U1 6
U2 38
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 2012
VL 13
IS 2
BP 188
EP 195
DI 10.1038/ni.2180
PG 8
WC Immunology
SC Immunology
GA 879FL
UT WOS:000299315000016
ER
PT J
AU Taveira-DaSilva, AM
Alford, CE
Levens, ED
Kotz, HL
Moss, J
AF Taveira-DaSilva, Angelo M.
Alford, Connie E.
Levens, Eric D.
Kotz, Herbert L.
Moss, Joel
TI Favorable Response to Antigonadal Therapy for a Benign Metastasizing
Leiomyoma
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID LYMPHANGIOLEIOMYOMATOSIS; UTERUS
AB BACKGROUND: Benign metastasizing leiomyoma and lymphangioleiomyomatosis (LAM) both are characterized by abnormal proliferation of smooth muscle-like cells in the lung.
CASE: A 32-year-old African woman with a diagnosis of LAM underwent myomectomy for uterine leiomyomas. An alternative diagnosis of benign metastasizing leiomy oma was made on repeat lung biopsy. Treatment with leuprolide acetate decreased pulmonary infiltrates and improved lung function and exercise tolerance.
CONCLUSION: Accurately diagnosing benign metastasizing leiomyoma has important implications for clinical outcome. Because its clinical presentation may be misleading, immunohistochemical techniques may assist in differentiating benign metastasizing leiomyoma from LAM. This is important because, in benign metastasizing leiomyoma, reduced tumor burden and improved pulmonary function may be achieved by suppressing gonadal steroids. (Obstet Gynecol 2012;119:438-42) DOI:10.1097/AOG.0b013e318240090e
C1 [Taveira-DaSilva, Angelo M.] NHLBI, Cardiovasc & Pulm Branch, Program Reprod & Adult Endocrinol,NIH, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Taveira-DaSilva, AM (reprint author), NHLBI, Cardiovasc & Pulm Branch, Program Reprod & Adult Endocrinol,NIH, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bldg 10,Room 6D05,MSC 1590, Bethesda, MD 20892 USA.
EM dasilvaa@nhlbi.nih.gov
FU NHLBI [protocol 96-H-0100]
FX Supported in part by the Intramural Research Programs of NHLBI (protocol
96-H-0100), PRAE NICHD, NIH, Bethesda, MD.
NR 8
TC 6
Z9 12
U1 0
U2 2
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 2012
VL 119
IS 2
BP 438
EP 442
DI 10.1097/AOG.0b013e318240090e
PN 2
PG 5
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 883AH
UT WOS:000299604500009
PM 22270431
ER
PT J
AU Kaushal, S
Merideth, M
Kopparthy, P
Pulanic, TK
Stratton, P
AF Kaushal, Suhasini
Merideth, Melissa
Kopparthy, Pallavi
Pulanic, Tajana Klepac
Stratton, Pamela
TI Treatment of Multifocal Bowen's Disease in Immunocompromised Women With
Surgery and Topical Imiquimod
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article; Proceedings Paper
CT Meeting of the Society-for-Gynecologic-Investigation
CY MAR 17-21, 2010
CL Orlando, FL
SP Soc Gynecol Invest
ID HIV-INFECTED PATIENTS; VULVAR INTRAEPITHELIAL NEOPLASIA; EXTERNAL
ANOGENITAL WARTS; THERAPY; CREAM
AB BACKGROUND: In human immunodeficiency virus (HIV)-infected women, Bowen's disease may be difficult to treat successfully with surgery alone. Imiquimod cream, effective in treating Bowen's disease in healthy women, may be a useful postsurgical treatment in immunocompromised women.
CASES: Two HIV-infected women had both Bowen's disease and severe cervical dysplasia. In both cases, Bowen's disease, but not cervical dysplasia, recurred after surgical treatment. When treated with topical 5% imiquimod cream twice weekly for 4 months, 70-80% reduction in lesions were observed in both patients. Follow-up biopsies of remaining lesions were vulvar intraepithelial neoplasia 1.
CONCLUSION: Imiquimod cream, in combination with surgical treatment, may be an appropriate strategy for treatment of Bowen's disease in HIV-infected and other immunocompromised women. (Obstet Gynecol 2012;119:442-4) DOI:10.1097/AOG.0b013e318236f1a0
C1 [Stratton, Pamela] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
NHLBI, Hematol Branch, Med Genet Branch,Off Director, Natl Human Genome Res Inst,Intramural Off Rare Di, Bethesda, MD 20892 USA.
RP Stratton, P (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bldg 10,Room 1-3140,10 Ctr Dr,MSC 7109, Bethesda, MD USA.
EM strattop@mail.nih.gov
FU Intramural NIH HHS [Z99 HD999999]
NR 11
TC 4
Z9 6
U1 0
U2 0
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 2012
VL 119
IS 2
BP 442
EP 444
DI 10.1097/AOG.0b013e318236f1a0
PN 2
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 883AH
UT WOS:000299604500010
PM 22270432
ER
PT J
AU Wu, M
Chason, R
Wong, M
AF Wu, Mae
Chason, Rebecca
Wong, Michelle
TI Raynaud's Phenomenon of the Nipple
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID VASOSPASM
AB BACKGROUND: Raynaud's phenomenon is a well-described pathologic state in which there is episodic vasospasm followed by vasodilation. It is described most commonly in the digits but also has been shown to affect the nipple vasculature. Raynaud's phenomenon of the nipple may result in discontinuation of breastfeeding secondary to pain and disruption of the maternal-infant bonding process.
CASES: We present the cases of two patients with painful breastfeeding associated with color changes of the nipple. Owing to a clinical presentation similar to fungal infections, the patients were treated repeatedly with antifungals before the correct diagnosis was made. Symptoms resolved with a course of nifedipine.
CONCLUSION: Increased awareness in the obstetric field will lead to appropriate diagnoses, earlier treatment and relief, and more successful breastfeeding experiences. (Obstel Gynecol 2012;119:447-9) DOI: 10.1097/AOG.0b013e31822c9a73
C1 [Wu, Mae] Natl Naval Med Ctr, Dept Obstet & Gynecol, Bethesda, MD 20889 USA.
Kennedy Shriver Natl Inst Child Hlth & Human Dev, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
RP Wu, M (reprint author), Natl Naval Med Ctr, Dept Obstet & Gynecol, 8901 Wisconsin Ave, Bethesda, MD 20889 USA.
EM Mae.Wu@med.navy.mil
NR 10
TC 2
Z9 3
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA TWO COMMERCE SQ, 2001 MARKET ST, PHILADELPHIA, PA 19103 USA
SN 0029-7844
J9 OBSTET GYNECOL
JI Obstet. Gynecol.
PD FEB
PY 2012
VL 119
IS 2
BP 447
EP 449
DI 10.1097/AOG.0b013e31822c9a73
PN 2
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 883AH
UT WOS:000299604500012
PM 22270434
ER
PT J
AU Maguire, M
Lungu, A
Gorden, P
Cochran, E
Stratton, P
AF Maguire, Marcy
Lungu, Andrea
Gorden, Phillip
Cochran, Elaine
Stratton, Pamela
TI Pregnancy in a Woman With Congenital Generalized Lipodystrophy
SO OBSTETRICS AND GYNECOLOGY
LA English
DT Article
ID HUMAN LEPTIN; OBESITY; WOMEN
AB BACKGROUND: Congenital generalized lipodystrophy is a rare disorder characterized by scant adipose tissue, profound leptin deficiency, and severe insulin resistance, resulting in multiple metabolic derangements, including hyperandrogenism, anovulation, and impaired fecundity.
CASE: A young woman with congenital generalized lipodystrophy receiving leptin therapy experienced menarche, conceived spontaneously, and delivered a liveborn male neonate.
CONCLUSION: Adipose tissue is important to normal female reproductive function. Leptin in particular appears to play a key role in adipose-mediated regulation of fertility. (Obstet Gynecol 2012;119:452-5) DOI: 10.1097/AOG.0b013e31822cecf7
C1 [Maguire, Marcy] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD 20814 USA.
NIDDK, Diabet Endocrinol & Obes Branch, Bethesda, MD USA.
RP Maguire, M (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, 1E-3140,Bldg 10 CRC,10 Ctr Dr, Bethesda, MD 20814 USA.
EM maguiremf@mail.nih.gov
FU Intramural NIH HHS [Z99 DK999999]
NR 10
TC 7
Z9 8
U1 0
U2 2
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 2012
VL 119
IS 2
BP 452
EP 455
DI 10.1097/AOG.0b013e31822cecf7
PN 2
PG 4
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 883AH
UT WOS:000299604500014
PM 22270436
ER
PT J
AU Rouleau, C
Sancho, J
Campos-Rivera, J
Teicher, BA
AF Rouleau, Cecile
Sancho, Jose
Campos-Rivera, Juanita
Teicher, Beverly A.
TI Endosialin expression in side populations in human sarcoma cell lines
SO ONCOLOGY LETTERS
LA English
DT Article
DE side populations; cancer stem cells; sarcoma marker
ID CANCER STEM-CELLS; IN-VITRO; TUMOR-CELLS; HUMAN OSTEOSARCOMA; INITIATING
CELLS; GROWTH; VIVO; IDENTIFICATION; GLYCOPROTEIN; CULTIVATION
AB The Hoechst 33342 exclusion side population (SP) assay is a validated method used to identify cells with stem cell-like properties. When isolated from tumors, SP cells have been shown to have high malignant potential. SPs have been found in both carcinomas and sarcomas. The molecular profile of sarcoma SP is poorly understood. The purpose of the present study was to determine whether endosialin is a suitable therapeutic target for sarcomas. Six cell lines (HT-1080 fibrosarcoma, SJSA-1 and HOS osteosarcoma, A-673 and SK-ES-1 Ewing sarcoma) were used for the SP analysis. Flow cytometry was used to count and examine the cells. Results showed for the first time that endosialin (CD248), which was previously identified as a sarcoma marker, is expressed in sarcoma SP cells. This observation supports the hypothesis that endosialin is a promising therapeutic target for sarcomas.
C1 [Rouleau, Cecile; Sancho, Jose; Campos-Rivera, Juanita; Teicher, Beverly A.] Genzyme Corp, Framingham, MA 01701 USA.
RP Teicher, BA (reprint author), NCI, Dev Therapeut Program, 6130 Execut Blvd, Rockville, MD 20852 USA.
EM beverly.teicher@nih.gov
NR 38
TC 8
Z9 9
U1 0
U2 1
PU SPANDIDOS PUBL LTD
PI ATHENS
PA POB 18179, ATHENS, 116 10, GREECE
SN 1792-1074
J9 ONCOL LETT
JI Oncol. Lett.
PD FEB
PY 2012
VL 3
IS 2
BP 325
EP 329
DI 10.3892/ol.2011.478
PG 5
WC Oncology
SC Oncology
GA 880KL
UT WOS:000299405900016
ER
PT J
AU Knapp, KM
Brogly, SB
Muenz, DG
Spiegel, HML
Conway, DH
Scott, GB
Talbot, JT
Shapiro, DE
Read, JS
AF Knapp, Katherine M.
Brogly, Susan B.
Muenz, Daniel G.
Spiegel, Hans M. L.
Conway, Daniel H.
Scott, Gwendolyn B.
Talbot, Jeffrey T.
Shapiro, David E.
Read, Jennifer S.
CA P1025 Team Int Maternal Pediat
TI Prevalence of Congenital Anomalies in Infants With In Utero Exposure to
Antiretrovirals
SO PEDIATRIC INFECTIOUS DISEASE JOURNAL
LA English
DT Article
DE congenital anomalies; in utero exposure; HIV; antiretroviral
ID HIV-INFECTED WOMEN; IMMUNODEFICIENCY-VIRUS TYPE-1; BIRTH-DEFECTS;
HIV-1-INFECTED WOMEN; ZIDOVUDINE TREATMENT; 1ST-TRIMESTER USE; THERAPY;
TRANSMISSION; RISK; COMBINATION
AB Background: Although use of efficacious interventions, including antiretrovirals (ARVs), has dramatically reduced the rate of mother-to-child transmission of human immunodeficiency virus, the safety of in utero ARV exposure remains of concern.
Methods: Data regarding 1112 infants enrolled in the International Maternal Pediatric Adolescent AIDS Clinical Trials Group protocol P1025 born between 2002 and 2007 were analyzed for this study. Congenital anomalies were classified based on the Metropolitan Atlanta Congenital Defects Program guidelines. Associations between congenital anomalies and timing of first in utero exposure to ARVs were evaluated by logistic regression analysis.
Results: Congenital anomalies were identified and confirmed in 61 of the 1112 infants, resulting in a prevalence of 5.49/100 live births (95% confidence interval, 4.22-6.99). Among the 80 anomalies identified, the organ systems involved included cardiovascular (n = 33), musculoskeletal (n = 15), renal (n = 9), genitourinary (n = 6), craniofacial (n = 4), and central nervous system (n = 2). First trimester exposure to efavirenz was associated with a significantly increased risk of congenital anomalies (odds ratio, 2.84; 95% confidence interval, 1.13-7.16). No significant associations were observed between exposure to other individual ARVs or classes of ARVs started at any time during pregnancy and infant congenital anomalies.
Conclusions: The observed rate of congenital anomalies in this cohort is higher than previously reported for the general population, but it is consistent with rates observed in other recent studies of children born to human immunodeficiency virus-infected women. Cardiovascular anomalies occurred most frequently. With the exception of a known teratogen (efavirenz), no statistically significant associations between in utero exposure to ARVs and congenital anomalies were identified.
C1 [Knapp, Katherine M.] St Jude Childrens Res Hosp, Dept Infect Dis, Memphis, TN 38105 USA.
[Brogly, Susan B.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Muenz, Daniel G.; Talbot, Jeffrey T.; Shapiro, David E.] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Spiegel, Hans M. L.] NIAID, Henry M Jackson Fdn Adv Mil Med, Prevent Sci Program, DAIDS,NIH, Bethesda, MD 20892 USA.
[Conway, Daniel H.] Drexel Univ, Coll Med, St Christophers Hosp Children, Dept Pediat, Philadelphia, PA 19104 USA.
[Scott, Gwendolyn B.] Univ Miami, Miller Sch Med, Div Pediat Infect Dis & Immunol, Miami, FL 33136 USA.
[Shapiro, David E.] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Read, Jennifer S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pediat Adolescent & Maternal AIDS PAMA Branch, NIH, Bethesda, MD USA.
RP Knapp, KM (reprint author), St Jude Childrens Res Hosp, Dept Infect Dis, 262 Danny Thomas Pl,Mail Stop 600, Memphis, TN 38105 USA.
EM katherine.knapp@stjude.org
FU National Institutes of Health (NIH); National Institute of Allergy and
Infectious Diseases (NIAID) [U01 AI068632]; Eunice Kennedy Shriver
National Institute of Child Health and Human Development (NICHD);
National Institute of Mental Health (NIMH) [AI068632]; Statistical and
Data Analysis Center at Harvard School of Public Health, under the
National Institute of Allergy and Infectious Diseases [5 U01 AI41110, 1
U01 AI068616]; National Institute of Allergy and Infectious Diseases
(NIAID); NICHD [N01-HD-9-001/HHSN267200800001C]
FX The authors received funding support for the research on which this
article is based from the National Institutes of Health (NIH). Overall
support for the International Maternal Pediatric Adolescent AIDS
Clinical Trials Group (IMPAACT) was provided by the National Institute
of Allergy and Infectious Diseases (NIAID) (grant U01 AI068632), the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD), and the National Institute of Mental Health (NIMH)
(grant AI068632). This work was supported by the Statistical and Data
Analysis Center at Harvard School of Public Health, under the National
Institute of Allergy and Infectious Diseases cooperative agreement
number 5 U01 AI41110 with the Pediatric AIDS Clinical Trials Group
(PACTG) and number 1 U01 AI068616 with the IMPAACT Group. Support of the
sites was provided by the National Institute of Allergy and Infectious
Diseases (NIAID) and the NICHD International and Domestic Pediatric and
Maternal HIV Clinical Trials Network funded by NICHD (contract number
N01-HD-9-001/HHSN267200800001C). The authors have no other funding or
conflicts of interest to disclose.
NR 34
TC 27
Z9 27
U1 1
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0891-3668
J9 PEDIATR INFECT DIS J
JI Pediatr. Infect. Dis. J.
PD FEB
PY 2012
VL 31
IS 2
BP 164
EP 170
DI 10.1097/INF.0b013e318235c7aa
PG 7
WC Immunology; Infectious Diseases; Pediatrics
SC Immunology; Infectious Diseases; Pediatrics
GA 879GA
UT WOS:000299316500014
PM 21983213
ER
PT J
AU Lopez-Class, M
Gomez-Duarte, J
Graves, K
Ashing-Giwa, K
AF Lopez-Class, Maria
Gomez-Duarte, Jessika
Graves, Kristi
Ashing-Giwa, Kimlin
TI A contextual approach to understanding breast cancer survivorship among
Latinas
SO PSYCHO-ONCOLOGY
LA English
DT Review
DE quality of life; Latinas; contextual-ecological perspective; breast
cancer survivors
ID QUALITY-OF-LIFE; TREATMENT DECISION-MAKING; SOCIAL SUPPORT; MULTIETHNIC
SAMPLE; PHYSICAL-ACTIVITY; EXERCISE INTERVENTION; HEALTH PROMOTION;
AFRICAN-AMERICAN; WHITE WOMEN; OLDER WOMEN
AB Objectives: The purpose of this review is to describe the empirical literature on the health-related quality of life (HRQOL) in Latina breast cancer survivors by exploring the social determinants of health. In framing the key domains of survivors' quality of life within a ecological-contextual model that evaluates individual and societal contributions to health outcomes, we provide a comprehensive landscape of the diverse factors constituting Latina survivors' lived experiences and their resultant quality of life outcomes.
Methods: We retrieved 244 studies via search engines and reference lists, of which 37 studies met the inclusion criteria.
Results: Findings document the importance of the social determinants of HRQOL, with studies documenting ecological and contextual factors accounting for significant variance in HRQOL outcomes. Our review identifies a dearth of research examining community-, institutional-, and policy-level factors, such as health care access, legal and immigration factors, physical and built environments, and health care affordability and policies affecting Latina breast cancer survivors' HRQOL.
Conclusions: Overall research on Latina breast cancer survivorship is sparse, with even greater underrepresentation within longitudinal and intervention studies. Results highlight a need for clear documentation of the comprehensive care needs of underserved cancer survivors and interventions considering integrated systems of care to address the medical and ecological factors known to impact the HRQOL of breast cancer survivors. Copyright (C) 2011 John Wiley & Sons, Ltd.
C1 [Lopez-Class, Maria] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
[Lopez-Class, Maria; Gomez-Duarte, Jessika; Graves, Kristi] Georgetown Univ, Med Ctr, Canc Control Program, Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
[Lopez-Class, Maria; Gomez-Duarte, Jessika; Graves, Kristi] Georgetown Univ, Med Ctr, Dept Oncol, Washington, DC 20007 USA.
[Ashing-Giwa, Kimlin] Beckman Res Inst City Hope, Ctr Community Alliance Res & Educ, Duarte, CA USA.
RP Lopez-Class, M (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, 6100 Execut Blvd,Room 5C01, Bethesda, MD 20892 USA.
EM lopezclassm@mail.nih.gov
FU NCI [5U01CA114593-03]; Susan G. Komen for the Cure [POP0601292]; The
Department of Defense [W81XWH-04-1-0548]
FX This research was funded by NCI Grant # 5U01CA114593-03 (the Latin
American Cancer Research Coalition) and Susan G. Komen for the Cure
Grant # POP0601292 and The Department of Defense Award #
W81XWH-04-1-0548. We would like to thank Ms. Susan Marx and Yasmin
Salehizadeh for their assistance with manuscript preparation.
NR 77
TC 17
Z9 17
U1 2
U2 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1057-9249
J9 PSYCHO-ONCOLOGY
JI Psycho-Oncol.
PD FEB
PY 2012
VL 21
IS 2
BP 115
EP 124
DI 10.1002/pon.1998
PG 10
WC Oncology; Psychology; Psychology, Multidisciplinary; Social Sciences,
Biomedical
SC Oncology; Psychology; Biomedical Social Sciences
GA 880NX
UT WOS:000299415200002
PM 21674680
ER
PT J
AU Yu, SC
Xiao, HL
Jiang, XF
Wang, QL
Li, Y
Yang, XJ
Ping, YF
Duan, JJ
Jiang, JY
Ye, XZ
Xu, SL
Xin, YH
Yao, XH
Chen, JH
Chu, WH
Sun, W
Wang, B
Wang, JM
Zhang, X
Bian, XW
AF Yu, Shi-Cang
Xiao, Hua-Liang
Jiang, Xue-Feng
Wang, Qing-Liang
Li, Yan
Yang, Xiao-Jun
Ping, Yi-Fang
Duan, Jiang Jie
Jiang, Jian-Yong
Ye, Xian-Zong
Xu, Sen-Lin
Xin, Yang-Hong
Yao, Xiao-Hong
Chen, Jian-Hong
Chu, Wei-Hua
Sun, Wei
Wang, Bing
Wang, Ji Ming
Zhang, Xia
Bian, Xiu-Wu
TI Connexin 43 Reverses Malignant Phenotypes of Glioma Stem Cells by
Modulating E-Cadherin
SO STEM CELLS
LA English
DT Article
DE Connexin 43; Glioma stem cells; E-Cadherin; Gap junctional intercellular
communication; Invasiveness; Tumorigenicity
ID JUNCTIONAL INTERCELLULAR COMMUNICATION; HUMAN GLIOBLASTOMA CELLS;
BREAST-CANCER CELLS; BETA-CATENIN; GAP-JUNCTIONS; EPIGENETIC REGULATION;
GENE-EXPRESSION; LUNG-CANCER; GROWTH; CX43
AB Malfunctioned gap junctional intercellular communication (GJIC) has been thought associated with malignant transformation of normal cells. However, the role of GJIC-related proteins such as connexins in sustaining the malignant behavior of cancer stem cells remains unclear. In this study, we obtained tumorspheres formed by glioma stem cells (GSCs) and adherent GSCs and then examined their GJIC. All GSCs showed reduced GJIC, and differentiated glioma cells had more gap junction-like structures than GSCs. GSCs expressed very low level of connexins, Cx43 in particular, which are key components of gap junction. We observed hypermethylation in the promoter of gap junction protein a1, which encodes Cx43 in GSCs. Reconstitution of Cx43 in GSCs inhibited their capacity of self-renewal, invasiveness, and tumorigenicity via influencing E-cadherin and its coding protein, which leads to changes in the expression of Wnt/beta-catenin targeting genes. Our results suggest that GSCs require the low expression of Cx43 for maintaining their malignant phenotype, and upregulation of Cx43 might be a potential strategy for treatment of malignant glioma. STEM CELLS 2012; 30:108-120.
C1 [Yu, Shi-Cang; Xiao, Hua-Liang; Jiang, Xue-Feng; Wang, Qing-Liang; Yang, Xiao-Jun; Ping, Yi-Fang; Duan, Jiang Jie; Jiang, Jian-Yong; Ye, Xian-Zong; Xu, Sen-Lin; Xin, Yang-Hong; Yao, Xiao-Hong; Chen, Jian-Hong; Wang, Bing; Zhang, Xia; Bian, Xiu-Wu] Third Mil Med Univ, Inst Pathol, Southwest Hosp, Chongqing 400038, Peoples R China.
[Yu, Shi-Cang; Xiao, Hua-Liang; Jiang, Xue-Feng; Wang, Qing-Liang; Yang, Xiao-Jun; Ping, Yi-Fang; Duan, Jiang Jie; Jiang, Jian-Yong; Ye, Xian-Zong; Xu, Sen-Lin; Xin, Yang-Hong; Yao, Xiao-Hong; Chen, Jian-Hong; Wang, Bing; Zhang, Xia; Bian, Xiu-Wu] Third Mil Med Univ, SW Canc Ctr, Southwest Hosp, Chongqing 400038, Peoples R China.
[Li, Yan] Third Mil Med Univ, Cent Lab, Southwest Hosp, Chongqing 400038, Peoples R China.
[Chu, Wei-Hua] Third Mil Med Univ, Dept Neurosurg, Southwest Hosp, Chongqing 400038, Peoples R China.
[Sun, Wei] Third Mil Med Univ, Cent Lab, Chongqing 400038, Peoples R China.
[Wang, Ji Ming] NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA.
RP Bian, XW (reprint author), Third Mil Med Univ, Inst Pathol, Southwest Hosp, Chongqing 400038, Peoples R China.
EM bianxiuwu@263.net
RI Zhang, Xia/B-8152-2008; ye, xianzong/G-6079-2011; Li, Yan/O-7342-2016;
Bian, Xiu-wu/D-4736-2017
OI Zhang, Xia/0000-0002-9040-1486; ye, xianzong/0000-0002-3640-0570; Bian,
Xiu-wu/0000-0003-4383-0197
FU National Basic Research Program of China (973 Program) [2010CB529403];
National Natural Science Foundation of China (NSFC) [30725035, 30700863]
FX This study was supported by grants from National Basic Research Program
of China (973 Program, No. 2010CB529403) and the National Natural
Science Foundation of China (NSFC, Nos. 30725035 and 30700863).
NR 76
TC 28
Z9 31
U1 1
U2 18
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PD FEB
PY 2012
VL 30
IS 2
BP 108
EP 120
DI 10.1002/stem.1685
PG 13
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 877UW
UT WOS:000299209200003
PM 22131169
ER
PT J
AU Nemeth, K
Wilson, T
Rada, B
Parmelee, A
Mayer, B
Buzas, E
Falus, A
Key, S
Masszi, T
Karpati, S
Mezey, E
AF Nemeth, Krisztian
Wilson, Todd
Rada, Balazs
Parmelee, Alissa
Mayer, Balazs
Buzas, Edit
Falus, Andras
Key, Sharon
Masszi, Tamas
Karpati, Sarolta
Mezey, Eva
TI Characterization and Function of Histamine Receptors in Human Bone
Marrow Stromal Cells
SO STEM CELLS
LA English
DT Article
DE Adult stem cells; Apoptosis; Bone marrow stromal cells; IL-6R; IL-6;
Mesenchymal stem cells
ID MESENCHYMAL STEM-CELLS; INNATE IMMUNITY; MAST-CELLS; MACROPHAGES;
INFLAMMATION; EXPRESSION; DISEASE; MODEL; BETA
AB There are several clinical trials worldwide using bone marrow stromal cells (BMSCs) as a cellular therapy to modulate immune responses in patients suffering from various inflammatory conditions. A deeper understanding of the molecular mechanisms involved in this modulatory effect could help us design better, more effective protocols to treat immune mediated diseases. In this study, we demonstrated that human BMSCs express H1, H2, and H4 histamine receptors and they respond to histamine stimulation with an increased interleukin 6 (IL-6) production both in vitro and in vivo. Using different receptor antagonists, we pinpointed the importance of the H1 histamine receptor, while Western blot analysis and application of various mitogen-activated protein kinase inhibitors highlighted the role of p38, extracellular signal-regulated kinase, and c-Jun N-terminal kinase kinases in the observed effect. When BMSCs were pretreated with either histamine or degranulated human mast cells, they exhibited an enhanced IL-6-dependent antiapoptotic effect on neutrophil granulocytes. Based on these observations, it is likely that introduction of BMSCs into a histamine-rich environment (such as any allergic setting) or pretreatment of these cells with synthetic histamine could have a significant modulatory effect on the therapeutic potential of BMSCs. STEM CELLS 2012; 30:222231.
C1 [Wilson, Todd; Rada, Balazs] NIAID, Host Def Lab, NIH, Rockville, MD USA.
[Buzas, Edit; Falus, Andras] Semmelweis Univ, Fac Med, Dept Genet Cell & Immunobiol, Budapest, Hungary.
[Karpati, Sarolta] Semmelweis Univ, Dept Dermatovenereol & Dermatooncol, Budapest, Hungary.
[Masszi, Tamas] Szent Laszlo Hosp, Dept Hematol & Stem Cell Transplantat, Budapest, Hungary.
EM nemethk@mail.nih.gov; mezeye@mail.nih.gov
RI Mayer, Balazs/B-7864-2013;
OI Mayer, Balazs/0000-0003-3577-3823; Masszi, Tamas/0000-0002-9038-302X;
Buzas, Edit/0000-0002-3744-206X
FU DIR, NIDCR, of the IRP, NIH, DHHS
FX We thank Dr. Dean Metcalfe for his help with the human mast cells and
Dr. Tamas Balla for his guidance and help with calcium measurements.
This work was supported by the DIR, NIDCR, of the IRP, NIH, DHHS.
NR 37
TC 10
Z9 10
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PD FEB
PY 2012
VL 30
IS 2
BP 222
EP 231
DI 10.1002/stem.771
PG 10
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 877UW
UT WOS:000299209200014
PM 22045589
ER
PT J
AU Hannas, BR
Lambright, CS
Furr, J
Evans, N
Foster, PMD
Gray, EL
Wilson, VS
AF Hannas, Bethany R.
Lambright, Christy S.
Furr, Johnathan
Evans, Nicola
Foster, Paul M. D.
Gray, Earl L.
Wilson, Vickie S.
TI Genomic Biomarkers of Phthalate-Induced Male Reproductive Developmental
Toxicity: A Targeted RT-PCR Array Approach for Defining Relative Potency
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE mixture toxicity; antiandrogen; PPAR; phthalate risk assessment
ID IN-UTERO EXPOSURE; FETAL-RAT TESTIS; N-BUTYL PHTHALATE; ALTERS
SEXUAL-DIFFERENTIATION; DOSE-DEPENDENT ALTERATIONS; LEYDIG-CELL
FUNCTION; DI(N-BUTYL) PHTHALATE; GENE-EXPRESSION; DIETHYLHEXYL
PHTHALATE; DIISOBUTYL PHTHALATE
AB Male rat fetuses exposed to certain phthalate esters (PEs) during sexual differentiation display reproductive tract malformations due to reductions in testosterone (T) production and the expression of steroidogenesis- and INSL3-related genes. In the current study, we used a 96-well real-time PCR array containing key target genes representing sexual determination and differentiation, steroidogenesis, gubernaculum development, and androgen signaling pathways to rank the relative potency of several PEs. We executed dose-response studies with diisobutyl (DIBP), dipentyl (DPeP), dihexyl (DHP), diheptyl (DHeP), diisononyl (DINP), or diisodecyl phthalate (DIDP) and serial dilutions of a mixture of nine phthalates. All phthalates, with the exception of DIDP, reduced fetal testicular T production. Several genes involved in cholesterol transport, androgen synthesis, and Insl3 also were downregulated in a dose-responsive manner by DIBP, DPeP, DHP, DHeP, DINP, and the 9-PE mixture. Despite speculation of peroxisome proliferator activated receptor (PPAR) involvement in the effects of PEs on the fetal testis, no PPAR-related genes were affected in the fetal testes by exposure to any of the tested PEs. Furthermore, the potent PPAR alpha agonist, Wy-14,643, did not reduce fetal testicular T production following gestational day 14-18 exposure, suggesting that the antiandrogenic activity of PEs is not PPAR alpha mediated. The overall sensitivity of the fetal endpoints (gene expression or T production) for the six phthalates from most to least was Cyp11b1 > Star = Scarb1 > Cyp17a1 = T production > Cyp11a1 = Hsd3b = Insl3 > Cyp11b2. The overall potency of the individual phthalates was DPeP > DHP > DIBP >= DHeP > DINP. Finally, the observed mixture interaction was adequately modeled by the dose-addition model for most of the affected genes. Together, these data advance our understanding of the collective reproductive toxicity of the PE compounds.
C1 [Hannas, Bethany R.; Lambright, Christy S.; Furr, Johnathan; Evans, Nicola; Gray, Earl L.; Wilson, Vickie S.] US EPA, Reprod Toxicol Branch, Toxicol Assessment Div, Natl Hlth & Environm Effects Res Lab,Off Res & De, Res Triangle Pk, NC 27711 USA.
[Foster, Paul M. D.] NIEHS, Dept Hlth & Human Serv, Natl Toxicol Program, NIH, Res Triangle Pk, NC 27709 USA.
RP Gray, EL (reprint author), US EPA, Reprod Toxicol Branch, Toxicol Assessment Div, Natl Hlth & Environm Effects Res Lab,Off Res & De, Mail Drop 72, Res Triangle Pk, NC 27711 USA.
EM gray.earl@epa.gov
OI Wilson, Vickie/0000-0003-1661-8481
FU United States Environmental Protection Agency; NTP at the National
Institute of Environmental Health Sciences [75-92285501-1]; National
Academy of Sciences
FX This project was provided by an Interagency Agreement between the United
States Environmental Protection Agency and the NTP at the National
Institute of Environmental Health Sciences (IA no. 75-92285501-1) and B.
R. H. was funded through a National Academy of Sciences postdoctoral
fellowship.
NR 59
TC 31
Z9 34
U1 5
U2 30
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 2012
VL 125
IS 2
BP 544
EP 557
DI 10.1093/toxsci/kfr315
PG 14
WC Toxicology
SC Toxicology
GA 879QD
UT WOS:000299346000021
PM 22112501
ER
PT J
AU Yuan, JP
Lee, KP
Hong, JH
Muallem, S
AF Yuan, J. P.
Lee, K. P.
Hong, J. H.
Muallem, S.
TI The closing and opening of TRPC channels by Homer1 and STIM1
SO ACTA PHYSIOLOGICA
LA English
DT Review
DE Ca2+influx; Homer1; STIM1
ID METABOTROPIC GLUTAMATE RECEPTORS; OPERATED CALCIUM-ENTRY; STROMAL
INTERACTION MOLECULE-1; FAST CA2+-DEPENDENT INACTIVATION; CAPACITATIVE
CA2+ ENTRY; ACTIVATES CRAC CHANNELS; PANCREATIC ACINAR-CELL; PROTEIN
SIGNALING RGS; PLASMA-MEMBRANE; INTRACELLULAR CALCIUM
AB Influx of Ca2+ is a central component of the receptor-evoked Ca2+ signal. A ubiquitous form of Ca2+ influx comes from Ca2+ channels that are activated in response to depletion of the endoplasmic reticulum Ca2+ stores and are thus named the store-operated Ca2+-influx channels (SOCs). One form of SOC is the transient receptor potential canonical (TRPC) channels. A major question in the field of Ca2+ signalling is the molecular mechanism that regulates the opening and closing of these channels. All TRPC channels have a Homer-binding ligand and two conserved negative charges that interact with two terminal lysines of the stromal interacting molecule 1 (STIM1). The Homer and STIM1 sites are separated by only four amino acid residues. Based on available results, we propose a molecular mechanism by which Homer couples TRPC channels to IP3 receptors (IP3Rs) to keep these channels in the closed state. Dissociation of the TRPCs-Homer-IP3Rs complex allows STIM1 access to the TRPC channels negative charges to gate open these channels.
C1 [Lee, K. P.; Hong, J. H.; Muallem, S.] NIDCR, Epithelial Signaling & Transport Sect, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Yuan, J. P.] Univ N Texas, Hlth Sci Ctr, Dept Integrat Physiol, Ft Worth, TX USA.
RP Muallem, S (reprint author), NIDCR, Epithelial Signaling & Transport Sect, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
EM joseph.yuan@unthsc.edu; shmuel.muallem@nih.gov
FU NHLBI NIH HHS [K99 HL093297, R00 HL093297]
NR 108
TC 32
Z9 33
U1 1
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1748-1708
J9 ACTA PHYSIOL
JI Acta Physiol.
PD FEB
PY 2012
VL 204
IS 2
SI SI
BP 238
EP 247
DI 10.1111/j.1748-1716.2011.02319.x
PG 10
WC Physiology
SC Physiology
GA 872EK
UT WOS:000298791400011
PM 21518270
ER
PT J
AU Gadalla, SM
Katki, HA
Shebl, FM
Giri, N
Alter, BP
Savage, SA
AF Gadalla, Shahinaz M.
Katki, Hormuzd A.
Shebl, Fatma M.
Giri, Neelam
Alter, Blanche P.
Savage, Sharon A.
TI The relationship between DNA methylation and telomere length in
dyskeratosis congenita
SO AGING CELL
LA English
DT Article
DE dyskeratosis congenita; epigenetic; human; methylation; telomere
ID MARROW FAILURE SYNDROMES; MAMMALIAN TELOMERES; EPIGENETIC REGULATION;
TINF2 MUTATIONS; HUMAN CANCER; ICF SYNDROME; HETEROCHROMATIN; CELLS;
TRANSCRIPTION; COHORT
AB The regulation of telomere length (TL) is a complex process, requiring the telomerase enzyme complex and numerous regulatory proteins. Epigenetic regulation may also be important in telomere maintenance. Specifically, methylation at subtelomeres is associated with changes in TL in vitro and in mouse models. Dyskeratosis congenita (DC) is an inherited bone marrow failure syndrome characterized by exceedingly short telomeres and mutations in telomere biology genes. To understand the interaction between methylation and TL in humans, we measured LINE-1, pericentromeric (NBL2), and subtelomeric (D4Z4) methylation in peripheral blood DNA derived from 40 patients with DC and 51 mutation-negative relatives. Pearsons correlation coefficient and linear regression models were used to evaluate the relationship between age-standardized lymphocyte TL measured by flow FISH and % DNA methylation. No differences in % subtelomeric, LINE-1, or pericentromeric methylation between patients with DC and relatives were noted except for an increase in % subtelomeric methylation in DC patients with a telomerase-complex mutation (TERC, TERT, DKC1, or TCAB1) (63.0% in DC vs. 61.8% in relatives, P = 0.03). Positive correlations between TL and DNA methylation at LINE-1 (r = 0.39, P = 0.01) and subtelomeric (r = 0.32, P = 0.05) sites were present in patients with DC. The positive correlation between TL and % LINE-1 methylation was restricted to TINF2 mutations. In contrast, statistically nonsignificant inverse correlations between TL and % LINE-1 (r = -0.17), subtelomeric (r = -0.20) were present in unaffected relatives. This study suggests an interaction between TL and both subtelomeric and LINE-1 methylation, which may be altered based on mutation status of telomere biology genes.
C1 [Gadalla, Shahinaz M.; Giri, Neelam; Alter, Blanche P.; Savage, Sharon A.] NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Gadalla, Shahinaz M.] NCI, Canc Prevent Fellowship Program, Rockville, MD 20852 USA.
[Katki, Hormuzd A.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Shebl, Fatma M.] NCI, Infect & Immunoepidemiol Branch, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
RP Savage, SA (reprint author), NCI, Clin Genet Branch, Div Canc Epidemiol & Genet, NIH, 6120 Executive Blvd,EPS 7018, Rockville, MD 20852 USA.
EM savagesh@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015; Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
FU National Cancer Institute; National Institutes of Health [N02-CP-11019,
N02-CP-65504, N02-CP-65501]
FX This work was funded by the intramural research program of the National
Cancer Institute and National Institutes of Health. We thank the
patients and their families for their generous participation in the
study. Lisa Leathwood, RN, Westat, Inc. (NIH contracts N02-CP-11019,
N02-CP-65504, and N02-CP-65501) provided outstanding study support.
NR 27
TC 9
Z9 9
U1 0
U2 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1474-9718
EI 1474-9726
J9 AGING CELL
JI Aging Cell
PD FEB
PY 2012
VL 11
IS 1
BP 24
EP 28
DI 10.1111/j.1474-9726.2011.00755.x
PG 5
WC Cell Biology; Geriatrics & Gerontology
SC Cell Biology; Geriatrics & Gerontology
GA 875LN
UT WOS:000299031500003
PM 21981348
ER
PT J
AU Bostrom, MA
Kao, WHL
Li, M
Abboud, HE
Adler, SG
Iyengar, SK
Kimmel, PL
Hanson, RL
Nicholas, SB
Rasooly, RS
Sedor, JR
Coresh, J
Kohn, OF
Leehey, DJ
Thornley-Brown, D
Bottinger, EP
Lipkowitz, MS
Meoni, LA
Klag, MJ
Lu, LY
Hicks, PJ
Langefeld, CD
Parekh, RS
Bowden, DW
Freedman, BI
AF Bostrom, Meredith A.
Kao, W. H. Linda
Li, Man
Abboud, Hanna E.
Adler, Sharon G.
Iyengar, Sudha K.
Kimmel, Paul L.
Hanson, Robert L.
Nicholas, Susanne B.
Rasooly, Rebekah S.
Sedor, John R.
Coresh, Josef
Kohn, Orly F.
Leehey, David J.
Thornley-Brown, Denyse
Bottinger, Erwin P.
Lipkowitz, Michael S.
Meoni, Lucy A.
Klag, Michael J.
Lu, Lingyi
Hicks, Pamela J.
Langefeld, Carl D.
Parekh, Rulan S.
Bowden, Donald W.
Freedman, Barry I.
CA Family Invest Nephropathy Diabet
TI Genetic Association and Gene-Gene Interaction Analyses in African
American Dialysis Patients With Nondiabetic Nephropathy
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE African American; APOL1; CFH; end-stage renal disease; Family
Investigation of Nephropathy and Diabetes (FIND); focal segmental
glomerulosclerosis (FSGS); hypertension
ID STAGE RENAL-DISEASE; FOCAL SEGMENTAL GLOMERULOSCLEROSIS; GENOME-WIDE
ASSOCIATION; HEMOLYTIC-UREMIC SYNDROME; NEPHROTIC SYNDROME;
SUSCEPTIBILITY LOCI; GLOMERULAR PROTEIN; KIDNEY-DISEASE; POLYMORPHISMS;
MUTATIONS
AB Background: African Americans have increased susceptibility to nondiabetic nephropathy relative to European Americans.
Study Design: Follow-up of a pooled genome-wide association study (GWAS) in African American dialysis patients with nondiabetic nephropathy; novel gene-gene interaction analyses.
Setting & Participants: Wake Forest sample: 962 African American nondiabetic nephropathy cases, 931 non-nephropathy controls. Replication sample: 668 Family Investigation of Nephropathy and Diabetes (FIND) African American nondiabetic nephropathy cases, 804 non-nephropathy controls.
Predictors: Individual genotyping of top 1,420 pooled GWAS-associated single-nucleotide polymorphisms (SNPs) and 54 SNPs in 6 nephropathy susceptibility genes.
Outcomes: APOL1 genetic association and additional candidate susceptibility loci interacting with or independently from APOL1.
Results: The strongest GWAS associations included 2 noncoding APOL1 SNPs, rs2239785 (OR, 0.33; dominant; P = 5.9 x 10(-24)) and rs136148 (OR, 0.54; additive; P = 1.1 x 10(-7)) with replication in FIND (P = 5.0 x 10(-21) and 1.9 x 10(-05), respectively). rs2239785 remained associated significantly after controlling for the APOL1 G1 and G2 coding variants. Additional top hits included a CFH SNP (OR from meta-analysis in the 3,367 African American cases and controls, 0.81; additive; P = 6.8 x 10(-4)). The 1,420 SNPs were tested for interaction with APOL1 G1 and G2 variants. Several interactive SNPs were detected; the most significant was rs16854341 in the podocin gene (NPHS2; P = 0.0001).
Limitations: Nonpooled GWASs have not been performed in African American patients with nondiabetic nephropathy.
Conclusions: This follow-up of a pooled GWAS provides additional and independent evidence that APOL1 variants contribute to nondiabetic nephropathy in African Americans and identified additional associated and interactive nondiabetic nephropathy susceptibility genes. Am J Kidney Dis. 59(2): 210-221. (C) 2012 by the National Kidney Foundation, Inc.
C1 [Bostrom, Meredith A.; Lu, Lingyi; Hicks, Pamela J.; Langefeld, Carl D.; Bowden, Donald W.; Freedman, Barry I.] Wake Forest Sch Med, Nephrol Sect, Winston Salem, NC 27157 USA.
[Kao, W. H. Linda; Li, Man; Coresh, Josef; Meoni, Lucy A.; Klag, Michael J.; Parekh, Rulan S.] Johns Hopkins Univ, Baltimore, MD USA.
[Abboud, Hanna E.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Adler, Sharon G.] Harbor UCLA Med Ctr, Los Angeles, CA USA.
[Iyengar, Sudha K.; Sedor, John R.] Case Western Reserve Univ, Sch Med, Cleveland, OH USA.
[Kimmel, Paul L.; Rasooly, Rebekah S.] NIDDK, NIH, Bethesda, MD USA.
[Hanson, Robert L.] NIDDK, NIH, Phoenix, AZ USA.
[Nicholas, Susanne B.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Kohn, Orly F.] Univ Chicago, Chicago, IL 60637 USA.
[Leehey, David J.] Loyola Univ, Chicago, IL 60611 USA.
[Thornley-Brown, Denyse] Univ Alabama, Birmingham, AL USA.
[Bottinger, Erwin P.] Mt Sinai Sch Med, New York, NY USA.
[Lipkowitz, Michael S.] Georgetown Univ, Sch Med, Washington, DC USA.
[Parekh, Rulan S.] Univ Toronto, Toronto, ON, Canada.
RP Freedman, BI (reprint author), Wake Forest Sch Med, Nephrol Sect, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM bfreedma@wakehealth.edu
RI Nelson, Robert/B-1470-2012;
OI Rasooly, Rebekah/0000-0002-6357-5528
FU National Institutes of Health (NIH) [R01 DK 070941, R01 DK 084149, R01
DK53591, N01-HG-65403]; National Institute of Diabetes and Digestive and
Kidney Diseases (NIDDK) [F32 DK080617, DK07024]; FIND [U01DK57292,
U01DK57329, U01DK057300, U01DK057298, U01DK057249, U01DK57295,
U01DK070657, U01DK057303, U01DK57304]; NIH National Cancer Institute
(NCI) [N01-CO-12400]; NIH-NCI Center for Cancer Research; National
Center for Research Resources for the General Clinical Research Center;
Case Western Reserve University [M01-RR-000080]; Wake Forest University
[M01-RR-07122]; Harbor-University of California, Los Angeles Medical
Center [M01-RR-00425]; College of Medicine, University of California,
Irvine [M01-RR-00827-29]; University of New Mexico [HSC M01-RR-00997];
Frederic C. Bartter [M01-RR-01346]; Agency for Healthcare Research and
Quality, Rockville, MD [HS08365]; National Heart, Lung, and Blood
Institute, Bethesda, MD [HL62985]
FX This study was supported in part by National Institutes of Health (NIH)
grants R01 DK 070941 and R01 DK 084149 (Dr Freedman) and R01 DK53591 (Dr
Bowden). Dr Bostrom was supported by F32 DK080617 from the National
Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).
Computing resources were provided by the Wake Forest University Health
Sciences Center for Public Health Genomics. This study was also
supported by FIND grants U01DK57292, U01DK57329, U01DK057300,
U01DK057298, U01DK057249, U01DK57295, U01DK070657, U01DK057303,
U01DK070657, U01DK57304 and CHOICE study DK07024 from the NIDDK and in
part by the Intramural Research Program of the NIDDK. This project has
been funded in whole or in part with federal funds from the NIH National
Cancer Institute (NCI) under contract N01-CO-12400 and the Intramural
Research Program of the NIH-NCI Center for Cancer Research. This work
also was supported by the National Center for Research Resources for the
General Clinical Research Center grants: Case Western Reserve
University, M01-RR-000080; Wake Forest University, M01-RR-07122;
Harbor-University of California, Los Angeles Medical Center,
M01-RR-00425; College of Medicine, University of California, Irvine,
M01-RR-00827-29; University of New Mexico, HSC M01-RR-00997; and
Frederic C. Bartter, M01-RR-01346. The CHOICE Study was supported in
part by HS08365 from the Agency for Healthcare Research and Quality,
Rockville, MD, and HL62985 from the National Heart, Lung, and Blood
Institute, Bethesda, MD. Genotyping was performed by the Center for
Inherited Disease Research, which is fully funded through a federal
contract from the NIH to Johns Hopkins University (N01-HG-65403).
NR 33
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U2 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD FEB
PY 2012
VL 59
IS 2
BP 210
EP 221
DI 10.1053/j.ajkd.2011.09.020
PG 12
WC Urology & Nephrology
SC Urology & Nephrology
GA 879GK
UT WOS:000299317500011
PM 22119407
ER
PT J
AU Textor, SC
Gloviczki, ML
Flessner, MF
Calhoun, DA
Glockner, J
Grande, JP
McKusick, MA
Cha, SS
Lerman, LO
AF Textor, Stephen C.
Gloviczki, Monika L.
Flessner, Michael F.
Calhoun, David A.
Glockner, James
Grande, Joseph P.
McKusick, Michael A.
Cha, Stephen S.
Lerman, Lilach O.
TI Association of Filtered Sodium Load With Medullary Volumes and Medullary
Hypoxia in Hypertensive African Americans as Compared With Whites
SO AMERICAN JOURNAL OF KIDNEY DISEASES
LA English
DT Article
DE Hypertension; ethnicity; glomerular filtration rate (GFR); oxidative
stress; blood oxygen level-dependent (BOLD) magnetic resonance (MR);
hemodynamics
ID STAGE RENAL-DISEASE; KIDNEY-DISEASE; GLOMERULAR-FILTRATION; OXIDATIVE
STRESS; ANGIOTENSIN-II; BLOOD-PRESSURE; BIRTH-WEIGHT; BOLD-MRI;
OXYGENATION; MEN
AB Background: African Americans develop hypertension earlier with more target manifestations than whites despite having a higher glomerular filtration rate (GFR) for any level of serum creatinine.
Study Design & Participants: This study tested the hypothesis that increased GFR and sodium reabsorption in African Americans is associated with increased metabolic work and medullary hypoxia in 49 nondiabetic patients with essential hypertension (29 whites and 20 African Americans) following a constant-sodium diet (150 mEq/d) and renin-angiotensin system blockade.
Predictors: Ethnicity, age, measured GFR, sodium excretion, and body mass index.
Outcomes: We examined cortical and medullary volumes and blood flows using multidetector computed tomography and intrarenal deoxyhemoglobin (R2*) using blood oxygen level-dependent magnetic resonance.
Results: Blood pressure and sodium excretion were similar, whereas African Americans were more obese and had higher iothalamate GFRs. Renal cortical volumes did not differ, but medullary volumes adjusted for body size and age were higher in African Americans (32.3 +/- 11.2 vs 25.1 +/- 7.4 cm(3)/m(2) body surface area; P < 0.001). Sodium reabsorption and blood flows were higher in African Americans. Basal cortical deoxyhemoglobin values were similar between ethnic groups, whereas medullary R2* was higher in African Americans (39.7 +/- 5.1 vs 36.3 +/- 6.5/s; P = 0.02), but decreased to levels similar to whites after furosemide treatment. Levels of the circulating isoprostane prostaglandin F(2 alpha) were higher in African Americans and daily urinary prostaglandin F(2 alpha) excretion in African Americans correlated directly with renal blood flow (R = 0.71; P < 0.01).
Limitations: Studies were limited to treated volunteers with normal kidney function without knowledge of prior nutrient intake.
Conclusions: These data show for the first time that increased sodium reabsorption in obese African American patients with hypertension was associated with enlarged medullary volumes, functional hypoxia related to solute reabsorption, and a direct relationship between blood flows and urinary isoprostane levels. Our results support a model of increased oxygen consumption and oxidative stress in African Americans that may accelerate hypertension and target-organ injury compared with white patients with essential hypertension. Am J Kidney Dis. 59(2): 229-237. (C) 2012 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
C1 [Textor, Stephen C.; Gloviczki, Monika L.; Glockner, James; Grande, Joseph P.; McKusick, Michael A.; Cha, Stephen S.; Lerman, Lilach O.] Mayo Clin, Rochester, MN 55905 USA.
[Flessner, Michael F.] NIH, Bethesda, MD 20892 USA.
[Flessner, Michael F.] Univ Mississippi, Jackson, MS 39216 USA.
[Calhoun, David A.] Univ Alabama, Birmingham, AL USA.
RP Textor, SC (reprint author), Mayo Clin, East 19,Mayo Bldg, Rochester, MN 55905 USA.
EM textor.stephen@mayo.edu
FU National Heart, Lung and Blood Institute (NHLBI) [PO1HL85307]; National
Institutes of Health (NIH)/National Center for Research Resources [UL1
RR024150]
FX The project described was supported by award PO1HL85307 from the
National Heart, Lung and Blood Institute (NHLBI) and National Institutes
of Health (NIH)/National Center for Research Resources CTSA grant UL1
RR024150. The content is solely the responsibility of the authors and
does not necessarily represent the official views of the NHLBI or the
NIH.
NR 41
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U1 0
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 0272-6386
J9 AM J KIDNEY DIS
JI Am. J. Kidney Dis.
PD FEB
PY 2012
VL 59
IS 2
BP 229
EP 237
DI 10.1053/j.ajkd.2011.09.023
PG 9
WC Urology & Nephrology
SC Urology & Nephrology
GA 879GK
UT WOS:000299317500013
PM 22130642
ER
PT J
AU Aung, PP
Sarlomo-Rikala, M
Lasota, J
Lai, JP
Wang, ZF
Miettinen, M
AF Aung, Phyu Phyu
Sarlomo-Rikala, Maarit
Lasota, Jerzy
Lai, Jin-Ping
Wang, Zeng-Feng
Miettinen, Markku
TI KBA62 and PNL2: 2 New Melanoma Markers-Immunohistochemical Analysis of
1563 Tumors Including Metastatic, Desmoplastic, and Mucosal Melanomas
and Their Mimics
SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY
LA English
DT Article
DE KBA62; PNL2; metastatic and desmoplastic melanoma; PEComa;
immunohistochemistry
ID SECTIONS; KBA.62
AB Identification of metastatic melanoma can be difficult because of its considerable morphologic variation and mimicry of a wide variety of other tumors. The more melanoma-specific melanoma markers, MelanA/MART-1, HMB45, and tyrosinase, used in addition to S100 protein, all have limitations in sensitivity and specificity. In this study, we evaluated 2 new melanoma markers, monoclonal antibodies KBA62 and PNL2 to yet unidentified antigens, using a large panel of metastatic melanomas (n = 214), desmoplastic melanomas (n = 34), gastrointestinal mucosal melanomas (n = 54), benign nevi (n = 27), clear cell sarcomas (n = 16), and nonmelanocytic tumors (n = 1218). Immunoreactivity for KBA62 and PNL2 was found in all pigmented nevi and in 86% and 90% of metastatic melanomas, respectively. Mucosal melanomas showed a similar rate of PNL2 immunoreactivity but somewhat less frequent KBA62 positivity (72%). In addition, KBA62 was found to be a sensitive diagnostic marker for desmoplastic melanoma (28 of 34; 82%), whereas PNL2 was only rarely positive (2 of 34; 6%). KBA62-positive normal tissues included pericytes, vascular and parenchymal smooth muscles, and basal cells of complex epithelia, including myoepithelia, whereas PNL2 labeled only melanocytes and neutrophils. Among nonmelanocytic tumors, those that were KBA62 positive were nodular fasciitis, leiomyoma and leiomyosarcoma, gastrointestinal stromal tumors, benign and malignant nerve sheath tumors, synovial sarcoma, and subsets of various carcinomas, especially those with squamous cell/stratified epithelial differentiation. PNL2 positivity in nonmelanocytic tumors was more restricted but occurred consistently in angiomyolipoma and other perivascular epitheloid cell tumor and in chronic myeloid leukemia tissue infiltrates. KBA62 may assist in the identification of desmoplastic melanomas, but its widespread occurrence in nonmelanomas limits utility. PNL2 is highly specific for melanomas but lacks reactivity with desmoplastic melanomas. It is also an excellent supplementary marker for perivascular epitheloid cell tumor at various sites.
C1 [Miettinen, Markku] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Sarlomo-Rikala, Maarit] Helsinki Univ Hosp, Helsinki, Finland.
[Sarlomo-Rikala, Maarit] HUSLab, Helsinki, Finland.
RP Miettinen, M (reprint author), NCI, Pathol Lab, NIH, 10 Ctr Dr,Room 2B50, Bethesda, MD 20892 USA.
EM miettinenmm@mail.nih.gov
FU NIH/NCI
FX This study was supported by the NIH/NCI Intramural Research Program. The
authors have disclosed that they have no significant relationships with,
or financial interest in, any commercial companies pertaining to this
article.
NR 9
TC 14
Z9 15
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0147-5185
J9 AM J SURG PATHOL
JI Am. J. Surg. Pathol.
PD FEB
PY 2012
VL 36
IS 2
BP 265
EP 272
DI 10.1097/PAS.0b013e31823651cb
PG 8
WC Pathology; Surgery
SC Pathology; Surgery
GA 879GD
UT WOS:000299316800012
PM 22067329
ER
PT J
AU Ascierto, ML
Kmieciak, M
Idowu, MO
Manjili, R
Zhao, YD
Grimes, M
Dumur, C
Wang, E
Ramakrishnan, V
Wang, XY
Bear, HD
Marincola, FM
Manjili, MH
AF Ascierto, Maria Libera
Kmieciak, Maciej
Idowu, Michael O.
Manjili, Rose
Zhao, Yingdong
Grimes, Margaret
Dumur, Catherine
Wang, Ena
Ramakrishnan, Viswanathan
Wang, Xiang-Yang
Bear, Harry D.
Marincola, Francesco M.
Manjili, Masoud H.
TI A signature of immune function genes associated with recurrence-free
survival in breast cancer patients
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Breast cancer prognosis; Tumor relapse; Tumor microenvironment; Immune
response; Neoadjuvant immunotherapy
ID SUPPRESSOR-CELLS; T-CELLS; COLORECTAL-CANCER; PREDICTS; RECEPTOR;
AMPLIFICATION; CHEMOTHERAPY; RECRUITMENT; METASTASIS; PROGNOSIS
AB The clinical significance of tumor-infiltrating immune cells has been reported in a variety of human carcinomas including breast cancer. However, molecular signature of tumor-infiltrating immune cells and their prognostic value in breast cancer patients remain elusive. We hypothesized that a distinct network of immune function genes at the tumor site can predict a low risk versus high risk of distant relapse in breast cancer patients regardless of the status of ER, PR, or HER-2/neu in their tumors. We conducted retrospective studies in a diverse cohort of breast cancer patients with a 1-5 year tumor relapse versus those with up to 7 years relapse-free survival. The RNAs were extracted from the frozen tumor specimens at the time of diagnosis and subjected to microarray analysis and real-time RT-PCR. Paraffin-embedded tissues were also subjected to immunohistochemistry staining. We determined that a network of immune function genes involved in B cell development, interferon signaling associated with allograft rejection and autoimmune reaction, antigen presentation pathway, and cross talk between adaptive and innate immune responses were exclusively upregulated in patients with relapse-free survival. Among the 299 genes, five genes which included B cell response genes were found to predict with > 85% accuracy relapse-free survival. Real-time RT-PCR confirmed the 5-gene prognostic signature that was distinct from an FDA-cleared 70-gene signature of MammaPrint panel and from the Oncotype DX recurrence score assay panel. These data suggest that neoadjuvant immunotherapy in patients with high risk of relapse may reduce tumor recurrence by inducing the immune function genes.
C1 [Kmieciak, Maciej; Manjili, Rose; Manjili, Masoud H.] Virginia Commonwealth Univ, Massey Canc Ctr, Dept Microbiol & Immunol, Richmond, VA 23298 USA.
[Ascierto, Maria Libera; Wang, Ena; Marincola, Francesco M.] NIH, IDIS, Dept Transfus Med, Bethesda, MD 20892 USA.
[Ascierto, Maria Libera; Wang, Ena; Marincola, Francesco M.] NIH, Ctr Human Immunol, Bethesda, MD 20892 USA.
[Idowu, Michael O.; Grimes, Margaret; Dumur, Catherine] Virginia Commonwealth Univ, Massey Canc Ctr, Dept Pathol, Richmond, VA 23298 USA.
[Zhao, Yingdong] NIH, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
[Ramakrishnan, Viswanathan] Virginia Commonwealth Univ, Massey Canc Ctr, Dept Biostat, Richmond, VA 23298 USA.
[Wang, Xiang-Yang] Virginia Commonwealth Univ, Dept Human & Mol Genet, Richmond, VA 23298 USA.
[Bear, Harry D.] Virginia Commonwealth Univ, Massey Canc Ctr, Dept Surg, Richmond, VA 23298 USA.
RP Manjili, MH (reprint author), Virginia Commonwealth Univ, Massey Canc Ctr, Dept Microbiol & Immunol, Med Coll Virginia Campus, Richmond, VA 23298 USA.
EM mmanjili@vcu.edu
RI Ascierto, Maria Libera/A-9239-2012
FU NIH [R01 CA104757]; Massey Cancer Center [2006FPP-04]; VCU; VCU Massey
Cancer Center; Commonwealth Foundation for Cancer Research
FX This study was supported by NIH R01 CA104757 Grant (M. H. Manjili),
Massey Cancer Center Pilot Project Program 2006FPP-04 (M. H. Manjili),
and VCU Technology Transfer Fund. We gratefully acknowledge the support
of VCU Massey Cancer Center and the Commonwealth Foundation for Cancer
Research. We thank Dr. K. Najarian for his review of the statistical
analysis.
NR 31
TC 48
Z9 50
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD FEB
PY 2012
VL 131
IS 3
BP 871
EP 880
DI 10.1007/s10549-011-1470-x
PG 10
WC Oncology
SC Oncology
GA 879QE
UT WOS:000299346100014
PM 21479927
ER
PT J
AU Gartner, EM
Silverman, P
Simon, M
Flaherty, L
Abrams, J
Ivy, P
LoRusso, PM
AF Gartner, Elaina M.
Silverman, Paula
Simon, Michael
Flaherty, Lawrence
Abrams, Judith
Ivy, Percy
LoRusso, Patricia M.
TI A phase II study of 17-allylamino-17-demethoxygeldanamycin in metastatic
or locally advanced, unresectable breast cancer
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE 17-AAG; 17-allylamino-17-demethoxygeldanamycin; Breast cancer; Hsp90;
Heat shock protein 90
ID REFRACTORY ADVANCED CANCERS; SOLID TUMORS; PEDIATRIC-PATIENTS; HSP90
INHIBITION; ADULT PATIENTS; TRIAL; EXPRESSION;
17-(ALLYLAMINO)-17-DEMETHOXYGELDANAMYCIN; HEAT-SHOCK-PROTEIN-90;
ACTIVATION
AB Heat shock protein 90 (Hsp90) is an attractive target for breast cancer treatment, as it is required for the proper folding and stabilization of several proteins known to be involved in breast cancer growth and development. These proteins include the epidermal growth factor receptor, human epidermal growth factor receptor 2 (HER2), estrogen receptor (ER), progesterone receptor (PR), and src. 17-Allylamino-17-demethoxygeldanamycin (17-AAG) is an intravenous Hsp90 inhibitor in development for breast cancer treatment. We conducted a phase II study of 17-AAG 220 mg/m(2) on days 1, 4, 8, and 11 every 21 days in patients with metastatic and locally advanced breast cancer. Since we expected the molecular effects of Hsp90 inhibition to extend beyond just ER, PR, and HER2 down regulation and to impact a variety of other cellular proteins, patients were not selected based on ER, PR, or HER2 status. Eleven patients, including 6 patients with triple negative breast cancer, were enrolled and treated. There were no responses and 3 patients had stable disease as their best response. Five patients developed grade 3/4 toxicities, which were primarily hepatic and pulmonary. Based on these results, we do not recommend further study of 17-AAG at this dosing schedule or in unselected breast cancer patients.
C1 [Gartner, Elaina M.; Simon, Michael; Flaherty, Lawrence; Abrams, Judith; LoRusso, Patricia M.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI 48201 USA.
[Silverman, Paula] Case Western Reserve Univ, Univ Hosp Seidman Canc Ctr, Cleveland, OH 44106 USA.
[Ivy, Percy] NCI, Canc Therapy Evaluat Program, NIH, Rockville, MD 20852 USA.
RP Gartner, EM (reprint author), Wayne State Univ, Karmanos Canc Inst, 4100 John R,4HWCRC, Detroit, MI 48201 USA.
EM gartnere@karmanos.org
FU National Institutes of Health [U01 CA062487]
FX This study was funded through a grant from the National Institutes of
Health, U01 CA062487.
NR 21
TC 35
Z9 35
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD FEB
PY 2012
VL 131
IS 3
BP 933
EP 937
DI 10.1007/s10549-011-1866-7
PG 5
WC Oncology
SC Oncology
GA 879QE
UT WOS:000299346100021
PM 22083229
ER
PT J
AU Neta, G
Anderson, WF
Gilbert, E
Berrington, A
AF Neta, Gila
Anderson, William F.
Gilbert, Ethel
Berrington, Amy
TI Variation in the risk of radiation-related contralateral breast cancer
by histology and estrogen receptor expression in SEER
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Contralateral breast cancer; Radiotherapy; Estrogen receptor status;
Histology
ID ATOMIC-BOMB SURVIVORS; RANDOMIZED-TRIALS; HORMONAL-THERAPY; 15-YEAR
SURVIVAL; POOLED ANALYSIS; RADIOTHERAPY; WOMEN; RECURRENCE; SUBTYPES
AB Radiation exposure, particularly at a young age, is an established cause of breast cancer. It is not known whether radiation-related breast cancer risk varies by molecular subtype. We characterized the relative risk (RR) of contralateral breast cancer (CBC) related to radiotherapy by histology and estrogen receptor (ER) status of the CBC in five-year survivors in the Surveillance, Epidemiology, and End Results database using Poisson regression models adjusted for attained age and calendar year, age at and year of treatment, ER status of the first breast cancer, and disease stage. 205,316 female breast cancer survivors were followed for an average of 10 years from 1973 until 2007, during which time 6924 women developed a subsequent primary invasive breast cancer in the contralateral breast. The overall RR (and 95% confidence interval (CI)) of radiotherapy-related CBC was 1.11 (1.05-1.16). There was no heterogeneity in risk according to histology of the CBC (P > 0.50) for all ages or young age at exposure, but case numbers were small for subtypes other than ductal and lobular carcinomas. Information on ER status was available from 1990 onwards for 3546 CBC cases, of which 2597 (73%) were ER+ and 949 (27%) were ER-. The RRs were 1.10 (1.02-1.19) for ER+ CBC and 1.19 (1.04-1.35) for ER- CBC (P (difference) = 0.33). Among women treated age < 35 years, radiation-related risk of CBC was non-significantly elevated for ER- (RR = 1.38, 95% CI: 0.96-1.97) but not for ER+ tumors (RR = 0.80, 95% CI: 0.47-1.35) (P (difference) = 0.09). We did not find clear evidence that radiation-related risk varies by histology or ER status, but our findings, which were the first to examine this question, were suggestive of possible differences by ER status that may merit further investigation.
C1 [Neta, Gila; Gilbert, Ethel; Berrington, Amy] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20852 USA.
[Anderson, William F.] NCI, Biostat Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20852 USA.
RP Neta, G (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd, Bethesda, MD 20852 USA.
EM netagil@mail.nih.gov
FU NIH; Division of Cancer Epidemiology and Genetics at the National Cancer
Institute
FX This research was supported by the Intramural Research program of the
NIH and the Division of Cancer Epidemiology and Genetics at the National
Cancer Institute.
NR 23
TC 8
Z9 8
U1 0
U2 5
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD FEB
PY 2012
VL 131
IS 3
BP 1021
EP 1027
DI 10.1007/s10549-011-1820-8
PG 7
WC Oncology
SC Oncology
GA 879QE
UT WOS:000299346100031
PM 22015617
ER
PT J
AU Simonyan, K
Ludlow, CL
AF Simonyan, Kristina
Ludlow, Christy L.
TI Abnormal Structure-Function Relationship in Spasmodic Dysphonia
SO CEREBRAL CORTEX
LA English
DT Article
DE cortical thickness; fMRI; laryngeal dystonia; VBM; voice production
ID IDIOPATHIC CERVICAL DYSTONIA; WHITE-MATTER CHANGES; WRITERS CRAMP;
BOTULINUM TOXIN; CORTICAL THICKNESS; CEREBRAL-CORTEX; FOCAL DYSTONIA;
RHESUS-MONKEY; ACTIVATION; SPEECH
AB Spasmodic dysphonia (SD) is a primary focal dystonia characterized by involuntary spasms in the laryngeal muscles during speech production. Although recent studies have found abnormal brain function and white matter organization in SD, the extent of gray matter alterations, their structure-function relationships, and correlations with symptoms remain unknown. We compared gray matter volume (GMV) and cortical thickness (CT) in 40 SD patients and 40 controls using voxel-based morphometry and cortical distance estimates. These measures were examined for relationships with blood oxygen level-dependent signal change during symptomatic syllable production in 15 of the same patients. SD patients had increased GMV, CT, and brain activation in key structures of the speech control system, including the laryngeal sensorimotor cortex, inferior frontal gyrus (IFG), superior/middle temporal and supramarginal gyri, and in a structure commonly abnormal in other primary dystonias, the cerebellum. Among these regions, GMV, CT and activation of the IFG and cerebellum showed positive relationships with SD severity, while CT of the IFG correlated with SD duration. The left anterior insula was the only region with decreased CT, which also correlated with SD symptom severity. These findings provide evidence for coupling between structural and functional abnormalities at different levels within the speech production system in SD.
C1 [Simonyan, Kristina] Mt Sinai Sch Med, Dept Neurol, New York, NY 10029 USA.
[Simonyan, Kristina] Mt Sinai Sch Med, Dept Otolaryngol, New York, NY 10029 USA.
[Simonyan, Kristina; Ludlow, Christy L.] Natl Inst Neurol Disorders & Stroke, Laryngeal & Speech Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Ludlow, Christy L.] James Madison Univ, Dept Commun Sci & Disorders, Harrisonburg, VA 22807 USA.
RP Simonyan, K (reprint author), Mt Sinai Sch Med, Dept Neurol, 1 Gustave L Levy Pl,Box 1137, New York, NY 10029 USA.
EM kristina.simonyan@mssm.edu
OI Simonyan, Kristina/0000-0001-7444-0437; Ludlow,
Christy/0000-0002-2015-6171
FU National Institute on Deafness and Other Communication Disorders;
National Institutes of Health [R00DC009620]; National Institute of
Neurological Disorders and Stroke [Z01NS00298]
FX National Institute on Deafness and Other Communication Disorders;
National Institutes of Health (R00DC009620 to K. S.); Intramural Program
of National Institute of Neurological Disorders and Stroke (Z01NS00298
to C.L.L.).
NR 54
TC 21
Z9 21
U1 2
U2 10
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 2012
VL 22
IS 2
BP 417
EP 425
DI 10.1093/cercor/bhr120
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 876RD
UT WOS:000299124400016
PM 21666131
ER
PT J
AU Kwon-Chung, KJ
AF Kwon-Chung, Kyung J.
TI Taxonomy of Fungi Causing Mucormycosis and Entomophthoramycosis
(Zygomycosis) and Nomenclature of the Disease: Molecular Mycologic
Perspectives
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID DISSEMINATED BASIDIOBOLOMYCOSIS; CONIDIOBOLUS-INCONGRUUS; UNITED-STATES;
EVOLUTION; INFECTION; CLASSIFICATION; PHYLOGENY; INDONESIA; SPECTRUM;
PATIENT
AB Molecular phylogenetic analysis confirmed the phylum Zygomycota to be polyphyletic, and the taxa conventionally classified in Zygomycota are now distributed among the new phylum Glomeromycota and 4 subphyla incertae sedis (uncertain placement). Because the nomenclature of the disease zygomycosis was based on the phylum Zygomycota (Zygomycetes) in which the etiologic agents had been classified, the new classification profoundly affects the name of the disease. Zygomycosis was originally described as a convenient and inclusive name for 2 clinicopathologically different diseases, mucormycosis caused by members of Mucorales and entomophthoramycosis caused by species in the order Entomophthorales of Zygomycota. Without revision of original definition, the name "zygomycosis," however, has more often been used as a synonym only for mucormycosis. This article reviews the progress and changes in taxonomy and nomenclature of Zygomycota and the disease zygomycosis. The article also reiterates the reasons why the classic names "mucormycosis" and "entomophthoramycosis" are more appropriate than "zygomycosis.".
C1 NIAID, Mol Microbiol Sect, LCID, NIH, Bethesda, MD 20892 USA.
RP Kwon-Chung, KJ (reprint author), NIAID, Mol Microbiol Sect, LCID, NIH, 9000 Rockville Pike,Bldg 10,Room 11N234, Bethesda, MD 20892 USA.
EM june_kwon-chung@nih.gov
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health; Henry Schueler 419 Foundation
FX This study was supported by funds from the intramural program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.; This article was published as part of a
supplement entitled "Advances Against Mucormycosis: A Tribute to the
Memory and Courage of Hank Schueler," sponsored by the Henry Schueler
41&9 Foundation.
NR 40
TC 61
Z9 61
U1 0
U2 11
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 1
PY 2012
VL 54
SU 1
BP S8
EP S15
DI 10.1093/cid/cir864
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 876GB
UT WOS:000299094500003
PM 22247451
ER
PT J
AU Simone, CB
Vapiwala, N
Hampshire, MK
Metz, JM
AF Simone, Charles B., II
Vapiwala, Neha
Hampshire, Margaret K.
Metz, James M.
TI Cancer Patient Attitudes Toward Analgesic Usage and Pain Intervention
SO CLINICAL JOURNAL OF PAIN
LA English
DT Article
DE pain; analgesic; quality of life; Internet; cancer
ID RADIATION ONCOLOGY PATIENTS; PHYSICIAN ATTITUDES; BREAST-CANCER;
MANAGEMENT; BARRIERS; PREVALENCE; INTERNET; RELIEF; INFORMATION;
MEDICATIONS
AB Objectives: Although pain is commonly experienced by cancer patients, many receive inadequate pain management. Little data exist quantifying analgesic usage among oncology patients. This study evaluates perceived causes of pain and investigates reasons why oncology patients fail to receive optimal pain management.
Methods: An institutional review board-approved questionnaire assessing pain control and analgesic usage was posted on OncoLink. Between November 2005 and July 2008, 1107 patients responded. Respondents were female (73%), white (74%), educated beyond high school (64%), and had surgery (69%), chemotherapy (64%), and radiation (47%). Most had breast (30%), gastrointestinal (12%), gynecologic (11%), and lung (8%) malignancies.
Results: Sixty-seven percent of respondents reported pain, with 48% reporting pain directly from their cancer and 47% reporting pain from their cancer treatment. Among patients in pain, 25% did not use analgesics. Analgesic usage was significantly less in men (44% vs. 52%, P=0.023), minorities (42% vs. 53%, P=0.001), and patients with lower education levels (45% vs. 53%, P=0.013). Usage varied by cancer diagnosis and was higher among patients who received chemotherapy (56% vs. 40%, P<0.001) and radiation (53% vs. 47%, P=0.058). Reasons for not taking analgesics included: health care provider not recommending medications (85%), fearing addiction/ dependence (80%), and inability to pay (76%). Many patients reporting pain, not taking analgesics, pursued alternative therapies (94%).
Discussion: Most cancer patients perceive pain from their disease or treatment, regardless of therapy received. Many, however, did not use analgesics due to concerns of addiction, cost, or lack of health care provider endorsement. Providers should regularly discuss pain symptoms and management with cancer patients.
C1 [Simone, Charles B., II; Vapiwala, Neha; Hampshire, Margaret K.; Metz, James M.] Hosp Univ Penn, Dept Radiat Oncol, Philadelphia, PA 19104 USA.
[Simone, Charles B., II] NCI, NIH, Radiat Oncol Branch, Bethesda, MD 20892 USA.
RP Simone, CB (reprint author), NCI, NIH, Radiat Oncol Branch, Bldg 10-CRC,Room B2-3500,10 Ctr Dr, Bethesda, MD 20892 USA.
EM csimone@alumni.upenn.edu
FU National Institutes of Health, National Cancer Institute, and Center for
Cancer Research, Bethesda, MD
FX Supported in part by the Intramural Research Program of the National
Institutes of Health, National Cancer Institute, and Center for Cancer
Research, Bethesda, MD. The authors declare no conflict of interest.
NR 48
TC 18
Z9 18
U1 0
U2 8
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0749-8047
J9 CLIN J PAIN
JI Clin. J. Pain
PD FEB
PY 2012
VL 28
IS 2
BP 157
EP 162
DI 10.1097/AJP.0b013e318223be30
PG 6
WC Anesthesiology; Clinical Neurology
SC Anesthesiology; Neurosciences & Neurology
GA 879JO
UT WOS:000299325700010
PM 21705874
ER
PT J
AU Shukla, S
Schwartz, C
Kapoor, K
Kouanda, A
Ambudkar, SV
AF Shukla, Suneet
Schwartz, Candice
Kapoor, Khyati
Kouanda, Abdul
Ambudkar, Suresh V.
TI Use of Baculovirus BacMam Vectors for Expression of ABC Drug
Transporters in Mammalian Cells
SO DRUG METABOLISM AND DISPOSITION
LA English
DT Article
ID HUMAN P-GLYCOPROTEIN; NORMAL HUMAN-TISSUES; MULTIDRUG-RESISTANCE;
RECOMBINANT BACULOVIRUS; MONOCLONAL-ANTIBODIES; CATALYTIC CYCLE;
FUNCTIONAL-ROLE; ATP HYDROLYSIS; LOCALIZATION; DISCOVERY
AB ATP-binding cassette (ABC) drug transporters ABCB1 [P-glycoprotein (Pgp)] and ABCG2 are expressed in many tissues including those of the intestines, the liver, the kidney and the brain and are known to influence the pharmacokinetics and toxicity of therapeutic drugs. In vitro studies involving their functional characteristics provide important information that allows improvements in drug delivery or drug design. In this study, we report use of the BacMam (baculovirus-based expression in mammalian cells) expression system to express and characterize the function of Pgp and ABCG2 in mammalian cell lines. BacMam-Pgp and BacMam-ABCG2 baculovirus-transduced cell lines showed similar cell surface expression (as detected by monoclonal antibodies with an external epitope) and transport function of these transporters compared to drug-resistant cell lines that overexpress the two transporters. Transient expression of Pgp was maintained in HeLa cells for up to 72 h after transduction (48 h after removal of the BacMam virus). These BacMam-baculovirus-transduced mammalian cells expressing Pgp or ABCG2 were used for assessing the functional activity of these transporters. Crude membranes isolated from these cells were further used to study the activity of these transporters by biochemical techniques such as photocross-linking with transport substrate and adenosine triphosphatase assays. In addition, we show that the BacMam expression system can be exploited to coexpress both Pgp and ABCG2 in mammalian cells to determine their contribution to the transport of a common anticancer drug substrate. Collectively, these data demonstrate that the BacMam-baculovirus-based expression system can be used to simultaneously study the transport function and biochemical properties of ABC transporters.
C1 [Shukla, Suneet; Schwartz, Candice; Kapoor, Khyati; Kouanda, Abdul; Ambudkar, Suresh V.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Ambudkar, SV (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM ambudkar@helix.nih.gov
RI shukla, suneet/B-4626-2012
FU National Institutes of Health National Cancer Institute; National
Institutes of Health Center for Cancer Research; National Institutes of
Health Office of Dietary Supplements [OD-09-101]
FX This work was supported by the Intramural Research program of the
National Institutes of Health National Cancer Institute; the National
Institutes of Health Center for Cancer Research; and the National
Institutes of Health Office of Dietary Supplements [Grant OD-09-101].
NR 33
TC 22
Z9 22
U1 0
U2 10
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0090-9556
J9 DRUG METAB DISPOS
JI Drug Metab. Dispos.
PD FEB
PY 2012
VL 40
IS 2
BP 304
EP 312
DI 10.1124/dmd.111.042721
PG 9
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 879KV
UT WOS:000299329000011
PM 22041108
ER
PT J
AU Nagaoka, T
Karasawa, H
Castro, NP
Rangel, MC
Salomon, DS
Bianco, C
AF Nagaoka, Tadahiro
Karasawa, Hideaki
Castro, Nadia Pereira
Rangel, Maria Cristina
Salomon, David S.
Bianco, Caterina
TI An evolving web of signaling networks regulated by Cripto-1
SO GROWTH FACTORS
LA English
DT Article
DE Cripto-1; Nodal-Cripto-1-dependent signaling pathway; MAPK/AKT signaling
pathway; Notch; Wnt/beta-catenin
ID MAMMARY EPITHELIAL-CELLS; LEFT-RIGHT ASYMMETRY; CANCER STEM-CELLS; A-P
AXIS; MOUSE EMBRYO; TYROSINE PHOSPHORYLATION; VERTEBRATE DEVELOPMENT;
MALIGNANT-MELANOMA; NODAL TRAFFICKING; XENOPUS EMBRYOS
AB Over the past few decades, our understanding of the embryonic gene Cripto-1 has considerably advanced through biochemical, cell biology, and animal studies. Cripto-1 performs key functions during embryonic development, while it dramatically disappears in adult tissues, except possibly in adult tissue stem cells. Cripto-1 is re-expressed in human tumors promoting cell proliferation, migration, invasion, epithelial to mesenchymal transition, and tumor angiogenesis. This diversity of biological effects is dependent upon interaction of Cripto-1 with an extensive array of signaling molecules. In fact, Cripto-1 modulates signaling of transforming growth factor-beta family members, including Nodal, GDF-1/-3, Activin, and TGF-beta 1, activates c-src/MAPK/Protein Kinase B (AKT) pathway in a Glypican-1 and GRP78-dependent manner, and cross-talks with erb B4, Wnt/beta-catenin, Notch, Caveolin-1, and Apelin/putative receptor protein related to Angiotensin-type I receptor (APJ) pathways. This article provides an updated survey of the various signaling pathways modulated by Cripto-1 with a focus on mechanistic insights in our understanding of the biological function of Cripto-1 in eukaryotic cells.
C1 [Nagaoka, Tadahiro; Karasawa, Hideaki; Castro, Nadia Pereira; Rangel, Maria Cristina; Salomon, David S.; Bianco, Caterina] NCI, Tumor Growth Factor Sect, Lab Canc Prevent, NIH, Bethesda, MD 20892 USA.
RP Bianco, C (reprint author), NCI, Tumor Growth Factor Sect, Lab Canc Prevent, NIH, 37 Convent Dr,Bldg 37,Room 1112, Bethesda, MD 20892 USA.
EM biancoc@mail.nih.gov
RI Rangel, Maria Cristina/P-7216-2014;
OI Rangel, Maria Cristina/0000-0002-8002-9617; Nagaoka,
Tadahiro/0000-0002-9391-0243
NR 66
TC 20
Z9 22
U1 0
U2 7
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0897-7194
J9 GROWTH FACTORS
JI Growth Factors
PD FEB
PY 2012
VL 30
IS 1
BP 13
EP 21
DI 10.3109/08977194.2011.641962
PG 9
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 875SA
UT WOS:000299053800002
PM 22149969
ER
PT J
AU Zanotti-Fregonara, P
Koroscil, TM
Mantil, J
Satter, M
AF Zanotti-Fregonara, Paolo
Koroscil, Thomas M.
Mantil, Joseph
Satter, Martin
TI RADIATION DOSE TO THE FETUS FROM [F-18]-FDG ADMINISTRATION DURING THE
SECOND TRIMESTER OF PREGNANCY
SO HEALTH PHYSICS
LA English
DT Article
DE dosimetry; internal; positron emission tomography; pregnancy; radiation;
medical
ID NUCLEAR-MEDICINE; F-18-FDG
AB The authors estimated the fetal radiation dose from [F-18]-FDG in a rare case of a woman who underwent a PET/CT scan during the second trimester of pregnancy. The patient, a 27-y-old female with a paraganglioma, received 181.3 MBq [F-18]-FDG. From the concentrations of radioactivity measured on the images, the time-integrated activity coefficients of the fetus and the placenta were derived. The time-integrated activity coefficients of the mother's organs were taken from the standard values of ICRP publication 106. The final fetal dose was calculated using the 6-mo pregnant model of the OLINDA/EXM software. The fetus showed an overall low and homogeneous [F-18]-FDG uptake, with an average concentration of 2.41 kBq cm(-3). The uptake in the placenta was generally higher (average concentration = 3.69 kBq cm(-3)). The estimated time-integrated activity coefficients were 0.0130 and 0.0058 Bq h Bq(-1) for the fetus and the placenta, respectively. The final average dose to the fetus was 1.97 x 10(-2) mGy MBq(-1) (3.6 mGy in this patient who received 181.3 MBq). Therefore, the dose to the fetus from [F-18]-FDG administration during the second trimester of pregnancy is low. When medically indicated, pregnancy should not be a categorical basis for withholding [F-18]-FDG PET scans. Health Phys. 102(2):217-219; 2012
C1 [Zanotti-Fregonara, Paolo] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Koroscil, Thomas M.] Wright State Univ, Boonshoft Sch Med, Dayton, OH 45435 USA.
[Mantil, Joseph; Satter, Martin] Kettering Med Ctr, Dept Nucl Med, PET, Dayton, OH USA.
RP Zanotti-Fregonara, P (reprint author), NIMH, Mol Imaging Branch, NIH, Bldg 10,Room B1D43,31 Ctr Dr,MSC 1026, Bethesda, MD 20892 USA.
EM zanottifregonp@mail.nih.gov
FU National Institute of Mental Health, National Institutes of Health,
Department of Health and Human Services (IRP-NIMH-NIH-DHHS)
FX The authors thank Michael G. Stabin for helpful discussion. This work
was supported by the Intramural Research Program of the National
Institute of Mental Health, National Institutes of Health, Department of
Health and Human Services (IRP-NIMH-NIH-DHHS).
NR 13
TC 8
Z9 8
U1 0
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 2012
VL 102
IS 2
BP 217
EP 219
DI 10.1097/HP.0b013e318226ebb4
PG 3
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 876LB
UT WOS:000299107900011
PM 22217594
ER
PT J
AU Bharmal, N
Tseng, CH
Kaplan, R
Wong, MD
AF Bharmal, Nazleen
Tseng, Chi-Hong
Kaplan, Robert
Wong, Mitchell D.
TI State-Level Variations in Racial Disparities in Life Expectancy
SO HEALTH SERVICES RESEARCH
LA English
DT Article
DE Life expectancy; disparity; black; United States
ID UNITED-STATES; HEALTH; MORTALITY
AB Objective. To explore state patterns in the racial life expectancy gap.
Data Sources. The 1997-2004 Multiple Cause of Death PUF, 2000 U.S. Census.
Study Design. We calculated life expectancy at birth for black and white men and women.
Data Extraction Methods. Data were obtained by the NCHS and U.S. Census Bureau.
Principal Findings. States with small racial differences are due to higher-than-expected life expectancy for blacks or lower-than-expected for whites. States with large disparity are explained by higher-than-average life expectancy among whites or lower-than-average life expectancy among blacks.
Conclusions. Heterogeneous state patterns in racial disparity in life expectancy exist. Eliminating disparity in states with large black populations would make the greatest impact nationally.
C1 [Bharmal, Nazleen] Univ Calif Los Angeles, UCLA David Geffen Sch Med, Div Gen Internal Med & Hlth Serv Res, AHA PRT Spina Outcomes Ctr, Los Angeles, CA 90095 USA.
[Kaplan, Robert] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
RP Bharmal, N (reprint author), Univ Calif Los Angeles, UCLA David Geffen Sch Med, Div Gen Internal Med & Hlth Serv Res, AHA PRT Spina Outcomes Ctr, 710Westwood Plaza,C109 RNRC, Los Angeles, CA 90095 USA.
EM nbharmal@mednet.ucla.edu
OI Wong, Mitchell/0000-0002-4800-8410
FU Robert Wood Johnson Clinical Scholars Program; UCLA National Service
[T32 PE19001]
FX The authors wish to thank Martin Shapiro, M. D., Ph. D., for his help in
the interpretation of the data, Patrick Heuveline, Ph. D., for his help
in life table methods, and Jenny Kotlerman, Ph. D., for her help in
programming codes. Dr. Bharmal was supported by the Robert Wood Johnson
Clinical Scholars Program and UCLA National Service Research Award (T32
PE19001).
NR 22
TC 10
Z9 10
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0017-9124
J9 HEALTH SERV RES
JI Health Serv. Res.
PD FEB
PY 2012
VL 47
IS 1
BP 544
EP 555
DI 10.1111/j.1475-6773.2011.01345.x
PN 2
PG 12
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 875OU
UT WOS:000299041600014
PM 22092060
ER
PT J
AU Rutledge, HR
Jiang, W
Yang, J
Warg, LA
Schwartz, DA
Pisetsky, DS
Yang, IV
AF Rutledge, Holly R.
Jiang, Weiwen
Yang, Jun
Warg, Laura A.
Schwartz, David A.
Pisetsky, David S.
Yang, Ivana V.
TI Gene expression profiles of RAW264.7 macrophages stimulated with
preparations of LPS differing in isolation and purity
SO INNATE IMMUNITY
LA English
DT Article
DE Lipopolysaccharide; endotoxin; LPS preparation; macrophage; gene
expression; microarray
ID SALMONELLA-ENTERITIDIS; IDENTIFICATION; LIPOPOLYSACCHARIDE;
INFLAMMATION; MICE; PERSISTENCE; ACTIVATION; INFECTION; DISEASE; TRAM
AB Lipopolysaccharide is a major component of the cell wall of Gram-negative bacteria and a potent stimulator of innate immune response via TLR4. Studies on the LPS action both in vivo and in vitro have used different preparations of LPS, including ultra-pure LPS (LIST) and a less pure but less expensive form (Sigma) isolated from Escherichia coli serotype O111:B4. The difference between the effects of these compounds has not been well studied although this information is important in understanding TLR stimulation. In this study, we compared response of RAW264.7 macrophage cells treated LIST or Sigma LPS for 6 h and 24 h. Gene expression data were analyzed to identify specific genes and pathways that are in common and unique to the two LPS preparations. Seven hundred fifty-five genes were differentially expressed at 6 h in response to Sigma LPS and 973 were differentially expressed following LIST LPS treatment, with 503 in common. At 24 h, Sigma LPS induced or repressed 901 genes while 1646 genes were differentially regulated by LIST LPS treatment; 701 genes were shared by two forms of LPS. Although considerably more genes were differentially expressed in response to LIST LPS, similar molecular pathways and transcriptional networks were activated by the two LPS preparations. We also treated bone marrow-derived macrophages (BMMs) from three strains of mice with different concentrations of LIST and Sigma LPS and showed that BMMs produced more IL-6 and TNF-alpha in response to LIST LPS at low LPS concentrations but, at higher LPS concentrations, more cytokines were produced in response to stimulation by Sigma LPS. Together, these findings suggest that, despite activation of similar molecular pathways by LIST and Sigma LPS preparations, residual protein impurities in the Sigma LPS preparation may nevertheless influence the transcriptional profile attributed to TLR4 stimulation.
C1 [Warg, Laura A.; Schwartz, David A.; Yang, Ivana V.] Natl Jewish Hlth, Dept Med, Denver, CO 80206 USA.
[Warg, Laura A.; Schwartz, David A.; Yang, Ivana V.] Natl Jewish Hlth, Ctr Genes Environm & Hlth, Denver, CO 80206 USA.
[Schwartz, David A.; Yang, Ivana V.] Univ Colorado Denver, Dept Med, Aurora, CO USA.
[Jiang, Weiwen; Pisetsky, David S.] Durham VA Med Ctr, Med Res Serv, Durham, NC USA.
[Jiang, Weiwen; Pisetsky, David S.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Rutledge, Holly R.; Yang, Jun] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Yang, IV (reprint author), Natl Jewish Hlth, Dept Med, 1400 Jackson St,Smith Bldg A651, Denver, CO 80206 USA.
EM yangi@njhealth.org
FU NIH; National Institute of the Environmental Health Sciences; National
Heart Lung and Blood Institute; VA Merit review
FX This study was funded by the Intramural Research Program of the NIH,
National Institute of the Environmental Health Sciences and National
Heart Lung and Blood Institute, and a VA Merit review grant.
NR 32
TC 7
Z9 7
U1 0
U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1753-4259
J9 INNATE IMMUN-LONDON
JI Innate Immun.
PD FEB
PY 2012
VL 18
IS 1
BP 80
EP 88
DI 10.1177/1753425910393540
PG 9
WC Biochemistry & Molecular Biology; Immunology; Medicine, Research &
Experimental; Microbiology
SC Biochemistry & Molecular Biology; Immunology; Research & Experimental
Medicine; Microbiology
GA 877FL
UT WOS:000299162600008
PM 21239457
ER
PT J
AU Singh, UP
Singh, NP
Busbee, B
Guan, H
Singh, B
Price, RL
Taub, DD
Mishra, MK
Nagarkatti, M
Nagarkatti, PS
AF Singh, Udai P.
Singh, Narendra P.
Busbee, Brandon
Guan, H.
Singh, Balwan
Price, Robert L.
Taub, Dennis D.
Mishra, Manoj K.
Nagarkatti, Mitzi
Nagarkatti, Prakash S.
TI Alternative Medicines as Emerging Therapies for Inflammatory Bowel
Diseases
SO INTERNATIONAL REVIEWS OF IMMUNOLOGY
LA English
DT Review
DE bromelain; Crohn disease (CD); curcumin; inflammation; inflammatory
bowel disease (IBD); polyphenols; pomegranate; resveratrol; rutin;
ulcerative colitis (UC)
ID AVIUM SUBSP PARATUBERCULOSIS; GENOME-WIDE ASSOCIATION; NF-KAPPA-B; RICH
POMEGRANATE EXTRACT; ACTIVE CROHNS-DISEASE; ULTRAVIOLET-INDUCED
PIGMENTATION; CHIMERIC MONOCLONAL-ANTIBODY; INDUCED EXPERIMENTAL
COLITIS; RANDOMIZED CONTROLLED-TRIAL; CHEMOKINE RECEPTOR CXCR3
AB Inflammatory bowel disease (IBD) can be divided into two major categories, ulcerative colitis (UC) and Crohn disease (CD). While the main cause(s) of IBD remain unknown, a number of interventional and preventive strategies have been proposed for use against CD and UC. Many reports have focused on the use of alternative natural medicines as potential therapeutic interventions in IBD patients with minimal side effects. While the use of alternative medicines may be effective in IBD patients that are refractory to corticosteroids or thiopurins, alternative treatment strategies are limited and require extensive clinical testing before being optimized for use in patients.
C1 [Singh, Udai P.; Singh, Narendra P.; Busbee, Brandon; Guan, H.] Univ S Carolina, Sch Med, Dept Pathol Microbiol & Immunol, Columbia, SC 29208 USA.
[Singh, Balwan] Emory Univ, Natl Primate Res Ctr, Atlanta, GA 30322 USA.
[Price, Robert L.] Univ S Carolina, Dept Cell & Dev Biol, Columbia, SC 29208 USA.
[Taub, Dennis D.] NIA IRP, Lab Mol Biol & Immunol, NIH, Baltimore, MD 21224 USA.
[Mishra, Manoj K.] Alabama State Univ, Dept Biol & Math Sci, Montgomery, AL 36101 USA.
RP Singh, UP (reprint author), Univ S Carolina, Sch Med, Dept Pathol Microbiol & Immunol, Columbia, SC 29208 USA.
EM Udai.singh@uscmed.sc.edu; taubd@grc.nia.nih.gov
FU NIH [P01AT003961]; National Institute on Aging, NIH
FX This study was supported in part by grants from NIH P01AT003961 and the
Intramural Research Program, National Institute on Aging, NIH.
NR 184
TC 11
Z9 11
U1 0
U2 10
PU TAYLOR & FRANCIS INC
PI PHILADELPHIA
PA 530 WALNUT STREET, STE 850, PHILADELPHIA, PA 19106 USA
SN 0883-0185
EI 1563-5244
J9 INT REV IMMUNOL
JI Int. Rev. Immunol.
PD FEB
PY 2012
VL 31
IS 1
BP 66
EP 84
DI 10.3109/08830185.2011.642909
PG 19
WC Immunology
SC Immunology
GA 877IT
UT WOS:000299171900005
PM 22251008
ER
PT J
AU Gardner, ER
Kelly, M
Springman, E
Lee, KJ
Li, HQ
Moore, W
Figg, WD
AF Gardner, Erin R.
Kelly, Martha
Springman, Eric
Lee, Kyoung-jin
Li, Haiqing
Moore, William
Figg, William D.
TI Antiangiogenic and antitumor activity of LP-261, a novel oral tubulin
binding agent, alone and in combination with bevacizumab
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Anticancer agent; Tubulin; In vitro; In vivo
ID PROSTATE-CANCER; PACLITAXEL
AB LP-261 is a novel tubulin targeting anticancer agent that binds at the colchicine site on tubulin, inducing G2/M arrest. Screening in the NCI60 cancer cell lines resulted in a mean GI50 of approximately 100 nM. Here, we report the results of testing in multiple mouse xenograft models and angiogenesis assays, along with bioavailability studies. To determine the antiangiogenic activity of LP-261, both in vitro and ex vivo experiments were performed. Human Umbilical Vein Endothelial cells (HUVECs) were incubated with LP-261 at 50 nM to 10 mu M. LP-261 was also tested in a rat aortic ring assay, from 20 nM to 10 mu M. Multiple mouse xenograft studies were performed to assess in vivo antitumor activity. LP-261 was tested as a single agent in colon adenocarcinoma (SW620) and prostate cancer (LNCaP and PC3) xenografts, evaluating several different dosing schedules. LP-261 was also used in combination with bevacizumab in the SW620 xenograft model. LP-261 also exhibited high oral bioavailability and apparent lack of efflux by intestinal transporters such as ABCB1. LP-261 is a very potent inhibitor of angiogenesis, preventing microvessel outgrowth in the rat aortic ring assay and HUVEC cell proliferation at nanomolar concentrations. Complete inhibition of tumor growth was achieved in the PC3 xenograft model and shown to be schedule dependent. Excellent inhibition of tumor growth in the SW620 model was observed, comparable with paclitaxel. Combining oral, low dose LP-261 with bevacizumab led to significantly improved tumor inhibition. Oral LP-261 is very effective at inhibiting tumor growth in multiple mouse xenograft models and is well tolerated.
C1 [Li, Haiqing; Figg, William D.] NCI, Med Oncol Branch, Mol Pharmacol Sect, Bethesda, MD 20892 USA.
[Gardner, Erin R.] NCI, Clin Pharmacol Program, SAIC Frederick, Frederick, MD 21702 USA.
[Kelly, Martha; Springman, Eric; Lee, Kyoung-jin; Moore, William] Ansaris, Blue Bell, PA 19422 USA.
RP Figg, WD (reprint author), NCI, Med Oncol Branch, Mol Pharmacol Sect, 9000 Rockville Pike,Bldg 10,Room 5A01, Bethesda, MD 20892 USA.
EM wdfigg@helix.nih.gov
RI Figg Sr, William/M-2411-2016
FU National Cancer Institute, National Institutes of Health [N01-CO-12400,
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, National Institutes of Health, under
contract N01-CO-12400 and HHSN261200800001E.1 The content of
this publication does not necessarily reflect the views or policies of
the Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the
U.S. Government.; This work was supported by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research.
NR 10
TC 3
Z9 3
U1 0
U2 4
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 2012
VL 30
IS 1
BP 90
EP 97
DI 10.1007/s10637-010-9520-5
PG 8
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 876QC
UT WOS:000299121500009
PM 20820910
ER
PT J
AU Kim, GP
Mahoney, MR
Szydlo, D
Mok, TSK
Marshke, R
Holen, K
Picus, J
Boyer, M
Pitot, HC
Rubin, J
Philip, PA
Nowak, A
Wright, JJ
Erlichman, C
AF Kim, George P.
Mahoney, Michelle R.
Szydlo, Daniel
Mok, Tony S. K.
Marshke, Robert
Holen, Kyle
Picus, Joel
Boyer, Michael
Pitot, Henry C.
Rubin, Joseph
Philip, Philip A.
Nowak, Anna
Wright, John J.
Erlichman, Charles
TI An international, multicenter phase II trial of bortezomib in patients
with hepatocellular carcinoma
SO INVESTIGATIONAL NEW DRUGS
LA English
DT Article
DE Boronic acids; Antineoplastic agents; Biologic agents; Treatment outcome
ID PROTEASOME INHIBITOR PS-341; FACTOR-KAPPA-B; COLORECTAL-CANCER;
ACTIVATION; SORAFENIB; MYELOMA; PROTEIN
AB Background and Rationale Bortezomib (PS-341, VELCADEA (R)) is a selective inhibitor of the 26S proteasome, an integral component of the ubiquitin-proteasome pathway. This phase II study evaluated the activity and tolerability of bortezomib in unresectable hepatocellular carcinoma (HCC) patients. Methods The primary endpoint was confirmed tumor response rate (RR) with secondary endpoints including duration of response, time to disease progression, survival and toxicity. Treatment consisted of bortezomib, 1.3 mg/m2 IV bolus on days 1, 4, 8, and 11 of each 21-day treatment cycle. Eligibility included: no prior systemic chemotherapy, ECOG PS 0-2, Child-Pugh A or B, preserved hematologic, hepatic and neurologic function; prior liver-directed therapy was permitted. Results Thirty-five patients enrolled and received a median of 2 cycles of treatment (range 1-12). Overall, 24 and 4 patients had a maximum severity of grade 3 and 4 adverse events (AEs), respectively. No treatment related deaths occurred. Only thrombocytopenia (11%) was seen in greater than 10% of patients. One patient achieved a partial response, lasting 13 weeks during treatment and progressed 11.6 months later; two patients received treatment for greater than 6 months. Median time-to-progression was 1.6 months and median survival was 6.0 months. Conclusions This international, multicenter trial evaluated bortezomib as monotherapy in unresectable HCC patients. And, despite the lack of significant activity, this report serves as a baseline clinical experience for the development of future dual biologic approaches including bortezomib.
C1 [Kim, George P.] Mayo Clin Florida, Jacksonville, FL USA.
[Mahoney, Michelle R.; Szydlo, Daniel; Pitot, Henry C.; Rubin, Joseph; Erlichman, Charles] Mayo Clin Rochester, Rochester, MN USA.
[Mok, Tony S. K.] Natl Univ Singapore Hosp, Singapore 117548, Singapore.
[Marshke, Robert] Mayo Clin Arizona, Scottsdale, AZ USA.
[Holen, Kyle] Univ Wisconsin Carbone Canc Ctr, Madison, WI USA.
[Picus, Joel] Washington Univ, St Louis, MO USA.
[Boyer, Michael] Royal Prince Alfred Hosp, Camperdown, NSW 2050, Australia.
[Philip, Philip A.] Karmanos Canc Inst, Detroit, MI USA.
[Nowak, Anna] Sir Charles Gairdner Hosp, Perth, WA, Australia.
[Wright, John J.] NCI, Rockville, MD USA.
RP Kim, GP (reprint author), Mayo Clin Florida, Jacksonville, FL USA.
EM kim.george@mayo.edu
RI Nowak, Anna/B-2487-2013
OI Nowak, Anna/0000-0002-9317-9526
FU Phase 2 Consortium [NCI N01 CM17104]
FX Supported by the Phase 2 Consortium Contract (NCI N01 CM17104).
NR 31
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U1 0
U2 4
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0167-6997
EI 1573-0646
J9 INVEST NEW DRUG
JI Invest. New Drugs
PD FEB
PY 2012
VL 30
IS 1
BP 387
EP 394
DI 10.1007/s10637-010-9532-1
PG 8
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 876QC
UT WOS:000299121500043
PM 20839030
ER
PT J
AU Veech, RL
Valeri, CR
VanItallie, TB
AF Veech, Richard L.
Valeri, C. Robert
VanItallie, Theodore B.
TI The mitochondrial permeability transition pore provides a key to the
diagnosis and treatment of traumatic brain injury
SO IUBMB LIFE
LA English
DT Article
DE TBI; ketone bodies; mPTP; cyclosporine A; brain energetics
ID CYCLOSPORINE-A; METABOLISM; GLUCOSE; PYROPHOSPHATE; DYSFUNCTION;
APOPTOSIS; DAMAGE
AB The pathological consequences of traumatic head injury result largely from the opening of the mitochondrial permeability transition pore (mPTP). The mPTP opens due to a decrease in brain phosphorylation energy resulting in a further decrease in brain ATP production and a measurable increase in brain heat generation and temperature. The increase in brain temperature can be measured transcranially by near infrared spectroscopy which can be used to diagnose traumatic brain injury (TBI) and to monitor treatment. Effective therapy of TBI can be achieved by closure of the mPTP by administration of cyclosporine A or by oral administration of ketone body esters. While ketosis has previously been known to prevent damage from TBI, the availability of oral ketone esters presents the first practical modality of achieving therapeutic levels of ketone bodies. (c) 2012 IUBMB Life, 2012
C1 [Veech, Richard L.] NIAAA, Lab Metab Control, NIH, Rockville, MD 20852 USA.
[Valeri, C. Robert] Naval Blood Res Lab Inc, Boston, MA USA.
[VanItallie, Theodore B.] Columbia Univ, Dept Med, St Lukes Roosevelt Hosp Ctr, Coll Phys & Surg, New York, NY USA.
RP Veech, RL (reprint author), NIAAA, Lab Metab Control, NIH, Rockville, MD 20852 USA.
EM rveech@mail.nih.gov
FU Defense Research Project Administration, DARPA
FX Support for development of the ketone ester from the Defense Research
Project Administration, DARPA, is gratefully acknowledged.
NR 25
TC 10
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U1 0
U2 5
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1521-6543
J9 IUBMB LIFE
JI IUBMB Life
PD FEB
PY 2012
VL 64
IS 2
BP 203
EP 207
DI 10.1002/iub.590
PG 5
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 875OE
UT WOS:000299039800013
PM 22241645
ER
PT J
AU Koonin, EV
AF Koonin, Eugene V.
TI Comment Defining Life: An Exercise in Semantics or A Route to Biological
Insights?
SO JOURNAL OF BIOMOLECULAR STRUCTURE & DYNAMICS
LA English
DT Editorial Material
ID EVOLUTION
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Koonin, EV (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov
NR 11
TC 2
Z9 2
U1 2
U2 10
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 2012
VL 29
IS 4
BP 603
EP 605
PG 3
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 876SN
UT WOS:000299128100004
PM 22208253
ER
PT J
AU Weinberger, DM
Simonsen, L
Jordan, R
Steiner, C
Miller, M
Viboud, C
AF Weinberger, Daniel M.
Simonsen, Lone
Jordan, Richard
Steiner, Claudia
Miller, Mark
Viboud, Cecile
TI Impact of the 2009 Influenza Pandemic on Pneumococcal Pneumonia
Hospitalizations in the United States
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID A H1N1 INFECTION; STREPTOCOCCUS-PNEUMONIAE; BACTERIAL PNEUMONIA;
DISEASE; VIRUS; ASSOCIATION; CHILDREN; COINFECTIONS; PATHOGENS; EFFICACY
AB Background. Infection with influenza virus increases the risk for developing pneumococcal disease. The A/H1N1 influenza pandemic in autumn 2009 provided a unique opportunity to evaluate this relationship.
Background. Infection with influenza virus increases the risk for developing pneumococcal disease. The A/H1N1 influenza pandemic in autumn 2009 provided a unique opportunity to evaluate this relationship.
Methods. Using weekly age-, state-, and cause-specific hospitalizations from the US State Inpatient Databases of the Healthcare Cost and Utilization Project 2003-2009, we quantified the increase in pneumococcal pneumonia hospitalization rates above a seasonal baseline during the pandemic period.
Results. We found a significant increase in pneumococcal hospitalizations from late August to mid-December 2009, which corresponded to the timing of highest pandemic influenza activity. Individuals aged 5-19 years, who have a low baseline level of pneumococcal disease, experienced the largest relative increase in pneumococcal hospitalizations (ratio, 1.6 [95% confidence interval {CI}, 1.4-1.7]), whereas the largest absolute increase was observed among individuals aged 40-64 years. In contrast, there was no excess disease in the elderly. Geographical variation in the timing of excess pneumococcal hospitalizations matched geographical patterns for the fall pandemic influenza wave.
Conclusions. The 2009 influenza pandemic had a significant impact on the rate of pneumococcal pneumonia hospitalizations, with the magnitude of this effect varying between age groups and states, mirroring observed variations in influenza activity.
C1 [Weinberger, Daniel M.; Simonsen, Lone; Miller, Mark; Viboud, Cecile] NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Simonsen, Lone] George Washington Univ, Dept Global Hlth, Washington, DC USA.
[Jordan, Richard] Social & Sci Syst Inc, Rockville, MD USA.
[Jordan, Richard; Steiner, Claudia] Agcy Healthcare Res & Qual, Healthcare Cost & Utilizat Project, Rockville, MD USA.
RP Weinberger, DM (reprint author), NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, Bldg 16,16 Ctr Dr, Bethesda, MD 20892 USA.
EM weinbergerdm@mail.nih.gov
OI Simonsen, Lone/0000-0003-1535-8526; Weinberger,
Daniel/0000-0003-1178-8086
FU International Influenza Unit, Office of Global Affairs, US Department of
Health and Human Services; RAPIDD program (Research And Policy for
Infectious Diseases Dynamics); Fogarty International Center, National
Institutes of Health (NIH); Department of Homeland Security; Pfizer
FX The MISMS study is funded by the International Influenza Unit, Office of
Global Affairs, US Department of Health and Human Services. L. S.
acknowledges support from the RAPIDD program (Research And Policy for
Infectious Diseases Dynamics) funded by the Fogarty International
Center, National Institutes of Health (NIH), and the Department of
Homeland Security.; L. S. has received research support from Pfizer for
an observational study of pneumococcal vaccine program benefits. All
other authors report no conflicts.
NR 42
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U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD FEB 1
PY 2012
VL 205
IS 3
BP 458
EP 465
DI 10.1093/infdis/jir749
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 876HA
UT WOS:000299097200015
PM 22158564
ER
PT J
AU Tobian, AAR
Kigozi, G
Redd, AD
Serwadda, D
Kong, XR
Oliver, A
Nalugoda, F
Quinn, TC
Gray, RH
Wawer, MJ
AF Tobian, Aaron A. R.
Kigozi, Godfrey
Redd, Andrew D.
Serwadda, David
Kong, Xiangrong
Oliver, Amy
Nalugoda, Fred
Quinn, Thomas C.
Gray, Ronald H.
Wawer, Maria J.
TI Male Circumcision and Herpes Simplex Virus Type 2 Infection in Female
Partners: A Randomized Trial in Rakai, Uganda
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID HUMAN-PAPILLOMAVIRUS; HIV PREVENTION; MEN; TRANSMISSION; SYPHILIS
AB Male circumcision reduces acquisition of herpes simplex virus type 2 (HSV-2) in men. We assessed whether male circumcision reduces HSV-2 infection among female partners. HSV-2-negative, human immunodeficiency virus-negative female partners of 368 males who were and 372 males who were not randomized to receive male circumcision were enrolled. The incidence of HSV-2 infection among females over a period of 2 years was 6.09 cases per 100 person-years in the intervention arm and 6.32 cases per 100 person-years in the control arm (incidence rate ratio [IRR], 0.96 [95% confidence interval {CI},.62-1.49]; P 5.87). Among female partners of HSV2- positive males, the incidence of HSV-2 infection was 9.55 cases per 100 person-years in the intervention arm and 11.17 cases per 100 person-years in the control arm (IRR, 0.85 [95% CI,.44-1.67]; P 5.62). Contrary to findings in males, male circumcision did not affect HSV-2 acquisition among female partners.
C1 [Tobian, Aaron A. R.] Johns Hopkins Univ, Dept Pathol, Sch Med, Baltimore, MD 21287 USA.
[Oliver, Amy; Quinn, Thomas C.] Johns Hopkins Univ, Dept Med, Sch Med, Baltimore, MD 21287 USA.
[Tobian, Aaron A. R.; Kong, Xiangrong; Gray, Ronald H.; Wawer, Maria J.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21287 USA.
[Kong, Xiangrong] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD 21287 USA.
[Redd, Andrew D.; Quinn, Thomas C.] NIAID, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Kigozi, Godfrey; Serwadda, David; Nalugoda, Fred; Gray, Ronald H.; Wawer, Maria J.] Rakai Hlth Sci Program, Entebbe, Uganda.
[Serwadda, David] Makerere Univ, Sch Publ Hlth, Kampala, Uganda.
RP Tobian, AAR (reprint author), Johns Hopkins Univ, Dept Pathol, Sch Med, Carnegie 667,600 N Wolfe St, Baltimore, MD 21287 USA.
EM atobian1@jhmi.edu
FU Bill and Melinda Gates Foundation [22006.02]; National Institutes of
Health (NIH) [U1AI51171, 1K23AI093152-01A1]; Doris Duke Charitable
Foundation [2011036]; Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, NIH; Fogarty International
Center [5D43TW001508, D43TW00015]; Doris Duke Charitable Foundation;
Johns Hopkins University
FX The trials were supported by the Bill and Melinda Gates Foundation
(22006.02) and the National Institutes of Health (NIH; U1AI51171); this
work was supported by the Doris Duke Charitable Foundation (2011036),
along with the Division of Intramural Research, National Institute of
Allergy and Infectious Diseases, NIH, for laboratory support; the
Fogarty International Center (5D43TW001508 and D43TW00015), for
contributions to training; and the Doris Duke Charitable Foundation, NIH
(1K23AI093152-01A1 to A. A. R. T.), and Johns Hopkins University
Clinician Scientist Development Award (to A. A. R. T.).
NR 15
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U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD FEB 1
PY 2012
VL 205
IS 3
BP 486
EP 490
DI 10.1093/infdis/jir767
PG 5
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 876HA
UT WOS:000299097200018
PM 22147796
ER
PT J
AU Markt, SC
Rodriguez, AC
Burk, RD
Hildesheim, A
Herrero, R
Wacholder, S
Hutchinson, M
Schiffman, M
AF Markt, Sarah Coseo
Rodriguez, Ana C.
Burk, Robert D.
Hildesheim, Allan
Herrero, Rolando
Wacholder, Sholom
Hutchinson, Martha
Schiffman, Mark
TI Longitudinal Analysis of Carcinogenic Human Papillomavirus Infection and
Associated Cytologic Abnormalities in the Guanacaste Natural History
Study: Looking Ahead to Cotesting
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID RISK HUMAN-PAPILLOMAVIRUS; CERVICAL-CANCER; COSTA-RICA; HPV DNA;
FOLLOW-UP; WOMEN; CLEARANCE; NEOPLASIA; SMEAR; LOAD
AB Background. Few studies have addressed the timing of cervical cytologic abnormalities and human papillomavirus (HPV) positivity during the course of an infection. It remains largely unknown how infections detected by HPV and cytology wax and wane relative to each other. The aim of this analysis was to assess the longitudinal relationship of abnormal cytology and HPV positivity in a 7-year prospective study of 2500 women in Guanacaste, Costa Rica.
Methods. At each semiannual or annual visit, cervical specimens were screened using liquid-based cytology and tested for > 40 HPV types with use of MY09/MY11 L1 degenerate primer polymerase chain reaction-based methods. On the basis of previous work, we separated prevalent and newly detected infections in younger and older women.
Results. Among newly detected HPV- and/or cytology-positive events, HPV and cytology appeared together similar to 60% of the time; when discordant, HPV tended to appear before cytology in younger and older women. Combining newly and prevalently detected events, HPV and cytology disappeared at the same time > 70% of the time. When discordant, HPV tended to disappear after cytology in younger and older women.
Conclusions. Detection of HPV DNA and associated cytological abnormalities tend to come and leave together; however, when discordant, detection of HPV DNA tends to precede and/or last longer than associated cytologic abnormalities.
C1 [Markt, Sarah Coseo] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Markt, Sarah Coseo; Hildesheim, Allan; Wacholder, Sholom; Schiffman, Mark] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Rodriguez, Ana C.; Herrero, Rolando] Fdn INCIENSA, Liberia, Costa Rica.
[Burk, Robert D.] Yeshiva Univ, Albert Einstein Coll Med, Bronx, NY USA.
[Hutchinson, Martha] Brown Univ, Women & Infants Hosp, Dept Pathol, Providence, RI USA.
RP Markt, SC (reprint author), Harvard Univ, Sch Publ Hlth, Dept Epidemiol, 677 Huntington Ave,9th Floor, Boston, MA 02115 USA.
EM scoseo@hsph.harvard.edu
RI Hildesheim, Allan/B-9760-2015
OI Hildesheim, Allan/0000-0003-0257-2363
FU National Institutes of Health research training grant (NIH) [R25
CA098566]; National Cancer Institute, NIH, Department of Health and
Human Services [NO1-CP-21081, NO1-CP-33061, NO1-CP-40542, NO1-CP-506535]
FX This work was supported in part by the National Institutes of Health
research training grant (NIH, R25 CA098566 to S. C. M.). The Guanacaste
Project was supported by National Cancer Institute, NIH, Department of
Health and Human Services (NO1-CP-21081, NO1-CP-33061, NO1-CP-40542, and
NO1-CP-506535).
NR 25
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U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD FEB 1
PY 2012
VL 205
IS 3
BP 498
EP 505
DI 10.1093/infdis/jir746
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 876HA
UT WOS:000299097200020
PM 22147792
ER
PT J
AU Hallett, M
AF Hallett, Mark
TI EMG analysis of stereotyped voluntary movements in man
SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
LA English
DT Editorial Material
C1 NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, NIH, 10 Ctr Dr MSC 1428, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
NR 7
TC 1
Z9 1
U1 3
U2 6
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-3050
J9 J NEUROL NEUROSUR PS
JI J. Neurol. Neurosurg. Psychiatry
PD FEB
PY 2012
VL 83
IS 2
BP 122
EP 123
DI 10.1136/jnnp-2011-301283
PG 2
WC Clinical Neurology; Psychiatry; Surgery
SC Neurosciences & Neurology; Psychiatry; Surgery
GA 877IC
UT WOS:000299170100002
PM 22228784
ER
PT J
AU Liberski, PP
Sikorska, B
Lindenbaum, S
Goldfarb, LG
McLean, C
Hainfellner, JA
Brown, P
AF Liberski, Pawel P.
Sikorska, Beata
Lindenbaum, Shirley
Goldfarb, Lev G.
McLean, Catriona
Hainfellner, Johannes A.
Brown, Paul
TI Kuru: Genes, Cannibals and Neuropathology
SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
LA English
DT Review
DE Kuru; Prion diseases; Transmissible spongiform encephalopathies
ID CREUTZFELDT-JAKOB-DISEASE; PRION PROTEIN; SPONGIFORM ENCEPHALOPATHIES;
TRANSMISSION; SCRAPIE; VARIANT; PATHOLOGY; GENOTYPE; BRAIN; CHIMPANZEES
AB Kuru was the first human transmissible spongiform encephalopathy (TSE) or prion disease identified, occurring in the Fore linguistic group of Papua New Guinea. Kuru was a uniformly fatal cerebellar ataxic syndrome, usually followed by choreiform and athetoid movements. Kuru imposed a strong balancing selection on the Fore population, with individuals homozygous for the 129 Met allele of the gene (PRNP) encoding for prion protein (PrP) being the most susceptible. The decline in the incidence of kuru in the Fore has been attributed to the exhaustion of the susceptible genotype and ultimately by discontinuation of exposure via cannibalism. Neuropathologically, kuru-affected brains were characterized by widespread degeneration of neurons, astroglial and microglial proliferation, and the presence of amyloid plaques. These early findings have been confirmed and extended by recent immunohistochemical studies for the detection of the TSE-specific PrP (PrPTSE). Confocal laser microscopy also showed the concentration of glial fibrillary acidic protein-positive astrocytic processes at the plaque periphery. The fine structure of plaques corresponds to that described earlier by light microscopy. The successful experimental transmission of kuru led to the awareness of its similarity to Creutzfeldt-Jakob disease and Gerstmann-Straussler-Scheinker disease and formed a background against which the recent epidemics of iatrogenic and variant Creutzfeldt-Jakob disease could be studied.
C1 [Liberski, Pawel P.; Sikorska, Beata] Med Univ Lodz, Dept Mol Pathol & Neuropathol, Lodz, Poland.
[Lindenbaum, Shirley] CUNY, Grad Ctr, New York, NY USA.
[Goldfarb, Lev G.] NINDS, NIH, Bethesda, MD 20892 USA.
[McLean, Catriona] Alfred Hosp, Dept Anat Pathol, Melbourne, Vic, Australia.
[Hainfellner, Johannes A.] Med Univ Vienna, Inst Neurol, Obersteiner Inst, Vienna, Austria.
[Brown, Paul] CEA DSV iMETI SEPIA, Inst Emerging Dis, Fontenay Aux Roses, France.
RP Liberski, PP (reprint author), Med Univ Lodz, Dept Mol Pathol & Neuropathol, Lodz, Poland.
EM ppliber@csk.umed.lodz.pl
FU Austrian Agency for International Cooperation in Education and Research
(OeAD)
FX Pawel Liberski, Beata Sikorska, and Johannes Hainfellner are supported
by the Austrian Agency for International Cooperation in Education and
Research (OeAD).
NR 89
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U2 59
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0022-3069
J9 J NEUROPATH EXP NEUR
JI J. Neuropathol. Exp. Neurol.
PD FEB
PY 2012
VL 71
IS 2
BP 92
EP 103
DI 10.1097/NEN.0b013e3182444efd
PG 12
WC Clinical Neurology; Neurosciences; Pathology
SC Neurosciences & Neurology; Pathology
GA 879IQ
UT WOS:000299323300001
PM 22249461
ER
PT J
AU Ma, WLD
Brenowitz, SD
AF Ma, Wei-Li Diana
Brenowitz, Stephan D.
TI Single-neuron recordings from unanesthetized mouse dorsal cochlear
nucleus
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
DE in vivo preparation; extracellular spike; auditory physiology
ID COMPLEX-SPIKING NEURONS; PHYSIOLOGICAL-RESPONSE PROPERTIES; LABELED
FUSIFORM CELLS; INFERIOR COLLICULUS; SOUND LOCALIZATION;
INTRACELLULAR-RECORDINGS; ULTRASONIC VOCALIZATIONS; DECEREBRATE GERBILS;
DISCHARGE PATTERNS; ACOUSTIC STRIAE
AB Ma WL, Brenowitz SD. Single-neuron recordings from unanesthetized mouse dorsal cochlear nucleus. J Neurophysiol 107: 824-835, 2012. First published November 9, 2011; doi:10.1152/jn.00427.2011.-Because of the availability of disease and genetic models, the mouse has become a valuable species for auditory neuroscience that will facilitate long-term goals of understanding neuronal mechanisms underlying the perception and processing of sounds. The goal of this study was to define the basic sound-evoked response properties of single neurons in the mouse dorsal cochlear nucleus (DCN). Neurons producing complex spikes were distinguished as cartwheel cells (CWCs), and other neurons were classified according to the response map scheme previously developed in DCN. Similar to observations in other rodent species, neurons of the mouse DCN exhibit relatively little sound-driven inhibition. As a result, type III was the most commonly observed response. Our findings are generally consistent with the model of DCN function that has been developed in the cat and the gerbil, suggesting that this in vivo mouse preparation will be a useful tool for future studies of auditory physiology.
C1 [Ma, Wei-Li Diana; Brenowitz, Stephan D.] Natl Inst Deafness & Other Commun Disorders, Sect Synapt Transmiss, NIDCD, NIH, Bethesda, MD 20892 USA.
RP Brenowitz, SD (reprint author), Natl Inst Deafness & Other Commun Disorders, Sect Synapt Transmiss, NIDCD, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM brenowitzs@nidcd.nih.gov
FU National Institute on Deafness and Other Communication Disorders
FX Funding for this research was provided by the National Institute on
Deafness and Other Communication Disorders Intramural Research Program.
NR 74
TC 5
Z9 5
U1 0
U2 4
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD FEB
PY 2012
VL 107
IS 3
BP 824
EP 835
DI 10.1152/jn.00427.2011
PG 12
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 879HI
UT WOS:000299319900009
PM 22072506
ER
PT J
AU Jacoby, J
Kreitzer, MA
Alford, S
Qian, HH
Tchernookova, BK
Naylor, ER
Malchow, RP
AF Jacoby, Jason
Kreitzer, Matthew A.
Alford, Simon
Qian, Haohua
Tchernookova, Boriana K.
Naylor, Ethan R.
Malchow, Robert Paul
TI Extracellular pH dynamics of retinal horizontal cells examined using
electrochemical and fluorometric methods
SO JOURNAL OF NEUROPHYSIOLOGY
LA English
DT Article
DE retina; feedback; lateral inhibition
ID CONE PHOTORECEPTORS; CALCIUM CURRENTS; LIGHT RESPONSES; PRIMATE RETINA;
FEEDBACK; INHIBITION; CATFISH; MODULATION; LANTHANUM; ATPASE
AB Jacoby J, Kreitzer MA, Alford S, Qian H, Tchernookova BK, Naylor ER, Malchow RP. Extracellular pH dynamics of retinal horizontal cells examined using electrochemical and fluorometric methods. J Neurophysiol 107: 868-879, 2012. First published November 16, 2011; doi:10.1152/jn.00878.2011.-Extracellular H+ has been hypothesized to mediate feedback inhibition from horizontal cells onto vertebrate photoreceptors. According to this hypothesis, depolarization of horizontal cells should induce extracellular acidification adjacent to the cell membrane. Experiments testing this hypothesis have produced conflicting results. Studies examining carp and goldfish horizontal cells loaded with the pH-sensitive dye 5-hexadecanoylaminofluorescein (HAF) reported an extracellular acidification on depolarization by glutamate or potassium. However, investigations using H+-selective microelectrodes report an extracellular alkalinization on depolarization of skate and catfish horizontal cells. These studies differed in the species and extracellular pH buffer used and the presence or absence of cobalt. We used both techniques to examine H+ changes from isolated catfish horizontal cells under identical experimental conditions (1 mM HEPES, no cobalt). HAF fluorescence indicated an acidification response to high extracellular potassium or glutamate. However, a clear extracellular alkalinization was found using H+-selective microelectrodes under the same conditions. Confocal microscopy revealed that HAF was not localized exclusively to the extracellular surface, but rather was detected throughout the intracellular compartment. A high degree of colocalization between HAF and the mitochondrion-specific dye MitoTracker was observed. When HAF fluorescence was monitored from optical sections from the center of a cell, glutamate produced an intracellular acidification. These results are consistent with a model in which depolarization allows calcium influx, followed by activation of a Ca2+/H+ plasma membrane ATPase. Our results suggest that HAF is reporting intracellular pH changes and that depolarization of horizontal cells induces an extracellular alkalinization, which may relieve H+-mediated inhibition of photoreceptor synaptic transmission.
C1 [Jacoby, Jason; Alford, Simon; Qian, Haohua; Tchernookova, Boriana K.; Malchow, Robert Paul] Univ Illinois, Dept Biol Sci, Chicago, IL 60607 USA.
[Kreitzer, Matthew A.; Naylor, Ethan R.] Indiana Wesleyan Univ, Dept Biol, Marion, IN USA.
[Qian, Haohua] NEI, Bethesda, MD 20892 USA.
[Malchow, Robert Paul] Univ Illinois, Dept Ophthalmol & Visual Sci, Chicago, IL 60607 USA.
RP Malchow, RP (reprint author), Univ Illinois, Dept Biol Sci, MC 067,Rm 4083 SEL,840 W Taylor St, Chicago, IL 60607 USA.
EM paulmalc@uic.edu
FU National Science Foundation [0924372, 0924383, 1005378]; National Eye
Institute (University ofIllinois at Chicago) [EY01792]; Marine
Biological Laboratory; Midwest Eye-Banks
FX This work was supported by National Science Foundation Grants 0924372,
0924383, and 1005378; National Eye Institute Grant EY01792 (University
of Illinois at Chicago); a Laura and Arthur Colwin Summer Fellowship
from the Marine Biological Laboratory; and the Midwest Eye-Banks.
NR 42
TC 11
Z9 11
U1 0
U2 11
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-3077
J9 J NEUROPHYSIOL
JI J. Neurophysiol.
PD FEB
PY 2012
VL 107
IS 3
BP 868
EP 879
DI 10.1152/jn.00878.2011
PG 12
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 879HI
UT WOS:000299319900013
PM 22090459
ER
PT J
AU Darbari, DS
Onyekwere, O
Nouraie, M
Minniti, CP
Luchtman-Jones, L
Rana, S
Sable, C
Ensing, G
Dham, N
Campbell, A
Arteta, M
Gladwin, MT
Castro, O
Taylor, JG
Kato, GJ
Gordeuk, V
AF Darbari, Deepika S.
Onyekwere, Onyinye
Nouraie, Mehdi
Minniti, Caterina P.
Luchtman-Jones, Lori
Rana, Sohail
Sable, Craig
Ensing, Gregory
Dham, Niti
Campbell, Andrew
Arteta, Manuel
Gladwin, Mark T.
Castro, Oswaldo
Taylor, James G.
Kato, Gregory J.
Gordeuk, Victor
TI Markers of Severe Vaso-Occlusive Painful Episode Frequency in Children
and Adolescents with Sickle Cell Anemia
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID ACUTE CHEST SYNDROME; ALPHA-THALASSEMIA; ADVERSE OUTCOMES; RISK-FACTORS;
DISEASE; CRISES; HYDROXYUREA; HEMOLYSIS; COHORT; HOSPITALIZATION
AB Objective To identify factors associated with frequent severe vaso-occlusive pain crises in a contemporary pediatric cohort of patients with sickle cell anemia (SCA) enrolled in a prospective study of pulmonary hypertension and the hypoxic response in sickle cell disease.
Study design Clinical and laboratory characteristics of children with SCA who had >= 3 severe pain crises requiring health care in the preceding year were compared with those of subjects with <3 such episodes.
Results Seventy-five children (20%) reported >= 3 severe pain episodes in the preceding year, and 232 (61%) had none. Frequent pain episodes were associated with older age (OR, 1.2; 95% CI, 1.1-1.3; P < .0001), alpha-thalassemia trait (OR 3.5; 1.6-6.7; P = .002), higher median hemoglobin (OR 1.7; 95% CI: 1.2-2.4; P < .003), and lower lactate dehydrogenase concentration (OR 1.82; 95% CI: 1.07-3.11; P = .027). Children with high pain frequency also had an increased iron burden (serum ferritin, 480 vs 198 mu g/L; P = .006) and higher median tricuspid regurgitation jet velocity (2.41 vs 2.31 m/s; P = .001). Neither hydroxyurea use nor fetal hemoglobin levels were significantly different according to severe pain history.
Conclusions In our cohort of children with SCA, increasing age was associated with higher frequency of severe pain episodes as were a-thalassemia, iron overload, higher hemoglobin and lower lactate dehydrogenase concentration, and higher tricuspid regurgitation velocity. (J Pediatr 2012; 160: 286-90).
C1 [Darbari, Deepika S.; Minniti, Caterina P.; Taylor, James G.; Kato, Gregory J.] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Onyekwere, Onyinye; Nouraie, Mehdi; Castro, Oswaldo; Gordeuk, Victor] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Darbari, Deepika S.; Luchtman-Jones, Lori] Div Pediat Hematol, Washington, DC USA.
[Darbari, Deepika S.; Luchtman-Jones, Lori] Div Oncol, Washington, DC USA.
[Rana, Sohail; Dham, Niti] Childrens Natl Med Ctr, Washington, DC 20010 USA.
Howard Univ Hosp, Dept Pediat, Washington, DC USA.
[Sable, Craig] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Ensing, Gregory] Univ Michigan, Div Pediat Hematol, Ann Arbor, MI 48109 USA.
[Campbell, Andrew] Univ Michigan, Div Pediat Pulmonol, Ann Arbor, MI 48109 USA.
[Arteta, Manuel] Univ Michigan, Div Pediat Cardiol, Ann Arbor, MI 48109 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
RP Darbari, DS (reprint author), NHLBI, Cardiovasc & Pulm Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014;
OI Kato, Gregory/0000-0003-4465-3217; Taylor, James/0000-0002-4421-1809
FU National Heart, Lung, and Blood Institute [2-R25 HL003679, 1-R01
HL079912]; Howard University General Clinic Research Center; National
Center for Research Resources [2MOI RR10284-10]; National Institutes of
Health, Bethesda, MD; National Institutes of Health
FX Supported in part by National Heart, Lung, and Blood Institute (grants
2-R25 HL003679 and 1-R01 HL079912), Howard University General Clinic
Research Center, National Center for Research Resources (grant 2MOI
RR10284-10), National Institutes of Health, Bethesda, MD, and the
Intramural Research Program of the National Institutes of Health. The
authors declare no conflicts of interest.
NR 30
TC 24
Z9 26
U1 0
U2 4
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD FEB
PY 2012
VL 160
IS 2
BP 286
EP 290
DI 10.1016/j.jpeds.2011.07.018
PG 5
WC Pediatrics
SC Pediatrics
GA 876MU
UT WOS:000299112400026
PM 21890147
ER
PT J
AU Borghese, CM
Blednov, YA
Quan, Y
Iyer, SV
Xiong, W
Mihic, SJ
Zhang, L
Lovinger, DM
Trudell, JR
Homanics, GE
Harris, RA
AF Borghese, Cecilia M.
Blednov, Yuri A.
Quan, Yu
Iyer, Sangeetha V.
Xiong, Wei
Mihic, S. John
Zhang, Li
Lovinger, David M.
Trudell, James R.
Homanics, Gregg E.
Harris, R. Adron
TI Characterization of Two Mutations, M287L and Q266I, in the alpha 1
Glycine Receptor Subunit That Modify Sensitivity to Alcohols
SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
LA English
DT Article
ID GATED ION-CHANNEL; FRAMESHIFT MUTATION; CHLORIDE CURRENTS;
SINGLE-CHANNEL; HYPEREKPLEXIA; MICE; ETHANOL; MUTANT; GABA(A); RESPONSES
AB Glycine receptors (GlyRs) are inhibitory ligand-gated ion channels. Ethanol potentiates glycine activation of the GlyR, and putative binding sites for alcohol are located in the transmembrane (TM) domains between and within subunits. To alter alcohol sensitivity of GlyR, we introduced two mutations in the GlyR alpha 1 subunit, M287L (TM3) and Q266I (TM2). After expression in Xenopus laevis oocytes, both mutants showed a reduction in glycine sensitivity and glycine-induced maximal currents. Activation by taurine, another endogenous agonist, was almost abolished in the M287L GlyR. The ethanol potentiation of glycine currents was reduced in the M287L GlyR and eliminated in Q266I. Physiological levels of zinc (100 nM) potentiate glycine responses in wild-type GlyR and also enhance the ethanol potentiation of glycine responses. Although zinc potentiation of glycine responses was unchanged in both mutants, zinc enhancement of ethanol potentiation of glycine responses was absent in M287L GlyRs. The Q266I mutation decreased conductance but increased mean open time (effects not seen in M287L). Two lines of knockin mice bearing these mutations were developed. Survival of homozygous knockin mice was impaired, probably as a consequence of impaired glycinergic transmission. Glycine showed a decreased capacity for displacing strychnine binding in heterozygous knockin mice. Electrophysiology in isolated neurons of brain stem showed decreased glycine-mediated currents and decreased ethanol potentiation in homozygous knockin mice. Molecular models of the wildtype and mutant GlyRs show a smaller water-filled cavity within the TM domains of the Q266I alpha 1 subunit. The behavioral characterization of these knockin mice is presented in a companion article (J Pharmacol Exp Ther 340:317-329, 2012).
C1 [Borghese, Cecilia M.; Blednov, Yuri A.; Quan, Yu; Iyer, Sangeetha V.; Harris, R. Adron] Univ Texas Austin, Waggoner Ctr Alcohol & Addict Res, Austin, TX 78712 USA.
[Iyer, Sangeetha V.] Univ Pittsburgh, Grad Program Mol Pharmacol, Pittsburgh, PA USA.
[Homanics, Gregg E.] Univ Pittsburgh, Dept Anesthesiol & Pharmacol, Pittsburgh, PA USA.
[Homanics, Gregg E.] Univ Pittsburgh, Dept Biol Chem, Pittsburgh, PA USA.
[Xiong, Wei; Zhang, Li; Lovinger, David M.] NIAAA, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
[Trudell, James R.] Stanford Univ, Dept Anesthesia, Stanford, CA 94305 USA.
[Trudell, James R.] Stanford Univ, Beckman Program Mol & Genet Med, Stanford, CA 94305 USA.
RP Harris, RA (reprint author), Univ Texas Austin, Waggoner Ctr Alcohol & Addict Res, 1 Univ Stn,A4800, Austin, TX 78712 USA.
EM harris@mail.utexas.edu
FU National Institutes of Health National Institute of Alcohol Abuse and
Alcoholism [AA06399, AA11525, AA10422]; National Institutes of Health
National Institute of General Medical Sciences [GM47818]
FX This work was supported by the National Institutes of Health National
Institute of Alcohol Abuse and Alcoholism [Grants AA06399, AA11525,
AA10422]; and the National Institutes of Health National Institute of
General Medical Sciences [Grant GM47818].
NR 42
TC 16
Z9 16
U1 0
U2 4
PU AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3995 USA
SN 0022-3565
J9 J PHARMACOL EXP THER
JI J. Pharmacol. Exp. Ther.
PD FEB
PY 2012
VL 340
IS 2
BP 304
EP 316
DI 10.1124/jpet.111.185116
PG 13
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 879IT
UT WOS:000299323600009
PM 22037201
ER
PT J
AU Mobley, CC
Stadler, DD
Staten, MA
El Ghormli, L
Gillis, B
Hartstein, J
Siega-Riz, AM
Virus, A
AF Mobley, Connie C.
Stadler, Diane D.
Staten, Myrlene A.
El Ghormli, Laure
Gillis, Bonnie
Hartstein, Jill
Siega-Riz, Anna Maria
Virus, Amy
CA HEALTHY Study Grp
TI Effect of Nutrition Changes on Foods Selected by Students in a Middle
School-Based Diabetes Prevention Intervention Program: The HEALTHY
Experience
SO JOURNAL OF SCHOOL HEALTH
LA English
DT Article
DE school food services; nutrition and diet; child and adolescent health
ID US PUBLIC-SCHOOLS; NUTRIENT CONTENT; ENVIRONMENTS; RATIONALE; COMPONENT;
DESIGN; CHILDREN; LUNCHES
AB BACKGOUND: The HEALTHY primary prevention trial developed an integrated multicomponent intervention program to moderate risk factors for type 2 diabetes in middle schools. The nutrition component aimed to improve the quality of foods and beverages served to students. Changes in the School Breakfast Program (SBP), National School Lunch Program (NSLP), and a la carte venues are compared to the experience of control schools. METHODS: The intervention was implemented in 21 middle schools from winter 2007 through spring 2009 (following a cohort of students from sixth through eighth grades); 21 schools acted as observed controls. The nutrition component targeted school food service environmental change. Data identifying foods and nutrients served (selected by students for consumption) were collected over a 20-day period at baseline and end of study. Analysis compared end of study values for intervention versus control schools. RESULTS: Intervention schools more successfully limited dessert and snack food portion size in NSLP and a la carte and lowered fat content of foods served. Servings of high-fiber grain-based foods and/ or legumes were improved in SBP but not NSLP. Intervention and control schools eliminated > 1% fat milk and added-sugar beverages in SBP, but intervention schools were more successful in NSLP and a la carte. CONCLUSION: The HEALTHY program demonstrated significant changes in the nutritional quality of foods and beverages served in the SBP, NSLP, and a la carte venues, as part of an effort to decrease childhood obesity and support beneficial effects in some secondary HEALTHY study outcomes.
C1 [Mobley, Connie C.] Univ Nevada, Las Vegas, NV 89106 USA.
[Stadler, Diane D.] Oregon Hlth & Sci Univ, Div Hlth Promot & Sports Med, Portland, OR 97239 USA.
[Stadler, Diane D.] Oregon Hlth & Sci Univ, Grad Programs Human Nutr, Portland, OR 97239 USA.
[Staten, Myrlene A.] NIDDK, NIH, Bethesda, MD 20892 USA.
[El Ghormli, Laure] George Washington Univ, Biostat Ctr, Rockville, MD 20852 USA.
[Gillis, Bonnie] Univ Pittsburgh, Med Ctr Hlth Plan, Hlth Promot Dept, Pittsburgh, PA 15219 USA.
[Hartstein, Jill] Univ Calif Irvine, Irvine, CA 92697 USA.
[Siega-Riz, Anna Maria] Univ N Carolina, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27599 USA.
[Virus, Amy] Temple Univ, Ctr Obes Res & Educ, Philadelphia, PA 19140 USA.
RP Mobley, CC (reprint author), Univ Nevada, 1001 Shadow Lane,MS 7425, Las Vegas, NV 89106 USA.
EM connie.mobley@unlv.edu; stadlerd@ohsu.edu; statenm@niddk.nih.gov;
elghorml@biostat.bsc.gwu.edu; gillisbp@upmc.edu; hartstej@uci.edu;
am_siegariz@unc.edu; amyvir@temple.edu
OI Stadler, Diane/0000-0002-4718-2054
NR 26
TC 13
Z9 13
U1 2
U2 24
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0022-4391
J9 J SCHOOL HEALTH
JI J. Sch. Health
PD FEB
PY 2012
VL 82
IS 2
BP 82
EP 90
DI 10.1111/j.1746-1561.2011.00670.x
PG 9
WC Education & Educational Research; Education, Scientific Disciplines;
Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Education & Educational Research; Health Care Sciences & Services;
Public, Environmental & Occupational Health
GA 875PO
UT WOS:000299044200004
ER
PT J
AU Pastrana, DV
Wieland, U
Silling, S
Buck, CB
Pfister, H
AF Pastrana, Diana V.
Wieland, Ulrike
Silling, Steffi
Buck, Christopher B.
Pfister, Herbert
TI Positive correlation between Merkel cell polyomavirus viral load and
capsid-specific antibody titer
SO MEDICAL MICROBIOLOGY AND IMMUNOLOGY
LA English
DT Article
DE MCV; MCPyV; Merkel cell polyomavirus; Neutralization; Viral load; Skin
ID BK-VIRUS; JC-VIRUS; DNA-SEQUENCES; HUMAN-TISSUES; INFECTION; CARCINOMA;
TRANSMISSION; INDIVIDUALS; PERSISTENCE; EXCRETION
AB Merkel cell polyomavirus (MCPyV or MCV) is the first polyomavirus to be clearly implicated as a causal agent underlying a human cancer, Merkel cell carcinoma (MCC). Infection with MCPyV is common in the general population, and a majority of adults shed MCPyV from the surface of their skin. In this study, we quantitated MCPyV DNA in skin swab specimens from healthy volunteers sampled at different anatomical sites over time periods ranging from 3 months to 4 years. The volunteers were also tested using a serological assay that detects antibodies specific for the MCPyV virion. There was a positive correlation between MCPyV virion-specific antibody titers and viral load at all anatomical sites tested (dorsal portion of the hands, forehead, and buttocks) (Spearman's r 0.644, P < 0.0001). The study results are consistent with previous findings suggesting that the skin is primary site of chronic MCPyV infection in healthy adults and suggest that the magnitude of an individual's seroresponsiveness against the MCPyV virion generally reflects the overall MCPyV DNA load across wide areas of the skin. In light of previous reports indicating a correlation between MCC and strong MCPyV-specific seroresponsiveness, this model suggests that poorly controlled chronic MCPyV infection might be a risk factor in the development of MCC.
C1 [Pastrana, Diana V.; Buck, Christopher B.] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
[Wieland, Ulrike; Silling, Steffi; Pfister, Herbert] Univ Cologne, Inst Virol, Natl Reference Ctr Papilloma & Polyomaviruses, D-50935 Cologne, Germany.
RP Buck, CB (reprint author), NCI, Cellular Oncol Lab, NIH, Bldg 37,Room 4118,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM Ulrike.Wieland@uni-koeln.de; BuckC@mail.nih.gov
OI Buck, Christopher/0000-0003-3165-8094
FU NIH; Center for Cancer Research; NCI; German National Reference Center
for Papilloma- and Polyomaviruses (German Federal Ministry of Health)
[FKZ 1369-401]
FX This work was funded in part by the Intramural Research Program of the
NIH, with support from the Center for Cancer Research and the NCI
Director's Intramural Innovation Award Program, and in part by the
German National Reference Center for Papilloma- and Polyomaviruses
(German Federal Ministry of Health, grant number FKZ 1369-401).
NR 28
TC 18
Z9 18
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0300-8584
J9 MED MICROBIOL IMMUN
JI Med. Microbiol. Immunol.
PD FEB
PY 2012
VL 201
IS 1
BP 17
EP 23
DI 10.1007/s00430-011-0200-7
PG 7
WC Immunology; Microbiology
SC Immunology; Microbiology
GA 876RN
UT WOS:000299125500003
PM 21614514
ER
PT J
AU Thompson, J
Pikis, A
AF Thompson, J.
Pikis, A.
TI Metabolism of sugars by genetically diverse species of oral Leptotrichia
SO MOLECULAR ORAL MICROBIOLOGY
LA English
DT Article
DE dental caries; glycosyl hydrolase family 4; Leptotrichia; oral
microbiology; phospho-a-glucosidase; sucrose isomers
ID PHOSPHO-ALPHA-GLUCOSIDASE; GLUCOSYL-D-FRUCTOSES; STREPTOCOCCUS-MUTANS;
BACILLUS-SUBTILIS; FUSOBACTERIUM-MORTIFERUM; KLEBSIELLA-PNEUMONIAE;
SUCROSE ISOMERS; ACID PRODUCTION; DENTAL-CARIES; BUCCALIS
AB Leptotrichia buccalis ATCC 14201 is a gram-negative, anaerobic rod-shaped bacterium resident in oral biofilm at the tooth surface. The sequenced genome of this organism reveals three contiguous genes at loci: Lebu_1525, Lebu_1526 and Lebu_1527. The translation products of these genes exhibit significant homology with phospho-a-glucosidase (Pagl), a regulatory protein (GntR) and a phosphoenol pyruvate-dependent sugar transport protein (EIICB), respectively. In non-oral bacterial species, these genes comprise the sim operon that facilitates sucrose isomer metabolism. Growth studies showed that L.buccalis fermented a wide variety of carbohydrates, including four of the five isomers of sucrose. Growth on the isomeric disaccharides elicited expression of a 50-kDa polypeptide comparable in size to that encoded by Lebu_1525. The latter gene was cloned, and the expressed protein was purified to homogeneity from Escherichia coli TOP10 cells. In the presence of two cofactors, NAD+ and Mn2+ ions, the enzyme readily hydrolyzed p-nitrophenyl-a-glucopyranoside 6-phosphate (pNPaG6P), a chromogenic analogue of the phosphorylated isomers of sucrose. By comparative sequence alignment, immunoreactivity and signature motifs, the enzyme can be assigned to the phospho-a-glucosidase (Pagl) clade of Family 4 of the glycosyl hydrolase super family. We suggest that the products of Lebu_1527 and Lebu_1525, catalyze the phosphorylative translocation and hydrolysis of sucrose isomers in L.buccalis, respectively. Four genetically diverse, but 16S rDNA-related, species of Leptotrichia have recently been described: L.goodfellowii, L.hofstadii, L.shahii and L.wadei. The phenotypic traits of these new species, with respect to carbohydrate utilization, have also been determined.
C1 [Thompson, J.; Pikis, A.] NIDCR, Microbial Biochem & Genet Unit, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA.
[Pikis, A.] US FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
RP Thompson, J (reprint author), NIDCR, Microbial Biochem & Genet Unit, Oral Infect & Immun Branch, NIH, Bldg 30,Rm 325,Convent Dr,MSC-4350, Bethesda, MD 20892 USA.
EM jthompson@dir.nidcr.nih.gov
FU NIDCR, National Institutes of Health, Bethesda, MD
FX We thank Rick Dreyfuss for assistance with photography and computer
graphics and Nga Nguyen for microsequence analyses. This work was
supported by the Intramural Research Program of the NIDCR, National
Institutes of Health, Bethesda, MD.
NR 42
TC 2
Z9 5
U1 0
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2041-1006
J9 MOL ORAL MICROBIOL
JI Mol. Oral Microbiol.
PD FEB
PY 2012
VL 27
IS 1
BP 34
EP 44
DI 10.1111/j.2041-1014.2011.00627.x
PG 11
WC Dentistry, Oral Surgery & Medicine; Microbiology
SC Dentistry, Oral Surgery & Medicine; Microbiology
GA 874II
UT WOS:000298948900004
PM 22230464
ER
PT J
AU Laggner, C
Kokel, D
Setola, V
Tolia, A
Lin, H
Irwin, JJ
Keiser, MJ
Cheung, CYJ
Minor, DL
Roth, BL
Peterson, RT
Shoichet, BK
AF Laggner, Christian
Kokel, David
Setola, Vincent
Tolia, Alexandra
Lin, Henry
Irwin, John J.
Keiser, Michael J.
Cheung, Chung Yan J.
Minor, Daniel L., Jr.
Roth, Bryan L.
Peterson, Randall T.
Shoichet, Brian K.
TI Chemical informatics and target identification in a zebrafish phenotypic
screen
SO NATURE CHEMICAL BIOLOGY
LA English
DT Article
ID SMALL MOLECULES; PHARMACOLOGY
AB Target identification is a core challenge in chemical genetics. Here we use chemical similarity to computationally predict the targets of 586 compounds that were active in a zebrafish behavioral assay. Among 20 predictions tested, 11 compounds had activities ranging from 1 nM to 10,000 nM on the predicted targets. The roles of two of these targets were tested in the original zebrafish phenotype. Prediction of targets from chemotype is rapid and may be generally applicable.
C1 [Setola, Vincent; Roth, Bryan L.] Univ N Carolina Chapel Hill Sch Med, Dept Pharmacol, Chapel Hill, NC 27515 USA.
[Laggner, Christian; Lin, Henry; Irwin, John J.; Keiser, Michael J.; Shoichet, Brian K.] Univ Calif San Francisco, Dept Pharmaceut Chem, San Francisco, CA USA.
[Kokel, David; Cheung, Chung Yan J.; Peterson, Randall T.] Harvard Univ, Sch Med, Cardiovasc Res Ctr, Dept Med,Massachusetts Gen Hosp, Charlestown, MA USA.
[Kokel, David; Cheung, Chung Yan J.; Peterson, Randall T.] Harvard Univ, Sch Med, Div Cardiol, Dept Med,Massachusetts Gen Hosp, Charlestown, MA USA.
[Kokel, David; Cheung, Chung Yan J.; Peterson, Randall T.] Broad Inst, Cambridge, MA USA.
[Setola, Vincent; Roth, Bryan L.] Univ N Carolina Chapel Hill Sch Med, Natl Inst Mental Hlth Psychoact Drug Screening Pr, Chapel Hill, NC USA.
[Tolia, Alexandra; Minor, Daniel L., Jr.] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA.
[Tolia, Alexandra; Minor, Daniel L., Jr.] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94143 USA.
RP Roth, BL (reprint author), Univ N Carolina Chapel Hill Sch Med, Dept Pharmacol, Chapel Hill, NC 27515 USA.
EM bryan_roth@med.unc.edu; peterson@cvrc.mgh.harvard.edu;
shoichet@cgl.ucsf.edu
RI Roth, Bryan/F-3928-2010; Keiser, Michael/F-2825-2016;
OI Keiser, Michael/0000-0002-1240-2192; kokel, david/0000-0002-1981-1511;
Irwin, John/0000-0002-1195-6417
FU US National Institutes of Health [GM71896, AG02132, MH085205, MH086867,
MH091449, R01 MH093603, R01 NS49272]; Rogers Family Foundation; National
Institutes of Mental Health [U19MH82441]; Michael Hooker Chair; Max Kade
Foundation; European Molecular Biology Organization
FX We thank S. Morris for help with Cytoscape. This work was supported by
US National Institutes of Health grants GM71896 (to J.J.I. and B.K.S.),
AG02132 (to S. Prusiner and B.K.S.), MH085205 and MH086867 (to R.P.),
MH091449 (to D.K.), R01 MH093603 and R01 NS49272 (to D.L.M.); a Rogers
Family Foundation award (to M.J.K.); the National Institutes of Mental
Health Psychoactive Drug Screening Program, grant U19MH82441; the
Michael Hooker Chair (to B.L.R.); and fellowships from the Max Kade
Foundation (to C.L.) and the European Molecular Biology Organization (to
A.T.).
NR 25
TC 63
Z9 63
U1 3
U2 21
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1552-4450
J9 NAT CHEM BIOL
JI Nat. Chem. Biol.
PD FEB
PY 2012
VL 8
IS 2
BP 144
EP 146
DI 10.1038/nchembio.732
PG 3
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 879IP
UT WOS:000299323200005
PM 22179068
ER
PT J
AU Barber, DL
Andrade, BB
Sereti, I
Sher, A
AF Barber, Daniel L.
Andrade, Bruno B.
Sereti, Irini
Sher, Alan
TI Immune reconstitution inflammatory syndrome: the trouble with immunity
when you had none
SO NATURE REVIEWS MICROBIOLOGY
LA English
DT Article
ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; HIV-INFECTED PATIENTS;
PNEUMOCYSTIS-CARINII-PNEUMONIA; ORGAN TRANSPLANT RECIPIENTS; CD4(+)
T-CELLS; ANTIRETROVIRAL THERAPY; RISK-FACTORS; RESTORATION DISEASE;
MYCOBACTERIUM-TUBERCULOSIS; HOMEOSTATIC PROLIFERATION
AB Some individuals who are infected with HIV rapidly deteriorate shortly after starting antiretroviral therapy, despite effective viral suppression. This reaction, referred to as immune reconstitution inflammatory syndrome ( IRIS), is characterized by tissue-destructive inflammation and arises as CD4(+) T cells re-emerge. It has been proposed that IRIS is caused by a dysregulation of the expanding population of CD4(+) T cells specific for a co-infecting opportunistic pathogen. Here, we argue that IRIS instead results from hyper-responsiveness of the innate immune system to T cell help, a mechanism that may be shared by the many manifestations of IRIS that occur following the reversal of other types of immunosuppression in pathogen-infected hosts.
C1 [Barber, Daniel L.; Andrade, Bruno B.; Sher, Alan] NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Sereti, Irini] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Barber, DL (reprint author), NIAID, Immunobiol Sect, Parasit Dis Lab, NIH, Rm 6146,50 South Dr, Bethesda, MD 20892 USA.
EM barberd@niaid.nih.gov
RI Andrade, Bruno/J-9111-2012
OI Andrade, Bruno/0000-0001-6833-3811
FU US National Institute for Allergy and Infectious Diseases, National
Institutes of Health
FX The authors thank J. Keane for stimulating discussions during the
preparation of this article. Work in the authors' laboratories is
supported by the intramural research programme of the US National
Institute for Allergy and Infectious Diseases, National Institutes of
Health.
NR 71
TC 58
Z9 60
U1 1
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1740-1526
J9 NAT REV MICROBIOL
JI Nat. Rev. Microbiol.
PD FEB
PY 2012
VL 10
IS 2
BP 150
EP 156
DI 10.1038/nrmicro2712
PG 7
WC Microbiology
SC Microbiology
GA 876NS
UT WOS:000299115000014
PM 22230950
ER
PT J
AU Rahimi, Z
Vaisi-Raygani, A
Rahimi, Z
Parsian, A
AF Rahimi, Zohreh
Vaisi-Raygani, Asad
Rahimi, Ziba
Parsian, Abbas
TI Concomitant presence of endothelial nitric oxide 894T and angiotensin
II-converting enzyme D alleles are associated with diabetic nephropathy
in a Kurdish population from Western Iran
SO NEPHROLOGY
LA English
DT Article
DE ACE I; D; eNOS G894T; macroalbuminuria; microalbuminuria; type 2
diabetes mellitus
ID STAGE RENAL-DISEASE; ENOS GLU298ASP POLYMORPHISM; SYNTHASE GENE;
INSERTION/DELETION POLYMORPHISM; ACE GENE; TYPE-2; HYPERTENSION; RISK;
CLEAVAGE; VARIANT
AB Aim: The present study investigated the influence of insertion (I)/deletion (D) polymorphism of the angiotensin II-converting enzyme (ACE) gene in combination with endothelial nitric oxide (eNOS) G894T polymorphism on the predisposition to diabetic nephropathy (DN). Methods: Using polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism (PCR-RFLP) method, the ACE and eNOS polymorphisms were genotyped in 72 microalbuminuric, 68 macroalbuminuric and 72 normoalbuinuric type 2 diabetes mellitus (T2DM) patients from Western Iran. Results: The presence of eNOS T or ACE D allele was not associated with increased risk of macroalbuminuria (odds ratio (OR) = 1.36, P = 0.27 and OR = 1.6, P = 0.062, respectively). However, in the presence of both alleles there was a trend towards increased risk of macroalbuminuria (fivefold, P = 0.05). Conclusion: Our study indicates that the concomitant presence of both ACE D and eNOS T alleles tends to be associated with an elevation risk of macroalbuminuria compared with the presence of each polymorphism alone. This risk could be attributed to the increasing activity of ACE and angiotensin II level in the presence of D allele and decreasing NO production in the presence of T allele accelerating diabetic nephropathy.
C1 [Rahimi, Zohreh; Rahimi, Ziba] Kermanshah Univ Med Sci, Med Biol Res Ctr, Sch Med, Kermanshah, Iran.
[Rahimi, Zohreh; Vaisi-Raygani, Asad] Kermanshah Univ Med Sci, Dept Biochem, Sch Med, Kermanshah, Iran.
[Parsian, Abbas] NIAAA, Div Neurosci & Behav, NIH, Rockville, MD 20852 USA.
RP Rahimi, Z (reprint author), Kermanshah Univ Med Sci, Med Biol Res Ctr, Sch Med, POB 67148-69914,Daneshgah Ave, Kermanshah, Iran.
EM zrahimi@kums.ac.ir; zrahimi@kums.ac.ir
OI Rahimi, Zohreh/0000-0001-7589-3307; Vaisi-Raygani,
Asad/0000-0002-3042-2832
FU Kermanshah University of Medical Sciences, Kermanshah, Iran
FX This work was financially supported by a grant from Vice Chancellor for
Research of Kermanshah University of Medical Sciences, Kermanshah, Iran.
NR 35
TC 12
Z9 12
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1320-5358
J9 NEPHROLOGY
JI Nephrology
PD FEB
PY 2012
VL 17
IS 2
BP 175
EP 181
DI 10.1111/j.1440-1797.2011.01533.x
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA 878JH
UT WOS:000299252400010
PM 22026967
ER
PT J
AU Yan, YJ
Pushparaj, A
Le Strat, Y
Gamaleddin, I
Barnes, C
Justinova, Z
Goldberg, SR
Le Foll, B
AF Yan, Yijin
Pushparaj, Abhiram
Le Strat, Yann
Gamaleddin, Islam
Barnes, Chanel
Justinova, Zuzana
Goldberg, Steven R.
Le Foll, Bernard
TI Blockade of Dopamine D4 Receptors Attenuates Reinstatement of
Extinguished Nicotine-Seeking Behavior in Rats
SO NEUROPSYCHOPHARMACOLOGY
LA English
DT Article
DE dopamine receptor D4; receptor antagonist; nicotine self-administration;
reinstatement of nicotine-seeking behavior; tobacco smoking; relapse
ID DRD4 VNTR POLYMORPHISM; CUE-INDUCED REINSTATEMENT; NUCLEUS-ACCUMBENS
SHELL; D-4 RECEPTOR; MENTAL-HEALTH; SMOKING CUES; D4 RECEPTORS; TOBACCO
USE; COCAINE DISCRIMINATION; PSYCHIATRIC-DISORDERS
AB Since cloning of the dopamine receptor D4 (DRD4), its role in the brain has remained unclear. It has been reported that polymorphism of the DRD4 gene in humans is associated with reactivity to cues related to tobacco smoking. However, the role of DRD4 in animal models of nicotine addiction has seldom been explored. In our study, male Long-Evans rats learned to intravenously self-administer nicotine under a fixed-ratio (FR) schedule of reinforcement. Effects of the selective DRD4 antagonist L-745,870 were evaluated on nicotine self-administration behavior and on reinstatement of extinguished nicotine-seeking behavior induced by nicotine-associated cues or by priming injections of nicotine. L-745,870 was also tested on reinstatement of extinguished food-seeking behavior as a control. In addition, the selective DRD4 agonist PD 168,077 was tested for its ability to reinstate extinguished nicotine-seeking behavior. Finally, L-745,870 was tested in Sprague Dawley rats trained to discriminate administration of 0.4 mg/kg nicotine from vehicle under an FR schedule of food delivery. L-745,870 significantly attenuated reinstatement of nicotine-seeking induced by both nicotine-associated cues and nicotine priming. In contrast, L-745,870 did not affect established nicotine self-administration behavior or reinstatement of food-seeking behavior induced by food cues or food priming. L-745,870 did not produce nicotine-like discriminative-stimulus effects and did not alter discriminative-stimulus effects of nicotine. PD 168,077 did not reinstate extinguished nicotine-seeking behavior. As DRD4 blockade by L-745,870 selectively attenuated both cue-and nicotine-induced reinstatement of nicotine-seeking behavior, without affecting cue-or food-induced reinstatement of food-seeking behavior, DRD4 antagonists are potential therapeutic agents against tobacco smoking relapse. Neuropsychopharmacology (2012) 37, 685-696; doi: 10.1038/npp.2011.245; published online 26 October 2011
C1 [Yan, Yijin; Pushparaj, Abhiram; Le Strat, Yann; Gamaleddin, Islam; Le Foll, Bernard] Univ Toronto, Translat Addict Res Lab, Ctr Addict & Mental Hlth Addict CAMH, Toronto, ON M5S 2S1, Canada.
[Barnes, Chanel; Justinova, Zuzana; Goldberg, Steven R.] Natl Inst Drug Abuse, Preclin Pharmacol Sect, Behav Neurosci Res Branch, Intramural Res Program,NIH,US Dept HHS, Baltimore, MD USA.
[Justinova, Zuzana] Univ Maryland, Sch Med, Maryland Psychiat Res Ctr, Dept Psychiat, Baltimore, MD 21201 USA.
[Le Foll, Bernard] Univ Toronto, Inst Med Sci, Dept Family & Community Med, Toronto, ON M5S 1A1, Canada.
RP Le Foll, B (reprint author), Univ Toronto, Translat Addict Res Lab, Ctr Addict & Mental Hlth Addict CAMH, 33 Russell St, Toronto, ON M5S 2S1, Canada.
EM bernard_lefoll@camh.net
RI Yan, Yijin/C-2733-2012; Justinova, Zuzana/A-9109-2011; Le Foll,
Bernard/K-2952-2014;
OI Justinova, Zuzana/0000-0001-5793-7484; Le Foll,
Bernard/0000-0002-6406-4973; Pushparaj, Abhiram/0000-0002-7109-9795
FU Canadian Tobacco Control Research Initiate (CTCRI) [20040]; Canadian
Institute of Health Research (CIHR) [200810MFE-193820-172560]; National
Institute on Drug Abuse
FX We thank Drs John Roder and Benoit Forget for their comments on our
experimental data. This study was supported partly by the Canadian
Tobacco Control Research Initiate (CTCRI) Student Research Grant (no.
20040), by the Canadian Institute of Health Research (CIHR) postdoctoral
fellowship (Code No. 200810MFE-193820-172560), by the CIHR Strategic
Training Program in Tobacco Use in Special Populations (TUSP)
postdoctoral fellowship and in part by the Intramural Research Program
of the National Institute on Drug Abuse.
NR 97
TC 30
Z9 30
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0893-133X
EI 1740-634X
J9 NEUROPSYCHOPHARMACOL
JI Neuropsychopharmacology
PD FEB
PY 2012
VL 37
IS 3
BP 685
EP 696
DI 10.1038/npp.2011.245
PG 12
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 876OV
UT WOS:000299117900011
PM 22030716
ER
PT J
AU Weyerbrock, A
Osterberg, N
Psarras, N
Baumer, B
Kogias, E
Werres, A
Bette, S
Saavedra, JE
Keefer, LK
Papazoglou, A
AF Weyerbrock, Astrid
Osterberg, Nadja
Psarras, Nikolaos
Baumer, Brunhilde
Kogias, Evangelos
Werres, Anna
Bette, Stefanie
Saavedra, Joseph E.
Keefer, Larry K.
Papazoglou, Anna
TI JS-K, a Glutathione S-Transferase-Activated Nitric Oxide Donor With
Antineoplastic Activity in Malignant Gliomas
SO NEUROSURGERY
LA English
DT Article
DE Glioma; GST; JS-K; Nitric oxide (NO); U87
ID CELLS IN-VITRO; SOLUBLE GUANYLYL CYCLASE; MYELOID-LEUKEMIA CELLS;
CYTOCHROME-C RELEASE; FACTOR-KAPPA-B; CASPASE ACTIVATION; TUMOR
PROGRESSION; DRUG-RESISTANCE; KINASE PATHWAYS; BRAIN-TUMORS
AB BACKGROUND: Glutathione S-transferases (GSTs) control multidrug resistance and are upregulated in many cancers, including malignant gliomas. The diazeniumdiolate JS-K generates nitric oxide (NO) on enzymatic activation by glutathione and GST, showing promising NO-based anticancer efficacy.
OBJECTIVE: To evaluate the role of NO-based antitumor therapy with JS-K in U87 gliomas in vitro and in vivo.
METHODS: U87 glioma cells and primary glioblastoma cell lines were exposed to JS-K and a variety of inhibitors to study cell death by necrosis, apoptosis, and other mechanisms. GST expression was evaluated by immunocytochemistry, polymerase chain reaction, and Western blot, and NO release from JS-K was studied with a NO assay. The growth-inhibitory effect of JS-K was studied in a U87 xenograft model in vivo.
RESULTS: Dose-dependent inhibition of cell proliferation was observed in human U87 glioma cells and primary glioblastoma cells in vitro. Cell death was partially induced by caspase-dependent apoptosis, which could be blocked by Z-VAD-FMK and Q-VD-OPH. Inhibition of GST by sulfasalazine, cGMP inhibition by ODQ, and MEK1/2 inhibition by UO126 attenuated the antiproliferative effect of JS-K, suggesting the involvement of various intracellular death signaling pathways. Response to JS-K correlated with mRNA and protein expression of GST and the amount of NO released by the glioma cells. Growth of U87 xenografts was reduced significantly, with immunohistochemical evidence for increased necrosis and apoptosis and reduced proliferation.
CONCLUSION: Our data show for the first time the potent antiproliferative effect of JS-K in gliomas in vitro and in vivo. These findings warrant further investigation of this novel NO-releasing prodrug in gliomas.
C1 [Weyerbrock, Astrid; Osterberg, Nadja; Psarras, Nikolaos; Baumer, Brunhilde; Kogias, Evangelos; Werres, Anna; Bette, Stefanie] Univ Med Ctr Freiburg, Dept Neurosurg, D-79106 Freiburg, Germany.
[Saavedra, Joseph E.] NCI, SAIC Frederick, Frederick, MD 21701 USA.
[Keefer, Larry K.] NCI, Comparat Carcinogenesis Lab, Frederick, MD 21701 USA.
[Papazoglou, Anna] Univ Med Ctr Freiburg, Dept Stereotact Neurosurg, D-79106 Freiburg, Germany.
RP Weyerbrock, A (reprint author), Univ Med Ctr Freiburg, Dept Neurosurg, Breisacher Str 64, D-79106 Freiburg, Germany.
EM astrid.weyerbrock@uniklinik-freiburg.de
RI Weyerbrock, Astrid/E-8493-2014; Keefer, Larry/N-3247-2014
OI Keefer, Larry/0000-0001-7489-9555
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research; National Cancer Institute, National Institutes of
Health [HHSN261200800001E]
FX This research was supported in part by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute, Center
for Cancer Research (Dr Saavedra) and by federal funds from the National
Cancer Institute, National Institutes of Health under contract
HHSN261200800001E. The authors have no personal financial or
institutional interest in any of the drugs, materials, or devices
described in this article.
NR 56
TC 13
Z9 16
U1 0
U2 11
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0148-396X
J9 NEUROSURGERY
JI Neurosurgery
PD FEB
PY 2012
VL 70
IS 2
BP 497
EP 510
DI 10.1227/NEU.0b013e31823209cf
PG 14
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 879IK
UT WOS:000299322700066
PM 21849924
ER
PT J
AU Cai, Y
Zhang, XM
Macklin, LN
Cai, HB
Luo, XG
Oddo, S
LaFerla, FM
Struble, RG
Rose, GM
Patrylo, PR
Yan, XX
AF Cai, Yan
Zhang, Xue-Mei
Macklin, Lauren N.
Cai, Huaibin
Luo, Xue-Gang
Oddo, Salvatore
LaFerla, Frank M.
Struble, Robert G.
Rose, Gregory M.
Patrylo, Peter R.
Yan, Xiao-Xin
TI BACE1 Elevation is Involved in Amyloid Plaque Development in the Triple
Transgenic Model of Alzheimer's Disease: Differential A beta Antibody
Labeling of Early-Onset Axon Terminal Pathology
SO NEUROTOXICITY RESEARCH
LA English
DT Article
DE Amyloid plaque; Axonal pathology; Synaptoplasticity; Aging; Dementia
ID BETA-SECRETASE-1 ELEVATION; CEREBRAL-CORTEX; MESSENGER-RNA; MOUSE-BRAIN;
MICE; PATHOGENESIS; EXPRESSION; PRESENILIN-1; SECRETASE;
IMMUNOREACTIVITY
AB beta-amyloid precursor protein (APP) and presenilins mutations cause early-onset familial Alzheimer's disease (FAD). Some FAD-based mouse models produce amyloid plaques, others do not. beta-Amyloid (A beta) deposition can manifest as compact and diffuse plaques; it is unclear why the same A beta molecules aggregate in different patterns. Is there a basic cellular process governing A beta plaque pathogenesis? We showed in some FAD mouse models that compact plaque formation is associated with a progressive axonal pathology inherent with increased expression of beta-secretase (BACE1), the enzyme initiating the amyloidogenic processing of APP. A monoclonal A beta antibody, 3D6, visualized distinct axon terminal labeling before plaque onset. The present study was set to understand BACE1 and axonal changes relative to diffuse plaque development and to further characterize the novel axonal A beta antibody immunoreactivity (IR), using triple transgenic AD (3xTg-AD) mice as experimental model. Diffuse-like plaques existed in the forebrain in aged transgenics and were regionally associated with increased BACE1 labeled swollen/sprouting axon terminals. Increased BACE1/3D6 IR at axon terminals occurred in young animals before plaque onset. These axonal elements were also co-labeled by other antibodies targeting the N-terminal and mid-region of A beta domain and the C-terminal of APP, but not co-labeled by antibodies against the A beta C-terminal and APP N-terminal. The results suggest that amyloidogenic axonal pathology precedes diffuse plaque formation in the 3xTg-AD mice, and that the early-onset axonal A beta antibody IR in transgenic models of AD might relate to a cross-reactivity of putative APP beta-carboxyl terminal fragments.
C1 [Cai, Yan; Luo, Xue-Gang; Yan, Xiao-Xin] Cent S Univ, Xiangya Sch Med, Dept Human Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
[Cai, Yan; Zhang, Xue-Mei; Rose, Gregory M.; Patrylo, Peter R.; Yan, Xiao-Xin] So Illinois Univ, Sch Med, Dept Anat, Carbondale, IL 62901 USA.
[Cai, Yan; Macklin, Lauren N.; Patrylo, Peter R.] So Illinois Univ, Sch Med, Dept Physiol, Carbondale, IL 62901 USA.
[Zhang, Xue-Mei] Harbin Med Coll, Affiliated Hosp 2, Dept Neurol, Harbin 150086, Peoples R China.
[Cai, Huaibin] NIA, Neurogenet Lab, Bethesda, MD 20892 USA.
[Oddo, Salvatore] Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA.
[Oddo, Salvatore] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, San Antonio, TX 78229 USA.
[LaFerla, Frank M.] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA.
[Struble, Robert G.] So Illinois Univ, Sch Med, Ctr Alzheimers Dis, Springfield, IL 62794 USA.
RP Yan, XX (reprint author), Cent S Univ, Xiangya Sch Med, Dept Human Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China.
EM yanxiaoxin@csu.edu.cn
RI Cai, Huaibin/H-3359-2013
OI Cai, Huaibin/0000-0002-8596-6108
FU Illinois Department of Public Health; National Institute of Health
[1R21NS056371]; Southern Illinois University Center for Alzheimer's
disease and related disorders; National Institute on Aging; Central
South University
FX This study was supported in part by Illinois Department of Public Health
(X.X.Y.), National Institute of Health (1R21NS056371 to P.R.P.),
Southern Illinois University Center for Alzheimer's disease and related
disorders (X.X.Y., P.R.P., R.G.S.), intramural program of the National
Institute on Aging (H.C.), and Central South University (X.X.Y.). We
thank Elan Pharmaceuticals and Drs. H. Akiyama, H. Mori, E. Koo, and P.
Davis for providing antibodies.
NR 34
TC 20
Z9 21
U1 2
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1029-8428
J9 NEUROTOX RES
JI Neurotox. Res.
PD FEB
PY 2012
VL 21
IS 2
BP 160
EP 174
DI 10.1007/s12640-011-9256-9
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 869NK
UT WOS:000298604700003
PM 21725719
ER
PT J
AU Li, M
Ivanov, V
Mizuuchi, M
Mizuuchi, K
Craigie, R
AF Li, Min
Ivanov, Vassili
Mizuuchi, Michiyo
Mizuuchi, Kiyoshi
Craigie, Robert
TI DNA requirements for assembly and stability of HIV-1 intasomes
SO PROTEIN SCIENCE
LA English
DT Article
DE FRET; anisotropy; site-specific recombination; retrovirus; integrase;
integration; nucleoprotein complex
ID RETROVIRAL DNA; STRAND TRANSFER; INTEGRATION; COMPLEX
AB Integration of viral DNA into the host genome is an essential step in retroviral replication that is mediated by a stable nucleoprotein complex comprising a tetramer of integrase bridging the two ends of the viral DNA in a stable synaptic complex (SSC) or intasome. Assembly of HIV-1 intasomes requires several hundred base pairs of nonspecific internal DNA in addition to the terminal viral DNA sequence that is protected in footprinting experiments. We find that only one of the viral DNA ends in the intasome requires long-nonspecific internal DNA for intasome assembly. Although intasomes are unstable in solution when the nonspecific internal DNA is cut off after assembly, they are stable in agarose gels. These complexes are indistinguishable from SSCs with nonspecific internal DNA in Forster resonance energy transfer (FRET) experiments suggesting the interactions with the viral DNA and integrase tetramer are the same regardless of the presence of nonspecific internal DNA. We discuss models of how the internal DNA contributes to intasome assembly and stability. FRET is exquisitely sensitive to the distance between the fluorophores and given certain assumptions can be translated to distance measurements. We anticipated that a set of such distance constraints would provide a map of the DNA path within the intasome. In reality, the constraints we could impose from the FRET data were quite weak allowing a wide envelope for the possible path. We discuss the difficulties of converting the FRET signal to absolute distance within nucleoprotein complexes.
C1 [Li, Min; Ivanov, Vassili; Mizuuchi, Michiyo; Mizuuchi, Kiyoshi; Craigie, Robert] NIDDK, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Craigie, R (reprint author), Bldg 5,Room 301,5 Mem Dr, Bethesda, MD 20892 USA.
EM bobc@helix.nih.gov
FU NIDDK, NIH; Office of the Director of the NIH
FX Grant sponsors: Intramural Program of NIDDK, NIH; AIDS Targeted
Antiviral Program of the Office of the Director of the NIH.
NR 13
TC 6
Z9 6
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0961-8368
J9 PROTEIN SCI
JI Protein Sci.
PD FEB
PY 2012
VL 21
IS 2
BP 249
EP 257
DI 10.1002/pro.2010
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 877UZ
UT WOS:000299209500011
PM 22124978
ER
PT J
AU Sahlberg, AS
Ruuska, M
Colbert, RA
Granfors, K
Penttinen, MA
AF Sahlberg, A. S.
Ruuska, M.
Colbert, R. A.
Granfors, K.
Penttinen, M. A.
TI Altered PKR Signalling and C?/?EBP ss Expression is Associated with
HLA-B27 Expression in Monocytic Cells
SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID PROTEIN-KINASE PKR; ENDOPLASMIC-RETICULUM STRESS; REACTIVE ARTHRITIS;
MESSENGER-RNA; SALMONELLA-ENTERITIDIS; YERSINIA ANTIGENS; TRANSGENIC
RATS; BREAST-CANCER; UP-REGULATION; B-POCKET
AB Infection caused by certain gram-negative bacteria, e.g. Salmonella, can trigger inflammatory joint disease reactive arthritis (ReA). It is suggested that the disease-triggering bacteria or bacterial components persist in patients for an abnormally long time. Development of ReA is strongly associated with tissue antigen HLA-B27. Previously, we reported an enhanced replication of Salmonella enteritidis and altered p38 MAP kinase signalling in HLA-B27-expressing monocytic cells. Here we aimed to investigate the role of HLA-B27 in regulation of double-stranded RNA-activated kinase (PKR)-related signalling in Salmonella-infected or Salmonella lipopolysaccharide (LPS)-stimulated human U937 monocytic cells, as PKR has been reported to modify p38 signalling in Salmonella-infected cells. In cells expressing HLA-B27, PKR is overexpressed and hypophosphorylated, and the expression of transcription factor CCAAT enhancer binding protein beta (C/EBP beta) is increased upon Salmonella infection and LPS stimulation. The expression of C/EBP beta is PKR-dependent in LPS-stimulated mock cells, whereas in LPS-stimulated B27 cells the majority of C/EBP beta is expressed in a PKR-independent manner. Our results show that the expression of HLA-B27 disturbs the PKR-mediated signalling pathway. Moreover, altered signalling is related to misfolding-linked Glu45 in the B pocket of the HLA-B27 heavy chain. We suggest that the expression of HLA-B27 HCs modulates the intracellular environment of monocyte/macrophages and the mechanisms that are important in eliminating intracellular S. enteritidis by altering the intracellular signalling. This phenomenon is at least partly dependent on the misfolding feature of the B27 molecule. These observations offer a novel mechanism by which HLA-B27 may modulate inflammatory response induced by ReA-triggering bacteria.
C1 [Sahlberg, A. S.] Natl Inst Hlth & Welf, Dept Infect Dis Surveillance & Control, FIN-20520 Turku, Finland.
[Colbert, R. A.] NIAMS, NIH, Bethesda, MD USA.
[Penttinen, M. A.] Univ Turku, Dept Med Microbiol, Turku, Finland.
RP Sahlberg, AS (reprint author), Natl Inst Hlth & Welf, Dept Infect Dis Surveillance & Control, Kiinamyllynkatu 13, FIN-20520 Turku, Finland.
EM anna.sahlberg@utu.fi
FU Academy of Finland; Sigrid Juselius Foundation; National Institutes of
Health (NIH) [R01-AR-46177, R01-AR-48372]
FX We thank Joel D. Taurog for providing the HLA-B27 genomic DNA. Tuija
Turjas and Tuula Rantasalo are warmly thanked for their skillful
technical assistance. Study was supported by grants from the Academy of
Finland, the Sigrid Juselius Foundation and National Institutes of
Health (NIH, R01-AR-46177 and R01-AR-48372).
NR 49
TC 3
Z9 3
U1 0
U2 2
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0300-9475
J9 SCAND J IMMUNOL
JI Scand. J. Immunol.
PD FEB
PY 2012
VL 75
IS 2
BP 184
EP 192
DI 10.1111/j.1365-3083.2011.02648.x
PG 9
WC Immunology
SC Immunology
GA 874VE
UT WOS:000298985400007
PM 21988375
ER
PT J
AU Peters, S
Kromhout, H
Olsson, AC
Wichmann, HE
Bruske, I
Consonni, D
Landi, MT
Caporaso, N
Siemiatycki, J
Richiardi, L
Mirabelli, D
Simonato, L
Gustavsson, P
Plato, N
Jockel, KH
Ahrens, W
Pohlabeln, H
Boffetta, P
Brennan, P
Zaridze, D
Cassidy, A
Lissowska, J
Szeszenia-Dabrowska, N
Rudnai, P
Fabianova, E
Forastiere, F
Bencko, V
Foretova, L
Janout, V
Stucker, I
Dumitru, RS
Benhamou, S
Bueno-de-Mesquita, B
Kendzia, B
Pesch, B
Straif, K
Bruning, T
Vermeulen, R
AF Peters, Susan
Kromhout, Hans
Olsson, Ann C.
Wichmann, Heinz-Erich
Brueske, Irene
Consonni, Dario
Landi, Maria Teresa
Caporaso, Neil
Siemiatycki, Jack
Richiardi, Lorenzo
Mirabelli, Dario
Simonato, Lorenzo
Gustavsson, Per
Plato, Nils
Joeckel, Karl-Heinz
Ahrens, Wolfgang
Pohlabeln, Hermann
Boffetta, Paolo
Brennan, Paul
Zaridze, David
Cassidy, Adrian
Lissowska, Jolanta
Szeszenia-Dabrowska, Neonila
Rudnai, Peter
Fabianova, Eleonora
Forastiere, Francesco
Bencko, Vladimir
Foretova, Lenka
Janout, Vladimir
Stuecker, Isabelle
Dumitru, Rodica Stanescu
Benhamou, Simone
Bueno-de-Mesquita, Bas
Kendzia, Benjamin
Pesch, Beate
Straif, Kurt
Bruening, Thomas
Vermeulen, Roel
TI Occupational exposure to organic dust increases lung cancer risk in the
general population
SO THORAX
LA English
DT Article
ID OBSTRUCTIVE PULMONARY-DISEASE; WORKERS; CARCINOGENS; EUROPE
AB Background Organic dust is a complex mixture of particulate matter from microbial, plant or animal origin. Occupations with exposure to animal products have been associated with an increased lung cancer risk, while exposure to microbial components (eg, endotoxin) has been associated with a decreased risk. To date there has not been a comprehensive evaluation of the possible association between occupational organic dust exposure (and its specific constituents) and lung cancer risk in the general population.
Methods The SYNERGY project has pooled information on lifetime working and smoking from 13 300 lung cancer cases and 16 273 controls from 11 case-control studies conducted in Europe and Canada. A newly developed general population job-exposure matrix (assigning no, low or high exposure to organic dust, endotoxin, and contact with animals or fresh animal products) was applied to determine level of exposure. ORs for lung cancer were estimated by logistic regression, adjusted for age, sex, study, cigarette pack-years, time since quitting smoking, and ever employment in occupations with established lung cancer risk.
Results Occupational organic dust exposure was associated with increased lung cancer risk. The second to the fourth quartile of cumulative exposure showed significant risk estimates ranging from 1.12 to 1.24 in a dose-dependent manner (p<0.001). This association remained in the highest quartile after restricting analyses to subjects without chronic obstructive pulmonary disease or asthma. No association was observed between lung cancer and exposure to endotoxin or contact with animals or animal products.
Conclusion Occupational exposure to organic dust was associated with increased lung cancer risk in this large pooled case-control study.
C1 [Peters, Susan; Kromhout, Hans; Vermeulen, Roel] Univ Utrecht, Inst Risk Assessment Sci, Environm Epidemiol Div, NL-3508 TD Utrecht, Netherlands.
[Olsson, Ann C.; Brennan, Paul; Straif, Kurt] Int Agcy Res Canc, F-69372 Lyon, France.
[Olsson, Ann C.; Gustavsson, Per; Plato, Nils] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
[Wichmann, Heinz-Erich; Brueske, Irene] Deutsch Forschungszentrum Gesundheit & Umwelt, Helmholtz Zentrum Munchen, Inst Epidemiol, Neuherberg, Germany.
[Wichmann, Heinz-Erich] Univ Munich, Inst Med Informat Biometrie Epidemiol, Munich, Germany.
[Consonni, Dario] Fdn IRCCS Ca Grandad Osped Maggiore Policlin, Epidemiol Unit, Milan, Italy.
[Landi, Maria Teresa; Caporaso, Neil] NCI, Bethesda, MD 20892 USA.
[Siemiatycki, Jack] Univ Montreal, Univ Montreal Hosp Ctr, Res Ctr, Montreal, PQ, Canada.
[Richiardi, Lorenzo; Mirabelli, Dario] CPO Piemonte, Canc Epidemiol Unit, Turin, Italy.
[Richiardi, Lorenzo; Mirabelli, Dario] Univ Turin, Turin, Italy.
[Simonato, Lorenzo] Univ Padua, Sch Med, Dept Environm Med & Publ Hlth, Padua, Italy.
[Joeckel, Karl-Heinz] Univ Duisburg Essen, Inst Med Informat Biometry & Epidemiol, Essen, Germany.
[Ahrens, Wolfgang; Pohlabeln, Hermann] Bremen Inst Prevent Res & Social Med, Bremen, Germany.
[Boffetta, Paolo] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA.
[Boffetta, Paolo] Int Prevent Res Inst, Lyon, France.
[Zaridze, David] Russian Canc Res Ctr, Moscow, Russia.
[Cassidy, Adrian] Univ Liverpool, Canc Res Ctr, Roy Castle Lung Canc Res Programme, Liverpool L69 3BX, Merseyside, England.
[Lissowska, Jolanta] M Sklodowska Curie Canc Ctr, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Szeszenia-Dabrowska, Neonila] Nofer Inst Occupat Med, Lodz, Poland.
[Rudnai, Peter] Natl Inst Environm Hlth, Budapest, Hungary.
[Fabianova, Eleonora] Reg Author Publ Hlth, Banska Bystrica, Slovakia.
[Forastiere, Francesco] Reg Hlth Serv, Dept Epidemiol, Rome, Italy.
[Bencko, Vladimir] Charles Univ Prague, Inst Hyg & Epidemiol, Fac Med 1, Prague, Czech Republic.
[Foretova, Lenka] Masaryk Mem Canc Inst, Brno, Czech Republic.
[Janout, Vladimir] Palacky Univ, Fac Med, CR-77147 Olomouc, Czech Republic.
[Stuecker, Isabelle] INSERM, IFR69, U754, Villejuif, France.
[Dumitru, Rodica Stanescu] Inst Publ Hlth, Bucharest, Romania.
[Benhamou, Simone] INSERM, U946, Paris, France.
[Bueno-de-Mesquita, Bas] Natl Inst Publ Hlth & Environm RIVM, Bilthoven, Netherlands.
[Kendzia, Benjamin; Pesch, Beate; Bruening, Thomas] Univ Bochum, German Social Accid Insuranced Inst, Inst Prevent & Occupat Med, Bochum, Germany.
[Vermeulen, Roel] Univ Med Ctr, Julius Ctr Hlth Sci & Primary Care, Utrecht, Netherlands.
RP Peters, S (reprint author), Univ Utrecht, Inst Risk Assessment Sci, Environm Epidemiol Div, POB 80178, NL-3508 TD Utrecht, Netherlands.
EM s.peters@uu.nl
RI Vermeulen, Roel/F-8037-2011; Peters, Susan/A-5845-2013; Zaridze,
David/K-5605-2013; Bruske, Irene/N-3125-2013; Janout,
Vladimir/M-5133-2014; Szeszenia-Dabrowska, Neonila/F-7190-2010; Bruning,
Thomas/G-8120-2015; Benhamou, Simone/K-6554-2015; Forastiere,
Francesco/J-9067-2016; Consonni, Dario/K-7943-2016;
OI Peters, Susan/0000-0001-5662-1971; Ahrens, Wolfgang/0000-0003-3777-570X;
richiardi, lorenzo/0000-0003-0316-9402; Vermeulen,
Roel/0000-0003-4082-8163; Bruning, Thomas/0000-0001-9560-5464;
Forastiere, Francesco/0000-0002-9162-5684; Consonni,
Dario/0000-0002-8935-3843; Lissowska, Jolanta/0000-0003-2695-5799
FU German Social Accident Insurance (DGUV); International Agency for
Research on Cancer (IARC); Institute for Prevention and Occupational
Medicine of the DGUV; Institute of the Ruhr-University Bochum (IPA);
Institute for Risk Assessment Sciences (IRAS) at Utrecht University
FX The SYNERGY project is funded by the German Social Accident Insurance
(DGUV), and is coordinated by the International Agency for Research on
Cancer (IARC), the Institute for Prevention and Occupational Medicine of
the DGUV, Institute of the Ruhr-University Bochum (IPA) and the
Institute for Risk Assessment Sciences (IRAS) at Utrecht University.
NR 22
TC 20
Z9 20
U1 1
U2 16
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0040-6376
EI 1468-3296
J9 THORAX
JI Thorax
PD FEB
PY 2012
VL 67
IS 2
BP 111
EP 116
DI 10.1136/thoraxjnl-2011-200716
PG 6
WC Respiratory System
SC Respiratory System
GA 879IA
UT WOS:000299321700006
PM 21856697
ER
PT J
AU O'Donghaile, D
Kelley, W
Klein, HG
Flegel, WA
AF O'Donghaile, Diarmaid
Kelley, Walter
Klein, Harvey G.
Flegel, Willy A.
TI Recommendations for transfusion in ABO-incompatible hematopoietic stem
cell transplantation
SO TRANSFUSION
LA English
DT Letter
ID PLATELETS
C1 [O'Donghaile, Diarmaid; Kelley, Walter; Klein, Harvey G.; Flegel, Willy A.] NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
RP O'Donghaile, D (reprint author), NIH, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
EM bill.flegel@nih.gov
OI Flegel, Willy Albrecht/0000-0002-1631-7198
FU Intramural NIH HHS [Z99 CL999999]
NR 5
TC 9
Z9 9
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0041-1132
J9 TRANSFUSION
JI Transfusion
PD FEB
PY 2012
VL 52
IS 2
BP 456
EP 458
DI 10.1111/j.1537-2995.2011.03465.x
PG 3
WC Hematology
SC Hematology
GA 875NO
UT WOS:000299038200035
PM 22239215
ER
PT J
AU Langenkamp, E
Zwiers, PJ
Moorlag, HE
Leenders, WP
Croix, BS
Molema, G
AF Langenkamp, Elise
Zwiers, Peter J.
Moorlag, Henk E.
Leenders, William P.
Croix, Brad St.
Molema, Grietje
TI Vascular endothelial growth factor receptor 2 inhibition in-vivo affects
tumor vasculature in a tumor type-dependent way and downregulates
vascular endothelial growth factor receptor 2 protein without a
prominent role for miR-296
SO ANTI-CANCER DRUGS
LA English
DT Article
DE receptor tyrosine kinase inhibitors; tumor angiogenesis; vascular gene
expression; vascular stabilization; vascular endothelial growth factor
receptor 2 inhibition
ID ANTIANGIOGENIC THERAPY; NEGATIVE REGULATOR; ANTITUMOR-ACTIVITY; KINASE
INHIBITORS; FACTOR-A; VEGF; ANGIOGENESIS; CANCER; CELLS; ZD6474
AB The precise molecular effects that antiangiogenic drugs exert on tumor vasculature remain to be poorly understood. We therefore set out to investigate the molecular and architectural changes that occur in the vasculature of two different tumor types that both respond to vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor therapy. Mice bearing Lewis lung carcinoma (LLC) or B16.F10 melanoma were treated with vandetanib (ZD6474), a VEGFR2/epidermal growth factor receptor (EGFR)/REarranged during Transfection (RET) kinase inhibitor, resulting in a significant 80% reduction in tumor outgrowth. Although in LLC the vascular density was not affected by vandetanib treatment, it was significantly decreased in B16.F10. In LLC, vandetanib treatment induced a shift in vascular gene expression toward stabilization, as demonstrated by upregulation of Tie2 and N-cadherin and downregulation of Ang2 and integrin beta 3. In contrast, only eNOS and P-selectin responded to vandetanib treatment in B16.F10 vasculature. Strikingly, vandetanib reduced protein expression of VEGFR2 in both models, whereas mRNA remained unaffected. Analysis of miR-296 expression allowed us to exclude a role for the recently proposed microRNA-296 in VEGFR2 posttranslational control in LLC and B16.F10 in vivo. Our data demonstrate that VEGFR2/EGFR inhibition through vandetanib slows down both LLC and B16.F10 tumor growth. Yet, the underlying molecular changes in the vasculature that orchestrate the antitumor effect differ between tumor types. Importantly, in both models, vandetanib treatment induced loss of its pharmacological target, which was not directly related to miR-296 expression. Validation of our observations in tumor biopsies from VEGFR2 inhibitor-treated patients will be essential to unravel the effects of VEGFR2 inhibitor therapy on tumor vasculature in relation to therapeutic efficacy. Anti-Cancer Drugs 23: 161-172 (C) 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins.
C1 [Langenkamp, Elise; Zwiers, Peter J.; Moorlag, Henk E.; Molema, Grietje] Univ Groningen, Univ Med Ctr Groningen, Dept Pathol & Med Biol, Med Biol Sect, NL-9713 GZ Groningen, Netherlands.
[Leenders, William P.] Univ Med Ctr Nijmegen, Dept Pathol, Nijmegen, Netherlands.
[Croix, Brad St.] NCI, Mouse Canc Genet Program, Tumor Angiogenesis Sect, Frederick, MD 21701 USA.
RP Molema, G (reprint author), Univ Groningen, Univ Med Ctr Groningen, Dept Pathol & Med Biol, Med Biol Sect, Internal Postal Code EA11,Hanzepl 1, NL-9713 GZ Groningen, Netherlands.
EM g.molema01@umcg.nl
OI Molema, Grietje/0000-0002-4147-6676
FU University of Groningen
FX This research was funded by the University of Groningen.
NR 45
TC 4
Z9 5
U1 1
U2 7
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0959-4973
J9 ANTI-CANCER DRUG
JI Anti-Cancer Drugs
PD FEB
PY 2012
VL 23
IS 2
BP 161
EP 172
DI 10.1097/CAD.0b013e32834dc279
PG 12
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 870AY
UT WOS:000298642700004
PM 22075979
ER
PT J
AU Malinouski, M
Kehr, S
Finney, L
Vogt, S
Carlson, BA
Seravalli, J
Jin, R
Handy, DE
Park, TJ
Loscalzo, J
Hatfield, DL
Gladyshev, VN
AF Malinouski, Mikalai
Kehr, Sebastian
Finney, Lydia
Vogt, Stefan
Carlson, Bradley A.
Seravalli, Javier
Jin, Richard
Handy, Diane E.
Park, Thomas J.
Loscalzo, Joseph
Hatfield, Dolph L.
Gladyshev, Vadim N.
TI High-Resolution Imaging of Selenium in Kidneys: A Localized Selenium
Pool Associated with Glutathione Peroxidase 3
SO ANTIOXIDANTS & REDOX SIGNALING
LA English
DT Article
ID NAKED MOLE-RAT; PREVENTION TRIAL SELECT; TUBULE CELLS; VITAMIN-E;
CANCER; MOUSE; SPERMATOGENESIS; SELENOPROTEINS; SELENOCYSTEINE;
RESISTANCE
AB Aim: Recent advances in quantitative methods and sensitive imaging techniques of trace elements provide opportunities to uncover and explain their biological roles. In particular, the distribution of selenium in tissues and cells under both physiological and pathological conditions remains unknown. In this work, we applied high-resolution synchrotron X-ray fluorescence microscopy (XFM) to map selenium distribution in mouse liver and kidney. Results: Liver showed a uniform selenium distribution that was dependent on selenocysteine tRNA([Ser]Sec) and dietary selenium. In contrast, kidney selenium had both uniformly distributed and highly localized components, the latter visualized as thin circular structures surrounding proximal tubules. Other parts of the kidney, such as glomeruli and distal tubules, only manifested the uniformly distributed selenium pattern that co-localized with sulfur. We found that proximal tubule selenium localized to the basement membrane. It was preserved in Selenoprotein P knockout mice, but was completely eliminated in glutathione peroxidase 3 (GPx3) knockout mice, indicating that this selenium represented GPx3. We further imaged kidneys of another model organism, the naked mole rat, which showed a diminished uniformly distributed selenium pool, but preserved the circular proximal tubule signal. Innovation: We applied XFM to image selenium in mammalian tissues and identified a highly localized pool of this trace element at the basement membrane of kidneys that was associated with GPx3. Conclusion: XFM allowed us to define and explain the tissue topography of selenium in mammalian kidneys at submicron resolution. Antioxid. Redox Signal. 16, 185-192.
C1 [Gladyshev, Vadim N.] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA.
[Malinouski, Mikalai; Jin, Richard; Handy, Diane E.; Loscalzo, Joseph; Gladyshev, Vadim N.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Malinouski, Mikalai; Kehr, Sebastian; Seravalli, Javier] Univ Nebraska, Dept Biochem, Lincoln, NE 68583 USA.
[Finney, Lydia; Vogt, Stefan] Argonne Natl Lab, X Ray Sci Div, Argonne, IL 60439 USA.
[Finney, Lydia] Argonne Natl Lab, Biosci Div, Argonne, IL 60439 USA.
[Carlson, Bradley A.; Hatfield, Dolph L.] NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Park, Thomas J.] Univ Illinois, Dept Biol Sci, Chicago, IL 60680 USA.
RP Gladyshev, VN (reprint author), Harvard Univ, Sch Med, Dept Med, New Res Bldg,Room 435,77 Ave Louis Pasteur, Boston, MA 02115 USA.
EM vgladyshev@rics.bwh.harvard.edu
RI Gladyshev, Vadim/A-9894-2013; Vogt, Stefan/B-9547-2009; Vogt,
Stefan/J-7937-2013
OI Vogt, Stefan/0000-0002-8034-5513; Vogt, Stefan/0000-0002-8034-5513
FU National Institutes of Health [GM061603, CA080946, HL061795, HL070819,
HL048743]; National Institutes of Health, National Cancer Institute,
Center for Cancer Research; U.S. DOE [DE-AC02-06CH11357]
FX We thank Drs. Raymond Burk and Kristina Hill (Vanderbilt University) for
providing tissues of SelP knockout mice. This work was supported by
National Institutes of Health grants to VNG (GM061603 and CA080946) and
JL (HL061795, HL070819, and HL048743), and the Intramural Research
Program of the National Institutes of Health, National Cancer Institute,
Center for Cancer Research, to DLH. Use of the Advanced Photon Source,
an Office of Science User Facility operated for the U.S. Department of
Energy (DOE) Office of Science by Argonne National Laboratory, was
supported by the U.S. DOE under Contract No. DE-AC02-06CH11357.
NR 33
TC 22
Z9 22
U1 3
U2 11
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1523-0864
J9 ANTIOXID REDOX SIGN
JI Antioxid. Redox Signal.
PD FEB
PY 2012
VL 16
IS 3
BP 185
EP 192
DI 10.1089/ars.2011.3997
PG 8
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 863HM
UT WOS:000298153400001
PM 21854231
ER
PT J
AU Rose, EJ
Ross, TJ
Salmeron, BJ
Lee, M
Shakleya, DM
Huestis, M
Stein, EA
AF Rose, Emma Jane
Ross, Thomas J.
Salmeron, Betty Jo
Lee, Mary
Shakleya, Diaa M.
Huestis, Marilyn
Stein, Elliot A.
TI Chronic Exposure to Nicotine Is Associated with Reduced Reward-Related
Activity in the Striatum but not the Midbrain
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE fMRI; nicotine; reward; smoking; striatum; temporal difference error
ID VENTRAL TEGMENTAL AREA; EVENT-RELATED FMRI; CIGARETTE-SMOKING; DOPAMINE
RELEASE; ACETYLCHOLINE-RECEPTORS; TEMPORAL PREDICTION; DECISION-MAKING;
NEURAL RESPONSE; FAGERSTROM TEST; HUMAN BRAIN
AB Background: The reinforcing effects of nicotine are mediated by brain regions that also support temporal difference error (TDE) processing; yet, the impact of nicotine on TDE is undetermined.
Methods: Dependent smokers (n = 21) and matched control subjects (n = 21) were trained to associate a juice reward with a visual cue in a classical conditioning paradigm. Subjects subsequently underwent functional magnetic resonance imaging sessions in which they were exposed to trials where they either received juice as temporally predicted or where the juice was withheld (negative TDE) and later received unexpectedly (positive TDE). Subjects were scanned in two sessions that were identical, except that smokers had a transdermal nicotine (21 mg) or placebo patch placed before scanning. Analysis focused on regions along the trajectory of mesocorticolimbic and nigrostriatal dopaminergic pathways.
Results: There was a reduction in TDE-related function in smokers in the striatum, which did not differ as a function of patch manipulation but was predicted by the duration (years) of smoking. Activation in midbrain regions was not impacted by group or drug condition.
Conclusions: These data suggest a differential effect of smoking status on the neural substrates of reward in distinct dopaminergic pathway regions, which may be partially attributable to chronic nicotine exposure. The failure of transdermal nicotine to alter reward-related functional processes, either within smokers or between smokers and control subjects, implies that acute nicotine patch administration is insufficient to modify reward processing, which has been linked to abstinence-induced anhedonia in smokers and may play a critical role in smoking relapse.
C1 [Rose, Emma Jane; Ross, Thomas J.; Salmeron, Betty Jo; Lee, Mary; Stein, Elliot A.] Natl Inst Drug Abuse, Neuroimaging Res Branch, NIH, Baltimore, MD USA.
[Shakleya, Diaa M.; Huestis, Marilyn] Natl Inst Drug Abuse, Chem & Drug Metab Branch, NIH, Baltimore, MD USA.
RP Rose, EJ (reprint author), Trinity Coll Dublin, Dept Psychiat, Neuropsychiat Genet Grp, Dublin, Ireland.
EM rosee@tcd.ie
RI Ross, Thomas/B-7469-2008; Rose, Emma/A-9960-2010; Salmeron, Betty
Jo/M-1793-2016
OI Ross, Thomas/0000-0002-7745-3572; Rose, Emma/0000-0001-5365-4794;
Salmeron, Betty Jo/0000-0003-1699-9333
FU National Institute on Drug Abuse (NIDA)
FX This study was supported by the National Institute on Drug Abuse (NIDA),
Intramural Research Program.
NR 79
TC 25
Z9 25
U1 1
U2 6
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 2012
VL 71
IS 3
BP 206
EP 213
DI 10.1016/j.biopsych.2011.09.013
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 875DP
UT WOS:000299010900006
PM 22032832
ER
PT J
AU Elking, DM
Perera, L
Pedersen, LG
AF Elking, Dennis M.
Perera, Lalith
Pedersen, Lee G.
TI HPAM: Hirshfeld partitioned atomic multipoles
SO COMPUTER PHYSICS COMMUNICATIONS
LA English
DT Article
DE Atomic multipoles; Hirshfeld charges; Dipole; Quadrupole
ID MOLECULAR ELECTROSTATIC POTENTIALS; FORCE-FIELD; CHARGE-DISTRIBUTION;
FLUCTUATING CHARGE; WATER; SIMULATION; MOMENTS; QUANTUM; MODELS;
PARAMETERIZATION
AB An implementation of the Hirshfeld (HD) and Hirshfeld-Iterated (HD-I) atomic charge density partitioning schemes is described. Atomic charges and atomic multipoles are calculated from the HD and HD-I atomic charge densities for arbitrary atomic multipole rank I(max) on molecules of arbitrary shape and size. The HD and HD-I atomic charges/multipoles are tested by comparing molecular multipole moments and the electrostatic potential (ESP) surrounding a molecule with their reference ab initio values. In general. the HD-I atomic charges/multipoles are found to better reproduce ab initio electrostatic properties over HD atomic charges/multipoles. A systematic increase in precision for reproducing ab initio electrostatic properties is demonstrated by increasing the atomic multipole rank from I(max) = 0 (atomic charges) to I(max) = 4 (atomic hexadecapoles). Both HD and HD-I atomic multipoles up to rank I(max) are shown to exactly reproduce ab initio molecular multipole moments of rank L for L <= I(max) In addition, molecular dipole moments calculated by HD, HD-I, and ChelpG atomic charges only (I(max) = 0) are compared with reference ab initio values. Significant errors in reproducing ab initio molecular dipole moments are found if only HD or HD-I atomic charges used.
Program summary
Program title: HPAM
Catalogue identifier: AEKP_v1_0
Program summary URL: http://cpc.cs.qub.ac.uk/summaries/AEKP_v1_0.html
Program obtainable from: CPC Program Library, Queen's University, Belfast, N. Ireland
Licensing provisions: GNU General Public License v2
No. of lines in distributed program, including test data, etc.: 500 809
No. of bytes in distributed program, including test data, etc.: 13 424 494
Distribution format: tarp
Programming language: C
Computer: Any
Operating system: Linux
RAM: Typically, a few hundred megabytes
Classification: 16.13
External routines: The program requires 'formatted checkpoint' files obtained from the Gaussian 03 or Gaussian 09 quantum chemistry program.
Nature of problem: An ab initio molecular charge density rho(mol)(r) is partitioned into Hirshfeld (HD) and Hirshfeld-lterated (HD-I) atomic charge densities rho(a)(r) on a grid. Atomic charges q(a) and multipoles Q(lm)(a) are calculated from the partitioned atomic charge densities rho(a)(r) by numerical integration.
Solution method: Molecular and isolated atomic grids are generated for the molecule of interest. The ab initio density matrix P(mu nu) and basis functions chi(mu)(r) are read in from 'formatted checkpoint' files obtained from the Gaussian 03 or 09 quantum chemistry programs. The ab initio density is evaluated for the molecule and the isolated atoms/atomic ions on grids and used to construct Hirshfeld (HD) and Hirshfeld-1 (HD-I) partitioned atomic charges densities rho(a)(r), which are used to calculate atomic charges qa and atomic multipoles Q(lm)(a), by integration.
Restrictions: The ab initio density matrix can be calculated at the HF, DEL MP2, or CCSD levels with ab initio Gaussian basis sets that include up to s, p, d, f, g functions for either closed shell or open shell molecules.
Running time: The running time varies with the size of the molecule, the size of the ab initio basis set, and the coarseness of the desired grid. The run time can range from a minute or less for water to similar to 15 minutes for neopentane. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Elking, Dennis M.; Pedersen, Lee G.] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
[Perera, Lalith; Pedersen, Lee G.] Natl Inst Environm Hlth Sci, Struct Biol Lab, Res Triangle Pk, NC 27709 USA.
RP Elking, DM (reprint author), Openeye Sci Software, 9 Bisbee Court,Suite D, Santa Fe, NM 87508 USA.
EM denny@eyesopen.com
RI perera, Lalith/B-6879-2012; Pedersen, Lee/E-3405-2013
OI perera, Lalith/0000-0003-0823-1631; Pedersen, Lee/0000-0003-1262-9861
FU National Institute of Health [HL-06350]; National Science Foundation
[FRG DMR 084549]; NIH-National Institute of Environmental Health
Sciences [Z01 ES125392]
FX This research was supported by the National Institute of Health
(HL-06350) and National Science Foundation (FRG DMR 084549) to LGP This
research was supported (in part) by the Intramural Research Program of
the NIH-National Institute of Environmental Health Sciences (Z01
ES125392). DME thanks the NIEHS, RIP, NC for providing visitor status
for the year this work was accomplished.
NR 51
TC 7
Z9 7
U1 1
U2 26
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0010-4655
J9 COMPUT PHYS COMMUN
JI Comput. Phys. Commun.
PD FEB
PY 2012
VL 183
IS 2
BP 390
EP 397
DI 10.1016/j.cpc.2011.10.003
PG 8
WC Computer Science, Interdisciplinary Applications; Physics, Mathematical
SC Computer Science; Physics
GA 868OA
UT WOS:000298531400020
PM 22140274
ER
PT J
AU Walford, GA
Green, T
Neale, B
Isakova, T
Rotter, JI
Grant, SFA
Fox, CS
Pankow, JS
Wilson, JG
Meigs, JB
Siscovick, DS
Bowden, DW
Daly, MJ
Florez, JC
AF Walford, G. A.
Green, T.
Neale, B.
Isakova, T.
Rotter, J. I.
Grant, S. F. A.
Fox, C. S.
Pankow, J. S.
Wilson, J. G.
Meigs, J. B.
Siscovick, D. S.
Bowden, D. W.
Daly, M. J.
Florez, J. C.
TI Common genetic variants differentially influence the transition from
clinically defined states of fasting glucose metabolism
SO DIABETOLOGIA
LA English
DT Article
DE Common genetic variants; Diabetes mellitus; Genetics; Glycaemic
progression; Impaired fasting glucose; Normal fasting glucose; Single
nucleotide polymorphism; Type 2 diabetes
ID TYPE-2 DIABETES RISK; FOLLOW-UP; ASSOCIATION ANALYSIS; TRIGLYCERIDE
LEVELS; INSULIN-SECRETION; PLASMA-GLUCOSE; MTNR1B; LOCI; MELLITUS;
DESIGN
AB Common genetic variants have been associated with type 2 diabetes. We hypothesised that a subset of these variants may have different effects on the transition from normal fasting glucose (NFG) to impaired fasting glucose (IFG) than on that from IFG to diabetes.
We identified 16 type 2 diabetes risk variants from the Illumina Broad Candidate-gene Association Resource (CARe) array genotyped in 26,576 CARe participants. Participants were categorised at baseline as NFG, IFG or type 2 diabetic (n = 16,465, 8,017 or 2,291, respectively). Using Cox proportional hazards and likelihood ratio tests (LRTs), we compared rates of progression by genotype for 4,909 (NFG to IFG) and 1,518 (IFG to type 2 diabetes) individuals, respectively. We then performed multinomial regression analyses at baseline, comparing the risk of assignment to the NFG, IFG or diabetes groups by genotype.
The rate of progression from NFG to IFG was significantly greater in participants carrying the risk allele at MTNR1B (p = 1 x 10(-4)), nominally greater at GCK and SLC30A8 (p < 0.05) and nominally smaller at IGF2BP2 (p = 0.01) than the rate of progression from IFG to diabetes by the LRT. Results of the baseline, multinomial regression model were consistent with these findings.
Common genetic risk variants at GCK, SLC30A8, IGF2BP2 and MTNR1B influence to different extents the development of IFG and the transition from IFG to type 2 diabetes. Our findings may have implications for understanding the genetic contribution of these variants to the development of IFG and type 2 diabetes.
C1 [Walford, G. A.; Green, T.; Neale, B.; Daly, M. J.; Florez, J. C.] Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA 02114 USA.
[Walford, G. A.; Florez, J. C.] Massachusetts Gen Hosp, Diabet Res Ctr, Diabet Unit, Boston, MA 02114 USA.
[Walford, G. A.; Green, T.; Neale, B.; Daly, M. J.; Florez, J. C.] Broad Inst, Program Med & Populat Genet, Cambridge, MA USA.
[Walford, G. A.; Isakova, T.; Florez, J. C.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Isakova, T.] Massachusetts Gen Hosp, Renal Unit, Boston, MA 02114 USA.
[Grant, S. F. A.] Childrens Hosp Philadelphia, Res Inst, Div Human Genet, Ctr Appl Genom, Philadelphia, PA 19104 USA.
[Grant, S. F. A.] Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA.
[Siscovick, D. S.] Univ Washington, Cardiovasc Hlth Res Unit, Seattle, WA 98195 USA.
[Siscovick, D. S.] Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA.
[Wilson, J. G.] Univ Mississippi, Med Ctr, Dept Med, Jackson, MS 39216 USA.
[Wilson, J. G.] VA Med Ctr, Dept Med, Jackson, MS USA.
[Fox, C. S.] Natl Heart Lung & Blood Inst Framingham Heart Stu, Framingham, MA USA.
[Fox, C. S.] Harvard Univ, Brigham & Womens Hosp, Sch Med, Div Endocrinol Diabet & Hypertens, Boston, MA 02115 USA.
[Meigs, J. B.] Massachusetts Gen Hosp, Div Gen Med, Boston, MA 02114 USA.
[Meigs, J. B.] Harvard Univ, Sch Med, Dept Med, Boston, MA USA.
[Pankow, J. S.] Univ Minnesota, Div Epidemiol & Community Hlth, Minneapolis, MN USA.
[Bowden, D. W.] Wake Forest Univ, Bowman Gray Sch Med, Dept Biochem, Ctr Human Genom, Winston Salem, NC 27103 USA.
[Bowden, D. W.] Wake Forest Univ, Bowman Gray Sch Med, Dept Biochem, Ctr Diabet Res, Winston Salem, NC 27103 USA.
[Rotter, J. I.] Cedars Sinai Med Ctr, Inst Med Genet, Los Angeles, CA 90048 USA.
RP Florez, JC (reprint author), Massachusetts Gen Hosp, Ctr Human Genet Res, Simches Res Bldg CPZN 5-250,185 Cambridge St, Boston, MA 02114 USA.
EM jcflorez@partners.org
OI Pankow, James/0000-0001-7076-483X
FU NIH [DK007028]; Scholars in Clinical Science programme of Harvard
Catalyst-The Harvard Clinical and Translational Science Center [UL1 RR
025758]; Harvard University; NIDDK [K24 DK080140]; Doris Duke Charitable
Foundation; National Heart, Lung, and Blood Institute
FX G.A. Walford (Massachusetts General Hospital) received support from NIH
training grant DK007028 and from the Scholars in Clinical Science
programme of Harvard Catalyst-The Harvard Clinical and Translational
Science Center (award UL1 RR 025758 and financial contributions from
Harvard University and its affiliated academic healthcare centres). J.B.
Meigs (Massachusetts General Hospital) is supported in part by NIDDK K24
DK080140. J.C. Florez (Massachusetts General Hospital) is supported by a
Clinical Scientist Development Award from the Doris Duke Charitable
Foundation. The authors wish to acknowledge the support of the National
Heart, Lung, and Blood Institute and the contributions of the research
institutions, study investigators, field staff and study participants
involved in creating this resource for biomedical research. Specific
funding information for the nine parent studies contributing to CARe can
be found in the ESM text. This study was presented in poster form as a
late-breaking abstract at the 2010 American Diabetes Association
Scientific Sessions in Orlando, FL, USA.
NR 34
TC 13
Z9 14
U1 0
U2 7
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0012-186X
J9 DIABETOLOGIA
JI Diabetologia
PD FEB
PY 2012
VL 55
IS 2
BP 331
EP 339
DI 10.1007/s00125-011-2353-8
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 866OZ
UT WOS:000298392000008
PM 22038522
ER
PT J
AU Augusto, DG
Zehnder-Alves, L
Pincerati, MR
Martin, MP
Carrington, M
Petzl-Erler, ML
AF Augusto, D. G.
Zehnder-Alves, L.
Pincerati, M. R.
Martin, M. P.
Carrington, M.
Petzl-Erler, Maria Luiza
TI Diversity of the KIR gene cluster in an urban Brazilian population
SO IMMUNOGENETICS
LA English
DT Article
DE KIR genes; KIR diversity; Brazilian population; HLA ligands; 2DL4 allele
frequencies
ID IMMUNOGLOBULIN-LIKE RECEPTOR; NATURAL-KILLER-CELLS; CHROMOSOME 19Q13.4;
HAPLOTYPE ANALYSIS; NK CELLS; HLA-C; KIR2DL4; ALLELES; POLYMORPHISMS;
DISEASE
AB The activity of natural killer cells depends on the balance between activating and inhibitory signals coming from their receptors. Among these are the killer cell immunoglobulin-like receptors (KIR) that recognize specific HLA class I allotypes. Here we characterized KIR genetic diversity and their HLA ligands in the population of Curitiba, Parana State (n = 164), and compared it with other worldwide populations. The distribution of 2DL4 alleles was also analyzed. The Curitiba population did not differ significantly from European and Euro-descendant populations, but as an admixed population showed higher genetic diversity. We found 27 KIR profiles, many of them uncommon in European populations, in agreement with the elevated historically recent gene flow in the study population. The frequencies of KIR genes and their respective HLA ligands were distributed independently and none of the analyzed individuals lacked functional KIR-HLA ligand combinations. KIR gene frequencies of 33 worldwide populations were consistent with geographic and ethnic distribution, in agreement with demography being the major factor shaping the observed gene content diversity of the KIR locus.
C1 [Augusto, D. G.; Zehnder-Alves, L.; Petzl-Erler, Maria Luiza] Univ Fed Parana, Dept Genet, Lab Genet Mol Humana, BR-81531980 Curitiba, Parana, Brazil.
[Pincerati, M. R.] Univ Sao Paulo, Dept Genet & Biol Evolut, BR-05508090 Sao Paulo, Brazil.
[Martin, M. P.; Carrington, M.] NCI Frederick, SAIC Frederick Inc, Canc & Inflammat Program, Expt Immunol Lab, Frederick, MD 21702 USA.
[Carrington, M.] MIT, Gen Hosp, Ragon Inst Massachusetts, Boston, MA 02114 USA.
RP Petzl-Erler, ML (reprint author), Univ Fed Parana, Dept Genet, Lab Genet Mol Humana, Caixa Postal 19071, BR-81531980 Curitiba, Parana, Brazil.
EM perler@ufpr.br
RI Augusto, Danillo/F-3147-2013; Petzl-Erler, Maria-Luiza/H-8221-2012
OI Petzl-Erler, Maria-Luiza/0000-0002-0345-5276
FU Laboratory of Human Molecular Genetics at the Department of Genetics of
the Federal University of Parana; Conselho Nacional de Desenvolvimento
Cientifico e Tecnologico (CNPq); PRONEX; Institutos do Milenio; Fundacao
Araucaria; Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior
(CAPES); National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; NIH, National Cancer Institute, Center for Cancer
Research
FX We thank the staff of the Laboratory of Human Molecular Genetics at the
Department of Genetics of the Federal University of Parana for
assistance and support. Special thanks to Liana Alves de Oliveira for
her expertise and valuable comments. We also thank Fuh-Mei Duh and Colm
O'huigin for helpful advice and Maria Dias da Silva for reading this
manuscript. This project received financial support from the Conselho
Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), PRONEX,
Institutos do Milenio, Fundacao Araucaria, Coordenacao de
Aperfeicoamento de Pessoal de Nivel Superior (CAPES). This project was
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 US Government. This Research was supported in part by
the Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research.
NR 52
TC 13
Z9 14
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0093-7711
J9 IMMUNOGENETICS
JI Immunogenetics
PD FEB
PY 2012
VL 64
IS 2
BP 143
EP 152
DI 10.1007/s00251-011-0565-1
PG 10
WC Genetics & Heredity; Immunology
SC Genetics & Heredity; Immunology
GA 876AT
UT WOS:000299079900007
PM 21850526
ER
PT J
AU Little, MP
Kleinerman, RA
Stiller, CA
Li, GQ
Kroll, ME
Murphy, MFG
AF Little, Mark P.
Kleinerman, Ruth A.
Stiller, Charles A.
Li, Guangquan
Kroll, Mary E.
Murphy, Michael F. G.
TI Analysis of retinoblastoma age incidence data using a fully stochastic
cancer model
SO INTERNATIONAL JOURNAL OF CANCER
LA English
DT Article
DE retinoblastoma; carcinogenesis modeling; two-hit theory; stochastic MVK
model; RB1 gene
ID HEREDITARY RETINOBLASTOMA; GENOMIC INSTABILITY; CHILDHOOD-CANCER; RB1
MUTATIONS; GENE; CARCINOGENESIS; HITS; HETEROZYGOSITY; IDENTIFICATION;
PROGRESSION
AB Retinoblastoma (RB) is an important ocular malignancy of childhood. It has been commonly accepted for some time that knockout of the two alleles of the RB1 gene is the principal molecular target associated with the occurrence of RB. In this article, we examine the validity of the two-hit theory for RB by comparing the fit of a stochastic model with two or more mutational stages. Unlike many such models, our model assumes a fully stochastic stem cell compartment, which is crucial to its behavior. Models are fitted to a population-based dataset comprising 1,553 cases of RB for the period 1962-2000 in Great Britain (England, Scotland and Wales). The population incidence of RB is best described by a fully stochastic model with two stages, although models with a deterministic stem cell compartment yield equivalent fit; models with three or more stages fit much less well. The results strongly suggest that knockout of the two alleles of the RB1 gene is necessary and may be largely sufficient for the development of RB, in support of Knudson's two-hit hypothesis.
C1 [Little, Mark P.; Kleinerman, Ruth A.] NCI, Radiat Epidemiol Branch, DHHS, NIH,Div Canc Epidemiol & Genet, Bethesda, MD 20852 USA.
[Stiller, Charles A.; Kroll, Mary E.; Murphy, Michael F. G.] Univ Oxford, Dept Paediat, Childhood Canc Res Grp, Oxford, England.
[Li, Guangquan] Univ London Imperial Coll Sci Technol & Med, Fac Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
[Kroll, Mary E.] Univ Oxford, Nuffield Dept Clin Med, Canc Epidemiol Unit, Oxford, England.
RP Little, MP (reprint author), NCI, Radiat Epidemiol Branch, DHHS, NIH,Div Canc Epidemiol & Genet, Bethesda, MD 20852 USA.
EM mark.little@nih.gov
OI Kleinerman, Ruth/0000-0001-7415-2478; Little, Mark/0000-0003-0980-7567
FU European Commission [FI6R-CT-2003-508842, FP6-036465]; National
Institutes of Health; National Cancer Institute; Division of Cancer
Epidemiology and Genetics; Department of Health and the Scottish
Ministers; Children with Leukaemia; Higher Education Funding Council for
England
FX Grant sponsor: European Commission; Grant numbers: FI6R-CT-2003-508842
(RISC-RAD), FP6-036465 (NOTE); Grant sponsors: National Institutes of
Health, the National Cancer Institute, Division of Cancer Epidemiology
and Genetics (Intramural Research Program), Department of Health and the
Scottish Ministers, Children with Leukaemia, Higher Education Funding
Council for England (Overseas Research Students Awards Schemes)
NR 49
TC 8
Z9 8
U1 0
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0020-7136
J9 INT J CANCER
JI Int. J. Cancer
PD FEB 1
PY 2012
VL 130
IS 3
BP 631
EP 640
DI 10.1002/ijc.26039
PG 10
WC Oncology
SC Oncology
GA 869MP
UT WOS:000298602500015
PM 21387305
ER
PT J
AU Lin, FR
Maas, P
Chien, W
Carey, JP
Ferrucci, L
Thorpe, R
AF Lin, Frank R.
Maas, Paige
Chien, Wade
Carey, John P.
Ferrucci, Luigi
Thorpe, Roland
TI Association of Skin Color, Race/Ethnicity, and Hearing Loss Among Adults
in the USA
SO JARO-JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY
LA English
DT Article
DE hearing loss; race; melanocytes; epidemiology
ID PIGMENTED GUINEA-PIGS; THRESHOLD SHIFT; DIFFERENTIAL SUSCEPTIBILITY;
STRIA VASCULARIS; HUMAN ALBINOS; NOISE; MELANIN; PREVALENCE; CISPLATIN;
HEALTH
AB Epidemiologic studies of hearing loss in adults have demonstrated that the odds of hearing loss are substantially lower in black than in white individuals. The basis of this association is unknown. We hypothesized that skin pigmentation as a marker of melanocytic functioning mediates this observed association and that skin pigmentation is associated with hearing loss independent of race/ethnicity. We analyzed cross-sectional data from 1,258 adults (20-59 years) in the 2003-2004 cycle of the National Health and Nutritional Examination Survey who had assessment of Fitzpatrick skin type and pure-tone audiometric testing. Audiometric thresholds in the worse hearing ear were used to calculate speech- (0.5-4 kHz) and high-frequency (3-8 kHz) pure-tone averages (PTA). Regression models were stratified by Fitzpatrick skin type or race/ethnicity to examine the association of each factor with hearing loss independent of the other. Models were adjusted for potential confounders (demographic, medical, and noise exposure covariates). Among all participants, race/ethnicity was associated with hearing thresholds (black participants with the best hearing followed by Hispanics and then white individuals), but these associations were not significant in analyses stratified by skin color. In contrast, in race-stratified analyses, darker-skinned Hispanics had better hearing than lighter-skinned Hispanics by an average of -2.5 dB hearing level (HL; 95% CI, -4.8 to -0.2) and -3.1 dB HL (95% CI, -5.3 to -0.8) for speech and high-frequency PTA, respectively. Associations between skin color and hearing loss were not significant in white and black participants. Our results demonstrate that skin pigmentation is independently associated with hearing loss in Hispanics and suggest that skin pigmentation as a marker of melanocytic functioning may mediate the strong association observed between race/ethnicity and hearing loss.
C1 [Lin, Frank R.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21287 USA.
[Lin, Frank R.] Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Aging & Hlth, Baltimore, MD 21287 USA.
[Lin, Frank R.; Chien, Wade; Carey, John P.] Johns Hopkins Sch Med, Dept Otolaryngol Head & Neck Surg, Baltimore, MD 21287 USA.
[Lin, Frank R.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Lin, Frank R.] Johns Hopkins Bloomberg Sch Publ Hlth, Ctr Aging & Hlth, Baltimore, MD 21205 USA.
[Maas, Paige] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD 21205 USA.
[Ferrucci, Luigi] NIA, Longitudinal Studies Sect, Baltimore, MD 21225 USA.
[Thorpe, Roland] Johns Hopkins Bloomberg Sch Publ Hlth, Johns Hopkins Ctr Hlth Dispar Solut, Baltimore, MD 21205 USA.
[Thorpe, Roland] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Hlth Policy & Management, Baltimore, MD 21205 USA.
RP Lin, FR (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, 2024 Monument St,Suite 2-700, Baltimore, MD 21287 USA.
EM flin1@jhmi.edu
FU NIDCD NIH HHS [K23 DC011279]
NR 35
TC 19
Z9 19
U1 2
U2 8
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1525-3961
J9 JARO-J ASSOC RES OTO
JI JARO
PD FEB
PY 2012
VL 13
IS 1
BP 109
EP 117
DI 10.1007/s10162-011-0298-8
PG 9
WC Neurosciences; Otorhinolaryngology
SC Neurosciences & Neurology; Otorhinolaryngology
GA 876FF
UT WOS:000299092200009
PM 22124888
ER
PT J
AU Lozito, TP
Tuan, RS
AF Lozito, Thomas P.
Tuan, Rocky S.
TI Endothelial cell microparticles act as centers of matrix
metalloproteinsase-2 (MMP-2) activation and vascular matrix remodeling
SO JOURNAL OF CELLULAR PHYSIOLOGY
LA English
DT Article
ID MESENCHYMAL STEM-CELLS; IN-VITRO; TISSUE INHIBITORS; MEMBRANE; SURFACE;
MT1-MMP; GENERATION; COMPONENTS; MECHANISM; DISEASE
AB Endothelial cell (EC)-derived microparticles (MPs) are small membrane vesicles associated with various vascular pathologies. Here, we investigated the role of MPs in matrix remodeling by analyzing their interactions with the extracellular matrix. MPs were shown to bind preferentially to surfaces coated with matrix molecules, and MPs bound fibronectin via integrin aV. MPs isolated from EC-conditioned medium (Sup) were significantly enriched for matrix-altering proteases, including matrix metalloproteinases (MMPs). MPs lacked the MMP inhibitors TIMP-1 and TIMP-2 found in the Sup and, while Sup strongly inhibited MMP activities but MPs did not. In fact, MPs were shown to bind and activate both endogenous and exogenous proMMP-2. Taken together, these results indicate that MPs interact with extracellular matrices, where they localize and activate MMP-2 to modify the surrounding matrix molecules. These findings provide insights into the cellular mechanisms of vascular matrix remodeling and identify new targets of vascular pathologies. J. Cell. Physiol. 227: 534549, 2012. (C) 2011 Wiley Periodicals, Inc.
C1 [Lozito, Thomas P.; Tuan, Rocky S.] Univ Pittsburgh, Sch Med, Ctr Cellular & Mol Engn, Dept Orthopaed Surg, Pittsburgh, PA 15219 USA.
[Lozito, Thomas P.; Tuan, Rocky S.] NIAMSD, Cartilage Biol & Orthopaed Branch, NIH, US Dept HHS, Bethesda, MD 20892 USA.
RP Tuan, RS (reprint author), Univ Pittsburgh, Sch Med, Ctr Cellular & Mol Engn, Dept Orthopaed Surg, 450 Technol Dr,Room 221, Pittsburgh, PA 15219 USA.
EM rst13@pitt.edu
FU NIAMS IRP [Z01AR41131]
FX Contract grant sponsor: NIAMS IRP;; Contract grant number: Z01AR41131.
NR 33
TC 19
Z9 22
U1 2
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0021-9541
J9 J CELL PHYSIOL
JI J. Cell. Physiol.
PD FEB
PY 2012
VL 227
IS 2
BP 534
EP 549
DI 10.1002/jcp.22744
PG 16
WC Cell Biology; Physiology
SC Cell Biology; Physiology
GA 862LQ
UT WOS:000298092800016
PM 21437907
ER
PT J
AU Bornstein, MH
Putnick, DL
Suwalsky, JTD
Venuti, P
de Falco, S
de Galperin, CZ
Gini, M
Tichovolsky, MH
AF Bornstein, Marc H.
Putnick, Diane L.
Suwalsky, Joan T. D.
Venuti, Paola
de Falco, Simona
Zingman de Galperin, Celia
Gini, Motti
Tichovolsky, Marianne Heslington
TI Emotional Relationships in Mothers and Infants: Culture-Common and
Community-Specific Characteristics of Dyads From Rural and Metropolitan
Settings in Argentina, Italy, and the United States
SO JOURNAL OF CROSS-CULTURAL PSYCHOLOGY
LA English
DT Article
DE cultural psychology; child/adolescent development; social development
ID EUROPEAN-AMERICAN FAMILIES; CHILD-REARING VALUES; AVAILABILITY SCALES;
PRESCHOOL-CHILDREN; YOUNG-CHILDREN; ATTACHMENT; PERSPECTIVE; BEHAVIOR;
QUALITY; PERCEPTION
AB This study uses country and regional contrasts to examine culture-common and community-specific variation in mother-infant emotional relationships. Altogether, 220 Argentine, Italian, and U.S. American mothers and their daughters and sons, living in rural and metropolitan settings, were observed at home at infant age 5 months. Both variable- and person-centered perspectives of dyadic emotional relationships were analyzed. Supporting the notion that adequate emotional relationships are a critical and culture-common characteristic of human infant development, across all samples most dyads scored in the adaptive range in terms of emotional relationships. Giving evidence of community-specific characteristics, Italian mothers were more sensitive, and Italian infants more responsive, than Argentine and U.S. mothers and infants; in addition, rural mothers were more intrusive than metropolitan mothers and rural dyads more likely than expected to be classified as midrange in emotional relationships and less likely to be classified as high in emotional relationships. Adaptive emotional relationships appear to be a culture-common characteristic of mother-infant dyads near the beginning of life, but this relational construct is moderated by a community-specific (country and regional) context.
C1 [Bornstein, Marc H.; Putnick, Diane L.; Suwalsky, Joan T. D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Venuti, Paola; de Falco, Simona] Univ Trent, Cognit Sci & Educ Dept, Trento, Italy.
[Zingman de Galperin, Celia] Univ Belgrano, Buenos Aires, DF, Argentina.
[Gini, Motti] Univ Haifa, IL-31999 Haifa, Israel.
[Tichovolsky, Marianne Heslington] Univ Massachusetts, Amherst, MA 01003 USA.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv, Suite 8030,6705 Rockledge Dr, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov
OI Putnick, Diane/0000-0002-6323-749X
FU Intramural NIH HHS [Z99 HD999999]
NR 138
TC 11
Z9 11
U1 3
U2 19
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-0221
J9 J CROSS CULT PSYCHOL
JI J. Cross-Cult. Psychol.
PD FEB
PY 2012
VL 43
IS 2
BP 171
EP 197
DI 10.1177/0022022110388563
PG 27
WC Psychology, Social
SC Psychology
GA 873XN
UT WOS:000298918900001
PM 22247569
ER
PT J
AU Setse, R
Siberry, GK
Moss, WJ
Gravitt, P
Wheeling, T
Bohannon, B
Dominguez, K
AF Setse, Rosanna
Siberry, George K.
Moss, William J.
Gravitt, Patti
Wheeling, Travis
Bohannon, Beverly
Dominguez, Kenneth
CA Legacy Consortium
TI Cervical Pap Screening Cytological Abnormalities among HIV-Infected
Adolescents in the LEGACY Cohort
SO JOURNAL OF PEDIATRIC AND ADOLESCENT GYNECOLOGY
LA English
DT Article
DE Cervical Pap screening; HIV infection; Adolescents
ID HUMAN-IMMUNODEFICIENCY-VIRUS; SQUAMOUS INTRAEPITHELIAL LESIONS;
HUMAN-PAPILLOMAVIRUS INFECTION; CANCER-SOCIETY GUIDELINE; RISK-FACTORS;
PAPANICOLAOU SMEARS; SEROPOSITIVE WOMEN; NEGATIVE WOMEN; UNITED-STATES;
SELF-REPORT
AB Objectives: To determine the prevalence of cervical Pap screening (CPAP-S), identify factors associated with CPAP-S, and explore risk factors for abnormal cervical cytology in female adolescents with perinatally and behaviorally acquired HIV infection.
Design: Cross-sectional.
Setting: LEGACY is a national observational cohort chart review study of 1478 HIV-infected persons (0% (consistent with a cytostatic effect) were observed in 8 cell lines and 15 cell lines showed Relative I/O values ranging from -4.7 to -92.2% (consistent with varying degrees of cytotoxic activity). In vivo AZD8055 induced significant differences in EFS distribution compared to controls in 23 of 36 (64%) evaluable solid tumor xenografts, and 1 of 6 evaluable ALL xenografts. Intermediate activity for the time to event activity measure (EFS T/C >2) was observed in 5 of 32 (16%) solid tumor xenografts evaluable. The best response was stable disease. PD2 (progressive disease with growth delay) was observed in 20 of 36 (55.6%) evaluable solid tumor xenografts. AZD8055 significantly inhibited 4E-BP1, S6, and Akt phosphorylation following day 1 and day 4 dosing, but suppression of mTORC1 or mTORC2 signaling did not predict tumor sensitivity.
C1 [Houghton, Peter J.] Nationwide Childrens Hosp, Ctr Childhood Canc, Columbus, OH 43204 USA.
[Gorlick, Richard] Childrens Hosp Montefiore, Bronx, NY USA.
[Kolb, E. Anders] Alfred I DuPont Hosp Children, Wilmington, DE USA.
[Lock, Richard; Carol, Hernan] Childrens Canc Inst Australia Med Res, Randwick, NSW, Australia.
[Morton, Christopher L.; Billups, Catherine] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Keir, Stephen T.] Duke Univ, Med Ctr, Durham, NC USA.
[Reynolds, C. Patrick; Kang, Min H.] Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
[Maris, John M.] Univ Penn, Childrens Hosp, Sch Med, Philadelphia, PA 19104 USA.
[Maris, John M.] Univ Penn, Childrens Hosp, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
[Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Houghton, PJ (reprint author), Nationwide Childrens Hosp, Ctr Childhood Canc, 700 Childrens Dr, Columbus, OH 43204 USA.
EM peter.houghton@nationwidechildrens.org
RI Houghton, Peter/E-3265-2011; Carol, Hernan/F-5750-2013; Lock,
Richard/G-4253-2013;
OI Carol, Hernan/0000-0002-9443-8032; Reynolds, C.
Patrick/0000-0002-2827-8536
FU National Cancer Institute [NO1-CM-42216, NO1-CM91001-03, CA21765,
CA108786]
FX Grant sponsor: National Cancer Institute; Grant numbers: NO1-CM-42216;
NO1-CM91001-03; CA21765; CA108786.
NR 34
TC 19
Z9 20
U1 0
U2 2
PU WILEY PERIODICALS, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN STREET, MALDEN, MA 02148-529 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD FEB
PY 2012
VL 58
IS 2
BP 191
EP 199
DI 10.1002/pbc.22935
PG 9
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 864RZ
UT WOS:000298259000008
PM 21337679
ER
PT J
AU Houghton, PJ
Lock, R
Carol, H
Morton, CL
Gorlick, R
Kolb, EA
Keir, ST
Reynolds, CP
Kang, H
Maris, JM
Billups, CA
Zhang, MX
Madden, SL
Teicher, BA
Smith, MA
AF Houghton, Peter J.
Lock, Richard
Carol, Hernan
Morton, Christopher L.
Gorlick, Richard
Kolb, E. Anders
Keir, Stephen T.
Reynolds, C. Patrick
Kang, H.
Maris, John M.
Billups, Catherine A.
Zhang, Mindy X.
Madden, Stephen L.
Teicher, Beverly A.
Smith, Malcolm A.
TI Testing of the topoisomerase 1 inhibitor Genz-644282 by the pediatric
preclinical testing program
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE developmental therapeutics; Genz-644282; preclinical testing
ID REFRACTORY SOLID TUMORS; PHASE-I TRIAL; CANCER MODELS; IRINOTECAN;
TOPOTECAN; XENOGRAFTS; CAMPTOTHECIN; EFFICACY; DRUG; CHILDREN
AB Background Genz-644282 is a novel non-camptothecin topoisomerase I poison that is in clinical development. Procedures. Genz-644282 was tested against the PPTP in vitro panel (0.1 nM to 1 mu M), and in vivo using three times per week x 2 schedule repeated at day 21 at its maximum tolerated dose (MTD) of 4 mg/kg. Subsequently Genz-644282 was tested at 4, 3, 2, and 1 mg/kg in 3 models to assess the dose-response relationship. mRNA gene signatures predictive for Genz-644282 response in vitro were applied to select 15 tumor models that were evaluated prospectively. Results. In vitro, Genz-644282 demonstrated potent cytotoxic activity with a median IC(50) of 1.2 nM (range 0.2-21.9 nM). In vivo, Genz-644282 at its MTD (4 mg/kg) induced maintained complete responses (MCR) in 6/6 evaluable solid tumor models. At 2 mg/kg Genz-644282 induced CR or MCR in 3/3 tumor models relatively insensitive to topotecan, but there were no objective responses at 1 mg/kg. Further testing at 2 mg/kg showed that Genz-644282 induced objective regressions in 7 of 17 (41%) models. There was a significant correlation between predictive response scores based on Affymetrix U133Plus2 baseline tumor expression profiles and the observed in vivo responses to Genz-644282. Conclusions. Genz-644282 was highly active within a narrow dose range (2-4 mg/kg), typical of other topoisomerase I poisons. As with other topoisomerase I poisons, how accurately these data will translate to clinical activity will depend upon the drug exposures that can be achieved in children treated with this agent. Pediatr Blood Cancer 2012; 58: 200-209. (C) 2011 Wiley Periodicals, Inc.
C1 [Houghton, Peter J.] Nationwide Childrens Hosp, Ctr Childhood Canc, Res Inst, Columbus, OH 43205 USA.
[Lock, Richard; Carol, Hernan; Billups, Catherine A.] Childrens Canc Inst Australia Med Res, Randwick, NSW, Australia.
[Morton, Christopher L.] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Gorlick, Richard] Childrens Hosp Montefiore, Bronx, NY USA.
[Kolb, E. Anders] Alfred I DuPont Hosp Children, Wilmington, DE USA.
[Keir, Stephen T.] Duke Univ, Med Ctr, Durham, NC USA.
[Reynolds, C. Patrick; Kang, H.] Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
[Maris, John M.] Univ Penn, Childrens Hosp, Sch Med, Philadelphia, PA 19104 USA.
[Maris, John M.] Univ Penn, Childrens Hosp, Abramson Family Canc Res Inst, Philadelphia, PA 19104 USA.
[Zhang, Mindy X.; Madden, Stephen L.] Genzyme Corp, Framingham, MA 01701 USA.
[Teicher, Beverly A.] NCI, Dev Therapeut Program, Bethesda, MD 20892 USA.
[Smith, Malcolm A.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Houghton, PJ (reprint author), Nationwide Childrens Hosp, Ctr Childhood Canc, Res Inst, 700 Childrens Dr, Columbus, OH 43205 USA.
EM Peter.Houghton@nationwidechildrens.org
RI Houghton, Peter/E-3265-2011; Carol, Hernan/F-5750-2013; Lock,
Richard/G-4253-2013;
OI Carol, Hernan/0000-0002-9443-8032; Reynolds, C.
Patrick/0000-0002-2827-8536
FU National Cancer Institute [NO1-CM-42216, CA21765, CA108786]
FX Grant sponsor: National Cancer Institute; Grant numbers: NO1-CM-42216,
CA21765, CA108786.
NR 39
TC 2
Z9 2
U1 0
U2 2
PU WILEY PERIODICALS, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN STREET, MALDEN, MA 02148-529 USA
SN 1545-5009
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD FEB
PY 2012
VL 58
IS 2
BP 200
EP 209
DI 10.1002/pbc.23016
PG 10
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 864RZ
UT WOS:000298259000009
PM 21548007
ER
PT J
AU Phipps, S
Buckholdt, KE
Fernandez, L
Wiener, L
Kupst, MJ
Madan-Swain, A
Mullins, L
Robert, R
Sahler, OJ
Vincent, N
Noll, RB
AF Phipps, Sean
Buckholdt, Kelly E.
Fernandez, Laly
Wiener, Lori
Kupst, Mary Jo
Madan-Swain, Avi
Mullins, Larry
Robert, Rhonda
Sahler, Olle Jane
Vincent, Nicole
Noll, Robert B.
TI Pediatric oncologists' practices of prescribing selective serotonin
reuptake inhibitors (SSRIs) for children and adolescents with cancer: A
multi-site study
SO PEDIATRIC BLOOD & CANCER
LA English
DT Article
DE antidepressants; depression; FDA; psychology; supportive care
ID DEPRESSIVE SYMPTOMS; ADAPTIVE STYLE; METAANALYSIS; PREVALENCE;
MEDICATION
AB Objective To survey pediatric oncologists regarding prescription of selective serotonin reuptake inhibitors (SSRIs) and related medications for the treatment of depression and anxiety disorders in children with cancer. Specifically, we sought to determine (a) how frequently pediatric oncologists prescribed SSRIs and what were the most commonly prescribed agents; (b) how decisions were made to prescribe, particularly whether mental health professionals were consulted; (c) how patients were monitored while on the agents; and (d) how the FDA black box warning has affected prescribing practices. Method. Oncologists from nine children's cancer centers (N = 151) from across the U.S. were surveyed, responding to either on- line or paper versions of a questionnaire developed for this study. Results. A majority of oncologists (71%) reported prescribing SSRIs for their patients. Oncologists reported difficulties differentiating symptoms of depression from aspects of cancer treatment. Mental health practitioners are consulted occasionally but not routinely, and oncologists reported a need for increased mental health resources. Approximately half of oncologists (51%) reported that the FDA black box warning had not affected their practice. In addition, only 28% reported monitoring patients on SSRIs at FDA recommended intervals, and only 9% indicated assessing for suicidality. Conclusions. Prescription of SSRIs is a common practice of pediatric oncologists, often without consultation with mental health professionals. Post- prescription monitoring appears to be suboptimal, and does not follow FDA guidelines. Pediatr Blood Cancer. Pediatr Blood Cancer 2012: 58: 210- 215. (C) 2011 Wiley Periodicals, Inc.
C1 [Phipps, Sean; Buckholdt, Kelly E.] St Jude Childrens Res Hosp, Dept Behav Med, Memphis, TN 38105 USA.
[Fernandez, Laly; Noll, Robert B.] Childrens Hosp Pittsburgh, Child Dev Unit, Pittsburgh, PA 15213 USA.
[Wiener, Lori] NCI, Bethesda, MD 20892 USA.
[Kupst, Mary Jo] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Madan-Swain, Avi] Univ Alabama Birmingham, Dept Pediat, Birmingham, AL USA.
[Mullins, Larry] Oklahoma State Univ, Dept Psychol, Stillwater, OK 74078 USA.
[Robert, Rhonda] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Sahler, Olle Jane] Univ Rochester, Med Ctr, Golisano Childrens Hosp, Rochester, NY 14642 USA.
[Vincent, Nicole] Childrens Hosp Orange Cty, Orange, CA 92668 USA.
RP Phipps, S (reprint author), St Jude Childrens Res Hosp, Dept Psychol, 262 Danny Thomas Pl, Memphis, TN 38105 USA.
EM sean.phipps@stjude.org
NR 21
TC 4
Z9 4
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1545-5009
EI 1545-5017
J9 PEDIATR BLOOD CANCER
JI Pediatr. Blood Cancer
PD FEB
PY 2012
VL 58
IS 2
BP 210
EP 215
DI 10.1002/pbc.22788
PG 6
WC Oncology; Hematology; Pediatrics
SC Oncology; Hematology; Pediatrics
GA 864RZ
UT WOS:000298259000010
PM 21284076
ER
PT J
AU Wilson, ST
Stanley, B
Brent, DA
Oquendo, MA
Huang, YY
Haghighi, F
Hodgkinson, CA
Mann, JJ
AF Wilson, Scott T.
Stanley, Barbara
Brent, David A.
Oquendo, Maria A.
Huang, Yung-yu
Haghighi, Fatemeh
Hodgkinson, Colin A.
Mann, J. John
TI Interaction between tryptophan hydroxylase I polymorphisms and childhood
abuse is associated with increased risk for borderline personality
disorder in adulthood
SO PSYCHIATRIC GENETICS
LA English
DT Article
DE A218C; borderline personality disorder; childhood abuse; G-6526A;
suicide; tryptophan hydroxylase I
ID POSTTRAUMATIC-STRESS-DISORDER; DELIBERATE SELF-HARM; DORSAL RAPHE
NUCLEUS; A218C POLYMORPHISM; SUICIDAL-BEHAVIOR; COMMUNITY SAMPLE;
MESSENGER-RNA; TPH GENE; SEROTONIN; PSYCHOPATHOLOGY
AB Introduction Borderline personality disorder (BPD) is a severe disorder with high morbidity and mortality, but unknown etiology. Childhood abuse has been proposed as an etiological factor, but the mechanism by which an abuse history could influence the risk for BPD has not been determined. The aim of this study was to determine whether the tryptophan hydroxylase 1 (TPH1) gene is related to BPD in a clinical sample, and whether TPH1 genotypes or haplotypes moderate the relationship between abuse history and BPD.
Methods Three hundred and ninety-eight patients diagnosed with mood disorders were genotyped for TPH1 G-6526A promoter polymorphism (rs4537731) and the A218C intron 7 polymorphism (rs1800532) and a set of ancestry informative markers, assessed for Diagnostic and Statistical Manual of Mental Disorders, 4th edition diagnoses, and assessed for a history of physical and sexual abuse.
Results Patients with a diagnosis of BPD were more likely to be risk allele carriers (A alleles at both loci) than the non-BPD group. Logistic regression analysis predicting BPD diagnosis with both single-nucleotide polymorphisms and haplotypes showed significant interaction effects between genotype and abuse history. Poisson regression predicting the number of BPD diagnostic criteria met with the same predictor set also included a significant interaction term. Risk allele carriers with a history of abuse had an increased likelihood of a BPD diagnosis.
Conclusion Variation in TPH1may increase risk for developing BPD as a result of childhood abuse. Elements of BPD pathology may be due in part to a genetically influenced serotonergic dysfunction, which in turn may lead to a differential response to environmental stressors. Psychiatr Genet 22: 15-24 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
C1 [Wilson, Scott T.] New York State Psychiat Inst & Hosp, Dept Mol Imaging & Neuropathol, Unit 42, Div Mol Imaging & Neuropathol, New York, NY 10032 USA.
[Wilson, Scott T.; Stanley, Barbara; Oquendo, Maria A.; Huang, Yung-yu; Mann, J. John] Columbia Univ Coll Phys & Surg, Dept Psychiat, New York, NY 10032 USA.
[Stanley, Barbara] CUNY, John Jay Coll, Dept Psychol, New York, NY 10021 USA.
[Brent, David A.] Univ Pittsburgh, Med Ctr, Dept Psychiat, New York, NY USA.
[Hodgkinson, Colin A.] NIAAA, Neurogenet Lab, New York, NY USA.
RP Wilson, ST (reprint author), New York State Psychiat Inst & Hosp, Dept Mol Imaging & Neuropathol, Unit 42, Div Mol Imaging & Neuropathol, 1051 Riverside Dr, New York, NY 10032 USA.
EM stw16@columbia.edu
RI Stanley, Barbara/J-8736-2013
FU National Institute of Mental Health [MH 48514, MH62185, MH59710,
MH61017, MH62665]; National Institute on Alcohol Abuse and Alcoholism
[AA15630]
FX This study was funded in part by grants from the National Institute of
Mental Health (MH 48514, MH62185, MH59710, MH61017, and MH62665) and the
National Institute on Alcohol Abuse and Alcoholism (AA15630).
NR 62
TC 10
Z9 10
U1 2
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0955-8829
J9 PSYCHIAT GENET
JI Psychiatr. Genet.
PD FEB
PY 2012
VL 22
IS 1
BP 15
EP 24
DI 10.1097/YPG.0b013e32834c0c4c
PG 10
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 866JN
UT WOS:000298376800002
PM 21989108
ER
PT J
AU Feng, Y
He, XZ
Yang, YL
Chao, DM
Lazarus, LH
Xia, Y
AF Feng, Yuan
He, Xiaozhou
Yang, Yilin
Chao, Dongman
Lazarus, Lawrence H.
Xia, Ying
TI Current Research on Opioid Receptor Function
SO CURRENT DRUG TARGETS
LA English
DT Article
DE Opioids; opioid receptors; neurotransmitters; function; brain; heart;
lung; ionic homeostasis; neuroprotection; hibernation; pain; hypoxia;
ischemia
ID MESSENGER-RNA EXPRESSION; INTRACELLULAR FREE CALCIUM; DIET-INDUCED
OBESITY; GUINEA-PIG HEART; PROTEIN-KINASE-C; HIPPOCAMPAL
HYPOXIA/HYPOGLYCEMIA MODEL; NOCICEPTIN/ORPHANIN FQ RECEPTOR;
MORPHINE-INDUCED ANALGESIA; ACUTE CEREBRAL-ISCHEMIA; TEMPORAL-LOBE
EPILEPSY
AB The use of opioid analgesics has a long history in clinical settings, although the comprehensive action of opioid receptors is still less understood. Nonetheless, recent studies have generated fresh insights into opioid receptor-mediated functions and their underlying mechanisms. Three major opioid receptors (mu-opioid receptor, MOR; delta-opioid receptor, DOR; and kappa-opioid receptor, KOR) have been cloned in many species. Each opioid receptor is functionally sub-classified into several pharmacological subtypes, although, specific gene corresponding each of these receptor subtypes is still unidentified as only a single gene has been isolated for each opioid receptor.
In addition to pain modulation and addiction, opioid receptors are widely involved in various physiological and pathophysiological activities, including the regulation of membrane ionic homeostasis, cell proliferation, emotional response, epileptic seizures, immune function, feeding, obesity, respiratory and cardiovascular control as well as some neurodegenerative disorders. In some species, they play an essential role in hibernation. One of the most exciting findings of the past decade is the opioid-receptor, especially DOR, mediated neuroprotection and cardioprotection. The upregulation of DOR expression and DOR activation increase the neuronal tolerance to hypoxic/ischemic stress. The DOR signal triggers (depending on stress duration and severity) different mechanisms at multiple levels to preserve neuronal survival, including the stabilization of homeostasis and increased pro-survival signaling (e.g., PKC-ERK-Bcl 2) and anti-oxidative capacity. In the heart, PKC and KATP channels are involved in the opioid receptor-mediated cardioprotection. The DOR-mediated neuroprotection and cardioprotection have the potential to significantly alter the clinical pharmacology in terms of prevention and treatment of life-threatening conditions like stroke and myocardial infarction.
The main purpose of this article is to review the recent work done on opioids and their receptor functions. It shall provide an informative reference for better understanding the opioid system and further elucidation of the opioid receptor function from a physiological and pharmacological point of view.
C1 [Feng, Yuan; Chao, Dongman; Xia, Ying] Yale Univ, Sch Med, New Haven, CT USA.
[He, Xiaozhou; Yang, Yilin] Soochow Univ, Clin Coll 3, Changzhou, Jiangsu, Peoples R China.
[Chao, Dongman; Xia, Ying] Univ Texas Houston, Med Sch Houston, Houston, TX 77030 USA.
[Lazarus, Lawrence H.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Feng, Yuan] Nanjing Med Univ, Affiliated Hosp 1, Nanjing, Jiangsu, Peoples R China.
RP Xia, Y (reprint author), Univ Texas Houston, Med Sch Houston, 6431 Fannin St, Houston, TX 77030 USA.
EM ying.xia@uth.tmc.edu
FU NIH [HD-34852, AT-004422]; Vivian L Smith Neurologic Foundation;
Intramural Research Program of the NIH; NIEHS
FX This work was supported by NIH (HD-34852 and AT-004422), Vivian L Smith
Neurologic Foundation and in part by the Intramural Research Program of
the NIH and NIEHS.
NR 314
TC 69
Z9 78
U1 2
U2 28
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1389-4501
J9 CURR DRUG TARGETS
JI Curr. Drug Targets
PD FEB
PY 2012
VL 13
IS 2
BP 230
EP 246
PG 17
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 204ND
UT WOS:000323371100009
PM 22204322
ER
PT J
AU Hoffert, JD
Pisitkun, T
Saeed, F
Song, JH
Chou, CL
Knepper, MA
AF Hoffert, Jason D.
Pisitkun, Trairak
Saeed, Fahad
Song, Jae H.
Chou, Chung-Lin
Knepper, Mark A.
TI Dynamics of the G Protein-coupled Vasopressin V2 Receptor Signaling
Network Revealed by Quantitative Phosphoproteomics
SO MOLECULAR & CELLULAR PROTEOMICS
LA English
DT Article
ID MEDULLARY COLLECTING DUCT; RENAL PRINCIPAL CELLS; BETA-CATENIN;
KINASE-A; IN-VIVO; AQUAPORIN-2 TRAFFICKING; LC-MS/MS; PHOSPHORYLATION;
IDENTIFICATION; ACTIVATION
AB G protein-coupled receptors (GPCRs) regulate diverse physiological processes, and many human diseases are due to defects in GPCR signaling. To identify the dynamic response of a signaling network downstream from a prototypical G(s)-coupled GPCR, the vasopressin V2 receptor, we have carried out multireplicate, quantitative phosphoproteomics with iTRAQ labeling at four time points following vasopressin exposure at a physiological concentration in cells isolated from rat kidney. A total of 12,167 phosphopeptides were identified from 2,783 proteins, with 273 changing significantly in abundance with vasopressin. Two-dimensional clustering of phosphopeptide time courses and Gene Ontology terms revealed that ligand binding to the V2 receptor affects more than simply the canonical cyclic adenosine monophosphate-protein kinase A and arrestin pathways under physiological conditions. The regulated proteins included key components of actin cytoskeleton remodeling, cell-cell adhesion, mitogen-activated protein kinase signaling, Wnt/beta-catenin signaling, and apoptosis pathways. These data suggest that vasopressin can regulate an array of cellular functions well beyond its classical role in regulating water and solute transport. These results greatly expand the current view of GPCR signaling in a physiological context and shed new light on potential roles for this signaling network in disorders such as polycystic kidney disease. Finally, we provide an online resource of physiologically regulated phosphorylation sites with dynamic quantitative data (http://helixweb.nih.gov/ESBL/Database/TiPD/index.html). Molecular & Cellular Proteomics 11: 10.1074/mcp.M111.014613, 1-15, 2012.
C1 [Hoffert, Jason D.; Pisitkun, Trairak; Saeed, Fahad; Song, Jae H.; Chou, Chung-Lin; Knepper, Mark A.] NHLBI, Epithelial Syst Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Hoffert, JD (reprint author), NHLBI, Epithelial Syst Biol Lab, NIH, Bldg 10,Rm 6N260,10 Ctr Dr, Bethesda, MD 20892 USA.
EM hoffertj@nhlbi.nih.gov
RI Saeed, Fahad/D-1545-2013;
OI Pisitkun, Trairak/0000-0001-6677-2271
FU National Institutes of Health, NHLBI [ZO1-HL001285]
FX This work was supported by the National Institutes of Health, NHLBI
intramural budget Grant ZO1-HL001285. The costs of publication of this
article were defrayed in part by the payment of page charges. This
article must therefore be hereby marked "advertisement" in accordance
with 18 U.S.C. Section 1734 solely to indicate this fact.
NR 79
TC 9
Z9 9
U1 1
U2 2
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 1535-9476
EI 1535-9484
J9 MOL CELL PROTEOMICS
JI Mol. Cell. Proteomics
PD FEB
PY 2012
VL 11
IS 2
AR M111.014613
DI 10.1074/mcp.M111.014613
PG 15
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 889EL
UT WOS:000300056200027
PM 22108457
ER
PT J
AU Wilke, M
Dechent, P
Schmidt-Samoa, C
AF Wilke, Melanie
Dechent, Peter
Schmidt-Samoa, Carsten
TI Experimental models for spatials Neglect (Studies in humans and
non-humans Primates)
SO NEUROFORUM
LA German
DT Article
DE spatial neglect; pulvinar; eye movements; visual awareness; attention
AB Spatial neglect is a debilitating neuropsychological disorder that is characterized by an impaired or lost ability to explore the space contralateral to the lesion and to react to stimuli presented on this side. Lesion sites that have been implicated in spatial neglect form a widely distributed network consisting of a number of cortical (i.e. fronto-parietal) and subcortical (i.e. thalamic) areas which are in healthy individuals activated during attentional and visuomotor tasks. While a detailed understanding of the brain circuits and mechanisms involved in spatial neglect is a prerequisite for the development of effective therapies, this has proven to be difficult in human patients, partly due to the extent and variability between lesion sites. Therefore, experimental models where pre-defined brain regions can be systematically inactivated are of great advantage. Neglect models have been developed in non-human primates where it is possible to pharmacologically inactivate small brain regions and in humans by means of non-invasive stimulation/inactivation methods such as transcranial magnetic stimulation. In this paper, we discuss theories about the mechanisms of spatial neglect such as the hemispheric imbalance model and the supporting experimental evidence, with an emphasis on imaging experiments that combined lesions with measures of dynamic brain activity.
C1 [Wilke, Melanie] NIMH, Bethesda, MD 20892 USA.
[Wilke, Melanie] CALTECH, Pasadena, CA 91125 USA.
[Wilke, Melanie] UMG, Abt Kognit Neurol, D-37075 Gottingen, Germany.
[Dechent, Peter] Biomed NMR Forsch GmbH, Munich, Germany.
[Dechent, Peter] UMG, Abt Kognit Neurol, Forsch Grp, D-37075 Gottingen, Germany.
[Schmidt-Samoa, Carsten] UMG, D-37075 Gottingen, Germany.
RP Wilke, M (reprint author), UMG, Abt Kognit Neurol, Robert Koch Str 40, D-37075 Gottingen, Germany.
EM melanie.wilke@med.uni-goettingen.de; pdechen@gwdg.de;
casten.schmidt-samoa@med.uni-goettingen.de
NR 9
TC 0
Z9 0
U1 1
U2 2
PU SPEKTRUM AKADEMISCHER VERLAG-SPRINGER-VERLAG GMBH
PI HEILDEBERG
PA TIERGARTENSTRASSE 17, HEILDEBERG, 69121, GERMANY
SN 0947-0875
EI 1868-856X
J9 NEUROFORUM
JI Neuroforum
PD FEB
PY 2012
VL 18
IS 1
BP 178
EP +
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA V33SH
UT WOS:000209038000002
ER
PT J
AU Guo, M
Lu, Y
Garza, JC
Li, Y
Chua, SC
Zhang, W
Lu, B
Lu, XY
AF Guo, M.
Lu, Y.
Garza, J. C.
Li, Y.
Chua, S. C.
Zhang, W.
Lu, B.
Lu, X-Y
TI Forebrain glutamatergic neurons mediate leptin action on depression-like
behaviors and synaptic depression
SO TRANSLATIONAL PSYCHIATRY
LA English
DT Article
DE behavioral depression; GluN2B subunit; glutamatergic neurons; leptin
receptor; NMDA receptors; synaptic depression
ID LONG-TERM DEPRESSION; PITUITARY-ADRENOCORTICAL AXIS; D-ASPARTATE
ANTAGONIST; TAIL SUSPENSION TEST; IN-VIVO; MOOD DISORDERS; RECEPTOR
GENE; ANIMAL-MODEL; ANTIDEPRESSANT ACTIVITY; HIPPOCAMPAL FUNCTION
AB The glutamatergic system has been implicated in the pathophysiology of depression and the mechanism of action of antidepressants. Leptin, an adipocyte-derived hormone, has antidepressant-like properties. However, the functional role of leptin receptor (Lepr) signaling in glutamatergic neurons remains to be elucidated. In this study, we generated conditional knockout mice in which the long form of Lepr was ablated selectively in glutamatergic neurons located in the forebrain structures, including the hippocampus and prefrontal cortex (Lepr cKO). Lepr cKO mice exhibit normal growth and body weight. Behavioral characterization of Lepr cKO mice reveals depression-like behavioral deficits, including anhedonia, behavioral despair, enhanced learned helplessness and social withdrawal, with no evident signs of anxiety. In addition, loss of Lepr in forebrain glutamatergic neurons facilitates N-methyl-D-aspartate (NMDA)-induced hippocampal long-term synaptic depression (LTD), whereas conventional LTD or long-term potentiation (LTP) was not affected. The facilitated LTD induction requires activation of the NMDA receptor GluN2B (NR2B) subunit as it was completely blocked by a selective GluN2B antagonist. Moreover, Lepr cKO mice are highly sensitive to the antidepressant-like behavioral effects of the GluN2B antagonist but resistant to leptin. These results support important roles for Lepr signaling in glutamatergic neurons in regulating depression-related behaviors and modulating excitatory synaptic strength, suggesting a possible association between synaptic depression and behavioral manifestation of behavioral depression. Translational Psychiatry (2012) 2, e83; doi:10.1038/tp.2012.9; published online 21 February 2012
C1 [Guo, M.; Garza, J. C.; Zhang, W.; Lu, X-Y] Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, San Antonio, TX 78229 USA.
[Lu, Y.; Lu, B.] NIMH, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
[Li, Y.] Univ Alabama Birmingham, Sch Med, Dept Neurol, Birmingham, AL USA.
[Chua, S. C.] Albert Einstein Coll Med, Dept Med, New York, NY USA.
[Chua, S. C.] Albert Einstein Coll Med, Dept Neurosci, New York, NY USA.
[Lu, B.] GlaxoSmithKline, R&D China, Shanghai 201203, Peoples R China.
[Lu, X-Y] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
RP Lu, XY (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Pharmacol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM bai.b.lu@gsk.com; lux3@uthscsa.edu
RI Li, Yuqing/G-1596-2011; Lu, Xin-Yun/M-8657-2016
OI Li, Yuqing/0000-0003-1211-5529;
FU NIH [NIMH 076929, NIMH 073844]; NRSA [NIMH 83442]; NICHD; NIMH
FX This work was supported by the NIH Grants NIMH 076929 and NIMH 073844
(to X-YL), the NRSA predoctoral fellowship award NIMH 83442 (to JCG) and
funds from intramural research programs of the NICHD and NIMH (to BL).
NR 113
TC 30
Z9 31
U1 1
U2 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2158-3188
J9 TRANSL PSYCHIAT
JI Transl. Psychiatr.
PD FEB
PY 2012
VL 2
AR e83
DI 10.1038/tp.2012.9
PG 15
WC Psychiatry
SC Psychiatry
GA 104JW
UT WOS:000315989800008
PM 22408745
ER
PT J
AU Ambatipudi, S
Gerstung, M
Pandey, M
Samant, T
Patil, A
Kane, S
Desai, RS
Schaffer, AA
Beerenwinkel, N
Mahimkar, MB
AF Ambatipudi, Srikant
Gerstung, Moritz
Pandey, Manishkumar
Samant, Tanuja
Patil, Asawari
Kane, Shubhada
Desai, Rajiv S.
Schaeffer, Alejandro A.
Beerenwinkel, Niko
Mahimkar, Manoj B.
TI Genome-wide expression and copy number analysis identifies driver genes
in gingivobuccal cancers
SO GENES CHROMOSOMES & CANCER
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; LYMPH-NODE METASTASIS; ORAL-CANCER; MICROARRAY
ANALYSIS; TUMOR-ANGIOGENESIS; DNA AMPLIFICATION; CDNA MICROARRAY;
DOWN-REGULATION; POOR SURVIVAL; TONGUE CANCER
AB The molecular mechanisms contributing to the development and progression of gingivobuccal complex (GBC) cancersa sub-site of oral cancer, comprising the buccal mucosa, the gingivobuccal sulcus, the lower gingival region, and the retromolar trigoneremain poorly understood. Identifying the GBC cancer-related gene expression signature and the driver genes residing on the altered chromosomal regions is critical for understanding the molecular basis of its pathogenesis. Genome-wide expression profiling of 27 GBC cancers with known chromosomal alterations was performed to reveal differentially expressed genes. Putative driver genes were identified by integrating copy number and gene expression data. A total of 315 genes were found differentially expressed (P = 0.05, logFC > 2.0) of which 11 genes were validated by real-time quantitative reverse transcriptase-PCR (qRT-PCR) in tumors (n = 57) and normal GBC tissues (n = 18). Overexpression of LY6K, in chromosome band 8q24.3, was validated by immunohistochemical (IHC) analysis. We found that 78.5% (2,417/3,079) of the genes located in regions of recurrent chromosomal alterations show copy number dependent expression indicating that copy number alteration has a direct effect on global gene expression. The integrative analysis revealed BIRC3 in 11q22.2 as a candidate driver gene associated with poor clinical outcome. Our study identified previously unreported differentially expressed genes in a homogeneous subtype of oral cancer and the candidate driver genes that may contribute to the development and progression of the disease. (C) 2011 Wiley Periodicals, Inc.
C1 [Ambatipudi, Srikant; Pandey, Manishkumar; Samant, Tanuja; Mahimkar, Manoj B.] TMC, ACTREC, CRI, Kharghar 410210, Navi Mumbai, India.
[Gerstung, Moritz; Beerenwinkel, Niko] Swiss Fed Inst Technol, Dept Biosyst Sci & Engn, CH-4058 Basel, Switzerland.
[Gerstung, Moritz; Beerenwinkel, Niko] Swiss Inst Bioinformat, CH-4058 Basel, Switzerland.
[Patil, Asawari; Kane, Shubhada] Tata Mem Hosp, TMC, Dept Pathol, Bombay 400012, Maharashtra, India.
[Desai, Rajiv S.] Nair Hosp Dent Coll, Dept Oral Pathol & Microbiol, Bombay 400008, Maharashtra, India.
[Schaeffer, Alejandro A.] NIH, Computat Biol Branch, Natl Ctr Biotechnol Informat, DHHS, Bethesda, MD 20894 USA.
RP Mahimkar, MB (reprint author), TMC, ACTREC, CRI, Kharghar 410210, Navi Mumbai, India.
EM mmahimkar@actrec.gov.in
RI Schaffer, Alejandro/F-2902-2012; Ambatipudi, Srikant/J-4648-2012;
OI Gerstung, Moritz/0000-0001-6709-963X; AMBATIPUDI,
SRIKANT/0000-0003-3102-3603
FU Lady Tata Memorial Trust, Mumbai; Council of Scientific and Industrial
Research [27(0207)/09/EMR-II]; National Institutes of Health, NLM;
SystemsX.ch [2009/024]
FX Supported by: Lady Tata Memorial Trust, Mumbai, and the Council of
Scientific and Industrial Research, Grant number: 27(0207)/09/EMR-II;
Intramural Research program of the National Institutes of Health, NLM;
SystemsX.ch, Grant number: 2009/024.
NR 61
TC 17
Z9 18
U1 0
U2 3
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1045-2257
J9 GENE CHROMOSOME CANC
JI Gene Chromosomes Cancer
PD FEB
PY 2012
VL 51
IS 2
BP 161
EP 173
DI 10.1002/gcc.20940
PG 13
WC Oncology; Genetics & Heredity
SC Oncology; Genetics & Heredity
GA 857QS
UT WOS:000297734400006
PM 22072328
ER
PT J
AU Follmann, D
Proschan, M
AF Follmann, Dean
Proschan, Michael
TI A test of location for exchangeable multivariate normal data with
unknown correlation
SO JOURNAL OF MULTIVARIATE ANALYSIS
LA English
DT Article
DE Confidence interval; Within cluster resampling; Likelihood ratio test
ID MULTIPLE END-POINTS; P-VALUES
AB We consider the problem of testing whether the common mean of a single n-vector of multivariate normal random variables with known variance and unknown common correlation rho is zero. We derive the standardized likelihood ratio test for known rho and explore different ways of proceeding with rho unknown. We evaluate the performance of the standardized statistic where rho is replaced with an estimate of rho and determine the critical value c(n) that controls the type I error rate for the least favorable rho in [0,1]. The constant c(n) increases with n and this procedure has pathological behavior if rho depends on n and rho(n) converges to zero at a certain rate. As an alternate approach, we replace rho with the upper limit of a (1 - beta(n)) confidence interval chosen so that c(n) = c for all n. We determine beta(n) so that the type I error rate is exactly controlled for all rho in [0,1]. We also investigate a simpler approach where we bound the type I error rate. The former method performs well for all n while the less powerful bound method may be a useful in some settings as a simple approach. The proposed tests can be used in different applications, including within-cluster resampling and combining exchangeable p-values. Published by Elsevier Inc.
C1 [Follmann, Dean; Proschan, Michael] NIAID, Biostat Res Branch, Bethesda, MD 20892 USA.
RP Follmann, D (reprint author), NIAID, Biostat Res Branch, 6700B Rockledge Dr,MSC 7609, Bethesda, MD 20892 USA.
EM dfollmann@niaid.nih.gov
FU Intramural NIH HHS [Z99 AI999999]
NR 8
TC 0
Z9 0
U1 1
U2 3
PU ELSEVIER INC
PI SAN DIEGO
PA 525 B STREET, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0047-259X
J9 J MULTIVARIATE ANAL
JI J. Multivar. Anal.
PD FEB
PY 2012
VL 104
IS 1
BP 115
EP 125
DI 10.1016/j.jmva.2011.07.003
PG 11
WC Statistics & Probability
SC Mathematics
GA 826KR
UT WOS:000295353500008
PM 22125347
ER
PT J
AU Tyagi, M
Thangudu, RR
Zhang, DC
Bryant, SH
Madej, T
Panchenko, AR
AF Tyagi, Manoj
Thangudu, Ratna R.
Zhang, Dachuan
Bryant, Stephen H.
Madej, Thomas
Panchenko, Anna R.
TI Homology Inference of Protein-Protein Interactions via Conserved Binding
Sites
SO PLOS ONE
LA English
DT Article
ID INTERACTION NETWORKS; PREDICTION; SEQUENCE; CLASSIFICATION; ANNOTATION;
DIVERGENCE; INTEROLOGS; COMPLEXES; DATABASE; SERVER
AB The coverage and reliability of protein-protein interactions determined by high-throughput experiments still needs to be improved, especially for higher organisms, therefore the question persists, how interactions can be verified and predicted by computational approaches using available data on protein structural complexes. Recently we developed an approach called IBIS (Inferred Biomolecular Interaction Server) to predict and annotate protein-protein binding sites and interaction partners, which is based on the assumption that the structural location and sequence patterns of protein-protein binding sites are conserved between close homologs. In this study first we confirmed high accuracy of our method and found that its accuracy depends critically on the usage of all available data on structures of homologous complexes, compared to the approaches where only a non-redundant set of complexes is employed. Second we showed that there exists a trade-off between specificity and sensitivity if we employ in the prediction only evolutionarily conserved binding site clusters or clusters supported by only one observation (singletons). Finally we addressed the question of identifying the biologically relevant interactions using the homology inference approach and demonstrated that a large majority of crystal packing interactions can be correctly identified and filtered by our algorithm. At the same time, about half of biological interfaces that are not present in the protein crystallographic asymmetric unit can be reconstructed by IBIS from homologous complexes without the prior knowledge of crystal parameters of the query protein.
C1 [Tyagi, Manoj; Thangudu, Ratna R.; Zhang, Dachuan; Bryant, Stephen H.; Madej, Thomas; Panchenko, Anna R.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Tyagi, M (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM madej@ncbi.nlm.nih.gov; panch@ncbi.nlm.nih.gov
RI Tyagi, Manoj/K-8438-2014
FU National Institutes of Health/Department of Health and Human Services of
the National Library of Medicine
FX This work was supported by the National Institutes of Health/Department
of Health and Human Services Intramural Research program of the National
Library of Medicine. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 47
TC 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 1932-6203
J9 PLOS ONE
JI PLoS One
PD JAN 31
PY 2012
VL 7
IS 1
AR e28896
DI 10.1371/journal.pone.0028896
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 912BY
UT WOS:000301770700003
PM 22303436
ER
PT J
AU Todd, CA
Greene, KM
Yu, XS
Ozaki, DA
Gao, HM
Huang, YD
Wang, M
Li, G
Brown, R
Wood, B
D'Souza, MP
Gilbert, P
Montefiori, DC
Sarzotti-Kelsoe, M
AF Todd, Christopher A.
Greene, Kelli M.
Yu, Xuesong
Ozaki, Daniel A.
Gao, Hongmei
Huang, Yunda
Wang, Maggie
Li, Gary
Brown, Ronald
Wood, Blake
D'Souza, M. Patricia
Gilbert, Peter
Montefiori, David C.
Sarzotti-Kelsoe, Marcella
TI Development and implementation of an international proficiency testing
program for a neutralizing antibody assay for HIV-1 in TZM-bl cells
SO JOURNAL OF IMMUNOLOGICAL METHODS
LA English
DT Article
DE Neutralizing; Antibody; Assay; Proficiency; HIV; TZM-bl
ID IMMUNODEFICIENCY-VIRUS TYPE-1; FUSION INHIBITOR T-20; ENV CLONES;
INFECTIONS; NETWORK; CCR5
AB Recent advances in assay technology have led to major improvements in how HIV-1 neutralizing antibodies are measured. A luciferase reporter gene assay performed in TZM-bl (JC53bl-13) cells has been optimized and validated. Because this assay has been adopted by multiple laboratories worldwide, an external proficiency testing program was developed to ensure data equivalency across laboratories performing this neutralizing antibody assay for HIV/AIDS vaccine clinical trials.
The program was optimized by conducting three independent rounds of testing, with an increased level of stringency from the first to third round. Results from the participating domestic and international laboratories improved each round as factors that contributed to interassay variability were identified and minimized. Key contributors to increased agreement were experience among laboratories and standardization of reagents.
A statistical qualification rule was developed using a simulation procedure based on the three optimization rounds of testing, where a laboratory qualifies if at least 25 of the 30 ID50 values lie within the acceptance ranges. This ensures no more than a 20% risk that a participating laboratory fails to qualify when it should, as defined by the simulation procedure. Five experienced reference laboratories were identified and tested a series of standardized reagents to derive the acceptance ranges for pass-fail criteria. This Standardized Proficiency Testing Program is the first available for the evaluation and documentation of assay equivalency for laboratories performing HIV-1 neutralizing antibody assays and may provide guidance for the development of future proficiency testing programs for other assay platforms. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Todd, Christopher A.; Greene, Kelli M.; Ozaki, Daniel A.; Gao, Hongmei; Montefiori, David C.; Sarzotti-Kelsoe, Marcella] Duke Univ, Med Ctr, Durham, NC 27705 USA.
[Yu, Xuesong; Huang, Yunda; Wang, Maggie; Wood, Blake; Gilbert, Peter] Fred Hutchinson Canc Res Ctr, Stat Ctr HIV AIDS Res & Prevent, Seattle, WA 98104 USA.
[Li, Gary; Brown, Ronald] Qual Biol Inc, Gaithersburg, MD USA.
[D'Souza, M. Patricia] NIAID, NIH, Div Aids, Bethesda, MD 20892 USA.
RP Sarzotti-Kelsoe, M (reprint author), Duke Univ, Med Ctr, 2812 Erwin Rd,Ste 301,Erwin Terrace 2, Durham, NC 27705 USA.
EM chris.todd@duke.edu; kelli.greene@duke.edu; xyu@scharp.org;
daniel.ozaki@dm.duke.edu; hongmei.gao@duke.edu; yunda@scharp.org;
maggie@fhcrc.org; lig@qualitybiological.com;
brownr@qualitybiological.com; geebeewood@gmail.com;
pdsouza@niaid.nih.gov; pgilbert@scharp.org; monte@duke.edu;
marcella.sarzottikelsoe@dm.duke.edu
FU Bill & Melinda Gates Foundation [38619]; Collaboration for AIDS Vaccine
Discovery/Vaccine Immunology Statistical Center [38744]; National
Institutes of Health [AI30034]; NIH/NIAID, Quality Biological, Inc.
FX This program is jointly supported by the Bill & Melinda Gates
Foundation's Collaboration for AIDS Vaccine Discovery/Comprehensive
Antibody Vaccine Immune Monitoring Consortium, grant number 38619,
Collaboration for AIDS Vaccine Discovery/Vaccine Immunology Statistical
Center, grant number 38744, National Institutes of Health grant AI30034,
and the NIH/NIAID Reagent Resource Support Program for AIDS Vaccine
Development, Quality Biological, Inc., Gaithersburg, MD. This paper was
submitted by one author in her capacity as an employee of NIH, but the
views expressed in this paper do not necessarily represent those of NIH.
We also thank all of the laboratories that participated in the
development of this program.
NR 17
TC 18
Z9 18
U1 0
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-1759
J9 J IMMUNOL METHODS
JI J. Immunol. Methods
PD JAN 31
PY 2012
VL 375
IS 1-2
BP 57
EP 67
DI 10.1016/j.jim.2011.09.007
PG 11
WC Biochemical Research Methods; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 900TO
UT WOS:000300913300008
PM 21968254
ER
PT J
AU Weiss, GE
Ndungu, FM
McKittrick, N
Li, SP
Kimani, D
Crompton, PD
Marsh, K
Pierce, SK
AF Weiss, Greta E.
Ndungu, Francis M.
McKittrick, Noah
Li, Shanping
Kimani, Domtila
Crompton, Peter D.
Marsh, Kevin
Pierce, Susan K.
TI High efficiency human memory B cell assay and its application to
studying Plasmodium falciparum-specific memory B cells in natural
infections
SO JOURNAL OF IMMUNOLOGICAL METHODS
LA English
DT Article
DE Memory B cells; B cell ELISPOT; Plasmodium falciparum; Malaria
ID MALARIA-ENDEMIC AREA; PLASMA-CELLS; DIFFERENTIATION; INDIVIDUALS;
ANTIGENS; IMMUNITY
AB Memory B cells (MBCs) are a key component of long term humoral immunity to many human infectious diseases. Despite their importance, we know little about the generation or maintenance of antigen-(Ag)-specific MBCs in humans in response to infection. A frequently employed method for quantifying Ag-specific MBCs in human peripheral blood (Crotty et al., 2004) relies on the ability of MBCs but not naive B cells to differentiate into antibody secreting cells (ASCs) in response to polyclonal activators and Toll-like receptor agonists in vitro and the measurement of Ag-specific ASCs by ELISPOT assays. Here we report on studies to optimize the efficiency of this ELISPOT-based assay and to apply this assay to the detection of Plasmodium falciparum (PP-specific MBCs in adults living in a malaria endemic area where immunity to Pf is acquired through natural infection. We show that the addition of IL-10 to in vitro cultures of human peripheral blood mononuclear cells increased the efficiency of the assay from 10% to over 90% without increasing the ASC burst size and without any substantial increase in background from naive B cells or plasma cells (PCs). Using this assay we were able to quantify the frequency of Pf-specific MBCs in peripheral blood of adults living in a malaria endemic area. Thus, this highly efficient assay appears to be well suited to field studies of the generation and maintenance of MBCs where the volumes of blood obtainable are often limiting. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Weiss, Greta E.; Li, Shanping; Crompton, Peter D.; Pierce, Susan K.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Ndungu, Francis M.; Kimani, Domtila; Marsh, Kevin] Kenya Govt Med Res Ctr, Ctr Geog Med Res Coast, Kilifi 80108, Kenya.
[McKittrick, Noah] Univ Penn, Philadelphia, PA 19104 USA.
RP Weiss, GE (reprint author), NIAID, Immunogenet Lab, NIH, Twinbrook 2,12441 Parklawn Dr,Room 213, Rockville, MD 20852 USA.
EM weiss@burnet.edu.au
RI Crompton, Peter/N-1130-2016;
OI McKittrick, Noah/0000-0001-6277-2733
FU Intramural NIH HHS [ZIA AI000949-06]; Wellcome Trust [092654]
NR 20
TC 14
Z9 14
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-1759
J9 J IMMUNOL METHODS
JI J. Immunol. Methods
PD JAN 31
PY 2012
VL 375
IS 1-2
BP 68
EP 74
DI 10.1016/j.jim.2011.09.006
PG 7
WC Biochemical Research Methods; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 900TO
UT WOS:000300913300009
PM 21963949
ER
PT J
AU Memon, SA
Sportes, C
Flomerfelt, FA
Gress, RE
Hakim, FT
AF Memon, Sarfraz A.
Sportes, Claude
Flomerfelt, Francis A.
Gress, Ronald E.
Hakim, Frances T.
TI Quantitative analysis of T cell receptor diversity in clinical samples
of human peripheral blood
SO JOURNAL OF IMMUNOLOGICAL METHODS
LA English
DT Article
DE TCR V beta CDR3 repertoire diversity in human peripheral blood;
Spectratype; Immune reconstitution; Hematopoietic stem cell
transplantation
ID TUMOR-INFILTRATING LYMPHOCYTES; MULTIPLE-SCLEROSIS PATIENTS; V-BETA
REPERTOIRE; MARROW-TRANSPLANTATION; ANTIRETROVIRAL THERAPY; IMMUNE
RECONSTITUTION; STATISTICAL-ANALYSIS; SPECTRATYPE ANALYSIS; CLONAL
DOMINANCE; THYMIC FUNCTION
AB The analysis of T cell receptor diversity provides a clinically relevant and sensitive marker of repertoire loss, gain, or skewing. Spectratyping is a broadly utilized technique to measure global TCR diversity by the analysis of the lengths of CDR3 fragments in each V beta family. However the common use of large numbers of T cells to obtain a global view of TCR V beta CDR3 diversity has restricted spectratyping analyses when limited T-cell numbers are available in clinical setting, such as following transplant regimens.
We here demonstrate that one hundred thousand T cells are sufficient to obtain a robust, highly reproducible measure of the global TCR V beta repertoire diversity among twenty V beta families in human peripheral blood. We also show that use of lower cell number results not in a dwindling of observed diversity but rather in non-reproducible patterns in replicate spectratypes. Finally, we report here a simple to use but sensitive method to quantify repertoire divergence in patient samples by comparison to a standard repertoire profile we generated from fifteen normal donors. We provide examples using this method to statistically evaluate the changes in the global TCR V beta repertoire diversity that may take place during T subset immune reconstitution after hematopoietic stem cell transplantation or after immune modulating therapies. Published by Elsevier B.V.
C1 [Memon, Sarfraz A.; Sportes, Claude; Flomerfelt, Francis A.; Gress, Ronald E.; Hakim, Frances T.] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Memon, SA (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, 10 Ctr Dr,CRC Room 3-3288, Bethesda, MD 20892 USA.
EM memons@mail.nih.gov
RI Memon, Sarfraz/E-1198-2013;
OI Memon, Sarfraz/0000-0002-0164-9739
FU NIH, National Cancer Institute, Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research.
NR 51
TC 9
Z9 9
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-1759
J9 J IMMUNOL METHODS
JI J. Immunol. Methods
PD JAN 31
PY 2012
VL 375
IS 1-2
BP 84
EP 92
DI 10.1016/j.jim.2011.09.012
PG 9
WC Biochemical Research Methods; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 900TO
UT WOS:000300913300011
PM 21986106
ER
PT J
AU Oliveira, TY
Resch, W
Jankovic, M
Casellas, R
Nussenzweig, MC
Klein, IA
AF Oliveira, Thiago Y.
Resch, Wolfgang
Jankovic, Mila
Casellas, Rafael
Nussenzweig, Michel C.
Klein, Isaac A.
TI Translocation capture sequencing: A method for high throughput mapping
of chromosomal rearrangements
SO JOURNAL OF IMMUNOLOGICAL METHODS
LA English
DT Article
DE Chromosomal translocations; Genomic instability; Activation-induced
cytidine deaminase; B lymphocytes; Lymphoma
ID CLASS-SWITCH RECOMBINATION; CYTIDINE DEAMINASE AID; DOUBLE-STRAND
BREAKS; SOMATIC HYPERMUTATION; B-LYMPHOCYTES; CELL LYMPHOMAS; IG GENES;
C-MYC; ACTIVATION; DNA
AB Chromosomal translocations require formation and joining of DNA double strand breaks (DSBs). These events disrupt the integrity of the genome and are involved in producing leukemias, lymphomas and sarcomas. Translocations are frequent, clonal and recurrent in mature B cell lymphomas, which bear a particularly high DNA damage burden by virtue of activation-induced cytidine deaminase (AID) expression. Despite the ubiquity of genomic rearrangements, the forces that underlie their genesis are not well understood. Here, we provide a detailed description of a new method for studying these events, translocation capture sequencing (TC-Seq). TC-Seq provides the means to document chromosomal rearrangements genome-wide in primary cells, and to discover recombination hotspots. Demonstrating its effectiveness, we successfully estimate the frequency of c-myc/IgH translocations in primary B cells, and identify hotspots of AID-mediated recombination. Furthermore. TC-Seq can be adapted to generate genome-wide rearrangement maps in any cell type and under any condition. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Oliveira, Thiago Y.; Jankovic, Mila; Nussenzweig, Michel C.; Klein, Isaac A.] Rockefeller Univ, Lab Mol Immunol, New York, NY 10065 USA.
[Resch, Wolfgang; Casellas, Rafael] NIAMS, NIH, Bethesda, MD 20892 USA.
[Casellas, Rafael] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Oliveira, Thiago Y.] Univ Sao Paulo, Med Sch Ribeirao Preto, Dept Genet, Natl Inst Sci & Technol Stem Cells & Cell Therapy, BR-14051140 Ribeirao Preto, SP, Brazil.
[Oliveira, Thiago Y.] Ctr Cell Based Therapy, BR-14051140 Ribeirao Preto, SP, Brazil.
[Nussenzweig, Michel C.] Rockefeller Univ, Howard Hughes Med Inst, New York, NY 10065 USA.
RP Klein, IA (reprint author), Rockefeller Univ, Lab Mol Immunol, 1230 York Ave,Box 220, New York, NY 10065 USA.
EM iklein@rockefeller.edu
OI Oliveira, Thiago/0000-0002-2654-0879
FU NIH [AI037526]; NYSTEM [C023046]; The Starr Cancer Consortium; National
Institute of Arthritis and Musculoskeletal and Skin Diseases of the
National Institutes of Health; NIH MSTP [GM07739]
FX We thank all the members of the Nussenzweig and Casellas labs for
valuable input and advice, Klara Velinzon and Svetlana Mazel for
FACSorting and David Bosque and Thomas Eisenreich for animal management.
We also thank Scott Dewell of the Rockefeller Genomics Resource Center
and Gustavo Gutierrez of the NIAMS genome facility for high-throughput
sequencing and guidance. This work was supported by NIH grant #AI037526
to M.C.N., NYSTEM #C023046, The Starr Cancer Consortium and the
Intramural Research Program of the National Institute of Arthritis and
Musculoskeletal and Skin Diseases of the National Institutes of Health.
M.C.N. is an HHMI investigator. I.A.K. was supported by NIH MSTP grant
GM07739, and is a Cancer Research Institute Predoctoral Fellow and a
William Randolph Hearst Foundation Fellow.
NR 27
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U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0022-1759
J9 J IMMUNOL METHODS
JI J. Immunol. Methods
PD JAN 31
PY 2012
VL 375
IS 1-2
BP 176
EP 181
DI 10.1016/j.jim.2011.10.007
PG 6
WC Biochemical Research Methods; Immunology
SC Biochemistry & Molecular Biology; Immunology
GA 900TO
UT WOS:000300913300021
PM 22033343
ER
PT J
AU Gao, Y
Baccarelli, A
Shu, XO
Ji, BT
Yu, K
Tarantini, L
Yang, G
Li, HL
Hou, L
Rothman, N
Zheng, W
Gao, YT
Chow, WH
AF Gao, Y.
Baccarelli, A.
Shu, X. O.
Ji, B-T
Yu, K.
Tarantini, L.
Yang, G.
Li, H-L
Hou, L.
Rothman, N.
Zheng, W.
Gao, Y-T
Chow, W-H
TI Blood leukocyte Alu and LINE-1 methylation and gastric cancer risk in
the Shanghai Women's Health Study
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE gastric cancer; DNA methylation; leukocyte
ID GLOBAL DNA METHYLATION; HELICOBACTER-PYLORI INFECTION; CPG ISLAND
METHYLATION; GENOMIC DNA; PROMOTER METHYLATION; ENVIRONMENTAL
EPIGENOMICS; DISEASE SUSCEPTIBILITY; BLADDER-CANCER; GENE PROMOTER;
BREAST-CANCER
AB BACKGROUND: Recent data suggest a link between blood leukocyte DNA methylation, and cancer risk. However, reports on DNA methylation from a prospective study are unavailable for gastric cancer.
METHODS: We explored the association between methylation in pre-diagnostic blood leukocyte DNA and gastric cancer risk in a case-control study nested in the prospective Shanghai Women's Health Study cohort. Incident gastric cancer cases (n = 192) and matched controls (n = 384) were included in the study. Methylation of Alu and long interspersed nucleotide elements (LINE)-1 were evaluated using bisulphite pyrosequencing. Odds ratios (ORs) and 95% confidence intervals (CI) were calculated from logistic regression adjusting for potential confounders.
RESULTS: Alu methylation was inversely associated with gastric cancer risk, mainly among cases diagnosed one or more years after blood collection. After excluding cases diagnosed during the first year of follow-up, the ORs for the third, second, and first quartiles of Alu methylation compared with the highest quartile were 2.43 (1.43-4.13), 1.47 (0.85-2.57), and 2.22 (1.28-3.84), respectively. This association appeared to be modified by dietary intake, particularly isoflavone. In contrast, LINE-1 methylation levels were not associated with gastric cancer risk.
CONCLUSION: Evidence from this prospective study is consistent with the hypothesis that DNA hypomethylation in blood leukocytes may be related to cancer risk, including risk of gastric cancer. British Journal of Cancer (2012) 106, 585-591. doi: 10.1038/bjc.2011.562 www.bjcancer.com Published online 15 December 2011 (C) 2012 Cancer Research UK
C1 [Gao, Y.; Ji, B-T; Yu, K.; Li, H-L; Rothman, N.; Chow, W-H] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Baccarelli, A.] Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
[Shu, X. O.; Yang, G.; Zheng, W.] Vanderbilt Univ, Sch Med, Vanderbilt Epidemiol Ctr, Nashville, TN 37203 USA.
[Tarantini, L.] Univ Milan, Mangiagalli & Regina Elena IRCCS Fdn, Maggiore Policlin Hosp, Dept Environm & Occupat Hlth,Ctr Mol & Genet Epid, I-20122 Milan, Italy.
[Hou, L.] Northwestern Univ, Feinberg Sch Med, Dept Prevent Med, Chicago, IL 60611 USA.
[Hou, L.] Northwestern Univ, Feinberg Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Gao, Y-T] Shanghai Canc Inst, Dept Epidemiol, Shanghai 200032, Peoples R China.
RP Gao, Y (reprint author), NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd,Bldg EPS,Room 7110, Bethesda, MD 20892 USA.
EM gaoying@mail.nih.gov
OI Baccarelli, Andrea/0000-0002-3436-0640
FU Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health; NIEHS [ES00002]
FX This study was supported by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute,
National Institutes of Health. Dr Baccarelli is partially supported by
New Investigator funding from NIEHS (ES00002). Finally, we acknowledge
the study participants for donating their time and making this study
possible.
NR 54
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U1 0
U2 10
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 JAN 31
PY 2012
VL 106
IS 3
BP 585
EP 591
DI 10.1038/bjc.2011.562
PG 7
WC Oncology
SC Oncology
GA 892RC
UT WOS:000300302300021
PM 22173668
ER
PT J
AU Blank, MM
Wentzensen, N
Murphy, MA
Hollenbeck, A
Park, Y
AF Blank, M. M.
Wentzensen, N.
Murphy, M. A.
Hollenbeck, A.
Park, Y.
TI Dietary fat intake and risk of ovarian cancer in the NIH-AARP Diet and
Health Study
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE dietary fat; ovarian cancer; cohort studies
ID RETIRED-PERSONS DIET; AMERICAN-ASSOCIATION; LOGISTIC-REGRESSION;
NATIONAL-INSTITUTES; HISTOLOGIC TYPE; COHORT; METAANALYSIS; VALIDATION
AB BACKGROUND: Fat intake has been postulated to increase risk of ovarian cancer, but previous studies have reported inconsistent results.
METHODS: The NIH-AARP Diet and Health Study, a large prospective cohort, assessed diet using a food frequency questionnaire at baseline in 1995-1996. During an average of 9 years of follow-up, 695 ovarian cancer cases were ascertained through the state cancer registry database. The relative risks (RRs) and 95% confidence interval (CI) were estimated using a Cox proportional hazard model.
RESULTS: Women in the highest vs the lowest quintile of total fat intake had a 28% increased risk of ovarian cancer (RRQ5 (vs Q1) = 1.28, 95% CI: 1.01-1.63). Fat intake from animal sources (RRQ5 (vs Q1) = 1.30; 95% CI: 1.02-1.66), but not from plant sources, was positively associated with ovarian cancer risk. Saturated and monounsaturated fat intakes were not related to risk of ovarian cancer, but polyunsaturated fat intake showed a weak positive association. The association between total fat intake and ovarian cancer was stronger in women who were nulliparous or never used oral contraceptives.
CONCLUSION: Fat intake, especially from animal sources, was related to an increased risk of ovarian cancer. The association may be modified by parity and oral contraceptive use, which warrants further investigation. British Journal of Cancer (2012) 106, 596-602. doi: 10.1038/bjc.2011.572 www.bjcancer.com Published online 5 January 2012 (C) 2012 Cancer Research UK
C1 [Blank, M. M.; Wentzensen, N.; Murphy, M. A.; Park, Y.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD 20852 USA.
[Murphy, M. A.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Hollenbeck, A.] AARP, Washington, DC 20049 USA.
RP Park, Y (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, 6120 Execut Blvd, Rockville, MD 20852 USA.
EM parkyik@mail.nih.gov
OI Park, Yikyung/0000-0002-6281-489X
FU Florida Department of Health (FDOH); National Cancer Institute, National
Institutes of Health; NIH [5 T32 CA09001-35]
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). 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. We are deeply saddened by the loss of Dr
Arthur Schatzkin, the principal investigator for the NIH-AARP Diet and
Health Study, who passed away on 20 January 2011. The study was
supported by the Intramural Research Program of the National Cancer
Institute, National Institutes of Health. Megan A Murphy is supported in
part by a training grant NIH 5 T32 CA09001-35.
NR 27
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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 JAN 31
PY 2012
VL 106
IS 3
BP 596
EP 602
DI 10.1038/bjc.2011.572
PG 7
WC Oncology
SC Oncology
GA 892RC
UT WOS:000300302300023
PM 22223086
ER
PT J
AU Ferrucci, LM
Sinha, R
Huang, WY
Berndt, SI
Katki, HA
Schoen, RE
Hayes, RB
Cross, AJ
AF Ferrucci, L. M.
Sinha, R.
Huang, W-Y
Berndt, S. I.
Katki, H. A.
Schoen, R. E.
Hayes, R. B.
Cross, A. J.
TI Meat consumption and the risk of incident distal colon and rectal
adenoma
SO BRITISH JOURNAL OF CANCER
LA English
DT Article
DE colorectal adenoma; diet; meat; haeme iron; meat mutagens; nitrate;
nitrite
ID COLORECTAL-CANCER RISK; EPOXIDE HYDROLASE POLYMORPHISMS; HETEROCYCLIC
AMINE CONTENT; N-NITROSO COMPOUNDS; BODY IRON STORES; GRILLED RED MEAT;
DIETARY IRON; WELL-DONE; HEME IRON; ALCOHOL-CONSUMPTION
AB BACKGROUND: Most studies of meat and colorectal adenoma have investigated prevalent events from a single screening, thus limiting our understanding of the role of meat and meat-related exposures in early colorectal carcinogenesis.
METHODS: Among participants in the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial who underwent baseline and follow-up sigmoidoscopy (n = 17 072), we identified 1008 individuals with incident distal colorectal adenoma. We calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for associations between meat and meat-related components and incident distal colorectal adenoma using multivariate logistic regression.
RESULTS: We observed suggestive positive associations for red meat, processed meat, haeme iron, and nitrate/nitrite with distal colorectal adenoma. Grilled meat (OR = 1.56, 95% CI = 1.04-2.36), well or very well-done meat (OR = 1.59, 95% CI = 1.05-2.43), 2-amino-1-methyl-6-phenyl-imidazo[4,5-b] pyridine (PhIP) (OR = 1.75, 95% CI = 1.17-2.64), benzo[a] pyrene (OR = 1.53, 95% CI = 1.06-2.20), and total mutagenic activity (OR = 1.57, 95% CI = 1.03-2.40) were positively associated with rectal adenoma. Total iron (diet and supplements) (OR = 0.69, 95% CI = 0.56-0.86) and iron from supplements (OR = 0.65, 95% CI = 0.44-0.97) were inversely associated with any distal colorectal adenoma.
CONCLUSION: Our findings indicate that several meat-related components may be most relevant to early neoplasia in the rectum. In contrast, total iron and iron from supplements were inversely associated with any distal colorectal adenoma. British Journal of Cancer (2012) 106, 608-616. doi: 10.1038/bjc.2011.549 www.bjcancer.com Published online 13 December 2011 (C) 2012 Cancer Research UK
C1 [Ferrucci, L. M.; Sinha, R.; Huang, W-Y; Berndt, S. I.; Katki, H. A.; Cross, A. J.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Ferrucci, L. M.] Yale Univ, Sch Publ Hlth, Div Chron Dis Epidemiol, New Haven, CT USA.
[Schoen, R. E.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Hayes, R. B.] NYU, Dept Environm Med, Sch Med, New York, NY 10016 USA.
RP Cross, AJ (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM crossa@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015; Sinha, Rashmi/G-7446-2015;
OI Sinha, Rashmi/0000-0002-2466-7462; Hayes, Richard/0000-0002-0918-661X
FU National Institutes of Health, National Cancer Institute; National
Cancer Institute [TU2 CA105666]; Division of Cancer Prevention, National
Cancer Institute, National Institutes of Health, Department of Health
and Human Services
FX This research was supported (in part) by the Intramural Research Program
of the National Institutes of Health, National Cancer Institute, by
grant TU2 CA105666 from the National Cancer Institute, and by contracts
from the Division of Cancer Prevention, National Cancer Institute,
National Institutes of Health, Department of Health and Human Services.
We thank Drs Christine Berg, Paul Pinsky, and Philip Prorok, Division of
Cancer Prevention, National Cancer Institute, the Screening Center
investigators and staff of the Prostate, Lung, Colorectal, and Ovarian
(PLCO) Cancer Screening Trial, and Mr Tom Riley and staff, Information
Management Services Inc.
NR 63
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U1 0
U2 18
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 JAN 31
PY 2012
VL 106
IS 3
BP 608
EP 616
DI 10.1038/bjc.2011.549
PG 9
WC Oncology
SC Oncology
GA 892RC
UT WOS:000300302300025
PM 22166801
ER
PT J
AU Xia, D
Esser, L
Tang, WK
Zhang, MQ
Yu, LD
Yu, CA
AF Xia, Di
Esser, Lothar
Tang, Wai-kwan
Zhang, Mingquan
Yu, Linda
Yu, Chang-an
TI Redox Coupled Conformational Changes in Cytochrome BC1 Complex:
Implication to the Bifurcated Electron Transfer at the Quinol Oxidation
Site
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Xia, Di] NCI, Cell Biol Lab, Bethesda, MD 20892 USA.
[Esser, Lothar; Tang, Wai-kwan] NCI, Bethesda, MD 20892 USA.
[Zhang, Mingquan; Yu, Linda; Yu, Chang-an] Oklahoma State Univ, Stillwater, OK 74078 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 3A
EP 3A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200015
ER
PT J
AU Hammer, JA
Wagner, W
Brenowitz, SD
Wu, XFS
Jung, G
AF Hammer, John A.
Wagner, Wolfgang
Brenowitz, Stefan D.
Wu, Xufeng S.
Jung, Goeh
TI Myosin V as a Point-to-Point Organelle Transporter
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Hammer, John A.] NIH, Cell Biol Lab, Bethesda, MD 20892 USA.
[Wagner, Wolfgang; Brenowitz, Stefan D.; Wu, Xufeng S.; Jung, Goeh] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 5A
EP 5A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200028
ER
PT J
AU Taraska, JW
AF Taraska, Justin W.
TI Imaging the Nanometer-Scale Architecture of Microvesicle Release and
Recapture
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Taraska, Justin W.] NHLBI, 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 9A
EP 9A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200048
ER
PT J
AU Koefinger, J
Hummer, G
AF Koefinger, Juergen
Hummer, Gerhard
TI Simple and Efficient Calculation of Scattering Intensities of Proteins
in Solution from Atomistically Detailed Structures
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Koefinger, Juergen; Hummer, Gerhard] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 21A
EP 21A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200109
ER
PT J
AU Kraft, ML
Frisz, JF
Lou, KY
Klitzing, HA
Hanafin, WP
Weber, PK
Zimmerberg, J
AF Kraft, Mary L.
Frisz, Jessica F.
Lou, Kaiyan
Klitzing, Haley A.
Hanafin, William P.
Weber, Peter K.
Zimmerberg, Joshua
TI Chemical Imaging of the Lipid and Cholesterol Distribution in the Plasma
Membranes of Intact Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Kraft, Mary L.; Frisz, Jessica F.; Lou, Kaiyan; Klitzing, Haley A.; Hanafin, William P.] Univ Illinois, Urbana, IL 61801 USA.
[Weber, Peter K.] Lawrence Livermore Natl Lab, Livermore, CA USA.
[Zimmerberg, Joshua] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 26A
EP 26A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200132
ER
PT J
AU King, KE
Blaih-Isler, YE
Jiang, ZP
Gericke, A
AF King, Katrice E.
Blaih-Isler, Yasmin E.
Jiang, Zhiping
Gericke, Arne
TI Cholesterol Dependent and Independent Domain Formation in Mixed
Phosphatidylinositol/Phosphoinositide Model Membranes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [King, Katrice E.; Gericke, Arne] Worcester Polytech, Worcester, MA USA.
[Blaih-Isler, Yasmin E.] Kent State Univ, Kent, OH 44242 USA.
[Jiang, Zhiping] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 27A
EP 27A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200135
ER
PT J
AU Itoh, SG
Damjanovic, A
Brooks, BR
AF Itoh, Satoru G.
Damjanovic, Ana
Brooks, Bernard R.
TI pH Replica-Exchange Method Based on Discrete Protonation States
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Itoh, Satoru G.] Inst Mol Sci, Okazaki, Aichi 444, Japan.
[Itoh, Satoru G.] Grad Univ Adv Studies, Okazaki, Aichi, Japan.
[Damjanovic, Ana] Johns Hopkins Univ, Baltimore, MD USA.
[Damjanovic, Ana; Brooks, Bernard R.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
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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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 40A
EP 40A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200200
ER
PT J
AU Maciejewski, M
Tjandra, N
Barlow, PN
AF Maciejewski, Mateusz
Tjandra, Nico
Barlow, Paul N.
TI Decoding the Components of Dynamics in Three-Domain Proteins
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Maciejewski, Mateusz; Tjandra, Nico] NIH, Bethesda, MD 20892 USA.
[Maciejewski, Mateusz; Barlow, Paul N.] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
NR 0
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U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 53A
EP 53A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200264
ER
PT J
AU Wu, H
McCauley, MJ
Gorelick, RJ
Rouzina, I
Musier-Forsyth, K
Williams, MC
AF Wu, Hao
McCauley, Micah J.
Gorelick, Robert J.
Rouzina, Ioulia
Musier-Forsyth, Karin
Williams, Mark C.
TI Nucleic Acid Chaperone Activity of Wild Type and Mutant FIV Nucleocapsid
Proteins
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Wu, Hao; McCauley, Micah J.; Williams, Mark C.] Northeastern Univ, Boston, MA 02115 USA.
[Gorelick, Robert J.] SAIC Frederick Inc, AIDS & Canc Virus Program, NCI Frederick, Frederick, MD USA.
[Rouzina, Ioulia] Univ Minnesota, Minneapolis, MN USA.
[Musier-Forsyth, Karin] Ohio State Univ, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 60A
EP 60A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200304
ER
PT J
AU Perera, HD
Keffer, J
Bewley, C
AF Perera, Hettiarachchige D.
Keffer, Jessica
Bewley, Carole
TI The Mode of Action of FtsZ Inhibitors
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Perera, Hettiarachchige D.; Keffer, Jessica; Bewley, Carole] NIH, Rockville, 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 64A
EP 64A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200325
ER
PT J
AU Jensen, MK
Fei, JY
Richard, AC
Sternberg, SH
Gonzalez, RL
AF Jensen, Madeleine K.
Fei, Jingyi
Richard, Arianne C.
Sternberg, Samuel H.
Gonzalez, Ruben L., Jr.
TI The Magnesium Dependence of Ribosome and tRNA Dynamics in Single
Pre-Translocation Ribosomal Complexes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Jensen, Madeleine K.; Richard, Arianne C.; Sternberg, Samuel H.; Gonzalez, Ruben L., Jr.] Columbia Univ, New York, NY USA.
[Fei, Jingyi] Univ Illinois, Urbana, IL 61801 USA.
[Richard, Arianne C.] NIH, Bathesda, MD USA.
[Sternberg, Samuel H.] Univ Calif Berkeley, Berkeley, CA 94720 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 69A
EP 69A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200347
ER
PT J
AU Dimitriadis, EK
Qian, Z
Adhya, S
AF Dimitriadis, Emilios K.
Qian, Zhong
Adhya, Sankar
TI GalR Mediated Interactions Across the E. Coli Chromosome
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Dimitriadis, Emilios K.] NIBIB, NIH, Bethesda, MD USA.
[Qian, Zhong; Adhya, Sankar] NCI, NIH, Bethesda, MD 20892 USA.
RI Qian, Zhong/N-2266-2014
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 73A
EP 73A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200370
ER
PT J
AU DeRouchey, JE
Rau, D
AF DeRouchey, Jason E.
Rau, Donald
TI Role of Amino Acid Insertions on Intermolecular Forces Between Arginine
Peptide Condensed DNA Helices: Implications for Protamine-DNA Packaging
in Sperm
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [DeRouchey, Jason E.] Univ Kentucky, Lexington, KY USA.
[Rau, Donald] NIH, Bethesda, MD 20892 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 75A
EP 75A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200380
ER
PT J
AU Walker, RL
Pfefferkorn, CM
He, Y
Lee, JC
AF Walker, Robert L.
Pfefferkorn, Candace M.
He, Yi
Lee, Jennifer C.
TI Tryptophan Probes at the Apolipoprotein C-III and Membrane Interface
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Walker, Robert L.; Pfefferkorn, Candace M.; He, Yi; Lee, Jennifer C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 77A
EP 77A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200389
ER
PT J
AU Rostovtseva, TK
Gurnev, PA
Jacobs, D
Weinrich, M
Weinrich, M
Bezrukov, SM
AF Rostovtseva, Tatiana K.
Gurnev, Philip A.
Jacobs, Daniel
Weinrich, Michael
Weinrich, Michael
Bezrukov, Sergey M.
TI Interaction of Novel Anticancer Drug Erastin with Lipid Bilayers Probed
by Gramicidin A
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Rostovtseva, Tatiana K.; Gurnev, Philip A.; Jacobs, Daniel; Bezrukov, Sergey M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Bethesda, MD USA.
[Weinrich, Michael; Weinrich, Michael] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Natl Ctr Med Rehabil Res, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 85A
EP 85A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200430
ER
PT J
AU Roark, TC
Palacio, LA
Gurnev, PA
Ray, BD
Petrache, HI
AF Roark, Torri C.
Palacio, Luis A.
Gurnev, Philip A.
Ray, Bruce D.
Petrache, Horia I.
TI Interactions of Lithium Ions with Lipid Membranes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Roark, Torri C.; Palacio, Luis A.; Ray, Bruce D.; Petrache, Horia I.] Indiana Univ Purdue Univ Indianapolis, Indianapolis, IN USA.
[Gurnev, Philip A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 96A
EP 96A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200484
ER
PT J
AU Song, KC
Venable, RM
Maliniak, A
Im, W
Gawrisch, K
Pastor, RW
AF Song, Kevin C.
Venable, Richard M.
Maliniak, Arnold
Im, Wonpil
Gawrisch, Klaus
Pastor, Richard W.
TI Molecular Dynamics Simulation, 31P-NMR Spectroscopy, and
Microelectrophoretic Studies of Cardiolipin Bilayers
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Song, Kevin C.; Im, Wonpil] Univ Kansas, Lawrence, KS 66045 USA.
[Venable, Richard M.] NIH, Betheda, MD USA.
[Maliniak, Arnold] Stockholm Univ, S-10691 Stockholm, Sweden.
[Gawrisch, Klaus; Pastor, Richard W.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 2
Z9 2
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 97A
EP 97A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200490
ER
PT J
AU Monfredi, O
Lakatta, EG
Maltsev, VA
AF Monfredi, Oliver
Lakatta, Edward G.
Maltsev, Victor A.
TI Synchronization of Local Calcium Releases by Beta-Adrenergic Stimulation
in Cardiac Pacemaker Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Monfredi, Oliver] Univ Manchester, Manchester, Lancs, England.
[Monfredi, Oliver; Lakatta, Edward G.; Maltsev, Victor A.] NIA, NIH, Baltimore, MD 21224 USA.
NR 0
TC 1
Z9 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 103A
EP 103A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200519
ER
PT J
AU Kumar, J
Zhang, JJ
Mayer, ML
AF Kumar, Janesh
Zhang, Jinjin
Mayer, Mark L.
TI Optimization of Constructs for Expression, Purification and
Crystallization of Glutamate Receptor Ion Channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Kumar, Janesh; Zhang, Jinjin; Mayer, Mark L.] NICHD, NIH, Bethesda, MD USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 116A
EP 116A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200584
ER
PT J
AU Lopez-Rodriguez, AM
Holmgren, M
AF Lopez-Rodriguez, Angelica M.
Holmgren, Miguel
TI Rescuing Proper Trafficking of Cysteine Mutant Proteins
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Lopez-Rodriguez, Angelica M.; Holmgren, Miguel] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 130A
EP 130A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200654
ER
PT J
AU Raghunathan, M
Zubovski, Y
Venable, RM
Pastor, RW
Nagle, JF
Tristram-Nagle, S
AF Raghunathan, Mohit
Zubovski, Yuriy
Venable, Richard M.
Pastor, Richard W.
Nagle, John F.
Tristram-Nagle, Stephanie
TI Structure and Elasticity of Genistein and Daidzein in Lipid Membranes
using X-Ray Scattering and MD Simulations
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Raghunathan, Mohit; Zubovski, Yuriy; Nagle, John F.; Tristram-Nagle, Stephanie] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.
[Venable, Richard M.; Pastor, Richard W.] NHLBI, Bethesda, MD 20892 USA.
RI Nagle, John/B-1917-2015; Tristram-Nagle, Prof. Stephanie/N-7811-2014
OI Nagle, John/0000-0002-9844-5934; Tristram-Nagle, Prof.
Stephanie/0000-0003-2271-7056
NR 1
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 136A
EP 136A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561200683
ER
PT J
AU Gurnev, PA
Martin, MQ
Aguilella, VM
Rostovtseva, TK
Bezrukov, SM
AF Gurnev, Philip A.
Martin, Maria Queralt
Aguilella, Vicente M.
Rostovtseva, Tatiana K.
Bezrukov, Sergey M.
TI Tubulin-Blocked State of VDAC Probed by Polymer Partitioning and Bilayer
Surface Charge
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Gurnev, Philip A.; Rostovtseva, Tatiana K.; Bezrukov, Sergey M.] NICHHD, Bethesda, MD 20892 USA.
[Martin, Maria Queralt; Aguilella, Vicente M.] Univ Jaume 1, Dept Phys, Lab Mol Biophys, Castellon De La Plama 12071, Castellon, Spain.
RI Aguilella, Vicente/B-7592-2008
OI Aguilella, Vicente/0000-0002-2420-2649
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 161A
EP 161A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201103
ER
PT J
AU Hermida, OT
Bezrukov, SM
Rostovtseva, TK
AF Hermida, Oscar Teijido
Bezrukov, Sergey M.
Rostovtseva, Tatiana K.
TI A Putative Role of Voltage-Dependent Anion Channel in Ischemia
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Hermida, Oscar Teijido; Bezrukov, Sergey M.; Rostovtseva, Tatiana K.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 161A
EP 161A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201101
ER
PT J
AU Rostovtseva, TK
Sheldon, KL
Gurnev, PA
Bezrukov, SM
AF Rostovtseva, Tatiana K.
Sheldon, Kely L.
Gurnev, Philip A.
Bezrukov, Sergey M.
TI VDAC Regulation by Tubulin and its Physiological Implications
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Rostovtseva, Tatiana K.; Sheldon, Kely L.; Gurnev, Philip A.; Bezrukov, Sergey M.] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 161A
EP 161A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201102
ER
PT J
AU Wu, XW
Hodoscek, M
Brooks, BR
AF Wu, Xiongwu
Hodoscek, Milan
Brooks, Bernard R.
TI Replica Exchange of Self-Guided Langevin Dynamics Simulation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Wu, Xiongwu; Brooks, Bernard R.] NIH, Bethesda, MD 20892 USA.
[Hodoscek, Milan] Natl Inst Chem, Hajdrihova, Slovenia.
NR 0
TC 0
Z9 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 171A
EP 171A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201153
ER
PT J
AU Zhao, HY
Brown, PH
Magone, MT
Schuck, P
AF Zhao, Huaying
Brown, Patrick H.
Magone, M. Teresa
Schuck, Peter
TI The Molecular Refractive Function of Lens Gamma Crystallins
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Zhao, Huaying; Brown, Patrick H.; Magone, M. Teresa; Schuck, Peter] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 185A
EP 185A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201230
ER
PT J
AU Lee, JY
Tokumasu, F
Sackett, D
Nossal, R
Hwang, J
AF Lee, Ji Youn
Tokumasu, Fuyuki
Sackett, Dan
Nossal, Ralph
Hwang, Jeeseong
TI Label-Free Hyperspectral Imaging of Intracellular Hemoglobin in Human
Erythrocytes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Lee, Ji Youn; Hwang, Jeeseong] NIST, Gaithersburg, MD 20899 USA.
[Tokumasu, Fuyuki; Sackett, Dan; Nossal, Ralph] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 195A
EP 195A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201280
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 Measurement of Average Transition-Path Time for Protein Folding in
Single Molecule FRET Experiments
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Chung, Hoi Sung; Gopich, Irina V.; McHale, Kevin; Louis, John M.; Eaton, William A.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 217A
EP 218A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201400
ER
PT J
AU Johnson, ME
Hummer, G
AF Johnson, Margaret E.
Hummer, Gerhard
TI Refining Protein Interaction Networks with Protein Structure and Kinetic
Modeling
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Johnson, Margaret E.; Hummer, Gerhard] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 226A
EP 226A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201442
ER
PT J
AU Stasevich, TJ
Hayashi-Takanaka, Y
Nozaki, N
McNally, JG
Kimura, H
AF Stasevich, Timothy J.
Hayashi-Takanaka, Yoko
Nozaki, Naohito
McNally, James G.
Kimura, Hiroshi
TI Visualizing the Transcription Cycle of Endogenous RNA Polymerase II in
Single Living Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Stasevich, Timothy J.; Hayashi-Takanaka, Yoko; Kimura, Hiroshi] Osaka Univ, Osaka, Japan.
[Nozaki, Naohito] MAB Inst Inc, Sapporo, Hokkaido, Japan.
[McNally, James G.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 228A
EP 228A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201452
ER
PT J
AU Adhya, S
AF Adhya, Sankar
TI Bacterial Chromosome Structure and Function
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Adhya, Sankar] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 233A
EP 233A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201475
ER
PT J
AU Gopich, IV
Szabo, A
AF Gopich, Irina V.
Szabo, Attila
TI Single-Molecule FRET: Theory and Analysis of Photon Sequences
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Gopich, Irina V.; Szabo, Attila] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 235A
EP 235A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201487
ER
PT J
AU Nguyen, TA
Sarkar, P
Veetil, JV
Koushik, SV
Thaler, C
Vogel, SS
AF Nguyen, Tuan A.
Sarkar, Pabak
Veetil, Jithesh V.
Koushik, Srinagesh V.
Thaler, Christopher
Vogel, Steven S.
TI Polarized Fluorescence Correlation Spectroscopy (pFCS): A
Single-Molecule Method for Simultaneously Measuring Homo-FRET,
Brightness, and the Diffusion of Protein Complexes in Living Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Nguyen, Tuan A.; Sarkar, Pabak; Veetil, Jithesh V.; Koushik, Srinagesh V.; Thaler, Christopher; Vogel, Steven S.] NIAAA, NIH, Rockville, MD 20852 USA.
NR 0
TC 0
Z9 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 235A
EP 235A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201485
ER
PT J
AU Renner, LD
Eswaramoorthy, P
Ramamurthi, KS
Weibel, DB
AF Renner, Lars D.
Eswaramoorthy, Prahathees
Ramamurthi, Kumaran S.
Weibel, Douglas B.
TI Curvature as a Mechanism for Biomolecule Localization in Bacterial Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Renner, Lars D.; Weibel, Douglas B.] Univ Wisconsin, Madison, WI USA.
[Eswaramoorthy, Prahathees; Ramamurthi, Kumaran S.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 237A
EP 237A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201498
ER
PT J
AU Kimura, T
Macke, L
Gawrisch, K
Yeliseev, A
AF Kimura, Tomohiro
Macke, Laura
Gawrisch, Klaus
Yeliseev, Alexei
TI Effect of Anionic Lipids on Structure and Function of Cannabinoid CB2
Receptor in Micelles and in Reconstituted Liposomes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Kimura, Tomohiro; Macke, Laura; Gawrisch, Klaus; Yeliseev, Alexei] NIAAA, NIH, Bethesda, MD 90034 USA.
NR 0
TC 0
Z9 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 240A
EP 240A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201513
ER
PT J
AU Brown, PH
AF Brown, Patrick H.
TI Density Contrast Sedimentation Velocity for the Determination of Protein
Partial-Specific Volumes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Brown, Patrick H.] NIBIB, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 2
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 258A
EP 258A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561201609
ER
PT J
AU Ishibashi, T
Bintu, L
Dangkulwanich, M
Gloria, W
Lubkowska, L
Kashlev, M
Bustamante, C
AF Ishibashi, Toyotaka
Bintu, Lacramioara
Dangkulwanich, Manchuta
Gloria, Wu
Lubkowska, Lucyna
Kashlev, Mikhail
Bustamante, Carlos
TI Dissecting the Nucleosomal Barrier to Transcription
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Ishibashi, Toyotaka; Bintu, Lacramioara; Dangkulwanich, Manchuta; Gloria, Wu; Bustamante, Carlos] Univ Calif Berkeley, Berkeley, CA USA.
[Lubkowska, Lucyna; Kashlev, Mikhail] NCI, Frederick Canc Res & Dev Ctr, Frederick, MD USA.
[Bustamante, Carlos] Univ Calif Berkeley, Howard Hughes Med Inst, Berkeley, CA 94720 USA.
OI Ishibashi, Toyotaka/0000-0001-8015-2319
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 284A
EP 284A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202027
ER
PT J
AU Nanda, H
Weinrich, M
Majkrzak, CF
Maranville, BB
Worcester, DL
Bezrukov, SM
AF Nanda, Hirsh
Weinrich, Michael
Majkrzak, Charles F.
Maranville, Brian B.
Worcester, David L.
Bezrukov, Sergey M.
TI Anesthetic Concentrations of Halothane Change the Domain Structure of
Mixed Lipid Membranes
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Nanda, Hirsh; Majkrzak, Charles F.; Maranville, Brian B.; Worcester, David L.; Bezrukov, Sergey M.] NIST, Gaithersburg, MD 20899 USA.
[Weinrich, Michael] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 288A
EP 288A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202049
ER
PT J
AU Sodt, AJ
Pastor, RW
AF Sodt, Alex J.
Pastor, Richard W.
TI Lipid Mechanical Properties from Computer Simulation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sodt, Alex J.; Pastor, Richard W.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 291A
EP 291A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202065
ER
PT J
AU Galimzyanov, TR
Molotkovsky, RJ
Jimmerberg, J
Akimov, SA
Cohen, FS
AF Galimzyanov, Timur R.
Molotkovsky, Rodion J.
Jimmerberg, Joshua
Akimov, Sergey A.
Cohen, Fredric S.
TI Elastic Deformations at a Boundary Stabilizes Opposion of Monolayer
Rafts in the Structure of a Bilayer Raft
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Galimzyanov, Timur R.] Natl Univ Sci & Technol MISiS, Moscow, Russia.
[Molotkovsky, Rodion J.; Akimov, Sergey A.] Russian Acad Sci, AN Frumkin Inst Phys Chem & Electrochem, Moscow, Russia.
[Jimmerberg, Joshua] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Bethesda, MD USA.
[Cohen, Fredric S.] Rush Univ, Med Ctr, Dept Mol Biophys & Physiol, Chicago, IL 60612 USA.
RI Akimov, Sergey/L-2001-2013; Galimzyanov, Timur/I-6297-2015; Akimov,
Sergey/I-6432-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 295A
EP 295A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202088
ER
PT J
AU Lee, KI
Kim, T
Pastor, RW
Andersen, OS
Im, W
AF Lee, Kyu Il
Kim, Taehoon
Pastor, Richard W.
Andersen, Olaf S.
Im, Wonpil
TI Assessment of Membrane Deformation Continuum Elastic Models Based on
Molecular Simulations of Gramicidin A
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Lee, Kyu Il; Kim, Taehoon; Im, Wonpil] Univ Kansas, Lawrence, KS 66045 USA.
[Pastor, Richard W.] NIH, Bethesda, MD 20892 USA.
[Andersen, Olaf S.] Weill Cornell Med Coll, New York, NY 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 296A
EP 296A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202090
ER
PT J
AU Lizunov, VA
Stenkula, K
Cushman, S
Zimmerberg, J
AF Lizunov, Vladimir A.
Stenkula, Karin
Cushman, Samuel
Zimmerberg, Joshua
TI Fence Model for Dynamic Exchange and Retention of GLUT4 in Plasma
Membrane Domains
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Lizunov, Vladimir A.; Cushman, Samuel; Zimmerberg, Joshua] NIH, Bethesda, MD 20892 USA.
[Stenkula, Karin] Lund Univ, Lund, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 320A
EP 321A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202206
ER
PT J
AU Banerjee, A
Nossal, R
AF Banerjee, Anand
Nossal, Ralph
TI Stochastic Nature of Clathrin-Coated Pit Assembly
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Banerjee, Anand; Nossal, Ralph] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 321A
EP 321A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202209
ER
PT J
AU Hinshaw, JE
Chappie, JS
Mears, JA
Fang, SM
Leonard, M
Schmid, SL
Milligan, RA
Dyda, F
AF Hinshaw, Jenny E.
Chappie, Joshua S.
Mears, Jason A.
Fang, Shunming
Leonard, Marilyn
Schmid, Sandra L.
Milligan, Ronald A.
Dyda, Fred
TI Structural Analysis of Dynamin Reveals Power Stroke
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Hinshaw, Jenny E.; Chappie, Joshua S.; Fang, Shunming; Dyda, Fred] NIDDK, NIH, Bethesda, MD USA.
[Mears, Jason A.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Leonard, Marilyn; Schmid, Sandra L.; Milligan, Ronald A.] Scripps Res Inst, La Jolla, CA 92037 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 321A
EP 321A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202211
ER
PT J
AU Shnyrova, A
Bashkirov, PV
Hortelano, ER
Zimmerberg, J
Frolov, VA
AF Shnyrova, Anna
Bashkirov, Pavel V.
Rodriguez Hortelano, Eva
Zimmerberg, Joshua
Frolov, Vadim A.
TI Spatio-Temporal Organization of a Minimal Dynamin Machinery Producing
Membrane Fission
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Shnyrova, Anna; Rodriguez Hortelano, Eva; Frolov, Vadim A.] Univ Basque Country, Dept Bioquim, EHU, Unidad Biofis,Ctr Mixto,CSIC,UPV, E-48080 Bilbao, Spain.
[Bashkirov, Pavel V.] AN Frumkin Inst Phys Chem & Elecrochem, Moscow, Russia.
[Zimmerberg, Joshua] Eunice Kennedy Schriver Natl Inst Child Hlth & Hu, Program Phys Biol, NIH, Bethesda, MD USA.
[Frolov, Vadim A.] Basque Fdn Sci, IKERBASQUE, Bilbao, Spain.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 322A
EP 322A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202214
ER
PT J
AU Bosmans, F
Swartz, KJ
AF Bosmans, Frank
Swartz, Kenton J.
TI Sodium Channel Voltage Sensor Movements Are Influenced by the Auxiliary
beta 1 Subunit
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Bosmans, Frank; Swartz, Kenton J.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 326A
EP 326A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202235
ER
PT J
AU Berger, AJ
Brown, P
Zhao, HY
Schuck, P
Mayer, M
AF Berger, Anthony J.
Brown, Patrick
Zhao, Huaying
Schuck, Peter
Mayer, Mark
TI Analysis of Oligomer Assembly for the GluA2 Amino Terminal Domain
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
ID CRYSTAL-STRUCTURE
C1 [Berger, Anthony J.; Brown, Patrick; Zhao, Huaying; Schuck, Peter; Mayer, Mark] NIH, Bethesda, MD 20892 USA.
NR 3
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 335A
EP 336A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202282
ER
PT J
AU Li, MF
Silberberg, SD
Swartz, KJ
AF Li, Mufeng
Silberberg, Shai D.
Swartz, Kenton J.
TI Subtype Specific Activation of P2X Receptors by Free and Magnesium-Bound
ATP
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Li, Mufeng; Silberberg, Shai D.; Swartz, Kenton J.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 336A
EP 337A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202287
ER
PT J
AU Khadra, A
AF Khadra, Anmar
TI Understanding the Kinetics of ATP-Activated P2X2A and P2X2B Receptor
Channels using a Markov State Model
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Khadra, Anmar] NIH, Bethesda, MD USA.
[Khadra, Anmar] McGill Univ, Montreal, PQ, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 337A
EP 337A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202289
ER
PT J
AU Ladt, KC
Bae, C
Yu, J
Kim, JI
Swartz, K
AF Ladt, Kelsey C.
Bae, Chanhyung
Yu, JeongHeon
Kim, Jae Il
Swartz, Kenton
TI Activation of TRPV1 by a Recombinant Double-Knot Toxin from a Chinese
Bird Spider
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Ladt, Kelsey C.; Swartz, Kenton] NIH, Bethesda, MD 20892 USA.
[Bae, Chanhyung; Yu, JeongHeon; Kim, Jae Il] Gwangju Inst Sci & Technol, Kwangju, South Korea.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 342A
EP 342A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202312
ER
PT J
AU Smith, DB
Liu, J
AF Smith, Daniel B.
Liu, Jian
TI The Geometry of Branching Actin Networks from Capping Branching and
Filament Growth
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Smith, Daniel B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Liu, Jian] NHBLI, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 348A
EP 348A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202348
ER
PT J
AU Toepfer, C
Caorsi, V
Mansfield, C
West, TG
Kampourakis, T
Leung, J
Sellers, JR
Ferenczi, MA
AF Toepfer, Christopher
Caorsi, Valentina
Mansfield, Catherine
West, Timothy G.
Kampourakis, Thomas
Leung, Judy
Sellers, James R.
Ferenczi, Michael A.
TI A Method to Exchange Recombinant Differentially Phosphorylated
Rhodamine-Labeled Cardiac RLC into Permeabilized Cardiac Trabeculae
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Toepfer, Christopher; Caorsi, Valentina; Mansfield, Catherine; Leung, Judy; Ferenczi, Michael A.] Univ London Imperial Coll Sci Technol & Med, London, England.
[West, Timothy G.] Univ London Royal Vet Coll, London, England.
[Kampourakis, Thomas] Kings Coll London, London WC2R 2LS, England.
[Sellers, James R.] NIH, Bethesda, MD 20892 USA.
RI Ferenczi, Michael/F-9510-2015
OI Ferenczi, Michael/0000-0002-0349-331X
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 359A
EP 359A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202398
ER
PT J
AU Vecchiarelli, A
Mizuuchi, K
AF Vecchiarelli, Anthony
Mizuuchi, Kiyoshi
TI Visualizing Bacterial DNA Segregation in a Cell Free System
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Vecchiarelli, Anthony; Mizuuchi, Kiyoshi] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 380A
EP 381A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202514
ER
PT J
AU Hwang, LC
Han, YW
Vecchiarelli, AG
Harada, Y
Funnell, BE
Mizuuchi, K
AF Hwang, Ling Chin
Han, Yong-Woon
Vecchiarelli, Anthony G.
Harada, Yoshie
Funnell, Barbara E.
Mizuuchi, Kiyoshi
TI Dynamic Self-Organization of Bacterial DNA Segregation Machinery in a
Cell-Free Reaction
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Hwang, Ling Chin; Vecchiarelli, Anthony G.; Mizuuchi, Kiyoshi] NIH, Bethesda, MD 20892 USA.
[Han, Yong-Woon; Harada, Yoshie] Inst Integrated Cell Mat Sci, Kyoto, Japan.
[Funnell, Barbara E.] Dept Mol Genet, Toronto, ON, Canada.
RI Hwang, Ling Chin/G-4078-2014
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 381A
EP 381A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202515
ER
PT J
AU Sharma, G
Stupina, V
Pallesen, J
Shapiro, B
Simon, A
Dinman, J
Frank, J
AF Sharma, Gyanesh
Stupina, Vera
Pallesen, Jesper
Shapiro, Bruce
Simon, Anne
Dinman, Jonathan
Frank, Joachim
TI Cryo-Electron Microscopy (Cryo-EM) Structure of a Cap-Independent
Translational Enhancer of the Turnip Crinkle Virus (TCV) Bound to the
Eukaryotic Ribosome
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sharma, Gyanesh; Pallesen, Jesper; Frank, Joachim] Columbia Univ, New York, NY USA.
[Stupina, Vera; Simon, Anne; Dinman, Jonathan] Univ Maryland, College Pk, MD 20742 USA.
[Shapiro, Bruce] NCI, Frederick, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 393A
EP 393A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202575
ER
PT J
AU Sousa, AA
Winters, CA
Cox, D
Chen, XB
Reese, TS
Leapman, RD
AF Sousa, Alioscka A.
Winters, Christine A.
Cox, Daniel
Chen, Xiaobing
Reese, Thomas S.
Leapman, Richard D.
TI Three-Dimensional Ultrastructure of Micrometer Thick Cellular Subvolumes
by STEM Tomography
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sousa, Alioscka A.; Cox, Daniel; Leapman, Richard D.] NIBIB, NIH, Bethesda, MD USA.
[Winters, Christine A.; Chen, Xiaobing; Reese, Thomas S.] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 393A
EP 393A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202574
ER
PT J
AU Hayakawa, EH
Tokumasu, F
Usukura, J
Tsuboi, T
Matsuoka, H
Wellems, TE
AF Hayakawa, Eri H.
Tokumasu, Fuyuki
Usukura, Jiro
Tsuboi, Takafumi
Matsuoka, Hiroyuki
Wellems, Thomas E.
TI Three Dimensional Imaging of Maurer's Clefts in "Unroofed" Plasmodium
Falciparum-Infected Erythrocytes by Transmission Electron Microscopy
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Hayakawa, Eri H.; Matsuoka, Hiroyuki] Jichi Med Univ, Dept Infect & Immun, Lab Med Zool & Parasitol, Shimotsuke, Japan.
[Tokumasu, Fuyuki; Wellems, Thomas E.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Usukura, Jiro] Nagoya Univ, Div Integrated Project, EcoTopia Sci Inst, Nagoya, Aichi 4648601, Japan.
[Tsuboi, Takafumi] Ehime Univ, Cell Free Sci & Technol Res Ctr, Malaria Res Unit, Matsuyama, Ehime, Japan.
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 395A
EP 395A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202585
ER
PT J
AU Heymann, J
Fontainhas, A
Fang, SM
Hinshaw, JE
AF Heymann, Jurgen
Fontainhas, Aurora
Fang, Shunming
Hinshaw, Jenny E.
TI Molecular Architecture of OPA1, the Dynamin-Related GTPase Involved in
Mitochondrial Fusion
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Heymann, Jurgen; Fontainhas, Aurora; Fang, Shunming; Hinshaw, Jenny E.] NIDDK, NIH, LCBB, Bethesda, MD USA.
NR 1
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 395A
EP 395A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202587
ER
PT J
AU Drobizhev, M
Hughes, TE
Rebane, A
Davis, B
Topol, I
Scott, N
Callis, PR
AF Drobizhev, Mikhail
Hughes, Thomas E.
Rebane, Aleksander
Davis, Bret
Topol, Igor
Scott, Nathan
Callis, Patrik R.
TI Unified Description of Optical Properties and Photostability of
Fluorescent Proteins by Means of the Chromophore-Protein Electrostatic
Interactions
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Drobizhev, Mikhail; Hughes, Thomas E.; Rebane, Aleksander; Davis, Bret; Scott, Nathan; Callis, Patrik R.] Montana State Univ, Bozeman, MT 59717 USA.
[Topol, Igor] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 403A
EP 404A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202630
ER
PT J
AU Yu, XZ
Taraska, J
AF Yu, Xiaozhen
Taraska, Justin
TI High-Throughput Protein Structural Mapping using Transition Metal FRET
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Yu, Xiaozhen; Taraska, Justin] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 403A
EP 403A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202625
ER
PT J
AU Teague, WE
Soubias, O
Fuller, NL
Rand, RP
Gawrisch, K
AF Teague, Walter E.
Soubias, Olivier
Fuller, Nola L.
Rand, R. Peter
Gawrisch, Klaus
TI Curvature Elastic Properties of Phosphatidylethanolamines with Mono- and
Polyunsaturated Hydrocarbon Chains - An NMR and X-Ray Diffraction Study
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Teague, Walter E.; Soubias, Olivier; Gawrisch, Klaus] NIAAA, NIH, Bethesda, MD 90034 USA.
[Fuller, Nola L.; Rand, R. Peter] Brock Univ, St Catharines, ON L2S 3A1, Canada.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 413A
EP 413A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561202676
ER
PT J
AU Renz, M
Daniels, B
Vamosi, G
Arias, I
Lippincott-Schwartz, J
AF Renz, Malte
Daniels, Brian
Vamosi, Gyorgy
Arias, Irwin
Lippincott-Schwartz, Jennifer
TI Plasticity of the Asialoglycoprotein Receptor Deciphered by Ensemble
FRET and Single-Molecule Counting PALM
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Renz, Malte; Daniels, Brian; Arias, Irwin; Lippincott-Schwartz, Jennifer] NIH, Bethesda, MD 20892 USA.
[Vamosi, Gyorgy] Univ Debrecen, H-4012 Debrecen, Hungary.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
EI 1542-0086
J9 BIOPHYS J
JI Biophys. J.
PD JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 430A
EP 430A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203052
ER
PT J
AU Jiang, ZP
McGlinchey, RP
Pfefferkorn, CM
Lee, JC
AF Jiang, Zhiping
McGlinchey, Ryan P.
Pfefferkorn, Candace M.
Lee, Jennifer C.
TI Effects of Lipids on the Conformation and Aggregation of the Repeat
Domain of a Functional Amyloid, Pmel17
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Jiang, Zhiping; McGlinchey, Ryan P.; Pfefferkorn, Candace M.; Lee, Jennifer C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 434A
EP 434A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203072
ER
PT J
AU Soubias, O
Teague, WE
Hines, KG
Gawrisch, K
AF Soubias, Olivier
Teague, Walter E.
Hines, Kirk G.
Gawrisch, Klaus
TI Cholesterol Enhances or Reduces Metarhodopsin II Formation Depending on
Bilayer Thickness
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
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 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 434A
EP 435A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203075
ER
PT J
AU Sheldon, KL
Maldonado, EN
Lemasters, JJ
Bezrukov, SM
Rostovtseva, TK
AF Sheldon, Kely L.
Maldonado, Eduardo N.
Lemasters, John J.
Bezrukov, Sergey M.
Rostovtseva, Tatiana K.
TI VDAC Phosphorylation in Control of Mitochondrial Respiration
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sheldon, Kely L.; Bezrukov, Sergey M.; Rostovtseva, Tatiana K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD USA.
[Sheldon, Kely L.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, W Harry Feinstone Dept Mol Microbiol & Immunol, Baltimore, MD USA.
[Maldonado, Eduardo N.; Lemasters, John J.] Med Univ S Carolina, Charleston, SC 29425 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 436A
EP 437A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203084
ER
PT J
AU Dejean, LM
Renault, TT
Teijido, O
Velours, G
Ganesan, YT
Camougrand, N
Antonsson, B
Manon, S
AF Dejean, Laurent M.
Renault, Thibaud T.
Teijido, Oscar
Velours, Gisele
Ganesan, Yogesh Tengarai
Camougrand, Nadine
Antonsson, Bruno
Manon, Stephen
TI Bcl-xL Increases Bax Mitochondrial Localization and Activation in
Non-Apoptotic Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Dejean, Laurent M.] Calif State Univ Fresno, Fresno, CA 93740 USA.
[Renault, Thibaud T.; Velours, Gisele; Camougrand, Nadine; Manon, Stephen] CNRS, Inst Biochim & Genet Cellulaires, Bordeaux, France.
[Teijido, Oscar] NICHD, NIH, Bethesda, MD USA.
[Ganesan, Yogesh Tengarai] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[Antonsson, Bruno] Merck Serrono SA, Geneva Res Ctr, Geneva, Switzerland.
RI Manon, Stephen/C-7088-2017
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 437A
EP 437A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203088
ER
PT J
AU Jang, H
Capone, R
Kotler, SA
Arce, FT
Connelly, L
Ramachandran, S
Kagan, BL
Lal, R
Nussinov, R
AF Jang, Hyunbum
Capone, Ricardo
Kotler, Samuel A.
Arce, Fernando Teran
Connelly, Laura
Ramachandran, Srinivasan
Kagan, Bruce L.
Lal, Ratnesh
Nussinov, Ruth
TI Modeling Alzheimer's Ion Channel Structures in Lipid Bilayers Formed by
D- and L-Enantiomers of Beta-Amyloid (1-42) Peptide
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Jang, Hyunbum; Nussinov, Ruth] NCI, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Capone, Ricardo; Kotler, Samuel A.; Arce, Fernando Teran; Connelly, Laura; Ramachandran, Srinivasan; Lal, Ratnesh] Univ Calif San Diego, La Jolla, CA 92093 USA.
[Kagan, Bruce L.] Univ Calif Los Angeles, Los Angeles, CA USA.
RI Ramachandran, Srinivasan/G-5300-2010
OI Ramachandran, Srinivasan/0000-0002-4912-0279
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 440A
EP 440A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203101
ER
PT J
AU Musselman, CA
Ramirez, J
Sims, JK
Mansfield, RE
Oliver, SS
Denu, JM
Mackay, JP
Wade, PA
Hagman, J
Kutateladze, TG
AF Musselman, Catherine A.
Ramirez, Julita
Sims, Jennifer K.
Mansfield, Robyn E.
Oliver, Samuel S.
Denu, John M.
Mackay, Joel P.
Wade, Paul A.
Hagman, James
Kutateladze, Tatiana G.
TI Bivalent Recognition of a Single Nucleosome by the Tandem PHD Fingers of
CHD4 is Required for CHD4-Mediated Repression
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Musselman, Catherine A.; Kutateladze, Tatiana G.] Univ Colorado Denver, Aurora, CO USA.
[Ramirez, Julita; Hagman, James] Natl Jewish Hlth, Denver, CO USA.
[Sims, Jennifer K.; Wade, Paul A.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
[Mansfield, Robyn E.; Mackay, Joel P.] Univ Sydney, Sydney, NSW 2006, Australia.
[Oliver, Samuel S.; Denu, John M.] Univ Wisconsin, Madison, WI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 480A
EP 480A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203312
ER
PT J
AU Zhurkin, V
Nikitina, T
Wang, DF
Cui, F
Gomberg, M
Grigoryev, S
AF Zhurkin, Victor
Nikitina, Tatiana
Wang, Difei
Cui, Feng
Gomberg, Michael
Grigoryev, Sergei
TI Sequence-Specific Asymmetric Binding of Linker Histone to Nucleosome
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Zhurkin, Victor; Nikitina, Tatiana; Wang, Difei; Cui, Feng] NIH, Bethesda, MD 20892 USA.
[Gomberg, Michael; Grigoryev, Sergei] Penn State Univ, Coll Med, Hershey, PA USA.
RI Wang, Difei/E-7066-2010
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 481A
EP 481A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203319
ER
PT J
AU Ma, BY
Xu, Y
Nussinov, R
AF Ma, Buyong
Xu, Yu
Nussinov, Ruth
TI Structural and Functional Consequences of Phosphate-Arsenate
Substitutions in Selected Nucleotides: DNA, RNA, and ATP
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Ma, Buyong; Nussinov, Ruth] NCI, SAIC Frederick, NIH, Frederick, MD 21701 USA.
[Xu, Yu] Minzu Univ China, Beijing, 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 483A
EP 483A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203329
ER
PT J
AU Sidorova, NY
Hung, S
Rau, DC
AF Sidorova, Nina Y.
Hung, Stevephen
Rau, Donald C.
TI Stabilizing Labile DNA-Protein Complexes in Polyacrylamide Gels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sidorova, Nina Y.; Hung, Stevephen; Rau, Donald C.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 484A
EP 484A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203336
ER
PT J
AU Seol, Y
Zhang, HL
Dalla Rosa, I
Pommier, Y
Neuman, KC
AF Seol, Yeonee
Zhang, Hongliang
Dalla Rosa, Ilaria
Pommier, Yves
Neuman, Keir C.
TI Distinct Uncoiling Mechanisms of Human Nuclear and Mitochondrial Type IB
Topoisomerases
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Seol, Yeonee; Neuman, Keir C.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Zhang, Hongliang; Dalla Rosa, Ilaria; Pommier, Yves] NCI, NIH, Bethesda, MD 20892 USA.
RI Neuman, Keir/F-7400-2011
OI Neuman, Keir/0000-0002-0863-5671
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 485A
EP 485A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203339
ER
PT J
AU Seol, Y
Hardin, AH
Charvin, G
Neuman, KC
AF Seol, Yeonee
Hardin, Ashley H.
Charvin, Gilles
Neuman, Keir C.
TI Non-Equilibrium Topology Simplification by Type II Topoisomerases: A
Test of Kinetic Proofreading
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
ID DNA
C1 [Seol, Yeonee; Hardin, Ashley H.; Neuman, Keir C.] NIH, Bethesda, MD 20892 USA.
[Charvin, Gilles] Inst Biol Mol & Cellulaire, Illkirch Graffenstaden, France.
RI Neuman, Keir/F-7400-2011
OI Neuman, Keir/0000-0002-0863-5671
NR 2
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 486A
EP 487A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203348
ER
PT J
AU Franquelim, HG
Veiga, AS
Santos, NC
Castanho, MA
AF Franquelim, Henri G.
Veiga, A. Salome
Santos, Nuno C.
Castanho, Miguel A.
TI Decoding Distinct Membrane Interactions of HIV-1 Inhibitors Enfuvirtide
and T-1249 using Atomic Force Microscopy Combined with Fluorescence
Methodologies
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Franquelim, Henri G.; Veiga, A. Salome; Santos, Nuno C.; Castanho, Miguel A.] Inst Mol Med, Lisbon, Portugal.
[Veiga, A. Salome] NCI, Frederick, MD 21701 USA.
RI Santos, Nuno/N-7248-2013
OI Santos, Nuno/0000-0002-0580-0475
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 490A
EP 490A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203365
ER
PT J
AU Zhang, LQ
Sodt, A
Venable, R
Pastor, RW
Buck, M
AF Zhang, Liqun
Sodt, Alexander
Venable, Rick
Pastor, Richard W.
Buck, Matthias
TI Molecular Dynamics Prediction and Refinement of Transmembrane Helix
Dimers
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Zhang, Liqun; Buck, Matthias] Case Western Reserve Univ, Cleveland, OH 44106 USA.
[Sodt, Alexander; Venable, Rick] NHLBI, Bethesda, MD 20892 USA.
[Pastor, Richard W.] NHBLI, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 497A
EP 498A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203402
ER
PT J
AU Chen, Y
Lippincott-Schwartz, J
AF Chen, Yu
Lippincott-Schwartz, Jennifer
TI Tirfing Insulin-Stimulated GLUT4 Translocation with a Quench-Based
Mehtod
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Chen, Yu; Lippincott-Schwartz, Jennifer] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 500A
EP 500A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203418
ER
PT J
AU Molotkovsky, R
Zimmerberg, J
Cohen, FS
Akimov, S
AF Molotkovsky, Rodion
Zimmerberg, Joshua
Cohen, Fredric S.
Akimov, Sergey
TI A Quantitative Model for Formation of Protein-Mediated Protrusions,
Based on Continuum Elasticity Theory
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Molotkovsky, Rodion; Akimov, Sergey] RAS, IPCE, Moscow 117901, Russia.
[Zimmerberg, Joshua] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Cohen, Fredric S.] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
RI Akimov, Sergey/L-2001-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 500A
EP 500A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203417
ER
PT J
AU Vinogradova, TM
Lakatta, EG
AF Vinogradova, Tatiana M.
Lakatta, Edward G.
TI Basal PKC Activity Regulates Spontaneous Firing of Cardiac Pacemaker
Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Vinogradova, Tatiana M.; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 511A
EP 511A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203473
ER
PT J
AU Yaniv, Y
Maltsev, VA
Lakatta, EG
AF Yaniv, Yael
Maltsev, Victor A.
Lakatta, Edward G.
TI How Ca2+-Activated, cAMP/PKA-Dependent Phosphorylation Signaling
Mediates Pacemaker Cell Activity: Experimental and In Silico Biochemical
and Biophysics Perspectives
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Yaniv, Yael; Maltsev, Victor A.; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 USA.
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 511A
EP 511A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203474
ER
PT J
AU Kalia, J
Swartz, KJ
AF Kalia, Jeet
Swartz, Kenton J.
TI Mechanism of Inhibition of Voltage-Gated Potassium Channels by Guanidine
Compounds
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Kalia, Jeet; Swartz, Kenton J.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 533A
EP 533A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203584
ER
PT J
AU Ganapathi, SB
Wei, SG
Lamb, FS
Shears, SB
AF Ganapathi, Sindura B.
Wei, Shun-Guang
Lamb, Fred S.
Shears, Stephen B.
TI Functional Regulation of ClC-3 in the Migration of Vascular Smooth
Muscle Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Ganapathi, Sindura B.; Shears, Stephen B.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Wei, Shun-Guang] Univ Iowa, Dept Internal Med, Carver Coll Med, Iowa City, IA 52242 USA.
[Lamb, Fred S.] Vanderbilt Univ, Nashville, TN 37235 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 549A
EP 549A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561203661
ER
PT J
AU Sunyer, R
Jin, AJ
Nossal, R
Sackett, DL
AF Sunyer, Raimon
Jin, Albert J.
Nossal, Ralph
Sackett, Dan L.
TI Fabrication of Hydrogels with Gradient of Compliance: Application to
Cell Mechanotaxis and Durotaxis
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sunyer, Raimon; Jin, Albert J.; Nossal, Ralph; Sackett, Dan L.] NIH, Bethesda, MD 20892 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 565A
EP 565A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204033
ER
PT J
AU Wu, ZH
Plotnikov, S
Waterman, CM
Liu, J
AF Wu, Zhanghan
Plotnikov, Sergey
Waterman, Clare M.
Liu, Jian
TI A Mechanochemistry Model of Focal Adhesion Dynamics in Cell Migration
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Wu, Zhanghan; Plotnikov, Sergey; Waterman, Clare M.; Liu, Jian] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 8
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 566A
EP 566A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204037
ER
PT J
AU Swenson, AM
Trivedi, D
Takagi, Y
Sellers, JR
Yengo, CM
AF Swenson, Anja M.
Trivedi, Darshan
Takagi, Yasuharu
Sellers, James R.
Yengo, Christopher M.
TI Differential Impact of Temperature and Magnesium on Myosin V and Myosin
II
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Swenson, Anja M.] Gustavus Adolphus Coll, St Peter, MN 56082 USA.
[Trivedi, Darshan; Yengo, Christopher M.] Penn State Univ, Coll Med, Hershey, PA USA.
[Takagi, Yasuharu; Sellers, James R.] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 567A
EP 567A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204043
ER
PT J
AU Bond, LM
Kendrick-Jones, J
Buss, F
Sellers, JR
AF Bond, Lisa M.
Kendrick-Jones, John
Buss, Folma
Sellers, James R.
TI Examination of the Kinetics of Myosin VI during Endocytosis
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Bond, Lisa M.] Univ Cambridge, NIH, Bethesda, MD USA.
[Kendrick-Jones, John] MRC, Mol Biol Lab, Cambridge CB2 2QH, England.
[Buss, Folma] Univ Cambridge, Cambridge, England.
[Sellers, James R.] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 569A
EP 569A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204056
ER
PT J
AU Maldonado, EN
DeHart, DN
Patnaik, JR
Sheldon, KL
Rostovtseva, TK
Manevich, Y
Townsend, D
Lemasters, JJ
AF Maldonado, Eduardo N.
DeHart, David N.
Patnaik, Jyoti R.
Sheldon, Kely L.
Rostovtseva, Tatiana K.
Manevich, Yefim
Townsend, Danyelle
Lemasters, John J.
TI Voltage Dependent Anion Channel-3 (VDAC3) is the Major Isoform
Contributing to Mitochondrial Metabolism in HepG2 Cells and is Regulated
by Free Tubulin and Erastin
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Maldonado, Eduardo N.; DeHart, David N.; Patnaik, Jyoti R.; Lemasters, John J.] Med Univ S Carolina, Ctr Cell Death Injury & Regenerat, Charleston, SC 29425 USA.
[Maldonado, Eduardo N.; DeHart, David N.; Patnaik, Jyoti R.; Manevich, Yefim; Townsend, Danyelle; Lemasters, John J.] Med Univ S Carolina, Dept Pharmaceut & Biomed Sci, Charleston, SC 29425 USA.
[Sheldon, Kely L.; Rostovtseva, Tatiana K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Sheldon, Kely L.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, W Harry Feinstein Dept Mol Microbiol & Immunol, Baltimore, MD USA.
[Lemasters, John J.] Med Univ S Carolina, Dept Biochem & Mol Biol, Charleston, SC 29425 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 573A
EP 573A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204072
ER
PT J
AU Connelly, LS
Arce, FT
Jang, H
Capone, R
Kotler, S
Kagan, B
Nussinov, R
Lal, R
AF Connelly, Laura S.
Arce, Fernando Teran
Jang, Hyunbum
Capone, Ricardo
Kotler, Samuel
Kagan, Bruce
Nussinov, Ruth
Lal, Ratnesh
TI Alzheimer's beta-Amyloid All-D-Enantiomers and Native All-L-Enantiomers
Exhibit Similar Pore Structures in Lipid Bilayers: Atomic Force
Microscopy
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Connelly, Laura S.; Arce, Fernando Teran; Capone, Ricardo; Kotler, Samuel; Lal, Ratnesh] Univ Calif San Diego, San Diego, CA 92103 USA.
[Jang, Hyunbum; Nussinov, Ruth] SAIC Frederick Inc, Ctr Canc Res, Nanobiol Program, NCI Frederick, Frederick, MD USA.
[Kagan, Bruce] Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst Neurosci & Human Behav, Dept Psychiat, Los Angeles, CA 90095 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Human Mol Genet & Biochem 4Dept, IL-69978 Tel Aviv, Israel.
NR 0
TC 0
Z9 0
U1 2
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 588A
EP 589A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204156
ER
PT J
AU Chaurasiya, KR
Geertsema, H
Qualley, DF
Wu, TY
Iwatani, Y
Chan, D
Hertz, A
Levin, JG
Musier-Forsyth, K
Rouzina, I
Williams, MC
AF Chaurasiya, Kathy R.
Geertsema, Hylkje
Qualley, Dominic F.
Wu, Tiyun
Iwatani, Yasumasa
Chan, Denise
Hertz, Amber
Levin, Judith G.
Musier-Forsyth, Karin
Rouzina, Ioulia
Williams, Mark C.
TI Oligomerization of HIV-1 Restriction Factor APOBEC3G Transforms it from
a Fast Enzyme to a Slow Nucleic Acid Binding Protein
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Chaurasiya, Kathy R.; Geertsema, Hylkje; Williams, Mark C.] Northeastern Univ, Boston, MA 02115 USA.
[Qualley, Dominic F.; Musier-Forsyth, Karin] Ohio State Univ, Columbus, OH 43210 USA.
[Wu, Tiyun; Iwatani, Yasumasa; Hertz, Amber; Levin, Judith G.] NIH, Bethesda, MD 20892 USA.
[Iwatani, Yasumasa] Natl Hosp Org Nagoya Med Ctr, Nagoya, Aichi, Japan.
[Chan, Denise] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Rouzina, Ioulia] Univ Minnesota, Minneapolis, MN USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 601A
EP 601A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204217
ER
PT J
AU Bhatnagar, J
Sim, HM
Georgieva, E
Kapoor, K
Chufan, E
Ohnuma, S
Borbat, PP
Freed, JH
Sauna, ZE
Ambudkar, SV
AF Bhatnagar, Jaya
Sim, Hong-May
Georgieva, Elka
Kapoor, Khyati
Chufan, Eduardo
Ohnuma, Shinobu
Borbat, Peter P.
Freed, Jack H.
Sauna, Zuben E.
Ambudkar, Suresh V.
TI Mapping Conformational Changes Associated with the Catalytic Cycle of
Human P-Glycoprotein (ABCB1)
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Bhatnagar, Jaya; Sim, Hong-May; Kapoor, Khyati; Chufan, Eduardo; Ohnuma, Shinobu; Ambudkar, Suresh V.] NCI, NIH, Bethesda, MD 20892 USA.
[Georgieva, Elka; Borbat, Peter P.; Freed, Jack H.] Cornell Univ, Natl Biomed Ctr Adv ESR Technol, ACERT, Ithaca, NY USA.
[Sauna, Zuben E.] US FDA, Div Hematol, CBER, Bethesda, MD 20014 USA.
RI Borbat, Petr/A-8658-2014; borbat, peter/B-1616-2016
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 606A
EP 607A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204245
ER
PT J
AU Sandtner, W
Egwolf, B
Khalili-Araghi, F
Sanchez-Rodriguez, JE
Roux, B
Bezanilla, F
Holmgren, M
AF Sandtner, Walter
Egwolf, Bernhard
Khalili-Araghi, Fatemeh
Sanchez-Rodriguez, Jorge E.
Roux, Benoit
Bezanilla, Francisco
Holmgren, Miguel
TI Ouabain Binding Site in a Functioning Na plus /K plus -ATPase
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sandtner, Walter] Med Univ Vienna, Vienna, Austria.
[Egwolf, Bernhard] Max Planck Inst Biophys Chem, D-37077 Gottingen, Germany.
[Khalili-Araghi, Fatemeh; Sanchez-Rodriguez, Jorge E.; Roux, Benoit; Bezanilla, Francisco] Univ Chicago, Chicago, IL 60637 USA.
[Holmgren, Miguel] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 607A
EP 607A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204246
ER
PT J
AU Capone, R
Jang, H
Kotler, SA
Connelly, L
Williams, M
Reddy, SR
Kagan, BL
Nussinov, R
Lal, R
AF Capone, Ricardo
Jang, Hyunbum
Kotler, Samuel A.
Connelly, Laura
Williams, Michael
Reddy, Srinivasan Ramachandra
Kagan, Bruce L.
Nussinov, Ruth
Lal, Ratnesh
TI All D-Amino Acids Amyloid beta Forms Ion Channels in Lipid Bilayers and
is Toxic to Cells
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Capone, Ricardo; Kotler, Samuel A.; Connelly, Laura; Reddy, Srinivasan Ramachandra; Lal, Ratnesh] UCSD, Dept Bioengn, La Jolla, SD USA.
[Capone, Ricardo; Kotler, Samuel A.; Connelly, Laura; Reddy, Srinivasan Ramachandra; Lal, Ratnesh] UCSD, Dept Mech & Aerosp Engn, La Jolla, SD USA.
[Jang, Hyunbum; Nussinov, Ruth] SAIC Frederick, Ctr Canc Res, Natl Canc Inst, Nanobiol Program, Frederick, MD USA.
[Williams, Michael] Univ Calif San Diego, IMSD Program, La Jolla, SD USA.
[Kagan, Bruce L.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Tel Aviv, Israel.
NR 0
TC 0
Z9 0
U1 2
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 616A
EP 617A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204293
ER
PT J
AU Carter, M
Voth, A
Ho, S
AF Carter, Megan
Voth, Andrea
Ho, Shing
TI Structure-Energy Relationship of Biological Halogen Bonds: Development
of Anisotropic Force Fields
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Carter, Megan; Ho, Shing] Colorado State Univ, Ft Collins, CO 80523 USA.
[Voth, Andrea] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 620A
EP 620A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204308
ER
PT J
AU Emileh, A
Tuzer, F
Moreira, DR
LaLonde, JM
Bewley, CA
Chaiken, IM
Abrams, CF
AF Emileh, Ali
Tuzer, Ferit
Moreira, Diogo R.
LaLonde, Judith M.
Bewley, Carole A.
Chaiken, Irwin M.
Abrams, Cameron F.
TI A Molecular Dynamics Simulation of Peptide-Triazole HIV Entry Inhibitor
Binding to gp120 Hydrophobic Core
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Emileh, Ali; Abrams, Cameron F.] Drexel Univ, Philadelphia, PA 19104 USA.
[Emileh, Ali; Tuzer, Ferit; Moreira, Diogo R.; Chaiken, Irwin M.] Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
[LaLonde, Judith M.] Bryn Mawr Coll, Bryn Mawr, PA 19010 USA.
[Bewley, Carole A.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 621A
EP 621A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204314
ER
PT J
AU Lee, KI
McLaughlin, SG
Im, W
Pastor, RW
AF Lee, Kyu Il
McLaughlin, Stuart G.
Im, Wonpil
Pastor, Richard W.
TI Langevin Dynamics Simulations of Protein Fencing of PIP2
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Lee, Kyu Il; Im, Wonpil] Univ Kansas, Lawrence, KS 66045 USA.
[McLaughlin, Stuart G.] SUNY Stony Brook, Stony Brook, NY 11794 USA.
[Pastor, Richard W.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 624A
EP 624A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204329
ER
PT J
AU Ball, KA
Phillips, AH
Fawzi, NL
Wemmer, DE
Head-Gordon, T
AF Ball, K. Aurelia
Phillips, Aaron H.
Fawzi, Nicolas L.
Wemmer, David E.
Head-Gordon, Teresa
TI Amyloid-Beta Heterogeneous Conformational Ensembles: Differences Between
the 40-and 42-Residue Peptides and Implications for Dimer Polyamorphism
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Ball, K. Aurelia; Phillips, Aaron H.; Wemmer, David E.; Head-Gordon, Teresa] Univ Calif Berkeley, Berkeley, CA USA.
[Fawzi, Nicolas L.] 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 631A
EP 631A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204365
ER
PT J
AU Tolchard, JL
Eaglen, LA
Morris, L
Hackstadt, T
Blumenschein, TM
AF Tolchard, James L.
Eaglen, Lawrence A.
Morris, Leah
Hackstadt, Ted
Blumenschein, Tharin M.
TI Insights into the Dynamics and Actin Interaction of the Intrinsically
Disordered Tarp Protein from Chlamydia
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Tolchard, James L.; Eaglen, Lawrence A.; Morris, Leah; Blumenschein, Tharin M.] Univ E Anglia, Norwich NR4 7TJ, Norfolk, England.
[Hackstadt, Ted] NIAID, Rocky Mt Labs, Hamilton, MT 59840 USA.
RI Tolchard, Julian/B-7889-2010
OI Tolchard, Julian/0000-0003-0934-4515
NR 0
TC 0
Z9 0
U1 3
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 634A
EP 634A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204378
ER
PT J
AU Kim, T
Afonin, K
Heldman, E
Blumenthal, R
Shapiro, B
AF Kim, Taejin
Afonin, Kirill
Heldman, Eliahu
Blumenthal, Robert
Shapiro, Bruce
TI In Silico and in Ex-Vivo Experiments Indicate the Potential of
Nanoparticles Composed of RNA-Bolaamphiphile Complexes as a Therapeutic
siRNA Delivery Vehicle
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Kim, Taejin; Afonin, Kirill; Heldman, Eliahu; Blumenthal, Robert; Shapiro, Bruce] NCI, Frederick, MD 21701 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 638A
EP 638A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204399
ER
PT J
AU Ivanov, V
Mizuuchi, K
AF Ivanov, Vassili
Mizuuchi, Kiyoshi
TI Alternating Two Different Diffusion States of Min Proteins on the Lipid
Bilayer Revealed by Single Molecule Tracking
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Ivanov, Vassili; Mizuuchi, Kiyoshi] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 652A
EP 652A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204474
ER
PT J
AU Simakova, O
Arispe, NJ
AF Simakova, Olga
Arispe, Nelson J.
TI Phosphatidyl-Serine-Positive Cells with High Sensitivity to the
Alzheimer's Disease A beta Peptides Display Distinctive Mitochondrial
Characteristics
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Simakova, Olga] NIH, Bethesda, MD 20892 USA.
[Arispe, Nelson J.] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 657A
EP 657A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204497
ER
PT J
AU Sirenko, S
Vinogradova, TM
Maltsev, V
Lakatta, EG
AF Sirenko, Syevda
Vinogradova, Tatiana M.
Maltsev, Victor
Lakatta, Edward G.
TI An Inherent Ability of Ventricular Myocytes to Self-Organize Spontaneous
RyRs Activation that Generate Synchronized Local Ca2+ Releases is
Physiologically Suppressed by Constitutive Phosphodiesterase and Protein
Phosphatase Activity
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sirenko, Syevda; Vinogradova, Tatiana M.; Maltsev, Victor; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 671A
EP 672A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204573
ER
PT J
AU Yaniv, Y
Spurgeon, HA
Ziman, BD
Lakatta, EG
AF Yaniv, Yael
Spurgeon, Harold A.
Ziman, Bruce D.
Lakatta, Edward G.
TI Ca2+/Calmodulin-Dependent Protein Kinase II (CaMKII) Activity Modulates
Sinoatrial Nodal Pacemaker Cell Energetics
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Yaniv, Yael; Spurgeon, Harold A.; Ziman, Bruce D.; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 USA.
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
NR 0
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 671A
EP 671A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204572
ER
PT J
AU Maltsev, VA
Yaniv, Y
Lakatta, EG
AF Maltsev, Victor A.
Yaniv, Yael
Lakatta, Edward G.
TI Numerical Modeling of Flash-Induced Ca2+ Release in Sa Node Cells (SANC)
Supports the "Coupled-Clock'' Hypothesis of Cardiac Pacemaker Cell
Function
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Maltsev, Victor A.; Yaniv, Yael; Lakatta, Edward G.] NIA, Gerontol Res Ctr, NIH, Baltimore, MD 21224 USA.
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 673A
EP 673A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204578
ER
PT J
AU Yang, DM
Zahanich, I
Lyashkov, AE
Lakatta, EG
AF Yang, Dongmei
Zahanich, Ihor
Lyashkov, Alexey E.
Lakatta, Edward G.
TI Action Potential (AP) Cycle Length in Connexin-43-Negative and Positive
Single Isolated Sinoatrial Node Cells (SANC) does not Differ in the
Basal State or during High-Level Beta-AR Stimulation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Yang, Dongmei; Zahanich, Ihor; Lyashkov, Alexey E.; Lakatta, Edward G.] NIA, NIH, Baltimore, MD 21224 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 674A
EP 675A
PG 2
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204586
ER
PT J
AU Krepkiy, D
Gawrisch, K
Swartz, KJ
AF Krepkiy, Dmitriy
Gawrisch, Klaus
Swartz, Kenton J.
TI Protein- Lipid Interactions in Lipid Reconstituted Potassium Channel
Voltage-Sensing Domains
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Krepkiy, Dmitriy; Gawrisch, Klaus; Swartz, Kenton J.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 685A
EP 685A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204635
ER
PT J
AU Smith, JJ
AF Smith, Jaime J.
TI Characterization of a Novel Voltage-Sensing Protein
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Smith, Jaime J.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 685A
EP 685A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204636
ER
PT J
AU Miranda, P
Contreras, JE
Wesch, D
Sigworth, FJ
Holmgren, M
Giraldez, T
AF Miranda, Pablo
Contreras, Jorge E.
Wesch, Diana
Sigworth, Fred J.
Holmgren, Miguel
Giraldez, Teresa
TI State-Dependent FRET Reports Large Gating-Ring Motions in BK Channels
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Miranda, Pablo; Wesch, Diana; Giraldez, Teresa] Univ Hosp NS Candelaria, Div Res, Tenerife, Spain.
[Miranda, Pablo; Wesch, Diana] Univ La Laguna, Dept Physiol, Tenerife, Spain.
[Contreras, Jorge E.] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
[Sigworth, Fred J.] Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06510 USA.
[Holmgren, Miguel] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 687A
EP 687A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204647
ER
PT J
AU Chen, J
Lippicott-Schwartz, J
Liu, J
AF Chen, Jing
Lippicott-Schwartz, Jennifer
Liu, Jian
TI Intracellular Spatial Localization Regulated by the Microtubule Network
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Chen, Jing; Lippicott-Schwartz, Jennifer; Liu, Jian] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 698A
EP 698A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561204700
ER
PT J
AU Hung, SH
Arce, SH
Wu, PH
Tseng, Y
AF Hung, Shen-Hsiu
Arce, Stephen Hugo
Wu, Pei-Hsun
Tseng, Yiider
TI A Biophysical Analysis of Cell and Nucleus Relation
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Hung, Shen-Hsiu; Arce, Stephen Hugo; Wu, Pei-Hsun; Tseng, Yiider] Univ Flordia, Dept Chem Engn, Gainseville, FL USA.
[Hung, Shen-Hsiu; Wu, Pei-Hsun; Tseng, Yiider] NCI, Phys Sci Oncol Ctr, Gainesville, FL USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 707A
EP 707A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561205044
ER
PT J
AU Holmgren, M
Gadsby, DC
Bezanilla, F
Rakowski, RF
De Weer, P
AF Holmgren, Miguel
Gadsby, David C.
Bezanilla, Francisco
Rakowski, Robert F.
De Weer, Paul
TI Na+ Access Kinetics in the Na+/K+-Atpase Pump
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Holmgren, Miguel] NIH, Bethesda, MD 20892 USA.
[Gadsby, David C.; Bezanilla, Francisco; Rakowski, Robert F.; De Weer, Paul] Marine Biol Lab, Woods Hole, MA 02543 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 708A
EP 708A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561205050
ER
PT J
AU Sanchez-Rodriguez, JE
Khalili-Araghi, F
Roux, B
Holmgren, M
Bezanilla, F
AF Sanchez-Rodriguez, Jorge E.
Khalili-Araghi, Fatemeh
Roux, Benoit
Holmgren, Miguel
Bezanilla, Francisco
TI Changes of Intramolecular Distances in the Na+/K+ Atpase upon Ouabain
Binding
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sanchez-Rodriguez, Jorge E.; Khalili-Araghi, Fatemeh; Roux, Benoit; Bezanilla, Francisco] Univ Chicago, Dept Biochem & Mol Biol, Gordon Ctr Integrat Sci, Chicago, IL 60637 USA.
[Holmgren, Miguel] NINDS, Mol Neurophysiol Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 708A
EP 708A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561205049
ER
PT J
AU Chandran, PL
Dimitriadis, EK
Horkay, F
AF Chandran, Preethi L.
Dimitriadis, Emilios K.
Horkay, Ferenc
TI Structure, Assembly and Mechanical Properties of DNA Nanoparticles
Condensed with Peim
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Chandran, Preethi L.] NIH, Bethesda, MD 20892 USA.
[Dimitriadis, Emilios K.] NIBIB, Lab Bioengn & Phys Sci, NIH, Bethesda, MD USA.
[Horkay, Ferenc] NICHD, Sect Tissue Biophys & Biomimet, 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 719A
EP 719A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561205103
ER
PT J
AU Sarkar, SK
Bumb, A
Wu, XFS
Brechbiel, MW
Neuman, KC
AF Sarkar, Susanta K.
Bumb, Ambika
Wu, Xufeng S.
Brechbiel, Martin W.
Neuman, Keir C.
TI Quantitative Characterization of Dyes Embedded in Nanoparticles by
Single-Molecule Fluorescence
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Sarkar, Susanta K.; Bumb, Ambika; Wu, Xufeng S.; Brechbiel, Martin W.; Neuman, Keir C.] NIH, Bethesda, MD 20892 USA.
RI Neuman, Keir/F-7400-2011
OI Neuman, Keir/0000-0002-0863-5671
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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 725A
EP 725A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561205136
ER
PT J
AU Balijepalli, A
Lee, KI
Im, W
Pastor, RW
AF Balijepalli, Arvind
Lee, Kyu Il
Im, Wonpil
Pastor, Richard W.
TI Modeling Polymer Interactions with Nanopores for DNA Sequencing and
Proteomics Applications
SO BIOPHYSICAL JOURNAL
LA English
DT Meeting Abstract
CT 56th Annual Meeting of the Biophysical-Society
CY FEB 25-29, 2012
CL San Diego, CA
SP Biophys Soc
C1 [Balijepalli, Arvind; Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[Balijepalli, Arvind] NIST, Div Semicond Elect, Phys Measurement Lab, Gaithersburg, MD 20899 USA.
[Lee, Kyu Il; Im, Wonpil] Univ Kansas, Dept Mol Biosci, Lawrence, KS 66045 USA.
[Lee, Kyu Il; Im, Wonpil] Univ Kansas, Ctr Bioinformat, Lawrence, KS 66045 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 JAN 31
PY 2012
VL 102
IS 3
SU 1
BP 732A
EP 732A
PG 1
WC Biophysics
SC Biophysics
GA 179ZF
UT WOS:000321561205170
ER
PT J
AU Diesner, SC
Olivera, A
Dillahunt, S
Schultz, C
Watzlawek, T
Forster-Waldl, E
Pollak, A
Jensen-Jarolim, E
Untersmayr, E
Rivera, J
AF Diesner, Susanne C.
Olivera, Ana
Dillahunt, Sandra
Schultz, Cornelia
Watzlawek, Thomas
Foerster-Waldl, Elisabeth
Pollak, Arnold
Jensen-Jarolim, Erika
Untersmayr, Eva
Rivera, Juan
TI Sphingosine-kinase 1 and 2 contribute to oral sensitization and effector
phase in a mouse model of food allergy
SO IMMUNOLOGY LETTERS
LA English
DT Article
DE Sphingosine-1-phosphate; Food allergy; Sphingosine kinase; Mast cells;
Anti-ulcer medication; Ovalbumin
ID MAST-CELLS; BARRIER FUNCTION; SPHINGOSINE-1-PHOSPHATE; 1-PHOSPHATE;
RECEPTORS; ANAPHYLAXIS; SUPPRESSION; PROTEINS; ASTHMA; MICE
AB Background: Sphingosine-1-phosphate (S1P) influences activation, migration and death of immune cells. Further, S1P was proposed to play a major role in the induction and promotion of allergic diseases. However, to date only limited information is available on the role of S1P in food allergy.
Objective: We aimed to investigate the role of sphingosine-kinase (SphK) 1 and 2, the enzymes responsible for endogenous S1P production, on the induction of food allergy.
Methods and results: Human epithelial colorectal CaCo2 cells stimulated in vitro with S1P revealed a decrease of transepithelial resistance and enhanced transport of FITC labeled OVA. We studied the effect of genetic deletion of the enzymes involved in S1P production on food allergy induction using a mouse model of food allergy based on intragastrically (i.g.) administered ovalbumin (OVA) with concomitant acid-suppression. Wild-type (WT), SphK1(-/-) and SphK2(-/-) mice immunized with OVA alone i.g. or intraperitoneally (i.p.) were used as negative or positive controls, respectively. SphK1- and SphK2-deficient mice fed with OVA under acid-suppression showed reduced induction of OVA specific IgE and IgG compared to WT mice, but had normal responses when immunized by the intraperitoneal route. Flow cytometric analysis of spleen cells revealed a significantly reduced proportion of CD4(+) effector T-cells in both SphK deficient animals after oral sensitization. This was accompanied by a reduced accumulation of mast cells in the gastric mucosa in SphK-deficient animals compared to WT mice. Furthermore, mouse mast cell protease-1 (mMCP-1) levels, an IgE-mediated anaphylaxis marker, were reliably elevated in allergic WT animals.
Conclusion: Modulation of the S1P homeostasis by deletion of either SphK1 or SphK2 alters the sensitization and effector phase of food allergy. (C) 2011 Elsevier B.V. All rights reserved.
C1 [Diesner, Susanne C.; Schultz, Cornelia; Watzlawek, Thomas; Jensen-Jarolim, Erika; Untersmayr, Eva] Med Univ Vienna, Ctr Pathophysiol Infectiol & Immunol, Dept Pathophysiol & Allergy Res, A-1090 Vienna, Austria.
[Diesner, Susanne C.; Foerster-Waldl, Elisabeth; Pollak, Arnold] Med Univ Vienna, Dept Pediat & Adolescent Med, A-1090 Vienna, Austria.
[Diesner, Susanne C.; Olivera, Ana; Dillahunt, Sandra; Rivera, Juan] NIAMS, Immunogenet Mol Lab, NIH, Bethesda, MD 20892 USA.
[Jensen-Jarolim, Erika] Univ Vienna, Messerli Inst Med Univ Vienna, A-1090 Vienna, Austria.
[Jensen-Jarolim, Erika] Vet Univ Vienna, A-1090 Vienna, Austria.
RP Untersmayr, E (reprint author), Med Univ Vienna, Ctr Pathophysiol Infectiol & Immunol, Dept Pathophysiol & Allergy Res, Waehringer Guertel 18-20,E3Q, A-1090 Vienna, Austria.
EM eva.untersmayr@meduniwien.ac.at; juan_rivera@nih.gov
FU NIAMS, NIH; Austrian Science fund FWF [P21577, P21884]; European
Molecular Biology Organization (EMBO) [ASTF 374-2008]; Flow Cytometry
Section, Laboratory Animal Care and Use Section, and the Light Imaging
Section, of the Office of Science and Technology, NIAMS
FX This work was supported by the Intramural Research Program of NIAMS, NIH
and grants of the Austrian Science fund FWF (P21577 and P21884). Susanne
C. Diesner was supported by a short-term fellowship (ASTF 374-2008) of
the European Molecular Biology Organization (EMBO). We also acknowledge
the support of the Flow Cytometry Section, Laboratory Animal Care and
Use Section, and the Light Imaging Section, of the Office of Science and
Technology, NIAMS and Dr. Sonja Zehetmayer for statistical advise in
data presentation.
NR 42
TC 15
Z9 15
U1 0
U2 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-2478
J9 IMMUNOL LETT
JI Immunol. Lett.
PD JAN 30
PY 2012
VL 141
IS 2
BP 210
EP 219
DI 10.1016/j.imlet.2011.10.006
PG 10
WC Immunology
SC Immunology
GA 900AR
UT WOS:000300859500009
PM 22020265
ER
PT J
AU Jacobson, O
Weiss, ID
Szajek, LP
Niu, G
Ma, Y
Kiesewetter, DO
Peled, A
Eden, HS
Farber, JM
Chen, XY
AF Jacobson, Orit
Weiss, Ido D.
Szajek, Lawrence P.
Niu, Gang
Ma, Ying
Kiesewetter, Dale O.
Peled, Amnon
Eden, Henry S.
Farber, Joshua M.
Chen, Xiaoyuan
TI Improvement of CXCR4 tracer specificity for PET imaging
SO JOURNAL OF CONTROLLED RELEASE
LA English
DT Article
DE T140; CXCR4 imaging; PET; Copper-64
ID CHEMOKINE RECEPTORS; BONE-MARROW; CELL MOBILIZATION; CANCER METASTASIS;
G-CSF; TUMOR; EXPRESSION; MICROENVIRONMENT; ANTAGONIST; XENOGRAFTS
AB Tumors expressing the chemokine receptor CXCR4 have been reported to be more aggressive and to produce more metastatic seeding in specific organs, such as the bone marrow. However, evaluation of tumors for CXCR4 expression requires testing of ex vivo biopsy samples, and is not routinely done in cancer management. In prior work to address this issue, we and others have developed tracers for positron emission tomography (PET) that targeted CXCR4, but in addition to binding to CXCR4 these tracers also bound to red blood cells (and to other unrelated targets) in vivo. Here we report two new tracers based on the CXCR4 peptide antagonist 4F-benzoyl-TN14003 (T140) that bind to CXCR4, but not to undesired targets. These tracers, NOTA-NFB and DOTA-NFB, show slight reductions in both 1) binding affinities for CXCR4 and 2) inhibition of CXCL12 induced migration, compared to T140, in vitro. Both NOTA-NFB and DOTA-NFB specifically accumulate in CXCR4-positive, but not CXCR4-negative, tumor xenografts in mice and allow clear visualization of CXCR4 expression by PET. Evaluation of NOTA-NFB and DOTA-NFB for their potential to mobilize immune cells and progenitor cells from the bone marrow to the peripheral blood revealed slightly reduced, but still comparable, results to the parent molecule T140. The tracers reported here may allow the evaluation of CXCR4 expression in primary tumors and metastatic nodules, and enable better informed, more personalized treatment for patients with cancer. Published by Elsevier B.V.
C1 [Jacobson, Orit; Niu, Gang; Ma, Ying; Kiesewetter, Dale O.; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
[Weiss, Ido D.; Farber, Joshua M.] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
[Szajek, Lawrence P.] NIH, Warren Grant Magnuson Clin Ctr, Positron Emiss Tomog Dept, Bethesda, MD 20892 USA.
[Peled, Amnon] Hadassah Hebrew Univ Hosp, Goldyne Savad Inst Gene Therapy, Jerusalem, Israel.
[Eden, Henry S.] NIBIB, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
RP Chen, XY (reprint author), NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bldg 31,Room 1C22, Bethesda, MD 20892 USA.
EM shawn.chen@nih.gov
FU National Institute of Biomedical Imaging and Bioengineering (NIBIB);
National Institute of Allergy and Infectious Diseases (NIAID), National
Institutes of Health (NIH); National Science Foundation of China (NSFC)
[81028009]
FX This research was supported in part by the Intramural Research Programs
(IRPs) of the National Institute of Biomedical Imaging and
Bioengineering (NIBIB) and the National Institute of Allergy and
Infectious Diseases (NIAID), National Institutes of Health (NIH), and by
the International Cooperative Program of the National Science Foundation
of China (NSFC) (81028009).
NR 35
TC 19
Z9 19
U1 0
U2 16
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0168-3659
J9 J CONTROL RELEASE
JI J. Control. Release
PD JAN 30
PY 2012
VL 157
IS 2
BP 216
EP 223
DI 10.1016/j.jconrel.2011.09.076
PG 8
WC Chemistry, Multidisciplinary; Pharmacology & Pharmacy
SC Chemistry; Pharmacology & Pharmacy
GA 902NO
UT WOS:000301045400007
PM 21964282
ER
PT J
AU Simons, SS
Chow, CC
AF Simons, S. Stoney, Jr.
Chow, Carson C.
TI The road less traveled: New views of steroid receptor action from the
path of dose-response curves
SO MOLECULAR AND CELLULAR ENDOCRINOLOGY
LA English
DT Review
DE Steroid hormone action; Potency (EC50); Efficacy (A(max)); Partial
agonist activity (PAA); New insight for steroid receptor mechanism
ID LIGAND-BINDING DOMAIN; GLUCOCORTICOID-RECEPTOR; GENE-EXPRESSION; NUCLEAR
RECEPTOR; COACTIVATOR BINDING; INDUCTION PROPERTIES; ANDROGEN RECEPTOR;
TRANSCRIPTION; TRANSACTIVATION; PROMOTER
AB Conventional studies of steroid hormone action proceed via quantitation of the maximal activity for gene induction at saturating concentrations of agonist steroid (i.e., A(max)). Less frequently analyzed parameters of receptor-mediated gene expression are EC50 and PAA. The EC50 is the concentration of steroid required for half-maximal agonist activity and is readily determined from the dose-response curve. The PAA is the partial agonist activity of an antagonist steroid, expressed as percent of A(max) under the same conditions. Recent results demonstrate that new and otherwise inaccessible mechanistic information is obtained when the EC50 and/or PAA are examined in addition to the A(max). Specifically, A(max), EC50, and PAA can be independently regulated, which suggests that novel pathways and factors may preferentially modify the EC50 and/or PAA with little effect on A(max). Other approaches indicate that the activity of receptor-bound factors can be altered without changing the binding of factors to receptor. Finally, a new theoretical model of steroid hormone action not only permits a mechanistically based definition of factor activity but also allows the positioning of when a factor acts, as opposed to binds, relative to a kinetically defined step. These advances illustrate some of the benefits of expanding the mechanistic studies of steroid hormone action to routinely include EC50 and PAA. Published by Elsevier Ireland Ltd.
C1 [Simons, S. Stoney, Jr.] NIDDK, Steroid Hormones Sect, CEB, NIH, Bethesda, MD 20892 USA.
[Chow, Carson C.] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD 20892 USA.
RP Simons, SS (reprint author), NIDDK, Steroid Hormones Sect, CEB, NIH, Bldg 10,Room 8N-307B, Bethesda, MD 20892 USA.
EM steroids@helix.nih.gov
RI Chow, Carson/A-7970-2009
FU NIH, NIDDK
FX We thank members of the Steroid Hormones Section for valuable comments
and insight. This research was supported by the Intramural Research
Program of the NIH, NIDDK.
NR 47
TC 11
Z9 11
U1 0
U2 3
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0303-7207
J9 MOL CELL ENDOCRINOL
JI Mol. Cell. Endocrinol.
PD JAN 30
PY 2012
VL 348
IS 2
SI SI
BP 373
EP 382
DI 10.1016/j.mce.2011.05.030
PG 10
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 891BF
UT WOS:000300190500004
PM 21664235
ER
PT J
AU Conway-Campbell, BL
Pooley, JR
Hager, GL
Lightman, SL
AF Conway-Campbell, Becky L.
Pooley, John R.
Hager, Gordon L.
Lightman, Stafford L.
TI Molecular dynamics of ultradian glucocorticoid receptor action
SO MOLECULAR AND CELLULAR ENDOCRINOLOGY
LA English
DT Review
DE Glucocorticoid receptor; Ultradian; Transcription; CBP; P300;
Acetylation
ID PITUITARY-ADRENAL AXIS; LIGAND-SPECIFIC DYNAMICS; TARGET GENE PROMOTERS;
ESTROGEN-RECEPTOR; LIVING CELLS; HISTONE ACETYLATION; IN-VIVO; STRESS
RESPONSIVENESS; ANDROGEN RECEPTOR; FEMALE RATS
AB In recent years it has become evident that glucocorticoid receptor (GR) action in the nucleus is highly dynamic, characterized by a rapid exchange at the chromatin template. This stochastic mode of GR action couples perfectly with a deterministic pulsatile availability of endogenous ligand in vivo. The endogenous glucocorticoid hormone (cortisol in man and corticosterone in rodent) is secreted from the adrenal gland with an ultradian rhythm made up of pulses at approximately hourly intervals. These two components the rapidly fluctuating ligand and the rapidly exchanging receptor - appear to have evolved to establish and maintain a system that is exquisitely responsive to the physiological demands of the organism. In this review, we discuss recent and innovative work that questions the idea of steady state, static hormone receptor responses, and replaces them with new concepts of stochastic mechanisms and oscillatory activity essential for optimal function in molecular and cellular systems. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
C1 [Conway-Campbell, Becky L.; Pooley, John R.; Lightman, Stafford L.] Univ Bristol, Henry Wellcome Labs Integrat Neurosci & Endocrino, Bristol BS1 3NY, Avon, England.
[Pooley, John R.; Hager, Gordon L.] NCI, Lab Receptor Biol & Gene Express, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Conway-Campbell, BL (reprint author), Univ Bristol, Henry Wellcome Labs Integrat Neurosci & Endocrino, Dorothy Hodgkin Bldg,Whitson St, Bristol BS1 3NY, Avon, England.
EM b.conway-campbell@bristol.ac.uk
FU Medical Research Council [MR/J008893/1]
NR 119
TC 25
Z9 28
U1 0
U2 15
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0303-7207
J9 MOL CELL ENDOCRINOL
JI Mol. Cell. Endocrinol.
PD JAN 30
PY 2012
VL 348
IS 2
SI SI
BP 383
EP 393
DI 10.1016/j.mce.2011.08.014
PG 11
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 891BF
UT WOS:000300190500005
PM 21872640
ER
PT J
AU Albert, PS
AF Albert, Paul S.
TI A linear mixed model for predicting a binary event from longitudinal
data under random effects misspecification
SO STATISTICS IN MEDICINE
LA English
DT Article
DE longitudinal data; prediction; random effects distribution
ID MAXIMUM-LIKELIHOOD ESTIMATION; GROWTH
AB The use of longitudinal data for predicting a subsequent binary event is often the focus of diagnostic studies. This is particularly important in obstetrics, where ultrasound measurements taken during fetal development may be useful for predicting various poor pregnancy outcomes. We propose a modeling framework for predicting a binary event from longitudinal measurements where a shared random effect links the two processes together. Under a Gaussian random effects assumption, the approach is simple to implement with standard statistical software. Using asymptotic and simulation results, we show that estimates of predictive accuracy under a Gaussian random effects distribution are robust to severe misspecification of this distribution. However, under some circumstances, estimates of individual risk may be sensitive to severe random effects misspecification. We illustrate the methodology with data from a longitudinal fetal growth study. Copyright (C) 2011 John Wiley & Sons, Ltd.
C1 Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA.
RP Albert, PS (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA.
EM albertp@mail.nih.gov
FU National Institutes of Health, Eunice Kennedy Shriver National Institute
of Child Health and Human Development
FX I thank the associate editor and two reviewers for their constructive
comments on this article. I also thank Dr. Jun Zhang for the helpful
comments on this manuscript and the Center for Information Technology,
National Institutes of Health, for providing access to the
high-performance computational capabilities of the Biowulf cluster
computer system. The Intramural Research Program of the National
Institutes of Health, Eunice Kennedy Shriver National Institute of Child
Health and Human Development supported this research.
NR 24
TC 8
Z9 8
U1 0
U2 6
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0277-6715
J9 STAT MED
JI Stat. Med.
PD JAN 30
PY 2012
VL 31
IS 2
BP 143
EP 154
DI 10.1002/sim.4405
PG 12
WC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Medicine, Research &
Experimental; Statistics & Probability
SC Mathematical & Computational Biology; Public, Environmental &
Occupational Health; Medical Informatics; Research & Experimental
Medicine; Mathematics
GA 869JY
UT WOS:000298595400004
PM 22081439
ER
PT J
AU Lee, KI
Jo, S
Rui, H
Egwolf, B
Roux, B
Pastor, RW
Im, W
AF Lee, Kyu Il
Jo, Sunhwan
Rui, Huan
Egwolf, Bernhard
Roux, Benoit
Pastor, Richard W.
Im, Wonpil
TI Web interface for brownian dynamics simulation of ion transport and its
applications to beta-barrel pores
SO JOURNAL OF COMPUTATIONAL CHEMISTRY
LA English
DT Article
DE grand canonical Monte Carlo; Brownian dynamics; channel conductance; ion
selectivity; voltage dependent anion channel; a-hemolysin; anthrax toxin
protective antigen pore
ID STAPHYLOCOCCAL ALPHA-HEMOLYSIN; NONCOVALENT MOLECULAR ADAPTER;
PROTECTIVE ANTIGEN; ELECTRODIFFUSION THEORY; OMPF PORIN; CHANNEL;
PERMEATION; CYCLODEXTRIN; SELECTIVITY; ANTHRAX
AB Brownian dynamics (BD) based on accurate potential of mean force is an efficient and accurate method for simulating ion transport through wide ion channels. Here, a web-based graphical user interface (GUI) is presented for carrying out grand canonical Monte Carlo (GCMC) BD simulations of channel proteins: . The webserver is designed to help users avoid most of the technical difficulties and issues encountered in setting up and simulating complex pore systems. GCMC/BD simulation results for three proteins, the voltage dependent anion channel (VDAC), a-Hemolysin (a-HL), and the protective antigen pore of the anthrax toxin (PA), are presented to illustrate the system setup, input preparation, and typical output (conductance, ion density profile, ion selectivity, and ion asymmetry). Two models for the input diffusion constants for potassium and chloride ions in the pore are compared: scaling of the bulk diffusion constants by 0.5, as deduced from previous all-atom molecular dynamics simulations of VDAC, and a hydrodynamics based model (HD) of diffusion through a tube. The HD model yields excellent agreement with experimental conductances for VDAC and a-HL, while scaling bulk diffusion constants by 0.5 leads to underestimates of 1020%. For PA, simulated ion conduction values overestimate experimental values by a factor of 1.57 (depending on His protonation state and the transmembrane potential), implying that the currently available computational model of this protein requires further structural refinement. (C) 2011 Wiley Periodicals, Inc. J Comput Chem, 2012
C1 [Lee, Kyu Il; Jo, Sunhwan; Rui, Huan; Im, Wonpil] Univ Kansas, Ctr Bioinformat, Lawrence, KS 66045 USA.
[Lee, Kyu Il; Jo, Sunhwan; Rui, Huan; Im, Wonpil] Univ Kansas, Dept Mol Biosci, Lawrence, KS 66045 USA.
[Egwolf, Bernhard] Max Planck Inst Biophys Chem, Dept Theoret & Computat Biophys, Gottingen, Germany.
[Roux, Benoit] Univ Chicago, Dept Biochem & Mol Biol, Chicago, IL 60637 USA.
[Pastor, Richard W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
RP Lee, KI (reprint author), Univ Kansas, Ctr Bioinformat, Lawrence, KS 66045 USA.
EM wonpil@ku.edu
FU University of Kansas [2301388-003]; Kansas-COBRE NIH [P20 RR-17708];
National Science Foundation [NSF OCI-0503992]; NIH [GM062342]; German
Research Foundation; National Heart, Lung, and Blood Institute in the
National Institutes of Health
FX Contract grant sponsor: University of Kansas General Research Fund
allocation; Contract grant number: 2301388-003; Contract grant sponsor:
Kansas-COBRE NIH; Contract grant number: P20 RR-17708; Contract grant
sponsor: National Science Foundation (TeraGrid resources provided by
Purdue University); Contract grant number: NSF OCI-0503992; Contract
grant sponsor: NIH; Contract grant number: GM062342; Contract grant
sponsors: German Research Foundation; Intramural Research Program of the
National Heart, Lung, and Blood Institute in the National Institutes of
Health
NR 43
TC 23
Z9 23
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0192-8651
J9 J COMPUT CHEM
JI J. Comput. Chem.
PD JAN 30
PY 2012
VL 33
IS 3
BP 331
EP 339
DI 10.1002/jcc.21952
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA 861ZA
UT WOS:000298058400011
PM 22102176
ER
PT J
AU Auffray, C
Caulfield, T
Khoury, MJ
Lupski, JR
Schwab, M
Veenstra, T
AF Auffray, Charles
Caulfield, Timothy
Khoury, Muin J.
Lupski, James R.
Schwab, Matthias
Veenstra, Timothy
TI Looking back at genomic medicine in 2011
SO GENOME MEDICINE
LA English
DT Editorial Material
ID REARRANGEMENTS; HLA-A-ASTERISK-3101; POPULATION; MICROBIOME; DISEASE
C1 [Auffray, Charles] Univ Lyon 1, European Inst Syst Biol & Med, CNRS Inst Biol Sci, F-69007 Lyon, France.
[Caulfield, Timothy] Univ Alberta, Fac Law, Edmonton, AB T6G 2H5, Canada.
[Caulfield, Timothy] Univ Alberta, Law Ctr 461, Sch Publ Hlth, Edmonton, AB T6G 2H5, Canada.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA 30333 USA.
[Lupski, James R.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Lupski, James R.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
[Lupski, James R.] Texas Childrens Hosp, Houston, TX 77030 USA.
[Schwab, Matthias] Dr Margarete Fischer Bosch Inst Clin Pharmacol, D-70367 Stuttgart, Germany.
[Schwab, Matthias] Univ Tubingen Hosp, Inst Expt & Clin Pharmacol & Toxicol, Dept Clin Pharmacol, D-72076 Tubingen, Germany.
[Veenstra, Timothy] NCI, Lab Prote & Analyt Technol, Frederick, MD 21702 USA.
RP Auffray, C (reprint author), Univ Lyon 1, European Inst Syst Biol & Med, CNRS Inst Biol Sci, F-69007 Lyon, France.
EM auffray@vjf.cnrs.fr
FU NCRR NIH HHS [M01 RR000188]; NINDS NIH HHS [R01 NS058529]
NR 37
TC 5
Z9 5
U1 1
U2 11
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-994X
J9 GENOME MED
JI Genome Med.
PD JAN 30
PY 2012
VL 4
AR 9
DI 10.1186/gm308
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 084UQ
UT WOS:000314565000001
PM 22293121
ER
PT J
AU French, M
Kinter, A
AF French, Martyn
Kinter, Audrey
TI Regulatory T cells are converts in simian immunodeficiency virus
infection
SO AIDS
LA English
DT Editorial Material
DE dendritic cells; lymphoid tissue; simian immunodeficiency virus
ID DENDRITIC CELLS; IMMUNE ACTIVATION; HIV-INFECTION; INDOLEAMINE
2,3-DIOXYGENASE; RHESUS MACAQUES; INDUCTION; MECHANISM; MUCOSAL; GUT
C1 [Kinter, Audrey] NIAID, LMM, NIH, Bethesda, MD 20982 USA.
[French, Martyn] Univ Western Australia, Royal Perth Hosp, Perth CBD Western Australia, Sch Pathol & Lab Med, Nedlands, WA 6009, Australia.
RP Kinter, A (reprint author), NIAID, LMM, NIH, Bldg 4,Rm 341,9000 Rockville Pike, Bethesda, MD 20982 USA.
EM akinter@niaid.nih.gov
NR 20
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0269-9370
J9 AIDS
JI Aids
PD JAN 28
PY 2012
VL 26
IS 3
BP 395
EP 396
DI 10.1097/QAD.0b013e32834ee778
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 876NV
UT WOS:000299115300016
PM 22217503
ER
PT J
AU Yan, CG
Zhu, M
Staiger, J
Johnson, PF
Gao, HW
AF Yan, Chunguang
Zhu, Mei
Staiger, Jennifer
Johnson, Peter F.
Gao, Hongwei
TI C5a-regulated CCAAT/Enhancer-binding Proteins beta and delta Are
Essential in Fc gamma Receptor-mediated Inflammatory Cytokine and
Chemokine Production in Macrophages
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID C/EBP-BETA; PROINFLAMMATORY CYTOKINES; KINASE ACTIVATION;
IMMUNE-COMPLEXES; LUNG INJURY; GENE; EXPRESSION; INDUCTION; CELLS; C5A
AB CCAAT/enhancer-binding protein beta (C/EBP beta) and C/EBP delta are known to participate in the regulation of many genes associated with inflammation. However, little is known about the activation and function of C/EBP beta and -delta in inflammatory responses elicited by Fc gamma receptor (Fc gamma R) activation. Here we show that C/EBP beta and -delta activation are induced in IgG immune complex (IC)-treated macrophages. The increased expression of C/EBP beta and -delta occurred at both mRNA and protein levels. Furthermore, induction of C/EBP beta and -delta was mediated, to a large extent, by activating Fc gamma Rs. Using siRNA-mediated knockdown as well as macrophages deficient for C/EBP beta and/or -delta, we demonstrate that C/EBP beta and -delta play a critical role in the production of TNF-alpha, MIP-2, and MIP-1 alpha in IgG IC-stimulated macrophages. Moreover, both ERK1/2 and p38 MAPK are involved in C/EBP induction and TNF-alpha, MIP-2, and MIP-1 alpha production induced by IgGIC. We provide the evidence that C5a regulates IgGIC-induced inflammatory responses by enhancing ERK1/2 and p38 MAPK activities as well as C/EBP beta and -delta activities. Collectively, these data suggest that C/EBP beta and -delta are key regulators for Fc gamma R-mediated induction of cytokines and chemokines in macrophages. Furthermore, C/EBPs may play an important regulatory role in IC-associated inflammatory responses.
C1 [Yan, Chunguang; Gao, Hongwei] Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, Dept Anesthesiol Perioperat & Pain Med,Sch Med, Boston, MA 02115 USA.
[Zhu, Mei] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Staiger, Jennifer] Mt St Marys Univ, Dept Sci, Sch Nat Sci & Math, Emmitsburg, MD 21727 USA.
[Johnson, Peter F.] NCI, Lab Canc Prevent, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
RP Gao, HW (reprint author), Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, Dept Anesthesiol,Sch Med, 20 Shattuck St, Boston, MA 02115 USA.
EM hgao@zeus.bwh.harvard.edu
FU National Institutes of Health (NIH) [5R01HL092905-04,
3R01HL092905-02S1]; NIH, NCI, Center for Cancer Research
FX This work was supported, in whole or in part, by National Institutes of
Health (NIH) Grants 5R01HL092905-04 and 3R01HL092905-02S1 (to H. G.) and
the Intramural Research Program of the NIH, NCI, Center for Cancer
Research.
NR 53
TC 18
Z9 19
U1 1
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD JAN 27
PY 2012
VL 287
IS 5
BP 3217
EP 3230
DI 10.1074/jbc.M111.280834
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 892OI
UT WOS:000300295100027
PM 22147692
ER
PT J
AU Mburu, YK
Egloff, AM
Walker, WH
Wang, L
Seethala, RR
van Waes, C
Ferris, RL
AF Mburu, Yvonne K.
Egloff, Ann Marie
Walker, William H.
Wang, Lin
Seethala, Raja R.
van Waes, Carter
Ferris, Robert L.
TI Chemokine Receptor 7 (CCR7) Gene Expression Is Regulated by NF-kappa B
and Activator Protein 1 (AP1) in Metastatic Squamous Cell Carcinoma of
Head and Neck (SCCHN)
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID CANCER; PROLIFERATION; TRANSCRIPTION; PATHWAYS; APOPTOSIS; CYTOKINES;
BIOLOGY; LINES; IL-8; AP-1
AB The chemokine receptor CCR7 is a seven-transmembrane domain G-protein-coupled receptor that facilitates leukocyte migration to regional lymph nodes. Aberrant CCR7 expression in a number of human malignancies has been linked to prosurvival, -invasive, and -metastatic pathways. We demonstrate here that up-regulation of CCR7 in squamous cell carcinoma of the head and neck (SCCHN) patient tumors correlates with lower survival because of metastatic disease. Because of this important oncogenic phenotype, we investigated the mechanisms that regulate CCR7 expression in these tumors. Interestingly, the inflammatory transcription factor NF-kappa B has been associated with a more aggressive SCCHN phenotype. Immunohistochemical staining of a SCCHN tumor cohort (n = 47) strongly linked NF-kappa B staining and CCR7 expression in SCCHN. Thus, we investigated whether NF-kappa B contributes to metastatic disease by promoting CCR7 expression in SCCHN tumor cells. Wecharacterized four novel, potential NF-kappa B binding sites in the 1000-bp promoter region upstream of the CCR7 gene, using luciferase, ChIP, and EMSA. However, NF-kappa B inhibition only resulted in partial reduction in CCR7 expression, prompting consideration of other co-regulators of CCR7. Indeed, cooperation between NF-kappa B and AP1 transcription factors, which are often co-activated, is crucial to the regulation of CCR7 mRNA expression in metastatic SCCHN cells. Thus, our findings support an important biological role for inflammatory NF-kappa B and AP1 in the regulation of CCR7 expression in metastatic SCCHN. As such, CCR7, NF-kappa B, and AP1 could be potentially useful therapeutic targets in controlling the progression and metastasis of SCCHN tumors.
C1 [Ferris, Robert L.] Univ Pittsburgh, Inst Canc, Hillman Canc Ctr, Pittsburgh, PA 15213 USA.
[Mburu, Yvonne K.; Ferris, Robert L.] Univ Pittsburgh, Dept Immunol, Pittsburgh, PA 15261 USA.
[Egloff, Ann Marie; Ferris, Robert L.] Univ Pittsburgh, Med Ctr, Dept Otolaryngol, Pittsburgh, PA 15213 USA.
[Walker, William H.] Univ Pittsburgh, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA 15213 USA.
[Wang, Lin; Seethala, Raja R.] Univ Pittsburgh, Dept Pathol, Pittsburgh, PA 15261 USA.
[van Waes, Carter] Natl Inst Deafness & Other Commun Disorders, Head & Neck Surg Branch, Bethesda, MD 20892 USA.
RP Ferris, RL (reprint author), Univ Pittsburgh, Inst Canc, Hillman Canc Ctr, Res Wing,Rm 2-26B,5117 Ctr Ave, Pittsburgh, PA 15213 USA.
EM ferrisrl@upmc.edu
FU National Institutes of Health [1R01 CA115902]
FX This work was supported, in whole or in part, by National Institutes of
Health Grant 1R01 CA115902 (to R. L. F.).
NR 28
TC 21
Z9 22
U1 1
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD JAN 27
PY 2012
VL 287
IS 5
BP 3581
EP 3590
DI 10.1074/jbc.M111.294876
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 892OI
UT WOS:000300295100062
PM 22158872
ER
PT J
AU Chen, WZ
Streaker, ED
Russ, DE
Feng, Y
Prabakaran, P
Dimitrov, DS
AF Chen, Weizao
Streaker, Emily D.
Russ, Daniel E.
Feng, Yang
Prabakaran, Ponraj
Dimitrov, Dimiter S.
TI Characterization of germline antibody libraries from human umbilical
cord blood and selection of monoclonal antibodies to viral envelope
glycoproteins: Implications for mechanisms of immune evasion and design
of vaccine immunogens
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE HIV-1; Human monoclonal antibody; IgM; gp120; Envelope glycoprotein;
Immunogen
ID NEUTRALIZING ANTIBODIES; HIV-1 GP120; CONSTRUCTION; VIRUS; EXPRESSION;
BINDING; HENDRA; DOMAIN
AB We have previously observed that all known HIV-1 broadly neutralizing antibodies (bnAbs) are highly divergent from germline antibodies in contrast to bnAbs against Hendra virus, Nipah virus and SARS coronavirus (SARS CoV). We have hypothesized that because the germline antibodies are so different from the mature HIV-1-specific bnAbs they may not bind the epitopes of the mature antibodies and provided the first evidence to support this hypothesis by using individual putative germline-like predecessor antibodies. To further validate the hypothesis and understand initial immune responses to different viruses, two phage-displayed human cord blood-derived IgM libraries were constructed which contained mostly germline antibodies or antibodies with very low level of somatic hypermutations. They were panned against different HIV-1 envelope glycoproteins (Envs), SARS Coy protein receptor-binding domain (RBD), and soluble Hendra virus G protein (sG). Despite a high sequence and combinatorial diversity observed in the cord blood-derived IgM antibody repertoire, no enrichment for binders of Envs was observed in contrast to considerable specific enrichments produced with panning against RBD and sG; one of the selected monoclonal antibodies (against the RBD) was of high (nM) affinity with only few somatic mutations. These results further support and expand our initial hypothesis for fundamental differences in immune responses leading to elicitation of bnAbs against HIV-1 compared to SARS CoV and Hendra virus. HIV-1 uses a strategy to minimize or eliminate strong binding of germline antibodies to its Env; in contrast, SARS CoV and Hendra virus, and perhaps other viruses causing acute infections, can bind germline antibody or minimally somatically mutated antibodies with relatively high affinity which could be one of the reasons for the success of sG and RBD as vaccine immunogens. Published by Elsevier Inc.
C1 [Chen, Weizao; Streaker, Emily D.; Feng, Yang; Prabakaran, Ponraj; Dimitrov, Dimiter S.] NCI, Prot Interact Grp, Ctr Canc Res Nanobiol Program, NIH, Frederick, MD 21702 USA.
[Streaker, Emily D.; Prabakaran, Ponraj] NCI, Basic Res Program, Sci Applicat Int Corp Frederick, Frederick, MD 21702 USA.
[Russ, Daniel E.] NIH, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Dimitrov, DS (reprint author), NCI, Prot Interact Grp, Ctr Canc Res Nanobiol Program, NIH, Bldg 469,Rm 150B, Frederick, MD 21702 USA.
EM dimiter.dimitrov@nih.gov
OI Russ, Daniel/0000-0003-4040-4416
FU NIH, National Cancer Institute, Center for Cancer Research; Gates
Foundation; NIH, National Cancer Institute [NO1-CO-12400]
FX We thank Drs. C. Broder, B. Haynes, H. Liao and T. Fouts for reagents.
This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research, and the
Gates Foundation to DSD, and by Federal funds from the NIH, National
Cancer Institute, under Contract No. NO1-CO-12400. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor does the mention of trade
names, commercial products, or organizations imply endorsement by the US
Government.
NR 23
TC 16
Z9 17
U1 0
U2 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD JAN 27
PY 2012
VL 417
IS 4
BP 1164
EP 1169
DI 10.1016/j.bbrc.2011.12.089
PG 6
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 891DG
UT WOS:000300196100010
PM 22226962
ER
PT J
AU Bera, TK
Walker, DA
Sherins, RJ
Pastan, I
AF Bera, Tapan K.
Walker, Dawn A.
Sherins, Richard J.
Pastan, Ira
TI POTE protein, a cancer-testis antigen, is highly expressed in spermatids
in human testis and is associated with apoptotic cells
SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
LA English
DT Article
DE POTE gene family; Spermatids; Apoptosis; Cleaved Caspase-3
ID SPERMATOGENESIS; ANTIBODIES; PARALOGS; PROSTATE
AB The POTE gene family encodes very closely related proteins that are highly expressed in testis and in many cancers. Recent studies indicate that the POTE proteins have a pro-apoptotic function. To examine if POTE is associated with cells that are undergoing apoptosis in testis, we determined the cellular location of POTE and of Cleaved Caspase-3 in testicular tissues from 26 azoospermic men. We found intense expression of POTE in round spermatids that are undergoing apoptosis, which are positive for Cleaved Caspase-3. This study suggests POTE may have a role in apoptosis in the human testis. Published by Elsevier Inc.
C1 [Bera, Tapan K.; Walker, Dawn A.; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Sherins, Richard J.] NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
RP Pastan, I (reprint author), NCI, Mol Biol Lab, Ctr Canc Res, NIH, 37 Convent Dr,Room 5106, Bethesda, MD 20892 USA.
EM BeraT@mail.nih.gov; walkerd@mail.nih.gov; rsherins@comcast.net;
pastani@mail.nih.gov
FU NIH, National Cancer Institute; National Institute of Child Health and
Human Development, National Institutes of Health
FX T.K.B., D.A.W., and I.P.'s research was supported by the Intramural
Research Program of the NIH, National Cancer Institute; R.J.S.'s
research was supported by the National Institute of Child Health and
Human Development, National Institutes of Health.
NR 12
TC 5
Z9 5
U1 0
U2 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0006-291X
J9 BIOCHEM BIOPH RES CO
JI Biochem. Biophys. Res. Commun.
PD JAN 27
PY 2012
VL 417
IS 4
BP 1271
EP 1274
DI 10.1016/j.bbrc.2011.12.125
PG 4
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 891DG
UT WOS:000300196100028
PM 22234308
ER
PT J
AU Pearce, MS
Salotti, JA
McHugh, K
Kim, KP
Craft, AW
Lubin, J
Ron, E
Parker, L
AF Pearce, Mark S.
Salotti, Jane A.
McHugh, Kieran
Kim, Kwang Pyo
Craft, Alan W.
Lubin, Jay
Ron, Elaine
Parker, Louise
TI Socio-economic variation in CT scanning in Northern England, 1990-2002
SO BMC HEALTH SERVICES RESEARCH
LA English
DT Article
ID RADIATION-EXPOSURE; PEDIATRIC CT; CANCER-RISKS; INJURIES; CHILDREN; UK;
PATTERNS; SCANS
AB Background: Socio-economic status is known to influence health throughout life. In childhood, studies have shown increased injury rates in more deprived settings. Socio-economic status may therefore be related to rates of certain medical procedures, such as computed tomography (CT) scans. This study aimed to assess socio-economic variation among young people having CT scans in Northern England between 1990 and 2002 inclusive.
Methods: Electronic data were obtained from Radiology Information Systems of all nine National Health Service hospital Trusts in the region. CT scan data, including sex, date of scan, age at scan, number and type of scans were assessed in relation to quintiles of Townsend deprivation scores, obtained from linkage of postcodes with census data, using chi(2) tests and Spearman rank correlations.
Results: During the study period, 39,676 scans were recorded on 21,089 patients, with 38,007 scans and 19,485 patients (11344 male and 8132 female) linkable to Townsend scores. The overall distributions of both scans and patients by quintile of Townsend deprivation scores were significantly different to the distributions of Townsend scores from the census wards included in the study (p < 0.0001). There was a significant association between type of scan and deprivation quintile (p < 0.0001), primarily due to the higher proportions of head scans in the three most deprived quintiles, and slightly higher proportions of chest scans and abdomen and pelvis scans in the least deprived groups. There was also a significant association (p < 0.0001) between the patient's age at the time of the CT scan and Townsend deprivation quintiles, with slightly increasing proportions of younger children with increasing deprivation. A similar association with age (p < 0.0001) was seen when restricting the data to include only the first scan of each patient. The number of scans per patient was also associated with Townsend deprivation quintiles (p = 0.014).
Conclusions: Social inequalities exist in the numbers of young people undergoing CT scans with those from deprived areas more likely to do so. This may reflect the rates of injuries in these individuals and implies that certain groups within the population may receive higher radiation doses than others due to medical procedures.
C1 [Pearce, Mark S.; Salotti, Jane A.] Newcastle Univ, Royal Victoria Infirm, Sir James Spence Inst, Inst Hlth & Soc, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England.
[McHugh, Kieran] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
[Kim, Kwang Pyo] Kyung Hee Univ, Dept Nucl Engn, Gyeonggi Do, South Korea.
[Craft, Alan W.] Newcastle Univ, Royal Victoria Infirm, Sir James Spence Inst, No Inst Canc Res, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England.
[Lubin, Jay] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Parker, Louise] Dalhousie Univ, Dept Med & Paediat, Populat Canc Res Program, Halifax, NS, Canada.
[Parker, Louise] Canc Care Nova Scotia, Halifax, NS, Canada.
RP Pearce, MS (reprint author), Newcastle Univ, Royal Victoria Infirm, Sir James Spence Inst, Inst Hlth & Soc, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England.
EM mark.pearce@ncl.ac.uk
FU US National Cancer Institute [NO2-CP-75501]; UK Department of Health
[RRX 119]
FX This study was supported by contract NO2-CP-75501 from the US National
Cancer Institute and through the Radiation Research Programme of the UK
Department of Health (RRX 119). We thank the staff in radiology
departments across the Northern England who contributed data and to
Katharine Kirton, Wenhua Metcalf and Richard Hardy for their assistance.
NR 22
TC 8
Z9 8
U1 0
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1472-6963
J9 BMC HEALTH SERV RES
JI BMC Health Serv. Res.
PD JAN 27
PY 2012
VL 12
AR 24
DI 10.1186/1472-6963-12-24
PG 6
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 889GH
UT WOS:000300061100001
PM 22283843
ER
PT J
AU Wang, XH
Zhang, YB
Yang, XXO
Nurieva, RI
Chang, SH
Ojeda, SS
Kang, HS
Schluns, KS
Gui, JF
Jetten, AM
Dong, C
AF Wang, Xiaohu
Zhang, Yibing
Yang, Xuexian O.
Nurieva, Roza I.
Chang, Seon Hee
Ojeda, Sandra S.
Kang, Hong S.
Schluns, Kimberly S.
Gui, Jianfang
Jetten, Anton M.
Dong, Chen
TI Transcription of Il17 and Il17f Is Controlled by Conserved Noncoding
Sequence 2
SO IMMUNITY
LA English
DT Article
ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; RANGE INTRACHROMOSOMAL
INTERACTIONS; CD4(+) T-CELLS; ROR-GAMMA-T; NUCLEAR RECEPTORS;
GENE-EXPRESSION; DIFFERENTIATION; CYTOKINE; LOCUS; LINEAGE
AB T helper 17 (Th17) cells specifically transcribe the Il17 and Il17f genes, which are localized in the same chromosome region, but the underlying mechanism is unclear. Here, we report a cis element that we previously named conserved noncoding sequence 2 (CNS2) physically interacted with both Il17 and Il17f gene promoters and was sufficient for regulating their selective transcription in Th17 cells. Targeted deletion of CNS2 resulted in impaired retinoic acid-related orphan receptor gammat (ROR gamma t)-driven IL-17 expression in vitro. CNS2-deficient T cells also produced substantially decreased amounts of IL-17F. These cytokine defects were associated with defective chromatin remodeling in the Ild17-Il17f gene locus, possibly because of effects on CNS2-mediated recruitment of histone-modifying enzymes p300 and JmjC domain-containing protein 3 (JMJD3). CNS2-deficient animals were also shown to be resistant to experimental autoimmune encephalomyelitis (EAE). Our results thus suggest that CNS2 is sufficient and necessary for Il17 and optimal Il17f gene transcription in Th17 cells.
C1 [Wang, Xiaohu; Zhang, Yibing; Yang, Xuexian O.; Nurieva, Roza I.; Chang, Seon Hee; Ojeda, Sandra S.; Schluns, Kimberly S.; Dong, Chen] Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
[Zhang, Yibing; Gui, Jianfang] Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Peoples R China.
[Kang, Hong S.; Jetten, Anton M.] NIEHS, Cell Biol Sect, LRB, NIH, Res Triangle Pk, NC 27709 USA.
RP Dong, C (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
EM cdong@mdanderson.org
RI dong, chen /B-3181-2009;
OI dong, chen /0000-0002-0084-9130; Jetten, Anton/0000-0003-0954-4445
FU NIH; American Heart Association; 973 National Basic Research Program of
China [2010CB126301]; National Multiple Sclerosis Society; Chinese
Academy of Sciences; MD Anderson Cancer Center; Leukemia and Lymphoma
Society
FX We thank the C.D. laboratory members for their help. The work is
supported by research grants from NIH (to C.D. and R.I.N.), American
Heart Association (to X.O.Y.), and 973 National Basic Research Program
of China (2010CB126301). X.W. receives a postdoctoral fellowship from
the National Multiple Sclerosis Society, Y.Z. was supported by a
fellowship from Chinese Academy of Sciences, and C.D. receives a
Research Trust Fellowship from MD Anderson Cancer Center and is a
Leukemia and Lymphoma Society Scholar. C.D. and X.W. designed the
research and analyzed the data. X.W., Y.Z., X.O.Y., RN., S.H.C., S.S.O.,
and H.S.K. performed the experiments, and X.W., J.G., K.S.S., A.M.J.,
and C.D. prepared the manuscript.
NR 37
TC 37
Z9 42
U1 0
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD JAN 27
PY 2012
VL 36
IS 1
BP 23
EP 31
DI 10.1016/j.immuni.2011.10.019
PG 9
WC Immunology
SC Immunology
GA 885GG
UT WOS:000299766000007
PM 22244845
ER
PT J
AU Tikhonova, AN
Van Laethem, F
Hanada, K
Lu, JH
Pobezinsky, LA
Hong, CW
Guinter, TI
Jeurling, SK
Bernhardt, G
Park, JH
Yang, JC
Sun, PD
Singer, A
AF Tikhonova, Anastasia N.
Van Laethem, Francois
Hanada, Ken-ichi
Lu, Jinghua
Pobezinsky, Leonid A.
Hong, Changwan
Guinter, Terry I.
Jeurling, Susanna K.
Bernhardt, Guenter
Park, Jung-Hyun
Yang, James C.
Sun, Peter D.
Singer, Alfred
TI alpha beta T Cell Receptors that Do Not Undergo Major Histocompatibility
Complex-Specific Thymic Selection Possess Antibody-like Recognition
Specificities
SO IMMUNITY
LA English
DT Article
ID NECTIN-LIKE MOLECULES; CLASS-I; IMMUNOGLOBULIN SUPERFAMILY;
CRYSTAL-STRUCTURE; MHC INTERACTION; AMINO-ACIDS; PEPTIDE; ANTIGEN;
BINDING; CD4
AB Major histocompatibility complex (MHC) restriction is the cardinal feature of T cell antigen recognition and is thought to be intrinsic to alpha beta T cell receptor (TCR) structure because of germline-encoded residues that impose MHC specificity. Here, we analyzed alpha beta TCRs from T cells that had not undergone MHC-specific thymic selection. Instead of recognizing peptide-MHC complexes, the two alpha beta TCRs studied here resembled antibodies in recognizing glycosylation-dependent conformational epitopes on a native self-protein, CD155, and they did so with high affinity independently of MHC molecules. Ligand recognition was via the alpha beta TCR combining site and involved the identical germline-encoded residues that have been thought to uniquely impose MHC specificity, demonstrating that these residues do not only promote MHC binding. This study demonstrates that, without MHC-specific thymic selection, alpha beta TCRs can resemble antibodies in recognizing conformational epitopes on MHC-independent ligands.
C1 [Tikhonova, Anastasia N.; Van Laethem, Francois; Pobezinsky, Leonid A.; Hong, Changwan; Guinter, Terry I.; Jeurling, Susanna K.; Park, Jung-Hyun; Singer, Alfred] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Hanada, Ken-ichi; Yang, James C.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
[Tikhonova, Anastasia N.] Univ Penn, Sch Med, Immunol Grad Grp, Philadelphia, PA 19104 USA.
[Lu, Jinghua; Sun, Peter D.] NIAID, Struct Immunol Sect, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Bernhardt, Guenter] Hannover Med Sch, Inst Immunol, D-30625 Hannover, Germany.
RP Singer, A (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM singera@nih.gov
RI lu, jinghua/G-5872-2012; Hanada, Ken-ichi/L-2481-2013; Bernhardt,
Gunter/F-6946-2012; Tikhonova, Anastasia/F-1186-2015; Park, Jung Hyun
/B-5712-2015
OI Hanada, Ken-ichi/0000-0003-2959-1257; Park, Jung Hyun
/0000-0002-9547-9055
FU National Institutes of Health, National Cancer Institute, Center for
Cancer Research
FX We thank R. Bosselut, W. Pear, and A. Chervonsky for providing reagents
and N. Taylor, J. Di Santo, M. Kimura, T. McCaughtry, X. Tai, and D.
Margulies for critically reading the manuscript. This work was supported
by the Intramural Research Program of the National Institutes of Health,
National Cancer Institute, Center for Cancer Research.
NR 37
TC 51
Z9 51
U1 0
U2 5
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD JAN 27
PY 2012
VL 36
IS 1
BP 79
EP 91
DI 10.1016/j.immuni.2011.11.013
PG 13
WC Immunology
SC Immunology
GA 885GG
UT WOS:000299766000012
PM 22209676
ER
EF