FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Beach, JR
Billington, N
Remmert, K
Barzik, M
Heissler, SM
Shao, L
Li, D
Friedman, TB
Betzig, E
Sellers, JR
Hammer, JA
AF Beach, J. R.
Billington, N.
Remmert, K.
Barzik, M.
Heissler, S. M.
Shao, L.
Li, D.
Friedman, T. B.
Betzig, E.
Sellers, J. R.
Hammer, J. A.
TI Myosin 18A Co-assembles with Myosin II to Drive the Functional Diversity
of Myosin II Bipolar Filaments.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Beach, J. R.; Remmert, K.; Hammer, J. A.] NHLBI, LCB, NIH, Bethesda, MD 20892 USA.
[Billington, N.; Heissler, S. M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Barzik, M.] NIDCD, NIH, Bethesda, MD USA.
[Shao, L.; Li, D.; Betzig, E.] HHMI, Ashburn, VA USA.
[Friedman, T. B.] NIDCD, NIH, Rockville, MD USA.
[Sellers, J. R.] NHLBI, LMP, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P107
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100108
ER
PT J
AU Bruun, K
Beach, JR
Murugesan, S
Remmert, K
Hammer, JA
AF Bruun, K.
Beach, J. R.
Murugesan, S.
Remmert, K.
Hammer, J. A.
TI Investigating the Role of Myosin 18A in Golgi Morphology.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Bruun, K.] St Josephs Univ, Dept Biol, Philadelphia, PA 19131 USA.
[Beach, J. R.] NHLBI, CBPC, NIH, Bethesda, MD 20892 USA.
[Murugesan, S.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Remmert, K.; Hammer, J. A.] NHLBI, LCB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2096
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105125
ER
PT J
AU Case, L
Baird, M
Shtengel, G
Campbell, S
Hess, H
Davidson, MW
Waterman, C
AF Case, L.
Baird, M.
Shtengel, G.
Campbell, S.
Hess, H.
Davidson, M. W.
Waterman, C.
TI iPALM and FRET reveal the mechanism of vinculin activation and
nano-scale spatial organization in focal adhesions
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Case, L.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
[Baird, M.] Florida State Univ, Tallahassee, FL 32306 USA.
[Shtengel, G.; Hess, H.] HHMI, Janelia Farm, Ashburn, VA USA.
[Campbell, S.] UNC, Biochem & Biophys, Chapel Hill, NC USA.
[Davidson, M. W.] Florida State Univ, Natl High Magnet Field Lab, Tallahassee, FL 32306 USA.
[Davidson, M. W.] Florida State Univ, Dept Biol Sci, Tallahassee, FL 32306 USA.
[Waterman, C.] Natl Inst Hlth, Natl Heart Lung & Blood Inst, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1463
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103314
ER
PT J
AU Cekan, P
Ryu, S
Hasegawa, K
Lee, J
Kalab, P
AF Cekan, P.
Ryu, S.
Hasegawa, K.
Lee, J.
Kalab, P.
TI Ran GTPase activates DNA damage response and cell cycle resumption,
driving the evasion of cell senescence in normal and cancer cells
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Cekan, P.; Ryu, S.; Hasegawa, K.; Lee, J.; Kalab, P.] NCI, NIH, Bethesda, MD 20892 USA.
[Ryu, S.] Samsung Adv Inst Technol, Well Aging Res Ctr, Osan, South Korea.
[Hasegawa, K.] Amherst Coll, Biochem Biophys, Amherst, MA 01002 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P219
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100220
ER
PT J
AU Cervantes, CBL
Tokuhiro, K
Zhang, Y
Conti, M
Bae, DH
Daniels, M
Dean, J
Adelstein, RS
AF Cervantes, C. B. Lerma
Tokuhiro, K.
Zhang, Y.
Conti, M.
Bae, D. H.
Daniels, M.
Dean, J.
Adelstein, R. S.
TI A Point Mutation in Nonmuscle Myosin II-A Disrupts Mouse Spermatogenesis
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Cervantes, C. B. Lerma; Zhang, Y.; Conti, M.; Adelstein, R. S.] NHLBI, Mol Cardiol Lab, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Tokuhiro, K.; Dean, J.] NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
[Bae, D. H.; Daniels, M.] NHLBI, Electron Microscopy Core, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2317
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105347
ER
PT J
AU Chang, J
Lee, S
Blackstone, CD
AF Chang, J.
Lee, S.
Blackstone, C. D.
TI Spastic paraplegia proteins spastizin and spatacsin mediate autophagic
lysosome reformation
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Chang, J.; Lee, S.; Blackstone, C. D.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1224
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103075
ER
PT J
AU Chen, J
Liu, J
AF Chen, J.
Liu, J.
TI Spatio-temporal Model for Silencing of the Mitotic Spindle Assembly
Checkpoint.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Chen, J.] NIH, Bethesda, MD 20892 USA.
[Liu, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P178
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100179
ER
PT J
AU Chua, J
Senft, J
Lockett, S
Brett, P
Burtnick, M
Deshazer, D
Friedlander, A
AF Chua, J.
Senft, J.
Lockett, S.
Brett, P.
Burtnick, M.
Deshazer, D.
Friedlander, A.
TI pH Alkalinization by Chloroquine Suppresses Burkholderia T6SS-1 Gene
Expression, Phagosomal Escape and Multi-Nucleated Giant Cell Formation.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Chua, J.; Senft, J.; Deshazer, D.; Friedlander, A.] USAMRIID, Bacteriol, Ft Detrick, MD USA.
[Lockett, S.] Frederick Natl Lab Canc Res, Opt Microscopy & Anal Lab, Frederick, MD USA.
[Brett, P.] Univ S Alabama, Microbiol & Immunol, Mobile, AL 36688 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P746
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101374
ER
PT J
AU Cohen-Fix, O
Walters, A
May, C
Dauster, E
Cinquin, B
Smith, E
Larabell, C
AF Cohen-Fix, O.
Walters, A.
May, C.
Dauster, E.
Cinquin, B.
Smith, E.
Larabell, C.
TI The budding yeast polo kinase, Cdc5, regulates domain-specific expansion
of the nuclear envelope
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Cohen-Fix, O.; Walters, A.; May, C.; Dauster, E.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Cinquin, B.; Smith, E.; Larabell, C.] Univ Calif San Francisco, Sch Med, Dept Anat, San Francisco, CA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA M100
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094106197
ER
PT J
AU Conti, M
Saleh, A
Cornelius, S
Van Waes, C
Adelstein, RS
AF Conti, M.
Saleh, A.
Cornelius, S.
Van Waes, C.
Adelstein, R. S.
TI Conditional Deletion of Nonmuscle Myosin II-A Leads to Squamous Cell
Carcinoma of the Tongue
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Conti, M.; Adelstein, R. S.] NHLBI, Mol Cardiol Lab, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Saleh, A.; Cornelius, S.; Van Waes, C.] NIDCD, Clin Genom Unit, NIH, Bethesda, MD USA.
[Saleh, A.; Cornelius, S.; Van Waes, C.] NIDCD, Tumor Biol Sect, Head & Neck Surg Branch, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P926
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102171
ER
PT J
AU Cruz, LA
Vedula, P
Gutierrez, N
Abramczyk, R
Ocegueda, M
Petrie, RJ
Rodriguez, AJ
AF Cruz, L. A.
Vedula, P.
Gutierrez, N.
Abramczyk, R.
Ocegueda, M.
Petrie, R. J.
Rodriguez, A. J.
TI Compartmentalized 3D colocalization analysis - a method to quantify
epithelial adherens junction assembly.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Cruz, L. A.; Vedula, P.; Gutierrez, N.; Abramczyk, R.; Ocegueda, M.; Rodriguez, A. J.] Rutgers State Univ, Federated Dept Biol, Newark, NJ 07102 USA.
[Petrie, R. J.] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P578
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101206
ER
PT J
AU Das, A
Waterman, C
AF Das, A.
Waterman, C.
TI Cytoskeletal integrity and acto-myosin contractility act by distinct
pathways to regulate nuclear Yap1 localization and phosphorylation
during mechanotransduction.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Das, A.] NHLBI, Cell Biol & Physiol, NIH, Bethesda, MD 20892 USA.
[Waterman, C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P524
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101153
ER
PT J
AU Dasso, M
Arnaoutov, A
AF Dasso, M.
Arnaoutov, A.
TI IRBIT is a novel regulator of Ribonucleotide reductase in high
eucaryotes
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Dasso, M.; Arnaoutov, A.] NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P218
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100219
ER
PT J
AU Dhingra, A
Frost, LS
Lopes, VS
Rodriguez, IR
Williams, DS
Boesze-Battaglia, K
AF Dhingra, A.
Frost, L. S.
Lopes, V. S.
Rodriguez, I. R.
Williams, D. S.
Boesze-Battaglia, K.
TI The Contribution of Melanoregulin to Microtubule-Associated Protein 1
Light Chain 3 (LC3) Associated Phagocytosis.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Dhingra, A.; Frost, L. S.; Boesze-Battaglia, K.] Univ Penn, Biochem, Philadelphia, PA 19104 USA.
[Lopes, V. S.; Williams, D. S.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Rodriguez, I. R.] NEI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1365
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103216
ER
PT J
AU Dorward, DW
Raae-Nielsen, J
Hansen, BT
Nair, V
Fischer, ER
AF Dorward, D. W.
Raae-Nielsen, J.
Hansen, B. T.
Nair, V.
Fischer, E. R.
TI Device for microwave-enhanced processing of cryo-substitution for light
and electron microscopy.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Dorward, D. W.; Raae-Nielsen, J.; Hansen, B. T.; Nair, V.; Fischer, E. R.] NIAID, RTB, Microscopy Unit, NIH,Rocky Mt Labs, Hamilton, MT USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P13
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100014
ER
PT J
AU Doyle, AD
Yamada, KM
Matsumoto, K
AF Doyle, A. D.
Yamada, K. M.
Matsumoto, K.
TI The local 3D microenvironment controls adhesion dynamics and cell
motility by balancing forces at the leading edge.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Doyle, A. D.; Yamada, K. M.; Matsumoto, K.] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P522
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101151
ER
PT J
AU Dutta, D
Donaldson, JG
AF Dutta, D.
Donaldson, J. G.
TI Cross-talk between clathrin-mediated and clathrin-independent endosomal
membrane systems coordinated by Rab35 and Arf6
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Dutta, D.; Donaldson, J. G.] NLHBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1201
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103052
ER
PT J
AU Fabritius, AS
Golden, A
AF Fabritius, A. S.
Golden, A.
TI Defining genetic pathways of disease through genetic suppression screens
in Caenorhabditis elegans.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Fabritius, A. S.; Golden, A.] NIDDK NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P780
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102026
ER
PT J
AU Fischer, RS
Elliott, HL
Myers, KA
Desai, RA
Chen, CS
Adelstein, RS
Waterman, C
Danuser, G
AF Fischer, R. S.
Elliott, H. L.
Myers, K. A.
Desai, R. A.
Chen, C. S.
Adelstein, R. S.
Waterman, C.
Danuser, G.
TI Myosin II controls cellular branching morphogenesis and migration in 3D
by responding to and minimizing cell surface curvature
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Fischer, R. S.] NHLBI, Cell & Tissue Morphogenesis, Bethesda, MD 20892 USA.
[Elliott, H. L.] Harvard Univ, Sch Med, Image & Data Anal Core, Boston, MA USA.
[Myers, K. A.] Univ Sci, Misher Coll Arts & Sci, Dept Biol Sci, Philadelphia, PA USA.
[Desai, R. A.] MRC NIMR, London, England.
[Chen, C. S.] Boston Univ, Biomed Engn, Boston, MA 02215 USA.
[Chen, C. S.] Harvard Univ, Wyss Inst Biologically Inspired Engn, Boston, MA USA.
[Adelstein, R. S.] NHLBI, Mol Cardiol Lab, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Waterman, C.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Danuser, G.] Univ Texas SW Med Ctr Dallas, Dept Cell Biol, Dallas, TX 75390 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P940
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102185
ER
PT J
AU Fuentes, R
Escobar-Aguirre, M
Kugath, A
Montecinos-Franjola, F
Lopez, P
Fernandez, J
Mullins, MC
AF Fuentes, R.
Escobar-Aguirre, M.
Kugath, A.
Montecinos-Franjola, F.
Lopez, P.
Fernandez, J.
Mullins, M. C.
TI Cation/proton exchanger 1 protein (Cax1), a maternal-effect regulator of
zebrafish cytoplasmic segregation and mRNA localization.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Fuentes, R.; Escobar-Aguirre, M.; Kugath, A.; Mullins, M. C.] Univ Penn, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA.
[Montecinos-Franjola, F.] NIH, LIMB, Bethesda, MD 20892 USA.
[Lopez, P.; Fernandez, J.] Univ Chile, Dept Biol, Santiago, Chile.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P718
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101346
ER
PT J
AU Galletta, BJ
Jacobs, KC
Fagerstron, CJ
Slep, KC
Rusan, NM
AF Galletta, B. J.
Jacobs, K. C.
Fagerstron, C. J.
Slep, K. C.
Rusan, N. M.
TI A Detailed Centrosome Interactome Reveals a Novel Role for
Asterless/CEP152 in Controlling Centriole Length Via Cep97.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Galletta, B. J.; Jacobs, K. C.; Fagerstron, C. J.; Rusan, N. M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Slep, K. C.] Univ N Carolina, Dept Biol, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1738
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104203
ER
PT J
AU Gaspar, A
Lucas, M
Rojas, A
Hierro, A
Machner, M
AF Gaspar, A.
Lucas, M.
Rojas, A.
Hierro, A.
Machner, M.
TI A molecular mechanism for endosomal avoidance by the pathogen Legionella
pneumophila.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Gaspar, A.; Machner, M.] NIH, Bethesda, MD 20892 USA.
[Lucas, M.; Rojas, A.; Hierro, A.] CIC bioGUNE, Bilbao, Spain.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA M50
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094106099
ER
PT J
AU Gibbs, K
Griffin, K
AF Gibbs, K.
Griffin, K.
TI Biomedical Science Ph.D. Career Development and Interest Patterns by
Race/Ethnicity and Gender.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Gibbs, K.] NCI, Bethesda, MD 20892 USA.
[Griffin, K.] Univ Maryland, Counseling, Higher Educ, Special Educ, College Pk, MD 20742 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P791
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102037
ER
PT J
AU Glushakova, SE
Wirth, CC
Scheuermayer, M
Leikina, E
Humphrey, G
Balaban, A
Kachman, MM
Pradel, G
Zimmerberg, J
AF Glushakova, S. E.
Wirth, C. C.
Scheuermayer, M.
Leikina, E.
Humphrey, G.
Balaban, A.
Kachman, M. M.
Pradel, G.
Zimmerberg, J.
TI Release of malaria parasites from red blood cells requires
parasite-derived pore-forming proteins.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Glushakova, S. E.; Leikina, E.; Humphrey, G.; Balaban, A.; Kachman, M. M.; Zimmerberg, J.] NICHHD, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Wirth, C. C.; Pradel, G.] Rhein Westfal TH Aachen, Inst Mol Biotechnol, Aachen, Germany.
[Scheuermayer, M.] Univ Wurzburg, Res Ctr Infect Dis, D-97070 Wurzburg, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2364
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105393
ER
PT J
AU Guha, M
Srinivasan, S
Ruthel, G
Kashina, AS
Carstens, R
Mendoza, A
Khanna, C
Van Winkle, T
Avadhani, NG
AF Guha, M.
Srinivasan, S.
Ruthel, G.
Kashina, A. S.
Carstens, R.
Mendoza, A.
Khanna, C.
Van Winkle, T.
Avadhani, N. G.
TI Mitochondrial retrograde signaling induces epithelial-mesenchymal
transition and generates breast cancer stem cells
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Guha, M.] Univ Penn, Anim Biol, Philadelphia, PA 19104 USA.
[Srinivasan, S.; Ruthel, G.] Univ Penn, Philadelphia, PA 19104 USA.
[Kashina, A. S.; Avadhani, N. G.] Univ Penn, Sch Vet Med, Dept Anim Biol, Philadelphia, PA 19104 USA.
[Carstens, R.] Univ Penn, Dept Med, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Mendoza, A.; Khanna, C.] NIH, Tumor & Metastasis Biol Sect, Ctr Canc Res, Bethesda, MD 20892 USA.
[Van Winkle, T.] Univ Penn, Sch Vet Med, Dept Pathobiol 3, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1888
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104335
ER
PT J
AU Hanson, JC
Chen, Y
AF Hanson, J. C.
Chen, Y.
TI Induction of Carcinoma-Associated Fibroblasts in 3D Cell Coculture
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Hanson, J. C.; Chen, Y.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1899
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104346
ER
PT J
AU Hardeman, EC
Yang, L
Kee, AJ
Polishchuk, E
Polishchuk, R
Pleines, I
Kile, B
Weigert, R
Gunning, PW
AF Hardeman, E. C.
Yang, L.
Kee, A. J.
Polishchuk, E.
Polishchuk, R.
Pleines, I.
Kile, B.
Weigert, R.
Gunning, P. W.
TI A novel actin filament population defined by the tropomyosin Tm4
regulates ER-to-Golgi trafficking.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Hardeman, E. C.; Yang, L.; Kee, A. J.; Gunning, P. W.] UNSW, Sch Med Sci, Sydney, NSW, Australia.
[Polishchuk, E.; Polishchuk, R.] Telethon Inst Genet & Med, Naples, Italy.
[Pleines, I.; Kile, B.] Water & Eliza Hall Inst, Melbourne, Vic, Australia.
[Weigert, R.] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1640
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104105
ER
PT J
AU Hayakawa, EH
Tokumasu, F
Usukura, J
Matsuoka, H
Tsuboi, T
Wellems, TE
AF Hayakawa, E. H.
Tokumasu, F.
Usukura, J.
Matsuoka, H.
Tsuboi, T.
Wellems, T. E.
TI Three dimensional structure of Maurer's cleft with tiny filaments in
Plasmodium falciparum-infected Erythrocytes by "unroofing" method
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Hayakawa, E. H.; Matsuoka, H.] Jichi Med Univ, Lab Med Zool & Parasitol, Shimotsuke, Japan.
[Tokumasu, F.] Univ Tokyo, Dept Lipid, Tokyo, MD, Japan.
[Usukura, J.] Nagoya Univ, Struct Biol Ctr, Nagoya, Aichi 4648601, Japan.
[Tsuboi, T.] Ehime Univ, Cell Free Sci & Technol Res Ctr, Matsuyama, Ehime, Japan.
[Wellems, T. E.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2355
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105384
ER
PT J
AU Henderson, MJ
Wires, ES
Trychta, KA
Richie, CT
Yan, X
Harvey, BK
AF Henderson, M. J.
Wires, E. S.
Trychta, K. A.
Richie, C. T.
Yan, X.
Harvey, B. K.
TI Monitoring perturbations in endoplasmic reticulum calcium homeostasis
using a novel secreted reporter protein.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Henderson, M. J.; Wires, E. S.; Trychta, K. A.; Richie, C. T.; Yan, X.; Harvey, B. K.] NIDA, NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P43
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100044
ER
PT J
AU Hu, L
Liu, J
AF Hu, L.
Liu, J.
TI Mechanochemistry of persistent plasmid movement.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Hu, L.; Liu, J.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1513
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103364
ER
PT J
AU Insinna, C
Lu, Q
Ott, CM
Baxa, U
Lopes, S
Lippincott-Schwartz, J
Caplan, S
Jackson, PK
Westlake, CJ
AF Insinna (Kettenhofen), C.
Lu, Q.
Ott, C. M.
Baxa, U.
Lopes, S.
Lippincott-Schwartz, J.
Caplan, S.
Jackson, P. K.
Westlake, C. J.
TI EHD proteins coordinate membrane reorganization and fusion to initiate
early steps of ciliogenesis.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Insinna (Kettenhofen), C.; Lu, Q.] NCI, LCDS, Frederick, MD 21701 USA.
[Ott, C. M.] NICHD, NIH, Bethesda, MD USA.
[Baxa, U.] NCI, NIH, Leidos, Frederick, MD 21701 USA.
[Lopes, S.] CEDOC, Fac Ciencias Med, Lisbon, Portugal.
[Lippincott-Schwartz, J.] Physiol Course Marine Biol Lab, Woods Hole, MA USA.
[Lippincott-Schwartz, J.] NIH, Cell Biol & Metab program, NICHD, Bethesda, MD 20892 USA.
[Caplan, S.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Jackson, P. K.] Stanford Univ, Sch Med, Dept Microbiol & Immunol, Stanford, CA 94305 USA.
[Westlake, C. J.] NCI, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P993
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102238
ER
PT J
AU Jaramillo-Lambert, A
Golden, A
AF Jaramillo-Lambert, A.
Golden, A.
TI Identification and characterization of paternal-effect lethal mutants in
C. elegans.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Jaramillo-Lambert, A.; Golden, A.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P721
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101349
ER
PT J
AU Johnson, D
Wilson, JM
Donaldson, JG
AF Johnson, D.
Wilson, J. M.
Donaldson, J. G.
TI Clathrin Independent Endosomal Trafficking is required for T Cell
Conjugate Formation and Activation.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Johnson, D.] Univ Arizona, Tucson, AZ USA.
[Wilson, J. M.] Univ Arizona, Coll Med, Tucson, AZ USA.
[Donaldson, J. G.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2040
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105069
ER
PT J
AU Joshi, AS
Prinz, W
AF Joshi, A. S.
Prinz, W.
TI Novel ER shaping proteins Pex30 and Pex31 are involved in pre-peroxisome
vesicle biogenesis.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Joshi, A. S.; Prinz, W.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2095
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105124
ER
PT J
AU Jung, G
Alexander, CJ
Chen, B
Betzig, E
Hammer, JA
AF Jung, G.
Alexander, C. J.
Chen, B.
Betzig, E.
Hammer, J. A.
TI V-1/Myotrophin Regulates Capping Protein Activity in Vivo.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Jung, G.; Alexander, C. J.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Chen, B.; Betzig, E.] HHMI, Janelia Farm Res Campus, Ashburn, VA USA.
[Hammer, J. A.] NHLBI, LCB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P905
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102151
ER
PT J
AU Kane, LA
Lazarou, M
Fogel, AI
Li, Y
Yamano, K
Sarraf, SA
Banerjee, S
Youle, RJ
AF Kane, L. A.
Lazarou, M.
Fogel, A. I.
Li, Y.
Yamano, K.
Sarraf, S. A.
Banerjee, S.
Youle, R. J.
TI PINK1 is a ubiquitin kinase
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Kane, L. A.; Lazarou, M.; Fogel, A. I.; Li, Y.; Yamano, K.; Sarraf, S. A.; Banerjee, S.; Youle, R. J.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2140
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105169
ER
PT J
AU Kaushik, G
Spenlehauer, A
Sessions, AO
Trujillo, A
Fuhrmann, A
Fu, Z
Venkatraman, V
Pohl, D
Tuler, J
Wang, M
Lakatta, E
Ocorr, K
Bodmer, R
Bernstein, S
Van Eyk, J
Cammarato, A
Engler, AJ
AF Kaushik, G.
Spenlehauer, A.
Sessions, A. O.
Trujillo, A.
Fuhrmann, A.
Fu, Z.
Venkatraman, V.
Pohl, D.
Tuler, J.
Wang, M.
Lakatta, E.
Ocorr, K.
Bodmer, R.
Bernstein, S.
Van Eyk, J.
Cammarato, A.
Engler, A. J.
TI The vinculin network regulates cytoskeletal remodeling and contractile
function in aging myocardium.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Kaushik, G.; Fuhrmann, A.; Engler, A. J.] Univ Calif San Diego, Bioengn, La Jolla, CA 92093 USA.
[Spenlehauer, A.; Tuler, J.] Univ Calif San Diego, Bioengn, San Diego, CA 92103 USA.
[Sessions, A. O.] Univ Calif San Diego, Biomed Sci, La Jolla, CA 92093 USA.
[Trujillo, A.; Bernstein, S.] San Diego State Univ, San Diego, CA 92182 USA.
[Fu, Z.; Venkatraman, V.; Van Eyk, J.] Johns Hopkins Univ, Sch Med, Cardiol, Baltimore, MD USA.
[Pohl, D.] Iowa State Univ, Ames, IA USA.
[Wang, M.; Lakatta, E.] NIA, Bethesda, MD 20892 USA.
[Ocorr, K.; Bodmer, R.] Sanford Burnham Med Res Inst, La Jolla, CA USA.
[Cammarato, A.] Johns Hopkins Univ, Med, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1392
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103243
ER
PT J
AU Kim, LY
Thompson, P
Campbell, S
Alushin, GM
AF Kim, L. Y.
Thompson, P.
Campbell, S.
Alushin, G. M.
TI Structural Basis of the Vinculin-F-actin Interaction.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Kim, L. Y.; Alushin, G. M.] NHLBI, CBPC, NIH, Bethesda, MD 20892 USA.
[Thompson, P.; Campbell, S.] UNC, Biochem & Biophys, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P876
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102122
ER
PT J
AU Kim, YJ
Guzman-Hernandez, ML
Wisniewski, E
Balla, T
AF Kim, Yeun Ju
Guzman-Hernandez, Maria-Luisa
Wisniewski, Eva
Balla, Tamas
TI Nir2 plays a central role in ER-PM junctions maintaining
Phosphoinositide Signaling Competence.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Kim, Yeun Ju; Guzman-Hernandez, Maria-Luisa; Wisniewski, Eva; Balla, Tamas] NICHD, Sect Mol Signal Transduct, Program Dev Neurosci, NIH, Bethesda, MD USA.
RI Wisniewski, Eva/O-9233-2015
OI Wisniewski, Eva/0000-0001-8698-6867
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1332
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103183
ER
PT J
AU Kong, D
Farmer, V
Shukla, AK
Loncarek, J
AF Kong, D.
Farmer, V.
Shukla, A. K.
Loncarek, J.
TI Centriole maturation requires regulated Plk1 activity during two
consecutive cell cycles.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Kong, D.; Farmer, V.; Shukla, A. K.; Loncarek, J.] NCI, NIH, Lab Prot Dynam & Signaling, Frederick, MD 21701 USA.
RI Kong, Dong/O-4465-2016
OI Kong, Dong/0000-0002-7144-3808
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1020
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102265
ER
PT J
AU Korzeniowski, MK
Wisniewski, E
Holowka, DA
Baird, B
Balla, T
AF Korzeniowski, M. K.
Wisniewski, E.
Holowka, D. A.
Baird, B.
Balla, T.
TI Molecular Anatomy of Early Events in STIM1 Activation; Oligomerization
or Conformational Change?.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Korzeniowski, M. K.; Holowka, D. A.; Baird, B.] Cornell Univ, Chem & Chem Biol, Ithaca, NY USA.
[Wisniewski, E.; Balla, T.] NICHD, NIH, Bethesda, MD USA.
RI Wisniewski, Eva/O-9233-2015
OI Wisniewski, Eva/0000-0001-8698-6867
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P472
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101101
ER
PT J
AU Kotlyanskaya, L
Giniger, E
Kannan, R
AF Kotlyanskaya, L.
Giniger, E.
Kannan, R.
TI Disabled regulates Abelson nonreceptor tyrosine kinase localization and
kinase activity in Drosophila.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Kotlyanskaya, L.] Univ N Carolina, Neurobiol Curriculum, Bethesda, MD USA.
[Giniger, E.; Kannan, R.] NINDS Inst, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P77
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100078
ER
PT J
AU Lakdawala, S
Wu, Y
Wawrzusin, P
Broadbent, A
Kabat, J
Lamirande, E
Fodor, E
Altan-Bonnet, N
Shroff, H
Subbarao, K
AF Lakdawala, S.
Wu, Y.
Wawrzusin, P.
Broadbent, A.
Kabat, J.
Lamirande, E.
Fodor, E.
Altan-Bonnet, N.
Shroff, H.
Subbarao, K.
TI Influenza A Virus Assembly Intermediates Fuse in the Cytoplasm.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Lakdawala, S.; Broadbent, A.; Lamirande, E.; Subbarao, K.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Wu, Y.; Wawrzusin, P.; Shroff, H.] NIBIB, Sect High Resolut Opt Imaging, NIH, Bethesda, MD USA.
[Kabat, J.] NIAID, Res Technol Branch, NIH, Bethesda, MD 20892 USA.
[Fodor, E.] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England.
[Altan-Bonnet, N.] NHLBI, NIH, Bethesda, MD 20892 USA.
RI Shroff, Hari/E-7247-2016
OI Shroff, Hari/0000-0003-3613-8215
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA E38
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094106043
ER
PT J
AU Lakdawala, S
Wu, Y
Wawrzusin, P
Broadbent, A
Kabat, J
Lamirande, E
Fodor, E
Altan-Bonnet, N
Shroff, H
Subbarao, K
AF Lakdawala, S.
Wu, Y.
Wawrzusin, P.
Broadbent, A.
Kabat, J.
Lamirande, E.
Fodor, E.
Altan-Bonnet, N.
Shroff, H.
Subbarao, K.
TI Influenza A Virus Assembly Intermediates Fuse in the Cytoplasm.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Lakdawala, S.; Broadbent, A.; Lamirande, E.; Subbarao, K.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[Wu, Y.; Wawrzusin, P.; Shroff, H.] NIBIB, Sect High Resolut Opt Imaging, Bethesda, MD USA.
[Kabat, J.] NIAID, Res Technol Branch, NIH, Bethesda, MD 20892 USA.
[Fodor, E.] Univ Oxford, Sir William Dunn Sch Pathol, Oxford OX1 3RE, England.
[Altan-Bonnet, N.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1236
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103087
ER
PT J
AU Lee, S
Chang, J
Blackstone, CD
AF Lee, S.
Chang, J.
Blackstone, C. D.
TI FAM21 regulates recycling of SNX27-retromer cargoes to the plasma
membrane.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Lee, S.; Chang, J.; Blackstone, C. D.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2046
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105075
ER
PT J
AU Lerit, DA
Poulton, JS
Jordan, HA
Peifer, M
Rusan, NM
AF Lerit, D. A.
Poulton, J. S.
Jordan, H. A.
Peifer, M.
Rusan, N. M.
TI PLP forms novel centriole satellites and is critical for embryonic
development.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Lerit, D. A.; Jordan, H. A.; Rusan, N. M.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
[Poulton, J. S.; Peifer, M.] Univ N Carolina, Dept Biol, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1024
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102269
ER
PT J
AU Li, Z
AF Li, Z.
TI Regulation of synaptic vesicles by the mitochondria-caspase-autohpagy
pathway.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Li, Z.] NIMH, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1294
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103145
ER
PT J
AU Lin, M
Sheng, Z
AF Lin, M.
Sheng, Z.
TI Mechanism Removing Damaged Mitochondria from Axonal Terminals.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Lin, M.; Sheng, Z.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1339
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103190
ER
PT J
AU Liu, L
AF Liu, L.
TI Role of ER-Golgi contact sites in sphingolipid synthesis in yeast.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Liu, L.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1331
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103182
ER
PT J
AU Loew, M
Sackett, DL
Bane, SL
AF Loew, M.
Sackett, D. L.
Bane, S. L.
TI Interaction of Colchicine-Site Drugs with beta VI-Isotype of Tubulin.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Loew, M.; Bane, S. L.] SUNY Binghamton, Chem, Binghamton, NY USA.
[Sackett, D. L.] NICHD, Program Phys Biol, NIH, Bethesda, MD USA.
RI Bane, Susan/C-1414-2013
OI Bane, Susan/0000-0002-4270-6314
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P137
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100138
ER
PT J
AU Logue, J
Cartagena-Rivera, A
Chadwick, R
Waterman, C
AF Logue, J.
Cartagena-Rivera, A.
Chadwick, R.
Waterman, C.
TI Bundling of the actin cortex by Erk phosphorylated Eps8 is essential for
high cortex tension and the bleb-based migration of melanoma cells
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Logue, J.] NHLBI, NIDCD, NIH, Bethesda, MD 20892 USA.
[Cartagena-Rivera, A.; Chadwick, R.] NIDCD, NIH, Bethesda, MD USA.
[Waterman, C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P248
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100267
ER
PT J
AU Ma, X
Uchida, Y
Bowen, C
Mukoyama, Y
Adelstein, RS
AF Ma, X.
Uchida, Y.
Bowen, C.
Mukoyama, Y.
Adelstein, R. S.
TI The Role of Nonmuscle Myosin II-A and II-B in Coronary Vessel
Development in Mice.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Ma, X.; Bowen, C.] NHLBI, Lab Mol Cardiol, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Uchida, Y.; Mukoyama, Y.] NHLBI, Lab Stem Cell & Neuro Vasc Biol, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
[Adelstein, R. S.] NHLBI, Lab Mol Cardiol, Genet & Dev Biol Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P707
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101335
ER
PT J
AU MacGillavry, HD
Kerr, JM
Frost, NA
Blanpied, TA
AF MacGillavry, H. D.
Kerr, J. M.
Frost, N. A.
Blanpied, T. A.
TI Triple miRNA Shank knockdown shows that Shank-cortactin interactions
control actin dynamics in neuronal spines and synapses.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [MacGillavry, H. D.] Univ Utrecht, Cell Biol, Utrecht, Netherlands.
[Kerr, J. M.] NINDS, NIH, Bethesda, MD 20892 USA.
[Frost, N. A.] UCSF, Sch Med, Psychiat, San Francisco, CA USA.
[Blanpied, T. A.] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
[Blanpied, T. A.] Univ Maryland, Sch Med, Program Neurosci, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2090
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105119
ER
PT J
AU Majumdar, R
Tavakoli-Tameh, A
Kriebel, P
Parent, CA
AF Majumdar, R.
Tavakoli-Tameh, A.
Kriebel, P.
Parent, C. A.
TI Exosomes mediate LTB4 signal relay during neutrophil chemotaxis.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Majumdar, R.; Tavakoli-Tameh, A.; Kriebel, P.; Parent, C. A.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P553
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101182
ER
PT J
AU Malide, D
AF Malide, D.
TI In vivo tracking of label-free resident cells in murine tissues via
third harmonic generation microscopy.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Malide, D.] NHLBI, Light Microscopy Core Facil, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P23
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100024
ER
PT J
AU Manor, U
Bartholomew, S
Higgs, H
Spudich, JA
Lippincott-Schwartz, J
AF Manor, U.
Bartholomew, S.
Higgs, H.
Spudich, J. A.
Lippincott-Schwartz, J.
TI Spire1C promotes actin- and ER-mediated mitochondria constriction and
fission
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT Joint Annual Meeting of the American-Society-for-Cell-Biology (ASCB) /
International-Federation-for-Cell-Biology (IFCB)
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Manor, U.] NICHD, Cell Biol & Metab, NIH, Bethesda, MD USA.
[Bartholomew, S.; Spudich, J. A.] Stanford Univ, Stanford, CA 94305 USA.
[Higgs, H.] Dartmouth Coll, Geisel Sch Med, Dept Biochem, Hanover, NH 03755 USA.
[Lippincott-Schwartz, J.] Marine Biol Lab, Physiol Course, Woods Hole, MA 02543 USA.
[Lippincott-Schwartz, J.] NICHD, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2134
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105163
ER
PT J
AU Markossian, S
Arnaoutov, A
Larionov, V
Dasso, M
AF Markossian, S.
Arnaoutov, A.
Larionov, V.
Dasso, M.
TI Quantitative Assessment of Chromosome Instability Promoted by
Chemotherapeutic Agents.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Markossian, S.; Arnaoutov, A.; Dasso, M.] NICHHD, NIH, Bethesda, MD 20892 USA.
[Larionov, V.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1818
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104283
ER
PT J
AU Marteil, G
Guerrero, A
Godinho, S
Machado, P
Loncarek, J
Mendonca, S
Fonseca, I
Pellman, D
Bettencourt-Dias, M
AF Marteil, G.
Guerrero, A.
Godinho, S.
Machado, P.
Loncarek, J.
Mendonca, S.
Fonseca, I.
Pellman, D.
Bettencourt-Dias, M.
TI Cancer-wide survey of centrosomes reveals centriole fragmentation as a
novel origin of supernumerary centrosomes.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Marteil, G.; Machado, P.; Mendonca, S.; Fonseca, I.; Bettencourt-Dias, M.] Gulbenkian Inst Sci, Oeiras, Portugal.
[Guerrero, A.] Univ Nacl Autonoma Mexico, Inst Biotechnol, Oeiras, Portugal.
[Godinho, S.] Barts Canc Inst, London, England.
[Machado, P.] EMBL, Heidelberg, Germany.
[Loncarek, J.] NCI, NIH, Lab Prot Dynam & Signaling, Frederick, MD 21701 USA.
[Pellman, D.] Dana Farber Canc Inst, Pediat Oncol, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1026
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102271
ER
PT J
AU Martin, MM
Shimura, T
Redmon, C
Fu, H
Zhang, Y
Ryan, M
Kim, K
Epner, EM
Aladjem, MI
AF Martin, M. M.
Shimura, T.
Redmon, C.
Fu, H.
Zhang, Y.
Ryan, M.
Kim, K.
Epner, E. M.
Aladjem, M. I.
TI Characterization of nuclear cyclin D1 interactions with replication
regulatory elements in human cancer cells.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Martin, M. M.] Grambling State Univ, Ruston, LA USA.
[Shimura, T.] Natl Inst Publ Hlth, Environm Hlth, Wako, Saitama 3510197, Japan.
[Redmon, C.] Univ Maryland Baltimore Cty, Baltimore, MD 21228 USA.
[Fu, H.; Zhang, Y.; Aladjem, M. I.] NCI, Mol Pharmacol Lab, NIH, Bethesda, MD 20892 USA.
[Ryan, M.; Kim, K.] InSil Solut, Fairfax, VA USA.
[Epner, E. M.] Penn State Hershey Med Ctr, Hematol Oncol, Hershey, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1114
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102359
ER
PT J
AU Mendez, MG
Inglese, J
AF Mendez, M. G.
Inglese, J.
TI Phenotypic Assay Development Targeting Gigaxonin-mediated Intermediate
Filament Aggregation associated with Giant Axonal Neuropathy (GAN).
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Mendez, M. G.; Inglese, J.] NCATS, Assay Dev & Screening Technol ADST Lab, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P544
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101173
ER
PT J
AU Meng, L
Park, J
Kim, T
Lee, K
AF Meng, L.
Park, J.
Kim, T.
Lee, K.
TI Plk1 binds to the two distinct phospho-motifs on a centrosomal scaffold,
Cep192, to promote bipolar spindle formation.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Meng, L.] NIH, Bethesda, MD 20892 USA.
[Park, J.; Kim, T.; Lee, K.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P167
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100168
ER
PT J
AU Meseroll, RA
Cohen-Fix, O
AF Meseroll, R. A.
Cohen-Fix, O.
TI A genetic screen reveals the requirement for mRNA processing genes and
the topoisomerase TOP2 in nuclear morphology.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Meseroll, R. A.; Cohen-Fix, O.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1180
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103031
ER
PT J
AU Milgroom, A
Ralston, E
AF Milgroom, A.
Ralston, E.
TI Optical clearing of mouse skeletal muscle with the CLARITY method.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Milgroom, A.; Ralston, E.] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P42
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100043
ER
PT J
AU Mo, M
Dasso, M
Arnaoutov, A
AF Mo, M.
Dasso, M.
Arnaoutov, A.
TI Phosphorylation of Xenopus p31comet potentiates mitotic checkpoint exit
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Mo, M.] NIH, Bethesda, MD 20892 USA.
[Dasso, M.; Arnaoutov, A.] NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P231
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100232
ER
PT J
AU Molina, O
Shah, P
Kouprina, N
Larionov, V
Earnshaw, WC
AF Molina, O.
Shah, P.
Kouprina, N.
Larionov, V.
Earnshaw, W. C.
TI Construction of Human Artificial Chromosomes in a non-transformed cell
line.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Molina, O.; Shah, P.; Earnshaw, W. C.] Univ Edinburgh, Wellcome Trust Ctr Cell Biol, Edinburgh, Midlothian, Scotland.
[Kouprina, N.; Larionov, V.] NCI, NIH, Bethesda, MD 20892 USA.
RI Molina, Oscar/P-4516-2016
OI Molina, Oscar/0000-0001-7585-4519
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P340
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100359
ER
PT J
AU Morsci, N
Hall, DH
Driscoll, M
Sheng, Z
AF Morsci, N.
Hall, D. H.
Driscoll, M.
Sheng, Z.
TI Mitochondrial maintenance changes dynamically with age in Caenorhabditis
elegans adult neurons.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Morsci, N.; Sheng, Z.] NINDS, NIH, Bethesda, MD 20892 USA.
[Hall, D. H.] Albert Einstein Coll Med, Nrurosci, Bronx, NY 10467 USA.
[Driscoll, M.] Rutgers State Univ, Mol Biol & Biochem, Piscataway, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1338
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103189
ER
PT J
AU Mukherjee, K
Chio, TI
Sorrentino, AM
Sackett, DL
Bane, SL
AF Mukherjee, K.
Chio, T. I.
Sorrentino, A. M.
Sackett, D. L.
Bane, S. L.
TI One Step Detection of Oxidative Stress-Induced Carbonylation in Live
Mammalian Cells.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Mukherjee, K.; Chio, T. I.; Sorrentino, A. M.; Bane, S. L.] SUNY Binghamton, Chem, Binghamton, NY USA.
[Sackett, D. L.] NICHD, Program Phys Biol, NIH, Bethesda, MD USA.
RI Bane, Susan/C-1414-2013
OI Bane, Susan/0000-0002-4270-6314
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P670
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101298
ER
PT J
AU Murugesan, S
Yi, J
Li, D
Shao, L
Betzig, E
Wu, X
Hammer, JA
AF Murugesan, S.
Yi, J.
Li, D.
Shao, L.
Betzig, E.
Wu, X.
Hammer, J. A.
TI An Alternative Mechanism for Actin Arc Formation at the Immunological
Synapse of Jurkat T cells.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Murugesan, S.; Yi, J.; Wu, X.; Hammer, J. A.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Li, D.; Shao, L.; Betzig, E.] HHMI, Ashburn, VA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P44
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100045
ER
PT J
AU Nezich, C
Fogel, AI
Wang, C
Youle, RJ
AF Nezich, C.
Fogel, A. I.
Wang, C.
Youle, R. J.
TI Parkin regulates the activity of MiTF/TFE transcription factors
independent of mTORC1 during mitophagy
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Nezich, C.; Fogel, A. I.; Wang, C.; Youle, R. J.] NINDS, NIH, Bethesda, MD 20892 USA.
[Nezich, C.] Univ Cambridge, MRC Mitochondrial Biol Unit, Cambridge, England.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2139
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105168
ER
PT J
AU Oddoux, S
Liu, W
Zaal, KJ
Ralston, E
AF Oddoux, S.
Liu, W.
Zaal, K. J.
Ralston, E.
TI Changes in Golgi elements are responsible for the disordered microtubule
network of DMD muscle fibers.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Oddoux, S.] Aix Marseille Univ, Marseille, France.
[Liu, W.; Zaal, K. J.; Ralston, E.] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2394
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105422
ER
PT J
AU Ohman, R
Brubaker, L
Kawakami-Schulz, S
Lin, X
Subedi, K
Chow, I
Kaufman, J
Wingfield, P
Mankodi, AK
AF Ohman, R.
Brubaker, L.
Kawakami-Schulz, S.
Lin, X.
Subedi, K.
Chow, I.
Kaufman, J.
Wingfield, P.
Mankodi, A. K.
TI Isoform-specific oligomerization of ZASP, a myofibrillar myopathy gene
product, in vitro and in vivo.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Ohman, R.; Brubaker, L.; Kawakami-Schulz, S.; Lin, X.; Subedi, K.; Chow, I.; Mankodi, A. K.] NINDS, NIH, Bethesda, MD 20892 USA.
[Kaufman, J.; Wingfield, P.] NIAMS, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P79
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100080
ER
PT J
AU Ojha, N
Choudhary, V
Prinz, W
AF Ojha, N.
Choudhary, V.
Prinz, W.
TI A dynamin-like ER-shaping protein and FIT proteins regulate lipid
droplet biogenesis in yeast
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Ojha, N.; Choudhary, V.; Prinz, W.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2118
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105147
ER
PT J
AU Ott, CM
Battle, C
Lippincott-Schwartz, J
Schmidt, CF
AF Ott, C. M.
Battle, C.
Lippincott-Schwartz, J.
Schmidt, C. F.
TI Primary cilia bend and pivot in response to intracellular and
extracellular forces.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT Joint Annual Meeting of the American-Society-for-Cell-Biology (ASCB) /
International-Federation-for-Cell-Biology (IFCB)
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Ott, C. M.] NICHD, NIH, Bethesda, MD USA.
[Battle, C.] Univ Gottingen, Drittes Phys Inst, Gottingen, Germany.
[Lippincott-Schwartz, J.] Marine Biol Lab, Physiol Course, Woods Hole, MA 02543 USA.
[Lippincott-Schwartz, J.] NICHD, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
[Schmidt, C. F.] Univ Gottingen, Phys Inst Biophys, D-37073 Gottingen, Germany.
RI Schmidt, Christoph/G-3787-2011
OI Schmidt, Christoph/0000-0003-2864-6973
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1764
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104229
ER
PT J
AU Park, C
Park, J
Kim, T
Lee, K
AF Park, C.
Park, J.
Kim, T.
Lee, K.
TI Plk1-dependent timely delocalization of the PBIP1-CENP-Q complex from
kinetochores is critical for proper chromosome segregation.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Park, C.] Korea Res Inst Chem Technol, Taejon 305606, South Korea.
[Park, J.; Kim, T.; Lee, K.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1052
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102297
ER
PT J
AU Park, J
Park, S
Kim, T
Kim, J
Kwak, M
Ku, B
Tian, L
Kim, S
Oh, B
Yang, W
Lee, K
AF Park, J.
Park, S.
Kim, T.
Kim, J.
Kwak, M.
Ku, B.
Tian, L.
Kim, S.
Oh, B.
Yang, W.
Lee, K.
TI Molecular basis of ordered Plk4 binding to two distinct scaffolds
critical for centriole biogenesis.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Park, J.; Park, S.; Kim, T.; Lee, K.] NCI, NIH, Bethesda, MD 20892 USA.
[Kim, J.; Ku, B.; Kim, S.] Korea Res Inst Biosci & Biotechnol, Taejon, South Korea.
[Kwak, M.; Oh, B.] Korea Adv Inst Sci & Technologycience & Biotechno, Daejeon, South Korea.
[Tian, L.; Yang, W.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1018
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102263
ER
PT J
AU Peel, N
Iyer, J
Naik, A
O'Connell, KF
AF Peel, N.
Iyer, J.
Naik, A.
O'Connell, K. F.
TI Protein phosphatase 1 regulates ZYG-1 levels to limit centrosome
duplication.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Peel, N.; Naik, A.] Coll New Jersey, Dept Biol, Ewing, NJ USA.
[Iyer, J.; O'Connell, K. F.] NIDDK, LBG, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1031
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102276
ER
PT J
AU Petrie, R
Koo, H
Yamada, K
AF Petrie, R.
Koo, H.
Yamada, K.
TI Myosin II pulls the nucleus forward to increase intracellular pressure
and drive 3D cell movement.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Petrie, R.; Yamada, K.] NIDCR, NIH, Bethesda, MD USA.
[Koo, H.] Univ Penn, Sch Dent Med, Dept Orthodont, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P523
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101152
ER
PT J
AU Plevock, KM
Guillen, RX
Galletta, BJ
Slep, KC
Rusan, NM
AF Plevock, K. M.
Guillen, R. X.
Galletta, B. J.
Slep, K. C.
Rusan, N. M.
TI CP190-microtubule association is mediated by a novel N-terminal region
that requires dimerization mediated by a flanking BTB domain.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Plevock, K. M.] Univ N Carolina, Chapel Hill, NC USA.
[Plevock, K. M.; Guillen, R. X.; Galletta, B. J.; Rusan, N. M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Slep, K. C.] Univ N Carolina, Dept Biol, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P119
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100120
ER
PT J
AU Porat-Shliom, N
Chen, Y
Shitara, A
Tora, M
Harding, O
Masedunskas, A
Weigert, R
AF Porat-Shliom, N.
Chen, Y.
Shitara, A.
Tora, M.
Harding, O.
Masedunskas, A.
Weigert, R.
TI In vivo tissue-wide synchronization of mitochondrial metabolic
oscillations
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Porat-Shliom, N.; Shitara, A.; Tora, M.; Harding, O.; Masedunskas, A.; Weigert, R.] NIDCR, NIH, Bethesda, MD USA.
[Chen, Y.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2144
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105173
ER
PT J
AU Porter, JR
Fisher, BE
Batchelor, E
AF Porter, J. R.
Fisher, B. E.
Batchelor, E.
TI Multiplexed transcriptional analysis of p53 targets in single cells
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Porter, J. R.; Fisher, B. E.; Batchelor, E.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2286
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105316
ER
PT J
AU Pronobis, M
Rusan, NM
Peifer, M
AF Pronobis, M.
Rusan, N. M.
Peifer, M.
TI Inside the destruction complex: APC's mechanistic role in downregulation
of Wnt signaling.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Pronobis, M.] UNC, GMB, Chapel Hill, NC USA.
[Pronobis, M.] HHMI, Chevy Chase, MD USA.
[Rusan, N. M.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
[Peifer, M.] Univ N Carolina, Dept Biol, Chapel Hill, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1387
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103238
ER
PT J
AU Rambold, A
Cohen, S
Lippincott-Schwartz, J
AF Rambold, A.
Cohen, S.
Lippincott-Schwartz, J.
TI Regulated by mitochondrial fusion dynamics, lipid droplets serve as
central fatty acid conduit to supply mitochondria with fatty acids for
oxidation during nutrient stress
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Rambold, A.] Max Planck Inst IE, Freiburg, Germany.
[Cohen, S.; Lippincott-Schwartz, J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2123
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105152
ER
PT J
AU Remmert, K
Beach, JR
Porat-Shliom, N
Weigert, R
Yang, Y
Sellers, JR
Hammer, JA
AF Remmert, K.
Beach, J. R.
Porat-Shliom, N.
Weigert, R.
Yang, Y.
Sellers, J. R.
Hammer, J. A.
TI Myosin 18A localizes with myosin II at cell: cell junctions in
epithelial cells and tissues.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Remmert, K.; Beach, J. R.; Hammer, J. A.] NHLBI, LCB, NIH, Bethesda, MD 20892 USA.
[Porat-Shliom, N.; Weigert, R.] NIDCR, NIH, Bethesda, MD USA.
[Yang, Y.] Hunan Agr Univ, Changsha, Hunan, Peoples R China.
[Sellers, J. R.] NHLBI, LMP, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P108
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100109
ER
PT J
AU Reveal, B
Lilly, M
AF Reveal, B.
Lilly, M.
TI The role of the TORC1 regulator IML1 in meiotic progression and the
response to cellular stress
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Reveal, B.; Lilly, M.] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2324
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105354
ER
PT J
AU Ricca, BL
Venugopalan, G
Tanner, K
Furata, S
Orellana, W
Reber, C
Brownfield, DG
Bissell, MJ
Fletcher, DA
AF Ricca, B. L.
Venugopalan, G.
Tanner, K.
Furata, S.
Orellana, W.
Reber, C.
Brownfield, D. G.
Bissell, M. J.
Fletcher, D. A.
TI Transient external force induces phenotypic reversion of malignant
epithelial structures via nitric oxide Signaling.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Ricca, B. L.; Venugopalan, G.; Reber, C.; Brownfield, D. G.; Fletcher, D. A.] Univ Calif Berkeley, Dept Bioengn, Berkeley, CA 94720 USA.
[Tanner, K.; Furata, S.; Orellana, W.; Brownfield, D. G.; Bissell, M. J.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Life Sci Div, Berkeley, CA 94720 USA.
[Tanner, K.; Orellana, W.] NCI, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Brownfield, D. G.] Stanford Univ, Biochem, Stanford, CA 94305 USA.
[Fletcher, D. A.] Univ Calif Berkeley, Biophys Grad Grp, Berkeley, CA 94720 USA.
[Fletcher, D. A.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Phys Biosci Div, Berkeley, CA 94720 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1915
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104362
ER
PT J
AU Ritter, AT
Betzig, E
Griffiths, GM
Lippincott-Schwartz, J
AF Ritter, A. T.
Betzig, E.
Griffiths, G. M.
Lippincott-Schwartz, J.
TI Dynamic modulation of cortical actin at the immunological synapse
controls cytotoxic granule secretion.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT Joint Annual Meeting of the American-Society-for-Cell-Biology (ASCB) /
International-Federation-for-Cell-Biology (IFCB)
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Ritter, A. T.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD 20892 USA.
[Ritter, A. T.] Univ Cambridge, Cambridge Inst Med Res, Cambridge, England.
[Betzig, E.] HHMI Janelia Farm Res Campus, Ashburn, VA USA.
[Griffiths, G. M.] Univ Cambridge, Cambridge, England.
[Lippincott-Schwartz, J.] Marine Biol Lab, Physiol Course, Woods Hole, MA 02543 USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1990
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105019
ER
PT J
AU Roney, JC
Gunay-Aygun, M
Gul, D
Vilboux, T
Maynard, DM
Toro, C
Introne, WJ
Mullikin, JC
Huizing, M
Gahl, WA
Cullinane, AR
AF Roney, J. C.
Gunay-Aygun, M.
Gul, D.
Vilboux, T.
Maynard, D. M.
Toro, C.
Introne, W. J.
Mullikin, J. C.
Huizing, M.
Gahl, W. A.
Cullinane, A. R.
TI Identification of a Mutation in a Novel Gene Causing a Chediak-Higashi
Syndrome-Like Phenotype.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Roney, J. C.; Gunay-Aygun, M.; Vilboux, T.; Maynard, D. M.; Toro, C.; Introne, W. J.; Huizing, M.; Gahl, W. A.; Cullinane, A. R.] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Gul, D.] Gulhane Mil Med Acad, Dept Med Genet, Ankara, Turkey.
[Mullikin, J. C.] NHGRI, Comparat Genom Anal Unit, Canc Genet & Comparat Genom Branch, NIH, Bethesda, MD 20892 USA.
[Mullikin, J. C.] NIH Intramural Sequencing Ctr, NHGRI, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P398
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101028
ER
PT J
AU Ryoo, M
Harding, O
Tangrea, MA
Weigert, R
Shitara, A
Hanson, JC
Rosenberg, A
Porat-Shliom, N
Chen, Y
AF Ryoo, M.
Harding, O.
Tangrea, M. A.
Weigert, R.
Shitara, A.
Hanson, J. C.
Rosenberg, A.
Porat-Shliom, N.
Chen, Y.
TI Developing Mitochondrial Enrichment for Targeted Analysis (META) to
Study Phosphorylation Kinetics
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Ryoo, M.; Tangrea, M. A.; Hanson, J. C.; Rosenberg, A.; Chen, Y.] NCI, NIH, Bethesda, MD 20892 USA.
[Ryoo, M.] Duke Univ, Durham, NC USA.
[Harding, O.; Weigert, R.; Shitara, A.; Porat-Shliom, N.] NIDCR, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1605
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104070
ER
PT J
AU Satpute-Krishnan, P
Lippincott-Schwartz, J
AF Satpute-Krishnan, P.
Lippincott-Schwartz, J.
TI Quality control of GPI-anchored proteins in the secretory pathway.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT Joint Annual Meeting of the American-Society-for-Cell-Biology (ASCB) /
International-Federation-for-Cell-Biology (IFCB)
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Satpute-Krishnan, P.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
[Lippincott-Schwartz, J.] Marine Biol Lab, Physiol Course, Woods Hole, MA 02543 USA.
[Lippincott-Schwartz, J.] NICHD, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
NR 2
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P650
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101278
ER
PT J
AU Schoborg, T
Guillen, RX
Rusan, NM
AF Schoborg, T.
Guillen, R. X.
Rusan, N. M.
TI Calmodulin and Abnormal Spindle Cooperate to Maintain Mitotic/Meiotic
Spindle Integrity in D. melanogaster
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Schoborg, T.; Rusan, N. M.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
[Guillen, R. X.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 2
U2 3
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1805
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104270
ER
PT J
AU Sengupta, P
van Engelenburg, S
Johnson, M
Lippincott-Schwartz, J
AF Sengupta, P.
van Engelenburg, S.
Johnson, M.
Lippincott-Schwartz, J.
TI Mechanism of protein incorporation into envelop of budding HIV particle.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT Joint Annual Meeting of the American-Society-for-Cell-Biology (ASCB) /
International-Federation-for-Cell-Biology (IFCB)
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Sengupta, P.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
[van Engelenburg, S.; Lippincott-Schwartz, J.] Marine Biol Lab, Physiol Course, Woods Hole, MA 02543 USA.
[van Engelenburg, S.; Lippincott-Schwartz, J.] NICHD, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
[Johnson, M.] Univ Missouri, Columbia, MO USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA M46
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094106095
ER
PT J
AU Sheldon, KL
Bezrukov, SM
Sackett, DL
AF Sheldon, K. L.
Bezrukov, S. M.
Sackett, D. L.
TI Not just charged strings: binding of Tubulin's disordered tails to VDAC
is regulated by small sequence changes and by posttranlational
modification.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Sheldon, K. L.; Bezrukov, S. M.; Sackett, D. L.] NICHD, Program Phys Biol, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P134
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100135
ER
PT J
AU Shomron, O
Nevo-Yassaf, I
Aviad, T
Patterson, GH
Hirschberg, K
AF Shomron, O.
Nevo-Yassaf, I.
Aviad, T.
Patterson, G. H.
Hirschberg, K.
TI Live cell microscopy of early ER export events underpins a new model for
COPII function at the ER-ER exit site boundary.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Shomron, O.; Nevo-Yassaf, I.; Aviad, T.; Hirschberg, K.] Tel Aviv Univ, Pathol, IL-69978 Tel Aviv, Israel.
[Patterson, G. H.] NIBIB, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P416
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101046
ER
PT J
AU Shu, S
Liu, X
Yu, S
Lee, D
Wang, G
Gucek, M
Korn, ED
AF Shu, S.
Liu, X.
Yu, S.
Lee, D.
Wang, G.
Gucek, M.
Korn, E. D.
TI Biochemical and Biological Properties of Dictyostelium Cortexillin III
and Its Complex(es) with DGAP1.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Shu, S.; Liu, X.; Yu, S.; Lee, D.; Wang, G.; Gucek, M.; Korn, E. D.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P899
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102145
ER
PT J
AU Shukla, AK
Kong, D
Sharma, M
Loncarek, J
AF Shukla, A. K.
Kong, D.
Sharma, M.
Loncarek, J.
TI Loss of block-to-centriole reduplication without a loss of centriole
orthogonal orientation in human cells.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Shukla, A. K.; Kong, D.; Sharma, M.; Loncarek, J.] NCI, NIH, Lab Prot Dynam & Signaling, Frederick, MD 21701 USA.
RI Kong, Dong/O-4465-2016
OI Kong, Dong/0000-0002-7144-3808
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1021
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102266
ER
PT J
AU Skau, CT
Waterman, C
AF Skau, C. T.
Waterman, C.
TI A novel actin-adhesion structure involved in nuclear positioning
requires the formin FMN2.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Skau, C. T.; Waterman, C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1649
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104114
ER
PT J
AU Skau, CT
Plotnikov, SV
Waterman, C
AF Skau, C. T.
Plotnikov, S. V.
Waterman, C.
TI The formin INF2 is a focal adhesion protein that promotes dorsal stress
fiber and fibrillar adhesion formation to drive extracellular matrix
assembly.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Skau, C. T.; Plotnikov, S. V.; Waterman, C.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Plotnikov, S. V.] Univ Toronto, Cell & Syst Biol, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P903
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102149
ER
PT J
AU Smith, GH
AF Smith, G. H.
TI Paracrine rescued lobulogenesis in PR null mammary outgrowths by
redirected testicular cells
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Smith, G. H.] NCI, BRL, NIH, CCR, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2351
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105380
ER
PT J
AU Sochacki, KA
Taraska, JW
AF Sochacki, K. A.
Taraska, J. W.
TI A nanometer-scale survey of the structure and organization of
clathrin-mediated endocytosis among mammalian cell lines
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Sochacki, K. A.; Taraska, J. W.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1192
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103043
ER
PT J
AU Sun, L
Vergarajauregui, S
Puertollano, R
AF Sun, L.
Vergarajauregui, S.
Puertollano, R.
TI Inducible expression of MCOLN2 in immune cells
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Sun, L.; Vergarajauregui, S.; Puertollano, R.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1216
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103067
ER
PT J
AU Sundborger, AC
Hinshaw, JE
AF Sundborger, A. C.
Hinshaw, J. E.
TI Super-constriction precedes GTP-hydrolysis dependent conformational
changes in dynamin polymers during plasma membrane fission
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Sundborger, A. C.; Hinshaw, J. E.] NIDDK, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P833
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102079
ER
PT J
AU Swaminathan, V
Waterman, C
AF Swaminathan, V.
Waterman, C.
TI Focal adhesion kinase links lamellipodial actin and nascent adhesions to
the ECM through the Arp2/3 complex to regulate leading edge dynamics.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Swaminathan, V.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
[Waterman, C.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2226
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105256
ER
PT J
AU Szyk, A
Deaconescu, A
Spector, J
Valenstein, M
Goodman, B
Kormendi, V
Grigorieff, N
Roll-Mecak, A
AF Szyk, A.
Deaconescu, A.
Spector, J.
Valenstein, M.
Goodman, B.
Kormendi, V.
Grigorieff, N.
Roll-Mecak, A.
TI Generating the chemical complexity of tubulin: insights into the
mechanism of tubulin post-translational modification enzymes
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Szyk, A.; Spector, J.; Valenstein, M.; Goodman, B.; Kormendi, V.; Roll-Mecak, A.] NINDS, Cell Biol & Biophys, NIH, Bethesda, MD 20892 USA.
[Deaconescu, A.] Brown Univ, Dept Mol Biol Cell Biol & Biochem, Providence, RI 02912 USA.
[Grigorieff, N.] Howard Hughes Med Inst, Ashburn, VA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P955
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102200
ER
PT J
AU Tanner, K
Afasizheva, A
AF Tanner, K.
Afasizheva, A.
TI Malignant melanoma cells dynamically construct a tumor biofilm that
promotes survival in response to drug treatment and hypoxia.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Tanner, K.; Afasizheva, A.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2241
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105271
ER
PT J
AU Traver, MK
Paul, S
Losert, W
Shroff, H
Schaefer, BC
AF Traver, M. K.
Paul, S.
Losert, W.
Shroff, H.
Schaefer, B. C.
TI Regulation of T cell receptor signaling to NF-kappa B by microtubule
transport of signalosomes.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Traver, M. K.; Schaefer, B. C.] Uniformed Serv Univ Hlth Sci, Microbiol & Immunol, Bethesda, MD USA.
[Paul, S.] Univ Toledo, Dept Internal Med, Med Ctr, Toledo, OH 43606 USA.
[Losert, W.] Univ Maryland, Dept Phys, College Pk, MD 20742 USA.
[Shroff, H.] NIBIB, Sect High Resolut Opt Imaging, NIH, Bethesda, MD USA.
RI Shroff, Hari/E-7247-2016
OI Shroff, Hari/0000-0003-3613-8215
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA M41
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094106090
ER
PT J
AU Trexler, AJ
Taraska, JW
AF Trexler, A. J.
Taraska, J. W.
TI Investigating the regulation of pulmonary surfactant secretion using
fluorescence microscopy.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Trexler, A. J.; Taraska, J. W.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1991
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105020
ER
PT J
AU Tsai, SA
Pokrass, MJ
Su, T
AF Tsai, S. A.
Pokrass, M. J.
Su, T.
TI Sigma-1 Receptor Deficiency Hinders p35 Degradation and Causes Impaired
Neuronal Circuitry.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Tsai, S. A.; Pokrass, M. J.; Su, T.] NIDA, NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1502
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103353
ER
PT J
AU Valm, AM
Cohen, S
Legant, WR
Davidson, MW
Betzig, E
Lippincott-Schwartz, J
AF Valm, A. M.
Cohen, S.
Legant, W. R.
Davidson, M. W.
Betzig, E.
Lippincott-Schwartz, J.
TI Novel spectral imaging and analysis to unravel the organelle interactome
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT Joint Annual Meeting of the American-Society-for-Cell-Biology (ASCB) /
International-Federation-for-Cell-Biology (IFCB)
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Valm, A. M.; Cohen, S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
[Legant, W. R.; Betzig, E.] HHMI Janelia Farm Res Campus, Ashburn, VA USA.
[Davidson, M. W.] Florida State Univ, Natl High Magnet Field Lab, Tallahassee, FL 32306 USA.
[Davidson, M. W.] Florida State Univ, Dept Biol Sci, Tallahassee, FL 32306 USA.
[Lippincott-Schwartz, J.] Marine Biol Lab, Physiol Course, Woods Hole, MA 02543 USA.
[Lippincott-Schwartz, J.] NICHD, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1600
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104065
ER
PT J
AU Vural, A
Al-Khodor, S
Cheung, GY
Shi, CS
Srinivasan, L
Briken, V
Otto, M
Fraser, ID
Kehrl, JH
AF Vural, A.
Al-Khodor, S.
Cheung, G. Y.
Shi, C. S.
Srinivasan, L.
Briken, V.
Otto, M.
Fraser, I. D.
Kehrl, J. H.
TI Activator of G-protein Signaling 3 (AGS3)-induced lysosomal biogenesis
mediates resistance against (antibiotic-resistant) intracellular
pathogens.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Vural, A.; Shi, C. S.; Kehrl, J. H.] NIAID, Immunoregulat Lab, Bethesda, MD 20892 USA.
[Al-Khodor, S.; Fraser, I. D.] NIAID, Lab Syst Biol, Bethesda, MD 20892 USA.
[Cheung, G. Y.; Otto, M.] NIAID, Lab Human Bacterial Pathogenesis, Bethesda, MD 20892 USA.
[Srinivasan, L.; Briken, V.] Univ Maryland, College Pk, MD 20742 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P411
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101041
ER
PT J
AU Walia, V
Insinna, C
Lu, Q
Specht, S
Westlake, CJ
AF Walia, V.
Insinna (Kettenhofen), C.
Lu, Q.
Specht, S.
Westlake, C. J.
TI PI3K/Akt signaling regulates ciliogenesis initiation via Rab11-effector
vesicular trafficking switch.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Walia, V.; Insinna (Kettenhofen), C.; Lu, Q.; Specht, S.] NCI, LCDS, Frederick, MD 21701 USA.
[Westlake, C. J.] NCI, Frederick, MD 21701 USA.
RI Lu, Quanlong/M-4436-2015
OI Lu, Quanlong/0000-0002-4261-5121
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P991
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102236
ER
PT J
AU Waterman, C
Case, L
Swaminathan, VS
Skau, CT
AF Waterman, C.
Case, L.
Swaminathan, V. S.
Skau, C. T.
TI Functional specificity of integrin-based adhesions in cell function is
defined by actin nucleators.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Waterman, C.; Case, L.; Swaminathan, V. S.; Skau, C. T.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA S5
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094106005
ER
PT J
AU Waxse, B
Hughes, AJ
Wojcik, M
Feliciano, D
van Engelenburg, S
Lippincott-Schwartz, J
AF Waxse, B.
Hughes, A. J.
Wojcik, M.
Feliciano, D.
van Engelenburg, S.
Lippincott-Schwartz, J.
TI Using microfluidic approaches to study gap junction intercellular
communication.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT Joint Annual Meeting of the American-Society-for-Cell-Biology (ASCB) /
International-Federation-for-Cell-Biology (IFCB)
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Waxse, B.; Hughes, A. J.; Wojcik, M.; Feliciano, D.; van Engelenburg, S.; Lippincott-Schwartz, J.] Marine Biol Lab, Physiol Course, Woods Hole, MA 02543 USA.
[Waxse, B.; van Engelenburg, S.; Lippincott-Schwartz, J.] NICHD, Cell Biol & Metab Program, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P588
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101216
ER
PT J
AU Webster, MR
Xu, M
Kinzler, KA
Kaur, A
Appleton, J
O'Connell, MP
Marchbank, K
Valiga, A
Dang, VM
Perego, M
Zang, G
Slipicevic, A
Keeney, F
Lehrmann, E
Wood, W
Becker, K
Kossenkov, A
Frederick, D
Flaherty, K
Xu, X
Herlyn, M
Murphy, ME
Weeraratna, AT
AF Webster, M. R.
Xu, M.
Kinzler, K. A.
Kaur, A.
Appleton, J.
O'Connell, M. P.
Marchbank, K.
Valiga, A.
Dang, V. M.
Perego, M.
Zang, G.
Slipicevic, A.
Keeney, F.
Lehrmann, E.
Wood, W., III
Becker, K.
Kossenkov, A.
Frederick, D.
Flaherty, K.
Xu, X.
Herlyn, M.
Murphy, M. E.
Weeraratna, A. T.
TI Wnt5A promotes an adaptive, senescent-like stress response, while
continuing to drive invasion in melanoma cells
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Webster, M. R.; Kaur, A.; Appleton, J.; O'Connell, M. P.; Marchbank, K.; Valiga, A.; Dang, V. M.; Perego, M.; Zang, G.; Slipicevic, A.; Herlyn, M.; Weeraratna, A. T.] Wistar Inst Anat & Biol, Tumor Microenvironm & Metastasis, Philadelphia, PA 19104 USA.
[Xu, M.; Kinzler, K. A.; Lehrmann, E.; Wood, W., III; Becker, K.] NIA, Baltimore, MD 21224 USA.
[Keeney, F.] Wistar Inst Anat & Biol, Microscopy, Philadelphia, PA 19104 USA.
[Kossenkov, A.] Wistar Inst Anat & Biol, Bioinformat, Philadelphia, PA 19104 USA.
[Frederick, D.; Flaherty, K.] Massachusetts Gen Hosp, Ctr Canc, Boston, MA USA.
[Xu, X.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Murphy, M. E.] Wistar Inst Anat & Biol, Mol & Cellular Oncogenesis, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1878
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104325
ER
PT J
AU Wei, Y
Lilly, M
AF Wei, Y.
Lilly, M.
TI The Drosophila SEA/GATOR complex controls meiotic progression and the
response to amino acid starvation by modulating TORC1 activity
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Wei, Y.] NICHD, NIH, Rockville, MD USA.
[Lilly, M.] NICHD, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2326
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105356
ER
PT J
AU Williams, C
Liu, Y
O'Connell, KF
AF Williams, C.
Liu, Y.
O'Connell, K. F.
TI A novel function for CDK--11 in fertilization and fecundity in C.
elegans
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Williams, C.; Liu, Y.; O'Connell, K. F.] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P2321
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094105351
ER
PT J
AU Williamson, CD
Donaldson, JG
AF Williamson, C. D.
Donaldson, J. G.
TI Macropinocytosis as a model for tracking clathrin-independent cargo
sorting in space and time.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Williamson, C. D.; Donaldson, J. G.] NHLBI, Cell Biol & Physiol Ctr, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P378
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101008
ER
PT J
AU Wu, X
Hammer, JA
AF Wu, X.
Hammer, J. A.
TI Melanoregulin may influence melanosome distribution through its effects
on the organization of lipids in the melanosome membrane.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Wu, X.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Hammer, J. A.] NHLBI, LCB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P395
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101025
ER
PT J
AU Wu, Z
Plotnikov, SV
Waterman, C
Liu, J
AF Wu, Z.
Plotnikov, S. V.
Waterman, C.
Liu, J.
TI Two distinct actin networks mediate traction oscillations to confer
mechanosensitivity of focal adhesions.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Wu, Z.; Plotnikov, S. V.; Waterman, C.; Liu, J.] Natl Inst Hlth, Natl Heart Lung & Blood Inst, Bethesda, MD USA.
[Plotnikov, S. V.] Univ Toronto, Cell & Syst Biol, Toronto, ON, Canada.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1470
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094103321
ER
PT J
AU Yamashita, RA
Marchler-Bauer, A
Bryant, S
AF Yamashita, R. A.
Marchler-Bauer, A.
Bryant, S.
TI Myosin Superfamily Classification using the Conserved Domain Database
(CDD) Resource at NCBI
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Yamashita, R. A.; Marchler-Bauer, A.; Bryant, S.] NCBI, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P937
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094102182
ER
PT J
AU Yasui, Y
Su, T
AF Yasui, Y.
Su, T.
TI PCAF is involved in acetylation and subcellular distribution of Sigma-1
receptors.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Yasui, Y.; Su, T.] NIDA, NIH, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P426
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101056
ER
PT J
AU Youle, RJ
AF Youle, R. J.
TI Damage control: how PINK1 and Parkin survey mitochondrial fidelity and
respond with selective autophagy
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Youle, R. J.] NINDS, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA S13
PG 1
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094106236
ER
PT J
AU Young, LE
Gauvin, TJ
Heimsath, EG
Higgs, H
AF Young, L. E.
Gauvin, T. J.
Heimsath, E. G.
Higgs, H.
TI Arp2/3 complex-dependent assembly of filopodia by the formin FMNL3
contributes to cell-cell adhesion.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Young, L. E.] Dartmouth Coll, Hanover, NH 03755 USA.
[Gauvin, T. J.] Dartmouth Geisel Sch Med, Hanover, NH USA.
[Heimsath, E. G.] NIDCD, NIH, Bethesda, MD USA.
[Higgs, H.] Dartmouth Coll, Geisel Sch Med, Dept Biochem, Hanover, NH 03755 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P1671
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094104136
ER
PT J
AU Zhang, F
Colavita, K
Rodionova, I
Buckley, B
Scott, D
Kumar, A
Shabalina, S
Saha, S
Chernov, M
Osterman, A
Kashina, AS
AF Zhang, F.
Colavita, K.
Rodionova, I.
Buckley, B.
Scott, D.
Kumar, A.
Shabalina, S.
Saha, S.
Chernov, M.
Osterman, A.
Kashina, A. S.
TI Arginylation Regulates Purine Biosynthesis by Facilitating the
Biological Activity of Phosphorybosyl Pyrophospate Synthase.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Zhang, F.; Kumar, A.] Univ Miami, Sch Med, Miami, FL USA.
[Colavita, K.] Univ Penn, Philadelphia, PA 19104 USA.
[Rodionova, I.] Sanford Burham Med Res Inst, La Jolla, CA USA.
[Buckley, B.] Roswell Pk Canc Res Ctr, Buffalo, NY USA.
[Scott, D.; Osterman, A.] 3Sanford Burnham Med Res Inst, La Jolla, CA USA.
[Shabalina, S.] NCBI, NIH, Bethesda, MD USA.
[Saha, S.] Tezpur Univ, Napaam, India.
[Chernov, M.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Kashina, A. S.] Univ Penn, Sch Vet Med, Dept Anim Biol, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P514
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094101143
ER
PT J
AU Zhang, M
Arnaoutov, A
Dasso, M
AF Zhang, M.
Arnaoutov, A.
Dasso, M.
TI RanBP1 governs spindle assembly by defining mitotic Ran-GTP production.
SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Meeting Abstract
CT ASCB/IFCB Meeting
CY DEC 06-10, 2014
CL Philadelphia, PA
SP Amer Soc Cell Biol, Int Federat Cell Biol
C1 [Zhang, M.; Arnaoutov, A.; Dasso, M.] NICHHD, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
EI 1939-4586
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD DEC
PY 2014
VL 25
MA P181
PG 2
WC Cell Biology
SC Cell Biology
GA CE8LP
UT WOS:000352094100182
ER
PT J
AU Said, M
AF Said, Maria
TI In Liberia, the End of the Ebola Epidemic will be the Beginning
SO ECOHEALTH
LA English
DT Editorial Material
C1 [Said, Maria] US PHS, LCDR, Washington, DC 20201 USA.
[Said, Maria] NIH, Div Int Training & Res, Fogarty Int Ctr, Rockville, MD 20852 USA.
[Said, Maria] US FDA, Div Epidemiol, Off Biostat & Epidemiol, Ctr Biol Evaluat & Res, Silver Spring, MD 20993 USA.
RP Said, M (reprint author), US PHS, LCDR, Washington, DC 20201 USA.
EM said.maria@gmail.com
NR 1
TC 0
Z9 0
U1 1
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1612-9202
EI 1612-9210
J9 ECOHEALTH
JI EcoHealth
PD DEC
PY 2014
VL 11
IS 4
BP 459
EP 460
DI 10.1007/s10393-015-1017-4
PG 2
WC Biodiversity Conservation; Ecology; Environmental Sciences
SC Biodiversity & Conservation; Environmental Sciences & Ecology
GA CE5HB
UT WOS:000351860800003
PM 25691142
ER
PT J
AU Perrings, C
Castillo-Chavez, C
Chowell, G
Daszak, P
Fenichel, EP
Finnoff, D
Horan, RD
Kilpatrick, AM
Kinzig, AP
Kuminoff, NV
Levin, S
Morin, B
Smith, KF
Springborn, M
AF Perrings, Charles
Castillo-Chavez, Carlos
Chowell, Gerardo
Daszak, Peter
Fenichel, Eli P.
Finnoff, David
Horan, Richard D.
Kilpatrick, A. Marm
Kinzig, Ann P.
Kuminoff, Nicolai V.
Levin, Simon
Morin, Benjamin
Smith, Katherine F.
Springborn, Michael
TI Merging Economics and Epidemiology to Improve the Prediction and
Management of Infectious Disease
SO ECOHEALTH
LA English
DT Article
DE economic epidemiology; epidemiological economics; incentives; infectious
disease
ID PANDEMIC INFLUENZA; WILDLIFE DISEASE; UNITED-KINGDOM; REPRODUCTION
NUMBER; MATHEMATICAL-MODELS; COST-EFFECTIVENESS; AVIAN INFLUENZA;
HUMAN-BEHAVIOR; SPREAD; TRADE
AB Mathematical epidemiology, one of the oldest and richest areas in mathematical biology, has significantly enhanced our understanding of how pathogens emerge, evolve, and spread. Classical epidemiological models, the standard for predicting and managing the spread of infectious disease, assume that contacts between susceptible and infectious individuals depend on their relative frequency in the population. The behavioral factors that underpin contact rates are not generally addressed. There is, however, an emerging a class of models that addresses the feedbacks between infectious disease dynamics and the behavioral decisions driving host contact. Referred to as "economic epidemiology" or "epidemiological economics," the approach explores the determinants of decisions about the number and type of contacts made by individuals, using insights and methods from economics. We show how the approach has the potential both to improve predictions of the course of infectious disease, and to support development of novel approaches to infectious disease management.
C1 [Perrings, Charles; Kinzig, Ann P.; Morin, Benjamin] Arizona State Univ, Sch Life Sci, Tempe, AZ 85287 USA.
[Castillo-Chavez, Carlos] Arizona State Univ, Math Computat & Modeling Sci Ctr, Tempe, AZ 85287 USA.
[Castillo-Chavez, Carlos; Chowell, Gerardo] Arizona State Univ, Sch Human Evolut & Social Change, Tempe, AZ 85287 USA.
[Chowell, Gerardo] NIH, Div Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Daszak, Peter] EcoHlth Alliance, New York, NY 10001 USA.
[Fenichel, Eli P.] Yale Univ, Sch Forestry & Environm Studies, New Haven, CT 06511 USA.
[Finnoff, David] Univ Wyoming, Dept Econ & Finance, Laramie, WY 82071 USA.
[Horan, Richard D.] Michigan State Univ, Dept Agr Food & Resource Econ, E Lansing, MI 48824 USA.
[Kilpatrick, A. Marm] Univ Calif Santa Cruz, Dept Ecol & Evolutionary Biol, Santa Cruz, CA 95064 USA.
[Kuminoff, Nicolai V.] Arizona State Univ, Dept Econ, Tempe, AZ 85287 USA.
[Levin, Simon] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Smith, Katherine F.] Brown Univ, Dept Ecol & Evolutionary Biol, Providence, RI 02912 USA.
[Springborn, Michael] Univ Calif Davis, Dept Environm Sci & Policy, Davis, CA 95616 USA.
RP Perrings, C (reprint author), Arizona State Univ, Sch Life Sci, Tempe, AZ 85287 USA.
EM charles.perrings@asu.edu; ccchavez@asu.edu; gchowell@asu.edu;
daszak@ecohealthalliance.org; eli.fenichel@yale.edu; finnoff@uwyo.edu;
horan@msu.edu; akilpatr@ucsc.edu; kinzig@asu.edu; kuminoff@asu.edu;
slevin@princeton.edu; brmorin@asu.edu; katherine_smith@brown.edu;
mspringborn@ucdavis.edu
OI Fenichel, Eli/0000-0002-7649-8250; Castillo-Chavez,
Carlos/0000-0002-1046-3901
FU National Institute of General Medical Sciences (NIGMS) at the National
Institutes of Health [1R01GM100471-01]; USDA National Institute of Food
and Agriculture [2011-67023-30872]; NSF [81140 - 443559]; American
people through the United States Agency for International Development
(USAID) Emerging Pandemic Threats PREDICT
FX This publication was made possible by grant #1R01GM100471-01 from the
National Institute of General Medical Sciences (NIGMS) at the National
Institutes of Health. In addition, Rick Horan acknowledges funding from
the USDA National Institute of Food and Agriculture, grant
#2011-67023-30872. Marm Kilpatrick acknowledges NSF grant #81140 -
443559. Peter Daszak acknowledges the generous support of the American
people through the United States Agency for International Development
(USAID) Emerging Pandemic Threats PREDICT.
NR 131
TC 11
Z9 11
U1 6
U2 33
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1612-9202
EI 1612-9210
J9 ECOHEALTH
JI EcoHealth
PD DEC
PY 2014
VL 11
IS 4
BP 464
EP 475
DI 10.1007/s10393-014-0963-6
PG 12
WC Biodiversity Conservation; Ecology; Environmental Sciences
SC Biodiversity & Conservation; Environmental Sciences & Ecology
GA CE5HB
UT WOS:000351860800005
PM 25233829
ER
PT J
AU Dunleavy, K
AF Dunleavy, Kieron
TI Double-hit lymphomas: current paradigms and novel treatment approaches
SO HEMATOLOGY-AMERICAN SOCIETY OF HEMATOLOGY EDUCATION PROGRAM
LA English
DT Article
ID B-CELL LYMPHOMA; RITUXIMAB PLUS CYCLOPHOSPHAMIDE; BURKITT-LYMPHOMA;
GERMINAL CENTER; MOLECULAR SUBTYPES; ANTITUMOR-ACTIVITY; PREDICTS
SURVIVAL; GENE-EXPRESSION; POOR-PROGNOSIS; PHASE-II
AB Double-hit lymphomas (DHLs) are a heterogeneous group of mature B-cell lymphomas that harbor concurrent rearrangements of MYC and BCL2 or, occasionally, BCL6. Several studies have now shown that they are associated with a very aggressive clinical course and poor outcome after standard R-CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, with few patients surviving beyond 2 years. Due to their rarity, there is a paucity of data evaluating patient outcomes with alternative strategies to R-CHOP and no consensus on how they should be optimally managed. Recent studies have demonstrated that a significant proportion of diffuse large B-cell lymphoma (DLBCL) cases have high protein expression of MYC and BCL2 as detected by IHC. These so-called "double-expressor" DLBCLs are also associated with a poor outcome after R-CHOP, even when MYC and BCL2 rearrangements are absent. There is much interest in developing new strategies for DHL and better characterizing the underlying biology that drives their poor prognosis. Alternative chemotherapy platforms to R-CHOP, such as DA-EPOCH-R (dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin and rituximab), are under investigation for MYC-rearranged DLBCL, including DHL, and several novel small-molecule inhibitors of MYC and BCL2 are in development.
C1 [Dunleavy, Kieron] NCI, Lymphoid Malignancies Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Dunleavy, K (reprint author), NCI, Lymphoid Malignancies Branch, 9000 Rockville Pike,Bldg 10,Room 4N-115, Bethesda, MD 20892 USA.
EM dunleavk@mail.nih.gov
FU intramural program of the National Cancer Institute
FX This work was supported by the intramural program of the National Cancer
Institute.
NR 45
TC 0
Z9 1
U1 2
U2 8
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 1520-4391
EI 1520-4383
J9 HEMATOL-AM SOC HEMAT
JI Hematol.-Am. Soc. Hematol. Educ. Program
PD DEC
PY 2014
BP 107
EP 112
DI 10.1182/asheducation-2014.1.107
PG 6
WC Education, Scientific Disciplines; Hematology
SC Education & Educational Research; Hematology
GA CC9XN
UT WOS:000350724600015
ER
PT J
AU Wiestner, A
AF Wiestner, Adrian
TI BCR pathway inhibition as therapy for chronic lymphocytic leukemia and
lymphoplasmacytic lymphoma
SO HEMATOLOGY-AMERICAN SOCIETY OF HEMATOLOGY EDUCATION PROGRAM
LA English
DT Article
ID B-CELL-RECEPTOR; TYROSINE KINASE INHIBITOR; L265P SOMATIC MUTATION;
NON-HODGKIN-LYMPHOMA; WALDENSTROM MACROGLOBULINEMIA; TUMOR
PROLIFERATION; PHOSPHATIDYLINOSITOL 3-KINASE-DELTA; ANTIGEN RECEPTORS;
T-LYMPHOCYTES; TARGETING BTK
AB Chronic lymphocytic leukemia (CLL) and lymphoplasmacytic lymphoma (LPL) are malignancies of mature B cells. In LPL, mutations of the adaptor protein MYD88 (L265P) in the Toll-like receptor pathway have been recognized recently as being a hallmark of the disease and indicate a dependence of the tumor on this pathway. In CLL, functional studies have implicated BCR activation in the tissue microenvironment as a pivotal pathway in the pathogenesis. Bruton's tyrosine kinase (BTK) and the PI3K delta isoform are essential for BCR signaling and also seem to be required for signal transduction in LPL cells, even if the role of BCR signaling in this disease remains less well defined. Ibrutinib, a covalent inhibitor of BTK approved by the Food and Drug Administration as a second-line treatment for CLL, and idelalisib, a selective inhibitor of PI3K delta, achieve excellent clinical responses in both diseases irrespective of classic markers indicating high-risk disease. Several additional inhibitors targeting BTK and PI3K delta, as well as the spleen tyrosine kinase, have entered clinical trials. This review discusses the biologic basis for kinase inhibitors as targeted therapy for CLL and LPL and summarizes the clinical experience with these agents.
C1 NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Wiestner, A (reprint author), NHLBI, Hematol Branch, NIH, Bldg 10,CRC 3-5140,10 Ctr Dr, Bethesda, MD 20892 USA.
EM wiestnea@nhlbi.nih.gov
FU National Heart, Lung, and Blood Institute of the National Institutes of
Health
FX The author is supported by the intramural research program of the
National Heart, Lung, and Blood Institute of the National Institutes of
Health.
NR 107
TC 1
Z9 1
U1 0
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 1520-4391
EI 1520-4383
J9 HEMATOL-AM SOC HEMAT
JI Hematol.-Am. Soc. Hematol. Educ. Program
PD DEC
PY 2014
BP 125
EP 134
DI 10.1182/asheducation-2014.1.125
PG 10
WC Education, Scientific Disciplines; Hematology
SC Education & Educational Research; Hematology
GA CC9XN
UT WOS:000350724600018
ER
PT J
AU Bollard, CM
Barrett, AJ
AF Bollard, Catherine M.
Barrett, A. John
TI Cytotoxic T lymphocytes for leukemia and lymphoma
SO HEMATOLOGY-AMERICAN SOCIETY OF HEMATOLOGY EDUCATION PROGRAM
LA English
DT Article
ID EPSTEIN-BARR-VIRUS; MINOR HISTOCOMPATIBILITY ANTIGENS; HODGKIN-LYMPHOMA;
CELL THERAPY; LYMPHOPROLIFERATIVE DISEASE; TRANSPLANT RECIPIENTS;
COMPLETE RESPONSES; DONOR LYMPHOCYTES; IMMUNOTHERAPY; TUMORS
AB This chapter focuses on the recent advances in adoptive T-cell immunotherapies, not only for patients after hematopoietic stem cell transplantation, but also in the autologous setting using T cells early in the disease process for the treatment of the highest-risk patients with leukemias and lymphomas. The particular emphasis is to highlight the role of T-cell therapies for hematologic malignancies using a non-gene-transfer approach to direct specificity, including the clinical use of T-cell therapies for EBV-associated lymphomas and strategies for targeting nonviral lymphoma-and leukemia-associated antigens.
C1 [Bollard, Catherine M.] Childrens Natl Hlth Syst, Washington, DC 20010 USA.
[Bollard, Catherine M.] George Washington Univ, Washington, DC USA.
[Barrett, A. John] NHLBI, NIH, Bethesda, MD 20892 USA.
RP Bollard, CM (reprint author), Childrens Natl Hlth Syst, 111 Michigan Ave NW, Washington, DC 20010 USA.
EM cbollard@cnmc.org
NR 37
TC 0
Z9 0
U1 1
U2 4
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA
SN 1520-4391
EI 1520-4383
J9 HEMATOL-AM SOC HEMAT
JI Hematol.-Am. Soc. Hematol. Educ. Program
PD DEC
PY 2014
BP 565
EP 569
DI 10.1182/asheducation-2014.1.565
PG 5
WC Education, Scientific Disciplines; Hematology
SC Education & Educational Research; Hematology
GA CC9XN
UT WOS:000350724600085
ER
PT J
AU Zholdybayeva, EV
Rakhimova, SE
Baikara, BT
Nigmatullina, NB
Mustapayeva, NM
Momynaliev, KT
AF Zholdybayeva, Elena V.
Rakhimova, Saule E.
Baikara, Barshagul T.
Nigmatullina, Nazym B.
Mustapayeva, Nagima M.
Momynaliev, Kuvat T.
TI Alport syndrome in a Kazakh family: a case study
SO JOURNAL OF GENETICS
LA English
DT Article
DE Alport syndrome; COL4A5 gene; X-linked Alport syndrome
ID COLLAGEN; IDENTIFICATION; MUTATIONS; GENES
C1 [Zholdybayeva, Elena V.; Rakhimova, Saule E.; Baikara, Barshagul T.; Momynaliev, Kuvat T.] Natl Biotechnol Ctr, Astana 010000, Kazakhstan.
[Nigmatullina, Nazym B.; Mustapayeva, Nagima M.] Natl Res Ctr Maternal & Child Hlth, Astana 010000, Kazakhstan.
RP Zholdybayeva, EV (reprint author), Natl Biotechnol Ctr, 13-1 Valikhanov St, Astana 010000, Kazakhstan.
EM lenazhol@gmail.com
FU Ministry of Education and Science of the Republic of Kazakhstan
FX We are grateful to the XLAS family for their participation in this
study. This study was supported by Ministry of Education and Science of
the Republic of Kazakhstan.
NR 14
TC 0
Z9 0
U1 0
U2 3
PU INDIAN ACAD SCIENCES
PI BANGALORE
PA C V RAMAN AVENUE, SADASHIVANAGAR, P B #8005, BANGALORE 560 080, INDIA
SN 0022-1333
EI 0973-7731
J9 J GENET
JI J. Genet.
PD DEC
PY 2014
VL 93
IS 3
BP 855
EP 858
DI 10.1007/s12041-014-0448-y
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA CC4BZ
UT WOS:000350297100030
PM 25572247
ER
PT J
AU Deveney, CM
Brotman, MA
Thomas, LA
Hinton, KE
Muhrer, EM
Reynolds, RC
Adleman, NE
Zarate, CA
Pine, DS
Leibenluft, E
AF Deveney, Christen M.
Brotman, Melissa A.
Thomas, Laura A.
Hinton, Kendra E.
Muhrer, Eli M.
Reynolds, Richard C.
Adleman, Nancy E.
Zarate, Carlos A., Jr.
Pine, Daniel S.
Leibenluft, Ellen
TI Neural response during explicit and implicit face processing varies
developmentally in bipolar disorder
SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
LA English
DT Article
ID MAJOR DEPRESSIVE DISORDER; SEVERE MOOD DYSREGULATION; FACIAL
EXPRESSIONS; ANTERIOR CINGULATE; AMYGDALA ACTIVATION; LABELING DEFICITS;
EMOTIONAL FACES; NEUTRAL FACES; CHILDREN; CIRCUITRY
AB Both children and adults with bipolar disorder (BD) exhibit face emotion labeling deficits and neural circuitry dysfunction in response to emotional faces. However, few studies have compared these groups directly to distinguish effects of age and diagnosis. Such studies are important to begin to elucidate the developmental trajectory of BD and facilitate its diagnosis, prevention and treatment. This functional magnetic resonance imaging study compares 41 individuals with BD (19 children; 22 adults) and 44 age-matched healthy individuals (25 children; 19 adults) when making explicit or implicit judgments about angry or happy face morphs across a range of emotion intensity. Linear trend analyses revealed that BD patients, irrespective of age, failed to recruit the amygdala in response to increasing angry face. This finding was no longer significant when the group was restricted to euthymic youth or those without comorbid attention deficit hyperactivity disorder although this may reflect low statistical power. Deficits in subgenual anterior cingulate modulation were observed in both patient groups but were related to implicit processing for child patients and explicit processing for adult patients. Abnormalities in face emotion labeling and the circuitry mediating it may be biomarkers of BD that are present across development.
C1 [Deveney, Christen M.; Brotman, Melissa A.; Thomas, Laura A.; Hinton, Kendra E.; Muhrer, Eli M.; Adleman, Nancy E.; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Emot & Dev Branch, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
[Zarate, Carlos A., Jr.] NIMH, Sect Neurobiol & Treatment Mood Disorders, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
[Reynolds, Richard C.] NIMH, Sci & Stat Comp Core, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
RP Deveney, CM (reprint author), Wellesley Coll, Dept Psychol, 106 Cent St, Wellesley, MA 02481 USA.
EM cdeveney@wellesley.edu
RI Brotman, Melissa/H-7409-2013;
OI Thomas, Laura/0000-0002-4106-1358
FU Intramural Research Program at the National Institute of Mental Health,
part of the National Institutes of Health [ZIA MH002786 12]
FX This research was supported by the Intramural Research Program at the
National Institute of Mental Health, part of the National Institutes of
Health (ZIA MH002786 12). C.A.Z. is listed as a co-inventor on a patent
application for the use of ketamine in major depression; he has assigned
his rights in the patent to the US government but will share a
percentage of any royalties that may be received by the government. All
other authors report no financial relationships with commercial
interests. The authors gratefully acknowledge the efforts of members of
the Emotion and Development Branch, and the participation of the
patients and families in their research endeavors.
NR 52
TC 2
Z9 2
U1 5
U2 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1749-5016
EI 1749-5024
J9 SOC COGN AFFECT NEUR
JI Soc. Cogn. Affect. Neurosci.
PD DEC
PY 2014
VL 9
IS 12
BP 1984
EP 1992
DI 10.1093/scan/nsu014
PG 9
WC Neurosciences; Psychology; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA CC1MU
UT WOS:000350105900015
PM 24493839
ER
PT J
AU Sukal-Moulton, T
de Campos, AC
Stanley, CJ
Damiano, DL
AF Sukal-Moulton, Theresa
de Campos, Ana Carolina
Stanley, Christopher J.
Damiano, Diane L.
TI Functional Near Infrared Spectroscopy of the Sensory and Motor Brain
Regions with Simultaneous Kinematic and EMG Monitoring During Motor
Tasks
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Behavior; Issue 94; functional near infrared spectroscopy; fNIRS; brain
activity; gait; motor tasks; cerebral palsy; coordination
ID CEREBRAL-PALSY; CONGENITAL HEMIPARESIS; CHILDREN; REORGANIZATION;
TREADMILL; SYSTEM; FNIRS; FMRI
AB There are several advantages that functional near-infrared spectroscopy (fNIRS) presents in the study of the neural control of human movement. It is relatively flexible with respect to participant positioning and allows for some head movements during tasks. Additionally, it is inexpensive, light weight, and portable, with very few contraindications to its use. This presents a unique opportunity to study functional brain activity during motor tasks in individuals who are typically developing, as well as those with movement disorders, such as cerebral palsy. An additional consideration when studying movement disorders, however, is the quality of actual movements performed and the potential for additional, unintended movements. Therefore, concurrent monitoring of both blood flow changes in the brain and actual movements of the body during testing is required for appropriate interpretation of fNIRS results. Here, we show a protocol for the combination of fNIRS with muscle and kinematic monitoring during motor tasks. We explore gait, a unilateral multi-joint movement (cycling), and two unilateral single-joint movements (isolated ankle dorsiflexion, and isolated hand squeezing). The techniques presented can be useful in studying both typical and atypical motor control, and can be modified to investigate a broad range of tasks and scientific questions.
C1 [Sukal-Moulton, Theresa; de Campos, Ana Carolina; Stanley, Christopher J.; Damiano, Diane L.] NIH, Funct & Appl Biomech Sect, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Damiano, DL (reprint author), NIH, Funct & Appl Biomech Sect, Dept Rehabil Med, Ctr Clin, Bethesda, MD 20892 USA.
EM damianod@cc.nih.gov
FU Intramural Research Program at the National Institutes of Health
Clinical Center
FX This project was funded by the Intramural Research Program at the
National Institutes of Health Clinical Center. We acknowledge the
helpful discussions with Dr. Thomas Bulea, PhD and Laurie Ohlrich, PT in
refining the procedures presented in this protocol. Muyinat W. Osoba and
Andrew Gravunder, MS assisted with the animations.
NR 26
TC 1
Z9 1
U1 2
U2 9
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD DEC
PY 2014
IS 94
AR e52391
DI 10.3791/52391
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA CB1AE
UT WOS:000349358000069
ER
PT J
AU Baker, SG
Prorok, PC
Kramer, BS
AF Baker, Stuart G.
Prorok, Philip C.
Kramer, Barnett S.
TI Lead Time and Overdiagnosis
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID BREAST-CANCER; MORTALITY
C1 [Baker, Stuart G.; Prorok, Philip C.; Kramer, Barnett S.] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Baker, SG (reprint author), NCI, 9609 Med Ctr Dr,5E638 MSC 9789, Bethesda, MD 20892 USA.
EM sb16i@nih.gov
NR 10
TC 7
Z9 7
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD DEC
PY 2014
VL 106
IS 12
AR dju346
DI 10.1093/jnci/dju346
PG 3
WC Oncology
SC Oncology
GA CA0FU
UT WOS:000348593200024
ER
PT J
AU Gu, FY
Wacholder, S
Freedman, ND
Panagiotou, OA
Reyes-Guzman, C
Bertazzi, PA
Caporaso, NE
AF Gu, Fangyi
Wacholder, Sholom
Freedman, Neal D.
Panagiotou, Orestis A.
Reyes-Guzman, Carolyn
Bertazzi, Pier Alberto
Caporaso, Neil E.
TI RE: Time to Smoke First Morning Cigarette (TTFC) and Lung Cancer in a
Case-Control Study Response
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
C1 NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20850 USA.
[Bertazzi, Pier Alberto] Univ Milan, Milan, Italy.
RP Caporaso, NE (reprint author), NCI, Div Canc Epidemiol & Genet, Room 6E410,9609 Med Ctr Dr, Bethesda, MD 20850 USA.
EM caporaso@nih.gov
RI Freedman, Neal/B-9741-2015; Panagiotou, Orestis/I-5934-2015; bertazzi,
pietro alberto/D-5039-2017
OI Freedman, Neal/0000-0003-0074-1098; Panagiotou,
Orestis/0000-0001-9604-8380; bertazzi, pietro
alberto/0000-0003-3475-2449
NR 8
TC 1
Z9 1
U1 2
U2 3
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD DEC
PY 2014
VL 106
IS 12
AR dju350
DI 10.1093/jnci/dju350
PG 1
WC Oncology
SC Oncology
GA CA0FU
UT WOS:000348593200026
ER
PT J
AU Renfro, LA
Grothey, A
Xue, Y
Saltz, LB
Andre, T
Twelves, C
Labianca, R
Allegra, CJ
Alberts, SR
Loprinzi, CL
Yothers, G
Sargent, DJ
AF Renfro, Lindsay A.
Grothey, Axel
Xue, Yuan
Saltz, Leonard B.
Andre, Thierry
Twelves, Chris
Labianca, Roberto
Allegra, Carmen J.
Alberts, Steven R.
Loprinzi, Charles L.
Yothers, Greg
Sargent, Daniel J.
CA Adjuvant Colon Canc Endpoints
TI ACCENT-Based Web Calculators to Predict Recurrence and Overall Survival
in Stage III Colon Cancer
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID ADJUVANT TREATMENT; PLUS OXALIPLATIN; TRIAL; FLUOROURACIL; THERAPY;
BEVACIZUMAB; LEUCOVORIN; CARCINOMA
AB Background Current prognostic tools in colon cancer use relatively few patient characteristics. We constructed and validated clinical calculators for overall survival (OS) and time to recurrence (TTR) for stage III colon cancer and compared their performance against an existing tool (Numeracy) and American Joint Committee on Cancer (AJCC) version 7 staging.
Methods Data from 15 936 stage III patients accrued to phase III clinical trials since 1989 were used to construct Cox models for TTR and OS. Variables included age, sex, race, body mass index, performance status, tumor grade, tumor stage, ratio of positive lymph nodes to nodes examined, number and location of primary tumors, and adjuvant treatment (fluoropyrimidine single agent or in combination). Missing data were imputed, and final models internally validated for optimism-corrected calibration and discrimination and compared with AJCC. External validation and comparisons against Numeracy were performed using stage III patients from NSABP trial C-08. All statistical tests were two-sided.
Results All variables were statistically and clinically significant for OS prediction, while age and race did not predict TTR. No meaningful interactions existed. Models for OS and TTR were well calibrated and associated with C-indices of 0.66 and 0.65, respectively, compared with C-indices of 0.58 and 0.59 for AJCC. These tools, available online, better predicted patient outcomes than Numeracy, both overall and within patient subgroups, in external validation.
Conclusions The proposed ACCENT calculators are internally and externally valid, better discriminate patient risk than AJCC version 7 staging, and better predict patient outcomes than Numeracy. These tools have replaced Numeracy for online clinical use and will aid prognostication and patient/physician communication.
C1 [Renfro, Lindsay A.; Sargent, Daniel J.] Mayo Clin, Div Biomed Stat & Informat, Rochester, MN 55905 USA.
[Grothey, Axel; Alberts, Steven R.; Loprinzi, Charles L.] Mayo Clin, Dept Oncol, Rochester, MN 55905 USA.
[Xue, Yuan] Univ Virginia, Dept Stat, Charlottesville, VA USA.
[Saltz, Leonard B.] Mem Sloan Kettering Canc Ctr, Gastrointestinal Oncol Serv, New York, NY 10021 USA.
[Andre, Thierry] Hop St Antoine, F-75571 Paris, France.
[Andre, Thierry] Univ Paris 06, Paris, France.
[Twelves, Chris] Univ Leeds, Leeds Inst Canc & Pathol, Leeds LS2 9JT, W Yorkshire, England.
[Twelves, Chris] St James Univ Hosp, Leeds Canc Res UK Ctr, Leeds, W Yorkshire, England.
[Labianca, Roberto] Osped Giovanni 23, Oncol Unit, Bergamo, Italy.
[Allegra, Carmen J.] Univ Florida, Div Hematol & Oncol, Gainesville, FL USA.
[Yothers, Greg] Natl Surg Adjuvant Breast & Bowel Project, Ctr Biostat, Pittsburgh, PA USA.
RP Renfro, LA (reprint author), Mayo Clin, Harwick 8-43,200 First St SW, Rochester, MN 55905 USA.
EM renfro.lindsay@mayo.edu
RI Labianca, Roberto/N-1847-2016;
OI Labianca, Roberto/0000-0001-7149-822X; Yothers,
Greg/0000-0002-7965-7333; Saltz, Leonard/0000-0001-8353-4670
FU National Cancer Institute [CA 25224]
FX Funding was provided by National Cancer Institute Grant CA 25224.
NR 22
TC 4
Z9 4
U1 0
U2 1
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-J. Natl. Cancer Inst.
PD DEC
PY 2014
VL 106
IS 12
AR dju333
DI 10.1093/jnci/dju333
PG 9
WC Oncology
SC Oncology
GA CA0FU
UT WOS:000348593200009
ER
PT J
AU Falorni, A
Minarelli, V
Eads, CM
Joachim, CM
Persani, L
Rossetti, R
Beim, PY
Pellegrini, VA
Schnatz, PF
Rafique, S
Kissell, K
Calis, KA
Popat, V
Nelson, LM
AF Falorni, A.
Minarelli, V.
Eads, C. M.
Joachim, C. M.
Persani, L.
Rossetti, R.
Beim, P. Yurttas
Pellegrini, V. A.
Schnatz, P. F.
Rafique, S.
Kissell, K.
Calis, K. A.
Popat, V.
Nelson, L. M.
TI A clinical research integration special program (CRISP) for young women
with primary ovarian insufficiency
SO PANMINERVA MEDICA
LA English
DT Article
DE Autoimmune oophoritis; Community-based participatory research; Mobile
health units; Menopause; premature; Primary ovarian insufficiency; Rare
diseases
ID RANDOMIZED-CONTROLLED-TRIAL; BONE-MINERAL DENSITY; AUTOIMMUNE
POLYGLANDULAR SYNDROME; HORMONE REPLACEMENT THERAPY; IDIOPATHIC
ADDISONS-DISEASE; FRAGILE-X-SYNDROME; POSTMENOPAUSAL WOMEN; ADRENAL
INSUFFICIENCY; TURNER-SYNDROME; GONADOTROPIN RECEPTORS
AB Large-scale medical sequencing provides a focal point around which to reorganize health care and health care research. Mobile health (mHealth) is also currently undergoing explosive growth and could be another innovation that will change the face of future health care. We are employing primary ovarian insufficiency (POI) as a model rare condition to explore the intersection of these potentials. As both sequencing capabilities and our ability to intepret this information improve, sequencing for medical purposes will play an increasing role in health care beyond basic research: it will help guide the delivery of care to patients. POI is a serious chronic disorder and syndrome characterized by hypergonadotrophic hypogonadism before the age of 40 years and most commonly presents with amenorrhea. It may have adverse health effects that become fully evident years after the initial diagnosis. The condition is most commonly viewed as one of infertility, however, it may also be associated with adverse long-term outcomes related to inadequate bone mineral density, increased risk of cardiovascular disease, adrenal insufficiency, hypothyroidism and, if pregnancy ensues, having a child with Fragile X Syndrome. There may also be adverse outcomes related to increased rates of anxiety and depression. POI is also a rare disease, and accordingly, presents special challenges. Too often advances in research are not effectively integrated into community care at the point of service for those with rare diseases. There is a need to connect community health providers in real time with investigators who have the requisite knowledge and expertise to help manage the rare disease and to conduct ongoing research. Here we review the pathophysiology and management of POI and propose the development of an international Clinical Research Integration Special Program (CRISP) for the condition.
C1 [Falorni, A.; Minarelli, V.] Univ Perugia, Dept Med, I-06126 Perugia, Italy.
[Eads, C. M.; Joachim, C. M.] Rachels Well, Mclean, VA USA.
[Persani, L.; Rossetti, R.] Univ Milan, Dept Clin Sci & Community Hlth, Lab Endocrine & Metab Res, Milan, Italy.
[Persani, L.; Rossetti, R.] IRCCS, Ist Auxologico Italiano, Div Endocrine & Metab Dis, Milan, Italy.
[Beim, P. Yurttas] Celmatix Inc, New York, NY USA.
[Pellegrini, V. A.; Schnatz, P. F.] Reading Hosp, Dept Obstet & Gynecol, Reading, PA USA.
[Schnatz, P. F.] Reading Hosp, Dept Internal Med, Reading, PA USA.
[Schnatz, P. F.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Obstet & Gynecol, Philadelphia, PA 19107 USA.
[Schnatz, P. F.] Thomas Jefferson Univ, Jefferson Med Coll, Dept Internal Med, Philadelphia, PA 19107 USA.
[Schnatz, P. F.] FaithCare, Hartford, CT USA.
[Rafique, S.; Kissell, K.; Calis, K. A.; Popat, V.; Nelson, L. M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intramural Res Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Nelson, L. M.] US PHS, Rockville, MD USA.
RP Falorni, A (reprint author), Univ Perugia, Dept Med, Via E Dal Pozzo, I-06126 Perugia, Italy.
EM alberto.falorni@unipg.it
OI Persani, Luca/0000-0003-2068-9581
FU EU FP7 [201167]; Euradrenal and Fondazione Cassa di Risparmio di
Perugia; Mary Elizabeth Conover Foundation; Telethon Foundation, Italy
[GGP09126A]; Intramural Research Program of the Eunice Kennedy Schriver
National Institute of Child Health and Human Development, National
Institutes of Health, Bethesda, Maryland, USA
FX The associated research activity has been supported by EU FP7, Grant
number 201167, Euradrenal and Fondazione Cassa di Risparmio di Perugia
(to AF), a grant from the Mary Elizabeth Conover Foundation (to CME),
Telethon Foundation, Grant GGP09126A (to LP), Italy, and by the
Intramural Research Program of the Eunice Kennedy Schriver National
Institute of Child Health and Human Development, National Institutes of
Health, Bethesda, Maryland, USA. We thank Peter and Cindy Catches of
Oceti Wakan (http://www.ocetiwakan.org) for valuable discussions and
Mark Ferguson for valuable help in graphic design.
NR 147
TC 1
Z9 1
U1 1
U2 9
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 0031-0808
EI 1827-1898
J9 PANMINERVA MED
JI Panminerva Medica
PD DEC
PY 2014
VL 56
IS 4
BP 245
EP 261
PG 17
WC Medicine, General & Internal
SC General & Internal Medicine
GA CA9UK
UT WOS:000349270100001
PM 25288327
ER
PT J
AU Jacobson, KA
AF Jacobson, Kenneth A.
TI Structure-based discovery of novel ligands of GPCRs: adenosine and P2Y
receptors
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Jacobson, Kenneth A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
NR 7
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
BP 658
EP 658
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700015
ER
PT J
AU Jacobson, KA
Robaye, B
Boeynaems, JM
Balasubramanian, R
AF Jacobson, Kenneth A.
Robaye, Bernard
Boeynaems, Jean-Marie
Balasubramanian, Ramachandran
TI Beneficial effects of P2Y(6) receptor agonists on insulin release and
survival of pancreatic beta-islet cells and in target tissue:
involvement of 5 '-AMP-activated protein kinase (AMPK)
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Jacobson, Kenneth A.; Balasubramanian, Ramachandran] Natl Inst Diabet & Digest & Kidney Dis, Mol Recognit Sect, NIH, Bethesda, MD USA.
[Robaye, Bernard] Univ Libre Bruxelles, IRIBHM, Inst Interdisciplinary Res, Gosselies, Belgium.
[Boeynaems, Jean-Marie] Univ Libre Bruxelles, Brussels, Belgium.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
BP 668
EP 669
PG 2
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700039
ER
PT J
AU Yang, TH
Shen, JB
Yang, RH
Redden, J
Dodge-Kafka, K
Grady, J
Jacobson, KA
Liang, BT
AF Yang, Tiehong
Shen, Jian-Bing
Yang, Ronghua
Redden, John
Dodge-Kafka, Kimberley
Grady, James
Jacobson, Kenneth A.
Liang, Bruce T.
TI Novel protective role of endogenous cardiac myocyte P2X4 receptors in
heart failure
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Yang, Tiehong; Shen, Jian-Bing; Yang, Ronghua; Redden, John; Dodge-Kafka, Kimberley; Grady, James; Liang, Bruce T.] Univ Connecticut, Sch Med, Farmington, CT USA.
NIH, Bethesda, MD 20892 USA.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
BP 676
EP 676
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700062
ER
PT J
AU Kang, E
Sharma, K
Han, KL
Malech, H
AF Kang, Elizabeth
Sharma, Karlie
Han, Kyu Lee
Malech, Harry
TI Adenosine agonists for the management of graft versus host disease
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Kang, Elizabeth; Sharma, Karlie; Han, Kyu Lee; Malech, Harry] NIAID, NIH, Bethesda, MD 20892 USA.
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
BP 682
EP 682
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700077
ER
PT J
AU Zhao, Q
Zhang, KH
Zhang, J
Gao, ZG
Jiang, HL
Mueller, CE
Cherezov, V
Katritch, V
Stevens, R
Jacobson, KA
Wu, BL
AF Zhao, Qiang
Zhang, Kaihua
Zhang, Jin
Gao, Zhan-Guo
Jiang, Hualiang
Mueller, Christa E.
Cherezov, Vadim
Katritch, Vsevolod
Stevens, Raymond
Jacobson, Kenneth A.
Wu, Beili
TI Structure and functional implications of purinoceptor 12
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Zhao, Qiang; Zhang, Kaihua; Zhang, Jin; Jiang, Hualiang] Shanghai Inst Mat Med, Shanghai, Peoples R China.
[Mueller, Christa E.] Univ Bonn, Pharma Ctr Bonn, Bonn, Germany.
[Gao, Zhan-Guo; Jacobson, Kenneth A.] Natl Inst Diabet & Digest & Kidney Dis, Bethesda, MD USA.
[Cherezov, Vadim; Katritch, Vsevolod; Stevens, Raymond] Scripps Res Inst, La Jolla, CA 92037 USA.
RI Jacobson, Kenneth/A-1530-2009; Katritch, Vsevolod/Q-8357-2016
OI Jacobson, Kenneth/0000-0001-8104-1493;
NR 0
TC 0
Z9 0
U1 0
U2 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
BP 689
EP 689
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700095
ER
PT J
AU Du, LL
Gao, ZG
Paoletta, S
Wan, TN
van Veldhoven, J
IJzerman, A
Jacobson, K
Auchampach, J
AF Du, Lili
Gao, Zhan-Guo
Paoletta, Silvia
Wan, Tina
van Veldhoven, Jacobus
IJzerman, Adriaan
Jacobson, Kenneth
Auchampach, John
TI Species differences and molecular mechanism of action of A(3) adenosine
receptor allosteric modulators
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Du, Lili; Wan, Tina; Auchampach, John] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Gao, Zhan-Guo; Paoletta, Silvia; Jacobson, Kenneth] NIH, Mol Recognit Sect, Bethesda, MD 20892 USA.
[van Veldhoven, Jacobus; IJzerman, Adriaan] Leiden Univ, Div Med Chem, Leiden, Netherlands.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
MA C024
BP 755
EP 755
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700253
ER
PT J
AU Carlsson, J
Rodriguez, D
Ranganathan, A
Moss, SM
Gao, ZG
Stoddart, LA
Hill, SJ
Jacobson, KA
AF Carlsson, Jens
Rodriguez, David
Ranganathan, Anirudh
Moss, Steven M.
Gao, Zhan-Guo
Stoddart, Leigh A.
Hill, Stephen J.
Jacobson, Kenneth A.
TI Ligand discovery from adenosine receptor crystal structures and homology
models
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Carlsson, Jens; Rodriguez, David; Ranganathan, Anirudh] Stockholm Univ, S-10691 Stockholm, Sweden.
[Moss, Steven M.; Gao, Zhan-Guo; Jacobson, Kenneth A.] NIDDK, NIH, Mol Recognit Sect, Bioorgan Chem Lab, Bethesda, MD 20892 USA.
[Stoddart, Leigh A.; Hill, Stephen J.] Univ Nottingham, Inst Cell Signalling, Sch Biomed Sci, Nottingham NG7 2RD, England.
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
MA D059
BP 771
EP 772
PG 2
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700288
ER
PT J
AU Jacobson, KA
Kiselev, E
Jayasekara, PS
Barrett, MO
Katritch, V
Paoletta, S
Weitzer, C
Hammes, E
Balasubramanian, R
Gao, ZG
Zhao, Q
Stevens, RC
Harden, TK
AF Jacobson, Kenneth A.
Kiselev, Evgeny
Jayasekara, P. Suresh
Barrett, Matthew O.
Katritch, Vsevolod
Paoletta, Silvia
Weitzer, Clarissa
Hammes, Eva
Balasubramanian, Ramachandran
Gao, Zhan-Guo
Zhao, Qiang
Stevens, Raymond C.
Harden, T. Kendall
TI Design, synthesis and characterization of high affinity fluorescent
agonist and antagonist ligands of G protein-coupled P2Y receptors
SO PURINERGIC SIGNALLING
LA English
DT Meeting Abstract
C1 [Jacobson, Kenneth A.; Kiselev, Evgeny; Jayasekara, P. Suresh; Paoletta, Silvia; Hammes, Eva; Balasubramanian, Ramachandran; Gao, Zhan-Guo] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Barrett, Matthew O.; Weitzer, Clarissa; Harden, T. Kendall] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Zhao, Qiang] Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China.
[Katritch, Vsevolod; Stevens, Raymond C.] Scripps Res Inst, Dept Integrat Struct & Computat Biol, La Jolla, CA 92037 USA.
RI Jacobson, Kenneth/A-1530-2009; Katritch, Vsevolod/Q-8357-2016
OI Jacobson, Kenneth/0000-0001-8104-1493;
NR 1
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1573-9538
EI 1573-9546
J9 PURINERG SIGNAL
JI Purinergic Signal.
PD DEC
PY 2014
VL 10
IS 4
MA D074
BP 781
EP 781
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA CA0BF
UT WOS:000348578700303
ER
PT J
AU Trikalinos, TA
Hoaglin, DC
Small, KM
Terrin, N
Schmid, CH
AF Trikalinos, Thomas A.
Hoaglin, David C.
Small, Kevin M.
Terrin, Norma
Schmid, Christopher H.
TI Methods for the joint meta-analysis of multiple tests
SO RESEARCH SYNTHESIS METHODS
LA English
DT Article
DE joint meta-analysis; multinomial likelihood; multivariate normal;
regularized regression; restricted maximum likelihood; Bayesian analysis
ID SONOGRAPHIC SCORING INDEX; FEMUR LENGTH RATIO; DOWN-SYNDROME;
CHROMOSOMAL-ABNORMALITIES; 2ND-TRIMESTER FETUSES; TRISOMY-21;
ULTRASOUND; HUMERUS; RISK; IDENTIFICATION
AB Existing methods for meta-analysis of diagnostic test accuracy focus primarily on a single index test. We propose models for the joint meta-analysis of studies comparing multiple index tests on the same participants in paired designs. These models respect the grouping of data by studies, account for the within-study correlation between the tests' true-positive rates (TPRs) and between their false-positive rates (FPRs) (induced because tests are applied to the same participants), and allow for between-study correlations between TPRs and FPRs (such as those induced by threshold effects). We estimate models in the Bayesian setting. We demonstrate using a meta-analysis of screening for Down syndrome with two tests: shortened humerus (arm bone), and shortened femur (thigh bone). Separate and joint meta-analyses yielded similar TPR and FPR estimates. For example, the summary TPR for a shortened humerus was 35.3% (95% credible interval (CrI): 26.9, 41.8%) versus 37.9% (27.7, 50.3%) with joint versus separate meta-analysis. Joint meta-analysis is more efficient when calculating comparative accuracy: the difference in the summary TPRs was 0.0% (-8.9, 9.5%; TPR higher for shortened humerus) with joint versus 2.6% (-14.7, 19.8%) with separate meta-analyses. Simulation and empirical analyses are needed to refine the role of the proposed methodology. Copyright (c) 2014 John Wiley & Sons, Ltd.
C1 [Trikalinos, Thomas A.; Hoaglin, David C.; Schmid, Christopher H.] Brown Univ, Sch Publ Hlth, Ctr Evidence Based Med, Providence, RI 02912 USA.
[Trikalinos, Thomas A.] Brown Univ, Sch Publ Hlth, Dept Hlth Serv Policy & Practice, Providence, RI 02912 USA.
[Hoaglin, David C.] Univ Massachusetts, Sch Med, Dept Quantitat Hlth Sci, Worcester, MA USA.
[Hoaglin, David C.] Consulting Statistician, Sudbury, ON, Canada.
[Small, Kevin M.] NIH, Off Portfolio Anal, Bethesda, MD 20892 USA.
[Terrin, Norma] Tufts Univ, Clin & Translat Sci Inst, Biostat Res Ctr, Res Design Ctr, Boston, MA 02111 USA.
[Terrin, Norma] Tufts Med Ctr, Inst Clin Res & Hlth Policy Studies, Boston, MA USA.
[Schmid, Christopher H.] Brown Univ, Sch Publ Hlth, Dept Biostat, Providence, RI 02912 USA.
RP Trikalinos, TA (reprint author), Brown Univ, Ctr Evidence Based Med, 121 S Main St, Providence, RI 02912 USA.
EM thomas_trikalinos@brown.edu
OI Schmid, Christopher/0000-0002-0855-5313
FU Effective Healthcare Program of the Agency for Health Care Research and
Quality (AHRQ) [HHSA 290 2007 10055 I]; AHRQ [R01HS018574]
FX This manuscript is based on work performed under Contract No. HHSA 290
2007 10055 I to Tufts Medical Center in the context of the Effective
Healthcare Program of the Agency for Health Care Research and Quality
(AHRQ). The findings and conclusions expressed here are those of the
authors and do not necessarily represent the views of AHRQ. Therefore,
no statement should be construed as an official position of AHRQ or of
the U.S. Department of Health and Human Services. Authors TT and CS were
partly funded by grant R01HS018574 from AHRQ.
NR 52
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1759-2879
EI 1759-2887
J9 RES SYNTH METHODS
JI Res. Synth. Methods
PD DEC
PY 2014
VL 5
IS 4
BP 294
EP 312
DI 10.1002/jrsm.1115
PG 19
WC Mathematical & Computational Biology; Multidisciplinary Sciences
SC Mathematical & Computational Biology; Science & Technology - Other
Topics
GA CA6VH
UT WOS:000349053400002
PM 26052954
ER
PT J
AU Kiselev, E
Barrett, MO
Katritch, V
Paoletta, S
Weitzer, CD
Brown, KA
Hammes, E
Yin, AL
Zhao, Q
Stevens, RC
Harden, TK
Jacobson, KA
AF Kiselev, Evgeny
Barrett, Matthew O.
Katritch, Vsevolod
Paoletta, Silvia
Weitzer, Clarissa D.
Brown, Kyle A.
Hammes, Eva
Yin, Andrew L.
Zhao, Qiang
Stevens, Raymond C.
Harden, T. Kendall
Jacobson, Kenneth A.
TI Exploring a 2-Naphthoic Acid Template for the Structure-Based Design of
P2Y(14) Receptor Antagonist Molecular Probes
SO ACS CHEMICAL BIOLOGY
LA English
DT Article
ID HUMAN NEUTROPHILS; DERIVATIVES; AGONISTS; CHEMOTAXIS; ALKYLATION;
MECHANISM; ANALOGS; SCOPE; DRUG
AB The P2Y(14) receptor (P2Y(14)R), one of eight P2Y G protein-coupled receptors (GPCR), is involved in inflammatory, endocrine, and hypoxic processes and is an attractive pharmaceutical target. The goal of this research is to develop high-affinity P2Y(14)R fluorescent probes based on the potent and highly selective antagonist 4-(4-(piperidin-4-yl)-phenyl)-7-(4-(trifluoromethyl)-phenyl)-2-naphthoic acid (6, PPTN). A model of hP2Y(14)R based on recent hP2Y(12)R X-ray structures together with simulated antagonist docking suggested that the piperidine ring is suitable for fluorophore conjugation while preserving affinity. Chain-elongated alkynyl or amino derivatives of 6 for click or amide coupling were synthesized, and their antagonist activities were measured in hP2Y(14)R-expressing CHO cells. Moreover, a new Alexa Fluor 488 (AF488) containing derivative 30 (MRS4174, K-i = 80 pM) exhibited exceptionally high affinity, as compared to 13 nM for the alkyne precursor 22. A flow cytometry assay employing 30 as a fluorescent probe was used to quantify specific binding to P2Y(14)R. Known P2Y receptor ligands inhibited binding of 30 with properties consistent with their previously established receptor selectivities and affinities. These results illustrate that potency in this series of 2-naphthoic acid derivatives can be preserved by chain functionalization, leading to highly potent fluorescent molecular probes for P2Y(14)R. Such conjugates will be useful tools in expanding the SAR of this receptor, which still lacks chemical diversity in its collective ligands. This approach demonstrates the predictive power of GPCR homology modeling and the relevance of newly determined X-ray structures to GPCR medicinal chemistry.
C1 [Kiselev, Evgeny; Paoletta, Silvia; Hammes, Eva; Yin, Andrew L.; Jacobson, Kenneth A.] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Barrett, Matthew O.; Weitzer, Clarissa D.; Brown, Kyle A.; Harden, T. Kendall] Univ N Carolina, Sch Med, Dept Pharmacol, Chapel Hill, NC 27599 USA.
[Zhao, Qiang] Chinese Acad Sci, Shanghai Inst Mat Med, CAS Key Lab Receptor Res, Shanghai 201203, Peoples R China.
[Katritch, Vsevolod; Stevens, Raymond C.] Scripps Res Inst, Dept Integrat Struct & Computat Biol, La Jolla, CA 92037 USA.
RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM kajacobs@helix.nih.gov
RI Jacobson, Kenneth/A-1530-2009; Katritch, Vsevolod/Q-8357-2016; Stevens,
Raymond/K-7272-2015
OI Jacobson, Kenneth/0000-0001-8104-1493; Stevens,
Raymond/0000-0002-4522-8725
FU NIGMS Postdoctoral Research Associate (PRAT) Program; Intramural Program
of the National Institute of Diabetes and Digestive and Kidney Diseases;
National Institutes of Health [GM38213, U54GM094618]
FX Mass spectral measurements were carried out by J. Lloyd and N. Whittaker
(NIDDK). We acknowledge support from the NIGMS Postdoctoral Research
Associate (PRAT) Program and the Intramural Program of the National
Institute of Diabetes and Digestive and Kidney Diseases. This work was
supported by National Institutes of Health grant nos. GM38213 to T.K.H.
and U54GM094618 to V.K. and R.C.S.
NR 40
TC 10
Z9 10
U1 3
U2 8
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1554-8929
EI 1554-8937
J9 ACS CHEM BIOL
JI ACS Chem. Biol.
PD DEC
PY 2014
VL 9
IS 12
BP 2833
EP 2842
DI 10.1021/cb500614p
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AX2FS
UT WOS:000346759600017
PM 25299434
ER
PT J
AU Xu, J
Zhou, JY
Xu, ZF
Kho, DH
Zhuang, ZP
Raz, A
Wu, GS
AF Xu, Jing
Zhou, Jun-Ying
Xu, Zhengfan
Kho, Dhong-Hyo
Zhuang, Zhengping
Raz, Avraham
Wu, Gen Sheng
TI The role of Cullin3-mediated ubiquitination of the catalytic subunit of
PP2A in TRAIL signaling
SO CELL CYCLE
LA English
DT Article
DE apoptosis resistance; Cullin3; PP2A; TRAIL; ubiquitination
ID PROTEIN PHOSPHATASE 2A; INDUCED APOPTOSIS; DEATH RECEPTORS; CANCER
CELLS; PHASE-I; LIGASES; INHIBITION; FAMILY; LIGAND; IDENTIFICATION
AB Protein phosphatase 2A (PP2A) is the major serine-threonine phosphatase that regulates a number of cell signaling pathways. PP2A activity is controlled partially through protein degradation; however, the underlying mechanism is not fully understood. Here we show that PP2A/C, a catalytic subunit of PP2A, is degraded by the Cullin3 (Cul3) ligase-mediated ubiquitin-proteasome pathway. In response to death receptor signaling by tumor-necrosis factor-related apoptosis-inducing ligand (TRAIL), PP2A/C, caspase-8 and Cul3, a subunit of the cullin family of E3 ligases, are recruited into the death-inducing signaling complex (DISC) where the Cul3 ligase targets PP2A/C for ubiquitination and subsequent degradation. Functionally, knockdown of PP2A/C expression by siRNA or pharmacological inhibition of PP2A activity increases TRAIL-induced apoptosis. In cancer cells that have developed acquired TRAIL resistance, PP2A phosphatase activity is increased, and PP2A/C protein is resistant to TRAIL-induced degradation. Thus, this work identifies a new mechanism by which PP2A/C is regulated by Cul3 ligase-mediated degradation in response to death receptor signaling and suggests that inhibition of PP2A/C degradation may contribute to resistance of cancer cells to death receptor-induced apoptosis.
C1 [Xu, Jing; Zhou, Jun-Ying; Xu, Zhengfan; Kho, Dhong-Hyo; Raz, Avraham; Wu, Gen Sheng] Wayne State Univ, Sch Med, Karmanos Canc Inst, Dept Oncol, Detroit, MI 48202 USA.
[Xu, Jing; Zhou, Jun-Ying; Xu, Zhengfan; Kho, Dhong-Hyo; Raz, Avraham; Wu, Gen Sheng] Wayne State Univ, Sch Med, Dept Pathol, Karmanos Canc Inst, Detroit, MI 48201 USA.
[Zhuang, Zhengping] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Wu, GS (reprint author), Wayne State Univ, Sch Med, Karmanos Canc Inst, Dept Oncol, Detroit, MI 48202 USA.
EM wug@karmanos.org
FU NIH/NCI [R01CA174949-01A1]
FX This work was supported in part by NIH/NCI R01CA174949-01A1.
NR 40
TC 4
Z9 4
U1 0
U2 1
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
EI 1551-4005
J9 CELL CYCLE
JI Cell Cycle
PD DEC 1
PY 2014
VL 13
IS 23
BP 3750
EP 3758
DI 10.4161/15384101.2014.965068
PG 9
WC Cell Biology
SC Cell Biology
GA AZ6KQ
UT WOS:000348329200017
PM 25551360
ER
PT J
AU Onoye, JMM
Hishinuma, ES
McArdle, JJ
Zonderman, AB
Bumanglag, RJ
Takeshita, J
AF Onoye, Jane M. M.
Hishinuma, Earl S.
McArdle, John J.
Zonderman, Alan B.
Bumanglag, R. Janine
Takeshita, Junji
TI Cohort Profile: The Hawai'i Family Study of Cognition
SO INTERNATIONAL JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE Cognition; family; longitudinal studies; ethnic groups
ID JAPANESE-AMERICAN MEN; 2 ETHNIC-GROUPS; PARENT-OFFSPRING RESEMBLANCE;
OCCUPATIONAL ATTAINMENT; DEPRESSIVE SYMPTOMS; BETWEEN-FAMILY; LIFE-SPAN;
PERSONALITY; ABILITIES; INTELLIGENCE
AB Intergenerational longitudinal studies over the lifespan provide valuable information for understanding the contexts and dynamic relations among cognition, family and health in adults and the elderly. The Hawai'i Family Study of Cognition (HFSC), initiated in the early 1970s, included a cohort of over 6500 individuals representing over 1800 families of parents and their offspring. The HFSC gathered data on cognitive, personality, biological and other psychosocial variables, and provided novel information on the nature of cognitive abilities, especially on family issues. Some families were reassessed with short-term retesting in the 1970s. A select sample of offspring and their siblings and spouses were re-measured in the 1980s. Decades later, a 40-year follow-up of the original HFSC cohort was facilitated by the availability of contemporary tracking and tracing methods and internet-based testing. A subgroup of the original HFSC participants was re-contacted and retested on contemporary cognitive as well as socio-demographic and health measures. In this paper, we describe the original HFSC cohort and the design and methodology of the re-contact and retest studies of the HFSC, plans for expanding the re-contact and retesting, as well as directions for future research and collaborations. The Principal Investigator may be contacted for more information regarding the application, review and approval process for data access requests from qualified individuals outside the project.
C1 [Onoye, Jane M. M.; Hishinuma, Earl S.; Bumanglag, R. Janine; Takeshita, Junji] Univ Hawaii Manoa, Dept Psychiat, Honolulu, HI 96813 USA.
[Onoye, Jane M. M.; Takeshita, Junji] Queens Med Ctr, Honolulu, HI USA.
[Zonderman, Alan B.] Univ So Calif, Dept Psychol, Los Angeles, CA 90089 USA.
[McArdle, John J.] Longitudinal Res Inst, Charlottesville, VA USA.
[Zonderman, Alan B.] NIA, Behav Epidemiol Sect, Baltimore, MD 21224 USA.
RP Onoye, JMM (reprint author), Univ Hawaii Manoa, Dept Psychiat, 1356 Lusitana St,4th Floor, Honolulu, HI 96813 USA.
EM onoyej@dop.hawaii.edu
OI Zonderman, Alan B/0000-0002-6523-4778
FU National Institute on Aging at the National Institutes of Health
[HHSN311200900372P, HHSN311201000229P, HHSN271201100465P]; University of
Southern California [Y71692]; Queen's Medical Center
FX The present research and dissemination efforts were supported in part
by: the National Institute on Aging at the National Institutes of Health
[Contracts HHSN311200900372P; HHSN311201000229P; HHSN271201100465P];
University of Southern California [Contract Y71692]; and the Queen's
Medical Center.
NR 34
TC 0
Z9 0
U1 1
U2 3
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0300-5771
EI 1464-3685
J9 INT J EPIDEMIOL
JI Int. J. Epidemiol.
PD DEC
PY 2014
VL 43
IS 6
BP 1726
EP 1735
DI 10.1093/ije/dyu012
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA CA0AD
UT WOS:000348575500015
PM 24639439
ER
PT J
AU Wright, ME
Albanes, D
Moser, AB
Weinstein, SJ
Snyder, K
Mannisto, S
Gann, PH
AF Wright, Margaret E.
Albanes, Demetrius
Moser, Ann B.
Weinstein, Stephanie J.
Snyder, Kirk
Mannisto, Satu
Gann, Peter H.
TI Serum phytanic and pristanic acid levels and prostate cancer risk in
Finnish smokers
SO CANCER MEDICINE
LA English
DT Article
DE Biomarker; diet; phytanic acid; pristanic acid; prostate cancer
ID METHYLACYL-COA RACEMASE; PROSPECTIVE COHORT; BETA-CAROTENE; FATTY-ACID;
DISEASE; PLASMA; METAANALYSIS; CONSUMPTION; METABOLISM; BIOMARKERS
AB Phytanic acid is a saturated branched-chain fatty acid found predominantly in red meat and dairy products, and may contribute to the elevated risks of prostate cancer associated with higher consumption of these foods. Pristanic acid is formed during peroxisomal oxidation of phytanic acid, and is the direct substrate of a-Methyl-CoA-Racemase (AMACR)-an enzyme that is consistently overexpressed in prostate tumors relative to benign tissue. We measured phytanic and pristanic acids as percentages of total fatty acids by gas chromatography-mass spectrometry in prediagnostic blood samples from 300 prostate cancer cases and 300 matched controls, all of whom were participants in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study supplementation trial and follow-up cohort. In addition to providing a fasting blood sample at baseline, all men completed extensive diet, lifestyle, and medical history questionnaires. Among controls, the strongest dietary correlates of serum phytanic and pristanic acids were saturated fat, dairy fat, and butter (r = 0.50 and 0.40, 0.46 and 0.38, and 0.40 and 0.37, respectively; all P-values <0.001). There was no association between serum phytanic acid and risk of total or aggressive prostate cancer in multivariate logistic regression models (for increasing quartiles, odds ratios (OR) and 95% confidence intervals (CI) for aggressive cancer were 1.0 (referent), 1.62 (0.97-2.68), 1.12 (0.66-1.90), and 1.14 (0.67-1.94), P-trend = 0.87). Pristanic acid was strongly correlated with phytanic acid levels (r = 0.73, P < 0.0001), and was similarly unrelated to prostate cancer risk. Significant interactions between phytanic and pristanic acids and baseline circulating beta-carotene concentrations were noted in relation to total and aggressive disease among participants who did not receive beta-carotene supplements as part of the original ATBC intervention trial. In summary, we observed no overall association between serum phytanic and pristanic acid levels and prostate cancer risk. Findings indicating that the direction and magnitude of these associations depended upon serum levels of the antioxidant beta-carotene among men not taking beta-carotene supplements should be interpreted cautiously, as they are likely due to chance.
C1 [Wright, Margaret E.; Gann, Peter H.] Univ Illinois, Coll Med, Dept Pathol, Chicago, IL 60612 USA.
[Wright, Margaret E.] Amer Acad Pediat, Elk Grove Village, IL 60007 USA.
[Albanes, Demetrius; Weinstein, Stephanie J.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Moser, Ann B.] Kennedy Krieger Inst, Baltimore, MD USA.
[Snyder, Kirk] Informat Management Serv Inc, Silver Spring, MD USA.
[Mannisto, Satu] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
RP Wright, ME (reprint author), Amer Acad Pediat, 141 Northwest Point Blvd, Elk Grove Village, IL 60007 USA.
EM mwright@aap.org
RI Albanes, Demetrius/B-9749-2015;
OI Mannisto, Satu/0000-0002-8668-3046
FU American Cancer Society [MSRG-08-109-01-CCE]; Department of Defense
[PC050393]; Intramural Research Program of the NIH; National Cancer
Institute; U.S. Public Health Service from the National Cancer
Institute, Department of Health and Human Services [N01-CN-45165,
N01-RC-45035, N01-RC-37004, HHSN261201000006C]
FX Supported by American Cancer Society grant MSRG-08-109-01-CCE,
Department of Defense grant PC050393, the Intramural Research Program of
the NIH and the National Cancer Institute, and U.S. Public Health
Service contracts N01-CN-45165, N01-RC-45035, N01-RC-37004 and
HHSN261201000006C from the National Cancer Institute, Department of
Health and Human Services.
NR 34
TC 3
Z9 3
U1 1
U2 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD DEC
PY 2014
VL 3
IS 6
BP 1562
EP 1569
DI 10.1002/cam4.319
PG 8
WC Oncology
SC Oncology
GA AZ4YB
UT WOS:000348226000012
PM 25132681
ER
PT J
AU Owonikoko, TK
Zhang, GJ
Deng, XM
Rossi, MR
Switchenko, JM
Doho, GH
Chen, ZJ
Kim, S
Strychor, S
Christner, SM
Beumer, J
Li, CY
Yue, P
Chen, A
Sica, GL
Ramalingam, SS
Kowalski, J
Khuri, FR
Sun, SY
AF Owonikoko, Taofeek K.
Zhang, Guojing
Deng, Xingming
Rossi, Michael R.
Switchenko, Jeffrey M.
Doho, Gregory H.
Chen, Zhengjia
Kim, Sungjin
Strychor, Sandy
Christner, Susan M.
Beumer, Jan
Li, Chunyang
Yue, Ping
Chen, Alice
Sica, Gabriel L.
Ramalingam, Suresh S.
Kowalski, Jeanne
Khuri, Fadlo R.
Sun, Shi-Yong
TI Poly (ADP) ribose polymerase enzyme inhibitor, veliparib, potentiates
chemotherapy and radiation in vitro and in vivo in small cell lung
cancer
SO CANCER MEDICINE
LA English
DT Article
DE Carboplatin; cisplatin; etoposide; PARP; SCLC; veliparib (ABT-888)
ID DEPENDENT PROTEIN-KINASE; CHROMATIN TRANSCRIPTION FACT; POLY(ADP-RIBOSE)
POLYMERASE; DNA-REPAIR; THERAPEUTIC TARGETS; PARP INHIBITORS;
OVARIAN-CANCER; BREAST-CANCER; BMN 673; CISPLATIN
AB Poly (ADP) ribose polymerase (PARP) plays a key role in DNA repair and is highly expressed in small cell lung cancer (SCLC). We investigated the therapeutic impact of PARP inhibition in SCLC. In vitro cytotoxicity of veliparib, cisplatin, carboplatin, and etoposide singly and combined was determined by MTS in 9 SCLC cell lines (H69, H128, H146, H526, H187, H209, DMS53, DMS153, and DMS114). Subcutaneous xenografts in athymic nu/nu mice of H146 and H128 cells with relatively high and low platinum sensitivity, respectively, were employed for in vivo testing. Mechanisms of differential sensitivity of SCLC cell lines to PARP inhibition were investigated by comparing protein and gene expression profiles of the platinum sensitive and the less sensitive cell lines. Veliparib showed limited single-agent cytotoxicity but selectively potentiated (>= 50% reduction in IC50) cisplatin, carboplatin, and etoposide in vitro in five of nine SCLC cell lines. Veliparib with cisplatin or etoposide or with both cisplatin and etoposide showed greater delay in tumor growth than chemotherapy alone in H146 but not H128 xenografts. The potentiating effect of veliparib was associated with in vitro cell line sensitivity to cisplatin (CC = 0.672; P = 0.048) and DNA-PKcs protein modulation. Gene expression profiling identified differential expression of a 5-gene panel (GLS, UBEC2, HACL1, MSI2, and LOC100129585) in cell lines with relatively greater sensitivity to platinum and veliparib combination. Veliparib potentiates standard cytotoxic agents against SCLC in a cell-specific manner. This potentiation correlates with platinum sensitivity, DNA-PKcs expression and a 5-gene expression profile.
C1 [Owonikoko, Taofeek K.; Zhang, Guojing; Yue, Ping; Ramalingam, Suresh S.; Khuri, Fadlo R.; Sun, Shi-Yong] Emory Univ, Sch Med, Dept Hematol & Med Oncol, Atlanta, GA 30322 USA.
[Owonikoko, Taofeek K.; Deng, Xingming; Switchenko, Jeffrey M.; Chen, Zhengjia; Kim, Sungjin; Li, Chunyang; Ramalingam, Suresh S.; Kowalski, Jeanne; Khuri, Fadlo R.] Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
[Deng, Xingming; Rossi, Michael R.] Emory Univ, Sch Med, Dept Radiat Oncol, Atlanta, GA 30322 USA.
[Switchenko, Jeffrey M.; Chen, Zhengjia; Kowalski, Jeanne] Emory Univ, Rollins Sch Publ Hlth, Dept Biostat & Bioinformat, Atlanta, GA 30322 USA.
[Doho, Gregory H.] Emory Univ, Sch Med, Emory Integrated Genom Core Lab, Atlanta, GA 30322 USA.
[Strychor, Sandy; Christner, Susan M.; Beumer, Jan] Univ Pittsburgh, Mol Therapeut Drug Discovery Program, Inst Canc, Pittsburgh, PA USA.
[Chen, Alice] NCI, Invest Drug Branch, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Sica, Gabriel L.] Emory Univ, Sch Med, Dept Pathol, Atlanta, GA 30322 USA.
RP Owonikoko, TK (reprint author), Emory Univ, Sch Med, Dept Hematol & Med Oncol, 1365C Clifton Rd NE,Room C3080, Atlanta, GA 30322 USA.
EM towonik@emory.edu
OI Beumer, Jan/0000-0002-8978-9401
FU NIH [1K23CA164015, P01CA116676, P30CA138292, P30CA47904, U01CA099168];
Georgia Research Alliance Distinguished Cancer Scientist Award
FX This work was supported by NIH grants (1K23CA164015, P01CA116676,
P30CA138292, P30CA47904, and U01CA099168); and Georgia Research Alliance
Distinguished Cancer Scientist Award.
NR 52
TC 9
Z9 9
U1 2
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2045-7634
J9 CANCER MED-US
JI Cancer Med.
PD DEC
PY 2014
VL 3
IS 6
BP 1579
EP 1594
DI 10.1002/cam4.317
PG 16
WC Oncology
SC Oncology
GA AZ4YB
UT WOS:000348226000014
PM 25124282
ER
PT J
AU Richter, S
Seah, JA
Pond, GR
Gan, HK
Mackenzie, MJ
Hotte, SJ
Mukherjee, SD
Murray, N
Kollmannsberger, C
Heng, D
Haider, MA
Halford, R
Ivy, SP
Moore, MJ
Sridhar, SS
AF Richter, Suzanne
Seah, Jo-An
Pond, Gregory R.
Gan, Hui K.
Mackenzie, Mary J.
Hotte, Sebastien J.
Mukherjee, Som D.
Murray, Nevin
Kollmannsberger, Christian
Heng, Daniel
Haider, Masoom A.
Halford, Robert
Ivy, S. Percy
Moore, Malcolm J.
Sridhar, Srikala S.
TI Evaluation of second-line and subsequent targeted therapies in
metastatic renal cell cancer (mRCC) patients treated with first-line
cediranib
SO CUAJ-CANADIAN UROLOGICAL ASSOCIATION JOURNAL
LA English
DT Article
ID PHASE-III TRIAL; INTERFERON-ALPHA; CARCINOMA; SUNITINIB; SORAFENIB;
TEMSIROLIMUS
AB Introduction: Pivotal phase III trials have positioned angiogenesis inhibitors as first-line therapy for the management of most advanced or metastatic renal cell carcinomas (mRCC). Approaches to secondline therapy, however, remain more controversial with respect to drug selection and drug sequencing.
Methods: In this study we evaluated mRCC patients who were initially treated on the first-line National Cancer Institute (NCI) trial with the highly potent vascular endothelial growth factor receptor tyrosine kinase inhibitor (TKI), cediranib, to determine the efficacy and tolerability of subsequent therapies.
Results: Twenty-eight (65.1%) of the 43 patients enrolled on the first-line cediranib trial were known to receive second-line therapy, most commonly sunitinib (n = 21), with 4 (14%), 2 (7%) and 1 (3%) patients receiving temsirolimus, sorafenib, and interleukin, respectively. Of these, 14 (50%) went on to have 3 or more lines of therapy. The progression-free survival (PFS) proportion (PFS) at 1 year from starting second line was 30% (14.5%-47.9%). Longer duration of first-line cediranib treatment was modestly associated with longer duration of second-line treatment (Spearman rho 0.26). Patients who discontinued cediranib for toxicity were less likely to receive second-line sunitinib.
Conclusion: In this real world evaluation, sequential use of TKIs for the management of mRCC was common. PFS with sequential TKIs was similar to observed and published results for any secondline therapy. Prior toxicity affected treatment patterns and the frequent use of at least 3 lines of therapy underscores the need for prospective sequencing trials in this disease.
C1 [Richter, Suzanne; Seah, Jo-An; Halford, Robert; Moore, Malcolm J.; Sridhar, Srikala S.] Princess Margaret Canc Ctr, Toronto, ON, Canada.
[Pond, Gregory R.] McMaster Univ, Hamilton, ON, Canada.
[Gan, Hui K.] Ludwig Inst Canc Res, Austin Hlth, Melbourne, Vic 3050, Australia.
[Mackenzie, Mary J.] Western Univ, London Reg Canc Program, London, ON, Canada.
[Hotte, Sebastien J.; Mukherjee, Som D.] McMaster Univ, Juravinski Canc Ctr, Hamilton, ON, Canada.
[Murray, Nevin; Kollmannsberger, Christian] Univ British Columbia, BC Canc Agcy, Vancouver, BC V5Z 1M9, Canada.
[Heng, Daniel] Univ Alberta, Tom Baker Canc Ctr, Calgary, AB, Canada.
[Haider, Masoom A.] Univ Toronto, Sunnybrook Hlth Sci Ctr, Toronto, ON, Canada.
[Ivy, S. Percy] NCI, Canc Therapy Evaluat Program, Rockville, MD USA.
RP Sridhar, SS (reprint author), Univ Toronto, Princess Margaret Canc Ctr, 5-222,610 Univ Ave, Toronto, ON M5G 6M9, Canada.
EM srikala.sridhar@uhn.ca
FU NCI NIH HHS [N01CM62203]
NR 13
TC 2
Z9 2
U1 0
U2 1
PU CANADIAN UROLOGICAL ASSOCIATION
PI DORVAL
PA 185 DORVAL AVENUE, STE 401, DORVAL, QC H9S 5J9, CANADA
SN 1911-6470
EI 1920-1214
J9 CUAJ-CAN UROL ASSOC
JI CUAJ-Can. Urol. Assoc. J.
PD DEC
PY 2014
VL 8
IS 11-12
BP 398
EP 402
DI 10.5489/cuaj.2426
PG 5
WC Urology & Nephrology
SC Urology & Nephrology
GA AY6ZJ
UT WOS:000347710800024
PM 25553152
ER
PT J
AU Abate-Daga, D
Lagisetty, KH
Tran, E
Zheng, ZL
Gattinoni, L
Yu, ZY
Burns, WR
Miermont, AM
Teper, Y
Rudloff, U
Restifo, NP
Feldman, SA
Rosenberg, SA
Morgan, RA
AF Abate-Daga, Daniel
Lagisetty, Kiran H.
Tran, Eric
Zheng, Zhili
Gattinoni, Luca
Yu, Zhiya
Burns, William R.
Miermont, Anne M.
Teper, Yaroslav
Rudloff, Udo
Restifo, Nicholas P.
Feldman, Steven A.
Rosenberg, Steven A.
Morgan, Richard A.
TI A Novel Chimeric Antigen Receptor Against Prostate Stem Cell Antigen
Mediates Tumor Destruction in a Humanized Mouse Model of Pancreatic
Cancer
SO HUMAN GENE THERAPY
LA English
DT Article
ID ENGINEERED T-CELLS; EXPRESSING TUMORS; CLINICAL-TRIAL; ADVERSE EVENT;
PHASE-I; PSCA; THERAPY; MICE; CD28; ADENOCARCINOMA
AB Despite advances in the understanding of its molecular pathophysiology, pancreatic cancer remains largely incurable, highlighting the need for novel therapies. We developed a chimeric antigen receptor (CAR) specific for prostate stem cell antigen (PSCA), a glycoprotein that is overexpressed in pancreatic cancer starting at early stages of malignant transformation. To optimize the CAR design, we used antigen-recognition domains derived from mouse or human antibodies, and intracellular signaling domains containing one or two T cell costimulatory elements, in addition to CD3zeta. Comparing multiple constructs established that the CAR based on human monoclonal antibody Ha1-4.117 had the greatest reactivity in vitro. To further analyze this CAR, we developed a human pancreatic cancer xenograft model and adoptively transferred CAR-engineered T cells into animals with established tumors. CAR-engineered human lymphocytes induced significant antitumor activity, and unlike what has been described for other CARs, a second-generation CAR (containing CD28 cosignaling domain) induced a more potent antitumor effect than a third-generation CAR (containing CD28 and 41BB cosignaling domains). While our results provide evidence to support PSCA as a target antigen for CAR-based immunotherapy of pancreatic cancer, the expression of PSCA on selected normal tissues could be a source of limiting toxicity.
C1 [Abate-Daga, Daniel; Lagisetty, Kiran H.; Tran, Eric; Zheng, Zhili; Gattinoni, Luca; Yu, Zhiya; Burns, William R.; Miermont, Anne M.; Teper, Yaroslav; Rudloff, Udo; Restifo, Nicholas P.; Feldman, Steven A.; Rosenberg, Steven A.; Morgan, Richard A.] NCI, Surg Branch, NIH, Bethesda, MD 20892 USA.
RP Abate-Daga, D (reprint author), NIH, CRC, Bldg 10,Room 3W-3864,10 Ctr Dr, Bethesda, MD 20892 USA.
EM daniel.abate-daga@nih.gov
RI Gattinoni, Luca/A-2281-2008;
OI Gattinoni, Luca/0000-0003-2239-3282; Restifo, Nicholas
P./0000-0003-4229-4580
FU Milstein Family Foundation; Intramural Research Program of the Center
for Cancer Research, National Cancer Institute, Bethesda, MD
FX We would like to thank Arnold Mixon, Shawn Farid, and Dave Jones for
technical support. This project was supported in part by a generous
contribution from the Milstein Family Foundation and by the Intramural
Research Program of the Center for Cancer Research, National Cancer
Institute, Bethesda, MD.
NR 41
TC 25
Z9 25
U1 0
U2 11
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1043-0342
EI 1557-7422
J9 HUM GENE THER
JI Hum. Gene Ther.
PD DEC 1
PY 2014
VL 25
IS 12
BP 1003
EP 1012
DI 10.1089/hum.2013.209
PG 10
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research &
Experimental Medicine
GA AW6AT
UT WOS:000346352600077
PM 24694017
ER
PT J
AU Agochukwu, NB
Solomon, BD
Muenke, M
AF Agochukwu, Nneamaka B.
Solomon, Benjamin D.
Muenke, Maximilian
TI Hearing loss in syndromic craniosynostoses: Otologic manifestations and
clinical findings
SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY
LA English
DT Review
DE Craniosynostosis; Syndromic craniosynostosis; Hearing loss
craniosynostosis; Hearing loss syndromes; Hearing FGFR syndromes
ID BEARE-STEVENSON-SYNDROME; FIBROBLAST-GROWTH-FACTOR;
CUTIS-GYRATA-SYNDROME; JACKSON-WEISS-SYNDROME; FACTOR RECEPTOR-2 GENE;
PFEIFFER-SYNDROME; CROUZON-SYNDROME; APERT-SYNDROME; ACANTHOSIS
NIGRICANS; OTITIS-MEDIA
AB Objective: This review addresses hearing loss as it occurs and has been reported in Muenke syndrome as well as six additional FGFR related craniosynostosis syndromes (Apert syndrome, Pfeiffer syndrome, Crouzon syndrome, Beare-Stevenson syndrome, Crouzon syndrome with acanthosis nigricans, and Jackson-Weiss syndrome.
Data sources: Pub-Med, Medline, Cochrane Database, Science Direct, NLM Catalog.
Review methods: A Medline search was conducted to find all reported cases of the 7 FGFR related syndromic craniosynostosis. Special attention was paid to literature that reported hearing findings and the audiology literature.
Results: Hearing loss occurs in variable percentage as a component part of all FGFR related craniosynostosis syndromes. Our literature review revealed the following incidences of hearing loss in FGFR craniosynostoses: 61% in Muenlce syndrome, 80% in Apert Syndrome, 92% in Pfeiffer syndrome, 74% in Crouzon syndrome, 68% in Jackson Weiss syndrome, 4% in Beare Stevenson syndrome and 14% in Crouzon syndrome with Acanthosis Nigricans. The majority of the hearing loss is a conductive hearing loss, with the exception of Muenke syndrome where the majority of patients have a sensorineural hearing loss and Crouzon syndrome where almost half of patients have a pure or component of sensorineural hearing loss.
Conclusion: This manuscript presents a diagnostic and management algorithm for patients with syndromic craniosynostosis. It will aid clinicians in treating these patients and further, the recognition of a possible syndrome in patients with hearing loss who also have syndromic features. Published by Elsevier Ireland Ltd.
C1 [Agochukwu, Nneamaka B.; Solomon, Benjamin D.; Muenke, Maximilian] NHGRI, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Agochukwu, Nneamaka B.] NIH, Clin Res Training Program, Bethesda, MD 20892 USA.
RP Agochukwu, NB (reprint author), NHGRI, Med Genet Branch, NIH, MSC 3717,Bldg 35,Room 1B-202, Bethesda, MD 20892 USA.
EM agochukwunb@mail.nih.gov
FU Division of Intramural Research at the National Human Genome Research
Institute (National Institutes of Health, Department of Health and Human
Services, United States of America) [TTY8664111010]
FX We would like to express our gratitude to the patients who participate
in our ongoing studies of Muenke syndrome at the NIH. This research was
supported by the Division of Intramural Research at the National Human
Genome Research Institute (Grant no. TTY8664111010) (National Institutes
of Health, Department of Health and Human Services, United States of
America).
NR 97
TC 3
Z9 3
U1 0
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0165-5876
EI 1872-8464
J9 INT J PEDIATR OTORHI
JI Int. J. Pediatr. Otorhinolaryngol.
PD DEC
PY 2014
VL 78
IS 12
BP 2037
EP 2047
DI 10.1016/j.ijporl.2014.09.019
PG 11
WC Otorhinolaryngology; Pediatrics
SC Otorhinolaryngology; Pediatrics
GA AY6FY
UT WOS:000347663800002
PM 25441602
ER
PT J
AU Davis, BJK
Vidal, JS
Garcia, M
Aspelund, T
van Buchem, MA
Jonsdottir, MK
Sigurdsson, S
Harris, TB
Gudnason, V
Launer, LJ
AF Davis, Benjamin J. K.
Vidal, Jean-Sebastian
Garcia, Melissa
Aspelund, Thor
van Buchem, Mark A.
Jonsdottir, Maria K.
Sigurdsson, Sigurdur
Harris, Tamara B.
Gudnason, Vilmundur
Launer, Lenore J.
TI The Alcohol Paradox: Light-to-Moderate Alcohol Consumption, Cognitive
Function, and Brain Volume
SO JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL
SCIENCES
LA English
DT Article
DE Alcohol consumption; Brain aging; Epidemiology; Imaging; Cognitive aging
ID OLDER-ADULTS; CARDIOVASCULAR HEALTH; AGES-REYKJAVIK; DEMENTIA; RISK;
ASSOCIATION; DECLINE; PERFORMANCE; ROTTERDAM; COHORT
AB Background. Studies of older persons show consumption of light-to-moderate amounts of alcohol is positively associated with cognitive function and, separately, is negatively associated with total brain volume (TBV). This is paradoxical as generally, cognitive function is positively associated with TBV. We examined the relationships of TBV, global cognitive function (GCF), and alcohol consumption in a population-based cohort of 3,363 men and women (b. 1907-1935) participating in the Age Gene/Environment Susceptibility-Reykjavik Study (2002-2006) and who were free of dementia or mild cognitive impairment
Methods. Drinking status (never, former, and current) and current amount of alcohol consumed were assessed by questionnaire. GCF is a composite score derived from a battery of cognitive tests. TBV, standardized to head size, is estimated quantitatively from brain magnetic resonance imaging.
Results. Among women and not men, adjusting for demographic and cardiovascular risk factors, current drinkers had significantly higher GCF scores than abstainers and former drinkers (p < .0001); and GCF was associated with amount consumed. TBV was not associated with drinking status or amount consumed in men or women. GCF and TBV did significantly differ in their associations across alcohol categories (p(interaction) < .001). Within categories of alcohol intake, GCF and TBV were positively associated.
Conclusions. The difference in associations of alcohol intake to brain structure and function suggests there may be unmeasured factors that contribute to maintaining better GCF relative to TBV. However, at higher levels of reasonable alcohol consumption, there may be factors leading to reduced brain volume.
C1 [Davis, Benjamin J. K.; Vidal, Jean-Sebastian; Garcia, Melissa; Harris, Tamara B.; Launer, Lenore J.] NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, NIH, Bethesda, MD 20892 USA.
[Aspelund, Thor; Jonsdottir, Maria K.; Sigurdsson, Sigurdur] Iceland Heart Assoc, Kopavogur, Iceland.
[Aspelund, Thor; Gudnason, Vilmundur] Univ Iceland, Ctr Publ Hlth Sci, Reykjavik, Iceland.
[van Buchem, Mark A.] Leiden Univ Med Ctr, Dept Radiol, Leiden, Netherlands.
[Jonsdottir, Maria K.] Univ Iceland, Fac Psychol, Reykjavik, Iceland.
[Jonsdottir, Maria K.] Natl Univ Hosp Iceland, Geriatr Res Ctr Landsptiali, Reykjavik, Iceland.
[Gudnason, Vilmundur] Univ Iceland, Fac Med, Reykjavik, Iceland.
RP Launer, LJ (reprint author), NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, NIH, 7201 Wisconsin Ave, Bethesda, MD 20892 USA.
EM launerl@nia.nih.gov
RI Gudnason, Vilmundur/K-6885-2015; Vidal, Jean-Sebastien/D-1941-2016
OI Gudnason, Vilmundur/0000-0001-5696-0084; Vidal,
Jean-Sebastien/0000-0001-6770-0720
FU National Institutes of Health [N01-AG-12100]; National Institutes of
Health/National Institute on Aging Intramural Research Program;
Hjartavernd (the Icelandic Heart Association); Althingi (the Icelandic
Parliament); University of Iceland Research Fund
FX This work was supported by National Institutes of Health (N01-AG-12100),
the National Institutes of Health/National Institute on Aging Intramural
Research Program, Hjartavernd (the Icelandic Heart Association), the
Althingi (the Icelandic Parliament), and the University of Iceland
Research Fund.
NR 40
TC 6
Z9 6
U1 2
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1079-5006
EI 1758-535X
J9 J GERONTOL A-BIOL
JI J. Gerontol. Ser. A-Biol. Sci. Med. Sci.
PD DEC
PY 2014
VL 69
IS 12
BP 1528
EP 1535
DI 10.1093/gerona/glu092
PG 8
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AZ6OX
UT WOS:000348339800010
PM 24994845
ER
PT J
AU Su, JM
Thompson, P
Adesina, A
Li, XN
Kilburn, L
Onar-Thomas, A
Kocak, M
Chyla, B
McKeegan, E
Warren, KE
Goldman, S
Pollack, IF
Fouladi, M
Chen, A
Giranda, V
Boyett, J
Kun, L
Blaney, SM
AF Su, Jack M.
Thompson, Patrick
Adesina, Adekunle
Li, Xiao-Nan
Kilburn, Lindsay
Onar-Thomas, Arzu
Kocak, Mehmet
Chyla, Brenda
McKeegan, Evelyn
Warren, Katherine E.
Goldman, Stewart
Pollack, Ian F.
Fouladi, Maryam
Chen, Alice
Giranda, Vincent
Boyett, James
Kun, Larry
Blaney, Susan M.
TI A phase I trial of veliparib (ABT-888) and temozolomide in children with
recurrent CNS tumors: a Pediatric Brain Tumor Consortium report
SO NEURO-ONCOLOGY
LA English
DT Article
DE ABT-888; CNS tumors; PARP inhibition; pediatric phase I study; veliparib
ID POLY(ADP-RIBOSE) POLYMERASE INHIBITOR; ADP-RIBOSE POLYMERASE; HOMOLOGOUS
RECOMBINATION REPAIR; REFRACTORY SOLID TUMORS; HIGH-GRADE GLIOMA; PARP
INHIBITION; IONIZING-RADIATION; CLINICAL-TRIALS; OVARIAN-CANCER;
COMBINATION
AB Background. A phase I trial of veliparib (ABT-888), an oral poly(ADP-ribose) polymerase (PARP) inhibitor, and temozolomide (TMZ) was conducted in children with recurrent brain tumors to (i) estimate the maximum tolerated doses (MTDs) or recommended phase II doses (RP2Ds) of veliparib and TMZ; (ii) describe the toxicities of this regimen; and (iii) evaluate the plasma pharmacokinetic parameters and extent of PARP inhibition in peripheral blood mononuclear cells (PBMCs) following veliparib.
Methods. TMZ was given once daily and veliparib twice daily for 5 days every 28 days. Veliparib concentrations and poly(ADP-ribose) (PAR) levels in PBMCs were measured on days 1 and 4. Analysis of pharmacokinetic and PBMC PAR levels were performed twice during study conduct to rationally guide dose modifications and to determine biologically optimal MTD/RP2D.
Results. Twenty-nine evaluable patients were enrolled. Myelosuppression (grade 4 neutropenia and thrombocytopenia) were dose limiting. The RP2Ds are veliparib 25 mg/m(2) b.i.d. and TMZ 135 mg/m(2)/d. Only 2 out of 12 patients treated at RP2Ds experienced dose-limiting toxicities. Although no objective response was observed, 4 patients had stable disease >6 months in duration, including 1 with glioblastoma multiforme and 1 with ependymoma. At the RP2D of veliparib, pediatric pharmacokinetic parameters were similar to those in adults.
Conclusions. Veliparib and TMZ at the RP2D were well tolerated in children with recurrent brain tumors. A phase I/II trial to evaluate the tolerability and efficacy of veliparib, TMZ, and radiation in children with newly diagnosed brainstem gliomas is in progress.
C1 [Su, Jack M.; Thompson, Patrick; Adesina, Adekunle; Li, Xiao-Nan; Blaney, Susan M.] Baylor Coll Med, Texas Childrens Canc Ctr, Houston, TX 77030 USA.
[Kilburn, Lindsay] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Onar-Thomas, Arzu; Boyett, James; Kun, Larry] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Kocak, Mehmet] Univ Tennessee, Hlth Sci Ctr, Knoxville, TN 37996 USA.
[Warren, Katherine E.] NCI, Pediat Oncol Branch, Bethesda, MD 20892 USA.
[Goldman, Stewart] Childrens Hosp Chicago, Chicago, IL USA.
[Pollack, Ian F.] Childrens Hosp Pittsburgh, Pittsburgh, PA USA.
[Fouladi, Maryam] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
[Chen, Alice] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Su, JM (reprint author), 6701 Fannin St,CC1510, Houston, TX 77030 USA.
EM jmsu@txch.org
FU NIH [U01 CA81457]; American Lebanese Syrian Associated Charities
FX This work was supported in part by NIH grant U01 CA81457 for the
Pediatric Brain Tumor Consortium and American Lebanese Syrian Associated
Charities.
NR 37
TC 13
Z9 13
U1 1
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1522-8517
EI 1523-5866
J9 NEURO-ONCOLOGY
JI Neuro-Oncology
PD DEC
PY 2014
VL 16
IS 12
BP 1661
EP 1668
DI 10.1093/neuonc/nou103
PG 8
WC Oncology; Clinical Neurology
SC Oncology; Neurosciences & Neurology
GA CA0JK
UT WOS:000348604000013
PM 24908656
ER
PT J
AU de Dios, JKL
Shrader, JA
Joe, GO
McClean, JC
Williams, K
Evers, R
Malicdan, MCV
Ciccone, C
Mankodi, A
Huizing, M
McKew, JC
Bluemke, DA
Gahl, WA
Carrillo-Carrasco, N
AF de Dios, John Karl L.
Shrader, Joseph A.
Joe, Galen O.
McClean, Jeffrey C.
Williams, Kayla
Evers, Robert
Malicdan, May Christine V.
Ciccone, Carla
Mankodi, Ami
Huizing, Marjan
McKew, John C.
Bluemke, David A.
Gahl, William A.
Carrillo-Carrasco, Nuria
TI Atypical presentation of GNE myopathy with asymmetric hand weakness
SO NEUROMUSCULAR DISORDERS
LA English
DT Article
DE GNE myopathy; Inclusion body myopathy 2; Hereditary inclusion body
myopathy (HIBM); Nonaka myopathy; Distal myopathy with rimmed vacuoles
(DMRV); N-acetylmannosamine (ManNAc); Sialic acid
ID INCLUSION-BODY MYOPATHY; DISTAL MYOPATHY; REFERENCE VALUES; RIMMED
VACUOLES; ENDOSCOPISTS; SIALYLATION; STRENGTH; GENE
AB GNE myopathy is a rare autosomal recessive muscle disease caused by mutations in GNE, the gene encoding the rate-limiting enzyme in sialic acid biosynthesis. GNE myopathy usually manifests in early adulthood with distal myopathy that progresses slowly and symmetrically, first involving distal muscles of the lower extremities, followed by proximal muscles with relative sparing of the quadriceps. Upper extremities are typically affected later in the disease. We report a patient with GNE myopathy who presented with asymmetric hand weakness. He had considerably decreased left grip strength, atrophy of the left anterior forearm and fibro-fatty tissue replacement of left forearm flexor muscles on T1-weighted magnetic resonance imaging. The patient was an endoscopist and thus the asymmetric hand involvement may be associated with left hand overuse in daily repetitive pinching and gripping movements, highlighting the possible impact of environmental factors on the progression of genetic muscle conditions. Published by Elsevier B.V.
C1 [de Dios, John Karl L.; Malicdan, May Christine V.; Ciccone, Carla; Huizing, Marjan; Gahl, William A.] NHGRI, MGB, NIH, Bethesda, MD USA.
[Shrader, Joseph A.; Joe, Galen O.; Williams, Kayla] NIH, Dept Rehabil Med, Ctr Clin, Bethesda, MD USA.
[McClean, Jeffrey C.] San Antonio Mil Med Ctr, Dept Neurol, San Antonio, TX USA.
[Evers, Robert; Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD USA.
[Mankodi, Ami] NINDS, NIH, Bethesda, MD 20892 USA.
[McKew, John C.; Carrillo-Carrasco, Nuria] NIH, NCATS, Bethesda, MD USA.
RP Carrillo-Carrasco, N (reprint author), 9000 Rockville Pike,Bldg 31,Room 3B11, Bethesda, MD 20892 USA.
EM carrilln@mail.nih.gov
RI Carrillo-Carrasco, Nuria/B-9034-2009;
OI Carrillo-Carrasco, Nuria/0000-0003-0374-0808; Bluemke,
David/0000-0002-8323-8086
FU Intramural NIH HHS [Z99 TR999999]
NR 24
TC 3
Z9 3
U1 1
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-8966
EI 1873-2364
J9 NEUROMUSCULAR DISORD
JI Neuromusc. Disord.
PD DEC
PY 2014
VL 24
IS 12
BP 1063
EP 1067
DI 10.1016/j.nmd.2014.07.006
PG 5
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AY7XW
UT WOS:000347770100005
PM 25182749
ER
PT J
AU Lee, PT
Chao, PK
Ou, LC
Chuang, JY
Lin, YC
Chen, SC
Chang, HF
Law, PY
Loh, HH
Chao, YS
Su, TP
Yeh, SH
AF Lee, Pin-Tse
Chao, Po-Kuan
Ou, Li-Chin
Chuang, Jian-Ying
Lin, Yen-Chang
Chen, Shu-Chun
Chang, Hsiao-Fu
Law, Ping-Yee
Loh, Horace H.
Chao, Yu-Sheng
Su, Tsung-Ping
Yeh, Shiu-Hwa
TI Morphine drives internal ribosome entry site-mediated hnRNP K
translation in neurons through opioid receptor-dependent signaling
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID NUCLEAR RIBONUCLEOPROTEIN-K; PERIAQUEDUCTAL GRAY; MESSENGER-RNAS;
SPINAL-CORD; PAIN; RAT; PHOSPHORYLATION; TRANSCRIPTION; CONTRIBUTES;
ACTIVATION
AB Heterogeneous nuclear ribonucleoprotein K (hnRNP K) binds to the promoter region of mu-opioid receptor (MOR) to regulate its transcriptional activity. How hnRNP K contributes to the analgesic effects of morphine, however, is largely unknown. We provide evidence that morphine increases hnRNP K protein expression via MOR activation in rat primary cortical neurons and HEK-293 cells expressing MORs, without increasing mRNA levels. Using the bicistronic reporter assay, we examined whether morphine-mediated accumulation of hnRNP K resulted from translational control. We identified potential internal ribosome entry site elements located in the 5' untranslated regions of hnRNP K transcripts that were regulated by morphine. This finding suggests that internal translation contributes to the morphine-induced accumulation of hnRNP K protein in regions of the central nervous system correlated with nociceptive and antinociceptive modulatory systems in mice. Finally, we found that down-regulation of hnRNP K mediated by siRNA attenuated morphine-induced hyperpolarization of membrane potential in AtT20 cells. Silencing hnRNP K expression in the spinal cord increased nociceptive sensitivity in wild-type mice, but not in MOR-knockout mice. Thus, our findings identify the role of translational control of hnRNP K in morphine-induced analgesia through activation of MOR.
C1 [Lee, Pin-Tse; Chao, Po-Kuan; Ou, Li-Chin; Chen, Shu-Chun; Chang, Hsiao-Fu; Chao, Yu-Sheng; Yeh, Shiu-Hwa] Natl Hlth Res Inst, Inst Biotechnol & Pharmaceut Res, Zhunan 35053, Miaoli County, Taiwan.
[Chuang, Jian-Ying] Taipei Med Univ, PhD Program Neural Regenerat Med, Taipei 110, Taiwan.
[Lin, Yen-Chang] Chinese Culture Univ, Grad Inst Biotechnol, Taipei 11114, Taiwan.
[Law, Ping-Yee; Loh, Horace H.] Univ Minnesota, Sch Med, Dept Pharmacol, Minneapolis, MN 55455 USA.
[Su, Tsung-Ping] NIDA, Cellular Pathobiol Sect, Intramural Res Program, Baltimore, MD 21224 USA.
RP Yeh, SH (reprint author), Natl Hlth Res Inst, Inst Biotechnol & Pharmaceut Res, Zhunan 35053, Miaoli County, Taiwan.
EM bau9763@bp.nhri.org.tw
RI Yeh, Shiu-Hwa/D-2088-2010;
OI Law, Ping-Yee/0000-0002-5364-1093
FU Intramural Research Program of National Health Research Institutes,
Taiwan, Republic of China; Ministry of Science and Technology, Taiwan,
Republic of China [NSC 101-2325-B-400-005, NSC 102-2325-B-400-005, NSC
103-2325-B-400-018, NSC 101-2311-B-400-005-MY3, NSC 101-2320-B-034-001]
FX Intramural Research Program of National Health Research Institutes,
Taiwan, Republic of China; and Ministry of Science and Technology,
Taiwan, Republic of China [NSC 101-2325-B-400-005, NSC
102-2325-B-400-005, NSC 103-2325-B-400-018, NSC 101-2311-B-400-005-MY3
and NSC 101-2320-B-034-001]. Funding for open access charge: Ministry of
Science and Technology, Taiwan, Republic of China [NSC
103-2325-B-400-018].
NR 43
TC 5
Z9 5
U1 0
U2 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD DEC 1
PY 2014
VL 42
IS 21
BP 13012
EP 13025
DI 10.1093/nar/gku1016
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AZ0CS
UT WOS:000347914600012
PM 25361975
ER
PT J
AU Kononenko, AV
Bansal, R
Lee, NCO
Grimes, BR
Masumoto, H
Earnshaw, WC
Larionov, V
Kouprina, N
AF Kononenko, Artem V.
Bansal, Ruchi
Lee, Nicholas C. O.
Grimes, Brenda R.
Masumoto, Hiroshi
Earnshaw, William C.
Larionov, Vladimir
Kouprina, Natalay
TI A portable BRCA1-HAC (human artificial chromosome) module for analysis
of BRCA1 tumor suppressor function
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID TRANSFORMATION-ASSOCIATED RECOMBINATION; CANCER CELL-LINE; CONDITIONAL
CENTROMERE; GENE DELIVERY; IONIZING-RADIATION; SATELLITE ARRAYS; BARR
BODY; INSTABILITY; DNA; HETEROCHROMATIN
AB BRCA1 is involved in many disparate cellular functions, including DNA damage repair, cell-cycle checkpoint activation, gene transcriptional regulation, DNA replication, centrosome function and others. The majority of evidence strongly favors the maintenance of genomic integrity as a principal tumor suppressor activity of BRCA1. At the same time some functional aspects of BRCA1 are not fully understood. Here, a HAC (human artificial chromosome) module with a regulated centromere was constructed for delivery and expression of the 90 kb genomic copy of the BRCA1 gene into BRCA1-deficient human cells. A battery of functional tests was carried out to demonstrate functionality of the exogenous BRCA1. In separate experiments, we investigated the role of BRCA1 in maintenance of heterochromatin integrity within a human functional kinetochore. We demonstrated that BRCA1 deficiency results in a specific activation of transcription of higher-order alphasatellite repeats (HORs) assembled into heterochromatin domains flanking the kinetochore. At the same time no detectable elevation of transcription was observed within HORs assembled into centrochromatin domains. Thus, we demonstrated a link between BRCA1 deficiency and kinetochore dysfunction and extended previous observations that BRCA1 is required to silence transcription in heterochromatin in specific genomic loci. This supports the hypothesis that epigenetic alterations of the kinetochore initiated in the absence of BRCA1 may contribute to cellular transformation.
C1 [Kononenko, Artem V.; Lee, Nicholas C. O.; Larionov, Vladimir; Kouprina, Natalay] NCI, Dev Therapeut Branch, Bethesda, MD 20892 USA.
[Bansal, Ruchi; Grimes, Brenda R.] Indiana Univ Melvin & Bren Simon Canc Ctr, Indiana Univ Sch Med, Dept Med & Mol Genet, Indianapolis, IN 46202 USA.
[Masumoto, Hiroshi] Kazusa DNA, Dept Frontier Res, Lab Cell Engn, Res Inst, Kisarazu, Chiba 2920818, Japan.
[Earnshaw, William C.] Univ Edinburgh, Wellcome Trust Ctr Cell Biol, Edinburgh EH9 3JR, Midlothian, Scotland.
RP Kouprina, N (reprint author), NCI, Dev Therapeut Branch, Bethesda, MD 20892 USA.
EM kouprinn@mail.nih.gov
RI Lee, Nicholas/F-3668-2015;
OI lee, nicholas/0000-0003-2628-6599
FU Intramural Research Program of the National Institutes of Health (NIH),
National Cancer Institute, Center for Cancer Research, USA; Wellcome
Trust Principal Research Fellowship [073915]; Ministry of Education,
Culture, Sports, Science and Technology of Japan [23247030, 23114008];
Kazusa DNA Research Institute Foundation; Indiana Genomics Initiative
(INGEN); Lilly Endowment; NIH
FX Intramural Research Program of the National Institutes of Health (NIH),
National Cancer Institute, Center for Cancer Research, USA [to V.L. and
N.K]; Wellcome Trust Principal Research Fellowship [073915 to W. C.E.];
Grand-in-Aid for Scientific Research from Ministry of Education,
Culture, Sports, Science and Technology of Japan [23247030, 23114008 to
H.M.]; Kazusa DNA Research Institute Foundation [to H.M.]; Indiana
Genomics Initiative (INGEN) [to B. R.G.]. INGEN is supported in part by
the Lilly Endowment. Funding for open access charge: NIH.
NR 58
TC 4
Z9 4
U1 1
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
EI 1362-4962
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD DEC 1
PY 2014
VL 42
IS 21
AR e164
DI 10.1093/nar/gku870
PG 15
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AZ0CS
UT WOS:000347914600005
ER
PT J
AU Grammatikakis, I
Panda, AC
Abdelmohsen, K
Gorospe, M
AF Grammatikakis, Ioannis
Panda, Amaresh C.
Abdelmohsen, Kotb
Gorospe, Myriam
TI Long noncoding RNAs (lncRNAs) and the molecular hallmarks of aging
SO AGING-US
LA English
DT Article
DE long noncoding RNAs; senescence-associated lncRNAs; epigenetic control
by lncRNAs; lncRNA regulation of post-transcriptional gene expression;
lncRNA influencing aging phenotypes
ID PLURIPOTENT STEM-CELLS; HUMAN TUMOR-GROWTH; CELLULAR SENESCENCE;
DNA-DAMAGE; HEPATOCELLULAR-CARCINOMA; GENE-EXPRESSION; RIBOSOMAL-RNA;
IN-VIVO; TRANSCRIPTIONAL ENHANCERS; HETEROCHROMATIN FORMATION
AB During aging, progressive deleterious changes increase the risk of disease and death. Prominent molecular hallmarks of aging are genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, cellular senescence, stem cell exhaustion, and altered intercellular communication. Long noncoding RNAs (lncRNAs) play important roles in a wide range of biological processes, including age-related diseases like cancer, cardiovascular pathologies, and neurodegenerative disorders. Evidence is emerging that lncRNAs influence the molecular processes that underlie age-associated phenotypes. Here, we review our current understanding of lncRNAs that control the development of aging traits.
C1 [Grammatikakis, Ioannis; Panda, Amaresh C.; Abdelmohsen, Kotb; Gorospe, Myriam] NIA, Genet Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
RP Abdelmohsen, K (reprint author), NIA, Genet Lab, Intramural Res Program, NIH, Baltimore, MD 21224 USA.
EM abdelmohsenk@mail.nih.gov
OI PANDA, AMARESH/0000-0003-3189-8995
FU National Institute on Aging-Intramural Research Program of the National
Institutes of Health
FX This work was supported in its entirety by the National Institute on
Aging-Intramural Research Program of the National Institutes of Health.
NR 196
TC 22
Z9 23
U1 4
U2 16
PU IMPACT JOURNALS LLC
PI ALBANY
PA 6211 TIPTON HOUSE, STE 6, ALBANY, NY 12203 USA
SN 1945-4589
J9 AGING-US
JI Aging-US
PD DEC
PY 2014
VL 6
IS 12
BP 992
EP 1009
PG 18
WC Cell Biology
SC Cell Biology
GA AZ2HR
UT WOS:000348055500001
PM 25543668
ER
PT J
AU Rioux-Leclercq, N
Ferran, A
Mahul, A
Argani, P
Billis, A
Bonsib, S
Cheng, L
Cheville, J
Eble, J
Egevad, L
Epstein, J
Grignon, D
Hes, O
Humphrey, P
Magi-Galluzzi, C
Martignoni, G
McKenney, J
Merino, M
Moch, H
Montironi, R
Netto, G
Reuter, V
Samaratunga, H
Shen, S
Srigley, J
Tamboli, P
Tan, PH
Tickoo, S
Trpkov, K
Zhou, M
Delahunt, B
Comperat, E
AF Rioux-Leclercq, Nathalie
Ferran, Algaba
Mahul, Amin
Argani, Pedram
Billis, Athanase
Bonsib, Stephen
Cheng, Liang
Cheville, John
Eble, John
Egevad, Lars
Epstein, Jonathan
Grignon, David
Hes, Ondrej
Humphrey, Peter
Magi-Galluzzi, Cristina
Martignoni, Guido
McKenney, Jesse
Merino, Maria
Moch, Holger
Montironi, Rodolfo
Netto, George
Reuter, Viktor
Samaratunga, Hemamali
Shen, Steven
Srigley, John
Tamboli, Pheroze
Tan, Puay Hoon
Tickoo, Satish
Trpkov, Kiril
Zhou, Ming
Delahunt, Brett
Comperat, Eva
TI Renal tumors: The International Society of Urologic Pathology (ISUP)
2012 consensus conference recommendations
SO ANNALES DE PATHOLOGIE
LA French
DT Article
DE Renal cancer; ISUP; Recommedations; Consensus conference
ID ACQUIRED CYSTIC-DISEASE; COLLECTING DUCT CARCINOMA; CELL-CARCINOMA;
CLEAR-CELL; TUBULOCYSTIC CARCINOMA; HEREDITARY LEIOMYOMATOSIS;
CLINICOPATHOLOGICAL FEATURES; TRANSLOCATION CARCINOMAS;
DIFFERENTIAL-DIAGNOSIS; FOLLICULAR CARCINOMA
AB During the last 30 years many advances have been made in kidney tumor pathology. In 1981, 9 entities were recognized in the WHO Classification. In the latest classification of 2004, 50 different types have been recognized. Additional tumor entities have been described since and a wide variety of prognostic parameters have been investigated with variable success; however, much attention has centered upon the importance of features relating to both stage and grade. The International Society of Urological Pathology (ISUP) recommends after consensus conferences the development of reporting guidelines, which have been adopted worldwide ISUP undertook to review all aspects of the pathology of adult renal malignancy through an international consensus conference to be held in 2012. As in the past, participation in this consensus conference was restricted to acknowledged experts in the field. (C) 2014 Elsevier Masson SAS. All rights reserved.
C1 [Rioux-Leclercq, Nathalie] CHU Pontchailloux, F-35033 Rennes 9, France.
[Ferran, Algaba] Fdn Puigvert Univ Antonomous, Barcelona, Spain.
[Mahul, Amin] Cedars Sinai Med Ctr, Los Angeles, CA 90048 USA.
[Argani, Pedram] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Bonsib, Stephen] Univ Estadual Campinas, Unicamp, Sch Med Sci, Campinas, SP, Brazil.
[Cheville, John] Univ Arkansas Med Sci, Little Rock, AR 72212 USA.
[Magi-Galluzzi, Cristina] Indiana Univ, Sch Med, Indianapolis, IN 46204 USA.
[Cheville, John] Mayo Clin, Rochester, MN USA.
[Humphrey, Peter] Karolinska Univ Hosp, Stockholm, Sweden.
[Martignoni, Guido] Univ Hosp Plzen, Plzen, Czech Republic.
[McKenney, Jesse] Yale Univ, Sch Med, New Haven, CT USA.
[Netto, George] Canc Biol & Glickman Urol Inst, Cleveland, OH USA.
[Magi-Galluzzi, Cristina] Univ Verona, I-37100 Verona, Italy.
[Samaratunga, Hemamali] NCI, Bethesda, MD 20892 USA.
[Shen, Steven] Univ Zurich, Zurich, Switzerland.
[Cheville, John; Eble, John; Hes, Ondrej] Univ Ancona, Sch Med, Ancona, Italy.
[Humphrey, Peter; McKenney, Jesse] Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
[McKenney, Jesse; Moch, Holger] Univ Queensland, Brisbane, Qld, Australia.
[Grignon, David; Hes, Ondrej] Cornell Univ, Methodist Hosp, Houston, TX USA.
[Srigley, John] Cornell Univ, Weill Med Coll, Houston, TX USA.
[Srigley, John] McMaster Univ, Hamilton, ON, Canada.
[Tamboli, Pheroze] Univ Otago, Wellington Sch Med & Hlth Sci, Wellington, New Zealand.
[Tan, Puay Hoon] Univ Otago, Wellington Sch Med & Hlth Sci, Wellington, New Zealand.
[Tickoo, Satish] Univ Calgary, Calgary, AB, Canada.
[Trpkov, Kiril] Calgary Lab Serv, Calgary, AB, Canada.
[Zhou, Ming] NYU, Med Ctr, New York, NY USA.
[Delahunt, Brett] Univ Otago, Wellington Sch Med, Wellington, New Zealand.
[Comperat, Eva] UPMC, Hop Pitie Salpetriere, Dept Pathol, F-75651 Paris 13, France.
RP Comperat, E (reprint author), UPMC, Hop Pitie Salpetriere, Dept Pathol, 47-83 Blvd Hop, F-75651 Paris 13, France.
EM evacomperat@yahoo.fr
RI Samaratunga, Hemamali/D-1559-2013;
OI Samaratunga, Hemamali/0000-0001-5796-1791; Shen,
Steven/0000-0001-7725-1260
NR 63
TC 1
Z9 1
U1 0
U2 2
PU MASSON EDITEUR
PI MOULINEAUX CEDEX 9
PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE
SN 0242-6498
J9 ANN PATHOL
JI Ann. Pathol.
PD DEC
PY 2014
VL 34
IS 6
BP 448
EP 461
DI 10.1016/j.annpat.2014.10.003
PG 14
WC Pathology
SC Pathology
GA AY7IK
UT WOS:000347734000004
PM 25499860
ER
PT J
AU Zipunnikov, V
Greven, S
Shou, HC
Caffo, BS
Reich, DS
Crainiceanu, CM
AF Zipunnikov, Vadim
Greven, Sonja
Shou, Haochang
Caffo, Brian S.
Reich, Daniel S.
Crainiceanu, Ciprian M.
TI LONGITUDINAL HIGH-DIMENSIONAL PRINCIPAL COMPONENTS ANALYSIS WITH
APPLICATION TO DIFFUSION TENSOR IMAGING OF MULTIPLE SCLEROSIS
SO ANNALS OF APPLIED STATISTICS
LA English
DT Article
DE Principal components; linear mixed model; diffusion tensor imaging;
brain imaging data; multiple sclerosis
ID FUNCTIONAL MIXED MODELS; REGRESSION; PREDICTORS; FRAMEWORK; PCA
AB We develop a flexible framework for modeling high-dimensional imaging data observed longitudinally. The approach decomposes the observed variability of repeatedly measured high-dimensional observations into three additive components: a subject-specific imaging random intercept that quantifies the cross-sectional variability, a subject-specific imaging slope that quantifies the dynamic irreversible deformation over multiple realizations, and a subject-visit-specific imaging deviation that quantifies exchangeable effects between visits. The proposed method is very fast, scalable to studies including ultrahigh-dimensional data, and can easily be adapted to and executed on modest computing infrastructures. The method is applied to the longitudinal analysis of diffusion tensor imaging (DTI) data of the corpus callosum of multiple sclerosis (MS) subjects. The study includes 176 subjects observed at 466 visits. For each subject and visit the study contains a registered DTI scan of the corpus callosum at roughly 30,000 voxels.
C1 [Zipunnikov, Vadim; Caffo, Brian S.; Crainiceanu, Ciprian M.] Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
[Greven, Sonja] Univ Munich, Dept Stat, D-80539 Munich, Germany.
[Shou, Haochang] Univ Penn, Dept Biostat & Epidemiol, Philadelphia, PA 19104 USA.
[Reich, Daniel S.] NINDS, NIH, Bethesda, MD 20824 USA.
RP Zipunnikov, V (reprint author), Johns Hopkins Univ, Dept Biostat, Baltimore, MD 21205 USA.
EM vzipunn1@jhu.edu
RI Reich, Daniel/E-5701-2010
OI Reich, Daniel/0000-0002-2628-4334
FU National Institute of Neurological Disorders and Stroke [R01NS060910];
NIH National Institute of Biomedical Imaging and Bioengineering (NIBIB)
[EB012547]; German Research Foundation through the Emmy Noether
Programme, Grant [GR 3793/1-1]; Intramural Research Program of the
National Institute of Neurological Disorders and Stroke
FX Supported by Grant R01NS060910 from the National Institute of
Neurological Disorders and Stroke and by Award Number EB012547 from the
NIH National Institute of Biomedical Imaging and Bioengineering
(NIBIB).; Supported by the German Research Foundation through the Emmy
Noether Programme, Grant GR 3793/1-1.; Supported by the Intramural
Research Program of the National Institute of Neurological Disorders and
Stroke.
NR 44
TC 4
Z9 4
U1 1
U2 7
PU INST MATHEMATICAL STATISTICS
PI CLEVELAND
PA 3163 SOMERSET DR, CLEVELAND, OH 44122 USA
SN 1932-6157
J9 ANN APPL STAT
JI Ann. Appl. Stat.
PD DEC
PY 2014
VL 8
IS 4
BP 2175
EP 2202
DI 10.1214/14-AOAS748
PG 28
WC Statistics & Probability
SC Mathematics
GA AY4EF
UT WOS:000347530200014
PM 25663955
ER
PT J
AU Zhang, ZW
Nie, L
Soon, GX
Liu, AY
AF Zhang, Zhiwei
Nie, Lei
Soon, Guoxing
Liu, Aiyi
TI THE USE OF COVARIATES AND RANDOM EFFECTS IN EVALUATING PREDICTIVE
BIOMARKERS UNDER A POTENTIAL OUTCOME FRAMEWORK
SO ANNALS OF APPLIED STATISTICS
LA English
DT Article
DE Conditional independence; counterfactual; ROC regression; sensitivity
analysis; treatment effect heterogeneity; treatment selection
ID TREATMENT-SELECTION; TRIAL; CANCER
AB Predictive or treatment selection biomarkers are usually evaluated in a subgroup or regression analysis with focus on the treatment-by-marker interaction. Under a potential outcome framework (Huang, Gilbert and Janes [Biometrics 68 (2012) 687-696]), a predictive biomarker is considered a predictor for a desirable treatment benefit (defined by comparing potential outcomes for different treatments) and evaluated using familiar concepts in prediction and classification. However, the desired treatment benefit is unobservable because each patient can receive only one treatment in a typical study. Huang et al. overcome this problem by assuming monotonicity of potential outcomes, with one treatment dominating the other in all patients. Motivated by an HIV example that appears to violate the monotonicity assumption, we propose a different approach based on covariates and random effects for evaluating predictive biomarkers under the potential outcome framework. Under the proposed approach, the parameters of interest can be identified by assuming conditional independence of potential outcomes given observed covariates, and a sensitivity analysis can be performed by incorporating an unobserved random effect that accounts for any residual dependence. Application of this approach to the motivating example shows that baseline viral load and CD4 cell count are both useful as predictive biomarkers for choosing antiretroviral drugs for treatment-naive patients.
C1 [Zhang, Zhiwei] US FDA, Div Biostat, Off Surveillance & Biometr, Ctr Devices & Radiol Hlth, Silver Spring, MD 20993 USA.
[Nie, Lei] US FDA, Div Biometr 5, Off Biostat, Ctr Drug Evaluat & Res, Silver Spring, MD 20993 USA.
[Soon, Guoxing] US FDA, Div Biometr 4, Off Biostat, Ctr Drug Evaluat & Res, Silver Spring, MD 20993 USA.
[Liu, Aiyi] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Population Hlth Res, NIH, Bethesda, MD 20892 USA.
RP Zhang, ZW (reprint author), US FDA, Div Biostat, Off Surveillance & Biometr, Ctr Devices & Radiol Hlth, 10903 New Hampshire Ave, Silver Spring, MD 20993 USA.
EM zhiwei.zhang@fda.hhs.gov; lei.nie@fda.hhs.gov; guoxing.soon@fda.hhs.gov;
liua@mail.nih.gov
OI Liu, Aiyi/0000-0002-6618-5082
FU Intramural NIH HHS [ZIA HD008875-01]
NR 25
TC 1
Z9 1
U1 1
U2 6
PU INST MATHEMATICAL STATISTICS
PI CLEVELAND
PA 3163 SOMERSET DR, CLEVELAND, OH 44122 USA
SN 1932-6157
J9 ANN APPL STAT
JI Ann. Appl. Stat.
PD DEC
PY 2014
VL 8
IS 4
BP 2336
EP 2355
DI 10.1214/14-AOAS773
PG 20
WC Statistics & Probability
SC Mathematics
GA AY4EF
UT WOS:000347530200021
PM 26779295
ER
PT J
AU Bornstein, MH
Esposito, G
AF Bornstein, Marc H.
Esposito, Gianluca
TI Beyond cry and laugh: Toward a multilevel model of language production
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Editorial Material
ID DISORDER; INFANTS
AB Language production is a multilevel phenomenon, and human capacities to communicate vocally progress from early forms, based on projections of motor cortex to brainstem nuclei, to complex elaborations, mediated by high-order cognition and fostered by socially mediated feedback.
C1 [Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
[Esposito, Gianluca] Univ Trento, Dept Psychol & Cognit Sci, I-38068 Trento, Italy.
[Esposito, Gianluca] Nanyang Technol Univ, Div Psychol, Singapore 639798, Singapore.
RP Bornstein, MH (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Rockledge 1, Bethesda, MD 20892 USA.
EM Marc_H_Bornstein@nih.gov; gianluca.esposito@unitn.it
NR 9
TC 0
Z9 0
U1 0
U2 4
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0140-525X
EI 1469-1825
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD DEC
PY 2014
VL 37
IS 6
DI 10.1017/S0140525X13003968
PG 4
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA AZ2IE
UT WOS:000348056700004
ER
PT J
AU Maity, J
Bohr, VA
Laskar, A
Karmakar, P
AF Maity, Jyotirindra
Bohr, Vilhelm A.
Laskar, Aparna
Karmakar, Parimal
TI Transient overexpression of Werner protein rescues starvation induced
autophagy in Werner syndrome cells
SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
LA English
DT Article
DE Autophagy; Aging; Beclin-1; RecQ helicase; Werner protein; Werner
syndrome
ID RNA-POLYMERASE-I; RECQ HELICASES; MAMMALIAN TARGET; DNA-DAMAGE;
TRANSCRIPTION; WRN; EXPRESSION; DISEASE; CANCER; REPAIR
AB Reduced autophagy may be associated with normal and pathological aging. Here we report a link between autophagy and Werner protein (WRNp), mutated in Werner syndrome, the human premature aging Werner syndrome (WS). WRN mutant fibroblast AG11395 and AG05229 respond weakly to starvation induced autophagy compared to normal cells. While the fusion of phagosomes with lysosome is normal, WS cells contain fewer autophagy vacuoles. Cellular starvation autophagy in WS cells is restored after transfection with full length WRN. Further, siRNA mediated silencing of WRN in the normal fibroblast cell line WI-38 results in decreased autophagy and altered expression of autophagy related proteins. Thus, our observations suggest that WRN may have a role in controlling autophagy and hereby cellular maintenance. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Maity, Jyotirindra; Karmakar, Parimal] Jadavpur Univ, Dept Life Sci & Biotechnol, Kolkata 700032, India.
[Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Baltimore, MD 21224 USA.
[Laskar, Aparna] CSIR, Indian Inst Chem Biol, Kolkata 700032, India.
RP Karmakar, P (reprint author), Jadavpur Univ, Dept Life Sci & Biotechnol, Kolkata 700032, W Bengal, India.
EM pkarmakar_28@yahoo.co.in
FU Council for Scientific and Industrial Research (CSIR), Government of
India [37/(1442)/10/EMR-II]; National Institute on Aging, NIH
FX The authors would like to acknowledge for financial support for this
research work the Council for Scientific and Industrial Research (CSIR),
project no: [37/(1442)/10/EMR-II] Government of India. We sincerely
acknowledge Dr. Jayanta Debnath (Department of Pathology, University
California, San Francisco) for pBABE-puro mCherry-EGFP-LC3B and Prof.
Tamatsu Yoshimori (Osaka, Japan) for EGFP-LC3 plasmid. We also express
sincere thanks to Prof. S. Roy, Director, Indian Institute of Chemical
Biology, Kolkata, India, for his permission to use the transmission
electron microscope. This project was partially supported by funds from
the Intramural program of the National Institute on Aging, NIH.
NR 45
TC 2
Z9 2
U1 1
U2 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0925-4439
EI 0006-3002
J9 BBA-MOL BASIS DIS
JI Biochim. Biophys. Acta-Mol. Basis Dis.
PD DEC
PY 2014
VL 1842
IS 12
BP 2387
EP 2394
DI 10.1016/j.bbadis.2014.09.007
PN A
PG 8
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA AY5CK
UT WOS:000347590700005
PM 25257404
ER
PT J
AU Castoria, G
Giovannelli, P
Di Donato, M
Ciociola, A
Hayashi, R
Bernal, F
Appella, E
Auricchio, F
Migliaccio, A
AF Castoria, G.
Giovannelli, P.
Di Donato, M.
Ciociola, A.
Hayashi, R.
Bernal, F.
Appella, E.
Auricchio, F.
Migliaccio, A.
TI Role of non-genomic androgen signalling in suppressing proliferation of
fibroblasts and fibrosarcoma cells
SO CELL DEATH & DISEASE
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; DEPENDENT NUCLEAR EXPORT; BREAST-CANCER CELLS;
PROSTATE-CANCER; ESTRADIOL-RECEPTOR; CYCLE PROGRESSION; RAS ONCOGENES;
DNA-SYNTHESIS; STAPLED P53; IN-VIVO
AB The functions of androgen receptor (AR) in stromal cells are still debated in spite of the demonstrated importance of these cells in organ development and diseases. Here, we show that physiological androgen concentration (10 nM R1881 or DHT) fails to induce DNA synthesis, while it consistently stimulates cell migration in mesenchymal and transformed mesenchymal cells. Ten nanomolar R1881 triggers p27 Ser10 phosphorylation and its stabilization in NIH3T3 fibroblasts. Activation of Rac and its downstream effector DYRK 1B is responsible for p27 Ser10 phosphorylation and cell quiescence. Ten nanomolar androgen also inhibits transformation induced by oncogenic Ras in NIH3T3 fibroblasts. Overexpression of an AR mutant unable to interact with filamin A, use of a small peptide displacing AR/filamin A interaction, and filamin A knockdown indicate that the androgen-triggered AR/filamin A complex regulates the pathway leading to p27 Ser10 phosphorylation and cell cycle arrest. As the AR/filamin A complex is also responsible for migration stimulated by 10 nM androgen, our report shows that the androgen-triggered AR/filamin A complex controls, through Rac 1, the decision of cells to halt cell cycle and migration. This study reveals a new and unexpected role of androgen/AR signalling in coordinating stromal cell functions.
C1 [Castoria, G.; Giovannelli, P.; Di Donato, M.; Ciociola, A.; Auricchio, F.; Migliaccio, A.] Univ Naples Federico II, Dept Biochem Biophys & Gen Pathol, I-80138 Naples, Italy.
[Hayashi, R.; Appella, E.] NCI, Lab Cell Biol, Bethesda, MD 20892 USA.
[Bernal, F.] NCI, Metabol Branch, Bethesda, MD 20892 USA.
RP Castoria, G (reprint author), Univ Naples Federico II, Dept Biochem Biophys & Gen Pathol, Via L De Crecchio 7, I-80138 Naples, Italy.
EM gabriella.castoria@unina2.it; antimo.migliaccio@unina2.it
OI Migliaccio, Antimo/0000-0002-4197-2055; Di Donato,
Marzia/0000-0001-7207-826X; Castoria, Gabriella/0000-0002-0576-4494
FU Italian Association for Cancer Research [IG11520]; Italian Ministry of
University and Scientific Research (P.R.I.N.) [2010NFEB9L_002]; Italian
Ministry of University and Scientific Research
FX We thank M.V. Barone for Src- and Ras-transformed fibroblasts, F.
Claessens for 3416 and 3424 constructs, P. Coffer for pGL2-p27
construct, E.L. Yong for Delta 622-670 hAR mutant, P. Friedl for human
fibrosarcoma HT1080 cells, and M. Pagano for HA-tagged wt p27 and S10A
constructs. The Italian Association for Cancer Research (IG11520 to A.
M.) and the Italian Ministry of University and Scientific Research
(P.R.I.N. 2010-2011; 2010NFEB9L_002 to G.C.) supported this work. Pia
Giovannelli and Marzia Di Donato are supported by a fellowship of the
Italian Ministry of University and Scientific Research.
NR 52
TC 7
Z9 7
U1 0
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD DEC
PY 2014
VL 5
AR e1548
DI 10.1038/cddis.2014.497
PG 12
WC Cell Biology
SC Cell Biology
GA AY8YU
UT WOS:000347837400001
PM 25476896
ER
PT J
AU Li, Y
Hong, N
Zhang, A
Chen, W
Wang, RH
Xu, XL
Deng, CX
AF Li, Y.
Hong, N.
Zhang, A.
Chen, W.
Wang, R-H
Xu, X-L
Deng, C-X
TI Enhancing mammary differentiation by overcoming lineage-specific
epigenetic modification and signature gene expression of
fibroblast-derived iPSCs
SO CELL DEATH & DISEASE
LA English
DT Article
ID PLURIPOTENT STEM-CELLS; CLAUDIN-7 EXPRESSION; DNA-METHYLATION; MOUSE;
GLAND; HETEROGENEITY; MORPHOGENESIS; CARCINOMA; MEDICINE; BRCA1
AB Recent studies have shown that induced pluripotent stem cells (iPSCs) retain a memory of their origin and exhibit biased differentiation potential. This finding reveals a severe limitation in the application of iPSCs to cell-based therapy because it means that certain cell types are not available for reprogramming for patients. Here we show that the iPSC differentiation process is accompanied by profound gene expression and epigenetic modifications that reflect cells' origins. Under typical conditions for mammary differentiation, iPSCs reprogrammed from tail-tip fibroblasts (TF-iPSCs) activated a fibroblast-specific signature that was not compatible with mammary differentiation. Strikingly, under optimized conditions, including coculture with iPSCs derived from the mammary epithelium or in the presence of pregnancy hormones, the fibroblast-specific signature of TF-iPSCs obtained during differentiation was erased and cells displayed a mammary-specific signature with a markedly enhanced ability for mammary differentiation. These findings provide new insights into the precise control of differentiation conditions that may have applications in personalized cell-based therapy.
C1 [Li, Y.; Hong, N.; Zhang, A.; Wang, R-H; Xu, X-L; Deng, C-X] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA.
[Li, Y.] Third Mil Med Univ, Xin Qiao Hosp, Chongqing, Peoples R China.
[Chen, W.] NIDDK, Microarray Core Facil, NIH, Bethesda, MD 20892 USA.
[Wang, R-H; Xu, X-L; Deng, C-X] Univ Macau, Fac Hlth Sci, Macau, Macau Sar, Peoples R China.
RP Deng, CX (reprint author), NIDDK, Genet Dev & Dis Branch, NIH, 10-9N105, Bethesda, MD 20892 USA.
EM chuxiad@bdg10.niddk.nih.gov
FU Intramural Research Program of the National Institute of Diabetes,
Digestive and Kidney Diseases, National Institutes of Health, Bethesda,
MD, USA
FX We thank Dr Gertraud Robinson for technical assistance in mammary fat
pat implantation and members of the Deng laboratory for the critical
reading of and helpful discussion about this manuscript. This work was
supported by the Intramural Research Program of the National Institute
of Diabetes, Digestive and Kidney Diseases, National Institutes of
Health, Bethesda, MD, USA.
NR 41
TC 1
Z9 1
U1 0
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-4889
J9 CELL DEATH DIS
JI Cell Death Dis.
PD DEC
PY 2014
VL 5
AR e1550
DI 10.1038/cddis.2014.499
PG 12
WC Cell Biology
SC Cell Biology
GA AY8YU
UT WOS:000347837400003
PM 25476898
ER
PT J
AU Freedman, BR
Brindle, TJ
Sheehan, FT
AF Freedman, Benjamin R.
Brindle, Timothy J.
Sheehan, Frances T.
TI Re-evaluating the functional implications of the Q-angle and its
relationship to in-vivo patellofemoral kinematics
SO CLINICAL BIOMECHANICS
LA English
DT Article
DE Patellofemoral joint; Patellofemoral pain syndrome; Magnetic resonance
imaging; Kinematics; Knee
ID ANTERIOR KNEE PAIN; PHYSICAL-EXAMINATION; GENDER-DIFFERENCES; PATELLAR
TRACKING; BIOMECHANICS; POSITION; WOMEN; JOINT; MEN; DISORDERS
AB Background: The Q-angle is widely used clinically to evaluate individuals with anterior knee pain. Recent studies have questioned the utility of this measure and have suggested that a large Q-angle may not be associated with lateral patellofemoral translation, as often assumed. The objective of this study was to determine: 1) how accurately the Q-angle represents the line-of-action of the quadriceps and 2) if adding active quadriceps contraction or a bent knee position to the measurement of the Q-angle improves its reliability, accuracy, and association with patellofemoral kinematics.
Methods: The study included individuals diagnosed with chronic idiopathic patellofemoral pain and control subjects (n = 43 and n = 30 knees). Three measures of the clinical Q-angle (straight- and bent-knee with relaxed quadriceps and straight-knee with maximum isometric quadriceps contraction) were obtained with a goniometer and compared to a fourth MR-based measure of Q-angle. Patellofemoral kinematics were derived from dynamic cine-phase contrast images, acquired while subjects extended/flexed their knee from approximately 0 degrees and 45 degrees.
Findings: The Q-angle did not represent the line-of-action of the quadriceps. The average difference between each clinical and the MR-based Q-angle ranged from 5 degrees to 8 degrees. These differences varied greatly across subjects (range: -28.5 degrees to 3.9 degrees). Adding an active quadriceps contraction or a bent knee position, did not improve the reliability of the Q-angle. An increased Q-angle correlated to medial patellar displacement and tilt (r = 0.38-0.54, P < 0.001) in the cohort with anterior knee pain.
Interpretation: Clinicians are cautioned against using the Q-angle to infer patellofemoral kinematics. (C) 2014 Published by Elsevier Ltd.
C1 [Freedman, Benjamin R.; Sheehan, Frances T.] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Brindle, Timothy J.] Univ Maryland, College Pk, MD 20742 USA.
[Freedman, Benjamin R.] Univ Penn, Dept Bioengn, Philadelphia, PA 19104 USA.
RP Freedman, BR (reprint author), Univ Penn, McKay Orthopaed Res Lab, 424 Stemmler Hal,36th & Hamilton Walk, Philadelphia, PA 19104 USA.
EM bfreed@seas.upenn.edu
FU NIH Clinical Center Intramural Research Program; Biomedical Engineering
Summer Internship Program - National Institute of Biomedical Imaging and
Bioengineering; Diagnostic Radiology Department at the National
Institutes of Health
FX This research was supported by the NIH Clinical Center Intramural
Research Program and the Biomedical Engineering Summer Internship
Program (funded by the National Institute of Biomedical Imaging and
Bioengineering). Special thanks are given to Sara Sadeghi, Abrahm
Behnam, Cris Zampieri-Gallagher, Ching Yi Shieh, Bonnie Damaska, and the
Diagnostic Radiology Department at the National Institutes of Health for
their support and research time.
NR 42
TC 4
Z9 6
U1 1
U2 11
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0268-0033
EI 1879-1271
J9 CLIN BIOMECH
JI Clin. Biomech.
PD DEC
PY 2014
VL 29
IS 10
BP 1139
EP 1145
DI 10.1016/j.clinbiomech.2014.09.012
PG 7
WC Engineering, Biomedical; Orthopedics; Sport Sciences
SC Engineering; Orthopedics; Sport Sciences
GA AY5CW
UT WOS:000347591800009
PM 25451861
ER
PT J
AU Gao, X
Cao, HB
Ming, D
Qi, HZ
Wang, XM
Wang, XL
Chen, RG
Zhou, P
AF Gao, Xiang
Cao, Hongbao
Ming, Dong
Qi, Hongzhi
Wang, Xuemin
Wang, Xiaolu
Chen, Runge
Zhou, Peng
TI Analysis of EEG activity in response to binaural beats with different
frequencies
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Article
DE Binaural beat; Connectivity; RP; PLV; CMI
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; MUTUAL INFORMATION ANALYSIS;
FUNCTIONAL-ORGANIZATION; HYPNOTIC-SUSCEPTIBILITY;
SCHIZOPHRENIC-PATIENTS; AUDITORY BEATS; PHASE-LOCKING; BRAIN; COHERENCE;
NEUROFEEDBACK
AB When two coherent sounds with nearly similar frequencies are presented to each ear respectively with stereo headphones, the brain integrates the two signals and produces a sensation of a third sound called binaural beat (BB). Although earlier studies showed that BB could influence behavior and cognition, common agreement on the mechanism of BB has not been reached yet. In this work, we employed Relative Power (RP), Phase Locking Value (PLV) and Cross-Mutual Information (CMI) to track EEG changes during BB stimulations. EEG signals were acquired from 13 healthy subjects. Five-minute BBs with four different frequencies were tested: delta band (1 Hz), theta band (5 Hz), alpha band (10 Hz) and beta band (20 Hz). We observed RP increase in theta and alpha bands and decrease in beta band during delta and alpha BB stimulations. RP decreased in beta band during theta BB, while RP decreased in theta band during beta BB. However, no clear brainwave entrainment effect was identified. Connectivity changes were detected following the variation of RP during BB stimulations. Our observation supports the hypothesis that BBs could affect functional brain connectivity, suggesting that the mechanism of BB-brain interaction is worth further study. (C) 2014 Published by Elsevier B.V.
C1 [Gao, Xiang; Ming, Dong; Qi, Hongzhi; Wang, Xuemin; Wang, Xiaolu; Chen, Runge; Zhou, Peng] Tianjin Univ, Sch Precis Instruments & Optoelect Engn, Tianjin 300072, Peoples R China.
[Cao, Hongbao] NIMH, Unit Stat Genom, NIH, Bethesda, MD 20852 USA.
RP Zhou, P (reprint author), Tianjin Univ, Sch Precis Instruments & Optoelect Engn, Tianjin 300072, Peoples R China.
EM zpzpa@vip.sina.com
FU National Natural Science Foundation of China [51377120, 81222021,
31271062, 61172008, 81171423, 51007063]; National Key Technology R&D
Program of the Ministry of Science and Technology of China
[2012BAI34B02]; Program for New Century Excellent Talents in University
of the Ministry of Education of China [NCET-10-0618]
FX This research was supported by the National Natural Science Foundation
of China (No. 51377120, 81222021, 31271062, 61172008, 81171423,
51007063), the National Key Technology R&D Program of the Ministry of
Science and Technology of China (No. 2012BAI34B02) and the Program for
New Century Excellent Talents in University of the Ministry of Education
of China (No. NCET-10-0618).
NR 50
TC 10
Z9 11
U1 10
U2 40
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
EI 1872-7697
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD DEC
PY 2014
VL 94
IS 3
BP 399
EP 406
DI 10.1016/j.ijpsycho.2014.10.010
PG 8
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA AZ1RI
UT WOS:000348015200017
PM 25448376
ER
PT J
AU Karev, GP
AF Karev, Georgy P.
TI Non-linearity and heterogeneity in modeling of population dynamics
SO MATHEMATICAL BIOSCIENCES
LA English
DT Article
DE Non-exponential growth; Distributed parameters; Heterogeneous
population; Prebiological evolution
ID REPLICATORS; GROWTH; REPRODUCERS; TEMPLATES; SURVIVAL
AB The study of population growth reveals that the behaviors that follow the power law appear in numerous biological, demographical, ecological, physical and other contexts. Parabolic models appear to be realistic approximations of real-life replicator systems, while hyperbolic models were successfully applied to problems of global demography and appear relevant in quasispecies and hypercycle modeling. Nevertheless, it is not always clear why non-exponential growth is observed empirically and what possible origins of the non-exponential models are.
In this paper the power equation is considered within the frameworks of inhomogeneous population models; it is proven that any power equation describes the total population size of a frequency-dependent model with Gamma-distributed Malthusian parameter. Additionally, any super-exponential equation describes the dynamics of inhomogeneous Malthusian density-dependent population model. All statistical characteristics of the underlying inhomogeneous models are computed explicitly. The results of this analysis show that population heterogeneity can be a reasonable explanation for power law accurately describing total population growth. (C) 2014 Elsevier Inc. All rights reserved.
C1 NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA.
RP Karev, GP (reprint author), NIH, Natl Ctr Biotechnol Informat, Bldg 38A,8600 Rockville Pike, Bethesda, MD 20894 USA.
EM karev@ncbi.nlm.nih.gov
FU NIH, NCBI
FX This research was supported by the Intramural Research Program of the
NIH, NCBI.
NR 34
TC 2
Z9 2
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0025-5564
EI 1879-3134
J9 MATH BIOSCI
JI Math. Biosci.
PD DEC
PY 2014
VL 258
BP 85
EP 92
DI 10.1016/j.mbs.2014.09.010
PG 8
WC Biology; Mathematical & Computational Biology
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology
GA AZ1TN
UT WOS:000348020700009
PM 25262656
ER
PT J
AU Morissette, R
McDonnell, NB
Merke, DP
AF Morissette, Rachel
McDonnell, Nazli B.
Merke, Deborah P.
TI Tenascin-X gene defects and cardiovascular disease
SO MEDICAL HYPOTHESES
LA English
DT Letter
ID EHLERS-DANLOS-SYNDROME
C1 [Morissette, Rachel] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[McDonnell, Nazli B.] NIA, NIH, Baltimore, MD 21224 USA.
[Merke, Deborah P.] NIH, Ctr Clin, CRC, Bethesda, MD 20892 USA.
[Merke, Deborah P.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
RP Morissette, R (reprint author), NIH, Ctr Clin, Bethesda, MD 20892 USA.
EM dmerke@nih.gov
FU Intramural NIH HHS
NR 3
TC 0
Z9 0
U1 1
U2 3
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PD DEC
PY 2014
VL 83
IS 6
BP 844
EP 844
DI 10.1016/j.mehy.2014.01.027
PG 1
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AY5EJ
UT WOS:000347595600046
PM 24709065
ER
PT J
AU Li, QT
Zou, J
Wang, MJ
Ding, XL
Chepelev, I
Zhou, XK
Zhao, W
Wei, G
Cui, J
Zhao, KJ
Wang, HY
Wang, RF
AF Li, Qingtian
Zou, Jia
Wang, Mingjun
Ding, Xilai
Chepelev, Iouri
Zhou, Xikun
Zhao, Wei
Wei, Gang
Cui, Jun
Zhao, Keji
Wang, Helen Y.
Wang, Rong-Fu
TI Critical role of histone demethylase Jmjd3 in the regulation of CD4(+)
T-cell differentiation
SO NATURE COMMUNICATIONS
LA English
DT Article
ID EMBRYONIC STEM-CELLS; EPIGENETIC CONTROL; GENE-EXPRESSION;
MOLECULAR-MECHANISMS; TRANSCRIPTION FACTOR; MEDIATED REPRESSION; LINEAGE
COMMITMENT; HELPER TYPE-1; IMMUNE-SYSTEM; T(H)17 CELLS
AB Epigenetic factors have been implicated in the regulation of CD4(+) T-cell differentiation. Jmjd3 plays a role in many biological processes, but its in vivo function in T-cell differentiation remains unknown. Here we report that Jmjd3 ablation promotes CD4(+) T-cell differentiation into Th2 and Th17 cells in the small intestine and colon, and inhibits T-cell differentiation into Th1 cells under different cytokine-polarizing conditions and in a Th1-dependent colitis model. Jmjd3 deficiency also restrains the plasticity of the conversion of Th2, Th17 or Treg cells to Th1 cells. The skewing of T-cell differentiation is concomitant with changes in the expression of key transcription factors and cytokines. H3K27me3 and H3K4me3 levels in Jmjd3-deficient cells are correlated with altered gene expression through interactions with specific transcription factors. Our results identify Jmjd3 as an epigenetic factor in T-cell differentiation via changes in histone methylation and target gene expression.
C1 [Li, Qingtian; Zou, Jia; Wang, Mingjun; Ding, Xilai; Zhou, Xikun; Zhao, Wei; Cui, Jun; Wang, Helen Y.; Wang, Rong-Fu] Houston Methodist Res Inst, Ctr Inflammat & Epigenet, Houston, TX 77030 USA.
[Chepelev, Iouri] Cincinnati Childrens Hosp Med Ctr, Ctr Autoimmune Genom & Etiol, Cincinnati, OH 45229 USA.
[Wei, Gang] Chinese Acad Sci, Shanghai Inst Biol Sci, CAS MPG Partner Inst Computat Biol, Shanghai 200031, Peoples R China.
[Zhao, Keji] NHLBI, Syst Biol Ctr, NIH, Bethesda, MD 20892 USA.
RP Wang, RF (reprint author), Houston Methodist Res Inst, Ctr Inflammat & Epigenet, Houston, TX 77030 USA.
EM rwang3@tmhs.org
FU NIH [R01CA101795, R01CA090327]; GlaxoSmithKline
FX We thank Dr Alexander Rudensky (Sloan-Kettering Institute, NY) for the
Foxp3-GFP reporter mice, David Haviland (Houston Methodist Research
Institute) for his assistance with the FACS analysis, and Jana S.
Burchfield for editing the manuscript. This work is supported, in part,
by grants from the NIH (R01CA101795, R01CA090327) and GlaxoSmithKline.
NR 56
TC 21
Z9 21
U1 0
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2014
VL 5
AR 5780
DI 10.1038/ncomms6780
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AY5LI
UT WOS:000347613200001
PM 25531312
ER
PT J
AU Citrin, DE
Mitchell, JB
AF Citrin, Deborah E.
Mitchell, James B.
TI Altering the Response to Radiation: Sensitizers and Protectors
SO SEMINARS IN ONCOLOGY
LA English
DT Review
ID IN-VIVO RADIOSENSITIZATION; HUMAN TUMOR-CELLS; IONIZING-RADIATION;
RANDOMIZED-TRIAL; DNA-REPAIR; MOLECULAR-AGENTS; INDUCED FIBROSIS;
PROSTATE-CANCER; GENE-EXPRESSION; NORMAL-TISSUES
AB A number of agents are used clinically to enhance the efficacy of radiotherapy today, many of which are cytotoxic chemotherapies. Agents that enhance radiation induced tumor cell killing or protect normal tissues from the deleterious effects of ionizing radiation are collectively termed radiation modifiers. A significant effort in radiobiological research is geared towards describing and testing radiation modifiers with the intent of enhancing the therapeutic effects of radiation while minimizing normal tissue toxicity. In this review, we discuss the characteristics of these agents, the testing required to translate these agents into clinical trials, and highlight some challenges in these efforts. Published by Elsevier Inc.
C1 NCI, Radiat Oncol Branch, Bethesda, MD 20892 USA.
NCI, Radiat Biol Branch, Bethesda, MD 20892 USA.
RP Citrin, DE (reprint author), NCI, Sect Translat Radiat Oncol, Radiat Oncol Branch, Bethesda, MD 20892 USA.
EM citrind@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute.
NR 64
TC 3
Z9 3
U1 3
U2 9
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0093-7754
EI 1532-8708
J9 SEMIN ONCOL
JI Semin. Oncol.
PD DEC
PY 2014
VL 41
IS 6
BP 848
EP 859
DI 10.1053/j.seminoncol.2014.09.013
PG 12
WC Oncology
SC Oncology
GA AY6CQ
UT WOS:000347655600013
PM 25499642
ER
PT J
AU Snow, SJ
McGee, J
Miller, DB
Bass, V
Schladweiler, MC
Thomas, RF
Krantz, T
King, C
Ledbetter, AD
Richards, J
Weinstein, JP
Conner, T
Willis, R
Linak, WP
Nash, D
Wood, CE
Elmore, SA
Morrison, JP
Johnson, CL
Gilmour, MI
Kodavanti, UP
AF Snow, Samantha J.
McGee, John
Miller, Desinia B.
Bass, Virginia
Schladweiler, Mette C.
Thomas, Ronald F.
Krantz, Todd
King, Charly
Ledbetter, Allen D.
Richards, Judy
Weinstein, Jason P.
Conner, Teri
Willis, Robert
Linak, William P.
Nash, David
Wood, Charles E.
Elmore, Susan A.
Morrison, James P.
Johnson, Crystal L.
Gilmour, Matthew Ian
Kodavanti, Urmila P.
TI Inhaled Diesel Emissions Generated with Cerium Oxide Nanoparticle Fuel
Additive Induce Adverse Pulmonary and Systemic Effects
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE diesel exhaust; cerium oxide; cardiopulmonary; nanoparticle
ID SPRAGUE-DAWLEY RATS; OXIDATIVE STRESS; EXHAUST INHALATION; INTRATRACHEAL
INSTILLATION; PARTICULATE MATTER; PERIPHERAL-BLOOD; IMMUNE-RESPONSES;
EXPOSURE; PARTICLES; CELLS
AB Diesel exhaust (DE) exposure induces adverse cardiopulmonary effects. Cerium oxide nanoparticles added to diesel fuel (DECe) increases fuel burning efficiency but leads to altered emission characteristics and potentially altered health effects. Here, we evaluated whether DECe results in greater adverse pulmonary effects compared with DE. Male Sprague Dawley rats were exposed to filtered air, DE, or DECe for 5 h/day for 2 days. N-acetyl glucosaminidase activity was increased in bronchial alveolar lavage fluid (BALF) of rats exposed to DECe but not DE. There were also marginal but insignificant increases in several other lung injury biomarkers in both exposure groups (DECe>DE for all). To further characterize DECe toxicity, rats in a second study were exposed to filtered air or DECe for 5 h/day for 2 days or 4 weeks. Tissue analysis indicated a concentration-and time-dependent accumulation of lung and liver cerium followed by a delayed clearance. The gas-phase and high concentration of DECe increased lung inflammation at the 2-day time point, indicating that gas-phase components, in addition to particles, contribute to pulmonary toxicity. This effect was reduced at 4 weeks except for a sustained increase in BALF gamma-glutamyl transferase activity. Histopathology and transmission electron microscopy revealed increased alveolar septa thickness due to edema and increased numbers of pigmented macrophages after DECe exposure. Collectively, these findings indicate that DECe induces more adverse pulmonary effects on a mass basis than DE. In addition, lung accumulation of cerium, systemic translocation to the liver, and delayed clearance are added concerns to existing health effects of DECe.
C1 [Snow, Samantha J.; Miller, Desinia B.] Univ N Carolina, Curriculum Toxicol, Chapel Hill, NC 27599 USA.
[Snow, Samantha J.; McGee, John; Schladweiler, Mette C.; Thomas, Ronald F.; Krantz, Todd; King, Charly; Ledbetter, Allen D.; Richards, Judy; Gilmour, Matthew Ian; Kodavanti, Urmila P.] US EPA, Environm Publ Hlth Div, NHEERL, Res Triangle Pk, NC 27711 USA.
[Bass, Virginia] Univ N Carolina, Gillings Sch Publ Hlth, Dept Environm Sci & Engn, Chapel Hill, NC 27599 USA.
[Weinstein, Jason P.; Conner, Teri; Willis, Robert] US EPA, Environm Characterizat & Apportionment Branch, NERL, Res Triangle Pk, NC 27711 USA.
[Linak, William P.; Nash, David] US EPA, Air Pollut Prevent & Control Div, NRMRL, Res Triangle Pk, NC 27711 USA.
[Nash, David] Arcadis US Inc, Durham, NC 27713 USA.
[Wood, Charles E.] US EPA, Integrated Syst Toxicol Div, NHEERL, Res Triangle Pk, NC 27711 USA.
[Elmore, Susan A.] Natl Inst Environm Hlth Sci, Natl Toxicol Program Div, Res Triangle Pk, NC 27711 USA.
[Morrison, James P.; Johnson, Crystal L.] Pathol Associates Inc, Charles River Labs, Durham, NC 27703 USA.
RP Snow, SJ (reprint author), US EPA, Environm Publ Hlth Div, NHEERL, 109 TW Alexander Dr, Res Triangle Pk, NC 27711 USA.
EM snow.samantha@epa.gov
OI Bass, Virginia/0000-0001-6219-2448; Snow, Samantha/0000-0003-1812-8582
FU U.S. Environmental Protection Agency/University of North Carolina
Toxicology [CR835152010]; U.S. Environmental Protection Agency Senior
Environmental Employment Program; Division of the National Toxicology
Program of the National Institutes of Health
FX This work was supported by the U.S. Environmental Protection
Agency/University of North Carolina Toxicology Training Agreement
CR835152010 to S.J.S.; U.S. Environmental Protection Agency Senior
Environmental Employment Program to R.F.T.; and the Division of the
National Toxicology Program of the National Institutes of Health.
NR 66
TC 7
Z9 8
U1 2
U2 22
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2014
VL 142
IS 2
BP 403
EP 417
DI 10.1093/toxsci/kfu187
PG 15
WC Toxicology
SC Toxicology
GA AY5MZ
UT WOS:000347617800010
PM 25239632
ER
PT J
AU Ngalame, NNO
Tokar, EJ
Person, RJ
Waalkes, MP
AF Ngalame, Ntube N. O.
Tokar, Erik J.
Person, Rachel J.
Waalkes, Michael P.
TI Silencing KRAS Overexpression in Arsenic-Transformed Prostate Epithelial
and Stem Cells Partially Mitigates Malignant Phenotype
SO TOXICOLOGICAL SCIENCES
LA English
DT Article
DE arsenic; prostate cells; stem cells; shRNA; KRAS; cancer
ID RAS ONCOGENE ACTIVATION; MATRIX METALLOPROTEINASES; PANCREATIC-CANCER;
K-RAS; THERAPY; STEM/PROGENITOR; STATISTICS; KNOCKDOWN; MUTATIONS;
GROWTH
AB Inorganic arsenic is a human carcinogen that likely targets the prostate. Chronic arsenic exposure malignantly transforms the RWPE-1 human prostate epithelial line to chronic arsenic exposed-prostate epithelial (CAsE-PE) cells, and a derivative normal prostate stem cell (SC) line, WPE-stem to arsenic-cancer SCs (As-CSCs). The KRAS oncogene is highly overexpressed in CAsE-PE cells and activation precedes transformation, inferring mechanistic significance. As-CSCs also highly overexpress KRAS. Thus, we hypothesize KRAS activation is key in causing and maintaining an arsenic-induced malignant phenotype, and hence, KRAS knockdown (KD) may reverse this malignant phenotype. RNA interference using shRNAmirs to obtain KRAS KD was used in CAsE-PE and As-CSC cells. Cells analyzed 2 weeks post transduction showed KRAS protein decreased to 5% of control after KD, confirming stable KD. KRAS KD decreased phosphorylated ERK, indicating inhibition of RAS/ERK signaling, a proliferation/survival pathway activated with arsenic transformation. Secreted metalloproteinase (MMP) activity was increased by arsenic-induced malignant transformation, but KRAS KD from 4 weeks on decreased secreted MMP-9 activity by 50% in As-CSCs. Colony formation, a characteristic of cancer cells, was decreased in both KRAS KD transformants. KRAS KD also decreased the invasive capacity of both cell types. KRAS KD decreased proliferation in As-CSCs, consistent with loss of rapid tumor growth. Genes predicted to impact cell proliferation (eg, Cyclin D1, p16, and p21) changed accordingly in both KD cell types. Thus, KRAS silencing impacts aspects of arsenic-induced malignant phenotype, inducing loss of many typical cancer characteristics particularly in As-CSCs.
C1 [Ngalame, Ntube N. O.; Tokar, Erik J.; Person, Rachel J.; Waalkes, Michael P.] NIEHS, Inorgan Toxicol Grp, Natl Toxicol Program Lab, Div Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Waalkes, MP (reprint author), DNTP, Div Natl Toxicol Program, 111 TW Alexander Dr,MD E1-07, Res Triangle Pk, NC 27709 USA.
EM waalkes@niehs.nih.gov
FU National Institute of Environmental Health Sciences of the National
Institutes of Health (NIH); National Toxicology Program (NTP) [ES
102925]
FX The intramural program of the National Institute of Environmental Health
Sciences of the National Institutes of Health (NIH), and the National
Toxicology Program (NTP) under project ES 102925.
NR 36
TC 8
Z9 9
U1 1
U2 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1096-6080
EI 1096-0929
J9 TOXICOL SCI
JI Toxicol. Sci.
PD DEC
PY 2014
VL 142
IS 2
BP 489
EP 496
DI 10.1093/toxsci/kfu201
PG 8
WC Toxicology
SC Toxicology
GA AY5MZ
UT WOS:000347617800018
PM 25273566
ER
PT J
AU Kim, H
Hofstetter, CR
Hughes, S
Irvin, VL
Kang, S
Hovell, MF
AF Kim, Hyeongsu
Hofstetter, C. Richard
Hughes, Suzanne
Irvin, Veronica L.
Kang, Sunny
Hovell, Melbourne F.
TI Changes in and Factors Affecting Second-hand Smoke Exposure in
Nonsmoking Korean Americans in California: A Panel Study
SO ASIAN NURSING RESEARCH
LA English
DT Article
DE follow-up; immigrants; Korean Americans; second-hand smoke exposure
ID ENVIRONMENTAL TOBACCO-SMOKE; SECONDHAND SMOKE; UNITED-STATES; DESCENT;
ADULTS; ACCULTURATION; SEOUL
AB Purpose: We evaluated changes in and factors affecting second-hand smoke (SHS) exposure in a panel study of nonsmokers.
Methods: This study was based on data from a larger study of tobacco use among a representative sample of adults of Korean descent residing in California. Participants included 846 males and 1,399 females who were nonsmokers at baseline (2005-2006) and at follow-up (2007-2009). Participants were selected by probability sampling and were interviewed by telephone.
Results: At baseline, 50.0% were exposed to any SHS, and at follow-up 2 years later, 60.4% were exposed to any SHS (p < .001). SHS expbsure at baseline was associated with acculturation, employment, spousal smoking, and having a friend who smoked (p < .001). Employment, spousal smoking, and other family members smoking were associated with SHS at follow-up (p < .001). The odds ratio of SHS in the employed group declined from 2.01 at baseline to 1.53 at follow-up, that of the group having a smoking spouse increased from 1.88 to 2.36, and that of the group having other family members smoking increased from 1.20 to 1.69.
Conclusions: We showed that SHS exposure increased among Korean American nonsmokers in California, and the most important variables explaining the change in SHS exposure involved smoking among others with whom the subject is associated. These findings could be used as objective evidence for developing public health policies to reduce SHS exposure. Copyright (c) 2014, Korean Society of Nursing Science. Published by Elsevier. All rights reserved.
C1 [Kim, Hyeongsu] Konkuk Univ, Sch Med, Dept Prevent Med, Seoul 143701, South Korea.
[Hofstetter, C. Richard] San Diego State Univ, Grad Sch Publ Hlth, Dept Polit Sci, San Diego, CA 92182 USA.
[Hughes, Suzanne; Kang, Sunny; Hovell, Melbourne F.] San Diego State Univ, Grad Sch Publ Hlth, Ctr Behav Epidemiol & Community Hlth, San Diego, CA 92182 USA.
[Irvin, Veronica L.] NIH, Ctr Clin, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Irvin, Veronica L.] Off Behav & Social Sci Res, Bethesda, MD USA.
RP Kim, H (reprint author), Konkuk Univ, Sch Med, Dept Prevent Med, 120 Neungdong Ro, Seoul 143701, South Korea.
EM mubul@kku.ac.kr
NR 35
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 1976-1317
EI 2093-7482
J9 ASIAN NURS RES
JI Asian Nurs. Res.
PD DEC
PY 2014
VL 8
IS 4
BP 313
EP 318
DI 10.1016/j.anr.2014.07.004
PG 6
WC Nursing
SC Nursing
GA AZ1OO
UT WOS:000348008300012
PM 25529916
ER
PT J
AU Spagnolo, PA
Ramchandani, VA
Schwandt, ML
Zhang, LS
Blaine, SK
Usala, JM
Diamond, KA
Phillips, MJ
George, DT
Momenan, R
Heilig, M
AF Spagnolo, Primavera A.
Ramchandani, Vijay A.
Schwandt, Melanie L.
Zhang, Lishu
Blaine, Sara K.
Usala, Julie M.
Diamond, Kristie A.
Phillips, Monte J.
George, David T.
Momenan, Reza
Heilig, Markus
TI Effects of Naltrexone on Neural and Subjective Response to Alcohol in
Treatment-Seeking Alcohol-Dependent Patients
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Alcoholism; Dopamine; Ventral Striatum; Naltrexone; Opioid System
ID MU-OPIOID RECEPTOR; VENTRAL TEGMENTAL AREA; NUCLEUS-ACCUMBENS; DOPAMINE
RELEASE; CUE REACTIVITY; KNOCKOUT MICE; ETHANOL; REWARD; MECHANISMS; RAT
AB BackgroundPositively reinforcing properties of alcohol are in part mediated by activation of the ventral striatum (VS). Alcohol-induced release of endogenous opioids is thought to contribute to this response. Preclinical studies show that the opioid antagonist naltrexone (NTX) can block this cascade, but its ability to do so in treatment-seeking alcoholics has not been examined. Our objective was to study the effects of NTX on alcohol-induced VS activation and on amygdala response to affective stimuli in treatment-seeking alcohol-dependent inpatients.
MethodsSixty-three treatment-seeking alcoholics were randomized to receive NTX (50mg) or placebo (PLC) daily. On Day 7, participants underwent an alcohol cue reactivity session, and craving was measured using the Penn Alcohol Craving Scale. On Day 9, participants received a saline infusion followed by an alcohol infusion and also viewed affective stimuli in a magnetic resonance scanner.
ResultsIrrespective of medication treatment condition, the alcohol infusion did not activate the VS in the alcohol-dependent patients. Unexpectedly, VS activation was greater in NTX treated patients than in the PLC group. NTX treated patients also reported increased craving in response to alcohol cue exposure, and increased subjective response to alcohol (high and intoxicated) compared to PLC subjects. No significant effects of alcohol infusion on brain response to affective stimuli were in the NTX or PLC groups.
ConclusionsUnlike previous findings in social drinkers, a moderate level of intoxication did not activate the VS in treatment-seeking alcoholics. This is likely to reflect tolerance to the positively reinforcing properties of alcohol in this clinical population. Our findings may help explain the efficacy of NTX to reduce heavy drinking, but not to maintain abstinence.
C1 [Spagnolo, Primavera A.; Ramchandani, Vijay A.; Schwandt, Melanie L.; Zhang, Lishu; Blaine, Sara K.; Usala, Julie M.; Diamond, Kristie A.; Phillips, Monte J.; George, David T.; Momenan, Reza; Heilig, Markus] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
RP Spagnolo, PA (reprint author), NIAAA, Lab Clin & Translat Studies, NIH, Clin Res Ctr, Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM vera.spagnolo@nih.gov
RI Schwandt, Melanie/L-9866-2016;
OI Heilig, Markus/0000-0003-2706-2482
FU Division of Intramural Clinical and Biological Research, National
Institute on Alcohol Abuse and Alcoholism, National Institutes of Health
FX Supported by the Division of Intramural Clinical and Biological
Research, National Institute on Alcohol Abuse and Alcoholism, National
Institutes of Health. None of the authors has any conflict to disclose.
NR 50
TC 3
Z9 3
U1 0
U2 4
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 DEC
PY 2014
VL 38
IS 12
BP 3024
EP 3032
DI 10.1111/acer.12581
PG 9
WC Substance Abuse
SC Substance Abuse
GA AY4IN
UT WOS:000347541500019
PM 25581657
ER
PT J
AU Robinson, JC
Graham, BB
Rouault, TC
Tuder, RM
AF Robinson, Jeffrey C.
Graham, Brian B.
Rouault, Tracey C.
Tuder, Rubin M.
TI The Crossroads of Iron with Hypoxia and Cellular Metabolism Implications
in the Pathobiology of Pulmonary Hypertension
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Review
ID POSITRON-EMISSION-TOMOGRAPHY; ARTERIAL-HYPERTENSION; PLEXIFORM LESIONS;
CHUVASH POLYCYTHEMIA; REGULATORY PROTEIN-1; DISTRIBUTION WIDTH;
MESSENGER-RNA; HIF-ALPHA; DISEASE; DEFICIENCY
AB The pathologic hallmark of pulmonary arterial hypertension (PAH) is pulmonary vascular remodeling, characterized by endothelial cell proliferation, smooth muscle hypertrophy, and perivascular inflammation, ultimately contributing to increased pulmonary arterial pressures. Several recent studies have observed that iron deficiency in patients with various forms of PAH is associated with worsened clinical outcome. Iron plays a key role in many cellular processes regulating the response to hypoxia, oxidative stress, cellular proliferation, and cell metabolism. Given the potential importance of iron supplementation in patients with the disease and the broad cellular functions of iron, we review its role in processes that pertain to PAH.
C1 [Robinson, Jeffrey C.; Graham, Brian B.; Tuder, Rubin M.] Univ Colorado, Sch Med, Dept Med, Div Pulm Sci & Crit Care Med,Program Tradit Lung, Aurora, CO 80045 USA.
[Rouault, Tracey C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Mol Med, Bethesda, MD USA.
RP Robinson, JC (reprint author), Univ Colorado, Sch Med, Dept Med, Div Pulm Sci & Crit Care Med,Program Tradit Lung, Aurora, CO 80045 USA.
EM jeffrey.robinson@ucdenver.edu
FU NHLBI NIH HHS [K08 HL105536]
NR 92
TC 13
Z9 14
U1 0
U2 3
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1044-1549
EI 1535-4989
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD DEC
PY 2014
VL 51
IS 6
BP 721
EP 729
DI 10.1165/rcmb.2014-0021TR
PG 9
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA AY2KS
UT WOS:000347419700001
PM 24988529
ER
PT J
AU Martinu, T
Gowdy, KM
Nugent, JL
Sun, J
Kinnier, CV
Nelson, ME
Lyes, MA
Kelly, FL
Foster, WM
Gunn, MD
Palmer, SM
AF Martinu, Tereza
Gowdy, Kymberly M.
Nugent, Julia L.
Sun, Jesse
Kinnier, Christine V.
Nelson, Margaret E.
Lyes, Matthew A.
Kelly, Francine L.
Foster, W. Michael
Gunn, Michael D.
Palmer, Scott M.
TI Role of C-C Motif Ligand 2 and C-C Motif Receptor 2 in Murine Pulmonary
Graft-versus-Host Disease after Lipopolysaccharide Inhalations
SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
LA English
DT Article
DE graft-versus-host disease; lipopolysaccharide; dendritic cells; C-C
motif ligand 2; C-C motif receptor 2
ID CHEMOATTRACTANT PROTEIN-1 MCP-1; IDIOPATHIC PNEUMONIA SYNDROME;
STEM-CELL TRANSPLANTATION; INNATE IMMUNE ACTIVATION; DENDRITIC CELLS;
LUNG INJURY; AIRWAY HYPERRESPONSIVENESS; INHALED LIPOPOLYSACCHARIDE;
CHEMOKINE RECEPTOR-2; CCR2(-/-) MICE
AB Environmental exposures are a potential trigger of chronic pulmonary graft-versus-host disease (pGVHD) after successful recovery from hematopoietic cell transplant (HCT). We hypothesized that inhalations of LPS, a prototypic environmental stimulus, trigger pGVHD via increased pulmonary recruitment of donor-derived antigen-presenting cells (APCs) through the C-C motif ligand 2 (CCL2)-C-C motif receptor 2 (CCR2) chemokine axis. B10.BR(H2(k)) and C57BL/6(H2(b)) mice underwent allogeneic (Allo) or syngeneic (Syn) HCT with wild-type (WT) C57BL/6, CCL2(-/-), or CCR2(-/-) donors. After 4 weeks, recipient mice received daily inhaled LPS for 5 days and were killed at multiple time points. Allo mice exposed to repeated inhaled LPS developed prominent lymphocytic bronchiolitis, similar to human pGVHD. The increase in pulmonary T cells in Allo mice after LPS exposures was accompanied by increased CCL2, CCR2, and Type-1 T-helper cytokines as well as by monocytes and monocytederived dendritic cells (moDCs) compared with Syn and nontransplanted controls. Using CCL2(-/-) donors leads to a significant decrease in lungDCs but to only mildly reduced CD4 T cells. Using CCR2(-/-) donors significantly reduces lung DCs and moDCs but does not change T cells. CCL2 or CCR2 deficiency does not alter pGVHD pathology but increases airway hyperreactivity and IL-5 or IL-13 cytokines. Our results show that hematopoietic donor- derived CCL2 and CCR2 regulate recruitment of APCs to the Allo lung after LPS exposure. Although they do not alter pathologic pGVHD, their absence is associated with increased airway hyperreactivity and IL-5 and IL-13 cytokines. These results suggest that the APC changes that result from CCL2-CCR2 blockade may have unexpected effects on T cell differentiation and physiologic outcomes in HCT.
C1 [Martinu, Tereza; Nelson, Margaret E.; Lyes, Matthew A.; Kelly, Francine L.; Foster, W. Michael; Gunn, Michael D.; Palmer, Scott M.] Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA.
[Palmer, Scott M.] Duke Univ, Med Ctr, Duke Clin Res Inst, Durham, NC 27710 USA.
[Gowdy, Kymberly M.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
[Nugent, Julia L.; Sun, Jesse] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
[Kinnier, Christine V.] Massachusetts Gen Hosp, Dept Surg, Boston, MA 02114 USA.
RP Martinu, T (reprint author), Duke Univ, Med Ctr, DUMC Box 3221, Durham, NC 27710 USA.
EM tereza.martinu@duke.edu
FU National Institutes of Health [S10RR019145]
FX The authors thank Mr. Robert F. Beasley for help with lung DC isolation.
Flow cytometric sorting was performed in the Duke Human Vaccine
Institute Research Flow Cytometry Shared Resource Facility (Durham, NC)
supported by National Institutes of Health grant S10RR019145.
NR 36
TC 1
Z9 1
U1 0
U2 3
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1044-1549
EI 1535-4989
J9 AM J RESP CELL MOL
JI Am. J. Respir. Cell Mol. Biol.
PD DEC
PY 2014
VL 51
IS 6
BP 810
EP 821
DI 10.1165/rcmb.2013-0451OC
PG 12
WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System
GA AY2KS
UT WOS:000347419700010
PM 24921973
ER
PT J
AU Leja, M
You, WC
Camargo, MC
Saito, H
AF Leja, Marcis
You, Weicheng
Camargo, M. Constanza
Saito, Hiroshi
TI Implementation of gastric cancer screening - The global experience
SO BEST PRACTICE & RESEARCH IN CLINICAL GASTROENTEROLOGY
LA English
DT Article
DE Biomarkers; Gastric cancer; Helicobacter pylori; Precancerous lesions;
Screening
ID HELICOBACTER-PYLORI ERADICATION; SERUM PEPSINOGEN; STOMACH-CANCER;
HIGH-RISK; COST-EFFECTIVENESS; FOLLOW-UP; PRECANCEROUS LESIONS;
MULTIPLEX SEROLOGY; GENE POLYMORPHISMS; CHINESE POPULATION
AB Gastric cancer (GC) is still an important global healthcare problem, and in absolute figures it is going to remain at the present level in foreseeable future. In general, survival' of patients with GC is poor mainly due to advanced-stage diagnosis. Early-stage GC can be cured by endoscopic resection or less invasive surgical treatment. Unfortunately, there is no appropriate screening strategy available for global application. This article provides a description of established national and regional GC screening programs and the screening modalities used. This review also summarizes current approaches to develop cancer-screening biomarkers. Although candidates with initial promising results have been suggested, moving discovery into clinical practice is still a major challenge. Well-designed biomarker studies, with systematic validation steps, are needed to decrease the burden of this fatal disease. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Leja, Marcis] Univ Latvia, Fac Med, LV-1006 Riga, Latvia.
[You, Weicheng] Peking Univ Canc Hosp & Inst, Dept Canc Epidemiol, Key Lab Carcinogenesis & Translat Res, Minist Educ, Beijing 100142, Peoples R China.
[Camargo, M. Constanza] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Saito, Hiroshi] Natl Canc Ctr, Res Ctr Canc Prevent & Detect, Canc Screening Assessment & Management Div, Tokyo 1040045, Japan.
RP Leja, M (reprint author), Univ Latvia, Fac Med, 6 Linezera Iela, LV-1006 Riga, Latvia.
EM cei@latnet.lv; weichengyou@yahoo.com; camargomc@mail.nih.gov;
hrsaito@ncc.go.jp
RI Camargo, M. Constanza/R-9891-2016
FU National Research Program in Public Health priority [4]
FX ML has been supported in part for writing of the manuscript from the
project No. 4 'Evaluation of the possibilities to decrease the gastric
cancer caused mortality in Latvia' within the National Research Program
in Public Health priority.
NR 95
TC 8
Z9 9
U1 1
U2 12
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1521-6918
EI 1532-1916
J9 BEST PRACT RES CL GA
JI Best Pract. Res. Clin. Gastroenterol.
PD DEC
PY 2014
VL 28
IS 6
BP 1093
EP 1106
DI 10.1016/j.bpg.2014.09.005
PG 14
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AY1PK
UT WOS:000347364500013
PM 25439074
ER
PT J
AU Soubias, O
Teague, WE
Hines, KG
Gawrisch, K
AF Soubias, Olivier
Teague, Walter E.
Hines, Kirk G.
Gawrisch, Klaus
TI The role of membrane curvature elastic stress for function of
rhodopsin-like G protein-coupled receptors
SO BIOCHIMIE
LA English
DT Review
DE G protein-coupled membrane receptor; Rhodopsin; Membrane; Lipid;
Cholesterol
ID ACTIVATION; TRANSDUCIN; NETWORKS; SEQUENCE; DISTANCE; BILAYERS
AB The human genome encodes about 800 different G protein-coupled receptors (GPCR). They are key molecules in signal transduction pathways that transmit signals of a variety of ligands such as hormones and neurotransmitters to the cell interior. Upon ligand binding, the receptors undergo structural transitions that either enhance or inhibit transmission of a specific signal to the cell interior. Here we discuss results which indicate that transmission of such signals can be strongly modulated by the composition of the lipid matrix into which GPCR are imbedded. Experimental results have been obtained on rhodopsin, a prototype GPCR whose structure and function is representative for the great majority of GPCR in humans. The data shed light on the importance of curvature elastic stress in the lipid domain for function of GPCR. (C) Published by Elsevier B.V.
C1 [Soubias, Olivier; Teague, Walter E.; Hines, Kirk G.; Gawrisch, Klaus] Natl Inst Alcohol & Alcoholism, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD 20892 USA.
RP Gawrisch, K (reprint author), Natl Inst Alcohol & Alcoholism, Lab Membrane Biochem & Biophys, NIH, Bethesda, MD 20892 USA.
EM klausg@mail.nih.gov
FU Intramural Research Program of the National Institute on Alcohol Abuse
and Alcoholism, National Institutes of Health
FX This work was supported by the Intramural Research Program of the
National Institute on Alcohol Abuse and Alcoholism, National Institutes
of Health.
NR 28
TC 5
Z9 5
U1 2
U2 21
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0300-9084
EI 1638-6183
J9 BIOCHIMIE
JI Biochimie
PD DEC
PY 2014
VL 107
BP 28
EP 32
DI 10.1016/j.biochi.2014.10.011
PN A
PG 5
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AY6FA
UT WOS:000347661500006
PM 25447139
ER
PT J
AU Natarajan, B
Salahuddin, T
Sadek, A
Dave, J
Nanda, N
Le, B
Reddy, A
Gelfand, J
Mehta, N
AF Natarajan, B.
Salahuddin, T.
Sadek, A.
Dave, J.
Nanda, N.
Le, B.
Reddy, A.
Gelfand, J.
Mehta, N.
TI In vivo characterization of vascular diseases in psoriasis through
implementation of a multimodal imaging program
SO BRITISH JOURNAL OF DERMATOLOGY
LA English
DT Meeting Abstract
CT 7th International Congress of Psoriasis - From Gene to Clinic
CY DEC 11-13, 2014
CL London, ENGLAND
C1 [Natarajan, B.; Salahuddin, T.; Sadek, A.; Dave, J.; Nanda, N.; Le, B.; Reddy, A.; Mehta, N.] NIH, Bethesda, MD 20892 USA.
[Gelfand, J.] Univ Penn, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-0963
EI 1365-2133
J9 BRIT J DERMATOL
JI Br. J. Dermatol.
PD DEC
PY 2014
VL 171
IS 6
MA FC24
BP E116
EP E116
PG 1
WC Dermatology
SC Dermatology
GA AX9QD
UT WOS:000347236100025
ER
PT J
AU Filer, D
Patisaul, HB
Schug, T
Reif, D
Thayer, K
AF Filer, Dayne
Patisaul, Heather B.
Schug, Thaddeus
Reif, David
Thayer, Kristina
TI Test driving ToxCast: endocrine profiling for 1858 chemicals included in
phase II
SO CURRENT OPINION IN PHARMACOLOGY
LA English
DT Article
ID PROTECTION
AB Identifying chemicals, beyond those already implicated, to test for potential endocrine disruption is a challenge and high throughput approaches have emerged as a potential tool for this type of screening. This review focused the Environmental Protection Agency's (EPA) ToxCast (TM) high throughput in vitro screening (HTS) program. Utility for identifying compounds was assessed and reviewed by using it to run the recently expanded chemical library (from 309 compounds to 1858) through the ToxPi (TM) prioritization scheme for endocrine disruption. The analysis included metabolic and neuroendocrine targets. This investigative approach simultaneously assessed the utility of ToxCast, and helped identify novel chemicals which may have endocrine activity. Results from this exercise suggest the spectrum of environmental chemicals with potential endocrine activity is much broader than indicated, and that some aspects of endocrine disruption are not fully covered in ToxCast.
C1 [Filer, Dayne] US EPA, Natl Ctr Computat Toxicol, Off Res & Dev, Res Triangle Pk, NC 27709 USA.
[Patisaul, Heather B.] N Carolina State Univ, Dept Biol Sci, Ctr Human Hlth & Environm, Raleigh, NC 27695 USA.
[Schug, Thaddeus] NIEHS, Div Extramural Res, NIH, Dept Hlth & Human Serv, Morrisville, NC 27560 USA.
[Reif, David] N Carolina State Univ, Bioinformat Res Ctr, Dept Biol Sci, Raleigh, NC 27695 USA.
[Thayer, Kristina] NIEHS, Off Hlth Assessment & Translat, Div Natl Toxicol Program, NIH,Dept Hlth & Human Serv, Morrisville, NC 27560 USA.
RP Thayer, K (reprint author), NIEHS, Off Hlth Assessment & Translat, Div Natl Toxicol Program, NIH,Dept Hlth & Human Serv, 530 Davis Dr,Room 2150 Mail Drop K2-04, Morrisville, NC 27560 USA.
EM thayer@niehs.nih.gov
OI Reif, David/0000-0001-7815-6767
FU Intramural NIH HHS [ZIA ES103226-01]
NR 16
TC 13
Z9 13
U1 3
U2 14
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1471-4892
EI 1471-4973
J9 CURR OPIN PHARMACOL
JI Curr. Opin. Pharmacol.
PD DEC
PY 2014
VL 19
BP 145
EP 152
DI 10.1016/j.coph.2014.09.021
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AY3UO
UT WOS:000347508000023
PM 25460227
ER
PT J
AU Shaughnessy, DT
McAllister, K
Worth, L
Haugen, AC
Meyer, JN
Domann, FE
Van Houten, B
Mostoslavsky, R
Bultman, SJ
Baccarelli, AA
Begley, TJ
Sobol, RW
Hirschey, MD
Ideker, T
Santos, JH
Copeland, WC
Tice, RR
Balshaw, DM
Tyson, FL
AF Shaughnessy, Daniel T.
McAllister, Kimberly
Worth, Leroy
Haugen, Astrid C.
Meyer, Joel N.
Domann, Frederick E.
Van Houten, Bennett
Mostoslavsky, Raul
Bultman, Scott J.
Baccarelli, Andrea A.
Begley, Thomas J.
Sobol, Robert W.
Hirschey, Matthew D.
Ideker, Trey
Santos, Janine H.
Copeland, William C.
Tice, Raymond R.
Balshaw, David M.
Tyson, Frederick L.
TI Mitochondria, Energetics, Epigenetics, and Cellular Responses to Stress
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Review
ID DNA COPY NUMBER; PLURIPOTENT STEM-CELLS; COLON-CARCINOMA CELLS;
ENERGY-METABOLISM; EXCISION-REPAIR; OXIDATIVE-PHOSPHORYLATION;
ATAXIA-TELANGIECTASIA; HISTONE ACETYLATION; BUTYRATE METABOLISM; CANCER
METABOLISM
AB Background: Cells respond to environmental stressors through several key pathways, including response to reactive oxygen species (ROS), nutrient and ATP sensing, DNA damage response (DDR), and epigenetic alterations. Mitochondria play a central role in these pathways not only through energetics and ATP production but also through metabolites generated in the tricarboxylic acid cycle, as well as mitochondria-nuclear signaling related to mitochondria morphology, biogenesis, fission/fusion, mitophagy, apoptosis, and epigenetic regulation.
Objectives: We investigated the concept of bidirectional interactions between mitochondria and cellular pathways in response to environmental stress with a focus on epigenetic regulation, and we examined DNA repair and DDR pathways as examples of biological processes that respond to exogenous insults through changes in homeostasis and altered mitochondrial function.
Methods: The National Institute of Environmental Health Sciences sponsored the Workshop on Mitochondria, Energetics, Epigenetics, Environment, and DNA Damage Response on 25-26 March 2013. Here, we summarize key points and ideas emerging from this meeting.
Discussion: A more comprehensive understanding of signaling mechanisms (cross-talk) between the mitochondria and nucleus is central to elucidating the integration of mitochondrial functions with other cellular response pathways in modulating the effects of environmental agents. Recent studies have highlighted the importance of mitochondrial functions in epigenetic regulation and DDR with environmental stress. Development and application of novel technologies, enhanced experimental models, and a systems-type research approach will help to discern how environmentally induced mitochondrial dysfunction affects key mechanistic pathways.
Conclusions: Understanding mitochondria-cell signaling will provide insight into individual responses to environmental hazards, improving prediction of hazard and susceptibility to environmental stressors.
C1 [Shaughnessy, Daniel T.; McAllister, Kimberly; Worth, Leroy; Haugen, Astrid C.; Balshaw, David M.; Tyson, Frederick L.] NIEHS, Div Extramural Res & Training, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
[Meyer, Joel N.] Duke Univ, Nicholas Sch Environm, Durham, NC 27708 USA.
[Domann, Frederick E.] Univ Iowa, Carver Coll Med, Dept Radiat Oncol, Free Radical & Radiat Biol Program, Iowa City, IA USA.
[Van Houten, Bennett; Sobol, Robert W.] Univ Pittsburgh, Inst Canc, Hillman Canc Ctr, Pittsburgh, PA USA.
[Mostoslavsky, Raul] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Canc, Boston, MA USA.
[Bultman, Scott J.] Univ N Carolina, Dept Genet, Chapel Hill, NC USA.
[Baccarelli, Andrea A.] Harvard Univ, Sch Publ Hlth, Exposure Epidemiol & Risk Program, Lab Environm Epigenet, Boston, MA 02115 USA.
[Begley, Thomas J.] SUNY Albany, Coll Nanoscale Sci & Engn, Albany, NY 12222 USA.
[Sobol, Robert W.] Univ Pittsburgh, Sch Med, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA.
[Hirschey, Matthew D.] Duke Univ, Med Ctr, Durham, NC USA.
[Ideker, Trey] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA.
[Ideker, Trey] Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA.
[Santos, Janine H.] NIEHS, Mol Carcinogenesis Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Copeland, William C.] NIEHS, Mol Genet Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Tice, Raymond R.] NIEHS, Biomol Screening Branch, Div Natl Toxicol Program, NIH,DHHS, Res Triangle Pk, NC 27709 USA.
RP Shaughnessy, DT (reprint author), NIEHS, Div Extramural Res & Training, MD K3-12,POB 12233, Res Triangle Pk, NC 27709 USA.
EM shaughn1@niehs.nih.gov
OI Baccarelli, Andrea/0000-0002-3436-0640; Domann,
Frederick/0000-0002-0489-2179
FU NIA NIH HHS [R01 AG045351]; NIEHS NIH HHS [R01 ES017540, P30 ES005605,
P42 ES010356]
NR 105
TC 35
Z9 35
U1 7
U2 55
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
EI 1552-9924
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD DEC
PY 2014
VL 122
IS 12
BP 1271
EP 1278
DI 10.1289/ehp.1408418
PG 8
WC Environmental Sciences; Public, Environmental & Occupational Health;
Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
Health; Toxicology
GA AY1YC
UT WOS:000347384600012
PM 25127496
ER
PT J
AU Chia, R
Haddock, S
Beilina, A
Rudenko, IN
Mamais, A
Kaganovich, A
Li, Y
Kumaran, R
Nalls, MA
Cookson, MR
AF Chia, Ruth
Haddock, Sara
Beilina, Alexandra
Rudenko, Iakov N.
Mamais, Adamantios
Kaganovich, Alice
Li, Yan
Kumaran, Ravindran
Nalls, Michael A.
Cookson, Mark R.
TI Phosphorylation of LRRK2 by casein kinase 1 alpha regulates trans-Golgi
clustering via differential interaction with ARHGEF7
SO NATURE COMMUNICATIONS
LA English
DT Article
ID PARKINSONS-DISEASE; CYTOPLASMIC LOCALIZATION; 14-3-3 BINDING; PROTEIN;
INHIBITION; MUTATION; MUTANT; RISK
AB LRRK2, a gene relevant to Parkinson's disease, encodes a scaffolding protein with both GTPase and kinase activities. LRRK2 protein is itself phosphorylated and therefore is subject to regulation by cell signalling; however, the kinase(s) responsible for this event have not been definitively identified. Here using an unbiased siRNA kinome screen, we identify and validate casein kinase 1 alpha (CK1 alpha) as being responsible for LRRK2 phosphorylation, including in the adult mouse striatum. We further show that LRRK2 recruitment to TGN46-positive Golgi-derived vesicles is modulated by constitutive LRRK2 phosphorylation by CK1 alpha. These effects are mediated by differential protein interactions of LRRK2 with a guanine nucleotide exchange factor, ARHGEF7. These pathways are therefore likely involved in the physiological maintenance of the Golgi in cells, which may play a role in the pathogenesis of Parkinson's disease.
C1 [Chia, Ruth; Haddock, Sara; Beilina, Alexandra; Rudenko, Iakov N.; Mamais, Adamantios; Kaganovich, Alice; Kumaran, Ravindran; Cookson, Mark R.] NIA, Cell Biol & Gene Express Sect, Neurogenet Lab, Bethesda, MD 20892 USA.
[Nalls, Michael A.] NIA, Mol Genet Sect, Neurogenet Lab, Bethesda, MD 20892 USA.
[Li, Yan] NINDS, Peptide Sequencing Facil, NIH, Bethesda, MD 20892 USA.
RP Cookson, MR (reprint author), NIA, Cell Biol & Gene Express Sect, Neurogenet Lab, 35 Convent Dr, Bethesda, MD 20892 USA.
EM cookson@mail.nih.gov
FU National Institute on Aging, National Institutes of Health;
Bachmann-Strauss Dystonia and Parkinson Foundation REP
FX This work was supported by the Intramural Research Programme of the
National Institute on Aging, National Institutes of Health and the
Bachmann-Strauss Dystonia and Parkinson Foundation RFP 2012. We thank
our laboratory colleagues for their support, advice and critical reading
of the manuscript. We would also like to thank Dr Jean-Marc Taymans,
Leuven, for the gift of stable FLAG-tagged LRRK2 cell lines and Dr Dario
Alessi, Dundee, for antibodies and access to LRRK2-IN1.
NR 43
TC 16
Z9 16
U1 2
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2014
VL 5
AR 5827
DI 10.1038/ncomms6827
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AY5LU
UT WOS:000347614400002
PM 25500533
ER
PT J
AU Maleth, J
Choi, S
Muallem, S
Ahuja, M
AF Maleth, Jozsef
Choi, Seok
Muallem, Shmuel
Ahuja, Malini
TI Translocation between PI(4,5)P-2-poor and PI(4,5)P-2-rich microdomains
during store depletion determines STIM1 conformation and Orai1 gating
SO NATURE COMMUNICATIONS
LA English
DT Article
ID FAST CA2+-DEPENDENT INACTIVATION; STROMAL INTERACTION MOLECULE-1; CRAC
CHANNELS; CALCIUM-ENTRY; DOMAIN; ACTIVATION; PROTEINS; ER;
PHOSPHOINOSITIDES; STIM1-ORAI1
AB The Orai1-STIM1 current undergoes slow Ca2+-dependent inactivation (SCDI) mediated by the binding of SARAF to STIM1. Here we report the use of SCDI by SARAF as a probe of the conformation and microdomain localization of the Orai1-STIM1 complex. We find that the interaction of STIM1 with Orai1 carboxyl terminus (C terminus) and the STIM1 K-domain are required for the interaction of SARAF with STIM1 and SCDI. STIM1-Orai1 must be in a PM/ER microdomain tethered by E-Syt1, stabilized by septin4 and enriched in PI(4,5)P-2 for STIM1-SARAF interaction. Targeting STIM1 to PI(4,5)P-2-rich and -poor microdomains reveals that SARAF-dependent SCDI is observed only when STIM1-Orai1 are within the PI(4,5)P-2-rich microdomain. Notably, store depletion results in transient localization of STIM1-Orai1 in the PI(4,5)P-2-poor microdomain, which then translocates to the PI(4,5)P-2-rich domain. These findings reveal the role of PM/ER tethers in the regulation of Orai1 function and a mode of regulation by PI(4,5)P-2 involving translocation between PI(4,5)P-2 microdomains.
C1 [Maleth, Jozsef; Choi, Seok; Muallem, Shmuel; Ahuja, Malini] NIDCR, Epithelial Signaling & Transport Sect, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
[Maleth, Jozsef] Univ Szeged, Dept Med 1, H-6725 Szeged, Hungary.
[Choi, Seok] Chosun Univ, Coll Med, Dept Physiol, Chosun 501375, South Korea.
RP Muallem, S (reprint author), NIDCR, Epithelial Signaling & Transport Sect, Mol Physiol & Therapeut Branch, NIH, Bethesda, MD 20892 USA.
EM shmuel.muallem@nih.gov
FU NIH/NIDCR intramural grant [DE000735]
FX We thank Drs Pietro De Camilli (Yale) for providing the E-Syt1, E-Syt2
and E-Syt3 plasmids and Jen Liou (UT Southwestern Medical center,
Dallas) for providing E-Syt1. We thank Dr Tamas Balla for valuable
discussions and suggestions and for providing the PI(4,5)P2
depletion system. This work was supported by the NIH/NIDCR intramural
grant DE000735 to S. M.
NR 39
TC 21
Z9 21
U1 0
U2 6
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2014
VL 5
AR 5843
DI 10.1038/ncomms6843
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AY6NF
UT WOS:000347682200004
PM 25517631
ER
PT J
AU Yong, RL
Yang, CZ
Lu, J
Wang, HE
Schlaff, CD
Tandle, A
Graves, CA
Elkahloun, AG
Chen, XY
Zhuang, ZP
Lonser, RR
AF Yong, Raymund L.
Yang, Chunzhang
Lu, Jie
Wang, Huaien
Schlaff, Cody D.
Tandle, Anita
Graves, Christian A.
Elkahloun, Abdel G.
Chen, Xiaoyuan
Zhuang, Zhengping
Lonser, Russell R.
TI Cell transcriptional state alters genomic patterns of DNA double-strand
break repair in human astrocytes
SO NATURE COMMUNICATIONS
LA English
DT Article
ID RECURRENT CHROMOSOMAL TRANSLOCATIONS; CHILDHOOD-CANCER SURVIVOR;
SPINAL-CORD-INJURY; GENE FUSIONS; IONIZING-RADIATION; REACTIVE GLIOSIS;
GLIAL-CELLS; EXPRESSION; GAMMA-H2AX; GLIOBLASTOMA
AB The misrepair of DNA double-strand breaks in close spatial proximity within the nucleus can result in chromosomal rearrangements that are important in the pathogenesis of haematopoietic and solid malignancies. It is unknown why certain epigenetic states, such as those found in stem or progenitor cells, appear to facilitate neoplastic transformation. Here we show that altering the transcriptional state of human astrocytes alters patterns of DNA damage repair from ionizing radiation at a gene locus-specific and genome-wide level. Astrocytes induced into a reactive state exhibit increased DNA repair, compared with non-reactive cells, in actively transcribed chromatin after irradiation. In mapping these repair sites, we identify misrepair events and repair hotspots that are unique to each state. The precise characterization of genomic regions susceptible to mutation in specific transcriptional states provides new opportunities for addressing clonal evolution in solid cancers, in particular those where double-strand break induction is a cornerstone of clinical intervention.
C1 [Yong, Raymund L.; Wang, Huaien] Icahn Sch Med Mt Sinai, Dept Neurosurg, New York, NY 10029 USA.
[Yong, Raymund L.; Yang, Chunzhang; Lu, Jie; Zhuang, Zhengping; Lonser, Russell R.] NINDS, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA.
[Lu, Jie; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
[Schlaff, Cody D.; Tandle, Anita; Graves, Christian A.] NCI, Radiat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Elkahloun, Abdel G.] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Lonser, Russell R.] Ohio State Univ, Wexner Med Ctr, Dept Neurol Surg, Columbus, OH 43210 USA.
RP Yong, RL (reprint author), Icahn Sch Med Mt Sinai, Dept Neurosurg, 1463 Madison Ave,Box 1136, New York, NY 10029 USA.
EM raymund.yong@mountsinai.org; russell.lonser@osumc.edu
FU NINDS; NCI; NHGRI; Radiology and Imaging Sciences Department, NIH
Clinical Center; NIBIB
FX We thank P. Gallant, I. Gordon, R. Hanson, B. Ikejiri, S. Pack and K.
Camphausen for discussions and support, and K. Johnson for
bioinformatics assistance. This work was funded by the Intramural
Research Programs of NINDS, NCI and NHGRI. J.L. is in an Imaging
Sciences Training Fellowship jointly supported by the Radiology and
Imaging Sciences Department, NIH Clinical Center and the Intramural
Research Program of NIBIB.
NR 56
TC 4
Z9 5
U1 1
U2 12
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2014
VL 5
AR 5799
DI 10.1038/ncomms6799
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AY5LL
UT WOS:000347613500005
PM 25517576
ER
PT J
AU Metti, AL
Yaffe, K
Boudreau, RM
Simonsick, EM
Carnahan, RM
Satterfield, S
Harris, TB
Ayonayon, HN
Rosano, C
Cauley, JA
AF Metti, Andrea L.
Yaffe, Kristine
Boudreau, Robert M.
Simonsick, Eleanor M.
Carnahan, Ryan M.
Satterfield, Suzanne
Harris, Tamara B.
Ayonayon, Hilsa N.
Rosano, Caterina
Cauley, Jane A.
CA Hlth ABC Study
TI Trajectories of inflammatory markers and cognitive decline over 10 years
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Inflammatory markers; Cognitive decline; C-reactive protein;
Interleukin-6
ID C-REACTIVE PROTEIN; ALZHEIMERS-DISEASE; OLDER-ADULTS; CARDIOVASCULAR
HEALTH; HEART-DISEASE; RISK; DEMENTIA; ATHEROSCLEROSIS; INTERLEUKIN-6;
ASSOCIATION
AB We aimed to examine trajectories of inflammatory markers and cognitive decline over 10 years. Cox proportional hazards models were used to examine the association between interleukin-6 and C-reactive protein (CRP) trajectory components (slope, variability, and baseline level) and cognitive decline among 1323 adults, aged 70-79 years in the Health, Aging, and Body Composition Study. We tested for interactions by sex and apolipoprotein E (APOE) genotype. In models adjusted for multiple covariates and comorbidities, extreme CRP variability was significantly associated with cognitive decline (hazard ratio [HR] 1.6, 95% confidence interval [CI]: 1.1-2.3). This association was modified by sex and APOE e4 (p < 0.001 for both), such that the association remained among women (HR = 1.8; 95% CI: 1.1, 3.0) and among those with no APOE e4 allele (HR = 1.6; 95% CI: 1.1, 2.5). There were no significant associations between slope or baseline level of CRP and cognitive decline nor between interleukin-6 and cognitive decline. We believe CRP variability likely reflects poor control of or greater changes in vascular or metabolic disease over time, which in turn is associated with cognitive decline. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Metti, Andrea L.; Boudreau, Robert M.; Rosano, Caterina; Cauley, Jane A.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15213 USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Yaffe, Kristine] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Yaffe, Kristine; Ayonayon, Hilsa N.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Simonsick, Eleanor M.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Carnahan, Ryan M.] Univ Iowa, Coll Publ Hlth, Dept Epidemiol, Iowa City, IA USA.
[Satterfield, Suzanne] Univ Tennessee, Dept Prevent Med, Memphis, TN USA.
[Harris, Tamara B.] NIA, Lab Epidemiol & Populat Sci, Intramural Res Program, Bethesda, MD 20892 USA.
RP Metti, AL (reprint author), Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Ctr Aging & Populat Hlth, 130 N Bellefield,Fourth Floor 456, Pittsburgh, PA 15213 USA.
EM alw111@pitt.edu
RI Cauley, Jane/N-4836-2015;
OI Cauley, Jane/0000-0003-0752-4408; Rosano, Caterina/0000-0002-0909-1506;
Rosano, Caterina/0000-0002-4271-6010; Boudreau,
Robert/0000-0003-0162-5187; Carnahan, Ryan/0000-0002-7478-4739
FU National Institute on Aging [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106, R01-AG028050]; R01-AG028050 [R01-NR012459]; Intramural
Research Program on the National Institutes of Health, National
Institute on Aging; National Institutes of Health Training Grant
[2T32AG000181]
FX This work was supported by National Institute on Aging Contracts
N01-AG-6-2101; N01-AG-6-2103; N01-AG-6-2106; National Institute on Aging
grant R01-AG028050 and National Institute of Nursing Research grant
R01-NR012459. This research was supported in part by the Intramural
Research Program on the National Institutes of Health, National
Institute on Aging. Andrea Metti is supported by a National Institutes
of Health Training Grant 2T32AG000181. Andrea Metti would like to
acknowledge Dr Mary Ganguli and Dr Oscar Lopez who both provided
invaluable feedback and advice on this manuscript over multiple phases
of its developments.
NR 33
TC 5
Z9 5
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD DEC
PY 2014
VL 35
IS 12
BP 2785
EP 2790
DI 10.1016/j.neurobiolaging.2014.05.030
PG 6
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AX9PB
UT WOS:000347233200013
PM 24997674
ER
PT J
AU Borghero, G
Pugliatti, M
Marrosu, F
Marrosu, MG
Murru, MR
Floris, G
Cannas, A
Parish, LD
Occhineri, P
Cau, TB
Loi, D
Ticca, A
Traccis, S
Manera, U
Canosa, A
Moglia, C
Calvo, A
Barberis, M
Brunetti, M
Pliner, HA
Renton, AE
Nalls, MA
Traynor, BJ
Restagno, G
Chio, A
AF Borghero, Giuseppe
Pugliatti, Maura
Marrosu, Francesco
Marrosu, Maria Giovanna
Murru, Maria Rita
Floris, Gianluca
Cannas, Antonino
Parish, Leslie D.
Occhineri, Patrizia
Cau, Tea B.
Loi, Daniela
Ticca, Anna
Traccis, Sebastiano
Manera, Umberto
Canosa, Antonio
Moglia, Cristina
Calvo, Andrea
Barberis, Marco
Brunetti, Maura
Pliner, Hannah A.
Renton, Alan E.
Nalls, Mike A.
Traynor, Bryan J.
Restagno, Gabriella
Chio, Adriano
CA ITALSGEN & SARDINALS Consortia
TI Genetic architecture of ALS in Sardinia
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Amyotrophic lateral sclerosis; Sardinia; Phenotype; Genetics;
Penetrance; Prognosis
ID AMYOTROPHIC-LATERAL-SCLEROSIS; HEXANUCLEOTIDE REPEAT EXPANSION; TARDBP
GENE; C9ORF72; MUTATIONS; FTD
AB Conserved populations, such as Sardinians, displaying elevated rates of familial or sporadic amyotrophic lateral sclerosis (ALS) provide unique information on the genetics of the disease. Our aim was to describe the genetic profile of a consecutive series of ALS patients of Sardinian ancestry. All ALS patients of Sardinian ancestry, identified between 2008 and 2013 through the Italian ALS Genetic Consortium, were eligible to be included in the study. Patients and controls underwent the analysis of TARDBP, C9ORF72, SOD1, and FUS genes. Genetic mutations were identified in 155 out of 375 Sardinian ALS cases (41.3%), more commonly the p.A382T and p.G295S mutations of TARDBP and the GGGGCC hexanucleotide repeat expansion of C9ORF72. One patient had both p.G295S and p.A382T mutations of TARDBP and 8 carried both the heterozygous p.A382T mutation of TARDBP and a repeat expansion of C9ORF72. Patients carrying the p.A382T and the p.G295S mutations of TARDBP and the C9ORF72 repeat expansion shared distinct haplotypes across these loci. Patients with cooccurrence of C9ORF72 and TARDBP p.A382T missense mutation had a significantly lower age at onset and shorter survival. More than 40% of all cases on the island of Sardinia carry a mutation of an ALS-related gene, representing the highest percentage of ALS cases genetically explained outside of Scandinavia. Clinical phenotypes associated with different genetic mutations show some distinctive characteristics, but the heterogeneity between and among families carrying the same mutations implies that ALS manifestation is influenced by other genetic and nongenetic factors. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Borghero, Giuseppe; Marrosu, Francesco; Floris, Gianluca; Cannas, Antonino] Azienda Univ Osped Cagliari, Dept Neurol, Cagliari, Italy.
[Borghero, Giuseppe; Marrosu, Francesco; Floris, Gianluca; Cannas, Antonino] Univ Cagliari, Cagliari, Italy.
[Pugliatti, Maura; Parish, Leslie D.; Occhineri, Patrizia] Univ Sassari, Dept Clin & Expt Med, I-07100 Sassari, Italy.
[Marrosu, Maria Giovanna; Murru, Maria Rita] Univ Cagliari, Multiple Sclerosis Ctr Lab, Cagliari, Italy.
[Loi, Daniela] Azienda Sanit Locale 2, Olbia Tempio, Italy.
[Ticca, Anna] Azienda Osped San Francesco, Dept Neurol, Nuoro, Italy.
[Traccis, Sebastiano] Osped Antonio Segni, Dept Neurol, Ozieri, Italy.
[Manera, Umberto; Canosa, Antonio; Moglia, Cristina; Calvo, Andrea; Barberis, Marco; Brunetti, Maura; Chio, Adriano] Univ Turin, Amyotroph Lateral Sclerosis Ctr, Rita Levi Montalcini Dept Neurosci, Turin, Italy.
[Canosa, Antonio; Chio, Adriano] Univ Genoa, Dept Neurosci Ophthalmol Genet Rehabil & Child Hl, Genoa, Italy.
[Canosa, Antonio; Calvo, Andrea; Chio, Adriano] Azienda Osped Univ Citta Salute & Sci, Turin, Italy.
[Barberis, Marco; Brunetti, Maura; Restagno, Gabriella] Azienda Osped Univ Citta Salute & Sci, Mol Genet Lab, Turin, Italy.
[Pliner, Hannah A.; Renton, Alan E.; Traynor, Bryan J.] NIA, Neuromuscular Dis Res Sect, Neurogenet Lab, Bethesda, MD 20892 USA.
[Nalls, Mike A.] NIA, Mol Genet Sect, Neurogenet Lab, Bethesda, MD 20892 USA.
[Traynor, Bryan J.] Johns Hopkins Univ, Dept Neurol, Brain Sci Inst, Baltimore, MD 21218 USA.
[Chio, Adriano] NIT, Turin, Italy.
RP Chio, A (reprint author), ALS Ctr, Rita Levi Montalcini Dept Neurosci, Via Cherasco 15, I-10126 Turin, Italy.
EM achio@usa.net
RI Pliner, Hannah/F-3608-2015; Calvo, Andrea/K-4141-2016; MANDRIOLI,
JESSICA/K-7235-2016; Moglia, Cristina/K-4142-2016;
OI Pliner, Hannah/0000-0003-1484-6501; Calvo, Andrea/0000-0002-5122-7243;
MANDRIOLI, JESSICA/0000-0002-9244-9782; Moglia,
Cristina/0000-0001-7377-7222; Chio, Adriano/0000-0001-9579-5341;
Marrosu, Maria Giovanna/0000-0003-2334-2081
FU Italian Ministry of Health (Ministero della Salute, Ricerca Sanitaria
Finalizzata) [RF-2010-2309849]; European Community [259867]; Joint
Programme-Neurodegenerative Disease Research; Italian Ministry of
Health; Strength Project - Italian Ministry of University and Research;
Agenzia Italiana per la Ricerca sulla SLA (ARISLA) (SARDINIALS Project);
Fondazione Vialli e Mauro per la SLA onlus; Fondazione Mauro e Anna
Magnetto; Associazione Piemontese per l'Assistenza alla SLA; Assessorato
alla Sanita, dell'Igiene e dell'Assistenza; Regione Autonoma della
Sardegna; US National Institutes of Health, National Institute on Aging
[Z01-AG000949-02]; National Institute of Neurological Disorder and
Stroke; Center for Disease Control and Prevention/Agency for Toxic
Substances and Disease Registry
FX We thank the patients and research subjects who contributed samples for
this study. This work was in part supported by the Italian Ministry of
Health (Ministero della Salute, Ricerca Sanitaria Finalizzata, 2010,
grant RF-2010-2309849), the European Community's Health Seventh
Framework Programme (FP7/2007-2013 under grant agreement no. 259867),
and the Joint Programme-Neurodegenerative Disease Research (Sophia
Project, supported by the Italian Ministry of Health, and Strength
Project, supported by the Italian Ministry of University and Research),
Agenzia Italiana per la Ricerca sulla SLA (ARISLA) (SARDINIALS Project),
Fondazione Vialli e Mauro per la SLA onlus, Fondazione Mauro e Anna
Magnetto, Associazione Piemontese per l'Assistenza alla SLA, Assessorato
alla Sanita, dell'Igiene e dell'Assistenza, and Regione Autonoma della
Sardegna. This work was supported in part by the Intramural Research
Programs of the US National Institutes of Health, National Institute on
Aging (Z01-AG000949-02), and National Institute of Neurological Disorder
and Stroke. The work was also supported by the Center for Disease
Control and Prevention/Agency for Toxic Substances and Disease Registry.
Author contributions-study concept and design: GB, MP, BJT, GR, and AC;
acquisition of data: MRM, GF, AC, LDP, PO, TBC, DL, AT, UM, AC, CM, AC,
MBa, MBr, HAP, AER, and MAN; analysis and interpretation of data: GB,
MP, FM, MGM, MRM, AER, MAN, BJT, GR, and AC; drafting of the article:
GB, MP, BJT, and AC; critical revision of the article for important
intellectual content: GB, MP, FM, MGM, MRM, GF, AC, LDP, PC, TBC, DL,
AT, UM, AC, CM, AC, MBa, MBr, HAP, AER, MAN, BJT, GR, and AC; obtained
funding: GB, MP, GR, and AC; administrative, technical, and material
support: MRM, GF, AC, LDP, PC, TBC, DL, AT, UM, AC, CM, AC, MBa, MBr,
HAP, AER, and MAN; study supervision: GB, MP, BJT, GR, and AC. AC has
full access to data. The corresponding author confirms that all these
authors have read and approved the final draft of the article and given
written permission to include their names in it.
NR 25
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Z9 6
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD DEC
PY 2014
VL 35
IS 12
AR 2882.e7
DI 10.1016/j.neurobiolaging.2014.07.012
PG 6
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AX9PB
UT WOS:000347233200027
PM 25123918
ER
PT J
AU Sassi, C
Guerreiro, R
Gibbs, R
Ding, JH
Lupton, MK
Troakes, C
Al-Sarraj, S
Niblock, M
Gallo, JM
Adnan, J
Killick, R
Brown, KS
Medway, C
Lord, J
Turton, J
Bras, J
Morgan, K
Powell, JF
Singleton, A
Hardy, J
AF Sassi, Celeste
Guerreiro, Rita
Gibbs, Raphael
Ding, Jinhui
Lupton, Michelle K.
Troakes, Claire
Al-Sarraj, Safa
Niblock, Michael
Gallo, Jean-Marc
Adnan, Jihad
Killick, Richard
Brown, Kristelle S.
Medway, Christopher
Lord, Jenny
Turton, James
Bras, Jose
Morgan, Kevin
Powell, John F.
Singleton, Andrew
Hardy, John
CA Alzheimer's Res Uk Consortium
TI Investigating the role of rare coding variability in Mendelian dementia
genes (APP, PSEN1, PSEN2, GRN, MAPT, and PRNP) in late-onset Alzheimer's
disease
SO NEUROBIOLOGY OF AGING
LA English
DT Article
DE Alzheimer's disease; Neurodegenerative dementia; APP; PSEN1; PSEN2;
MAPT; GRN; PRNP; Exome sequencing
ID GENOME-WIDE ASSOCIATION; PRION PROTEIN GENE; IDENTIFIES VARIANTS; COMMON
VARIANTS; SEQUENCING DATA; MUTATIONS; DELETIONS; CD2AP; EPHA1; RISK
AB The overlapping clinical and neuropathologic features between late-onset apparently sporadic Alzheimer's disease (LOAD), familial Alzheimer's disease (FAD), and other neurodegenerative dementias (frontotemporal dementia, corticobasal degeneration, progressive supranuclear palsy, and Creutzfeldt-Jakob disease) raise the question of whether shared genetic risk factors may explain the similar phenotype among these disparate disorders. To investigate this intriguing hypothesis, we analyzed rare coding variability in 6 Mendelian dementia genes (APP, PSEN1, PSEN2, GRN, MAPT, and PRNP), in 141 LOAD patients and 179 elderly controls, neuropathologically proven, from the UK. In our cohort, 14 LOAD cases (10%) and 11 controls (6%) carry at least 1 rare variant in the genes studied. We report a novel variant in PSEN1 (p.I168T) and a rare variant in PSEN2 (p.A237V), absent in controls and both likely pathogenic. Our findings support previous studies, suggesting that (1) rare coding variability in PSEN1 and PSEN2 may influence the susceptibility for LOAD and (2) GRN, MAPT, and PRNP are not major contributors to LOAD. Thus, genetic screening is pivotal for the clinical differential diagnosis of these neurodegenerative dementias. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Sassi, Celeste; Guerreiro, Rita; Gibbs, Raphael; Bras, Jose; Hardy, John] UCL, UCL Inst Neurol, Dept Mol Neurosci, London, England.
[Sassi, Celeste; Guerreiro, Rita; Gibbs, Raphael; Ding, Jinhui; Singleton, Andrew] NIA, Neurogenet Lab, Bethesda, MD 20892 USA.
[Lupton, Michelle K.; Troakes, Claire; Al-Sarraj, Safa; Niblock, Michael; Gallo, Jean-Marc; Adnan, Jihad; Killick, Richard; Powell, John F.] Kings Coll London, Inst Psychiat, London, England.
[Brown, Kristelle S.; Medway, Christopher; Lord, Jenny; Turton, James; Morgan, Kevin] Univ Nottingham, Queens Med Ctr, Sch Life Sci, Nottingham NG7 2RD, England.
RP Sassi, C (reprint author), NIH, Neurogenet Lab, 35 Convent Dr, Bethesda, MD 20892 USA.
EM celeste.sassi.10@ucl.ac.uk
RI Powell, John/G-4412-2011; Hardy, John/C-2451-2009; Singleton,
Andrew/C-3010-2009; Troakes, Claire/K-4346-2015; Guerreiro,
Rita/A-1327-2011;
OI Powell, John/0000-0001-6124-439X; Bras, Jose/0000-0001-8186-0333;
Killick, Richard/0000-0002-8815-3436
FU Alzheimer's Research UK; Medical Research Council (MRC); Wellcome
Trust/MRC Joint Call in Neurodegeneration Award [WT089698]; National
Institute for Health Research Biomedical Research Unit in Dementia at
University College London Hospitals, University College London; National
Institute on Aging [ZO1 AG000950-10]; National Institute of Neurological
Disease and Stroke, National Institutes of Health (Department of Health
and Human Services) [ZO1 AG000950-10]; Alzheimer's Association; [P50
AG016574]; [U01 AG006786]; [R01 AG18023]
FX This study was supported by the Alzheimer's Research UK, the Medical
Research Council (MRC), and the Wellcome Trust/MRC Joint Call in
Neurodegeneration Award (WT089698) to the UK Parkinson's Disease
Consortium (whose members are from the University College London, the
National Institute for Health Research Biomedical Research Centre for
Mental Health and Biomedical Research Unit for Dementia at the South
London, and Maudsley NHS Foundation Trust and Kings College London;
Institute of Neurology, the University of Sheffield, and the MRC Protein
Phosphorylation Unit at the University of Dundee), grants (P50 AG016574,
U01 AG006786, and R01 AG18023), the National Institute for Health
Research Biomedical Research Unit in Dementia at University College
London Hospitals, University College London; an anonymous donor, the Big
Lottery (to Dr Morgan); a fellowship from Alzheimer's Research UK (to Dr
Guerreiro); and the Intramural Research Programs of the National
Institute on Aging and the National Institute of Neurological Disease
and Stroke, National Institutes of Health (Department of Health and
Human Services Project number, ZO1 AG000950-10). The MRC London
Neurodegenerative Diseases Brain Bank and the Manchester Brain Bank from
Brains for Dementia Research are jointly funded from Alzheimer's
Research UK and Alzheimer's Association. The views expressed are those
of the authors and not necessarily those of the NHS, the NIHR, or the
Department of Health.
NR 33
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U1 2
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0197-4580
EI 1558-1497
J9 NEUROBIOL AGING
JI Neurobiol. Aging
PD DEC
PY 2014
VL 35
IS 12
AR 2881.e1
DI 10.1016/j.neurobiolaging.2014.06.002
PG 6
WC Geriatrics & Gerontology; Neurosciences
SC Geriatrics & Gerontology; Neurosciences & Neurology
GA AX9PB
UT WOS:000347233200023
PM 25104557
ER
PT J
AU Nie, LM
Huang, P
Li, WT
Yan, XF
Jin, A
Wang, Z
Tang, YX
Wang, SJ
Zhang, XF
Niu, G
Chen, XY
AF Nie, Liming
Huang, Peng
Li, Weitao
Yan, Xuefeng
Jin, Albert
Wang, Zhe
Tang, Yuxia
Wang, Shouju
Zhang, Xiaofen
Niu, Gang
Chen, Xiaoyuan
TI Early-Stage Imaging of Nanocarrier-Enhanced Chemotherapy Response in
Living Subjects by Scalable Photoacoustic Microscopy
SO ACS NANO
LA English
DT Article
DE early prediction; chemotherapy response; nanocarrier; photoacoustic
microscopy; scalable imaging; graphene oxide; signal amplification
ID GRAPHENE OXIDE; GOLD NANOPARTICLES; PHOTOTHERMAL THERAPY; MOLECULAR
TOMOGRAPHY; CONTRAST AGENTS; DRUG-DELIVERY; BREAST-CANCER; IN-VITRO;
FUNCTIONALIZATION; GENERATION
AB Conventional evaluation methods of chemotherapeutic efficacy such as tissue biopsy and anatomical measurement are either invasive with potential complications or dilatory to capture the rapid pathological changes. Here, a sensitive and resolution-scalable photoacoustic microscopy (PAM) with theranostic nanoformulation was developed to noninvasively monitor the therapy response in a timely manner. Ultrasmall graphene oxide nanosheets were designed as both drug-loading vehicle and photoacoustic signal amplifier to the tumor. With the signal enhancement by the injected contrast agents, the subtle microvascular changes of the chemotherapy response in tumor were advantagely revealed by our PAM system, which was much earlier than the morphological measurement by standard imaging techniques. High tumor uptake of the enhanced nanodrug with Cy5.5 labeling was validated by fluorescence imaging. At different observation scales, PAM offered unprecedented sensitivity of optical absorption and high spatial resolution over optical imaging. Our studies demonstrate the PAM system with synergistic theranostic strategy to be a multiplexing platform for tumor diagnosis, drug delivery, and chemotherapy response monitoring at a very early stage and in an effective way.
C1 [Nie, Liming; Zhang, Xiaofen] Xiamen Univ, Sch Publ Hlth, State Key Lab Mol Vaccinol & Mol Diagnost, Xiamen 361102, Peoples R China.
[Nie, Liming; Zhang, Xiaofen] Xiamen Univ, Sch Publ Hlth, Ctr Mol Imaging & Translat Med, Xiamen 361102, Peoples R China.
[Huang, Peng; Li, Weitao; Yan, Xuefeng; Wang, Zhe; Tang, Yuxia; Wang, Shouju; Niu, Gang; Chen, Xiaoyuan] NIBIB, Lab Mol Imaging & Nanomed LOMIN, NIH, Bethesda, MD 20892 USA.
[Li, Weitao] Nanjing Univ Aeronaut & Astronaut, Coll Automat Engn, Dept Biomed Engn, Nanjing 210016, Jiangsu, Peoples R China.
[Jin, Albert] NIBIB, Lab Cellular Imaging & Macromol Biophys, NIH, Bethesda, MD 20982 USA.
RP Nie, LM (reprint author), Xiamen Univ, Sch Publ Hlth, State Key Lab Mol Vaccinol & Mol Diagnost, Xiamen 361102, Peoples R China.
EM nielm@xmu.edu.cn
RI Huang, Peng/H-9985-2013; Nie, Liming/F-7718-2016; Huang,
Peng/R-2480-2016;
OI Huang, Peng/0000-0003-3651-7813; Jin, Albert/0000-0003-3826-1081
FU National Science Foundation of China [81301257, 81371596, 51373144];
National Basic Research Program of China (973 Program) [2013CB733802,
2014CB744503]; Intramural Research Program (IRP) of the National
Institute of Biomedical Imaging and Bioengineering (NIBIB), National
Institutes of Health (NIH)
FX This work was supported by the National Science Foundation of China
(81301257, 81371596, 51373144), the National Basic Research Program of
China (973 Program 2013CB733802, 2014CB744503), and the Intramural
Research Program (IRP) of the National Institute of Biomedical Imaging
and Bioengineering (NIBIB), National Institutes of Health (NIH). The
authors also acknowledge instrumental and technical support from nanoPAM
Inc.
NR 45
TC 21
Z9 23
U1 2
U2 48
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1936-0851
EI 1936-086X
J9 ACS NANO
JI ACS Nano
PD DEC
PY 2014
VL 8
IS 12
BP 12141
EP 12150
DI 10.1021/nn505989e
PG 10
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA AX8CL
UT WOS:000347138000027
PM 25406986
ER
PT J
AU Wang, Z
Zhang, RL
Wang, ZL
Wang, HF
Wang, Y
Zhao, J
Wang, F
Li, WT
Niu, G
Kiesewetter, DO
Chen, XY
AF Wang, Zhe
Zhang, Ruili
Wang, Zhongliang
Wang, He-Fang
Wang, Yu
Zhao, Jun
Wang, Fu
Li, Weitao
Niu, Gang
Kiesewetter, Dale O.
Chen, Xiaoyuan
TI Bioinspired Nanocomplex for Spatiotemporal Imaging of Sequential mRNA
Expression in Differentiating Neural Stem Cells
SO ACS NANO
LA English
DT Article
DE mRNA; imaging; gold nanoparticle; drug delivery; neural stem cell
ID LIVING CELLS; MOLECULAR BEACON; MAMMALIAN-CELLS; MICELLE FLARES;
RETINOIC ACID; CANCER-CELLS; NANOPROBE; NANOPARTICLES; LOCALIZATION;
MONOLAYERS
AB Messenger RNA plays a pivotal role in regulating cellular activities. The expression dynamics of specific mRNA contains substantial information on the intracellular milieu. Unlike the imaging of stationary mRNAs, real-time intracellular imaging of the dynamics of mRNA expression is of great value for investigating mRNA biology and exploring specific cellular cascades. In addition to advanced imaging methods, timely extracellular stimulation is another key factor in regulating the mRNA expression repertoire. The integration of effective stimulation and imaging into a single robust system would significantly improve stimulation efficiency and imaging accuracy, producing fewer unwanted artifacts. In this study, we developed a multifunctional nanocomplex to enable self-activating and spatiotemporal imaging of the dynamics of mRNA sequential expression during the neural stem cell differentiation process. This nanocomplex showed improved enzymatic stability, fast recognition kinetics, and high specificity. With a mechanism regulated by endogenous cell machinery, this nanocomplex realized the successive stimulating motif release and the dynamic imaging of chronological mRNA expression during neural stem cell differentiation without the use of transgenetic manipulation. The dynamic imaging montage of mRNA expression ultimately facilitated genetic heterogeneity analysis. In vivo lateral ventricle injection of this nanocomplex enabled endogenous neural stem cell activation and labeling at their specific differentiation stages. This nanocomplex is highly amenable as an alternative tool to explore the dynamics of intricate mRNA activities in various physiological and pathological conditions.
C1 [Wang, Zhe; Zhang, Ruili; Wang, Zhongliang; Wang, He-Fang; Wang, Yu; Wang, Fu; Li, Weitao; Niu, Gang; Kiesewetter, Dale O.; Chen, Xiaoyuan] Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
[Zhang, Ruili; Wang, Zhongliang; Wang, Fu] Xidian Univ, Sch Life Sci & Technol, Xian 710071, Shaanxi, Peoples R China.
[Zhao, Jun] NIMH, Unit Synapse Dev & Plast, NIH, Bethesda, MD 20892 USA.
RP Wang, ZL (reprint author), Natl Inst Biomed Imaging & Bioengn, Lab Mol Imaging & Nanomed, NIH, Bethesda, MD 20892 USA.
EM zhongliang.wang@nih.gov; shawn.chen@nih.gov
RI Wang, He-Fang/D-7842-2011;
OI Wang, He-Fang/0000-0003-4127-5038; Wang, Fu/0000-0001-9222-0833
FU Center for Neuroscience and Regenerative Medicine (CNRM) program at
Henry M. Jackson Foundation; Intramural Research Program (IRP) of the
National Institute of Biomedical Imaging and Bioengineering (NIBIB) at
the National Institutes of Health (NIH)
FX This study was supported, in part, by the Center for Neuroscience and
Regenerative Medicine (CNRM) program at Henry M. Jackson Foundation and
the Intramural Research Program (IRP) of the National Institute of
Biomedical Imaging and Bioengineering (NIBIB) at the National Institutes
of Health (NIH).
NR 44
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Z9 5
U1 6
U2 66
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1936-0851
EI 1936-086X
J9 ACS NANO
JI ACS Nano
PD DEC
PY 2014
VL 8
IS 12
BP 12386
EP 12396
DI 10.1021/nn505047n
PG 11
WC Chemistry, Multidisciplinary; Chemistry, Physical; Nanoscience &
Nanotechnology; Materials Science, Multidisciplinary
SC Chemistry; Science & Technology - Other Topics; Materials Science
GA AX8CL
UT WOS:000347138000051
PM 25494492
ER
PT J
AU Spielberg, F
Levy, V
Lensing, S
Chattopadhyay, I
Venkatasubramanian, L
Acevedo, N
Wolff, P
Callabresi, D
Philip, S
Lopez, TP
Padian, N
Blake, DR
Gaydos, CA
AF Spielberg, Freya
Levy, Vivian
Lensing, Shelly
Chattopadhyay, Ishita
Venkatasubramanian, Lalitha
Acevedo, Nincoshka
Wolff, Peter
Callabresi, Debra
Philip, Susan
Lopez, Teresa P.
Padian, Nancy
Blake, Diane R.
Gaydos, Charlotte A.
TI Fully Integrated e-Services for Prevention, Diagnosis, and Treatment of
Sexually Transmitted Infections: Results of a 4-County Study in
California
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID CHLAMYDIA-TRACHOMATIS; VAGINAL SWABS; NEISSERIA-GONORRHOEAE; HOME;
INTERNET; ACCEPTABILITY; METAANALYSIS; URINE; COST
AB Objectives. We examined the acceptability, feasibility, and cost of a fully integrated online system (eSTI) for sexually transmitted infection (STI) testing, treatment, and linkage to care with 4 Northern California health departments.
Methods. In April 2012, we implemented the eSTI system, which provided education; testing of self-collected vaginal swabs for chlamydia, gonorrhea, and trichomoniasis; e-prescriptions; e-partner notification; and data integration with clinic electronic health records. We analyzed feasibility, acceptability, and cost measures.
Results. During a 3-month period, 217 women aged 18 to 30 years enrolled; 67% returned the kit. Of these, 92% viewed their results online. STI prevalence was 5.6% (chlamydia and trichomoniasis). All participants with STIs received treatment either the same day at a pharmacy (62%) or within 7 days at a clinic (38%). Among participants completing follow-up surveys, 99% would recommend the online eSTI system to a friend, and 95% preferred it over clinic-based testing within a study.
Conclusions. The fully integrated eSTI system has the potential to increase diagnosis and treatment of STIs with higher patient satisfaction at a potentially lower cost.
C1 [Spielberg, Freya] George Washington Univ, Dept Prevent & Community Hlth, Washington, DC 20052 USA.
[Levy, Vivian; Lopez, Teresa P.] San Mateo Cty Hlth Syst, San Mateo, CA USA.
[Lensing, Shelly] Univ Arkansas Med Sci, Dept Biostat, Little Rock, AR 72205 USA.
[Chattopadhyay, Ishita] Res Triangle Inst Int, Res Triangle Pk, NC USA.
[Venkatasubramanian, Lalitha; Acevedo, Nincoshka] FHI 360, Durham, NC USA.
[Wolff, Peter] NIAID, Bethesda, MD 20892 USA.
[Callabresi, Debra] N Ton, Los Angeles, CA USA.
[Philip, Susan] San Francisco Dept Publ Hlth, San Francisco, CA USA.
[Padian, Nancy] Berkeley Sch Publ Hlth, Berkeley, CA USA.
[Blake, Diane R.] Univ Massachusetts, Sch Med, Dept Pediat, Worcester, MA USA.
[Gaydos, Charlotte A.] Johns Hopkins Univ, Dept Med, Div Infect Dis, Baltimore, MD USA.
RP Spielberg, F (reprint author), George Washington Univ, Dept Prevent & Community Hlth, 2175 K St NW,Suite 700,Room 728, Washington, DC 20052 USA.
EM fspielberg@e-mail.gwu.edu
FU National Institute of Allergy and Infectious Diseases through the
Sexually Transmitted Infections Clinical Trials Group
[HHSN266200400074C]; National Institute of Biomedical Imaging and
Bioengineering, NIH [U54EB007958]; National Institute of Allergy and
Infectious Diseases, NIH [U-01 AI068613]
FX This work was supported by the National Institute of Allergy and
Infectious Diseases (HHSN266200400074C) through the Sexually Transmitted
Infections Clinical Trials Group. C.A. Gaydos was also supported by the
National Institute of Biomedical Imaging and Bioengineering, NIH
U54EB007958 and National Institute of Allergy and Infectious Diseases,
NIH U-01 AI068613.
NR 20
TC 6
Z9 6
U1 0
U2 3
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
EI 1541-0048
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD DEC
PY 2014
VL 104
IS 12
BP 2313
EP 2320
DI 10.2105/AJPH.2014.302302
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AX9GB
UT WOS:000347210500038
PM 25320878
ER
PT J
AU Han, B
Compton, WM
Gfroerer, J
McKeon, R
AF Han, Beth
Compton, Wilson M.
Gfroerer, Joseph
McKeon, Richard
TI Mental Health Treatment Patterns Among Adults With Recent Suicide
Attempts in the United States
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
ID COMMON OUTCOMES; RELATIVE RISK; SUBSTANCE USE; CARE; BEHAVIORS;
IDEATION; COHORT; MODEL; INDIVIDUALS; DISORDERS
AB Objectives. We examined mental health treatment patterns among adults with suicide attempts in the past 12 months in the United States.
Methods. We examined data from 2000 persons, aged 18 years or older, who participated in the 2008 to 2012 National Survey on Drug Use and Health and who reported attempting suicide in the past 12 months. We applied descriptive analyses and multivariable logistic regression models.
Results. In adults who attempted suicide in the past year, 56.3% received mental health treatment, but half of those who received treatment perceived unmet treatment needs, and of the 43.0% who did not receive mental health treatment, one fourth perceived unmet treatment needs. From 2008 to 2012, the mental health treatment rate among suicide attempters remained unchanged. Factors associated with receipt of mental health treatment varied by perceived unmet treatment need and receipt of medical attention that resulted from a suicide attempt.
Conclusions. Suicide prevention strategies that focus on suicide attempters are needed to increase their access to mental health treatments that meet their needs. To be effective, these strategies need to account for language and cultural differences and barriers to financial and treatment delivery.
C1 [Han, Beth; Gfroerer, Joseph; McKeon, Richard] Subst Abuse & Mental Hlth Serv Adm, Rockville, MD USA.
[Compton, Wilson M.] NIDA, NIH, Bethesda, MD 20892 USA.
RP Han, B (reprint author), 1 Choke Cherry Rd,Room 2-1079, Rockville, MD 20857 USA.
EM Beth.Han@SAMHSA.HHS.GOV
NR 37
TC 7
Z9 7
U1 1
U2 7
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
EI 1541-0048
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD DEC
PY 2014
VL 104
IS 12
BP 2359
EP 2368
DI 10.2105/AJPH.2014.302163
PG 10
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AX9GB
UT WOS:000347210500044
PM 25322299
ER
PT J
AU Garrison, AR
Giomarelli, BG
Lear-Rooney, CM
Saucedo, CJ
Yellayi, S
Krumpe, LRH
Rose, M
Paragas, J
Bray, M
Olinger, GG
McMahon, JB
Huggins, J
O'Keefe, BR
AF Garrison, Aura R.
Giomarelli, Barbara G.
Lear-Rooney, Calli M.
Saucedo, Carrie J.
Yellayi, Srikanth
Krumpe, Lauren R. H.
Rose, Maura
Paragas, Jason
Bray, Mike
Olinger, Gene G., Jr.
McMahon, James B.
Huggins, John
O'Keefe, Barry R.
TI The cyanobacterial lectin scytovirin displays potent in vitro and in
vivo activity against Zaire Ebola virus
SO ANTIVIRAL RESEARCH
LA English
DT Article
DE Ebola; Scytovirin; Lectin; Natural product; Cyanobacteria
ID ANTI-HIV PROTEIN; CYANOVIRIN-N; INACTIVATING PROTEIN; FILOVIRUS
INFECTION; SCYTONEMA-VARIUM; GLYCOPROTEIN; ENTRY; GRIFFITHSIN;
INHIBITOR; BINDS
AB The cyanobacterial lectin scytovirin (SVN) binds with high affinity to mannose-rich oligosaccharides on the envelope glycoprotein (GP) of a number of viruses, blocking entry into target cells. In this study, we assessed the ability of SVN to bind to the envelope GP of Zaire Ebola virus (ZEBOV) and inhibit its replication. SVN interacted specifically with the protein's mucin-rich domain. In cell culture, it inhibited ZEBOV replication with a 50% virus-inhibitory concentration (EC50) of 50 nM, and was also active against the Angola strain of the related Marburg virus (MARV), with a similar EC50. Injected subcutaneously in mice, SVN reached a peak plasma level of 100 nm in 45 min, but was cleared within 4 h. When ZEBOV-infected mice were given 30 mg/kg/day of SVN by subcutaneous injection every 6 h, beginning the day before virus challenge, 9 of 10 animals survived the infection, while all infected, untreated mice died. When treatment was begun one hour or one day after challenge, 70-90% of mice survived. Quantitation of infectious virus and viral RNA in samples of serum, liver and spleen collected on days 2 and 5 postinfection showed a trend toward lower titers in treated than control mice, with a significant decrease in liver titers on day 2. Our findings provide further evidence of the potential of natural lectins as therapeutic agents for viral infections. Published by Elsevier B.V.
C1 [Garrison, Aura R.; Lear-Rooney, Calli M.; Paragas, Jason; Bray, Mike; Olinger, Gene G., Jr.; Huggins, John] US Army, Med Res Inst Infect Dis, Dept Viral Therapeut, Div Virol, Ft Detrick, MD 21702 USA.
[Giomarelli, Barbara G.; Saucedo, Carrie J.; Krumpe, Lauren R. H.; Rose, Maura; McMahon, James B.; O'Keefe, Barry R.] NCI, Ctr Canc Res, Mol Targets Lab, NIH,Frederick Natl Lab Canc Res, Ft Detrick, MD 21702 USA.
[Saucedo, Carrie J.; Krumpe, Lauren R. H.] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, Basic Sci Program, Frederick, MD 21702 USA.
[Yellayi, Srikanth] NIAID, Off Chief Scientist, Integrated Res Facil, Div Clin Res, Frederick, MD USA.
[Bray, Mike] NIAID, Div Clin Res, NIH, Bethesda, MD 20892 USA.
RP O'Keefe, BR (reprint author), NCI, Mol Targets Lab, Bldg 562,Rm 201, Ft Detrick, MD 21702 USA.
EM okeefeba@mail.nih.gov
FU Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research and the NIAID Trans-NIH/FDA Biodefense Grant
Program; Frederick National Laboratory for Cancer Research, National
Institutes of Health [HHSN261200800001E]
FX This research was supported by the Intramural Research Program of the
NIH, National Cancer Institute, Center for Cancer Research and the NIAID
Trans-NIH/FDA Biodefense Grant Program. This project has been funded in
whole or in part with federal funds from the Frederick National
Laboratory for Cancer Research, National Institutes of Health, under
contract HHSN261200800001E. 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.
Opinions, interpretations, conclusions, and recommendations are those of
the author and are not necessarily endorsed by the U.S. Army.
NR 24
TC 11
Z9 13
U1 3
U2 26
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
EI 1872-9096
J9 ANTIVIR RES
JI Antiviral Res.
PD DEC
PY 2014
VL 112
BP 1
EP 7
DI 10.1016/j.antiviral.2014.09.012
PG 7
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA AX5CE
UT WOS:000346943900001
PM 25265598
ER
PT J
AU Smith, DR
Holbrook, MR
Gowen, BB
AF Smith, Darci R.
Holbrook, Michael R.
Gowen, Brian B.
TI Animal models of viral hemorrhagic fever
SO ANTIVIRAL RESEARCH
LA English
DT Review
DE Animal models; Viral hemorrhagic fever; Rodents; Non-human primates;
Medical countermeasures
ID RIFT-VALLEY-FEVER; EXPERIMENTAL YELLOW-FEVER; EBOLA-VIRUS INFECTION;
HANTAVIRUS PULMONARY SYNDROME; SYRIAN GOLDEN-HAMSTER; THROMBOCYTOPENIA
SYNDROME VIRUS; EXPERIMENTAL LASSA FEVER; KYASANUR-FOREST-DISEASE;
SIN-NOMBRE-VIRUS; LYMPHOCYTIC CHORIOMENINGITIS VIRUS
AB The term "viral hemorrhagic fever" (VHF) designates a syndrome of acute febrile illness, increased vascular permeability and coagulation defects which often progresses to bleeding and shock and may be fatal in a significant percentage of cases. The causative agents are some 20 different RNA viruses in the families Arenaviridae, Bunyaviridae, Filoviridae and Flaviviridae, which are maintained in a variety of animal species and are transferred to humans through direct or indirect contact or by an arthropod vector. Except for dengue, which is transmitted among humans by mosquitoes, the geographic distribution of each type of VHF is determined by the range of its animal reservoir. Treatments are available for Argentine HF and Lassa fever, but no approved countermeasures have been developed against other types of VHF. The development of effective interventions is hindered by the sporadic nature of most infections and their occurrence in geographic regions with limited medical resources. Laboratory animal models that faithfully reproduce human disease are therefore essential for the evaluation of potential vaccines and therapeutics. The goal of this review is to highlight the current status of animal models that can be used to study the pathogenesis of VHF and test new countermeasures. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Smith, Darci R.] So Res Inst, Frederick, MD 21701 USA.
[Holbrook, Michael R.] NIAID, Integrated Res Facil, NIH, Frederick, MD USA.
[Gowen, Brian B.] Utah State Univ, Inst Antiviral Res, Logan, UT 84322 USA.
[Gowen, Brian B.] Utah State Univ, Dept Anim Dairy & Vet Sci, Logan, UT 84322 USA.
RP Smith, DR (reprint author), So Res Inst, 431 Aviat Way, Frederick, MD 21701 USA.
EM smithdr@southernresearch.org
FU NIAID [HHSN272200200016I]
FX The authors would like to thank Jiro Wada for his illustration work. MRH
is an employee of Battelle Memorial Institute under its prime contract
with NIAID No. HHSN272200200016I. The information presented here is the
responsibility of the authors and does not necessarily represent views
or policies of the US Department of Health and Human Services or
Battelle Memorial Institute.
NR 336
TC 8
Z9 9
U1 2
U2 23
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-3542
EI 1872-9096
J9 ANTIVIR RES
JI Antiviral Res.
PD DEC
PY 2014
VL 112
BP 59
EP 79
DI 10.1016/j.antiviral.2014.10.001
PG 21
WC Pharmacology & Pharmacy; Virology
SC Pharmacology & Pharmacy; Virology
GA AX5CE
UT WOS:000346943900007
PM 25448088
ER
PT J
AU Kanevskiy, LM
Erokhina, SA
Streltsova, MA
Telford, WG
Sapozhnikov, AM
Kovalenko, EI
AF Kanevskiy, L. M.
Erokhina, S. A.
Streltsova, M. A.
Telford, W. G.
Sapozhnikov, A. M.
Kovalenko, E. I.
TI Bacterial Lipopolysaccharide Activates CD57-Negative Human NK Cells
SO BIOCHEMISTRY-MOSCOW
LA English
DT Article
DE NK cells; lipopolysaccharide; IFN-gamma production; CD57; cytotoxicity;
TLR4
ID NATURAL-KILLER-CELLS; TOLL-LIKE RECEPTOR; IMMUNE-RESPONSE; IFN-GAMMA;
RECOGNITION; MACROPHAGES; EXPRESSION; SEPSIS; SUBSET; MODEL
AB NK cells play an important regulatory role in sepsis by induction and augmentation of proinflammatory reactions in early stages of the septic process and by suppression of immune response in later stages of inflammation. The present work was aimed at the effect of bacterial lipopolysaccharide (LPS), the main pathogenic factor of sepsis development, on human NK cells ex vivo. We show that LPS activates immature CD57-negative NK cells, which typically constitute less than half of the normal NK cell population in human peripheral blood. Under conditions of NK cell stimulation with IL-2, addition of LPS provokes an increase in IFN-gamma production. However, LPS both increased and inhibited NK cell cytotoxic activity. It is important to note that the activation of NK cells on LPS addition was observed in the absence of TLR4 on the NK cell surface. These results confirm our previous data arguing for a direct interaction of LPS with NK cells and evidence an atypical mechanism of LPS-induced NK cell activation without the involvement of surface TLR4.
C1 [Kanevskiy, L. M.; Erokhina, S. A.; Streltsova, M. A.; Sapozhnikov, A. M.; Kovalenko, E. I.] Russian Acad Sci, Shemyakin & Ovchinnikov Inst Bioorgan Chem, Moscow 117997, Russia.
[Erokhina, S. A.; Sapozhnikov, A. M.] Moscow MV Lomonosov State Univ, Fac Biol, Moscow 119991, Russia.
[Telford, W. G.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Kovalenko, EI (reprint author), Russian Acad Sci, Shemyakin & Ovchinnikov Inst Bioorgan Chem, Ul Miklukho Maklaya 16-10, Moscow 117997, Russia.
EM leonid_kanewski@mail.ru; lenkovalen@mail.ru
RI Streltsova, Maria/S-2066-2016; Kovalenko, Elena/S-2086-2016
FU Russian Foundation for Basic Research [13-04-02041, 14-04-01842]
FX This work was supported by the Russian Foundation for Basic Research
grants (Nos. 13-04-02041 and 14-04-01842).
NR 30
TC 1
Z9 1
U1 1
U2 6
PU MAIK NAUKA/INTERPERIODICA/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA
SN 0006-2979
EI 0320-9725
J9 BIOCHEMISTRY-MOSCOW+
JI Biochem.-Moscow
PD DEC
PY 2014
VL 79
IS 12
BP 1339
EP 1348
DI 10.1134/S0006297914120074
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA AX4UE
UT WOS:000346926000007
PM 25716727
ER
PT J
AU Sissung, TM
Price, DK
Del Re, M
Ley, AM
Giovannetti, E
Figg, WD
Danesi, R
AF Sissung, Tristan M.
Price, Douglas K.
Del Re, Marzia
Ley, Ariel M.
Giovannetti, Elisa
Figg, William D.
Danesi, Romano
TI Genetic variation: effect on prostate cancer
SO BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
LA English
DT Review
DE Pharmacogenomics; Prostate cancer; Androgen deprivation therapy;
Chemotherapy; Steroid
ID ANDROGEN-DEPRIVATION THERAPY; ENDOTHELIAL GROWTH-FACTOR; SINGLE
NUCLEOTIDE POLYMORPHISMS; 5-ALPHA-REDUCTASE TYPE-II; GENOME-WIDE
ASSOCIATION; NORTH INDIAN POPULATION; VITAMIN-D-RECEPTOR; CAG REPEAT
LENGTH; REDUCTASE TYPE-II; CYP17 GENE
AB The crucial role of androgens in the development of prostate cancer is well established. The aim of this review is to examine the role of constitutional (germline) and tumor-specific (somatic) polymorphisms within important regulatory genes of prostate cancer. These include genes encoding enzymes of the androgen biosynthetic pathway, the androgen receptor gene, genes that encode proteins of the signal transduction pathways that may have a role in disease progression and survival, and genes involved in prostate cancer angiogenesis. Characterization of deregulated pathways critical to cancer cell growth have lead to the development of new treatments, including the CYP17 inhibitor abiraterone and clinical trials using novel drugs that are ongoing or recently completed [1]. The pharmacogenetics of the drugs used to treat prostate cancer will also be addressed. This review will define how germline polymorphisms are known affect a multitude of pathways, and therefore phenotypes, in prostate cancer etiology, progression, and treatment. Published by Elsevier B.V.
C1 [Sissung, Tristan M.; Price, Douglas K.; Ley, Ariel M.; Figg, William D.] NCI, NIH, Bethesda, MD 20892 USA.
[Del Re, Marzia; Giovannetti, Elisa; Danesi, Romano] Univ Pisa, Dept Clin & Expt Med, I-56100 Pisa, Italy.
RP Figg, WD (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
RI Figg Sr, William/M-2411-2016;
OI Del Re, Marzia/0000-0001-7343-6161
FU Intramural NIH HHS [ZIA BC010627-10]
NR 213
TC 8
Z9 8
U1 2
U2 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-419X
EI 0006-3002
J9 BBA-REV CANCER
JI Biochim. Biophys. Acta-Rev. Cancer
PD DEC
PY 2014
VL 1846
IS 2
BP 446
EP 456
DI 10.1016/j.bbcan.2014.08.007
PG 11
WC Biochemistry & Molecular Biology; Biophysics; Oncology
SC Biochemistry & Molecular Biology; Biophysics; Oncology
GA AY0BQ
UT WOS:000347263400014
PM 25199985
ER
PT J
AU Volkin, D
Turkbey, B
Hoang, AN
Rais-Bahrami, S
Yerram, N
Walton-Diaz, A
Nix, JW
Wood, BJ
Choyke, PL
Pinto, PA
AF Volkin, Dmitry
Turkbey, Baris
Hoang, Anthony N.
Rais-Bahrami, Soroush
Yerram, Nitin
Walton-Diaz, Annerleim
Nix, Jeffrey W.
Wood, Bradford J.
Choyke, Peter L.
Pinto, Peter A.
TI Multiparametric magnetic resonance imaging (MRI) and subsequent
MRI/ultrasonography fusion-guided biopsy increase the detection of
anteriorly located prostate cancers
SO BJU INTERNATIONAL
LA English
DT Article
DE prostatic adenocarcinoma; functional MRI; cancer screening; prostate
biopsy
ID CLINICAL-SIGNIFICANCE; TUMOR VOLUME
AB ObjectiveTo describe the detection rate of anteriorly located prostate cancer (PCa) with the addition of magnetic resonance imaging (MRI)/ultrasonography (US) fusion-guided biopsy (FGB) to the standard transrectal ultrasonography (TRUS)-guided biopsy.
Patients and MethodsAll patients, regardless of their biopsy history, who were referred for clinical suspicion of PCa (i.e elevated prostate-specific antigen (PSA) level and abnormal digital rectal examination) underwent 3T multiparametric-MRI (mpMRI) screening; and those with suspicious lesions in the anterior region of the prostate were identified. Patients then received a FGB of all suspicious lesions in addition to a systematic 12-core extended sextant TRUS-guided biopsy. We conducted a lesion-based analysis comparing cancer detection rates of anterior targets using FGB vs systematic cores taken from the same anatomic sextant within the prostate. Lengths of cancer in the most involved core were also compared between the two biopsy techniques used. Patients with only anterior targets were analysed separately.
ResultsOf 499 patients undergoing FGB, 162 had a total of 241 anterior lesions. The mean age, PSA level and prostate volume in this group were 62 years, 12.7ng/dL, and 57mL, respectively. In total, PCa was diagnosed in 121 anterior lesions (50.2%) identified on mpMRI. Sixty-two (25.7%) of these anterior lesions were documented as positive for cancer on systematic 12-core TRUS-guided biopsy cores, while 97 (40.2%) were positive on the targeted FGB cores (P = 0.001). In lesions that were positive on both FGB and TRUS biopsy, the most involved core was 112% longer on FGB (3.7 vs 1.6mm, P 0.01). Forty-two patients had only anterior lesions on mpMRI; of these, 24 (57.1%) were found to have cancer on the FGB + TRUS biopsy platform. Six patients were positive on FGB only and 13 were positive on both biopsy techniques; however, 7/13 patients were upgraded to a higher Gleason score after FGB. All five patients positive on TRUS biopsy only were candidates for active surveillance.
ConclusionThe results showed that FGB detects significantly more anteriorly located PCa than does TRUS-guided biopsy alone and it may serve as an effective tool for the subset of patients with such tumours.
C1 [Volkin, Dmitry; Hoang, Anthony N.; Rais-Bahrami, Soroush; Yerram, Nitin; Walton-Diaz, Annerleim; Nix, Jeffrey W.; Pinto, Peter A.] NCI, Urol Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Turkbey, Baris; Choyke, Peter L.] NCI, Mol Imaging Program, NIH, Bethesda, MD 20892 USA.
[Wood, Bradford J.; Pinto, Peter A.] NCI, Ctr Intervent Oncol, NIH, Bethesda, MD 20892 USA.
RP Pinto, PA (reprint author), NCI, Urol Oncol Branch, NIH, 10 Ctr Dr,MSC1210,Building10,CRCRoom2W-5940, Bethesda, MD 20892 USA.
EM pintop@mail.nih.gov
OI Rais-Bahrami, Soroush/0000-0001-9466-9925
NR 33
TC 24
Z9 24
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1464-4096
EI 1464-410X
J9 BJU INT
JI BJU Int.
PD DEC
PY 2014
VL 114
IS 6B
BP E43
EP E49
DI 10.1111/bju.12670
PG 7
WC Urology & Nephrology
SC Urology & Nephrology
GA AX5ST
UT WOS:000346988300006
PM 24712649
ER
PT J
AU Mitchell, SA
Hoffman, AJ
Clark, JC
DeGennaro, RM
Poirier, P
Robinson, CB
Weisbrod, BL
AF Mitchell, Sandra A.
Hoffman, Amy J.
Clark, Jane C.
DeGennaro, Regina M.
Poirier, Patricia
Robinson, Carolene B.
Weisbrod, Breanna L.
TI Putting Evidence Into Practice: An Update of Evidence-Based
Interventions for Cancer-Related Fatigue During and Following Treatment
SO CLINICAL JOURNAL OF ONCOLOGY NURSING
LA English
DT Article
DE cancer-related fatigue; cancer; management; nursing; evidence-based
practice
ID QUALITY-OF-LIFE; RANDOMIZED CONTROLLED-TRIAL; PATIENTS RECEIVING
CHEMOTHERAPY; PLACEBO-CONTROLLED TRIAL; ERYTHROPOIESIS-STIMULATING
AGENTS; COGNITIVE-BEHAVIOR THERAPY; L-CARNITINE SUPPLEMENTATION;
STEM-CELL TRANSPLANTATION; STAGE BREAST-CANCER; III CLINICAL-TRIAL
AB Cancer-related fatigue (CRF) has deleterious effects on physical, social, cognitive, and vocational functioning, and causes emotional and spiritual distress for patients and their families; however, it remains under-recognized and undertreated. This article critically reviews and integrates the available empirical evidence supporting the efficacy of pharmacologic and nonpharmacologic treatment approaches to CRF, highlighting new evidence since 2007 and 2009 Putting Evidence Into Practice publications. Interventions that are recommended for practice or likely to be effective in improving fatigue outcomes include exercise; screening for treatable risk factors; management of concurrent symptoms; yoga; structured rehabilitation; Wisconsin ginseng; cognitive-behavioral therapies for insomnia, pain, and depression; mindfulness-based stress reduction; and psychoeducational interventions such as anticipatory guidance, psychosocial support, and energy conservation and activity management. This information can be applied to improve the management of CRF, inform health policy and program development, shape the design of clinical trials of new therapies for CRF, and drive basic and translational research.
C1 [Mitchell, Sandra A.] Natl Canc Ctr, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Hoffman, Amy J.] Michigan State Univ, Coll Nursing, E Lansing, MI 48824 USA.
[Clark, Jane C.] Georgia Ctr Oncol Res & Educ, Atlanta, GA USA.
[DeGennaro, Regina M.] Univ Virginia, Sch Nursing, Charlottesville, VA 22903 USA.
[Poirier, Patricia] Univ Maine, Sch Nursing, Orono, ME USA.
[Robinson, Carolene B.] UnityPoint Hlth Trinity, Moline, IL USA.
[Weisbrod, Breanna L.] Univ Kansas Hosp, Dept Nursing, Kansas City, KS USA.
RP Mitchell, SA (reprint author), Natl Canc Ctr, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
EM mitchlls@mailnih.gov
NR 324
TC 20
Z9 21
U1 9
U2 44
PU ONCOLOGY NURSING SOC
PI PITTSBURGH
PA 125 ENTERPRISE DR, PITTSBURGH, PA 15275 USA
SN 1092-1095
EI 1538-067X
J9 CLIN J ONCOL NURS
JI Clin. J. Oncol. Nurs.
PD DEC
PY 2014
VL 18
SU S
BP 38
EP 58
DI 10.1188/14.CJON.S3.38-58
PG 21
WC Oncology; Nursing
SC Oncology; Nursing
GA AX9OP
UT WOS:000347232100005
PM 25427608
ER
PT J
AU Wester, JC
McBain, CJ
AF Wester, Jason C.
McBain, Chris J.
TI Behavioral state-dependent modulation of distinct interneuron subtypes
and consequences for circuit function
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID CHOLECYSTOKININ-POSITIVE INTERNEURONS; CORTICAL INTERNEURONS; GABAERGIC
NEURONS; VISUAL-CORTEX; BARREL CORTEX; CHOLINERGIC MODULATION;
SOMATOSENSORY CORTEX; NICOTINIC RECEPTORS; PYRAMIDAL NEURONS; RAT
HIPPOCAMPUS
AB Multiple neuromodulators regulate neuronal response properties and synaptic connections in order to adjust circuit function. Inhibitory interneurons are a diverse group of cells that are differentially modulated depending on neuronal subtype and play key roles in regulating local circuit activity. Importantly, new tools to target specific subtypes are greatly improving our understanding of interneuron circuits and their modulation. Indeed, recent work has demonstrated that during different behavioral states interneuron activity changes in a subtype specific manner in both neocortex and hippocampus. Furthermore, in neocortex, modulation of specific interneuron microcircuits results in pyramidal cell disinhibition with important consequences for synaptic plasticity and animal behavior. Thus, neuromodulators tune the output of different interneuron subtypes to provide neural circuits with great flexibility.
C1 [Wester, Jason C.; McBain, Chris J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Neurobiol, NIH, Bethesda, MD 20892 USA.
RP McBain, CJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Dev Neurobiol, NIH, Bethesda, MD 20892 USA.
EM mcbainc@mail.nih.gov
FU National Institute of Child Health and Human Development
[Z1A-HD001205-21]
FX We thank the National Institute of Child Health and Human Development
(Z1A-HD001205-21) for funding support. We also thank Ken Pelkey for
helpful comments on this manuscript, as well as Carl Petersen, Bernardo
Rudy, and Peyman Golshani for their kind permission to modify the
figures presented here.
NR 60
TC 11
Z9 11
U1 1
U2 12
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
EI 1873-6882
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD DEC
PY 2014
VL 29
BP 118
EP 125
DI 10.1016/j.conb.2014.07.007
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA AX7YS
UT WOS:000347128200017
PM 25058112
ER
PT J
AU Horvat, B
Berges, BK
Lusso, P
AF Horvat, Branka
Berges, Bradford K.
Lusso, Paolo
TI Recent developments in animal models for human herpesvirus 6A and 6B
SO CURRENT OPINION IN VIROLOGY
LA English
DT Article
ID IN-VITRO SUSCEPTIBILITY; MULTIPLE-SCLEROSIS; CELLULAR RECEPTOR; HIV-1
INFECTION; DOWN-REGULATION; T-LYMPHOCYTES; HUMAN-HERPESVIRUS-6; HHV-6;
MICE; ANTIGEN
AB Progress in the identification of suitable animal models for human herpesvirus (HHV)-6A and HHV-6B infections has been slow. Recently, new models have been established, mainly for HHV-6A, which reproduce some pathological features seen in humans. Neuroinflammatory signs were observed in infected marmosets and CD46-transgenic mice; although viral replication was not prominent, persistence of viral DNA and specific immunologic responses were detected, suggesting an immune-mediated pathogenic mechanism. Pig-tailed macaques showed robust viral replication concomitant with acute-phase symptoms, and provided a model to study the effects of HHV-6A on AIDS progression. In humanized mice, viral replication was less evident, but infection led to T-cell alterations. Altogether, these recent developments have opened new perspectives for studying the pathogenic role of HHV-6A in humans.
C1 [Horvat, Branka] INSERM, U1111, F-69008 Lyon, France.
[Horvat, Branka] CNRS, UMR5308, Lyon, France.
[Horvat, Branka] Univ Lyon 1, F-69365 Lyon, France.
[Horvat, Branka] Ecole Normale Super Lyon, F-69364 Lyon, France.
[Berges, Bradford K.] Brigham Young Univ, Dept Microbiol & Mol Biol, Provo, UT 84602 USA.
[Lusso, Paolo] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
RP Lusso, P (reprint author), NIAID, Immunoregulat Lab, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM plusso@niaid.nih.gov
RI Horvat, Branka/M-3504-2014
OI Horvat, Branka/0000-0003-0578-7765
FU Intramural Research Program of the NIAID; NIH; HHV-6 Foundation; INSERM
and ARSEP, France
FX This work was supported in part by the Intramural Research Program of
the NIAID, NIH (PL), the HHV-6 Foundation (BKB) and the INSERM and
ARSEP, France (BFI).
NR 27
TC 2
Z9 2
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD DEC
PY 2014
VL 9
BP 97
EP 103
DI 10.1016/j.coviro.2014.09.012
PG 7
WC Virology
SC Virology
GA AX5IC
UT WOS:000346958700017
PM 25462440
ER
PT J
AU Leibovitch, EC
Jacobson, S
AF Leibovitch, Emily C.
Jacobson, Steven
TI Evidence linking HHV-6 with multiple sclerosis: an update
SO CURRENT OPINION IN VIROLOGY
LA English
DT Article
ID HUMAN-HERPESVIRUS 6; POLYMERASE-CHAIN-REACTION; EPSTEIN-BARR-VIRUS;
INTERFERON-BETA; DISEASE PROGRESSION; CEREBROSPINAL-FLUID; OLIGOCLONAL
BANDS; CROSS-REACTIVITY; DNA-SEQUENCES; BRAIN-TISSUE
AB Following reports of elevated antiviral antibodies in MS patient sera and viral DNA detection in MS plaques nearly two decades ago, the neurovirology community has actively explored how herpesviruses such as HHV-6 might be involved in MS disease pathogenesis. Though findings across the field are non-uniform, an emerging consensus of viral correlates with disease course and evidence of HHV-6-specific immune responses in the CNS provide compelling evidence for a role, direct or indirect, of this virus in MS. Ultimately, the only way to demonstrate the involvement, or lack thereof, of HHV-6 or other herpesviruses in this disease is through a controlled clinical trial of an efficacious antiviral drug.
C1 [Leibovitch, Emily C.; Jacobson, Steven] NINDS, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Leibovitch, Emily C.] George Washington Univ, Sch Med & Hlth Sci, Inst Biomed Sci, Washington, DC 20052 USA.
RP Jacobson, S (reprint author), NINDS, Neuroimmunol Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM jacobsons@ninds.nih.gov
FU National Institutes of Health; National Institute of Neurologic Disease
and Stroke (NINDS)
FX Funding was provided by the intramural program of the National
Institutes of Health, National Institute of Neurologic Disease and
Stroke (NINDS). We thank Bridgette Jeanne Billioux and Breanna Caruso
for critical reading of the manuscript.
NR 52
TC 14
Z9 15
U1 1
U2 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1879-6257
J9 CURR OPIN VIROL
JI Curr. Opin. Virol.
PD DEC
PY 2014
VL 9
BP 127
EP 133
DI 10.1016/j.coviro.2014.09.016
PG 7
WC Virology
SC Virology
GA AX5IC
UT WOS:000346958700021
PM 25462444
ER
PT J
AU Boffetta, P
Bobak, M
Borsch-Supan, A
Brenner, H
Eriksson, S
Grodstein, F
Jansen, E
Jenab, M
Juerges, H
Kampman, E
Kee, F
Kuulasmaa, K
Park, Y
Tjonneland, A
van Duijn, C
Wilsgaard, T
Wolk, A
Trichopoulos, D
Bamia, C
Trichopoulou, A
AF Boffetta, Paolo
Bobak, Martin
Borsch-Supan, Axel
Brenner, Hermann
Eriksson, Sture
Grodstein, Fran
Jansen, Eugene
Jenab, Mazda
Juerges, Hendrik
Kampman, Ellen
Kee, Frank
Kuulasmaa, Kari
Park, Yikyung
Tjonneland, Anne
van Duijn, Cornelia
Wilsgaard, Tom
Wolk, Alicja
Trichopoulos, Dimitrios
Bamia, Christina
Trichopoulou, Antonia
TI The Consortium on Health and Ageing: Network of Cohorts in Europe and
the United States (CHANCES) project-design, population and data
harmonization of a large-scale, international study
SO EUROPEAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE Cohort; Ageing; Elderly; Meta-analysis
ID OSTEOPOROTIC FRACTURES; CARDIOVASCULAR-DISEASE; LIFE-STYLE;
EPIDEMIOLOGY; MORTALITY; WOMEN; DIET; CONSUMPTION; DISABILITY; CANCER
AB There is a public health demand to prevent health conditions which lead to increased morbidity and mortality among the rapidly-increasing elderly population. Data for the incidence of such conditions exist in cohort studies worldwide, which, however, differ in various aspects. The Consortium on Health and Ageing: Network of Cohorts in Europe and the United States (CHANCES) project aims at harmonizing data from existing major longitudinal studies for the elderly whilst focussing on cardiovascular diseases, diabetes mellitus, cancer, fractures and cognitive impairment in order to estimate their prevalence, incidence and cause-specific mortality, and identify lifestyle, socioeconomic, and genetic determinants and biomarkers for the incidence of and mortality from these conditions. A survey instrument assessing ageing-related conditions of the elderly will be also developed. Fourteen cohort studies participate in CHANCES with 683,228 elderly (and 150,210 deaths), from 23 European and three non-European countries. So far, 287 variables on health conditions and a variety of exposures, including biomarkers and genetic data have been harmonized. Different research hypotheses are investigated with meta-analyses. The results which will be produced can help international organizations, governments and policy-makers to better understand the broader implications and consequences of ageing and thus make informed decisions.
C1 [Boffetta, Paolo; Trichopoulos, Dimitrios; Bamia, Christina; Trichopoulou, Antonia] Hellen Hlth Fdn, Athens 11527, Greece.
[Boffetta, Paolo] Icahn Sch Med Mt Sinai, Inst Translat Epidemiol, New York, NY 10029 USA.
[Boffetta, Paolo] Icahn Sch Med Mt Sinai, Tisch Canc Inst, New York, NY 10029 USA.
[Bobak, Martin] UCL, Dept Epidemiol & Publ Hlth, London WC1E 6BT, England.
[Borsch-Supan, Axel] Max Planck Inst Social Law & Social Policy, Munich Ctr Econ Aging, Munich, Germany.
[Brenner, Hermann] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, D-69120 Heidelberg, Germany.
[Eriksson, Sture] Umea Univ, S-90185 Umea, Sweden.
[Grodstein, Fran] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
[Jansen, Eugene] Natl Inst Publ Hlth & Environm, Ctr Hlth Protect, NL-3720 BA Bilthoven, Netherlands.
[Jenab, Mazda] Int Agcy Res Canc IARC WHO, Lyon, France.
[Juerges, Hendrik] Univ Wuppertal, Schumpeter Sch Business & Econ, D-42119 Wuppertal, Germany.
[Kampman, Ellen] Wageningen Univ, Div Human Nutr, NL-6700 EV Wageningen, Netherlands.
[Kee, Frank] Queens Univ Belfast, Inst Clin Sci, UKCRC Ctr Excellence Publ Hlth Northern Ireland, Belfast BT12 6BJ, Antrim, North Ireland.
[Kuulasmaa, Kari] Natl Inst Hlth & Welf THL, Chron Dis Epidemiol & Prevent Unit, Helsinki 00271, Finland.
[Park, Yikyung] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Tjonneland, Anne] Danish Canc Soc, Res Ctr, DK-2100 Copenhagen O, Denmark.
[van Duijn, Cornelia] Erasmus Univ, Med Ctr, Dept Epidemiol, NL-3015 GE Rotterdam, Netherlands.
[Wilsgaard, Tom] UIT, Dept Community Med, N-9037 Tromso, Norway.
[Wolk, Alicja] Karolinska Inst, Inst Environm Med, S-10401 Stockholm, Sweden.
[Trichopoulos, Dimitrios] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Trichopoulos, Dimitrios] Acad Athens, Bur Epidemiol Res, Athens, Greece.
[Bamia, Christina; Trichopoulou, Antonia] Univ Athens, Sch Med, Dept Hyg Epidemiol & Med Stat, GR-11527 Athens, Greece.
RP Trichopoulou, A (reprint author), Hellen Hlth Fdn, 13 Kaisareias & Alexandroupoleos St, Athens 11527, Greece.
EM atrichopoulou@hhf-greece.gr
RI Kampman, E./H-8057-2014; Brenner, Hermann/B-4627-2017;
OI Brenner, Hermann/0000-0002-6129-1572; Kuulasmaa,
Kari/0000-0003-2165-1411; Park, Yikyung/0000-0002-6281-489X
FU European Community [HEALTH-F3-2010-242244]
FX The research leading to these results has received funding from the
European Community's Seventh Framework Programme (FP7/2007-2013)
DG-RESEARCH under Grant Agreement No. HEALTH-F3-2010-242244.
NR 40
TC 16
Z9 16
U1 0
U2 7
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0393-2990
EI 1573-7284
J9 EUR J EPIDEMIOL
JI Eur. J. Epidemiol.
PD DEC
PY 2014
VL 29
IS 12
BP 929
EP 936
DI 10.1007/s10654-014-9977-1
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA AX4PA
UT WOS:000346912900006
PM 25504016
ER
PT J
AU Sinai, P
Dozmorov, IM
Song, R
Schwartzberg, PL
Wakeland, EK
Wulfing, C
AF Sinai, Parisa
Dozmorov, Igor M.
Song, Ran
Schwartzberg, Pamela L.
Wakeland, Edward K.
Wuelfing, Christoph
TI T/B-cell interactions are more transient in response to weak stimuli in
SLE-prone mice
SO EUROPEAN JOURNAL OF IMMUNOLOGY
LA English
DT Article
DE Actin; Imaging; Immunological synapse; Protein kinase C; Systemic lupus
erythematosus
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; GERMINAL-CENTER; PKC-THETA; T-CELLS;
SPATIOTEMPORAL ORGANIZATION; IMMUNOLOGICAL SYNAPSE; IMMUNE-RESPONSES;
SLAM RECEPTORS; B-CELLS; ACTIVATION
AB Changes in immune function during the course of systemic lupus erythematosus (SLE) are well characterized. Class-switched antinuclear antibodies are the hallmark of SLE, and T/B-cell interactions are thus critical. However, changes in immune function contributing to disease susceptibility are unknown. Here, we have analyzed primary T and B cells from a mouse model of SLE prior to the onset of disease. To allow cognate T-cell activation with low affinity, we have developed a lower potency peptide ligand for the OTII TCR. T-and B-cell couples formed less frequently and retained their polarity less efficiently preferentially in response to low-affinity stimulation in SLE-prone mice. This matched decreased recruitment of actin and Vav1 and an enhanced PKC Theta recruitment to the cellular interface in T cells. The induction of the GC B-cell marker GL7 was increased in T/B cell couples from SLE-prone mice when the T-cell numbers were limited. However, the overall gene expression changes were marginal. Taken together, the enhanced cell-couple transience may allow a more efficient sampling of a large number of T/B cell couples, preferentially in response to limiting stimuli, therefore enhancing the immune reactivity in the development of SLE.
C1 [Sinai, Parisa; Wuelfing, Christoph] Univ Bristol, Sch Cellular & Mol Med, Bristol BS8 1TD, Avon, England.
[Sinai, Parisa; Dozmorov, Igor M.; Song, Ran; Wakeland, Edward K.; Wuelfing, Christoph] UT Southwestern Med Ctr, Dept Immunol, Dallas, TX USA.
[Schwartzberg, Pamela L.] NHGRI, NIH, Bethesda, MD 20892 USA.
[Wuelfing, Christoph] UT Southwestern Med Ctr, Dept Cell Biol, Dallas, TX USA.
RP Wulfing, C (reprint author), Univ Bristol, Sch Cellular & Mol Med, Bristol BS8 1TD, Avon, England.
EM Christoph.Wuelfing@bristol.ac.uk
FU National Institutes of Health [CA90436]; National Human Genome Research
Institute
FX This work was supported by grants from the National Institutes of Health
(CA90436) and in part by the intramural program of the National Human
Genome Research Institute. P.S., E.K.W., and C.W. designed the
experiments; P.S., I.M.D., and C.W. executed the experiments; P.L.S. and
E.K.W. provided critical mouse strains; P.S. and C.W. wrote the
manuscript.
NR 37
TC 3
Z9 3
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0014-2980
EI 1521-4141
J9 EUR J IMMUNOL
JI Eur. J. Immunol.
PD DEC
PY 2014
VL 44
IS 12
BP 3522
EP 3531
DI 10.1002/eji.201444602
PG 10
WC Immunology
SC Immunology
GA AX1IO
UT WOS:000346701200007
PM 25209945
ER
PT J
AU Brown, PR
Odet, F
Bortner, CD
Eddy, EM
AF Brown, Paula R.
Odet, Fanny
Bortner, Carl D.
Eddy, Edward M.
TI Reporter Mice Express Green Fluorescent Protein at Initiation of Meiosis
in Spermatocytes
SO GENESIS
LA English
DT Article
DE spermatogenesis; heat shock protein; variegated gene expression;
fluorescence activated cell sorting
ID MOUSE SPERMATOGENIC CELLS; TRANSGENIC MICE; SP-10 GENE; CENTRIFUGAL
ELUTRIATION; SEDIMENTATION-VELOCITY; STEM-CELLS; PROMOTER; TESTIS;
INSULATOR; P70
AB Transgenic mice were generated using a heat shock protein 2 (Hspa2) gene promoter to express green fluorescent protein (GFP) at the beginning of meiotic prophase I in spermatocytes. Expression was confirmed in four lines by in situ fluorescence, immunohistochemistry, western blotting, and PCR assays. The expression and distribution of the GFP and HSPA2 proteins co-localized in spermatocytes and spermatids in three lines, but GFP expression was variegated in one line (F46), being present in some clones of meiotic and post-meiotic germ cells and not in others. Fluorescence activated cell sorting (FACS) was used to isolate purified populations of spermatocytes and spermatids. Although bisulfite sequencing revealed differences in the DNA methylation patterns in the promoter regions of the transgene of the variegated expressing GFP line, a uniformly expressing GFP reporter line, and the Hspa2 gene, these differences did not correlate with variegated expression. The Hspa2-GFP reporter mice provide a novel tool for studies of meiosis by allowing detection of GFP in situ and in isolated spermatogenic cells. They will allow sorting of meiotic and post-meiotic germ cells for characterization of molecular features and correlation of expression of GFP with stage-specific spermatogenic cell proteins and developmental events. genesis 52:976-984, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [Brown, Paula R.; Odet, Fanny; Eddy, Edward M.] NIEHS, Gamete Biol Sect, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Odet, Fanny] GenOway, Lyon, France.
[Bortner, Carl D.] NIEHS, Mol Endocrinol Grp, Lab Signal Transduct, NIH, Res Triangle Pk, NC 27709 USA.
RP Eddy, EM (reprint author), NIEHS, Gamete Biol Sect, Reprod & Dev Toxicol Lab, NIH, POB 12233, Res Triangle Pk, NC 27709 USA.
EM eddy@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences
FX Supported by the Intramural Research Program of the NIH, National
Institute of Environmental Health Sciences
NR 28
TC 1
Z9 1
U1 0
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1526-954X
EI 1526-968X
J9 GENESIS
JI Genesis
PD DEC
PY 2014
VL 52
IS 12
BP 976
EP 984
DI 10.1002/dvg.22830
PG 9
WC Developmental Biology; Genetics & Heredity
SC Developmental Biology; Genetics & Heredity
GA AX1IY
UT WOS:000346702100007
PM 25293348
ER
PT J
AU Bai, HH
Guo, XS
Zhang, D
Narisu, N
Bu, JJ
Jirimutu, J
Liang, F
Zhao, X
Xing, YP
Wang, DZ
Li, TD
Zhang, YR
Guan, BZ
Yang, XK
Yang, ZL
Shuangshan, S
Su, Z
Wu, HG
Li, WJ
Chen, M
Zhu, SL
Bayinnamula, B
Chang, YQ
Gao, Y
Lan, TM
Suyalatu, S
Huang, H
Su, Y
Chen, YJ
Li, WQ
Yang, X
Feng, Q
Wang, J
Yang, HM
Wang, J
Wu, QZ
Yin, Y
Zhou, HM
AF Bai, Haihua
Guo, Xiaosen
Zhang, Dong
Narisu, Narisu
Bu, Junjie
Jirimutu, Jirimutu
Liang, Fan
Zhao, Xiang
Xing, Yanping
Wang, Dingzhu
Li, Tongda
Zhang, Yanru
Guan, Baozhu
Yang, Xukui
Yang, Zili
Shuangshan, Shuangshan
Su, Zhe
Wu, Huiguang
Li, Wenjing
Chen, Ming
Zhu, Shilin
Bayinnamula, Bayinnamula
Chang, Yuqi
Gao, Ying
Lan, Tianming
Suyalatu, Suyalatu
Huang, Hui
Su, Yan
Chen, Yujie
Li, Wenqi
Yang, Xu
Feng, Qiang
Wang, Jian
Yang, Huanming
Wang, Jun
Wu, Qizhu
Yin, Ye
Zhou, Huanmin
TI The Genome of a Mongolian Individual Reveals the Genetic Imprints of
Mongolians on Modern Human Populations
SO GENOME BIOLOGY AND EVOLUTION
LA English
DT Article
DE Mongolian genome; de novo assembly; genetic variations; patrilineal
origin; genetic imprints
ID Y-CHROMOSOME EVIDENCE; HUMAN MITOCHONDRIAL-DNA; SEQUENCING DATA;
CARNITINE DEFICIENCY; WIDE PATTERNS; EASTERN ASIA; NEW-WORLD; HISTORY;
PROTEIN; DATABASE
AB Mongolians have played a significant role in modern human evolution, especially after the rise of Genghis Khan (1162[?]-1227). Although the social cultural impacts of Genghis Khan and the Mongolian population have been well documented, explorations of their genome structure and genetic imprints on other human populations have been lacking. We here present the genome of a Mongolian male individual. The genome was de novo assembled using a total of 130.8-fold genomic data produced from massively parallel whole-genome sequencing. We identified high-confidence variation sets, including 3.7 million single nucleotide polymorphisms (SNPs) and 756,234 short insertions and deletions. Functional SNP analysis predicted that the individual has a pathogenic risk for carnitine deficiency. We located the patrilineal inheritance of the Mongolian genome to the lineage D3a through Y haplogroup analysis and inferred that the individual has a common patrilineal ancestor with Tibeto-Burman populations and is likely to be the progeny of the earliest settlers in East Asia. We finally investigated the genetic imprints of Mongolians on other human populations using different approaches. We found varying degrees of gene flows between Mongolians and populations living in Europe, South/Central Asia, and the Indian subcontinent. The analyses demonstrate that the genetic impacts of Mongolians likely resulted from the expansion of the Mongolian Empire in the 13th century. The genome will be of great help in further explorations of modern human evolution and genetic causes of diseases/traits specific to Mongolians.
C1 [Bai, Haihua; Jirimutu, Jirimutu; Wang, Dingzhu; Shuangshan, Shuangshan; Wu, Huiguang; Chen, Ming; Bayinnamula, Bayinnamula; Gao, Ying; Suyalatu, Suyalatu; Chen, Yujie; Wu, Qizhu] Inner Mongolia Univ Nationalities, Tongliao, Peoples R China.
[Guo, Xiaosen; Bu, Junjie; Liang, Fan; Zhao, Xiang; Li, Tongda; Yang, Xukui; Su, Zhe; Li, Wenjing; Zhu, Shilin; Chang, Yuqi; Lan, Tianming; Huang, Hui; Su, Yan; Li, Wenqi; Yang, Xu; Feng, Qiang; Wang, Jian; Yang, Huanming; Wang, Jun; Yin, Ye] BGI Shenzhen, Shenzhen, Peoples R China.
[Guo, Xiaosen; Feng, Qiang; Wang, Jun] Univ Copenhagen, Dept Biol, DK-1168 Copenhagen, Denmark.
[Zhang, Dong; Xing, Yanping; Zhang, Yanru; Yang, Zili; Zhou, Huanmin] Inner Mongolia Agr Univ, Inner Mongolia Autonomous Reg Key Lab Biomanufact, Hohhot, Peoples R China.
[Narisu, Narisu] NHGRI, Med Genom & Metab Genet Branch, NIH, Bethesda, MD 20892 USA.
[Bu, Junjie; Yang, Huanming] Univ Elect Sci & Technol China, Sch Life Sci & Technol, Minist Educ, Key Lab NeuroInformat, Chengdu 610054, Peoples R China.
[Li, Tongda] S China Univ Technol, Sch Biosci & Bioengn, Guangzhou, Guangdong, Peoples R China.
[Guan, Baozhu] Inner Mongolia Int Mongolian Hosp, Hohhot, Peoples R China.
[Shuangshan, Shuangshan] Baotou Normal Coll, Baotou, Peoples R China.
[Chen, Ming] Zhejiang Univ, Coll Life Sci, Dept Bioinformat, Hangzhou 310003, Zhejiang, Peoples R China.
[Wang, Jian; Yang, Huanming] James D Watson Inst Genome Sci, Hangzhou, Zhejiang, Peoples R China.
[Wang, Jun] Univ Copenhagen, Ctr Basic Metab Res, Novo Nordisk Fdn, DK-1168 Copenhagen, Denmark.
[Wang, Jun] King Abdulaziz Univ, Jeddah 21413, Saudi Arabia.
[Wang, Jun] Aarhus Univ, Ctr iSequencing, DK-8000 Aarhus C, Denmark.
RP Wu, QZ (reprint author), Inner Mongolia Univ Nationalities, Tongliao, Peoples R China.
EM qizhu_wu@sohu.com; yinye@genomics.cn; huanminzhou@gmail.com
RI Wang, Jun/C-8434-2016; Wang, Jun/B-9503-2016
OI Wang, Jun/0000-0002-8540-8931; Wang, Jun/0000-0002-2113-5874
FU National Basic Research Program of China (973 program) [2011CB809201,
2011CB809202, 2011CB809203]; Chinese 863 Program [2012AA02A201];
National Natural Science Foundation of China [30890032, 31161130357,
81060098, 81160101]; Foundation of the Inner Mongolia Department of
Education [NJZY13169]; Shenzhen Municipal Government of China
[ZYC200903240080A, ZYC201105170397A]; NHGRI [1ZIAHG000024]; National
Institute of Health (NIH)
FX The authors sincerely thank our sample donor for generously contributing
his blood. This project was supported by the National Basic Research
Program of China (973 program no. 2011CB809201, 2011CB809202, and
2011CB809203), the Chinese 863 Program (2012AA02A201), the National
Natural Science Foundation of China (30890032, 31161130357, 81060098,
and 81160101), Foundation of the Inner Mongolia Department of Education
(NJZY13169), and the Shenzhen Municipal Government of China (grants
ZYC200903240080A and ZYC201105170397A). It was also supported by the
intramural program of NHGRI (1ZIAHG000024), the National Institute of
Health (NIH) to N.N. The authors are indebted to the Mongolian
historians and anthropologists who contributed to this work, but are not
included in the author list, including Dr Yuqing Bao, Dr Ming Chen, Dr
Yongchun Fu, and others. They sincerely thank Dr David Reich for
generously providing the genotype data of India populations. They thank
Dr Francis S. Collins, Dr Steve C.J. Parker, Dr Lawrence Brody, and Dr
Kevin Stuart for helpful advice, comments, and editing. They also thank
two anonymous reviewers for critical comments. The authors declare that
they have no competing interest.
NR 70
TC 3
Z9 3
U1 3
U2 19
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1759-6653
J9 GENOME BIOL EVOL
JI Genome Biol. Evol.
PD DEC
PY 2014
VL 6
IS 12
BP 3122
EP 3136
DI 10.1093/gbe/evu242
PG 15
WC Evolutionary Biology; Genetics & Heredity
SC Evolutionary Biology; Genetics & Heredity
GA AX5YO
UT WOS:000347000800001
PM 25377941
ER
PT J
AU Manasanch, EE
Korde, N
Mailankody, S
Tageja, N
Bhutani, M
Roschewski, M
Landgren, O
AF Manasanch, Elisabet E.
Korde, Neha
Mailankody, Sham
Tageja, Nishant
Bhutani, Manisha
Roschewski, Mark
Landgren, Ola
TI Smoldering multiple myeloma: special considerations surrounding
treatment on versus off clinical trials
SO HAEMATOLOGICA
LA English
DT Editorial Material
ID STEM-CELL TRANSPLANTATION; MONOCLONAL GAMMOPATHY; UNDETERMINED
SIGNIFICANCE; COMPLETE RESPONSE; PROGRESSION; THERAPY; RISK
C1 [Manasanch, Elisabet E.] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma Myeloma, Houston, TX 77030 USA.
[Korde, Neha; Landgren, Ola] Mem Sloan Kettering Canc Ctr, Myeloma Serv, New York, NY 10021 USA.
[Mailankody, Sham; Tageja, Nishant; Bhutani, Manisha; Roschewski, Mark] NCI, Multiple Myeloma Sect, Lymphoid Malignancies Branch, NIH, Bethesda, MD 20892 USA.
RP Manasanch, EE (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Lymphoma Myeloma, Houston, TX 77030 USA.
EM EEManasanch@mdanderson.org; landgrec@mskcc.org
NR 17
TC 2
Z9 2
U1 0
U2 0
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOLOGICA
JI Haematologica
PD DEC
PY 2014
VL 99
IS 12
BP 1769
EP 1771
DI 10.3324/haematol.2014.107516
PG 3
WC Hematology
SC Hematology
GA AX6EP
UT WOS:000347016400001
PM 25472951
ER
PT J
AU Kim, SY
Le Rademacher, J
Antin, JH
Anderlini, P
Ayas, M
Battiwalla, M
Carreras, J
Kurtzberg, J
Nakamura, R
Eapen, M
Deeg, HJ
AF Kim, Sung-Yong
Le Rademacher, Jennifer
Antin, Joseph H.
Anderlini, Paolo
Ayas, Mouhab
Battiwalla, Minoo
Carreras, Jeanette
Kurtzberg, Joanne
Nakamura, Ryotaro
Eapen, Mary
Deeg, H. Joachim
TI Myelodysplastic syndrome evolving from aplastic anemia treated with
immunosuppressive therapy: efficacy of hematopoietic stem cell
transplantation
SO HAEMATOLOGICA
LA English
DT Article
ID ACUTE MYELOID-LEUKEMIA; UNRELATED DONOR TRANSPLANTATION; ANTITHYMOCYTE
GLOBULIN; TELOMERE LENGTH; RISK-FACTORS; CYCLOSPORINE; ASSOCIATION;
KARYOTYPE; RECIPIENT; CHILDREN
AB A proportion of patients with aplastic anemia who are treated with immunosuppressive therapy develop clonal hematologic disorders, including post-aplastic anemia myelodysplastic syndrome. Many will proceed to allogeneic hematopoietic stem cell transplantation. We identified 123 patients with post-aplastic anemia myelodysplastic syndrome who from 1991 through 2011 underwent allogeneic hematopoietic stem cell transplantation, and in a matched-pair analysis compared outcome to that in 393 patients with de novo myelodysplastic syndrome. There was no difference in overall survival. There were no significant differences with regard to 5-year probabilities of relapse, non-relapse mortality, relapse-free survival and overall survival; these were 14%, 40%, 46% and 49% for post-aplastic anemia myelodysplastic syndrome, and 20%, 33%, 47% and 49% for de novo myelodysplastic syndrome, respectively. In multivariate analysis, relapse (hazard ratio 0.71; P=0.18), non-relapse mortality (hazard ratio 1.28; P=0.18), relapse-free survival (hazard ratio 0.97; P=0.80) and overall survival (hazard ratio 1.02; P=0.88) of post-aplastic anemia myelodysplastic syndrome were similar to those of patients with de novo myelodysplastic syndrome. Cytogenetic risk was independently associated with overall survival in both groups. Thus, transplant success in patients with post-aplastic anemia myelodysplastic syndrome was similar to that in patients with de novo myelodysplastic syndrome, and cytogenetics was the only significant prognostic factor for post-aplastic anemia myelodysplastic syndrome patients.
C1 [Kim, Sung-Yong; Deeg, H. Joachim] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA.
[Kim, Sung-Yong] KonKuk Univ, Sch Med, Med Ctr, Seoul, South Korea.
[Le Rademacher, Jennifer; Carreras, Jeanette; Eapen, Mary] Med Coll Wisconsin, Ctr Int Blood & Marrow Transplant Res, Dept Med, Milwaukee, WI 53226 USA.
[Le Rademacher, Jennifer] Med Coll Wisconsin, Div Biostat, Milwaukee, WI 53226 USA.
[Antin, Joseph H.] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Anderlini, Paolo] Univ Texas MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cellular Therapy, Houston, TX 77030 USA.
[Ayas, Mouhab] King Faisal Specialist Hosp & Res Ctr, Dept Pediat Hematol Oncol, Riyadh 11211, Saudi Arabia.
[Carreras, Jeanette] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Kurtzberg, Joanne] Duke Univ, Med Ctr, Dept Pediat Pediat Blood & Marrow Transplant, Durham, NC USA.
[Nakamura, Ryotaro] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
RP Deeg, HJ (reprint author), Fred Hutchinson Canc Res Ctr, Div Clin Res, 1124 Columbia St, Seattle, WA 98104 USA.
EM jdeeg@fhcrc.org
FU National Cancer Institute (NCI) [U24-CA076518]; National Heart, Lung and
Blood Institute (NHLBI); National Institute of Allergy and Infectious
Diseases (NIAID); NHLBI [5U10HL069294]; NCI; Health Resources and
Services Administration (HRSA/DHHS) [HHSH250201200016C]; Office of Naval
Research [N00014-13-10039, N00014-14-1-0028]; Actinium Pharmaceuticals;
Allos Therapeutics, Inc.; Amgen, Inc.; [HL036444]; [HL095999];
[CA015704]
FX The CIBMTR which is supported by Public Health Service Grant/Cooperative
Agreement U24-CA076518 from the National Cancer Institute (NCI), the
National Heart, Lung and Blood Institute (NHLBI) and the National
Institute of Allergy and Infectious Diseases (NIAID); a
Grant/Cooperative Agreement 5U10HL069294 from NHLBI and NCI; a contract
HHSH250201200016C with Health Resources and Services Administration
(HRSA/DHHS); two Grants N00014-13-10039 and N00014-14-1-0028 from the
Office of Naval Research; and grants from *Actinium Pharmaceuticals;
Allos Therapeutics, Inc.; *Amgen, Inc.; anonymous donation to the
Medical College of Wisconsin; Ariad; Be the Match Foundation; Blue Cross
and Blue Shield Association; *Celgene Corporation; Chimerix, Inc.; Fred
Hutchinson Cancer Research Center; Fresenius-Biotech North America,
Inc.; *Gamida Cell Teva Joint Venture Ltd.; Genentech, Inc.;*Gentium
SpA; Genzyme Corporation; GlaxoSmithKline; Health Research, Inc. Roswell
Park Cancer Institute; HistoGenetics, Inc.; Incyte Corporation; Jeff
Gordon Children's Foundation; Kiadis Pharma; The Leukemia & Lymphoma
Society; Medac GmbH; The Medical College of Wisconsin; Merck & Co, Inc.;
Millennium: The Takeda Oncology Co.; *Milliman USA, Inc.; *Miltenyi
Biotec, Inc.; National Marrow Donor Program; Onyx Pharmaceuticals; Optum
Healthcare Solutions, Inc.; Osiris Therapeutics, Inc.; Otsuka America
Pharmaceutical, Inc.; Perkin Elmer, Inc.; *Remedy Informatics; *Sanofi
US; Seattle Genetics; Sigma-Tau Pharmaceuticals; Soligenix, Inc.; St.
Baldrick's Foundation; StemCyte, A Global Cord Blood Therapeutics Co.;
Stemsoft Software, Inc.; Swedish Orphan Biovitrum; *Tarix
Pharmaceuticals; *TerumoBCT; *Teva Neuroscience, Inc.; *THERAKOS, Inc.;
University of Minnesota; University of Utah; and *Wellpoint, Inc. The
views expressed in this article do not reflect the official policy or
position of the National Institute of Health, the Department of the
Navy, the Department of Defense, Health Resources and Services
Administration (HRSA) or any other agency of the U.S. Government.
*Corporate Members. SY K and HJD were supported by grants HL036444,
HL095999 and CA015704.
NR 28
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Z9 3
U1 2
U2 6
PU FERRATA STORTI FOUNDATION
PI PAVIA
PA VIA GIUSEPPE BELLI 4, 27100 PAVIA, ITALY
SN 0390-6078
J9 HAEMATOLOGICA
JI Haematologica
PD DEC
PY 2014
VL 99
IS 12
BP 1868
EP 1875
DI 10.3324/haematol.2014.108977
PG 8
WC Hematology
SC Hematology
GA AX6EP
UT WOS:000347016400013
PM 25107891
ER
PT J
AU Jelacic, TM
Chabot, DJ
Bozue, JA
Tobery, SA
West, MW
Moody, K
Yang, D
Oppenheim, JJ
Friedlander, AM
AF Jelacic, Tanya M.
Chabot, Donald J.
Bozue, Joel A.
Tobery, Steven A.
West, Michael W.
Moody, Krishna
Yang, De
Oppenheim, Joost J.
Friedlander, Arthur M.
TI Exposure to Bacillus anthracis Capsule Results in Suppression of Human
Monocyte-Derived Dendritic Cells (vol 82, pg 3405, 2014)
SO INFECTION AND IMMUNITY
LA English
DT Correction
C1 [Jelacic, Tanya M.; Chabot, Donald J.; Bozue, Joel A.; Tobery, Steven A.; West, Michael W.; Friedlander, Arthur M.] US Army, Med Res Inst Infect Dis, Frederick, MD 21702 USA.
[Yang, De; Oppenheim, Joost J.] Frederick Natl Lab Canc Res, Mol Immunoregulat Lab, Frederick, MD USA.
[Moody, Krishna] Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA.
RP Jelacic, TM (reprint author), US Army, Med Res Inst Infect Dis, Frederick, MD 21702 USA.
NR 1
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0019-9567
EI 1098-5522
J9 INFECT IMMUN
JI Infect. Immun.
PD DEC
PY 2014
VL 82
IS 12
BP 5347
EP 5347
DI 10.1128/IAI.02665-14
PG 1
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AX5HZ
UT WOS:000346958400043
ER
PT J
AU Zhang, XX
Ito, Y
Liang, JR
Liu, JL
He, J
Sun, WJ
AF Zhang, Xin-xin
Ito, Yoichiro
Liang, Jin-ru
Liu, Jian-li
He, Jiao
Sun, Wen-ji
TI Therapeutic effects of total steroid saponin extracts from the rhizome
of Dioscorea zingiberensis CHWright in Freund's complete adjuvant
induced arthritis in rats
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Dioscorea zingiberensis CHWright; Total steroid saponins;
Adjuvant-induced arthritis; Lipopolysaccharide; NF-kappa B
ID COLLAGEN-INDUCED ARTHRITIS; KAPPA-B; INFLAMMATORY MEDIATORS;
RHEUMATOID-ARTHRITIS; ACTIVATION; SUPPRESSES; IDENTIFICATION; PATHWAY;
DIOSCIN; WRIGHT
AB The aim of our present study is to explore the anti-arthritic potential effect of total steroid saponins (TSSNs) extracted from the rhizome of Dioscorea zingiberensis C.H.Wright (DZW) and to investigate the underlying mechanisms. This work was performed using adjuvant-induced arthritis (AIA) rats in vivo and lipopolysaccharide (LPS) simulated 264.7 macrophage cells in vitro. In ALA-induced arthritic rats, TSSN significantly alleviated the arthritic progression through evaluating arthritic score, immune organ indexes, paw swelling, and body weight This phenomenon was well correlated with significant suppression of the overproduction of inflammation cytokines (IL-1, IL-1 beta, IL-6, and TNF-alpha.), oxidant stress makers (MDA and NO), eicosanoids (LTB4 and PGE(2)), and inflammatory enzymes (5-LOX and COX-2) versus the ALA rats without treatment. On the contrary, the release of SOD and IL-10 was profoundly increased. What's more, TSSN could obviously ameliorate the translocation of NF-kappa B to the nucleus through phosphorylation of the p65 and I kappa B alpha in vivo and in vitro. The current findings demonstrated that TSSN could protect the injured ankle joint from further deterioration and exert its satisfactory anti-arthritis properties through anti-inflammatory and anti-oxidant effects via inactivating the NF-kappa B signal pathway. This research implies that DZW may be a useful therapeutic agent for the treatment of human arthritis. (C) 2014 Published by Elsevier B.V.
C1 [Zhang, Xin-xin; Liang, Jin-ru; Liu, Jian-li; He, Jiao; Sun, Wen-ji] NW Univ Xian, Biomed Key Lab Shaanxi Prov, Xian 710069, Peoples R China.
[Ito, Yoichiro] NHLBI, Lab Bioseparat Technol, Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Ito, Y (reprint author), NHLBI, Lab Bioseparat Technol, Biochem & Biophys Ctr, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM itoy@nhlbi.nih.gov; guoxiaolizhang@163.com
FU Intramural NIH HHS [Z99 HL999999]
NR 33
TC 5
Z9 5
U1 1
U2 18
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD DEC
PY 2014
VL 23
IS 2
BP 407
EP 416
DI 10.1016/j.intimp.2014.07.018
PG 10
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA AX5GF
UT WOS:000346954000006
PM 25066758
ER
PT J
AU Bode, C
Wang, J
Klinman, DM
AF Bode, Christian
Wang, Jing
Klinman, Dennis M.
TI Suppressive oligodeoxynucleotides promote the generation of regulatory T
cells by inhibiting STAT1 phosphorylation
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Suppressive oligonucleotides; Regulatory T cells; STAT transcription
factors
ID TRANSCRIPTION FACTOR FOXP3; IMMUNE TOLERANCE; COMMENSAL DNA; TTAGGG
MOTIFS; INDUCTION; EFFECTOR; MICE; OLIGONUCLEOTIDES; ACTIVATION; ANTIGEN
AB Suppressive oligodeoxynucleotides (Sup ODN) express repetitive TTAGGG motifs that have proven useful in the treatment/prevention of numerous inflammatory and autoimmune diseases. The mechanism underlying the immunosuppressive activity of Sup ODN is incompletely understood. Regulatory T cells (T-reg) Play a key role in controlling a variety of pathologic autoimmune responses. T-reg are generated from activated CD4(+) T cells in a process that involves the phosphorylation of STAT family members. Current studies demonstrate that Sup ODN promote the differentiation of CD4(+)CD25(-) T cells into functionally active iT(reg) in vitro. When administered in vivo, Sup ODN promote the generation of iT(reg) in response to peptide challenge. Central to this effect is the ability of Sup ODN to block the phosphorylation of STAT1. These findings clarify the mechanism underlying the therapeutic activity of Sup ODN and support their use in T-reg-based immunotherapy. Published by Elsevier B.V. All rights reserved.
C1 [Bode, Christian; Wang, Jing; Klinman, Dennis M.] NCI, Ctr Canc Res, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Bode, Christian] Univ Hosp Bonn, Dept Anesthesiol & Intens Care Med, Bonn, Germany.
RP Klinman, DM (reprint author), NCI, CCR, Bldg 567 Rm 205, Frederick, MD 21702 USA.
EM klinmand@mail.nih.gov
FU National Cancer Institute of the National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Cancer Institute of the National Institutes of Health.
NR 48
TC 3
Z9 3
U1 0
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD DEC
PY 2014
VL 23
IS 2
BP 516
EP 522
DI 10.1016/j.intimp.2014.09.027
PG 7
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA AX5GF
UT WOS:000346954000020
PM 25311665
ER
PT J
AU Yang, J
Lernmark, A
Uusitalo, UM
Lynch, KF
Veijola, R
Winkler, C
Larsson, HE
Rewers, M
She, JX
Ziegler, AG
Simell, OG
Hagopian, WA
Akolkar, B
Krischer, JP
Vehik, K
AF Yang, J.
Lernmark, A.
Uusitalo, U. M.
Lynch, K. F.
Veijola, R.
Winkler, C.
Larsson, H. E.
Rewers, M.
She, J-X
Ziegler, A. G.
Simell, O. G.
Hagopian, W. A.
Akolkar, B.
Krischer, J. P.
Vehik, K.
CA TEDDY Study Grp
TI Prevalence of obesity was related to HLA-DQ in 2-4-year-old children at
genetic risk for type 1 diabetes
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
DE body mass index; HLA genotype; type 1 diabetes; pediatric;
autoantibodies
ID BODY-MASS INDEX; INCREASED LINEAR GROWTH; ACCELERATOR HYPOTHESIS;
ENVIRONMENTAL DETERMINANTS; FINNISH CHILDREN; CELIAC-DISEASE; AGE;
DIAGNOSIS; OVERWEIGHT; GENOTYPES
AB OBJECTIVES: Body size is postulated to modulate type 1 diabetes as either a trigger of islet autoimmunity or an accelerator to clinical onset after seroconversion. As overweight and obesity continue to rise among children, the aim of this study was to determine whether human leukocyte antigen DQ (HLA-DQ) genotypes may be related to body size among children genetically at risk for type 1 diabetes.
METHODS: Repeated measures of weight and height were collected from 5969 children 2-4 years of age enrolled in The Environmental Determinants of Diabetes in the Young prospective study. Overweight and obesity was determined by the International Obesity Task Force cutoff values that correspond to body mass index (BMI) of 25 and 30 kg m(-2) at age 18.
RESULTS: The average BMI was comparable across specific HLA genotypes at every age point. The proportion of overweight was not different by HLA, but percent obesity varied by age with a decreasing trend among DQ2/8 carriers (P for trend = 0.0315). A multivariable regression model suggested DQ2/2 was associated with higher obesity risk at age 4 (odds ratio, 2.41; 95% confidence interval, 1.21-4.80) after adjusting for the development of islet autoantibody and/or type 1 diabetes.
CONCLUSIONS: The HLA-DQ2/2 genotype may predispose to obesity among 2-4-year-old children with genetic risk for type 1 diabetes.
C1 [Yang, J.; Uusitalo, U. M.; Lynch, K. F.; Krischer, J. P.; Vehik, K.] Univ S Florida, Dept Pediat, Morsani Coll Med, Pediat Epidemiol Ctr, Tampa, FL 33612 USA.
[Lernmark, A.; Larsson, H. E.] Lund Univ, CRC, Skane Univ Hosp SUS, Dept Clin Sci, Malmo, Sweden.
[Veijola, R.] Univ Oulu, Dept Pediat, Inst Clin Med, SF-90100 Oulu, Finland.
[Winkler, C.; Ziegler, A. G.] Helmholtz Zentrum Munchen, Inst Diabet Res, Neuherberg, Germany.
[Winkler, C.; Ziegler, A. G.] Tech Univ Munich, Klinikum Rechts Isar, Neuherberg, Germany.
[Winkler, C.; Ziegler, A. G.] Forschergrp Diabet eV, Neuherberg, Germany.
[Rewers, M.] Univ Colorado, Barbara Davis Ctr Childhood Diabet, Aurora, CO USA.
[She, J-X] Georgia Regents Univ, Med Coll Georgia, Ctr Biotechnol & Genom Med, Augusta, GA USA.
[Simell, O. G.] Univ Turku, Dept Pediat, Turku, Finland.
[Hagopian, W. A.] Pacific Northwest Diabet Res Inst, Seattle, WA USA.
[Akolkar, B.] NIDDK, Bethesda, MD USA.
RP Yang, J (reprint author), Univ S Florida, Dept Pediat, Morsani Coll Med, Pediat Epidemiol Ctr, 3650 Spectrum Blvd,Suite 100, Tampa, FL 33612 USA.
EM jimin.yang@epi.usf.edu
RI Ziegler, Anette-Gabriele/M-4614-2014;
OI Ziegler, Anette-Gabriele/0000-0002-6290-5548; Elding Larsson,
Helena/0000-0003-3306-1742
FU National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
[U01 DK63829, U01 DK63861, U01 DK63821, U01 DK63865, U01 DK63863, U01
DK63836, U01 DK63790, UC4 DK63829, UC4 DK63861, UC4 DK63821, UC4
DK63865, UC4 DK63863, UC4 DK63836, UC4 DK95300, HHSN267200700014C];
National Institute of Allergy and Infectious Diseases (NIAID); National
Institute of Child Health and Human Development (NICHD); National
Institute of Environmental Health Sciences (NIEHS); Juvenile Diabetes
Research Foundation (JDRF); Centers for Disease Control and Prevention
(CDC)
FX This study was funded by U01 DK63829, U01 DK63861, U01 DK63821, U01
DK63865, U01 DK63863, U01 DK63836, U01 DK63790, UC4 DK63829, UC4
DK63861, UC4 DK63821, UC4 DK63865, UC4 DK63863, UC4 DK63836 and UC4
DK95300 and Contract No. HHSN267200700014C from the National Institute
of Diabetes and Digestive and Kidney Diseases (NIDDK), National
Institute of Allergy and Infectious Diseases (NIAID), National Institute
of Child Health and Human Development (NICHD), National Institute of
Environmental Health Sciences (NIEHS), Juvenile Diabetes Research
Foundation (JDRF), and Centers for Disease Control and Prevention (CDC).
NR 42
TC 0
Z9 0
U1 4
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0307-0565
EI 1476-5497
J9 INT J OBESITY
JI Int. J. Obes.
PD DEC
PY 2014
VL 38
IS 12
BP 1491
EP 1496
DI 10.1038/ijo.2014.55
PG 6
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA AX7PL
UT WOS:000347107400002
PM 24694666
ER
PT J
AU Chrysovergis, K
Wang, X
Kosak, J
Lee, SH
Kim, JS
Foley, JF
Travlos, G
Singh, S
Baek, SJ
Eling, TE
AF Chrysovergis, K.
Wang, X.
Kosak, J.
Lee, S-H
Kim, J. S.
Foley, J. F.
Travlos, G.
Singh, S.
Baek, S. J.
Eling, T. E.
TI NAG-1/GDF-15 prevents obesity by increasing thermogenesis, lipolysis and
oxidative metabolism
SO INTERNATIONAL JOURNAL OF OBESITY
LA English
DT Article
DE NAG-1/GDF-15; insulin resistance; BAT; thermogenesis; lipolysis
ID BROWN ADIPOSE-TISSUE; DIET-INDUCED OBESITY; TGF-BETA SUPERFAMILY;
MACROPHAGE INHIBITORY CYTOKINE-1; INSULIN-RESISTANCE;
ENERGY-EXPENDITURE; ADIPOCYTE DIFFERENTIATION; ENDOCRINE ORGAN;
SENSITIVITY; MICE
AB OBJECTIVE: Obesity is a major health problem associated with high morbidity and mortality. NSAID-activated gene (NAG-1) is a TGF-beta superfamily member reported to alter adipose tissue levels in mice. We investigated whether hNAG-1 acts as a regulator of adiposity and energy metabolism.
DESIGN/SUBJECTS: hNAG-1 mice, ubiquitously expressing hNAG-1, were placed on a control or high-fat diet for 12 weeks. hNAG-1-expressing B16/F10 melanoma cells were used in a xenograft model to deliver hNAG-1 to obese C57BL/6 mice.
RESULTS: As compared with wild-type littermates, transgenic hNAG-1 mice have less white fat and brown fat despite equivalent food intake, improved glucose tolerance, lower insulin levels and are resistant to dietary-and genetic-induced obesity. hNAG-1 mice are more metabolically active with higher energy expenditure. Obese C57BL/6 mice treated with hNAG-1-expressing xenografts show decreases in adipose tissue and serum insulin levels. hNAG-1 mice and obese mice treated with hNAG-1-expressing xenografts show increased thermogenic gene expression (UCP1, PGC1 alpha, ECH1, Cox8b, Dio2, Cyc1, PGC1 beta, PPAR alpha, Elvol3) in brown adipose tissue (BAT) and increased expression of lipolytic genes (Adrb3, ATGL, HSL) in both white adipose tissue (WAT) and BAT, consistent with higher energy metabolism.
CONCLUSION: hNAG-1 modulates metabolic activity by increasing the expression of key thermogenic and lipolytic genes in BAT and WAT. hNAG-1 appears to be a novel therapeutic target in preventing and treating obesity and insulin resistance.
C1 [Chrysovergis, K.; Wang, X.; Kosak, J.; Kim, J. S.; Singh, S.; Eling, T. E.] NIEHS, Mol Carcinogenesis Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Lee, S-H; Baek, S. J.] Univ Tennessee, Coll Vet Med, Dept Biomed & Diagnost Sci, Knoxville, TN USA.
[Foley, J. F.; Travlos, G.] NIEHS, Cellular & Mol Pathol Branch, NIH, Res Triangle Pk, NC 27709 USA.
[Kim, J. S.] Andong Natl Univ, Dept Biol Sci, Andong, South Korea.
RP Eling, TE (reprint author), NIEHS, Mol Carcinogenesis Lab, NIH, 111 TW Alexander Dr,Bldg 101,Room D448B, Res Triangle Pk, NC 27709 USA.
EM eling@niehs.nih.gov
FU NIH, NIEHS Intramural Research Program [Z01- ES010016-14]; Center of
Excellence in Livestock Diseases and Human Health, University of
Tennessee
FX We thank David Goulding, Page Myers and the Necropsy core for their
technical help. We thank Drs Paul Wade and Xiaoling Li for critical
reading of this manuscript. There are no conflicts of interests. This
research was supported by NIH, NIEHS Intramural Research Program (Eling)
Z01- ES010016-14 and in part, the Center of Excellence in Livestock
Diseases and Human Health, University of Tennessee (Baek).
NR 50
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Z9 12
U1 0
U2 8
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0307-0565
EI 1476-5497
J9 INT J OBESITY
JI Int. J. Obes.
PD DEC
PY 2014
VL 38
IS 12
BP 1555
EP 1564
DI 10.1038/ijo.2014.27
PG 10
WC Endocrinology & Metabolism; Nutrition & Dietetics
SC Endocrinology & Metabolism; Nutrition & Dietetics
GA AX7PL
UT WOS:000347107400011
PM 24531647
ER
PT J
AU Weiss, DJ
Atkinson, PM
Bhatt, S
Mappin, B
Hay, SI
Gething, PW
AF Weiss, Daniel J.
Atkinson, Peter M.
Bhatt, Samir
Mappin, Bonnie
Hay, Simon I.
Gething, Peter W.
TI An effective approach for gap-filling continental scale remotely sensed
time-series
SO ISPRS JOURNAL OF PHOTOGRAMMETRY AND REMOTE SENSING
LA English
DT Article
DE Gap-filling; MODIS; EVI; LST; Africa
ID SLC-OFF IMAGES; GEOSTATISTICAL APPROACH; CLOUDED PIXELS; MODIS;
PRODUCTS; INTERPOLATION; COVER; VALIDATION
AB The archives of imagery and modeled data products derived from remote sensing programs with high temporal resolution provide powerful resources for characterizing inter- and intra-annual environmental dynamics. The impressive depth of available time-series from such missions (e.g., MODIS and AVHRR) affords new opportunities for improving data usability by leveraging spatial and temporal information inherent to longitudinal geospatial datasets. In this research we develop an approach for filling gaps in imagery time-series that result primarily from cloud cover, which is particularly problematic in forested equatorial regions. Our approach consists of two, complementary gap-filling algorithms and a variety of run-time options that allow users to balance competing demands of model accuracy and processing time. We applied the gap-filling methodology to MODIS Enhanced Vegetation Index (EVI) and daytime and nighttime Land Surface Temperature (LST) datasets for the African continent for 2000-2012, with a 1 km spatial resolution, and an 8-day temporal resolution. We validated the method by introducing and filling artificial gaps, and then comparing the original data with model predictions. Our approach achieved R-2 values above 0.87 even for pixels within 500 km wide introduced gaps. Furthermore, the structure of our approach allows estimation of the error associated with each gap-filled pixel based on the distance to the non-gap pixels used to model its fill value, thus providing a mechanism for including uncertainty associated with the gap-filling process in downstream applications of the resulting datasets. (C) 2014 The Authors. Published by Elsevier B.V. on behalf of International Society for Photogrammetry and Remote Sensing, Inc. (ISPRS).
C1 [Weiss, Daniel J.; Bhatt, Samir; Mappin, Bonnie; Hay, Simon I.; Gething, Peter W.] Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Oxford, England.
[Atkinson, Peter M.] Univ Southampton, Southampton SO17 1BJ, Hants, England.
[Hay, Simon I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Weiss, DJ (reprint author), Univ Oxford, Dept Zool, Spatial Ecol & Epidemiol Grp, Tinbergen Bldg, Oxford, England.
EM daniel.weiss@zoo.ox.ac.uk
RI Hay, Simon/F-8967-2015;
OI Hay, Simon/0000-0002-0611-7272; Mappin, Bonnie/0000-0002-1205-719X;
Gething, Peter/0000-0001-6759-5449
FU UK Medical Research Council (MRC) [K00669X]; UK Department for
International Development (DFID) under the MRC/DFID [K00669X]; Bill and
Melinda Gates Foundation [OPP1068048]
FX PWG is a Career Development Fellow (#K00669X) jointly funded by the UK
Medical Research Council (MRC) and the UK Department for International
Development (DFID) under the MRC/DFID Concordat agreement and also
receives support from the Bill and Melinda Gates Foundation
(#OPP1068048). These grants also support DW, SB, and BM.
NR 28
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U1 3
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-2716
EI 1872-8235
J9 ISPRS J PHOTOGRAMM
JI ISPRS-J. Photogramm. Remote Sens.
PD DEC
PY 2014
VL 98
BP 106
EP 118
DI 10.1016/j.isprsjprs.2014.10.001
PG 13
WC Geography, Physical; Geosciences, Multidisciplinary; Remote Sensing;
Imaging Science & Photographic Technology
SC Physical Geography; Geology; Remote Sensing; Imaging Science &
Photographic Technology
GA AX8BL
UT WOS:000347135500009
PM 25642100
ER
PT J
AU Cimino, JJ
Ayres, EJ
Remennik, L
Rath, S
Freedman, R
Beri, A
Chen, Y
Huser, V
AF Cimino, James J.
Ayres, Elaine J.
Remennik, Lyubov
Rath, Sachi
Freedman, Robert
Beri, Andrea
Chen, Yang
Huser, Vojtech
TI The National Institutes of Health's Biomedical Translational Research
Information System (BTRIS): Design, contents, functionality and
experience to date
SO JOURNAL OF BIOMEDICAL INFORMATICS
LA English
DT Article
DE Clinical research; Translational research; Research data repository;
Research data warehouse; Ontology
ID DATABASE; TERMINOLOGIES; DESIDERATA; KNOWLEDGE; SCIENCE; MODEL; WEB
AB The US National Institutes of Health (NIH) has developed the Biomedical Translational Research Information System (BTRIS) to support researchers' access to translational and clinical data. BTRIS includes a data repository, a set of programs for loading data from NIH electronic health records and research data management systems, an ontology for coding the disparate data with a single terminology, and a set of user interface tools that provide access to identified data from individual research studies and data across all studies from which individually identifiable data have been removed. This paper reports on unique design elements of the system, progress to date and user experience after five years of development and operation. Published by Elsevier Inc.
C1 [Cimino, James J.; Ayres, Elaine J.; Remennik, Lyubov; Huser, Vojtech] NIH, Lab Informat Dev, Ctr Clin, Bethesda, MD 20892 USA.
[Rath, Sachi; Freedman, Robert; Beri, Andrea; Chen, Yang] Comp Sci Corp, Falls Church, VA USA.
RP Cimino, JJ (reprint author), NIH, Lab Informat Dev, Ctr Clin, Room 6-2551,10 Ctr Dr, Bethesda, MD 20892 USA.
EM ciminoj@mail.nih.gov
OI Cimino, James/0000-0003-4101-1622
FU NIH Clinical Center; National Library of Medicine
FX The authors thank NIH Clinical Center Director John Gallin and former
NIH Director Elias Zerhouni for the vision to launch the BTRIS project.
We have had additional invaluable guidance from Dr. Richard Cannon and
Dr. Richard Davey on many design and policy decisions. We also thank all
the BTRIS staff, past and present, for their contributions to the
project, especially Mark Budd, James Rohrbaugh and Donald Griffin. We
are grateful to the National Cancer Institute's Center for Biomedical
Informatics and Information Technology (CBIIT) for sharing their
ontology development tools and experience. Drs. Cimino and Huser are
supported by research funding from the NIH Clinical Center and the
National Library of Medicine.
NR 41
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Z9 3
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 1532-0464
EI 1532-0480
J9 J BIOMED INFORM
JI J. Biomed. Inform.
PD DEC
PY 2014
VL 52
BP 11
EP 27
DI 10.1016/j.jbi.2013.11.004
PG 17
WC Computer Science, Interdisciplinary Applications; Medical Informatics
SC Computer Science; Medical Informatics
GA AY0HC
UT WOS:000347277000003
PM 24262893
ER
PT J
AU Shang, N
Xu, H
Rindflesch, TC
Cohen, T
AF Shang, Ning
Xu, Hua
Rindflesch, Thomas C.
Cohen, Trevor
TI Identifying plausible adverse drug reactions using knowledge extracted
from the literature
SO JOURNAL OF BIOMEDICAL INFORMATICS
LA English
DT Article
DE Pharmacovigilance; Distributional semantics; Literature-based discovery;
Predication-based semantic indexing; Reflective random indexing
ID LITERATURE-BASED DISCOVERY; ACTIVATED RECEPTOR-GAMMA; SPONTANEOUS
REPORTING SYSTEM; ELECTRONIC HEALTH RECORDS; TYPE-2 DIABETES-MELLITUS;
MIGRAINE-MAGNESIUM DISCOVERIES; UNDISCOVERED PUBLIC KNOWLEDGE;
MYOCARDIAL-INFARCTION; PPAR-GAMMA; CARDIOVASCULAR OUTCOMES
AB Pharmacovigilance involves continually monitoring drug safety after drugs are put to market. To aid this process; algorithms for the identification of strongly correlated drug/adverse drug reaction (ADR) pairs from data sources such as adverse event reporting systems or Electronic Health Records have been developed. These methods are generally statistical in nature, and do not draw upon the large volumes of knowledge embedded in the biomedical literature. In this paper, we investigate the ability of scalable Literature Based Discovery (LBD) methods to identify side effects of pharmaceutical agents. The advantage of LBD methods is that they can provide evidence from the literature to support the plausibility of a drug/ADR association, thereby assisting human review to validate the signal, which is an essential component of pharmacovigilance. To do so, we draw upon vast repositories of knowledge that has been extracted from the biomedical literature by two Natural Language Processing tools, MetaMap and SemRep. We evaluate two LBD methods that scale comfortably to the volume of knowledge available in these repositories. Specifically, we evaluate Reflective Random Indexing (RAI), a model based on concept-level co-occurrence, and Predication-based Semantic Indexing (PSI), a model that encodes the nature of the relationship between concepts to support reasoning analogically about drug-effect relationships. An evaluation set was constructed from the Side Effect Resource 2 (SIDER2), which contains known drug/ADR relations, and models were evaluated for their ability to "rediscover" these relations. In this paper, we demonstrate that both RRI and PSI can recover known drug-adverse event associations. However, PSI performed better overall, and has the additional advantage of being able to recover the literature underlying the reasoning pathways it used to make its predictions. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Shang, Ning; Xu, Hua; Cohen, Trevor] Univ Texas Hlth Sci Ctr Houston, Sch Biomed Informat, Houston, TX 77030 USA.
[Rindflesch, Thomas C.] Natl Lib Med, Bethesda, MD USA.
RP Shang, N (reprint author), Univ Texas Hlth Sci Ctr Houston, Sch Biomed Informat, Houston, TX 77030 USA.
EM sunnyshang001@gmail.com
FU U.S. National Library of Medicine [1R01LM011563]; Intramural Research
Program of the U.S. National Institutes of Health, National Library of
Medicine
FX The work was supported by the U.S. National Library of Medicine Grant
(1R01LM011563), Using Biomedical Knowledge to Identify Plausible Signals
for Pharmacovigilance. This work was also supported in part by the
Intramural Research Program of the U.S. National Institutes of Health,
National Library of Medicine. The authors would like to thank Peter
Davies for his comments on the paper, and for discussions regarding the
implications of these methods for the evaluation of potential ADRs.
NR 155
TC 9
Z9 9
U1 2
U2 13
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1532-0464
EI 1532-0480
J9 J BIOMED INFORM
JI J. Biomed. Inform.
PD DEC
PY 2014
VL 52
BP 293
EP 310
DI 10.1016/j.jbi.2014.07.011
PG 18
WC Computer Science, Interdisciplinary Applications; Medical Informatics
SC Computer Science; Medical Informatics
GA AY0HC
UT WOS:000347277000031
PM 25046831
ER
PT J
AU Mishra, R
Bian, JT
Fiszman, M
Weir, CR
Jonnalagadda, S
Mostafa, J
Del Fiol, G
AF Mishra, Rashmi
Bian, Jiantao
Fiszman, Marcelo
Weir, Charlene R.
Jonnalagadda, Siddhartha
Mostafa, Javed
Del Fiol, Guilherme
TI Text summarization in the biomedical domain: A systematic review of
recent research
SO JOURNAL OF BIOMEDICAL INFORMATICS
LA English
DT Review
DE Text summarization; Intrinsic evaluation; Language processing; Machine
learning; Biomedical domain
ID KNOWLEDGE; STRATEGIES; DOCUMENTS
AB Objective: The amount of information for clinicians and clinical researchers is growing exponentially. Text summarization reduces information as an attempt to enable users to find and understand relevant source texts more quickly and effortlessly. In recent years, substantial research has been conducted to develop and evaluate various summarization techniques in the biomedical domain. The goal of this study was to systematically review recent published research on summarization of textual documents in the biomedical domain.
Materials and methods: MEDLINE (2000 to October 2013), IEEE Digital Library, and the ACM digital library were searched. Investigators independently screened and abstracted studies that examined text summarization techniques in the biomedical domain. Information is derived from selected articles on five dimensions: input, purpose, output, method and evaluation.
Results: Of 10,786 studies retrieved, 34(0.3%) met the inclusion criteria. Natural language processing (17; 50%) and a hybrid technique comprising of statistical, Natural language processing and machine learning (15; 44%) were the most common summarization approaches. Most studies (28; 82%) conducted an intrinsic evaluation.
Discussion: This is the first systematic review of text summarization in the biomedical domain. The study identified research gaps and provides recommendations for guiding future research on biomedical text summarization.
Conclusion: Recent research has focused on a hybrid technique comprising statistical, language processing and machine learning techniques. Further research is needed on the application and evaluation of text summarization in real research or patient care settings. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Mishra, Rashmi; Bian, Jiantao; Weir, Charlene R.; Del Fiol, Guilherme] Univ Utah, Dept Biomed Informat, Salt Lake City, UT 84108 USA.
[Bian, Jiantao] Intermt Healthcare, Clin Modeling Team, Salt Lake City, UT USA.
[Fiszman, Marcelo] Natl Lib Med, Lister Hill Ctr, Bethesda, MD USA.
[Weir, Charlene R.] VA Med Ctr, Salt Lake City, UT USA.
[Jonnalagadda, Siddhartha] Northwestern Univ, Dept Prevent Med Hlth & Biomed Informat, Chicago, IL 60611 USA.
[Mostafa, Javed] Univ N Carolina, SILS, Chapel Hill, NC USA.
RP Del Fiol, G (reprint author), Univ Utah, Dept Biomed Informat, 421 Wakara Way, Salt Lake City, UT 84108 USA.
EM guilherme.delfiol@utah.edu
OI Bian, Jiantao/0000-0001-5989-5177; Del Fiol,
Guilherme/0000-0001-9954-6799
FU National Library of Medicine [1R01LM011416]
FX The authors would like to acknowledge Alice Weber for providing insights
on the search strategy of this systematic review. This project was
supported by Grant Number 1R01LM011416-01 from the National Library of
Medicine.
NR 52
TC 4
Z9 4
U1 0
U2 15
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1532-0464
EI 1532-0480
J9 J BIOMED INFORM
JI J. Biomed. Inform.
PD DEC
PY 2014
VL 52
BP 457
EP 467
DI 10.1016/j.jbi.2014.06.009
PG 11
WC Computer Science, Interdisciplinary Applications; Medical Informatics
SC Computer Science; Medical Informatics
GA AY0HC
UT WOS:000347277000046
PM 25016293
ER
PT J
AU Kuban, KCK
O'Shea, TM
Allred, EN
Paneth, N
Hirtz, D
Fichorova, RN
Leviton, A
AF Kuban, Karl C. K.
O'Shea, T. Michael
Allred, Elizabeth N.
Paneth, Nigel
Hirtz, Deborah
Fichorova, Raina N.
Leviton, Alan
CA ELGAN Study Investigators
TI Systemic Inflammation and Cerebral Palsy Risk in Extremely Preterm
Infants
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Article
DE cerebral palsy risk; inflammation
ID WHITE-MATTER DAMAGE; LOW GESTATIONAL-AGE; BRAIN-DAMAGE; PERIVENTRICULAR
LEUKOMALACIA; HISTOLOGIC CHARACTERISTICS; CHILDREN BORN; 28TH WEEK;
BLOOD; CYTOKINES; PROTEINS
AB The authors hypothesized that among extremely preterm infants, elevated concentrations of inflammation-related proteins in neonatal blood are associated with cerebral palsy at 24 months. In 939 infants born before 28 weeks gestation, the authors measured blood concentrations of 25 proteins on postnatal days 1, 7, and 14 and evaluated associations between elevated protein concentrations and cerebral palsy diagnosis. Protein elevations within 3 days of birth were not associated with cerebral palsy. Elevations of tumor necrosis factor-alpha, tumor necrosis factor-alpha-receptor-1, interleukin-8, and intercellular adhesion molecule-1 on at least 2 days were associated with diparesis. Recurrent-persistent elevations of interleukin-6, E-selectin, or insulin-like growth factor binding protein-1 were associated with hemiparesis. Diparesis and hemiparesis were more likely among infants who had at least 4 of 9 protein elevations that previously have been associated with cognitive impairment and microcephaly. Repeated elevations of inflammation-related proteins during the first 2 postnatal weeks are associated with increased risk of cerebral palsy.
C1 [Kuban, Karl C. K.] Boston Med Ctr, Dept Pediat, Boston, MA USA.
[O'Shea, T. Michael] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA.
[Allred, Elizabeth N.; Fichorova, Raina N.; Leviton, Alan] Harvard Univ, Sch Med, Boston, MA USA.
[Allred, Elizabeth N.; Leviton, Alan] Boston Childrens Hosp, Boston, MA USA.
[Allred, Elizabeth N.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Paneth, Nigel] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 USA.
[Hirtz, Deborah] NINDS, Bethesda, MD 20892 USA.
[Fichorova, Raina N.] Brigham & Womens Hosp, Dept Obstet Gynecol & Reprod Biol, Boston, MA 02115 USA.
RP Kuban, KCK (reprint author), Boston Univ, Sch Med, Boston Med Ctr, Dept Pediat, 771 Albany St, Boston, MA 02118 USA.
EM karl.kuban@bmc.org
FU National Institute of Neurological Disorders and Stroke
[5U01NS040069-05, 2R01NS040069-06A2]
FX The authors disclosed receipt of the following financial support for the
research, authorship, and/or publication of this article: This study was
completed as a cooperative agreement with the National Institute of
Neurological Disorders and Stroke (5U01NS040069-05 and
2R01NS040069-06A2). The study sponsor participated in the study design,
analyses, and manuscript writing.
NR 49
TC 12
Z9 12
U1 0
U2 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0883-0738
EI 1708-8283
J9 J CHILD NEUROL
JI J. Child Neurol.
PD DEC
PY 2014
VL 29
IS 12
BP 1692
EP 1698
DI 10.1177/0883073813513335
PG 7
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA AX4NB
UT WOS:000346908000024
PM 24646503
ER
PT J
AU Goswami, SC
Mishra, SK
Maric, D
Kaszas, K
Gonnella, GL
Clokie, SJ
Kominsky, HD
Gross, JR
Keller, JM
Mannes, AJ
Hoon, MA
Iadarola, MJ
AF Goswami, Samridhi C.
Mishra, Santosh K.
Maric, Dragan
Kaszas, Krisztian
Gonnella, Gian Luigi
Clokie, Samuel J.
Kominsky, Hal D.
Gross, Jacklyn R.
Keller, Jason M.
Mannes, Andrew J.
Hoon, Mark A.
Iadarola, Michael J.
TI Molecular Signatures of Mouse TRPV1-Lineage Neurons Revealed by RNA-Seq
Transcriptome Analysis
SO JOURNAL OF PAIN
LA English
DT Article
DE Pain; nociception; dorsal root ganglion; capsaicin; resiniferatoxin
ID DORSAL-ROOT GANGLION; PRIMARY SENSORY NEURONS; PRIMARY AFFERENT NEURONS;
MU-OPIOID RECEPTORS; SPINAL-CORD; NEUROPATHIC PAIN; GENE-EXPRESSION;
THERMAL STIMULI; C-KIT; DIFFERENTIAL EXPRESSION
AB Disorders of pain neural systems are frequently chronic and, when recalcitrant to treatment, can severely degrade the quality of life. The pain pathway begins with sensory neurons in dorsal root or trigeminal ganglia, and the neuronal subpopulations that express the transient receptor potential cation channel, subfamily V. member 1 (TRPV1) ion channel transduce sensations of painful heat and inflammation and play a fundamental role in clinical pain arising from cancer and arthritis. In the present study, we elucidate the complete transcriptomes of neurons from the TRPV1 lineage and a non-TRPV1 neuroglial population in sensory ganglia through the combined application of next-gen deep RNA-Seq, genetic neuronal labeling with fluorescence-activated cell sorting, or neuron-selective chemoablation. RNA-Seq accurately quantitates gene expression, a difficult parameter to determine with most other methods, especially for very low and very high expressed genes. Differentially expressed genes are present at every level of cellular function from the nucleus to the plasma membrane. We identified many ligand receptor pairs in the TRPV1 population, suggesting that autonomous presynaptic regulation may be a major regulatory mechanism in nociceptive neurons. The data define, in a quantitative, cell population-specific fashion, the molecular signature of a distinct and clinically important group of pain-sensing neurons and provide an overall framework for understanding the transcriptome of TRPV1 nociceptive neurons.
Perspective: Next-gen RNA-Seq, combined with molecular genetics, provides a comprehensive and quantitative measurement of transcripts in TRPV1 lineage neurons and a contrasting transcriptome from non-TRPV1 neurons and cells. The transcriptome highlights previously unrecognized protein families, identifies multiple molecular circuits for excitatory or inhibitory autocrine and paracrine signaling, and suggests new combinatorial approaches to pain control. Published by Elsevier Inc.
C1 [Goswami, Samridhi C.; Kaszas, Krisztian; Gonnella, Gian Luigi; Clokie, Samuel J.; Kominsky, Hal D.; Gross, Jacklyn R.; Keller, Jason M.; Mannes, Andrew J.; Iadarola, Michael J.] NIH, Ctr Clin, Dept Perioperat Med, Anesthesia Sect, Bethesda, MD 20892 USA.
[Mishra, Santosh K.; Hoon, Mark A.] Natl Inst Dent & Craniofacial Res, Lab Sensory Biol, Mol Genet Unit, Bethesda, MD USA.
[Maric, Dragan] NINDS, Neurophysiol Lab, NIH, Bethesda, MD 20892 USA.
RP Iadarola, MJ (reprint author), NIH, Ctr Clin, Dept Perioperat Med, Bldg 10,Room 2C401,10 Ctr Dr,MSC 1510, Bethesda, MD 20892 USA.
EM michael.iadarola@nih.gov
OI Clokie, Samuel/0000-0002-0025-3652
FU National Center for Complementary and Alternative Medicine; National
Institute of Dental and Craniofacial Research; Department of
Perioperative Medicine, Clinical Center of the National Institutes of
Health
FX This research was supported by the Intramural Research Programs of the
National Center for Complementary and Alternative Medicine, the National
Institute of Dental and Craniofacial Research, and the Department of
Perioperative Medicine, Clinical Center of the National Institutes of
Health. Supplementary data accompanying this article are available
online at www.jpain.org and www.sciencedirect.com.
NR 107
TC 15
Z9 15
U1 0
U2 8
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1526-5900
J9 J PAIN
JI J. Pain
PD DEC
PY 2014
VL 15
IS 12
BP 1338
EP 1359
DI 10.1016/j.jpain.2014.09.010
PG 22
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AX4HC
UT WOS:000346893100013
PM 25281809
ER
PT J
AU Hanson, LC
Bull, J
Wessell, K
Massie, L
Bennett, RE
Kutner, JS
Aziz, NM
Abernethy, A
AF Hanson, Laura C.
Bull, Janet
Wessell, Kathryn
Massie, Lisa
Bennett, Rachael E.
Kutner, Jean S.
Aziz, Noreen M.
Abernethy, Amy
TI Strategies to Support Recruitment of Patients With Life-Limiting Illness
for Research: The Palliative Care Research Cooperative Group
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Palliative care; recruitment; research networks; clinical trials
ID STATIN THERAPY; EVIDENCE BASE; DISCONTINUATION; METAANALYSIS;
MEDICATIONS; CHALLENGES; PATTERNS
AB Context. The Palliative Care Research Cooperative Group (PCRC) is the first clinical trials cooperative for palliative care in the U.S.
Objectives. To describe barriers and strategies for recruitment during the inaugural PCRC clinical trial.
Methods. The parent study was a multisite randomized controlled trial enrolling adults with life expectancy anticipated to be one to six months, randomized to discontinue statins (intervention) vs. to continue on statins (control). To study recruitment best practices, we conducted semistructured interviews with 18 site principal investigators (PIs) and clinical research coordinators (CRCs) and reviewed recruitment rates. Interviews covered three topics: 1) successful strategies for recruitment, 2) barriers to recruitment, and 3) optimal roles of the PI and CRC.
Results. All eligible site PIs and CRCs completed interviews and provided data on statin protocol recruitment. The parent study completed recruitment of 381 patients. Site enrollment ranged from 1 to 109 participants, with an average of 25 enrolled per site. Five major barriers included difficulty locating eligible patients, severity of illness, family and provider protectiveness, seeking patients in multiple settings, and lack of resources for recruitment activities. Five effective recruitment strategies included systematic screening of patient lists, thoughtful messaging to make research relevant, flexible protocols to accommodate patients' needs, support from clinical champions, and the additional resources of a trials cooperative group.
Conclusion. The recruitment experience from the multisite PCRC yields new insights into methods for effective recruitment to palliative care clinical trials. These results will inform training materials for the PCRC and may assist other investigators in the field. J Pain Symptom Manage 2014;48:1021-1030. (C) 2014 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.
C1 [Hanson, Laura C.] Univ N Carolina, Div Geriatr Med, Chapel Hill, NC 27599 USA.
[Hanson, Laura C.] Univ N Carolina, Palliat Care Program, Chapel Hill, NC 27599 USA.
[Hanson, Laura C.; Wessell, Kathryn] Univ N Carolina, Cecil B Sheps Ctr Hlth Serv Res, Chapel Hill, NC 27599 USA.
[Bull, Janet; Massie, Lisa] Four Seasons Hosp & Palliat Care, Flat Rock, NC USA.
[Bennett, Rachael E.; Kutner, Jean S.] Univ Colorado, Sch Med, Dept Med, Div Gen Internal Med, Denver, CO USA.
[Aziz, Noreen M.] NINR, NIH, Bethesda, MD 20892 USA.
[Abernethy, Amy] Duke Univ, Sch Med, Dept Med, Div Oncol, Durham, NC 27706 USA.
RP Hanson, LC (reprint author), Univ N Carolina, Div Geriatr Med, CB 7550, Chapel Hill, NC 27599 USA.
EM lhanson@med.unc.edu
OI Wessell, Kathryn/0000-0001-9127-7088
FU National Institutes of Health-National Institute of Nursing Research
[UC4 NR012584]; National Institute of Nursing Research; National
Institute on Aging; National Heart, Lung, and Blood Institute; National
Cancer Institute; Agency for Healthcare Research and Quality; DARA;
GlaxoSmithKline; Celgene; Helsinn; Dendreon; Pfizer; Informed Medical
Decisions Foundation
FX This study was supported by National Institutes of Health-National
Institute of Nursing Research grant UC4 NR012584. Dr. Hanson has
research funding from the National Institute of Nursing Research, the
National Institute on Aging, and the National Heart, Lung, and Blood
Institute. Funds are distributed to the University of North Carolina for
salary and research support. Further consulting is pending for the
Research Triangle Institute. Dr. Abernethy has research funding from the
National Institute of Nursing Research, National Cancer Institute,
Agency for Healthcare Research and Quality, DARA, GlaxoSmithKline,
Celgene, Helsinn, Dendreon, and Pfizer; these funds are all distributed
to Duke University Medical Center to support research including salary
support for Dr. Abernethy. Pending industry-funded projects include
Genentech, Bristol-Myers Squibb, Insys, and Kanglaite. In the last two
years, she has had nominal consulting agreements with or received
honoraria (<$10,000 annually) from Novartis, Bristol-Myers Squibb, and
Pfizer. Consulting with Bristol-Meyers Squibb in 2013, for role as
cochair of a Scientific Advisory Committee. Dr. Abernethy had a paid
leadership role with American Academy of Hospice & Palliative Medicine
(President). She has corporate leadership responsibility in AthenaHealth
(health IT company), Advoset (an education company that has a contract
with Novartis), and Orange Leaf Associates LLC (an IT development
company). Dr. Kutner has research funding from the National Institute of
Nursing Research, National Cancer Institute, and Agency for Healthcare
Research and Quality. She is supported by the Informed Medical Decisions
Foundation in her role as medical editor. All these funds are
distributed to University of Colorado School of Medicine to support
research including salary support for Dr. Kutner.
NR 30
TC 2
Z9 2
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD DEC
PY 2014
VL 48
IS 6
BP 1021
EP 1030
DI 10.1016/j.jpainsymman.2014.04.008
PG 10
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA AX1ZG
UT WOS:000346742300001
PM 24863152
ER
PT J
AU Hsiao, CP
Wang, D
Kaushal, A
Chen, MK
Saligan, L
AF Hsiao, Chao-Pin
Wang, Dan
Kaushal, Aradhana
Chen, Mei-Kuang
Saligan, Leorey
TI Differential Expression of Genes Related to Mitochondrial Biogenesis and
Bioenergetics in Fatigued Prostate Cancer Men Receiving External Beam
Radiation Therapy
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Fatigue; gene expression; mitochondria; biogenesis; bioenergetics;
prostate cancer; radiation therapy
ID ALPHA-SYNUCLEIN; RADIOTHERAPY; AUTOPHAGY; PATIENT; HOMEOSTASIS;
ACTIVATION; DEPRESSION; MITOPHAGY; MUTATION; FISSION
AB Objectives. This prospective study explored relationships between expression changes of genes related to mitochondrial biogenesis/bioenergetics and fatigue in men with prostate cancer receiving external beam radiation therapy (EBRT).
Methods. Fatigue and gene expression were measured before (Day 0), at midpoint (Days 19-21), and at completion (Days 38-42) of EBRT using the seven-item Patient-Reported Outcomes Measurement Information System-Fatigue short form and from whole blood cell RNA, respectively. The human mitochondria RT2 Profiler (TM) PCR Array System was used to identify differential expression of mitochondrial biogenesis/bioenergetics-related genes. Mixed linear modeling estimated the changes in fatigue and gene expression over time and determined significant associations between gene expression and fatigue.
Results. Subjects were 50 men with prostate cancer (scheduled for EBRT = 25, active surveillance as matched controls = 25). The mean Patient-Reported Outcomes Measurement Information System-Fatigue T-score (mean = 50 +/- 10 in a general population) for study subjects was 44.87 +/- 5.89 and for controls was 43.5 +/- 2.8 at baseline. Differential expression of two genes inside the mitochondria involved in critical mitochondrial complexes: BCS1L (beta = 1.30), SLC25A37 (beta = -2.44), and two genes on the outer mitochondrial membrane vital for mitochondrial integrity: BCL2L1 (beta = -1.68) and FIS1 (beta = -2.35) were significantly associated with changes in fatigue scores of study subjects during EBRT.
Conclusion. Genes related to oxidative phosphorylation, energy production, and mitochondrial membrane integrity are associated with worsening fatigue during EBRT. Further investigation of the pathways involved with this association may explain mechanisms behind the development of fatigue in this population. Published by Elsevier Inc. on behalf of American Academy of Hospice and Palliative Medicine.
C1 [Hsiao, Chao-Pin; Wang, Dan; Saligan, Leorey] NINR, NIH, Cleveland, OH 44106 USA.
[Kaushal, Aradhana] NCI, NIH, Cleveland, OH USA.
[Chen, Mei-Kuang] Univ Arizona, Tucson, AZ USA.
[Hsiao, Chao-Pin] Case Western Reserve Univ, Cleveland, OH 44106 USA.
RP Hsiao, CP (reprint author), NINR, 2120 Cornell Rd, Cleveland, OH 44106 USA.
EM cxh416@case.edu
OI Chen, Mei-kuang/0000-0002-0407-6788
FU Intramural Research Program of National Institute of Nursing Research,
National Institutes of Health, Bethesda, MD [09-NR-0088]
FX This study was supported by the Intramural Research Program of National
Institute of Nursing Research (Protocol # 09-NR-0088), National
Institutes of Health, Bethesda, MD. The authors have no consultant or
advisory positions and no stock or other ownership interests to
disclose.
NR 41
TC 4
Z9 4
U1 1
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD DEC
PY 2014
VL 48
IS 6
BP 1080
EP 1090
DI 10.1016/j.jpainsymman.2014.03.010
PG 11
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA AX1ZG
UT WOS:000346742300007
PM 24786901
ER
PT J
AU Abernethy, AP
Capell, WH
Aziz, NM
Ritchie, C
Prince-Paul, M
Bennett, RE
Kutner, JS
AF Abernethy, Amy P.
Capell, Warren H.
Aziz, Noreen M.
Ritchie, Christine
Prince-Paul, Maryjo
Bennett, Rachael E.
Kutner, Jean S.
TI Ethical Conduct of Palliative Care Research: Enhancing Communication
Between Investigators and Institutional Review Boards
SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT
LA English
DT Article
DE Palliative care; human subjects protection; research ethics;
institutional review boards
ID END-OF-LIFE; CLINICAL-RESEARCH; EVIDENCE BASE; ISSUES; CHALLENGES;
STRATEGIES; GUIDELINES; BARRIERS; SCIENCE; CANCER
AB Palliative care has faced moral and ethical challenges when conducting research involving human subjects. There are currently no resources to guide institutional review boards (IRBs) in applying standard ethical principles and terms-in a specific way-to palliative care research. Using as a case study a recently completed multisite palliative care clinical trial, this article provides guidance and recommendations for both IRBs and palliative care investigators to facilitate communication and attain the goal of conducting ethical palliative care research and protecting study participants while advancing the science. Beyond identifying current challenges faced by palliative care researchers and IRBs reviewing palliative care research, this article suggests steps that the palliative care research community can take to establish a scientifically sound, stable, productive, and well-functioning relationship between palliative care investigators and the ethical bodies that oversee their work. (C) 2014 American Academy of Hospice and Palliative Medicine. Published by Elsevier Inc. All rights reserved.
C1 [Abernethy, Amy P.] Duke Univ, Sch Med, Duke Clin Res Inst, Durham, NC USA.
[Abernethy, Amy P.] Duke Univ, Sch Med, Duke Canc Inst, Durham, NC USA.
[Capell, Warren H.; Bennett, Rachael E.] Univ Colorado, Sch Med, Aurora, CO USA.
[Aziz, Noreen M.] NINR, Div Extramural Act, NIH, Bethesda, MD 20892 USA.
[Ritchie, Christine] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Prince-Paul, Maryjo] Case Western Reserve Univ, Frances Payne Bolton Sch Nursing, Cleveland, OH 44106 USA.
RP Kutner, JS (reprint author), Univ Colorado, Sch Med, 12631 E 17th Ave,Mail Stop B180, Aurora, CO 80045 USA.
EM Jean.Kutner@ucdenver.edu
FU NINR [1UC4NR012584-01]; National Cancer Institute; Agency for Healthcare
Research and Quality; DARA; GlaxoSmithKline; Celgene; Helsinn; Dendreon;
Pfizer; National Institute on Aging; Commonwealth Fund; Retirement
Research Foundation; California Healthcare Foundation; Steven D.
Bechtel, Jr. Foundation; National Heart Lung Blood Institute; American
Cancer Society
FX This work was supported by the NINR (1UC4NR012584-01). Dr. Abernethy has
research funding from the NINR, National Cancer Institute, Agency for
Healthcare Research and Quality, DARA, GlaxoSmithKline, Celgene,
Helsinn, Dendreon, and Pfizer; all these funds are distributed to Duke
University Medical Center to support research including salary support
for Dr. Abernethy. Pending industry-funded projects include Genentech,
Bristol-Myers Squibb, Insys, and Kanglaite. In the last two years, she
has had nominal consulting agreements with or received honoraria
(<$10,000 annually) from Novartis, Bristol-Myers Squibb, and Pfizer. Dr.
Abernethy had a paid leadership role with American Academy of Hospice &
Palliative Medicine (President). She has corporate leadership
responsibility in AthenaHealth (health IT company), Advoset (an
education company that has a contract with Novartis), and Orange Leaf
Associates LLC (an IT development company). Dr. Ritchie has research
funding from the NINR, National Institute on Aging, the Commonwealth
Fund, the Retirement Research Foundation, the California Healthcare
Foundation, and the Steven D. Bechtel, Jr. Foundation. All these funds
are distributed to the University of California San Francisco to support
research including salary support for Dr. Ritchie. She is also Editor
for Up to Date Palliative Care.; Dr. Kutner has research funding from
the NINR, National Institute on Aging, National Cancer Institute, Agency
for Healthcare Research and Quality, the National Heart Lung Blood
Institute, and the American Cancer Society. Dr. Kutner is a Medical
Editor for the Informed Medical Decisions Foundation. All these funds
are distributed to the University of Colorado to support research
including salary support for Dr. Kutner. Drs. Capell, Prince-Paul and
Aziz and Ms. Bennett have no disclosures.
NR 44
TC 0
Z9 1
U1 1
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0885-3924
EI 1873-6513
J9 J PAIN SYMPTOM MANAG
JI J. Pain Symptom Manage.
PD DEC
PY 2014
VL 48
IS 6
BP 1211
EP 1221
DI 10.1016/j.jpainsymman.2014.05.005
PG 11
WC Health Care Sciences & Services; Medicine, General & Internal; Clinical
Neurology
SC Health Care Sciences & Services; General & Internal Medicine;
Neurosciences & Neurology
GA AX1ZG
UT WOS:000346742300019
PM 24879998
ER
PT J
AU Schmoll, HJ
Twelves, C
Sun, WJ
O'Connell, MJ
Cartwright, T
McKenna, E
Saif, M
Lee, S
Yothers, G
Haller, D
AF Schmoll, Hans-Joachim
Twelves, Chris
Sun, Weijing
O'Connell, Michael J.
Cartwright, Thomas
McKenna, Edward
Saif, Muhammad
Lee, Steve
Yothers, Greg
Haller, Daniel
TI Effect of adjuvant capecitabine or fluorouracil, with or without
oxaliplatin, on survival outcomes in stage III colon cancer and the
effect of oxaliplatin on post-relapse survival: a pooled analysis of
individual patient data from four randomised controlled trials
SO LANCET ONCOLOGY
LA English
DT Article
ID METASTATIC COLORECTAL-CANCER; ACID PLUS OXALIPLATIN; PHASE-III;
5-FLUOROURACIL/FOLINIC ACID; 1ST-LINE THERAPY; MONTHLY REGIMEN;
ONCOLOGY-GROUP; NSABP C-07; LEUCOVORIN; BEVACIZUMAB
AB Background Oxaliplatin-based adjuvant therapy is the standard of care for stage III colon cancer. Adjuvant capecitabine with or without oxaliplatin versus leucovorin and fluorouracil with or without oxaliplatin has not been directly compared; therefore, we aimed to analyse the efficacy and safety of these treatments using individual patient data pooled from four randomised controlled trials. We also assessed post-relapse survival, which has been postulated to be worse in patients receiving adjuvant oxaliplatin.
Methods Patients with resected stage III colon cancer who were 18 years of age or older, with an Eastern Cooperative Oncology Group performance status of 0 or 1, from four randomised controlled trials (NSABP C-08, XELOXA, X-ACT, and AVANT; 8734 patients in total) were pooled and analysed. The treatment regimens included in our analyses were: XELOX (oxaliplatin and capecitabine); leucovorin and fluorouracil; capecitabine; FOLFOX-4 (leucovorin, fluorouracil, and oxaliplatin); and modified FOLFOX-6 (mFOLFOX-6). Disease-free survival was the primary endpoint for all trials that supplied patients for this analysis. Here, we compared disease-free, relapse-free, and overall survival between the patient groups who received capecitabine with or without oxaliplatin and those who received leucovorin and fluorouracil with or without oxaliplatin. Post-relapse survival was compared between the combined XELOX and FOLFOX groups, and the leucovorin and fluorouracil groups. Post-relapse survival was also compared between the capecitabine with or without oxaliplatin and leucovorin and fluorouracil with or without oxaliplatin groups.
Findings Disease-free survival did not differ significantly between patients who received leucovorin and fluorouracil versus those who received capecitabine in adjusted analyses (hazard ratio [HR] 1.02 [0.93-1.11; p=0.72]) or in unadjusted analyses (HR 1.01 [95% CI 0.92-1.10; p= 0.86]). Relapse-free survival was similar (adjusted HR 1.02 [0.93-1.12; p=0.72] and unadjusted HR 1.01 [95% CI 0.92-1.11; p=0.86]), as was overall survival (adjusted HR 1.04 [95% CI 0.93-1.15; p=0.50] and unadjusted HR 1.02 [0.92-1.14]; p=0.65). For overall survival, a significant interaction between oxaliplatin and fluoropyrimidine was recorded in the multiple Cox regression analysis (p=0.014). Post-relapse survival was similar in adjusted (p=0.23) and unadjusted analyses (p=0.33) for the comparison of XELOX or FOLFOX versus leucovorin and fluorouracil, and was also similar for capecitabine-based regimens versus leucovorin and fluorouracil-based regimens (unadjusted p=0.26).
Interpretation Combination therapy with oxaliplatin provided consistently improved outcomes without adversely affecting post-relapse survival in the adjuvant treatment of stage III colon cancer, irrespective of whether the fluoropyrimidine backbone was capecitabine or leucovorin and fluorouracil. These data add to the existing evidence that oxaliplatin plus capecitabine or leucovorin and fluorouracil is the standard of care for the adjuvant treatment of stage III colon cancer, and offers physicians flexibility to treat patients according to the patients' overall physical performance and preference.
C1 [Schmoll, Hans-Joachim] Univ Halle Wittenberg, Univ Clin, D-06120 Halle, Germany.
[Twelves, Chris] Leeds Inst Canc & Pathol, Leeds, W Yorkshire, England.
[Twelves, Chris] St James Univ Hosp, Leeds, W Yorkshire, England.
[Sun, Weijing] Univ Pittsburgh, Inst Canc, Pittsburgh, PA USA.
[O'Connell, Michael J.] Natl Surg Adjuvant Breast & Bowel Project NSABP, Pittsburgh, PA USA.
[Cartwright, Thomas] Florida Canc Affiliates, New Port Richey, FL USA.
[McKenna, Edward] Genentech Inc, San Francisco, CA 94080 USA.
[Saif, Muhammad] Tufts Univ, Sch Med, Boston, MA 02111 USA.
[Yothers, Greg] NSABP, Biostat Ctr, Pittsburgh, PA USA.
[Yothers, Greg] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Biostat, Pittsburgh, PA 15261 USA.
[Haller, Daniel] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RP Schmoll, HJ (reprint author), Univ Halle Wittenberg, Univ Clin, Dept Internal Med, Ernst Grube Str 40, D-06120 Halle, Germany.
EM hans-joachim.schmoll@uk-halle.de
FU Genentech Inc.
FX Genentech Inc.
NR 30
TC 21
Z9 22
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1470-2045
EI 1474-5488
J9 LANCET ONCOL
JI Lancet Oncol.
PD DEC
PY 2014
VL 15
IS 13
BP 1481
EP 1492
DI 10.1016/S1470-2045(14)70486-3
PG 12
WC Oncology
SC Oncology
GA AX4OT
UT WOS:000346912300047
PM 25456367
ER
PT J
AU Anic, GM
Weinstein, SJ
Mondul, AM
Mannisto, S
Albanes, D
AF Anic, Gabriella M.
Weinstein, Stephanie J.
Mondul, Alison M.
Mannisto, Satu
Albanes, Demetrius
TI Serum vitamin D, vitamin D binding protein, and lung cancer survival
SO LUNG CANCER
LA English
DT Article
DE Serum vitamin D; Vitamin D binding protein; Lung cancer; Survival;
Cohort; 25-hydroxyvitamin D
ID CIRCULATING 25-HYDROXYVITAMIN D; PHYSICAL-ACTIVITY; RISK; COHORT;
REPRODUCIBILITY; POPULATION; PROGNOSIS; PLASMA; D-3; POLYMORPHISMS
AB Objectives: Vitamin D may prolong cancer survival by inhibiting tumor progression and metastasis, however, there are limited epidemiologic studies regarding the association between circulating 25-hydroxyvitamin D (25(OH)D) and lung cancer survival. The aim of this study was to examine the relationship between serum 25(OH)D and lung cancer specific survival and to evaluate whether vitamin D binding protein (DBP) concentration modified this association.
Materials and methods: 25(OH)D and DBP were measured in fasting serum samples from 500 male lung cancer cases in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CI) for lung cancer related death according to quartiles of season-specific 25(OH)D, DBP, and the molar ratio of 25(OH)D:DBP, a proxy for free circulating 25(OH)D.
Results: Comparing highest to lowest quartiles, serum 25(OH)D (HR=1.18; 95% CI: 0.89-1.56) and DBP (HR=0.95; 95% CI: 0.71-1.26) were not associated with lung cancer survival and DBP concentration did not modify the association with 25(OH)D (p for interaction=0.56). There was suggestion of an association between higher serum 25(OH)D and better survival from adenocarcinoma (HR=0.64; 95% CI: 0.17-2.45) and small cell carcinoma (HR=0.55; 95% CI: 0.21-1.45), but these estimates were based on a relatively small number of cases.
Conclusion: Serum 25(OH)D was not associated with overall lung cancer survival regardless of DBP concentration, however, these findings should be examined in other studies that include women and subjects with higher 25(OH)D levels. Published by Elsevier Ireland Ltd.
C1 [Anic, Gabriella M.] NCI, Canc Prevent Fellowship Program, Canc Prevent Div, Bethesda, MD 20892 USA.
[Anic, Gabriella M.; Weinstein, Stephanie J.; Mondul, Alison M.; Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Mannisto, Satu] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
RP Anic, GM (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,6E316, Bethesda, MD 20892 USA.
EM gabriella.anic@nih.gov
RI Albanes, Demetrius/B-9749-2015;
OI Mondul, Alison/0000-0002-8843-1416; Mannisto, Satu/0000-0002-8668-3046
FU US National Institutes of Health; National Cancer Institute; US Public
Health Service from the National Cancer Institute [N01-CN-45165,
N01-RC-45035, N01-RC-37004, HHSN261201000006C]
FX This work was supported in part by the Intramural Research Program of
the US National Institutes of Health and the National Cancer Institute.
Additionally, this research was supported by US Public Health Service
contracts N01-CN-45165, N01-RC-45035, N01-RC-37004, and
HHSN261201000006C from the National Cancer Institute.
NR 42
TC 6
Z9 6
U1 0
U2 10
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0169-5002
EI 1872-8332
J9 LUNG CANCER
JI Lung Cancer
PD DEC
PY 2014
VL 86
IS 3
BP 297
EP 303
DI 10.1016/j.lungcan.2014.10.008
PG 7
WC Oncology; Respiratory System
SC Oncology; Respiratory System
GA AX8BU
UT WOS:000347136400001
PM 25456734
ER
PT J
AU Beerli, RR
Bauer, M
Fritzer, A
Rosen, LB
Buser, RB
Hanner, M
Maudrich, M
Nebenfuehr, M
Toepfer, JAS
Mangold, S
Bauer, A
Holland, SM
Browne, SK
Meinke, A
AF Beerli, Roger R.
Bauer, Monika
Fritzer, Andrea
Rosen, Lindsey B.
Buser, Regula B.
Hanner, Markus
Maudrich, Melanie
Nebenfuehr, Mario
Toepfer, Jorge Alejandro Sepulveda
Mangold, Susanne
Bauer, Anton
Holland, Steven M.
Browne, Sarah K.
Meinke, Andreas
TI Mining the human autoantibody repertoire: Isolation of potent
IL17A-neutralizing monoclonal antibodies from a patient with thymoma
SO MABS
LA English
DT Article
DE AIN457; human autoantibodies; ixekizumab; IL17; mammalian cell display;
monoclonal antibodies; secukinumab; Sindbis virus; scFv-Fc
ID CHRONIC MUCOCUTANEOUS CANDIDIASIS; INFLUENZA-A VIRUSES; ANTI-CYTOKINE
AUTOANTIBODIES; SEVERE PLAQUE PSORIASIS; GM-CSF AUTOANTIBODIES;
CANCER-CELL GROWTH; RHEUMATOID-ARTHRITIS; NEUTRALIZING ANTIBODIES;
DOUBLE-BLIND; MOLECULAR CHARACTERIZATION
AB Anti-cytokine autoantibodies have been widely reported to be present in human plasma, both in healthy subjects and in patients with underlying autoimmune conditions, such as autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) or thymic epithelial neoplasms. While often asymptomatic, they can cause or facilitate a wide range of diseases including opportunistic infections. The potential therapeutic value of specific neutralizing anticytokine autoantibodies has not been thoroughly investigated. Here we used mammalian cell display to isolate IL17A-specific antibodies from a thymoma patient with proven high-titer autoantibodies against the same. We identified 3 distinct clonotypes that efficiently neutralized IL17A in a cell-based in vitro assay. Their potencies were comparable to those of known neutralizing antibodies, including 2, AIN457 (secukinumab) and ixekizumab that are currently in clinical development for the treatment of various inflammatory disorders. These data clearly demonstrate that the human autoantibody repertoire can be mined for antibodies with high therapeutic potential for clinical development.
C1 [Bauer, Monika; Fritzer, Andrea; Hanner, Markus; Nebenfuehr, Mario; Toepfer, Jorge Alejandro Sepulveda; Bauer, Anton; Meinke, Andreas] Valneva Austria GmbH, Vienna, Austria.
[Rosen, Lindsey B.; Holland, Steven M.; Browne, Sarah K.] NIAID, Bethesda, MD 20892 USA.
[Buser, Regula B.] ImmunoQure Res AG, Schlieren, Switzerland.
[Maudrich, Melanie] Univ Zurich Hosp, Dept Dermatol, CH-8091 Zurich, Switzerland.
[Mangold, Susanne] Andreasklin, Synlab, Cham, Switzerland.
[Beerli, Roger R.] NBE Therapeut LLC, Basel, Switzerland.
RP Meinke, A (reprint author), Valneva Austria GmbH, Campus Vienna Bioctr 3, Vienna, Austria.
EM andreas.meinke@valneva.com
FU Division of Intramural Research, National Institute of Allergy and
Infectious Diseases, National Institutes of Health
FX This work supported in part by the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.
NR 80
TC 1
Z9 1
U1 1
U2 4
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1942-0862
EI 1942-0870
J9 MABS-AUSTIN
JI mAbs
PD DEC
PY 2014
VL 6
IS 6
BP 1608
EP 1620
DI 10.4161/mabs.36292
PG 13
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AX4BH
UT WOS:000346878600025
PM 25484038
ER
PT J
AU You, XX
Bian, C
Zan, QJ
Xu, X
Liu, X
Chen, JM
Wang, JT
Qiu, Y
Li, WJ
Zhang, XH
Sun, Y
Chen, SX
Hong, WS
Li, YX
Cheng, SF
Fan, GY
Shi, CC
Liang, J
Tang, YT
Yang, CY
Ruan, ZQ
Bai, J
Peng, C
Mu, Q
Lu, J
Fan, MJ
Yang, S
Huang, ZY
Jiang, XT
Fang, XD
Zhang, GJ
Zhang, Y
Polgar, G
Yu, H
Li, J
Liu, ZJ
Zhang, GQ
Ravi, V
Coon, SL
Wang, J
Yang, HM
Venkatesh, B
Wang, J
Shi, Q
AF You, Xinxin
Bian, Chao
Zan, Qijie
Xu, Xun
Liu, Xin
Chen, Jieming
Wang, Jintu
Qiu, Ying
Li, Wujiao
Zhang, Xinhui
Sun, Ying
Chen, Shixi
Hong, Wanshu
Li, Yuxiang
Cheng, Shifeng
Fan, Guangyi
Shi, Chengcheng
Liang, Jie
Tang, Y. Tom
Yang, Chengye
Ruan, Zhiqiang
Bai, Jie
Peng, Chao
Mu, Qian
Lu, Jun
Fan, Mingjun
Yang, Shuang
Huang, Zhiyong
Jiang, Xuanting
Fang, Xiaodong
Zhang, Guojie
Zhang, Yong
Polgar, Gianluca
Yu, Hui
Li, Jia
Liu, Zhongjian
Zhang, Guoqiang
Ravi, Vydianathan
Coon, Steven L.
Wang, Jian
Yang, Huanming
Venkatesh, Byrappa
Wang, Jun
Shi, Qiong
TI Mudskipper genomes provide insights into the terrestrial adaptation of
amphibious fishes
SO NATURE COMMUNICATIONS
LA English
DT Article
ID GENE-EXPRESSION; PERIOPHTHALMODON-SCHLOSSERI; BOLEOPHTHALMUS-BODDAERTI;
RNA-SEQ; AMMONIA; RECEPTOR; HYPOXIA; TRANSCRIPTS; VERTEBRATES;
DIVERGENCE
AB Mudskippers are amphibious fishes that have developed morphological and physiological adaptations to match their unique lifestyles. Here we perform whole-genome sequencing of four representative mudskippers to elucidate the molecular mechanisms underlying these adaptations. We discover an expansion of innate immune system genes in the mudskippers that may provide defence against terrestrial pathogens. Several genes of the ammonia excretion pathway in the gills have experienced positive selection, suggesting their important roles in mudskippers' tolerance to environmental ammonia. Some vision-related genes are differentially lost or mutated, illustrating genomic changes associated with aerial vision. Transcriptomic analyses of mudskippers exposed to air highlight regulatory pathways that are up-or down-regulated in response to hypoxia. The present study provides a valuable resource for understanding the molecular mechanisms underlying water-to-land transition of vertebrates.
C1 [You, Xinxin; Bian, Chao; Chen, Jieming; Qiu, Ying; Li, Wujiao; Zhang, Xinhui; Ruan, Zhiqiang; Bai, Jie; Peng, Chao; Yu, Hui; Li, Jia; Shi, Qiong] State Key Lab Agr Genom, Shenzhen Key Lab Marine Genom, Shenzhen 518083, Peoples R China.
[You, Xinxin; Bian, Chao; Xu, Xun; Liu, Xin; Chen, Jieming; Wang, Jintu; Qiu, Ying; Zhang, Xinhui; Sun, Ying; Li, Yuxiang; Cheng, Shifeng; Fan, Guangyi; Shi, Chengcheng; Liang, Jie; Tang, Y. Tom; Yang, Chengye; Ruan, Zhiqiang; Bai, Jie; Peng, Chao; Mu, Qian; Lu, Jun; Yang, Shuang; Huang, Zhiyong; Jiang, Xuanting; Fang, Xiaodong; Zhang, Guojie; Zhang, Yong; Yu, Hui; Li, Jia; Wang, Jian; Yang, Huanming; Wang, Jun; Shi, Qiong] BGI Shenzhen, Shenzhen 518083, Peoples R China.
[Zan, Qijie] Shenzhen Wild Anim Rescue Ctr, Shenzhen 518040, Peoples R China.
[Chen, Shixi; Hong, Wanshu] Xiamen Univ, Coll Ocean & Earth Sci, Xiamen 361005, Peoples R China.
[Lu, Jun; Shi, Qiong] Shenzhen BGI Fisheries Sci & Tech Co Ltd, Shenzhen 518083, Peoples R China.
[Fan, Mingjun; Yang, Shuang; Shi, Qiong] BGI Wuhan, Ctr Fish Genom, Wuhan 430075, Peoples R China.
[Polgar, Gianluca] Univ Brunei Darussalam, Fac Sci, Environm & Life Sci Programme, BE-1410 Jln Tungku Link, Brunei.
[Liu, Zhongjian; Zhang, Guoqiang] Orchid Conservat & Res Ctr Shenzhen, Shenzhen Key Lab Orchid Conservat & Utilizat, Shenzhen 518114, Peoples R China.
[Ravi, Vydianathan; Venkatesh, Byrappa] ASTAR, Biopolis, Inst Mol & Cell Biol, Singapore 138673, Singapore.
[Coon, Steven L.] NIH, Mol Genom Lab, Bethesda, MD 20892 USA.
[Wang, Jian; Yang, Huanming] James D Watson Inst Genome Sci, Hangzhou 310008, Zhejiang, Peoples R China.
[Yang, Huanming; Wang, Jun] King Abdulaziz Univ, Princess Al Jawhara Ctr Excellence Res Hereditary, Jeddah 21413, Saudi Arabia.
[Wang, Jun] Univ Copenhagen, Dept Biol, DK-2200 Copenhagen, Denmark.
RP Bian, C (reprint author), State Key Lab Agr Genom, Shenzhen Key Lab Marine Genom, Shenzhen 518083, Peoples R China.
EM bianchao@genomics.cn; wangj@genomics.cn; shiqiong@genomics.cn
RI Zhang, Guojie/B-6188-2014; ASTAR, IMCB/E-2320-2012; Wang,
Jun/C-8434-2016; Vydianathan, Ravi/B-2759-2009; Wang, Jun/B-9503-2016;
OI Venkatesh, Byrappa/0000-0003-3620-0277; Zhang,
Guojie/0000-0001-6860-1521; Wang, Jun/0000-0002-8540-8931; Vydianathan,
Ravi/0000-0003-0807-7697; Wang, Jun/0000-0002-2113-5874; Polgar,
Gianluca/0000-0002-4901-6287
FU Shenzhen Key Lab of Marine Genomics [CXB201108250095A]; China National
High-Technology Research and Development Program [2012AA10A407]; State
Key Laboratory of Agricultural Genomics [ZDSY20120618171817275];
Biomedical Research Council of A*STAR, Singapore; Intramural Research
Program of the Eunice Kennedy Shriver National Institute of Child Health
and Human Development at the National Institutes of Health, USA; Xiamen
University President Research Award [2013121044]
FX We acknowledge L. Lin, R. You, C. Wang, H. Zhong and Yuen K. Ip for
their help in collecting mudskipper samples, S. He, H. Ye, Y. Kawabata,
A. Ishimatsu and J. Chung for fruitful discussions; L. Goodman for
manuscript revision. C. K. Ching provided the high-quality photo of
mudskippers for the Featured image. This study was supported by grants
from Shenzhen Key Lab of Marine Genomics (CXB201108250095A), China
National High-Technology Research and Development Program (2012AA10A407)
and State Key Laboratory of Agricultural Genomics
(ZDSY20120618171817275) to Q. Shi. It was also supported in part by the
Biomedical Research Council of A*STAR, Singapore (to B.V.), the
Intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development at the National
Institutes of Health, USA (to S.L.C.) and the Xiamen University
President Research Award (No. 2013121044) to S.C.
NR 56
TC 15
Z9 15
U1 5
U2 49
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD DEC
PY 2014
VL 5
AR 5594
DI 10.1038/ncomms6594
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AX9LO
UT WOS:000347224500001
PM 25463417
ER
PT J
AU Omonijo, O
Wongprayoon, P
Ladenheim, B
Mccoy, MT
Govitrapong, P
Jayanthi, S
Cadet, JL
AF Omonijo, Oluwaseyi
Wongprayoon, Pawaris
Ladenheim, Bruce
Mccoy, Michael T.
Govitrapong, Piyarat
Jayanthi, Subramaniam
Cadet, Jean Lud
TI Differential effects of binge methamphetamine injections on the mRNA
expression of histone deacetylases (HDACs) in the rat striatum
SO NEUROTOXICOLOGY
LA English
DT Article
DE Epigenetics; Sirtuins; Neurotoxicity; Gene expression
ID INDUCED NEURONAL APOPTOSIS; MYOCYTE-ENHANCER FACTOR-2; DEPENDENT
PROTEIN-KINASE; PHOSPHATE SYNTHETASE 1; GENE-EXPRESSION;
ENDOPLASMIC-RETICULUM; INDUCED NEUROTOXICITY; UP-REGULATION; CLONING;
SIRT5
AB Methamphetamine use disorder is characterized by recurrent binge episodes. Humans addicted to methamphetamine experience various degrees of cognitive deficits and show evidence of neurodegenerative processes in the brain. Binge injections of METH to rodents also cause significant toxic changes in the brain. In addition, this pattern of METH injections can alter gene expression in the dorsal striatum. Gene expression is regulated, in part, by histone deacetylation. We thus tested the possibility that METH toxic doses might cause changes in the mRNA levels of histone deacetylases (HDACs). We found that METH did produce significant decreases in the mRNA expression of HDAC8, which is a class I HDAC. METH also decreased expression of HDAC6, HDAC9, and HDAC10 that are class II HDACs. The expression of the class IV HDAC, HDAC11, was also suppressed by METH. The expression of Sirt2, Sirt5, and Sirt6 that are members of class III HDACs was also downregulated by METH injections. Our findings implicate changes in HDAC expression may be an early indicator of impending METH-induced neurotoxicity in the striatum. This idea is consistent with the accumulated evidence that some HDACs are involved in neurodegenerative processes in the brain. Published by Elsevier Inc.
C1 [Omonijo, Oluwaseyi; Ladenheim, Bruce; Mccoy, Michael T.; Jayanthi, Subramaniam; Cadet, Jean Lud] NIDA Intramural Res Program, Mol Neuropsychiat Res Branch, Baltimore, MD 21224 USA.
[Wongprayoon, Pawaris; Govitrapong, Piyarat] Mahidol Univ, Inst Mol Biosci, Res Ctr Neurosci, Bangkok 10700, Thailand.
RP Cadet, JL (reprint author), NIDA Intramural Res Program, Mol Neuropsychiat Res Branch, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM jcadet@intra.nida.nih.gov
FU Intramural Research Program of the DHHS/NIH/NIDA; Thailand Research Fund
(TRF) - Royal Golden Jubilee Ph.D. Program; Mahidol University
FX This research was supported by funds of the Intramural Research Program
of the DHHS/NIH/NIDA. Pawaris Wongprayoon and Dr. Piyarat Govitrapong
were supported by funds from the Thailand Research Fund (TRF) - Royal
Golden Jubilee Ph.D. Program and Mahidol University. The authors also
thank the comments of two reviewers who help make this a better paper.
NR 81
TC 5
Z9 5
U1 1
U2 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0161-813X
EI 1872-9711
J9 NEUROTOXICOLOGY
JI Neurotoxicology
PD DEC
PY 2014
VL 45
BP 178
EP 184
DI 10.1016/j.neuro.2014.10.008
PG 7
WC Neurosciences; Pharmacology & Pharmacy; Toxicology
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology
GA AX5GQ
UT WOS:000346955100019
PM 25452209
ER
PT J
AU Malik, N
Efthymiou, AG
Mather, K
Chester, N
Wang, XT
Nath, A
Rao, MS
Steiner, JP
AF Malik, Nasir
Efthymiou, Anastasia G.
Mather, Karly
Chester, Nathaniel
Wang, Xiantao
Nath, Avindra
Rao, Mahendra S.
Steiner, Joseph P.
TI Compounds with species and cell type specific toxicity identified in a
2000 compound drug screen of neural stem cells and rat mixed cortical
neurons
SO NEUROTOXICOLOGY
LA English
DT Article
DE Neurotoxicity screening; Neural stem cells; Cardiac glycosides
ID DEFINED CONDITIONS; SMALL-MOLECULE; NEUROTOXICITY; GENERATION;
EFFICIENT; LIGAND; DIFFERENTIATION; DERIVATION; INHIBITION; EXPRESSION
AB Human primary neural tissue is a vital component for the quick and simple determination of chemical compound neurotoxicity in vitro. In particular, such tissue would be ideal for high-throughput screens that can be used to identify novel neurotoxic or neurotherapeutic compounds. We have previously established a high-throughput screening platform using human induced pluripotent stem cell (iPSC)-derived neural stem cells (NSCs) and neurons. In this study, we conducted a 2000 compound screen with human NSCs and rat cortical cells to identify compounds that are selectively toxic to each group. Approximately 100 of the tested compounds showed specific toxicity to human NSCs. A secondary screen of a small subset of compounds from the primary screen on human iPSCs, NSC-derived neurons, and fetal astrocytes validated the results from >80% of these compounds with some showing cell specific toxicity. Amongst those compounds were several cardiac glycosides, all of which were selectively toxic to the human cells. As the screen was able to reliably identify neurotoxicants, many with species and cell-type specificity, this study demonstrates the feasibility of this NSC-driven platform for higher-throughput neurotoxicity screens. Published by Elsevier Inc.
C1 [Malik, Nasir; Efthymiou, Anastasia G.; Wang, Xiantao; Rao, Mahendra S.] NIAMS, NIH, Bethesda, MD 20892 USA.
[Mather, Karly; Chester, Nathaniel; Nath, Avindra; Steiner, Joseph P.] NINDS, NIH, Bethesda, MD 20892 USA.
[Rao, Mahendra S.] Natl Inst Hlth Ctr Regenerat Med, Natl Inst Hlth, Bethesda, MD USA.
RP Malik, N (reprint author), NIAMS, NIH, 50 South Dr,Room 1142, Bethesda, MD 20892 USA.
EM malikn@mail.nih.gov
OI Efthymiou, Anastasia/0000-0002-1769-5078
FU NIH Common Fund
FX This work was funded by the NIH Common Fund.
NR 37
TC 9
Z9 9
U1 1
U2 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0161-813X
EI 1872-9711
J9 NEUROTOXICOLOGY
JI Neurotoxicology
PD DEC
PY 2014
VL 45
BP 192
EP 200
DI 10.1016/j.neuro.2014.10.007
PG 9
WC Neurosciences; Pharmacology & Pharmacy; Toxicology
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology
GA AX5GQ
UT WOS:000346955100021
PM 25454721
ER
PT J
AU Buckland, RJ
Watt, DL
Chittoor, B
Nilsson, AK
Kunkel, TA
Chabes, A
AF Buckland, Robert J.
Watt, Danielle L.
Chittoor, Balasubramanyam
Nilsson, Anna Karin
Kunkel, Thomas A.
Chabes, Andrei
TI Increased and Imbalanced dNTP Pools Symmetrically Promote Both Leading
and Lagging Strand Replication Infidelity
SO PLOS GENETICS
LA English
DT Article
ID DNA MISMATCH-REPAIR; ESCHERICHIA-COLI; SACCHAROMYCES-CEREVISIAE;
RIBONUCLEOTIDE REDUCTASE; SPONTANEOUS MUTATION; BUDDING YEAST; CANCER;
GENE; FORK; MUTAGENESIS
AB The fidelity of DNA replication requires an appropriate balance of dNTPs, yet the nascent leading and lagging strands of the nuclear genome are primarily synthesized by replicases that differ in subunit composition, protein partnerships and biochemical properties, including fidelity. These facts pose the question of whether imbalanced dNTP pools differentially influence leading and lagging strand replication fidelity. Here we test this possibility by examining strand-specific replication infidelity driven by a mutation in yeast ribonucleotide reductase, rnr1-Y285A, that leads to elevated dTTP and dCTP concentrations. The results for the CAN1 mutational reporter gene present in opposite orientations in the genome reveal that the rates, and surprisingly even the sequence contexts, of replication errors are remarkably similar for leading and lagging strand synthesis. Moreover, while many mismatches driven by the dNTP pool imbalance are efficiently corrected by mismatch repair, others are repaired less efficiently, especially those in sequence contexts suggesting reduced proofreading due to increased mismatch extension driven by the high dTTP and dCTP concentrations. Thus the two DNA strands of the nuclear genome are at similar risk of mutations resulting from this dNTP pool imbalance, and this risk is not completely suppressed even when both major replication error correction mechanisms are genetically intact.
C1 [Buckland, Robert J.; Chittoor, Balasubramanyam; Nilsson, Anna Karin; Chabes, Andrei] Umea Univ, Dept Med Biochem & Biophys, S-90187 Umea, Sweden.
[Buckland, Robert J.; Chabes, Andrei] Umea Univ, Lab Mol Infect Med Sweden MIMS, Umea, Sweden.
[Watt, Danielle L.; Kunkel, Thomas A.] NIEHS, Mol Genet Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[Watt, Danielle L.; Kunkel, Thomas A.] NIEHS, Struct Biol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
RP Buckland, RJ (reprint author), Umea Univ, Dept Med Biochem & Biophys, S-90187 Umea, Sweden.
EM andrei.chabes@medchem.umu.se
RI Buckland, Robert/L-6137-2014
OI Buckland, Robert/0000-0001-9749-5422
FU Division of Intramural Research of the NIH, NIEHS [Z01 ES065070]; Knut
and Alice Wallenberg Foundation; Swedish Foundation for Strategic
Research; Swedish Cancer Society
FX This work was supported by Project Z01 ES065070 to TAK from the Division
of Intramural Research of the NIH, NIEHS, and by The Knut and Alice
Wallenberg Foundation, the Swedish Foundation for Strategic Research and
the Swedish Cancer Society to AC. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 42
TC 11
Z9 11
U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7390
EI 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD DEC
PY 2014
VL 10
IS 12
AR e1004846
DI 10.1371/journal.pgen.1004846
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA AX0NW
UT WOS:000346649900047
PM 25474551
ER
PT J
AU Bastian, H
AF Bastian, Hilda
TI A Stronger Post-Publication Culture Is Needed for Better Science
SO PLOS MEDICINE
LA English
DT Editorial Material
ID MEDICAL LITERATURE; GENDER; LANGUAGE; AUTHORS; WOMEN
C1 NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
RP Bastian, H (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bldg 10, Bethesda, MD 20892 USA.
EM hilda.bastian@nih.gov
OI Bastian, Hilda/0000-0001-8544-7386
FU Intramural NIH HHS
NR 33
TC 7
Z9 7
U1 0
U2 9
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1549-1676
J9 PLOS MED
JI PLos Med.
PD DEC
PY 2014
VL 11
IS 12
AR e1001772
DI 10.1371/journal.pmed.1001772
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA AX5ZD
UT WOS:000347002300010
PM 25548904
ER
PT J
AU Kim, JH
Sohn, BH
Lee, HS
Kim, SB
Yoo, JE
Park, YY
Jeong, W
Lee, SS
Park, ES
Kaseb, A
Kim, BH
Kim, WB
Yeon, JE
Byun, KS
Chu, IS
Kim, SS
Wang, XW
Thorgeirsson, SS
Luk, JM
Kang, KJ
Heo, J
Park, YN
Lee, JS
AF Kim, Ji Hoon
Sohn, Bo Hwa
Lee, Hyun-Sung
Kim, Sang-Bae
Yoo, Jeong Eun
Park, Yun-Yong
Jeong, Woojin
Lee, Sung Sook
Park, Eun Sung
Kaseb, Ahmed
Kim, Baek Hui
Kim, Wan Bae
Yeon, Jong Eun
Byun, Kwan Soo
Chu, In-Sun
Kim, Sung Soo
Wang, Xin Wei
Thorgeirsson, Snorri S.
Luk, John M.
Kang, Koo Jeong
Heo, Jeonghoon
Park, Young Nyun
Lee, Ju-Seog
TI Genomic Predictors for Recurrence Patterns of Hepatocellular Carcinoma:
Model Derivation and Validation
SO PLOS MEDICINE
LA English
DT Article
ID GENE-EXPRESSION; INTRAHEPATIC RECURRENCE; RISK-FACTORS; THERAPEUTIC
TARGET; CURATIVE RESECTION; SIGNALING PATHWAY; STAT3 ACTIVATION;
UNITED-STATES; TUMOR-GROWTH; LIVER
AB Background: Typically observed at 2 y after surgical resection, late recurrence is a major challenge in the management of hepatocellular carcinoma (HCC). We aimed to develop a genomic predictor that can identify patients at high risk for late recurrence and assess its clinical implications.
Methods and Findings: Systematic analysis of gene expression data fromhuman liver undergoing hepatic injury and regeneration revealed a 233-gene signature that was significantly associated with late recurrence of HCC. Using this signature, we developed a prognostic predictor that can identify patients at high risk of late recurrence, and tested and validated the robustness of the predictor in patients (n = 396) who underwent surgery between 1990 and 2011 at four centers (210 recurrences during a median of 3.7 y of follow-up). In multivariate analysis, this signature was the strongest risk factor for late recurrence (hazard ratio, 2.2; 95% confidence interval, 1.3-3.7; p = 0.002). In contrast, our previously developed tumor-derived 65-gene risk score was significantly associated with early recurrence (p = 0.005) but not with late recurrence (p = 0.7). In multivariate analysis, the 65-gene risk score was the strongest risk factor for very early recurrence (< 1 y after surgical resection) (hazard ratio, 1.7; 95% confidence interval, 1.1-2.6; p = 0.01). The potential significance of STAT3 activation in late recurrence was predicted by gene network analysis and validated later. We also developed and validated 4- and 20-gene predictors from the full 233-gene predictor. The main limitation of the study is that most of the patients in our study were hepatitis B virus-positive. Further investigations are needed to test our prediction models in patients with different etiologies of HCC, such as hepatitis C virus.
Conclusions: Two independently developed predictors reflected well the differences between early and late recurrence of HCC at the molecular level and provided new biomarkers for risk stratification.
C1 [Kim, Ji Hoon; Sohn, Bo Hwa; Lee, Hyun-Sung; Kim, Sang-Bae; Lee, Ju-Seog] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Syst Biol, Houston, TX 77030 USA.
[Kim, Ji Hoon; Sohn, Bo Hwa; Lee, Hyun-Sung; Kim, Sang-Bae; Lee, Ju-Seog] Univ Texas MD Anderson Canc Ctr, Kleberg Ctr Mol Markers, Houston, TX 77030 USA.
[Kim, Ji Hoon; Yeon, Jong Eun; Byun, Kwan Soo] Korea Univ, Coll Med, Dept Internal Med, Div Gastroenterol & Hepatol, Seoul 136705, South Korea.
[Yoo, Jeong Eun; Park, Young Nyun] Yonsei Univ, Coll Med, Dept Pathol, Seoul, South Korea.
[Yoo, Jeong Eun; Park, Young Nyun] Yonsei Univ, Coll Med, Brain Korea Project Med Sci 21, Seoul, South Korea.
[Park, Yun-Yong] Univ Ulsan, Coll Med, Dept Med, ASAN Inst Life Sci,Asan Med Ctr, Seoul, South Korea.
[Jeong, Woojin] Ewha Womans Univ, Dept Life Sci, Div Life & Pharmaceut Sci, Ctr Cell Signaling & Drug Discovery Res, Seoul, South Korea.
[Lee, Sung Sook] Inje Univ, Haeundae Paik Hosp, Dept Hematol Oncol, Pusan, South Korea.
[Park, Eun Sung] Yonsei Univ, Coll Med, Inst Med Convergence, Seoul, South Korea.
[Kaseb, Ahmed] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept GI Med Oncol, Houston, TX 77030 USA.
[Kim, Baek Hui] Korea Univ, Coll Med, Dept Internal Med, Dept Pathol, Seoul 136705, South Korea.
[Kim, Wan Bae] Korea Univ, Coll Med, Dept Internal Med, Dept Surg, Seoul 136705, South Korea.
[Chu, In-Sun] Korea Res Inst Biosci & Biotechnol, Korean Bioinformat Ctr, Taejon, South Korea.
[Kim, Sung Soo; Lee, Ju-Seog] Kyung Hee Univ, Med Res Ctr, Dept Biochem & Mol Biol, Seoul, South Korea.
[Kim, Sung Soo; Lee, Ju-Seog] Kyung Hee Univ, Sch Med, Inst Biomed Sci, Seoul, South Korea.
[Wang, Xin Wei] NCI, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Thorgeirsson, Snorri S.] NCI, Expt Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Luk, John M.] Natl Univ Singapore, Dept Pharmacol, Singapore 117548, Singapore.
[Kang, Koo Jeong] Keimyung Univ, Sch Med, Dept Surg, Taegu, South Korea.
[Heo, Jeonghoon] Kosin Univ, Coll Med, Dept Mol Biol, Pusan, South Korea.
[Heo, Jeonghoon] Kosin Univ, Coll Med, Dept Immunol, Pusan, South Korea.
RP Kim, JH (reprint author), Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Syst Biol, Houston, TX 77030 USA.
EM jlee@mdanderson.org
RI Wang, Xin/B-6162-2009; Luk, John/A-4085-2008;
OI Luk, John/0000-0002-6323-7940; Lee, Hyun-Sung/0000-0001-8259-046X
FU MD Anderson Sister Institute Network Fund; Bio & Medical Technology
Development Program [M10642040002-07N4204-00210]; Scientific Research
Center Program [2012R1A5A1048236]; GlaxoSmithKline Research Fund of the
Korean Association for the Study of the Liver; Center for Cancer
Research, National Cancer Institute; National Research Foundation (NSF)
of Korea by the Korea government (Ministry of Science, ICT, and Future
Planning) [2013R1A2A2A05005990]
FX This work is supported in part by 2011 and 2012 cycle of MD Anderson
Sister Institute Network Fund (JSL); Bio & Medical Technology
Development Program Grant M10642040002-07N4204-00210 (WJ); Scientific
Research Center Program Grant 2012R1A5A1048236 (WJ); the GlaxoSmithKline
Research Fund of the Korean Association for the Study of the Liver
(JHK); the intramural program of the Center for Cancer Research,
National Cancer Institute (XWW and SST); and the National Research
Foundation (NSF); of Korea grant by the Korea government (Ministry of
Science, ICT, and Future Planning) (No. 2013R1A2A2A05005990) (YNP). The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
NR 55
TC 8
Z9 8
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1549-1676
J9 PLOS MED
JI PLos Med.
PD DEC
PY 2014
VL 11
IS 12
AR e1001770
DI 10.1371/journal.pmed.1001770
PG 16
WC Medicine, General & Internal
SC General & Internal Medicine
GA AX5ZD
UT WOS:000347002300008
PM 25536056
ER
PT J
AU Schwarz, A
Medrano-Mercado, N
Schaub, GA
Struchiner, CJ
Bargues, MD
Levy, MZ
Ribeiro, JMC
AF Schwarz, Alexandra
Medrano-Mercado, Nora
Schaub, Guenter A.
Struchiner, Claudio J.
Dolores Bargues, M.
Levy, Michael Z.
Ribeiro, Jose M. C.
TI An Updated Insight into the Sialotranscriptome of Triatoma infestans:
Developmental Stage and Geographic Variations
SO PLOS NEGLECTED TROPICAL DISEASES
LA English
DT Article
ID PANSTRONGYLUS-MEGISTUS HEMIPTERA; INDUCED PLATELET-AGGREGATION; BUG
RHODNIUS-PROLIXUS; CHAGAS-DISEASE; NUCLEAR RDNA; SALIVARY PROTEINS;
PHYLOGENETIC-RELATIONSHIPS; BRAZILIAN POPULATIONS; ANOPHELES-GAMBIAE;
SERINE-PROTEASE
AB Background: Triatoma infestans is the main vector of Chagas disease in South America. As in all hematophagous arthropods, its saliva contains a complex cocktail that assists blood feeding by preventing platelet aggregation and blood clotting and promoting vasodilation. These salivary components can be immunologically recognized by their vector's hosts and targeted with antibodies that might disrupt blood feeding. These antibodies can be used to detect vector exposure using immunoassays. Antibodies may also contribute to the fast evolution of the salivary cocktail.
Methodology: Salivary gland cDNA libraries from nymphal and adult T. infestans of breeding colonies originating from different locations (Argentina, Chile, Peru and Bolivia), and cDNA libraries originating from F1 populations of Bolivia, were sequenced using Illumina technology. Coding sequences (CDS) were extracted from the assembled reads, the numbers of reads mapped to these CDS, sequences were functionally annotated and polymorphisms determined.
Main findings/Significance: Over five thousand CDS, mostly full length or near full length, were publicly deposited on GenBank. Transcripts that were over 10-fold overexpressed from different geographical regions, or from different developmental stages were identified. Polymorphisms were mapped to derived coding sequences, and found to vary between developmental instars and geographic origin of the biological material. This expanded sialome database from T. infestans should be of assistance in future proteomic work attempting to identify salivary proteins that might be used as epidemiological markers of vector exposure, or proteins of pharmacological interest.
C1 [Schwarz, Alexandra] Acad Sci Czech Republic, Inst Parasitol, Ctr Biol, CR-37005 Ceske Budejovice, Czech Republic.
[Medrano-Mercado, Nora] Univ Mayor San Simon, Lab Chagas Dis & Immunoparasitol, Cochabamba, Bolivia.
[Schaub, Guenter A.] Ruhr Univ Bochum, Zool Parasitol Grp, Bochum, Germany.
[Struchiner, Claudio J.] Fiocruz MS, Escola Nacl Saude Publ, BR-21045900 Rio De Janeiro, Brazil.
[Dolores Bargues, M.] Univ Valencia, Fac Farm, Dept Parasitol, E-46010 Valencia, Spain.
[Levy, Michael Z.] Univ Peruana Cayetano Heredia, Sede De Arequipa, Arequipa, Peru.
[Levy, Michael Z.] Univ Penn, Sch Med, Dept Biostat & Epidemiol, Ctr Clin Epidemiol & Biostat, Philadelphia, PA 19104 USA.
[Ribeiro, Jose M. C.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
RP Schwarz, A (reprint author), Acad Sci Czech Republic, Inst Parasitol, Ctr Biol, Branisovska 31, CR-37005 Ceske Budejovice, Czech Republic.
EM jribeiro@niaid.nih.gov
OI Ribeiro, Jose/0000-0002-9107-0818
FU National Institute of Allergy and Infectious Diseases [ZIA AI000810-16];
Ministry of Education, Youth and Sports of the Czech Republic [LH12002];
Academy of Sciences of the Czech Republic [Z60220518]; RETICS, Red de
Investigacion Cooperativa en Enfermedades Tropicales - RICET
[RD12/0018/0013]; VI National Plan of I+D+I, ISCIII - Subdireccion
General de Redes y Centros de Investigacion Cooperativa; Ministry of
Health, Madrid, Spain; PROMETEO Project, Programa of Ayudas para Grupos
de Investigacion de Excelencia, Generalitat Valenciana, Valencia, Spain
[2012/042]
FX This work was partially supported by grants ZIA AI000810-16 from the
National Institute of Allergy and Infectious Diseases to JMCR, by grant
KONTAKT II no. LH12002 from the Ministry of Education, Youth and Sports
of the Czech Republic and grant no. Z60220518 from the Academy of
Sciences of the Czech Republic to AS, and project No. RD12/0018/0013 of
RETICS, Red de Investigacion Cooperativa en Enfermedades Tropicales -
RICET, VI National Plan of I+D+I 2008-2011, ISCIII - Subdireccion
General de Redes y Centros de Investigacion Cooperativa, Ministry of
Health, Madrid, Spain and PROMETEO Project No. 2012/042, Programa of
Ayudas para Grupos de Investigacion de Excelencia, Generalitat
Valenciana, Valencia, Spain to MDB. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
NR 68
TC 5
Z9 5
U1 2
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1935-2735
J9 PLOS NEGLECT TROP D
JI Plos Neglect. Trop. Dis.
PD DEC
PY 2014
VL 8
IS 12
AR e3372
DI 10.1371/journal.pntd.0003372
PG 15
WC Infectious Diseases; Parasitology; Tropical Medicine
SC Infectious Diseases; Parasitology; Tropical Medicine
GA AX1IM
UT WOS:000346701000045
PM 25474469
ER
PT J
AU Malinowski, JR
Denny, JC
Bielinski, SJ
Basford, MA
Bradford, Y
Peissig, PL
Carrell, D
Crosslin, DR
Pathak, J
Rasmussen, L
Pacheco, J
Kho, A
Newton, KM
Li, RL
Kullo, IJ
Chute, CG
Chisholm, RL
Jarvik, GP
Larson, EB
McCarty, CA
Masys, DR
Roden, DM
de Andrade, M
Ritchie, MD
Crawford, DC
AF Malinowski, Jennifer R.
Denny, Joshua C.
Bielinski, Suzette J.
Basford, Melissa A.
Bradford, Yuki
Peissig, Peggy L.
Carrell, David
Crosslin, David R.
Pathak, Jyotishman
Rasmussen, Luke
Pacheco, Jennifer
Kho, Abel
Newton, Katherine M.
Li, Rongling
Kullo, Iftikhar J.
Chute, Christopher G.
Chisholm, Rex L.
Jarvik, Gail P.
Larson, Eric B.
McCarty, Catherine A.
Masys, Daniel R.
Roden, Dan M.
de Andrade, Mariza
Ritchie, Marylyn D.
Crawford, Dana C.
TI Genetic Variants Associated with Serum Thyroid Stimulating Hormone (TSH)
Levels in European Americans and African Americans from the eMERGE
Network
SO PLOS ONE
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ELECTRONIC MEDICAL-RECORDS; REFERENCE LIMITS;
NATIONAL-HEALTH; TWIN COHORT; FREE T4; POPULATION; CANCER; LOCI;
METAANALYSIS
AB Thyroid stimulating hormone (TSH) hormone levels are normally tightly regulated within an individual; thus, relatively small variations may indicate thyroid disease. Genome-wide association studies (GWAS) have identified variants in PDE8B and FOXE1 that are associated with TSH levels. However, prior studies lacked racial/ethnic diversity, limiting the generalization of these findings to individuals of non-European ethnicities. The Electronic Medical Records and Genomics (eMERGE) Network is a collaboration across institutions with biobanks linked to electronic medical records (EMRs). The eMERGE Network uses EMR-derived phenotypes to perform GWAS in diverse populations for a variety of phenotypes. In this report, we identified serum TSH levels from 4,501 European American and 351 African American euthyroid individuals in the eMERGE Network with existing GWAS data. Tests of association were performed using linear regression and adjusted for age, sex, body mass index (BMI), and principal components, assuming an additive genetic model. Our results replicate the known association of PDE8B with serum TSH levels in European Americans (rs2046045 p=1.85x10(-17), beta=0.09). FOXE1 variants, associated with hypothyroidism, were not genome-wide significant (rs10759944: p=1.08x10(-6), beta=-0.05). No SNPs reached genome-wide significance in African Americans. However, multiple known associations with TSH levels in European ancestry were nominally significant in African Americans, including PDE8B (rs2046045 p=0.03, beta=-0.09), VEGFA (rs11755845 p=0.01, beta=-0.13), and NFIA (rs334699 p=1.50x10(-3), beta=-0.17). We found little evidence that SNPs previously associated with other thyroid-related disorders were associated with serum TSH levels in this study. These results support the previously reported association between PDE8B and serum TSH levels in European Americans and emphasize the need for additional genetic studies in more diverse populations.
C1 [Denny, Joshua C.; Masys, Daniel R.; Ritchie, Marylyn D.] Vanderbilt Univ, Dept Biomed Informat, Nashville, TN 37235 USA.
[Denny, Joshua C.; Roden, Dan M.] Vanderbilt Univ, Dept Med, Nashville, TN USA.
[Ritchie, Marylyn D.; Crawford, Dana C.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
[Malinowski, Jennifer R.; Bradford, Yuki; Ritchie, Marylyn D.; Crawford, Dana C.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN 37235 USA.
[Bielinski, Suzette J.] Mayo Clin, Div Epidemiol, Dept Hlth Sci Res, Rochester, MN USA.
[Basford, Melissa A.] Vanderbilt Univ, Res Off, Nashville, TN 37235 USA.
[Pathak, Jyotishman; Chute, Christopher G.; de Andrade, Mariza] Mayo Clin, Div Biomed Stat & Informat, Dept Hlth Sci Res, Rochester, MN USA.
[Peissig, Peggy L.; Rasmussen, Luke] Marshfield Clin Res Fdn, Biomed Informat Res Ctr, Marshfield, WI USA.
[Carrell, David; Newton, Katherine M.; Larson, Eric B.] Grp Hlth Res Inst, Seattle, WA USA.
[Pacheco, Jennifer; Kho, Abel] Northwestern Univ, Dept Med, Chicago, IL 60611 USA.
[Li, Rongling] NHGRI, Div Genom Med, Bethesda, MD 20892 USA.
[Kullo, Iftikhar J.] Mayo Clin, Div Cardiovasc Dis, Dept Hlth Sci Res, Rochester, MN USA.
[Chisholm, Rex L.] Northwestern Univ, Ctr Genet Med, Chicago, IL 60611 USA.
[McCarty, Catherine A.] Essentia Inst Rural Hlth, Duluth, MN USA.
[Roden, Dan M.] Vanderbilt Univ, Dept Pharmacol, Nashville, TN USA.
[Crosslin, David R.; Jarvik, Gail P.] Univ Washington, Dept Med Med Genet, Seattle, WA 98195 USA.
[Crosslin, David R.; Jarvik, Gail P.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
RP Crawford, DC (reprint author), Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA.
EM dana.crawford@case.edu
RI Bielinski, Suzette/A-2238-2009;
OI Bielinski, Suzette/0000-0002-2905-5430; Rasmussen,
Luke/0000-0002-4497-8049
FU NHGRI; NIGMS [U01HG04599, U01HG006379, U01HG004610, U01HG006375,
U01HG004608, U01HG006389, U01HG004609, U01HG006388, U01HG04603,
U01HG006378, U01HG006385, U01HG006382, U01HG006380, U01HG006830,
U01HG006828]; Group Health/UW ADPR/ACT [UO1 AG 0681]
FX Funding: The eMERGE Network is funded by NHGRI, with additional funding
from NIGMS through the following grants: U01HG04599 and U01HG006379 to
Mayo Clinic; U01HG004610 and U01HG006375 to Group Health Cooperative;
U01HG004608 to Marshfield Clinic; U01HG006389 to Essentia Institute of
Rural Health; U01HG004609 and U01HG006388 to Northwestern University;
U01HG04603 and U01HG006378 to Vanderbilt University; U01HG006385 to the
Coordinating Center; U01HG006382 to Geisinger Clinic; U01HG006380 to
Icahn School of Medicine at Mount Sinai; U01HG006830 to The Children's
Hospital of Philadelphia; and U01HG006828 to Cincinnati Children's
Hospital and Boston Children's Hospital. Group Health/University of
Washington received additional funding through Group Health/UW ADPR/ACT
grant UO1 AG 0681. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 50
TC 4
Z9 4
U1 0
U2 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD DEC 1
PY 2014
VL 9
IS 12
AR e111301
DI 10.1371/journal.pone.0111301
PG 21
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AX7SK
UT WOS:000347114900008
PM 25436638
ER
PT J
AU Peters, NC
Pagan, AJ
Lawyer, PG
Hand, TW
Roma, EH
Stamper, LW
Romano, A
Sacks, DL
AF Peters, Nathan C.
Pagan, Antonio J.
Lawyer, Phillip G.
Hand, Timothy W.
Roma, Eric Henrique
Stamper, Lisa W.
Romano, Audrey
Sacks, David L.
TI Chronic Parasitic Infection Maintains High Frequencies of Short-Lived
Ly6C(+)CD4(+) Effector T Cells That Are Required for Protection against
Re-infection
SO PLOS PATHOGENS
LA English
DT Article
ID LEISHMANIA-MAJOR INFECTION; TUBERCULOSIS INFECTION; CONCOMITANT
IMMUNITY; IMMUNOLOGICAL MEMORY; PERSISTENCE; RESPONSES; CD4(+);
MIGRATION; ANTIBODY; TRANSMISSION
AB In contrast to the ability of long-lived CD8(+) memory T cells to mediate protection against systemic viral infections, the relationship between CD4(+) T cell memory and acquired resistance against infectious pathogens remains poorly defined. This is especially true for T helper 1 (Th1) concomitant immunity, in which protection against reinfection coincides with a persisting primary infection. In these situations, pre-existing effector CD4 T cells generated by ongoing chronic infection, not memory cells, may be essential for protection against reinfection. We present a systematic study of the tissue homing properties, functionality, and life span of subsets of memory and effector CD4 T cells activated in the setting of chronic Leishmania major infection in resistant C57Bl/6 mice. We found that pre-existing, CD44(+)CD62L(-)T-bet(+)Ly6C(+) effector (T-EFF) cells that are short-lived in the absence of infection and are not derived from memory cells reactivated by secondary challenge, mediate concomitant immunity. Upon adoptive transfer and challenge, non-dividing Ly6C(+) T-EFF cells preferentially homed to the skin, released IFN-gamma, and conferred protection as compared to CD44(+)CD62L(-)Ly6C(-) effector memory or CD44(+)CD62L(+)Ly6C(-) central memory cells. During chronic infection, Ly6C(+) T-EFF cells were maintained at high frequencies via reactivation of TCM and the T-EFF themselves. The lack of effective vaccines for many chronic diseases may be because protection against infectious challenge requires the maintenance of pre-existing T-EFF cells, and is therefore not amenable to conventional, memory inducing, vaccination strategies.
C1 [Peters, Nathan C.; Lawyer, Phillip G.; Hand, Timothy W.; Roma, Eric Henrique; Stamper, Lisa W.; Romano, Audrey; Sacks, David L.] NIAID, Intracellular Parasite Biol Sect, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Pagan, Antonio J.] Univ Minnesota, Sch Med, Dept Microbiol, Ctr Immunol, Minneapolis, MN 55455 USA.
RP Peters, NC (reprint author), Univ Calgary, Fac Vet Med, Dept Comparat Biol & Expt Med, Dept Microbiol Immunol & Infect Dis,Cumming Sch M, Calgary, AB, Canada.
EM ncpeters@ucalgary.ca
RI Roma, Eric /E-2752-2014
OI Roma, Eric /0000-0001-5265-5277
FU National Institute of Allergy and Infectious Diseases
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases. The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
NR 42
TC 19
Z9 19
U1 2
U2 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD DEC
PY 2014
VL 10
IS 12
AR e1004538
DI 10.1371/journal.ppat.1004538
PG 17
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA AX1JB
UT WOS:000346702400026
PM 25473946
ER
PT J
AU Schuetz, A
Deleage, C
Sereti, I
Rerknimitr, R
Phanuphak, N
Phuang-Ngern, Y
Estes, JD
Sandler, NG
Sukhumvittaya, S
Marovich, M
Jongrakthaitae, S
Akapirat, S
Fletscher, JLK
Kroon, E
Dewar, R
Trichavaroj, R
Chomchey, N
Douek, DC
O'Connell, RJ
Ngauy, V
Robb, ML
Phanuphak, P
Michael, NL
Excler, JL
Kim, JH
de Souza, MS
Ananworanich, J
AF Schuetz, Alexandra
Deleage, Claire
Sereti, Irini
Rerknimitr, Rungsun
Phanuphak, Nittaya
Phuang-Ngern, Yuwadee
Estes, Jacob D.
Sandler, Netanya G.
Sukhumvittaya, Suchada
Marovich, Mary
Jongrakthaitae, Surat
Akapirat, Siriwat
Fletscher, James L. K.
Kroon, Eugene
Dewar, Robin
Trichavaroj, Rapee
Chomchey, Nitiya
Douek, Daniel C.
O'Connell, Robert J.
Ngauy, Viseth
Robb, Merlin L.
Phanuphak, Praphan
Michael, Nelson L.
Excler, Jean-Louis
Kim, Jerome H.
de Souza, Mark S.
Ananworanich, Jintanat
CA RV254 SEARCH 010 Study Grp
RV304 SEARCH 013 Study Grp
TI Initiation of ART during Early Acute HIV Infection Preserves Mucosal
Th17 Function and Reverses HIV-Related Immune Activation
SO PLOS PATHOGENS
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; REGULATORY T-CELLS; ANTIRETROVIRAL
THERAPY; MICROBIAL TRANSLOCATION; TYPE-1 INFECTION; LYMPHOID-TISSUE;
PERIPHERAL LYMPHOCYTES; LENTIVIRAL INFECTIONS; DISEASE PROGRESSION;
GENE-EXPRESSION
AB Mucosal Th17 cells play an important role in maintaining gut epithelium integrity and thus prevent microbial translocation. Chronic HIV infection is characterized by mucosal Th17 cell depletion, microbial translocation and subsequent immune-activation, which remain elevated despite antiretroviral therapy (ART) correlating with increased mortality. However, when Th17 depletion occurs following HIV infection is unknown. We analyzed mucosal Th17 cells in 42 acute HIV infection (AHI) subjects (Fiebig (F) stage I-V) with a median duration of infection of 16 days and the short-term impact of early initiation of ART. Th17 cells were defined as IL-17+ CD4+ T cells and their function was assessed by the co-expression of IL-22, IL-2 and IFN gamma. While intact during FI/II, depletion of mucosal Th17 cell numbers and function was observed during FIII correlating with local and systemic markers of immune-activation. ART initiated at FI/II prevented loss of Th17 cell numbers and function, while initiation at FIII restored Th17 cell numbers but not their polyfunctionality. Furthermore, early initiation of ART in FI/II fully reversed the initially observed mucosal and systemic immune-activation. In contrast, patients treated later during AHI maintained elevated mucosal and systemic CD8+ T-cell activation post initiation of ART. These data support a loss of Th17 cells at early stages of acute HIV infection, and highlight that studies of ART initiation during early AHI should be further explored to assess the underlying mechanism of mucosal Th17 function preservation.
C1 [Schuetz, Alexandra; Phuang-Ngern, Yuwadee; Sukhumvittaya, Suchada; Jongrakthaitae, Surat; Akapirat, Siriwat; Kroon, Eugene; Trichavaroj, Rapee; O'Connell, Robert J.; Ngauy, Viseth; de Souza, Mark S.] Armed Forces Res Inst Med Sci US Component, Dept Retrovirol, Bangkok, Thailand.
[Schuetz, Alexandra; Robb, Merlin L.; Excler, Jean-Louis; Ananworanich, Jintanat] Henry M Jackson Fdn Adv Mil Med, Bethesda, MD USA.
[Deleage, Claire; Estes, Jacob D.] Frederick Natl Lab Canc Res, Leidos Biomed Res Inc, AIDS & Canc Virus Program, Frederick, MD USA.
[Sereti, Irini] NIAID, Clin & Mol Retrovirol Sect, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Rerknimitr, Rungsun; Phanuphak, Praphan] Chulalongkorn Univ, Fac Med, Dept Med, Bangkok 10330, Thailand.
[Phanuphak, Nittaya; Fletscher, James L. K.; Kroon, Eugene; Chomchey, Nitiya; Phanuphak, Praphan; Kim, Jerome H.; de Souza, Mark S.; Ananworanich, Jintanat] SEARCH, Bangkok, Thailand.
[Phanuphak, Nittaya; Chomchey, Nitiya; Phanuphak, Praphan; Ananworanich, Jintanat] Thai Red Cross AIDS Res Ctr, Bangkok, Thailand.
[Sandler, Netanya G.; Douek, Daniel C.] NIAID, Human Immunol Sect, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Marovich, Mary; Robb, Merlin L.; Michael, Nelson L.; Excler, Jean-Louis; Kim, Jerome H.; Ananworanich, Jintanat] Walter Reed Army Inst Res, US Mil HIV Res Program, Silver Spring, MD USA.
[Dewar, Robin] NCI, Virus Isolat & Serol Lab Appl & Dev Res Directora, Frederick Inc, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA.
RP Schuetz, A (reprint author), Armed Forces Res Inst Med Sci US Component, Dept Retrovirol, Bangkok, Thailand.
EM schuetza@afrims.org
OI Utay, Netanya/0000-0002-6407-8670
FU Henry M. Jackson Foundation for the Advancement of Military Medicine,
Inc. [W81XWH-07-2-0067]; U.S. Department of Defense (DOD)
[W81XWH-07-2-0067]; Thai Red Cross AIDS Research Center; UCLA CFAR grant
[5P30 AI028697]; NIAID/NIH
FX This work was supported by a cooperative agreement (W81XWH-07-2-0067)
between the Henry M. Jackson Foundation for the Advancement of Military
Medicine, Inc., and the U.S. Department of Defense (DOD) and by an
intramural grant from the Thai Red Cross AIDS Research Center.
Antiretroviral therapy was supported by the Thai Government
Pharmaceutical Organization, Gilead, Merck and ViiV Healthcare. The UCLA
CFAR Mucosal Immunology Core Laboratory is funded by UCLA CFAR grant
5P30 AI028697 and provided support and guidance regarding the isolation
of MMC. The work of Irini Sereti was supported by Intramural Research
Program of NIAID/NIH. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
NR 79
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U1 0
U2 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7366
EI 1553-7374
J9 PLOS PATHOG
JI PLoS Pathog.
PD DEC
PY 2014
VL 10
IS 12
AR e1004543
DI 10.1371/journal.ppat.1004543
PG 15
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA AX1JB
UT WOS:000346702400030
PM 25503054
ER
PT J
AU Looy, CV
Hotton, CL
AF Looy, Cindy V.
Hotton, Carol L.
TI Spatiotemporal relationships among Late Pennsylvanian plant assemblages:
Palynological evidence from the Markley Formation, West Texas, USA
SO REVIEW OF PALAEOBOTANY AND PALYNOLOGY
LA English
DT Article
DE Palaeoecology; Palynology; Environmental change; Pennsylvanian; Texas;
Markley Formation
ID PALEOZOIC ICE-AGE; NORTH-CENTRAL TEXAS; SEED FERN POLLEN; PERMIAN
PALEOBOTANY; CLIMATE-CHANGE; FORMING ENVIRONMENTS; APPALACHIAN BASIN;
MARATTIALEAN FERN; ATLANTIC CANADA; FOSSIL RECORD
AB The Pennsylvanian lowlands of western Pangea are best known for their diverse wetland floras of arborescent and herbaceous ferns, and arborescent horsetails and clubmosses. In apparent juxtaposition, a very different kind of flora, dominated by a xerophilous assemblage of conifers, taeniopterids and peltasperms, is occasionally glimpsed. Once believed to represent upland or extrabasinal floras from well-drained portions of the landscape, these dryland floras more recently have been interpreted as lowland assemblages growing during drier phases of glacial/interglacial cycles. Whether Pennsylvanian dryland and wetland floras were separated spatially or temporally remains an unsettled question, due in large part to taphonomic bias toward preservation of wetland plants. Previous paleobotanical and sedimentological analysis of the Markley Formation of latest Pennsylvanian (Gzhelian) age, from north central Texas, U.S.A, indicates close correlation between lithofacies and distinct dryland and wetland megaflora assemblages. Here we present a detailed analysis one of those localities, a section unusual in containing abundant palynomorphs, from the lower Markley Formation. Paleobotanical, palynological and lithological data from a section thought to represent a single interglacial/glacial phase are integrated and analyzed to create a complex picture of an evolving landscape. Megafloral data from throughout the Markley Formation show that conifer-dominated dryland floras occur exclusively in highly leached kaolinite beds, likely eroded from underlying soils, whereas a mosaic of wetland floras occupy histosols, ultisols, and fluvial overbank deposits. Palynological data largely conform to this pattern but reveal a more complex picture. An assemblage of mixed wetland and dryland palynofloral taxa is interpolated between a dryland assemblage and an overlying histosol containing wetland taxa. In this section, as well as elsewhere in the Markley Formation, kaolinite and overlying organic beds appear to have formed as a single genetic unit, with the kaolinite forming an impermeable aquiclude upon which a poorly drained wetland subsequently formed. Within a single inferred glacial/interglacial cycle, lithological data indicate significant fluctuations in water availability tracked by changes in palynofloral and megafloral taxa. Palynology reveals that elements of the dryland floras appear at low abundance even within wetland deposits. The combined data indicate a complex pattern of succession and suggest a mosaic of dryland and wetland plant communities in the Late Pennsylvanian. Our data alone cannot show whether dryland and wetland assemblages succeed one another temporally, or coexisted on the landscape. However, the combined evidence suggests relatively close spatial proximity within a fragmenting and increasingly arid environment. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Looy, Cindy V.] Univ Calif Berkeley, Dept Integrat Biol, Berkeley, CA 94720 USA.
[Looy, Cindy V.] Univ Calif Berkeley, Museum Paleontol, Berkeley, CA 94720 USA.
[Hotton, Carol L.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20892 USA.
[Hotton, Carol L.] Smithsonian Inst, Natl Museum Nat Hist, Dept Paleobiol, Washington, DC 20560 USA.
RP Looy, CV (reprint author), Univ Calif Berkeley, Dept Integrat Biol, 1005 Valley Life Sci Bldg 3140, Berkeley, CA 94720 USA.
EM looy@berkeley.edu; hotton@ncbi.nlm.nih.gov
FU Hellman Family Foundation; Intramural Research Program of the National
Institutes of Health, National Library of Medicine
FX We acknowledge William A. DiMichele for his generous sharing of samples
and field notes, helpful discussions and support for this work. Ivo
Duijnstee and Robert Stevenson assisted with imaging, figure and plate
preparation. Critiques by Henk Visscher, Tom van Hoof and especially
Hans Kerp greatly improved the manuscript. Cindy Looy was supported by
the Hellman Family Foundation. The research of Carol Hotton was
supported in part by the Intramural Research Program of the National
Institutes of Health, National Library of Medicine. This is ETE
publication 337, and UCMP Contribution 2055.
NR 158
TC 2
Z9 2
U1 2
U2 85
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0034-6667
EI 1879-0615
J9 REV PALAEOBOT PALYNO
JI Rev. Palaeobot. Palynology
PD DEC
PY 2014
VL 211
BP 10
EP 27
DI 10.1016/j.revpalbo.2014.09.007
PG 18
WC Plant Sciences; Paleontology
SC Plant Sciences; Paleontology
GA AX8BX
UT WOS:000347136600002
PM 26028779
ER
PT J
AU Allen, JD
Caspi, C
Yang, M
Leyva, B
Stoddard, AM
Tamers, S
Tucker-Seeley, RD
Sorensen, GC
AF Allen, Jennifer Dacey
Caspi, Caitlin
Yang, May
Leyva, Bryan
Stoddard, Anne M.
Tamers, Sara
Tucker-Seeley, Reginald D.
Sorensen, Glorian C.
TI Pathways between acculturation and health behaviors among residents of
low-income housing: The mediating role of social and contextual factors
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE United States; Acculturation; Health behavior; Immigrant; Public
housing; Social context
ID FOOD FREQUENCY QUESTIONNAIRE; SELF-REPORTED SMOKING; UNITED-STATES;
PHYSICAL-ACTIVITY; HISPANIC IMMIGRANTS; US HISPANICS; LIFE-COURSE;
VALIDITY; DISCRIMINATION; MODEL
AB Acculturation may influence health behaviors, yet mechanisms underlying its effect are not well understood. In this study, we describe relationships between acculturation and health behaviors among low-income housing residents, and examine whether these relationships are mediated by social and contextual factors. Residents of 20 low-income housing sites in the Boston metropolitan area completed surveys that assessed acculturative characteristics, social/contextual factors, and health behaviors. A composite acculturation scale was developed using latent class analysis, resulting in four distinct acculturative groups. Path analysis was used to examine interrelationships between acculturation, health behaviors, and social/contextual factors, specifically self-reported social ties, social support, stress, material hardship, and discrimination.
Of the 828 respondents, 69% were born outside of the U.S. Less acculturated groups exhibited healthier dietary practices and were less likely to smoke than more acculturated groups. Acculturation had a direct effect on diet and smoking, but not physical activity. Acculturation also showed an indirect effect on diet through its relationship with material hardship.
Our finding that material hardship mediated the relationship between acculturation and diet suggests the need to explicate the significant role of financial resources in interventions seeking to promote healthy diets among low-income immigrant groups. Future research should examine these social and contextual mediators using larger, population-based samples, preferably with longitudinal data. (C) 2014 The Authors. Published by Elsevier Ltd.
C1 [Allen, Jennifer Dacey; Tamers, Sara; Tucker-Seeley, Reginald D.; Sorensen, Glorian C.] Dana Farber Canc Inst, Boston, MA 02215 USA.
[Caspi, Caitlin] Univ Minnesota, Dept Family Med & Community Hlth, Minneapolis, MN 55455 USA.
[Yang, May; Stoddard, Anne M.] New England Res Inst, Watertown, MA USA.
[Leyva, Bryan] NCI, NIH, Bethesda, MD 20892 USA.
RP Allen, JD (reprint author), Dana Farber Canc Inst, Phyllis Cantor Ctr Nursing Res & Patient Care Ser, Ctr Community Based Res, 450 Brookline Ave, Boston, MA 02215 USA.
EM jennifer.allen@tufts.edu
RI Allen, Jennifer/M-2113-2015
FU National Cancer Institute [R01 CA111310-01A1, K05 CA108663-05]; Centers
for Disease Control and Prevention the NIH/NCI Harvard Education Program
in Cancer Prevention and Control [U48DP001946, R25 CA057713]; NIH/NCI
Cancer Related Health Disparities Education and Career Development
Program [R25 CA163184]; NIH/NCI Reducing Social Disparities in Cancer
Risk [K05 CA108663- 05]; NCI K01 career development award [CA169041-01]
FX This research was supported by the National Cancer Institute (grant
numbers R01 CA111310-01A1; K05 CA108663-05), Cooperative Agreement
Number U48DP001946 from the Centers for Disease Control and Prevention
the NIH/NCI Harvard Education Program in Cancer Prevention and Control
(R25 CA057713), the NIH/NCI Cancer Related Health Disparities Education
and Career Development Program (R25 CA163184), the NIH/NCI Reducing
Social Disparities in Cancer Risk (K05 CA108663- 05), and an NCI K01
career development award (Grant# CA169041-01).The findings and
conclusions in this journal article are those of the authors and do not
necessarily represent the official position of the Centers for Disease
Control and Prevention. The authors would like to thank the 20
low-income housing sites that participated in this research, and the
assistance from the Cambridge, Somerville and Chelsea Public Housing
Authorities. The authors also acknowledge the administrative and field
staff at the Harvard School of Public Health and Dana-Farber Cancer
Institute, and the study participants for their contributions to this
project. They also thank Gary Adamkiewicz, Marty Alvarez-Reeves, Amy
Harley, Ruth Lederman, Samuel Lipson, Carol Lowenstein, Hannah L Mills,
Laura Tom, Brianna Wadler, and Lorraine Wallace for their contributions
to the overall study design and implementation.
NR 69
TC 10
Z9 10
U1 8
U2 31
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD DEC
PY 2014
VL 123
BP 26
EP 36
DI 10.1016/j.socscimed.2014.10.034
PG 11
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA AX6GT
UT WOS:000347021800004
PM 25462602
ER
PT J
AU Chen, L
Mathema, B
Chavda, KD
DeLeo, FR
Bonomo, RA
Kreiswirth, BN
AF Chen, Liang
Mathema, Barun
Chavda, Kalyan D.
DeLeo, Frank R.
Bonomo, Robert A.
Kreiswirth, Barry N.
TI Carbapenemase-producing Klebsiella pneumoniae: molecular and genetic
decoding
SO TRENDS IN MICROBIOLOGY
LA English
DT Review
DE Klebsiella pneumoniae carbapenemase; carbapenem-resistant; ST258
ID SEQUENCE TYPE 258; COMPLETE NUCLEOTIDE-SEQUENCE; COMPLETE GENOME
SEQUENCE; NEW-YORK HOSPITALS; HYDROLYZING BETA-LACTAMASE; NEW-JERSEY;
PSEUDOMONAS-AERUGINOSA; ANTIBIOTIC-RESISTANCE; BLA(KPC) GENE; 1ST
DESCRIPTION
AB Klebsiella pneumoniae carbapenemases (KPCs) were first identified in 1996 in the USA. Since then, regional outbreaks of KPC-producing K. pneumoniae (KPC-Kp) have occurred in the USA, and have spread internationally. Dissemination of bla(KPC) involves both horizontal transfer of bla(KPC) genes and plasmids, and clonal spread. Of epidemiological significance, the international spread of KPC-producing K. pneumoniae is primarily associated with a single multilocus sequence type (ST), ST258, and its related variants. However, the molecular factors contributing to the success of ST258 largely remain unclear. In this review, we discuss the recent progresses in understanding KPC-producing K. pneumoniae that are contributing to our knowledge of plasmid and genome composition and structure among the KPC epidemic clone, and we identify possible factors that influence its epidemiological success.
C1 [Chen, Liang; Mathema, Barun; Chavda, Kalyan D.; Kreiswirth, Barry N.] Rutgers State Univ, New Jersey Med Sch, Publ Res Inst, TB Ctr, Newark, NJ 07103 USA.
[Mathema, Barun] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY 10032 USA.
[DeLeo, Frank R.] NIAID, Lab Human Bacterial Pathogenesis, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
[Bonomo, Robert A.] Vet Affairs Med Ctr, Louis Stokes Cleveland Dept, Res Serv, Cleveland, OH 44106 USA.
[Bonomo, Robert A.] Case Western Reserve Univ, Dept Med, Cleveland, OH 44106 USA.
[Bonomo, Robert A.] Case Western Reserve Univ, Dept Pharmacol, Cleveland, OH 44106 USA.
[Bonomo, Robert A.] Case Western Reserve Univ, Dept Mol Biol & Microbiol, Cleveland, OH 44106 USA.
RP Kreiswirth, BN (reprint author), Rutgers State Univ, New Jersey Med Sch, Publ Res Inst, TB Ctr, Newark, NJ 07103 USA.
EM kreiswba@njms.rutgers.edu
OI DeLeo, Frank/0000-0003-3150-2516
FU National Institutes of Health (NIH) [1R01AI090155]; Intramural Research
Program of the NIAID, NIH; Public Health Service [R01AI072219,
R01AI063517]; Cleveland Department of Veterans Affairs; Veterans Affairs
Merit Review Program; Geriatric Research Education and Clinical Center
[VISN 10]
FX This work was supported in part by National Institutes of Health (NIH)
Grant 1R01AI090155 (to B.N.K.), and by the Intramural Research Program
of the NIAID, NIH. This work was also supported by Public Health Service
grant R01AI072219 and R01AI063517 (to R.A. Bonomo) from the National
Institutes of Health and funds and/or facilities provided by the
Cleveland Department of Veterans Affairs, the Veterans Affairs Merit
Review Program and the Geriatric Research Education and Clinical Center
VISN 10 to R. A. Bonomo. The content is solely the responsibility of the
authors and does not necessarily represent the official views of the
National Institute of Health.
NR 80
TC 47
Z9 52
U1 5
U2 24
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0966-842X
EI 1878-4380
J9 TRENDS MICROBIOL
JI Trends Microbiol.
PD DEC
PY 2014
VL 22
IS 12
BP 686
EP 696
DI 10.1016/j.tim.2014.09.003
PG 11
WC Biochemistry & Molecular Biology; Microbiology
SC Biochemistry & Molecular Biology; Microbiology
GA AX8CF
UT WOS:000347137400006
PM 25304194
ER
PT J
AU Safdar, B
Greenberg, MR
Anise, A
Brown, J
Conwit, R
Filart, R
Scott, J
Choo, EK
AF Safdar, Basmah
Greenberg, Marna R.
Anise, Ayodola
Brown, Jeremy
Conwit, Robin
Filart, Rosemarie
Scott, Jane
Choo, Esther K.
TI Funding Mechanisms for Gender-specific Research: Proceedings from a
Panel Discussion at the 2014 Academic Emergency Medicine Consensus
Conference
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article
AB As part of the 2014 Academic Emergency Medicine (AEM) consensus conference Gender-Specific Research in Emergency Care: Investigate, Understand, and Translate How Gender Affects Patient Outcomes, we assembled a diverse panel of representatives from federal and nonfederal funding agencies to discuss future opportunities for sex- and gender-specific research. The discussion revolved around the mission and priorities of each organization, as well as its interest in promoting sex- and gender-specific research. The panelists were asked to provide specific examples of funding lines generated or planned for as pertinent to emergency care. Training opportunities for future researchers in this area were also discussed.
C1 [Safdar, Basmah] Yale Univ, Dept Emergency Med, New Haven, CT 06520 USA.
[Greenberg, Marna R.] Lehigh Valley Hlth Networks, Dept Emergency Med, Allentown, PA USA.
[Anise, Ayodola] Patient Ctr Outcome Res Inst, Addressing Dispar Program, Washington, DC USA.
[Brown, Jeremy] NIH, Off Emergency Care Res, Bethesda, MD 20892 USA.
[Conwit, Robin] NINDS, Off Clin Res, Bethesda, MD 20892 USA.
[Filart, Rosemarie] NIH, Off Res Womens Hlth, Bethesda, MD 20892 USA.
[Scott, Jane] NHLBI, DCVS, NIH, Bethesda, MD 20892 USA.
[Choo, Esther K.] Brown Univ, Dept Emergency Med, Providence, RI 02912 USA.
RP Safdar, B (reprint author), Yale Univ, Dept Emergency Med, New Haven, CT 06520 USA.
EM basmah.safdar@yale.edu
FU National Institute of Neurological Disorders and Stroke
[1R13NS087861-01]; Office of Research on Women's Health at the NIH
FX The consensus conference was supported by grant 1R13NS087861-01 from the
National Institute of Neurological Disorders and Stroke and the Office
of Research on Women's Health at the NIH. Additional funding was
provided by several organizational, institutional, and individual
donors. Non-CME events were supported by Janssen Pharmaceuticals and
Besins Critical Care/BH Pharma. See the Executive Summary elsewhere in
this issue for full funding information.
NR 8
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
EI 1553-2712
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD DEC
PY 2014
VL 21
IS 12
BP 1329
EP 1333
DI 10.1111/acem.12522
PG 5
WC Emergency Medicine
SC Emergency Medicine
GA AW9KS
UT WOS:000346576700005
PM 25413301
ER
PT J
AU Safdar, B
Nagurney, JT
Anise, A
DeVon, HA
D'Onofrio, G
Hess, EP
Hollander, JE
Legato, MJ
McGregor, AJ
Scott, J
Tewelde, S
Diercks, DB
AF Safdar, Basmah
Nagurney, John T.
Anise, Ayodola
DeVon, Holli A.
D'Onofrio, Gail
Hess, Erik P.
Hollander, Judd E.
Legato, Mariane J.
McGregor, Alyson J.
Scott, Jane
Tewelde, Semhar
Diercks, Deborah B.
TI Gender-specific Research for Emergency Diagnosis and Management of
Ischemic Heart Disease: Proceedings from the 2014 Academic Emergency
Medicine Consensus Conference Cardiovascular Research Workgroup
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; SYNDROME EVALUATION WISE; QUANTITATIVE PRETEST
PROBABILITY; ELEVATION MYOCARDIAL-INFARCTION; TAKO-TSUBO CARDIOMYOPATHY;
ACUTE CHEST-PAIN; DEPARTMENT PATIENTS; ANGINA-PECTORIS; SEX-DIFFERENCES;
TAKOTSUBO CARDIOMYOPATHY
AB Coronary artery disease (CAD) is the most common cause of death for both men and women. However, over the years, emergency physicians, cardiologists, and other health care practitioners have observed varying outcomes in men and women with symptomatic CAD. Women in general are 10 to 15 years older than men when they develop CAD, but suffer worse postinfarction outcomes compared to age-matched men. This article was developed by the cardiovascular workgroup at the 2014 Academic Emergency Medicine (AEM) consensus conference to identify sex- and gender-specific gaps in the key themes and research questions related to emergency cardiac ischemia care. The workgroup had diverse stakeholder representation from emergency medicine, cardiology, critical care, nursing, emergency medical services, patients, and major policy-makers in government, academia, and patient care. We implemented the nominal group technique to identify and prioritize themes and research questions using electronic mail, monthly conference calls, in-person meetings, and Web-based surveys between June 2013 and May 2014. Through three rounds of nomination and refinement, followed by an in-person meeting on May 13, 2014, we achieved consensus on five priority themes and 30 research questions. The overarching themes were as follows: 1) the full spectrum of sex-specific risk as well as presentation of cardiac ischemia may not be captured by our standard definition of CAD and needs to incorporate other forms of ischemic heart disease (IHD); 2) diagnosis is further challenged by sex/gender differences in presentation and variable sensitivity of cardiac biomarkers, imaging, and risk scores; 3) sex-specific pathophysiology of cardiac ischemia extends beyond conventional obstructive CAD to include other causes such as microvascular dysfunction, takotsubo, and coronary artery dissection, better recognized as IHD; 4) treatment and prognosis are influenced by sex-specific variations in biology, as well as patient-provider communication; and 5) the changing definitions of pathophysiology call for looking beyond conventionally defined cardiovascular outcomes to patient-centered outcomes. These emergency care priorities should guide future clinical and basic science research and extramural funding in an area that greatly influences patient outcomes.
C1 [Safdar, Basmah; D'Onofrio, Gail] Yale Univ, Dept Emergency Med, New Haven, CT 06520 USA.
[Nagurney, John T.] Massachusetts Gen Hosp, Dept Emergency Med, Boston, MA 02114 USA.
[Hess, Erik P.] Mayo Clin, Dept Emergency Med, Rochester, MN USA.
Thomas Jefferson Univ, Dept Emergency Med, Sidney Kimmel Med Coll, Philadelphia, PA 19107 USA.
[McGregor, Alyson J.] Brown Univ, Dept Emergency Med, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Tewelde, Semhar] Univ Maryland, Dept Emergency Med, College Pk, MD 20742 USA.
[Diercks, Deborah B.] Univ Calif Davis, Med Ctr, Dept Emergency Med, Davis, CA 95616 USA.
[Anise, Ayodola] Patient Ctr Outcomes Res Inst, Washington, DC USA.
[DeVon, Holli A.] Univ Illinois, Coll Nursing, Chicago, IL USA.
[Legato, Mariane J.] Columbia Univ, Cardiol Sect, Dept Med, New York, NY USA.
[Scott, Jane] NHLBI, Washington, DC USA.
RP Safdar, B (reprint author), Yale Univ, Dept Emergency Med, New Haven, CT 06520 USA.
EM basmah.safdar@yale.edu
OI Hollander, Judd/0000-0002-1318-2785; D'Onofrio, Gail/0000-0002-3833-1871
FU National Institute of Neurological Disorders and Stroke
[1R13NS087861-01]; Office of Research on Women's Health at the National
Institutes of Health
FX The consensus conference was supported by grant 1R13NS087861-01 from the
National Institute of Neurological Disorders and Stroke and the Office
of Research on Women's Health at the National Institutes of Health.
Additional funding was provided by several organizational,
institutional, and individual donors. Non-CME events were supported by
Janssen Pharmaceuticals and Besins Critical Care/BH Pharma. See the
executive summary elsewhere in this issue for full funding information.
NR 76
TC 4
Z9 5
U1 3
U2 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1069-6563
EI 1553-2712
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD DEC
PY 2014
VL 21
IS 12
BP 1350
EP 1360
DI 10.1111/acem.12527
PG 11
WC Emergency Medicine
SC Emergency Medicine
GA AW9KS
UT WOS:000346576700009
PM 25413468
ER
PT J
AU Wager, TT
Chandrasekaran, RY
Bradley, J
Rubitski, D
Berke, H
Mente, S
Butler, T
Doran, A
Chang, C
Fisher, K
Knafels, J
Liu, SP
Ohren, J
Marconi, M
DeMarco, G
Sneed, B
Walton, K
Horton, D
Rosado, A
Mead, A
AF Wager, Travis T.
Chandrasekaran, Ramalakshmi Y.
Bradley, Jenifer
Rubitski, David
Berke, Helen
Mente, Scot
Butler, Todd
Doran, Angela
Chang, Cheng
Fisher, Katherine
Knafels, John
Liu, Shenping
Ohren, Jeff
Marconi, Michael
DeMarco, George
Sneed, Blossom
Walton, Kevin
Horton, David
Rosado, Amy
Mead, Andy
TI Casein Kinase 1 delta/epsilon Inhibitor PF-5006739 Attenuates Opioid
Drug-Seeking Behavior
SO ACS CHEMICAL NEUROSCIENCE
LA English
DT Article
DE Casein kinase 1; CK1 delta; CK1 epsilon; PF-5006739; dual inhibitor;
circadian rhythm; phase-delaying; opioid reinstatement; drug addiction
ID CENTRAL-NERVOUS-SYSTEM; SLEEP-PHASE SYNDROME; CIRCADIAN CLOCK; DARPP-32;
MUTATION; RECEPTOR; DETERMINANTS; ADDICTION; ALIGNMENT; EPSILON
AB Casein kinase 1 delta (CK1 delta) and casein kinase 1 epsilon (CK1 epsilon) inhibitors are potential therapeutic agents for a range of psychiatric disorders. The feasibility of developing a CNS kinase inhibitor has been limited by an inability to identify safe brain-penetrant compounds with high kinome selectivity. Guided by structure-based drug design, potent and selective CK1 delta/epsilon inhibitors have now been identified that address this gap, through the design and synthesis of novel 4-[4-(4-fluoropheny1)-1-(piperidin-4-yl)-1H-imidazol-5-yl]pyrimidin-2-amine derivatives. PF-5006739 (6) possesses a desirable profile, with low nanomolar in vitro potency for CK1 delta/epsilon (IC50 = 3.9 and 17.0 nM, respectively) and high kinome selectivity. In vivo, 6 demonstrated robust centrally mediated circadian rhythm phase-delaying effects in both nocturnal and diurnal animal models. Further, 6 dose-dependently attenuated opioid drug-seeking behavior in a rodent operant reinstatement model in animals trained to self-administer fentanyl. Collectively, our data supports further development of 6 as a promising candidate to test the hypothesis of CK1 delta/epsilon inhibition in treating multiple indications in the clinic.
C1 [Wager, Travis T.; Rubitski, David; Mente, Scot; Fisher, Katherine; Marconi, Michael; DeMarco, George] Pfizer Worldwide Res & Dev, Cambridge, MA 02139 USA.
[Chandrasekaran, Ramalakshmi Y.; Bradley, Jenifer; Berke, Helen; Butler, Todd; Doran, Angela; Chang, Cheng; Knafels, John; Liu, Shenping; Ohren, Jeff; Sneed, Blossom; Horton, David; Rosado, Amy; Mead, Andy] Pfizer Worldwide Res & Dev, Groton, CT 06340 USA.
[Walton, Kevin] NIAID, Div Pharmacotherapies & Med Consequences Drug Abu, NIH, Rockville, MD 20852 USA.
RP Wager, TT (reprint author), Pfizer Worldwide Res & Dev, 610 Main St, Cambridge, MA 02139 USA.
EM travis.t.wager@pfizer.com
NR 37
TC 4
Z9 4
U1 0
U2 3
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1948-7193
J9 ACS CHEM NEUROSCI
JI ACS Chem. Neurosci.
PD DEC
PY 2014
VL 5
IS 12
BP 1253
EP 1265
DI 10.1021/cn500201x
PG 13
WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Neurosciences
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Neurosciences
& Neurology
GA AX1AY
UT WOS:000346682000015
PM 25299732
ER
PT J
AU Elias, AF
AF Elias, Abdallah F.
TI The Shodair Medical Genetics Department-Recent Past and Future
Developments
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Article
DE Shodair Hospital; Philip Pallister; medical genetics
ID DELETION; MUTATIONS
AB Philip Pallister and John Opitz laid the ground work for a unique genetic service model in Montana that continues to flourish through ongoing support by the Montana Legislature, the Montana Department of Public Health and Human Services and the Shodair Foundation. At the heart of the model are clinical and laboratory genetic specialists based at Shodair Children's Hospital in Helena providing genetic care for patients through outreach clinics. Clinical services are supported by a state-of-the-art cytogenetics and molecular genetic laboratory as well a fetal genetic pathology program. Over the years, the reach of regular genetics clinics expanded to include large geographic areas including northwest (Kalispell), west central (Missoula), southwest (Bozeman, Butte), north central (Great Falls), and south central Montana (Billings). Building on the foundation of its world-renowned pioneers, the next generation of medical geneticists at Shodair carries the responsibility of integrating genomic medicine in the diagnosis and care of their patients, reducing inequality of services within Montana and partnering with colleagues across specialties to develop a more personalized practice of medicine. (c) 2014 Wiley Periodicals, Inc.
C1 [Elias, Abdallah F.] Shodair Childrens Hosp, Helena, MT 59601 USA.
[Elias, Abdallah F.] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD 21218 USA.
[Elias, Abdallah F.] Univ Montana, Dept Biomed & Pharmaceut Sci, Missoula, MT 59812 USA.
[Elias, Abdallah F.] Western Montana Family Med Residency Program, Missoula, MT USA.
[Elias, Abdallah F.] NIAID, Rocky Mt Labs, NIH, Bethesda, MD USA.
RP Elias, AF (reprint author), Shodair Childrens Hosp, Dept Med Genet, 2755 Colonial Dr, Helena, MT 59601 USA.
EM aelias@shodair.org
NR 10
TC 0
Z9 0
U1 1
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4868
EI 1552-4876
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD DEC
PY 2014
VL 166
IS 4
BP 381
EP 386
DI 10.1002/ajmg.c.31417
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA AX1HW
UT WOS:000346699300003
PM 25424535
ER
PT J
AU Kobayashi, H
Turkbey, B
Watanabe, R
Choyke, PL
AF Kobayashi, Hisataka
Turkbey, Baris
Watanabe, Rira
Choyke, Peter L.
TI Cancer Drug Delivery: Considerations in the Rational Design of Nanosized
Bioconjugates
SO BIOCONJUGATE CHEMISTRY
LA English
DT Review
ID TRANSCAPILLARY PRESSURE-GRADIENT; HUMAN OSTEOSARCOMA XENOGRAFTS;
GROWTH-FACTOR VEGF; SOLID TUMORS; IN-VIVO; ENHANCED PERMEABILITY;
LIPOSOMAL DOXORUBICIN; VASCULAR-PERMEABILITY; BLOOD-VESSELS; SIZE
AB In order to efficiently deliver anticancer agents to tumors, biocompatible nanoparticles or bioconjugates, including antibody-drug conjugates (ADCs), have recently been designed, synthesized, and tested, some even in clinical trials. Controlled delivery can be enhanced by changing specific design characteristics of the bioconjugate such as its size, the nature of the payload, and the surface features. The delivery of macromolecular drugs to cancers largely relies on the leaky nature of the tumor vasculature compared with healthy vessels in normal organs. When administered intravenously, macromolecular bioconjugates and nanosized agents tend to circulate for prolonged times, unless they are small enough to be excreted by the kidney or stealthy enough to evade the macrophage phagocytic system (MPS), formerly the reticulo-endothelial system (RES). Therefore, macromolecular bioconjugates and nanosized agents with long circulation times leak preferentially into tumor tissue through permeable tumor vessels and are then retained in the tumor bed due to reduced lymphatic drainage. This process is known as the enhanced permeability and retention (EPR) effect. However, success of cancer drug delivery only relying on the EPR effect is still limited. To cure cancer patients, further improvement of drug delivery is required by both designing superior agents and enhancing EPR effects. In this Review, we describe the basis of macromolecular or nanosized bioconjugate delivery into cancer tissue and discuss current diagnostic methods for evaluating leakiness of the tumor vasculature. Then, we discuss methods to augment conventional "permeability and retention" effects for macromolecular or nanosized bioconjugates in cancer tissue.
C1 [Kobayashi, Hisataka; Turkbey, Baris; Watanabe, Rira; Choyke, Peter L.] NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Kobayashi, H (reprint author), NCI, Mol Imaging Program, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM Kobayash@mail.nih.gov
FU Intramural Research Program of the 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 75
TC 16
Z9 16
U1 8
U2 47
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 1043-1802
J9 BIOCONJUGATE CHEM
JI Bioconjugate Chem.
PD DEC
PY 2014
VL 25
IS 12
BP 2093
EP 2100
DI 10.1021/bc500481x
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA AX1BB
UT WOS:000346682300001
PM 25385142
ER
PT J
AU Huynh, D
Laeyendecker, O
Brookmeyer, R
AF Huynh, Dat
Laeyendecker, Oliver
Brookmeyer, Ron
TI A Serial Risk Score Approach to Disease Classification that Accounts for
Accuracy and Cost
SO BIOMETRICS
LA English
DT Article
DE Biomarkers; Classification; Diagnostic tests; HIV
ID HIV-INFECTION; BIOMARKERS; COHORT; ERROR
AB The performance of diagnostic tests for disease classification is often measured by accuracy (e.g., sensitivity or specificity); however, costs of the diagnostic test are a concern as well. Combinations of multiple diagnostic tests may improve accuracy, but incur additional costs. Here, we consider serial testing approaches that maintain accuracy while controlling costs of the diagnostic tests. We present a serial risk score classification approach. The basic idea is to sequentially test with additional diagnostic tests just until persons are classified. In this way, it is not necessary to test all persons with all tests. The methods are studied in simulations and compared with logistic regression. We applied the methods to data from HIV cohort studies to identify HIV infected individuals who are recently infected (<1 year) by testing with assays for multiple biomarkers. We find that the serial risk score classification approach can maintain accuracy while achieving a reduction in cost compared to testing all individuals with all assays.
C1 [Huynh, Dat; Brookmeyer, Ron] Univ Calif Los Angeles, Dept Biostat, Los Angeles, CA 90095 USA.
[Laeyendecker, Oliver] Johns Hopkins Univ, Sch Med, Dept Med, NIAID,NIH, Baltimore, MD 21205 USA.
RP Brookmeyer, R (reprint author), Univ Calif Los Angeles, Dept Biostat, Los Angeles, CA 90095 USA.
EM rbrookmeyer@ucla.edu
OI Laeyendecker, Oliver/0000-0002-6429-4760
FU National Institutes of Health [R01-AI095068]; Division of Intramural
Research, National Institute of Allergy and Infectious Diseases,
National Institutes of Health; HIVNET; NIAID; NIDA; NIAIDNational Cancer
Institute; National Heart, Lung, and Blood Institute
FX This work was supported by National Institutes of Health grant
R01-AI095068 and in part by the Division of Intramural Research,
National Institute of Allergy and Infectious Diseases, National
Institutes of Health.; The HIV Network for Prevention Trials (HIVNET)
001 Study was funded by the HIVNET and sponsored by the NIAID; the AIDS
Link to Intravenous Experience (ALIVE) Study was funded by the NIDA; and
the Multicenter AIDS Cohort Study (MACS) was funded by the NIAID, with
additional supplemental funding from the National Cancer Institute and
National Heart, Lung, and Blood Institute.
NR 21
TC 1
Z9 1
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-341X
EI 1541-0420
J9 BIOMETRICS
JI Biometrics
PD DEC
PY 2014
VL 70
IS 4
BP 1042
EP 1051
DI 10.1111/biom.12217
PG 10
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA AX3GF
UT WOS:000346827500028
PM 25156309
ER
PT J
AU McLain, AC
Albert, PS
AF McLain, Alexander C.
Albert, Paul S.
TI Modeling Longitudinal Data with a Random Change Point and No Time-Zero:
Applications to Inference and Prediction of the Labor Curve
SO BIOMETRICS
LA English
DT Article
DE Change point; Heterogeneity; Longitudinal analysis; Prediction
ID MIXED-EFFECTS MODEL
AB In some longitudinal studies the initiation time of the process is not clearly defined, yet it is important to make inference or do predictions about the longitudinal process. The application of interest in this article is to provide a framework for modeling individualized labor curves (longitudinal cervical dilation measurements) where the start of labor is not clearly defined. This is a well-known problem in obstetrics where the benchmark reference time is often chosen as the end of the process (individuals are fully dilated at 10cm) and time is run backwards. This approach results in valid and efficient inference unless subjects are censored before the end of the process, or if we are focused on prediction. Providing dynamic individualized predictions of the longitudinal labor curve prospectively (where backwards time is unknown) is of interest to aid obstetricians to determine if a labor is on a suitable trajectory. We propose a model for longitudinal labor dilation that uses a random-effects model with unknown time-zero and a random change point. We present a maximum likelihood approach for parameter estimation that uses adaptive Gaussian quadrature for the numerical integration. Further, we propose a Monte Carlo approach for dynamic prediction of the future longitudinal dilation trajectory from past dilation measurements. The methodology is illustrated with longitudinal cervical dilation data from the Consortium of Safe Labor Study.
C1 [McLain, Alexander C.] Univ S Carolina, Dept Epidemiol & Biostat, Columbia, SC 29208 USA.
[Albert, Paul S.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Biostat & Bioinformat Branch, Div Intramural Populat Hlth Res, NIH,DHHS, Rockville, MD 20852 USA.
RP McLain, AC (reprint author), Univ S Carolina, Dept Epidemiol & Biostat, 800 Sumter St, Columbia, SC 29208 USA.
EM mclaina@mailbox.sc.edu
FU Intramural Research Program of the National Institutes of Health Eunice
Kennedy Shriver National Institute of Child Health and Human
Development; Division of Intramural Population Health Research, Eunice
Kennedy Shriver National Institute of Child Health and Human Development
FX We thank the editor, associate editor, and referee for their helpful
comments. This study utilized the high-performance computational
capabilities of the Biowulf Linux cluster at the National Institutes of
Health, Bethesda, MD (http://biowulf.nih.gov). The research of Paul
Albert was supported by the Intramural Research Program of the National
Institutes of Health Eunice Kennedy Shriver National Institute of Child
Health and Human Development. The research by Alexander McLain was
supported, in part, by an Interpersonal Agreement with the Division of
Intramural Population Health Research, Eunice Kennedy Shriver National
Institute of Child Health and Human Development.
NR 16
TC 1
Z9 1
U1 2
U2 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0006-341X
EI 1541-0420
J9 BIOMETRICS
JI Biometrics
PD DEC
PY 2014
VL 70
IS 4
BP 1052
EP 1060
DI 10.1111/biom.12218
PG 9
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA AX3GF
UT WOS:000346827500029
PM 25156417
ER
PT J
AU Johnson, JO
Glynn, SM
Gibbs, R
Nalls, MA
Sabatelli, M
Restagno, G
Drory, VE
Chio, A
Rogaeva, E
Traynor, BJ
AF Johnson, Janel O.
Glynn, Shannon M.
Gibbs, Raphael
Nalls, Mike A.
Sabatelli, Mario
Restagno, Gabriella
Drory, Vivian E.
Chio, Adriano
Rogaeva, Ekaterina
Traynor, Bryan J.
TI Mutations in the CHCHD10 gene are a common cause of familial amyotrophic
lateral sclerosis
SO BRAIN
LA English
DT Letter
C1 [Johnson, Janel O.; Glynn, Shannon M.; Traynor, Bryan J.] NIA, Neuromuscular Dis Res Sect, Neurogenet Lab, Bethesda, MD 20892 USA.
[Gibbs, Raphael] NIA, Computat Biol Core, Neurogenet Lab, Bethesda, MD 20892 USA.
[Nalls, Mike A.] NIA, Mol Genet Sect, Neurogenet Lab, Bethesda, MD 20892 USA.
[Sabatelli, Mario] Univ Cattolica Sacro Cuore, Neurol Inst, I-00168 Rome, Italy.
[Sabatelli, Mario] Insieme Contro Malattie Motoneurone Assoc ALS Res, I-00168 Rome, Italy.
[Restagno, Gabriella] Azienda Sanit Osped Osped Infantile Reg Margher S, Dept Clin Pathol, Mol Genet Unit, I-10126 Turin, Italy.
[Drory, Vivian E.] Sourasky Med Ctr, Dept Neurol, IL-64239 Tel Aviv, Israel.
[Chio, Adriano] Univ Turin, Rita Levi Montalcini Dept Neurosci, I-10124 Turin, Italy.
[Rogaeva, Ekaterina] Univ Toronto, Div Neurol, Dept Med, Tanz Ctr Res Neurodegenerat Dis, Toronto, ON M5S 3H2, Canada.
RP Traynor, BJ (reprint author), NIA, Neurogenet Lab, NIH, 35 Convent Dr, Bethesda, MD 20892 USA.
EM traynorb@mail.nih.gov
OI Sabatelli, Mario/0000-0001-6635-4985; Chio, Adriano/0000-0001-9579-5341
FU Intramural NIH HHS; NIA NIH HHS [Z01-AG000949-02]
NR 5
TC 34
Z9 34
U1 2
U2 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
EI 1460-2156
J9 BRAIN
JI Brain
PD DEC
PY 2014
VL 137
AR e311
DI 10.1093/brain/awu265
PN 12
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AX2GJ
UT WOS:000346761200003
PM 25261972
ER
PT J
AU Chen, LY
Brown, PR
Willis, WB
Eddy, EM
AF Chen, Liang-Yu
Brown, Paula R.
Willis, William B.
Eddy, Edward M.
TI Peritubular Myoid Cells Participate in Male Mouse Spermatogonial Stem
Cell Maintenance
SO ENDOCRINOLOGY
LA English
DT Article
ID NEUROTROPHIC FACTOR; SERTOLI-CELLS; SEMINIFEROUS TUBULES; ANDROGEN
RECEPTOR; GENE-EXPRESSION; GROWTH-FACTOR; SELF-RENEWAL; RAT TESTIS;
IMMUNOHISTOCHEMICAL LOCALIZATION; UNDIFFERENTIATED SPERMATOGONIA
AB Peritubular myoid (PM) cells surround the seminiferous tubule and together with Sertoli cells form the cellular boundary of the spermatogonial stem cell (SSC) niche. However, it remains unclear what role PM cells have in determining the microenvironment in the niche required for maintenance of the ability of SSCs to undergo self-renewal and differentiation into spermatogonia. Mice with a targeted disruption of the androgen receptorgene(Ar) in PM cells experienced a progressive loss of spermatogonia, suggesting that PM cells require testosterone (T) action to produce factors influencing SSC maintenance in the niche. Other studies showed that glial cell line-derived neurotrophic factor (GDNF) is required for SSC self-renewal and differentiation of SSCs in vitro and in vivo. This led us to hypothesize that T-regulated GDNF expression by PM cells contributes to the maintenance of SSCs. This hypothesis was tested using an adult mouse PM cell primary culture system and germ cell transplantation. We found that T induced GDNF expression at the mRNA and protein levels in PM cells. Furthermore, when thymus cell antigen 1-positive spermatogonia isolated from neonatal mice were cocultured with PM cells with or without T and transplanted to the testes of germ cell-depleted mice, the number and length of transplant-derived colonies was increased considerably by in vitro T treatment. These results support the novel hypothesis that T-dependent regulation of GDNF expression in PM cells has a significant influence on the microenvironment of the niche and SSC maintenance.
C1 [Chen, Liang-Yu; Willis, William B.; Eddy, Edward M.] NIEHS, Gamete Biol Grp, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
[Brown, Paula R.] NIEHS, Reprod Dev Biol Grp, Lab Reprod & Dev Toxicol, NIH, Res Triangle Pk, NC 27709 USA.
RP Eddy, EM (reprint author), NIEHS, Reprod & Dev Toxicol Lab, NIH, 111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM eddy@niehs.nih.gov
FU Intramural Research Program of the 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 70
TC 15
Z9 16
U1 1
U2 9
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD DEC
PY 2014
VL 155
IS 12
BP 4964
EP 4974
DI 10.1210/en.2014-1406
PG 11
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AX0UN
UT WOS:000346668000034
PM 25181385
ER
PT J
AU Tamaresis, JS
Irwin, JC
Goldfien, GA
Rabban, JT
Burney, RO
Nezhat, C
DePaolo, LV
Giudice, LC
AF Tamaresis, John S.
Irwin, Juan C.
Goldfien, Gabriel A.
Rabban, Joseph T.
Burney, Richard O.
Nezhat, Camran
DePaolo, Louis V.
Giudice, Linda C.
TI Molecular Classification of Endometriosis and Disease Stage Using
High-Dimensional Genomic Data
SO ENDOCRINOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; GENE-EXPRESSION; EUTOPIC ENDOMETRIUM; MILD
ENDOMETRIOSIS; WOMEN; BIOMARKERS; MICROARRAY; DIAGNOSIS; PATHWAYS; FOS
AB Endometriosis (E), an estrogen-dependent, progesterone-resistant, inflammatory disorder, affects 10% of reproductive-age women. It is diagnosed and staged at surgery, resulting in an 11-year latency from symptom onset to diagnosis, underscoring the need for less invasive, less expensive approaches. Because the uterine lining (endometrium) in women with E has altered molecular profiles, we tested whether molecular classification of this tissue can distinguish and stage disease. We developed classifiers using genomic data from n = 148 archived endometrial samples from women with E or without E (normal controls or with other common uterine/pelvic pathologies) across the menstrual cycle and evaluated their performance on independent sample sets. Classifiers were trained separately on samples in specific hormonal milieu, using margin tree classification, and accuracies were scored on independent validation samples. Classification of samples from women with E or no E involved 2 binary decisions, each based on expression of specific genes. These first distinguished presence or absence of uterine/pelvic pathology and then no E from E, with the latter further classified according to severity (minimal/mild or moderate/severe). Best performing classifiers identified E with 90%-100% accuracy, were cycle phase-specific or independent, and used relatively few genes to determine disease and severity. Differential gene expression and pathway analyses revealed immune activation, altered steroid and thyroid hormone signaling/metabolism, and growth factor signaling in endometrium of women with E. Similar findings were observed with other disorders vs controls. Thus, classifier analysis of genomic data from endometrium can detect and stage pelvic E with high accuracy, dependent or independent of hormonal milieu. We propose that limited classifier candidate genes are of high value in developing diagnostics and identifying therapeutic targets. Discovery of endometrial molecular differences in the presence of E and other uterine/pelvic pathologies raises the broader biological question of their impact on the steroid hormone response and normal functions of this tissue.
C1 [Tamaresis, John S.; Irwin, Juan C.; Goldfien, Gabriel A.; Giudice, Linda C.] Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, Ctr Reprod Sci, San Francisco, CA 94143 USA.
[Rabban, Joseph T.] Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94143 USA.
[Burney, Richard O.] Madigan Healthcare Syst, Dept Obstet & Gynecol & Clin Invest, Tacoma, WA 98431 USA.
[Nezhat, Camran] Stanford Univ, Dept Obstet & Gynecol, Stanford, CA 94024 USA.
[DePaolo, Louis V.] NIH, Fertil & Infertil Branch, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
RP Giudice, LC (reprint author), Univ Calif San Francisco, Dept Obstet Gynecol & Reprod Sci, 505 Parnassus Ave,Room 1496, San Francisco, CA 94143 USA.
EM giudice@obgyn.ucsf.edu
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
of Child Health and Human Development Specialized Cooperative Centers
Program in Reproduction and Infertility Research Grant [U54HD 055764];
National Institutes of Health/University of California; San Francisco
Human Endometrial Tissue and DNA Bank; University of California, San
Francisco Clinical and Translational Research Institute Resource
Allocation Program; University of California Office of the President
Proof of Concept grant
FX This work was supported by the National Institutes of Health, Eunice
Kennedy Shriver National Institute of Child Health and Human Development
Specialized Cooperative Centers Program in Reproduction and Infertility
Research Grant U54HD 055764 (to L.C.G.), the National Institutes of
Health/University of California, San Francisco Human Endometrial Tissue
and DNA Bank, the University of California, San Francisco Clinical and
Translational Research Institute Resource Allocation Program (L.C.G.),
and a University of California Office of the President Proof of Concept
grant (L.C.G.).
NR 57
TC 17
Z9 17
U1 1
U2 6
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD DEC
PY 2014
VL 155
IS 12
BP 4986
EP 4999
DI 10.1210/en.2014-1490
PG 14
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AX0UN
UT WOS:000346668000036
PM 25243856
ER
PT J
AU Sun, GH
Fu, LZ
Wen, L
Shi, YB
AF Sun, Guihong
Fu, Liezhen
Wen, Luan
Shi, Yun-Bo
TI Activation of Sox3 Gene by Thyroid Hormone in the Developing Adult
Intestinal Stem Cell During Xenopus Metamorphosis
SO ENDOCRINOLOGY
LA English
DT Article
ID AMPHIBIAN METAMORPHOSIS; SONIC HEDGEHOG; POSTEMBRYONIC DEVELOPMENT;
EPITHELIAL DEVELOPMENT; CONNECTIVE-TISSUE; LAEVIS INTESTINE;
BETA-CATENIN; TR-ALPHA; RECEPTOR; DIFFERENTIATION
AB The maturation of the intestine into the adult form involves the formation of adult stem cells in a thyroid hormone (T-3)-dependent process in vertebrates. In mammals, this takes place during postembryonic development, a period around birth when the T-3 level peaks. Due to the difficulty of manipulating late-stage, uterus-enclosed embryos, very little is known about the development of the adult intestinal stem cells. Interestingly, the remodeling of the intestine during the T-3-dependent amphibian metamorphosis mimics the maturation of mammalian intestine. Our earlier microarray studies in Xenopus laevis revealed that the transcription factor SRY (sex-determining region Y)-box 3 (Sox3), well known for its involvement in neural development, was upregulated in the intestinal epithelium during metamorphosis. Here, we show that Sox3 is highly and specifically expressed in the developing adult intestinal progenitor/stem cells. We further show that its induction by T-3 is independent of new protein synthesis, suggesting that Sox3 is directly activated by liganded T-3 receptor. Thus, T-3 activates Sox3 as one of the earliest changes in the epithelium, and Sox3 in turn may facilitate the dedifferentiation of the larval epithelial cells into adult stem cells.
C1 [Sun, Guihong] Wuhan Univ, Sch Basic Med Sci, Wuhan 430072, Peoples R China.
[Fu, Liezhen; Wen, Luan; Shi, Yun-Bo] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Mol Morphogenesis, Program Cellular Regulat & Metab, NIH, Bethesda, MD 20892 USA.
RP Shi, YB (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Lab Gene Regulat & Dev, Bldg 18T Room 106,18 Lib Dr,MSC 5431, Bethesda, MD 20892 USA.
EM shi@helix.nih.gov
FU intramural Research Program of the Eunice Kennedy Shriver National
Institute of Child Health and Human Development, National Institutes of
Health; National Natural Science Foundation of China [31370187,
30870113]
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, and National Natural Science
Foundation of China (Grants 31370187 and 30870113).
NR 75
TC 3
Z9 3
U1 0
U2 5
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD DEC
PY 2014
VL 155
IS 12
BP 5024
EP 5032
DI 10.1210/en.2014-1316
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AX0UN
UT WOS:000346668000039
PM 25211587
ER
PT J
AU Feng, Y
Zhao, Q
Chen, WZ
Wang, YP
Crowder, K
Dimitrov, DS
AF Feng, Yang
Zhao, Qi
Chen, Weizao
Wang, Yanping
Crowder, Karalyne
Dimitrov, Dimiter S.
TI A new bispecific antibody targeting non-overlapping epitopes on IGF2:
Design, in vitro characterization and pharmacokinetics in macaques
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Article
DE IGF ligand; Bispecific antibodies; Half-life; Cynomolgus macaques
ID HUMAN MONOCLONAL-ANTIBODIES; GROWTH-FACTOR-II; PHASE-2 TRIAL; INSULIN;
CANCER; RECEPTOR; TUMORS; INHIBITION; BINDING
AB The insulin-like growth factor 2 (IGF2) is an important target for cancer therapy. We have previously proposed an approach for fast and irreversible removal of IGF2 from the circulation by using monoclonal antibodies (mAbs) that bind to two or more non-overlapping epitopes on the same molecule. We provided initial evidence for the formation of oligomeric antibody-ligand complexes that can bind to cells expressing Fc gamma receptors (Fc gamma Rs) with high avidity using an antibody domain with relatively low affinity as one of the anti-IGF2 mAbs. Recently, we identified a mAb, m708.5, in a scFv format which binds to both IGF2 and IGF1 with very high (pM) affinity. Interestingly, and rather surprisingly, this mAb did not compete with our other high affinity mAb, m610.27, for binding to IGF2. Therefore, we generated a new bispecific mAb, m67, by combining m708.5 and m610.27. As expected m67 potently inhibited binding of IGF2 to cells expressing the IGF1R and its phosphorylation, and resulted in formation of multimolecular complexes when incubated with IGF2 and bound with high avidity to cells expressing Fc gamma RII; the complexes were internalized in a macrophage-like cell line. However, although m67 exhibited a reasonably long half-life (6.4 +/- 0.6 days) in cynomolgus macaques and high stability in serum, its administration to three animals did not result in any measurable decrease in the IGF2 concentration likely due to the complexity of the IGF2 interactions in the blood and the relatively low (2 mg/kg) dose of the mAb leading to a relatively low maximal blood concentration of 120 nM. In spite of the lack of effect on the IGF2 concentration in this particular experimental setup, m67 exhibited good drugability properties and could be highly effective in other animal models and in humans. Studies with animal models of cancer are ongoing to evaluate the potential of m67 as a new candidate mAb-based therapeutic. Published by Elsevier Inc.
C1 [Feng, Yang; Chen, Weizao; Wang, Yanping; Dimitrov, Dimiter S.] NCI, Ctr Canc Res, Prot Interact Grp, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Zhao, Qi] Chinese Acad Sci, Shenzhen Inst Adv Technol, Guangzhou 518000, Guangdong, Peoples R China.
[Wang, Yanping] Geneva Fdn, Tacoma, WA 98402 USA.
[Crowder, Karalyne] SNBL USA, Everett, WA 98203 USA.
RP Feng, Y (reprint author), NCI, Bldg 567,Rm180,1050 Boyles St, Frederick, MD 21702 USA.
EM fengya@mail.nih.gov
FU Intramural Research Program of the Center for Cancer Research, National
Cancer Institute, National Institutes of Health [NO1-CO-12400,
HHSN261200800001E]
FX This work was supported by the Intramural Research Program of the Center
for Cancer Research, National Cancer Institute, National Institutes of
Health (Contract No. NO1-CO-12400 and HHSN261200800001E).
NR 22
TC 4
Z9 4
U1 1
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD DEC
PY 2014
VL 97
IS 3
BP 359
EP 367
DI 10.1016/j.yexmp.2014.09.007
PG 9
WC Pathology
SC Pathology
GA AX1CK
UT WOS:000346685700007
PM 25220345
ER
PT J
AU Neuman, MG
French, SW
French, BA
Seitz, HK
Cohen, LB
Mueller, S
Osna, NA
Kharbanda, KK
Seth, D
Bautista, A
Thompson, KJ
McKillop, IH
Kirpich, IA
McClain, CJ
Bataller, R
Nanau, RM
Voiculescu, M
Opris, M
Shen, H
Tillman, B
Li, J
Liu, H
Thomes, PG
Ganesan, M
Malnick, S
AF Neuman, Manuela G.
French, Samuel W.
French, Barbara A.
Seitz, Helmut K.
Cohen, Lawrence B.
Mueller, Sebastian
Osna, Natalia A.
Kharbanda, Kusum K.
Seth, Devanshi
Bautista, Abraham
Thompson, Kyle J.
McKillop, Iain H.
Kirpich, Irina A.
McClain, Craig J.
Bataller, Ramon
Nanau, Radu M.
Voiculescu, Mihai
Opris, Mihai
Shen, Hong
Tillman, Brittany
Li, Jun
Liu, Hui
Thomes, Paul G.
Ganesan, Murali
Malnick, Steve
TI Alcoholic and non-alcoholic steatohepatitis
SO EXPERIMENTAL AND MOLECULAR PATHOLOGY
LA English
DT Review
DE Alcoholic hepatitis; Nonalcoholic steatohepatitis; Alcoholic liver
disease; CYP2E1; Hangover; Hepatocarcinogenesis; Immunohistochemistry;
Laboratory markers; Mallory-Denk bodies; Methylation; Mitochondrion;
Micronutrients; Viral hepatitis; Human immunodeficiency virus
ID FATTY LIVER-DISEASE; CARBOHYDRATE-DEFICIENT TRANSFERRIN; HEPATITIS-C
VIRUS; HEPATOCYTE NUCLEAR FACTOR-4-ALPHA; HUMAN
HEPATOCELLULAR-CARCINOMA; GAMMA-GLUTAMYL-TRANSFERASE; CHRONIC ETHANOL
INGESTION; INDUCED OXIDATIVE STRESS; MALLORY-DENK BODIES; METABOLIC
SYNDROME
AB This paper is based upon the "Charles Lieber Satellite Symposia" organized by Manuela G. Neuman at the Research Society on Alcoholism (RSA) Annual Meetings, 2013 and 2014. The present review includes pre-clinical, translational and clinical research that characterize alcoholic liver disease (ALD) and non-alcoholic steatohepatitis (NASH). In addition, a literature search in the discussed area was performed.
Strong clinical and experimental evidence lead to recognition of the key toxic role of alcohol in the pathogenesis of ALD. The liver biopsy can confirm the etiology of NASH or alcoholic steatohepatitis (ASH) and assess structural alterations of cells, their organelles, as well as inflammatory activity. Three histological stages of ALD are simple steatosis, ASH, and chronic hepatitis with hepatic fibrosis or cirrhosis. These latter stages may also be associated with a number of cellular and histological changes, including the presence of Mallory's hyaline, megamitochondria, or perivenular and perisinusoidal fibrosis. Genetic polymorphisms of ethanol metabolizing enzymes such as cytochrome p450 (CYP) 2E1 activation may change the severity of ASH and NASH. Alcohol mediated hepatocarcinogenesis, immune response to alcohol in ASH, as well as the role of other risk factors such as its co-morbidities with chronic viral hepatitis in the presence or absence of human immunodeficiency virus are discussed. Dysregulation of hepatic methylation, as result of ethanol exposure, in hepatocytes transfected with hepatitis C virus (HCV), illustrates an impaired interferon signaling. The hepatotoxic effects of ethanol undermine the contribution of malnutrition to the liver injury. Dietary interventions such as micro and macronutrients, as well as changes to the microbiota are suggested. The clinical aspects of NASH, as part of metabolic syndrome in the aging population, are offered.
The integrative symposia investigate different aspects of alcohol-induced liver damage and possible repair. We aim to (1) determine the immuno-pathology of alcohol-induced liver damage, (2) examine the role of genetics in the development of ASH, (3) propose diagnostic markers of ASH and NASH, (4) examine age differences, (5) develop common research tools to study alcohol-induced effects in clinical and pre-clinical studies, and (6) focus on factors that aggravate severity of organ-damage. The intention of these symposia is to advance the international profile of the biological research on alcoholism. We also wish to further our mission of leading the forum to progress the science and practice of translational research in alcoholism. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Neuman, Manuela G.; Nanau, Radu M.; Opris, Mihai] Univ Toronto, Toronto, ON M5G 0A3, Canada.
[Neuman, Manuela G.] Univ Toronto, Fac Med, Dept Pharmacol & Toxicol, Toronto, ON M5G 0A3, Canada.
[French, Samuel W.; French, Barbara A.; Shen, Hong; Tillman, Brittany; Li, Jun; Liu, Hui] Harbor UCLA Med Ctr, Torrance, CA 90509 USA.
[Seitz, Helmut K.; Mueller, Sebastian] Heidelberg Univ, Alcohol Res Ctr, Heidelberg, Germany.
[Seitz, Helmut K.; Mueller, Sebastian] Salem Med Ctr, Dept Med Gastroenterol & Hepatol, Heidelberg, Germany.
[Cohen, Lawrence B.] Univ Toronto, Fac Med, Sunnybrook Hlth Sci Ctr, Dept Med,Div Gastroenterol, Toronto, ON M5G 0A3, Canada.
[Osna, Natalia A.; Kharbanda, Kusum K.; Thomes, Paul G.; Ganesan, Murali] Univ Nebraska, Med Ctr, Vet Affairs Nebraska Western Iowa Hlth Care Syst, Res Serv, Omaha, NE 68182 USA.
[Seth, Devanshi] Royal Prince Alfred Hosp, Centenary Inst Canc Med & Cell Biol, Drug Hlth Serv, Camperdown, NSW 2050, Australia.
[Seth, Devanshi] Univ Sydney, Fac Med, Sydney, NSW 2006, Australia.
[Bautista, Abraham] NIAAA, Off Extramural Activ, NIH, Rockville, MD 20852 USA.
[Thompson, Kyle J.; McKillop, Iain H.] NIAAA, Off Extramural Activ, NIH, Rockville, MD 20852 USA.
[McClain, Craig J.] Univ Louisville, Sch Med, Louisville, KY 40292 USA.
[Bataller, Ramon] Robley Rex Vet Med Ctr, Louisville, KY USA.
[Bataller, Ramon] Univ N Carolina, Dept Med, Div Gastroenterol & Hepatol, Chapel Hill, NC USA.
[Malnick, Steve] Univ N Carolina, Dept Nutr, Chapel Hill, NC USA.
[Malnick, Steve] Kaplan Med Ctr, Dept Internal Med, Rehovot, Israel.
[Voiculescu, Mihai] Hebrew Univ Jerusalem, IL-76100 Rehovot, Israel.
[Opris, Mihai] Fundeni Clin Inst, Div Nephrol & Internal Med, Bucharest, Romania.
[Opris, Mihai] Univ Med & Pharm Carol Davila, Bucharest, Romania.
[Opris, Mihai] Family Med Clin CAR, Bucharest, Romania.
RP Neuman, MG (reprint author), Univ Toronto, Fac Med, Vitro Drug Safety & Biotechnol Banting Inst, Dept Pharmacol & Toxicol, 100 Coll St,Lab 217, Toronto, ON M5G 0A3, Canada.
EM manuela.neuman@utoronto.ca
FU NIH [AAUOI-021848-02, P50-11999]; Merit Review grants from the
Department of Veterans Affairs, Office of Research and Development
(Biomedical Laboratory and Development) [BX001673, BX001155]; In Vitro
Drug Safety and Biotechnology; Mahaffy Grant, Sunnybrook HSC
FX S. French and his team thank Adriana Flores for typing the manuscript
and thank NIH for the grant support (AAUOI-021848-02 and P50-11999
Morphology Core).; Drs. Osna and Kharbanda acknowledge that their
research reported here was supported by Merit Review grants BX001673
(NAO) and BX001155 (KKK) from the Department of Veterans Affairs, Office
of Research and Development (Biomedical Laboratory and Development).;
Drs. Neuman and Cohen thank In Vitro Drug Safety and Biotechnology and
Mahaffy Grant, Sunnybrook HSC for the funding.
NR 243
TC 16
Z9 16
U1 9
U2 40
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0014-4800
EI 1096-0945
J9 EXP MOL PATHOL
JI Exp. Mol. Pathol.
PD DEC
PY 2014
VL 97
IS 3
BP 492
EP 510
DI 10.1016/j.yexmp.2014.09.005
PG 19
WC Pathology
SC Pathology
GA AX1CK
UT WOS:000346685700024
PM 25217800
ER
PT J
AU Kang, E
Gennery, A
AF Kang, Elizabeth
Gennery, Andrew
TI Hematopoietic Stem Cell Transplantation for Primary Immunodeficiencies
SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA
LA English
DT Article
DE Immunodeficiency; Immune reconstitution; Infection; Immunosuppression;
Inflammation
ID BONE-MARROW-TRANSPLANTATION; CHRONIC GRANULOMATOUS-DISEASE;
WISKOTT-ALDRICH-SYNDROME; TERM IMMUNE RECONSTITUTION; IN-UTERO
TRANSPLANTATION; CERNUNNOS-XLF DEFICIENCY; SINGLE-CENTER EXPERIENCE;
HYPER-IGE SYNDROME; DNA-LIGASE-IV; DOCK8 DEFICIENCY
AB Allogeneic hematopoietic stem cell transplantation has been shown to be curative for well-described as well as newly discovered immunodeficiencies. However, it is difficult to define a universal transplant regimen given the rarity of these disorders and the varied pathophysiology these disorders encompass. This article discusses those primary immunodeficiencies most commonly treated by hematopoietic stem cell transplant and describes the transplant issues specific to these disorders.
C1 [Kang, Elizabeth] NIAID, Hematotherapeut Unit, Lab Host Def, NIH, Bethesda, MD 20892 USA.
[Gennery, Andrew] Great North Childrens Hosp, Inst Cellular Med, Paediat Immunol Dept, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England.
RP Kang, E (reprint author), NIAID, Hematotherapeut Unit, Lab Host Def, NIH, 10-CRC Room 6-3752,10 Ctr Dr, Bethesda, MD 20892 USA.
EM ekang@niaid.nih.gov
FU Intramural NIH HHS [Z99 AI999999]
NR 97
TC 1
Z9 2
U1 1
U2 11
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0889-8588
EI 1558-1977
J9 HEMATOL ONCOL CLIN N
JI Hematol. Oncol. Clin. North Am.
PD DEC
PY 2014
VL 28
IS 6
BP 1157
EP +
DI 10.1016/j.hoc.2014.08.006
PG 15
WC Oncology; Hematology
SC Oncology; Hematology
GA AX1CS
UT WOS:000346686500013
PM 25459185
ER
PT J
AU Bras, J
Guerreiro, R
Darwent, L
Parkkinen, L
Ansorge, O
Escott-Price, V
Hernandez, DG
Nalls, MA
Clark, LN
Honig, LS
Marder, K
Van Der Flier, WM
Lemstra, A
Scheltens, P
Rogaeva, E
St George-Hyslop, P
Londos, E
Zetterberg, H
Ortega-Cubero, S
Pastor, P
Ferman, TJ
Graff-Radford, NR
Ross, OA
Barber, I
Braae, A
Brown, K
Morgan, K
Maetzler, W
Berg, D
Troakes, C
Al-Sarraj, S
Lashley, T
Compta, Y
Revesz, T
Lees, A
Cairns, N
Halliday, GM
Mann, D
Pickering-Brown, S
Dickson, DW
Singleton, A
Hardy, J
AF Bras, Jose
Guerreiro, Rita
Darwent, Lee
Parkkinen, Laura
Ansorge, Olaf
Escott-Price, Valentina
Hernandez, Dena G.
Nalls, Michael A.
Clark, Lorraine N.
Honig, Lawrence S.
Marder, Karen
Van Der Flier, Wiesje M.
Lemstra, Afina
Scheltens, Philip
Rogaeva, Ekaterina
St George-Hyslop, Peter
Londos, Elisabet
Zetterberg, Henrik
Ortega-Cubero, Sara
Pastor, Pau
Ferman, Tanis J.
Graff-Radford, Neill R.
Ross, Owen A.
Barber, Imelda
Braae, Anne
Brown, Kristelle
Morgan, Kevin
Maetzler, Walter
Berg, Daniela
Troakes, Claire
Al-Sarraj, Safa
Lashley, Tammaryn
Compta, Yaroslau
Revesz, Tamas
Lees, Andrew
Cairns, Nigel
Halliday, Glenda M.
Mann, David
Pickering-Brown, Stuart
Dickson, Dennis W.
Singleton, Andrew
Hardy, John
TI Genetic analysis implicates APOE, SNCA and suggests lysosomal
dysfunction in the etiology of dementia with Lewy bodies
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE;
GLUCOCEREBROSIDASE MUTATIONS; IDENTIFIES VARIANTS; DIAGNOSIS;
MULTICENTER; PATHOLOGY; RISK; DLB
AB Clinical and neuropathological similarities between dementia with Lewy bodies (DLB), Parkinson's and Alzheimer's diseases (PD and AD, respectively) suggest that these disorders may share etiology. To test this hypothesis, we have performed an association study of 54 genomic regions, previously implicated in PD or AD, in a large cohort of DLB cases and controls. The cohort comprised 788 DLB cases and 2624 controls. To minimize the issue of potential misdiagnosis, we have also performed the analysis including only neuropathologically proven DLB cases (667 cases). The results show that the APOE is a strong genetic risk factor for DLB, confirming previous findings, and that the SNCA and SCARB2 loci are also associated after a study-wise Bonferroni correction, although these have a different association profile than the associations reported for the same loci in PD. We have previously shown that the p.N370S variant in GBA is associated with DLB, which, together with the findings at the SCARB2 locus, suggests a role for lysosomal dysfunction in this disease. These results indicate that DLB has a unique genetic risk profile when compared with the two most common neurodegenerative diseases and that the lysosome may play an important role in the etiology of this disorder. We make all these data available.
C1 [Bras, Jose; Guerreiro, Rita; Darwent, Lee] UCL Inst Neurol, Dept Mol Neurosci, London WC1N 3BG, England.
[Lashley, Tammaryn; Compta, Yaroslau; Revesz, Tamas; Lees, Andrew] UCL Inst Neurol, Queen Sq Brain Bank, Dept Mol Neurosci, London WC1N 3BG, England.
[Hardy, John] UCL Inst Neurol, Reta Lila Weston Res Labs, Dept Mol Neurosci, London WC1N 3BG, England.
[Parkkinen, Laura; Ansorge, Olaf] Univ Oxford, Nuffield Dept Clin Neurosci, Oxford Parkinsons Dis Ctr, Oxford, England.
[Escott-Price, Valentina] Cardiff Univ, Sch Med, MRC Ctr Neuropsychiatr Genet & Genom, Cardiff CF10 3AX, S Glam, Wales.
[Hernandez, Dena G.; Nalls, Michael A.; Singleton, Andrew] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Clark, Lorraine N.; Honig, Lawrence S.; Marder, Karen] Columbia Univ, Taub Inst Alzheimer Dis & Aging Brain, New York, NY USA.
[Clark, Lorraine N.] Columbia Univ, Dept Pathol & Cell Biol, New York, NY USA.
[Honig, Lawrence S.; Marder, Karen] Columbia Univ, Dept Neurol, New York, NY USA.
[Van Der Flier, Wiesje M.; Lemstra, Afina; Scheltens, Philip] Vrije Univ Amsterdam, Med Ctr, Dept Neurol, Amsterdam, Netherlands.
[Van Der Flier, Wiesje M.; Lemstra, Afina; Scheltens, Philip] Vrije Univ Amsterdam, Med Ctr, Alzheimer Ctr, Amsterdam, Netherlands.
[Rogaeva, Ekaterina; St George-Hyslop, Peter] Univ Toronto, Dept Med, Tanz Ctr Res Neurodegenerat Dis, Toronto, ON, Canada.
[St George-Hyslop, Peter] Univ Cambridge, Cambridge Inst Med Res, Cambridge CB2 0XY, England.
[St George-Hyslop, Peter] Univ Cambridge, Cambridge Natl Inst Hlth Res Biomed Res Unit Deme, Cambridge CB2 0XY, England.
[Londos, Elisabet] Lund Univ, Clin Memory Res Unit, Inst Clin Sci Malmo, S-22100 Lund, Sweden.
[Zetterberg, Henrik] Univ Gothenburg, Clin Neurochem Lab, Dept Psychiat & Neurochem, Inst Neurosci & Physiol,Sahlgrenska Acad, Molndal, Sweden.
[Ortega-Cubero, Sara; Pastor, Pau] Univ Navarra, Neurogenet Lab, Div Neurosci, Ctr Appl Med Res, E-31080 Pamplona, Spain.
[Ortega-Cubero, Sara; Pastor, Pau] Univ Navarra, Sch Med, Dept Neurol, Univ Navarra Clin, E-31080 Pamplona, Spain.
[Ortega-Cubero, Sara; Pastor, Pau] Inst Salud Carlos III, CIBERNED, Ctr Invest Biomed Red Enfermedades Neurodegenerat, Madrid, Spain.
[Ferman, Tanis J.] Mayo Clin, Dept Psychiat, Jacksonville, FL 32224 USA.
[Ferman, Tanis J.] Mayo Clin, Dept Psychol, Jacksonville, FL 32224 USA.
[Graff-Radford, Neill R.] Mayo Clin, Dept Neurol, Jacksonville, FL 32224 USA.
[Ross, Owen A.; Dickson, Dennis W.] Mayo Clin, Dept Neurosci, Jacksonville, FL 32224 USA.
[Barber, Imelda; Braae, Anne; Brown, Kristelle; Morgan, Kevin] Univ Nottingham, Sch Life Sci, Queens Med Ctr, Nottingham NG7 2RD, England.
[Maetzler, Walter; Berg, Daniela] Univ Tubingen, Hertie Inst Clin Brain Res, Dept Neurodegenerat, Ctr Neurol, Tubingen, Germany.
[Maetzler, Walter; Berg, Daniela] German Ctr Neurodegenerat Dis, DZNE, Tubingen, Germany.
[Troakes, Claire; Al-Sarraj, Safa] Kings Coll London, Inst Psychiat, MRC London Neurodegenerat Dis Brain Bank, Dept Clin Neurosci, London WC2R 2LS, England.
[Cairns, Nigel] Washington Univ, Sch Med, Knight Alzheimers Dis Res Ctr, St Louis, MO USA.
[Cairns, Nigel] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
[Halliday, Glenda M.] Neurosci Res Australia, Sydney, NSW, Australia.
[Halliday, Glenda M.] Univ New S Wales, Sch Med Sci, Fac Med, Sydney, NSW, Australia.
[Mann, David; Pickering-Brown, Stuart] Univ Manchester, Fac Med & Human Sci, Inst Brain Behav & Mental Hlth, Manchester, Lancs, England.
[Compta, Yaroslau] Hosp Clin Barcelona, Parkinsons Dis & Movement Disorders Unit, Neurol Serv, IDIBAPS,CIBERNED, Barcelona, Catalonia, Spain.
RP Bras, J (reprint author), UCL Inst Neurol, Dept Mol Neurosci, Queen Sq House,Queen Sq, London WC1N 3BG, England.
EM j.bras@ucl.ac.uk
RI Pastor, Pau/C-9834-2009; Lashley, Tammaryn/D-2583-2009; Hardy,
John/C-2451-2009; Singleton, Andrew/C-3010-2009; Halliday,
Glenda/E-8555-2011; Pickering-Brown, Stuart/D-4008-2009; Troakes,
Claire/K-4346-2015; Maetzler, Walter/A-6796-2011; Guerreiro,
Rita/A-1327-2011; Revesz, Tamas/A-8732-2010;
OI Pastor, Pau/0000-0002-7493-8777; Bras, Jose/0000-0001-8186-0333;
Halliday, Glenda/0000-0003-0422-8398; Pickering-Brown,
Stuart/0000-0003-1561-6054; Revesz, Tamas/0000-0003-2501-0259;
Escott-Price, Valentina/0000-0003-1784-5483
FU Parkinson's UK [K-1204]; Wellcome Trust/MRC [WT089698]; Alzheimer's
Research UK; Spanish Ministry of Science and Innovation [SAF2006-10126,
SAF2010-22329-C02-01]; UTE project FIMA; Stichting Dioraphte; Stichting
VUMC fonds; Wellcome Trust; Medical Research Council; Canadian
Institutes of Health Research; Ontario Research Fund; ARUK; Big Lottery
Fund; Taub Institute; Panasci Fund; Parkinson's Disease Foundation; NIH
[NS060113, P50AG008702, P50NS038370, UL1TR000040]; Michael J. Fox
Foundation; NINDS [NS078086]; Mangurian Foundation for Lewy body
research; Queen Square Brain Bank at the UCL Institute of Neurology;
Alzheimer's Society; NIHR UCLH Biomedical Research Centre; Queen Square
Dementia Biomedical Research Unit; National Institute on Aging, National
Institutes of Health, Department of Health and Human Services
[AG000951-12]
FX This work was supported in part by a Parkinson's UK Innovation Award
(K-1204) and by the Wellcome Trust/MRC Joint Call in Neurodegeneration
award (WT089698) to the UK Parkinson's Disease Consortium whose members
are from the UCL Institute of Neurology, the University of Sheffield,
and the MRC Protein Phosphorylation Unit at the University of Dundee and
by an anonymous Foundation. R.G. is supported by an Alzheimer's Research
UK Travelling Fellowship. The authors would like to acknowledge Elena
Lorenzo for her technical assistance. This study was supported in part
by grants from the Spanish Ministry of Science and Innovation
SAF2006-10126 (2006-2009) and SAF2010-22329-C02-01 (2011-2013) to P.P.
and by the UTE project FIMA to P.P. The sample collection and database
of the Amsterdam Dementia Cohort was funded by Stichting Dioraphte and
Stichting VUMC fonds. G.M.H. is a Senior Principal Research Fellow of
the National Health and Medical Research Council of Australia. For the
neuropathologically confirmed samples from Australia, brain tissue was
received from the Sydney Brain Bank, which is supported by Neuroscience
Research Australia, the University of New South Wales and the National
Health and Medical Research Council of Australia. This study was also
partially funded by the Wellcome Trust, Medical Research Council,
Canadian Institutes of Health Research, Ontario Research Fund. The
Nottingham Genetics Group is supported by ARUK and The Big Lottery Fund.
The effort from Columbia University was supported by the Taub Institute,
the Panasci Fund, the Parkinson's Disease Foundation, and NIH grants
NS060113 (L. Clark), P50AG008702 (P.I. Scott Small), P50NS038370 (P.I.
R. Burke), and UL1TR000040 (P.I. H. Ginsberg). O.A.R. is supported by
the Michael J. Fox Foundation, NINDS R01# NS078086. The Mayo Clinic
Jacksonville is a Morris K. Udall Parkinson's Disease Research Center of
Excellence (NINDS P50 #NS072187) and is supported by the Mangurian
Foundation for Lewy body research. This work has received support from
The Queen Square Brain Bank at the UCL Institute of Neurology. Some of
the tissue samples studied were provided by the MRC London
Neurodegenerative Diseases Brain Bank and the Brains for Dementia
Research project (funded by Alzheimer's Society and ARUK). This research
was supported in part by both the NIHR UCLH Biomedical Research Centre
and the Queen Square Dementia Biomedical Research Unit. This work was
supported in part by the Intramural Research Program of the National
Institute on Aging, National Institutes of Health, Department of Health
and Human Services; project AG000951-12. Funding to pay the Open Access
publication charges for this article was provided by the Wellcome Trust
and the Medical Research Council.
NR 31
TC 39
Z9 39
U1 2
U2 11
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD DEC 1
PY 2014
VL 23
IS 23
BP 6139
EP 6146
DI 10.1093/hmg/ddu334
PG 8
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA AX2MF
UT WOS:000346777400001
PM 24973356
ER
PT J
AU Squires, RB
Pickett, BE
Das, S
Scheuermann, RH
AF Squires, R. Burke
Pickett, Brett E.
Das, Sajal
Scheuermann, Richard H.
TI Toward a method for tracking virus evolutionary trajectory applied to
the pandemic H1N1 2009 influenza virus
SO INFECTION GENETICS AND EVOLUTION
LA English
DT Article
DE Influenza; Virus; Evolution; Metadata; Swine flu; Pandemic
ID A VIRUS; MUTATION-RATES; ORIGIN; GENES; PERFORMANCE
AB In 2009 a novel pandemic H1N1 influenza virus (H1N1pdm09) emerged as the first official influenza pandemic of the 21st century. Early genomic sequence analysis pointed to the swine origin of the virus. Here we report a novel computational approach to determine the evolutionary trajectory of viral sequences that uses data-driven estimations of nucleotide substitution rates to track the gradual accumulation of observed sequence alterations over time. Phylogenetic analysis and multiple sequence alignments show that sequences belonging to the resulting evolutionary trajectory of the H1N1pdm09 lineage exhibit a gradual accumulation of sequence variations and tight temporal correlations in the topological structure of the phylogenetic trees. These results suggest that our evolutionary trajectory analysis (ETA) can more effectively pinpoint the evolutionary history of viruses, including the host and geographical location traversed by each segment, when compared against either BLAST or traditional phylogenetic analysis alone. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Squires, R. Burke] NIAID, Bioinformat & Computat Biosci Branch, Off Cyber Infrastruct & Computat Biol, NIH, Bethesda, MD 20892 USA.
[Pickett, Brett E.; Scheuermann, Richard H.] J Craig Venter Inst, La Jolla, CA USA.
[Das, Sajal] Missouri Univ Sci & Technol, Dept Comp Sci, Rolla, MO USA.
[Scheuermann, Richard H.] Univ Calif San Diego, Dept Pathol, San Diego, CA 92103 USA.
RP Squires, RB (reprint author), NIAID, Bioinformat & Computat Biosci Branch, Off Cyber Infrastruct & Computat Biol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM richard.squires@nih.gov
OI Squires, R Burke/0000-0001-9666-6285
FU NIAID [N01AI40041]
FX Thanks to Megan Coakley for critical reading of the manuscript. We also
acknowledge the generous support received from the NIAID - N01AI40041.
NR 16
TC 1
Z9 1
U1 5
U2 31
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-1348
EI 1567-7257
J9 INFECT GENET EVOL
JI Infect. Genet. Evol.
PD DEC
PY 2014
VL 28
BP 351
EP 357
DI 10.1016/j.meegid.2014.07.015
PG 7
WC Infectious Diseases
SC Infectious Diseases
GA AX1YI
UT WOS:000346739500053
PM 25064525
ER
PT J
AU Huestis, DL
Lehmann, T
AF Huestis, Diana L.
Lehmann, Tovi
TI Ecophysiology of Anopheles gambiae s.l.: Persistence in the Sahel
SO INFECTION GENETICS AND EVOLUTION
LA English
DT Article
DE Aestivation; Diapause; Dormancy; Geographic variation; Malaria; Vector
ecology
ID MOSQUITO CULEX-PIPIENS; OVIPOSITION-SITE DEPRIVATION; DISCONTINUOUS
GAS-EXCHANGE; METABOLIC-RATE DEPRESSION; MOTH CYMBALOPHORA-PUDICA;
NORTHERN HOUSE MOSQUITO; DRY SEASON; DESICCATION RESISTANCE;
CULISETA-INORNATA; SUMMER DIAPAUSE
AB The dry-season biology of malaria vectors is poorly understood, especially in arid environments when no surface waters are available for several months, such as during the dry season in the Sahel. Here we reappraise results on the dry-season physiology of members of the Anopheles gambiae s.l. complex in the broad context of dormancy in insects and especially in mosquitoes. We examine evidence on seasonal changes in reproduction, metabolism, stress tolerance, nutrition, molecular regulation, and environmental conditions and determine if the current results are compatible with dry-season diapause (aestivation) as the primary strategy for persistence throughout the dry season in the Sahel. In the process, we point out critical gaps in our knowledge that future studies can fill. We find compelling evidence that members of the An. gambiae s.l. complex undergo a form of aestivation during the Sahelian dry season by shifting energetic resources away from reproduction and towards increased longevity. Considering the differences between winter at temperate latitudes, which entails immobility of the insect and hence reliance on physiological solutions, as opposed to the Sahelian dry season, which restricts reproduction exclusively, we propose that behavioral changes play an important role in complementing physiological changes in this strategy. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Huestis, Diana L.; Lehmann, Tovi] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
RP Huestis, DL (reprint author), 12735 Twinbrook Pkwy,Room 2W-13A, Rockville, MD 20852 USA.
EM diana.huestis@nih.gov
FU Division of Intramural Research, NIAID, NIH
FX We thank Dia Elnaiem, Peter Armbruster, Phil Lounibos, and 1 anonymous
reviewer for their comments on earlier versions of this manuscript.
Research conducted by the authors mentioned throughout was supported by
the Division of Intramural Research, NIAID, NIH.
NR 145
TC 9
Z9 9
U1 2
U2 18
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-1348
EI 1567-7257
J9 INFECT GENET EVOL
JI Infect. Genet. Evol.
PD DEC
PY 2014
VL 28
BP 648
EP 661
DI 10.1016/j.meegid.2014.05.027
PG 14
WC Infectious Diseases
SC Infectious Diseases
GA AX1YI
UT WOS:000346739500084
PM 24933461
ER
PT J
AU Abdeladhim, M
Kamhawi, S
Valenzuela, JG
AF Abdeladhim, Maha
Kamhawi, Shaden
Valenzuela, Jesus G.
TI What's behind a sand fly bite? The profound effect of sand fly saliva on
host hemostasis, inflammation and immunity
SO INFECTION GENETICS AND EVOLUTION
LA English
DT Article
DE Sand flies; Salivary protein; Immunity; Leishmaniasis; Vaccine;
Transcriptomes
ID LUTZOMYIA-LONGIPALPIS SALIVA; TRANSMITTED LEISHMANIA-MAJOR; POSSIBLE
ETIOLOGIC LINK; VISCERAL LEISHMANIASIS; PHLEBOTOMUS-PAPATASI; CUTANEOUS
LEISHMANIASIS; ANTI-DESMOGLEIN-1 ANTIBODIES; BRAZILIENSIS INFECTION;
VASODILATORY PEPTIDE; GLAND TRANSCRIPTOMES
AB Sand flies are blood-feeding insects and vectors of the Leishmania parasite. For many years, saliva of these insects has represented a gold mine for the discovery of molecules with anti- hemostatic and immunomodulatory activities. Furthermore, proteins in sand fly saliva have been shown to be a potential vaccine against leishmaniasis and also markers of vector exposure. A bottleneck to progress in these areas of research has been the identification of molecules responsible for the observed activities and properties of saliva. Over the past decade, rapid advances in transcriptomics and proteomics resulted in the completion of a number of sialomes (salivary gland transcriptomes) and the expression of several recombinant salivary proteins from different species of sand fly vectors. This review will provide readers with a comprehensive update of recent advances in the characterization of these salivary molecules and their biological activities and offer insights pertaining to their protective effect against leishmaniasis and their potential as markers of vector exposure. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license
C1 [Abdeladhim, Maha; Kamhawi, Shaden; Valenzuela, Jesus G.] NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
RP Kamhawi, S (reprint author), NIAID, Vector Mol Biol Sect, Lab Malaria & Vector Res, NIH, Rockville, MD 20852 USA.
EM skamhawi@niaid.nih.gov; jvalenzuela@niaid.nih.gov
FU Intramural Research Program of the NIH; National Institute of Allergy
and Infectious Diseases, United States
FX M.A., S.K. and J.G.V. were supported by the Intramural Research Program
of the NIH, National Institute of Allergy and Infectious Diseases,
United States.
NR 90
TC 14
Z9 14
U1 0
U2 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-1348
EI 1567-7257
J9 INFECT GENET EVOL
JI Infect. Genet. Evol.
PD DEC
PY 2014
VL 28
BP 691
EP 703
DI 10.1016/j.meegid.2014.07.028
PG 13
WC Infectious Diseases
SC Infectious Diseases
GA AX1YI
UT WOS:000346739500089
PM 25117872
ER
PT J
AU Saag, MS
Masur, H
AF Saag, Michael S.
Masur, Henry
TI HIV/AIDS Preface
SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA
LA English
DT Editorial Material
C1 [Saag, Michael S.] Univ Alabama Birmingham, Ctr AIDS Res, Birmingham, AL 35294 USA.
[Masur, Henry] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
RP Saag, MS (reprint author), Univ Alabama Birmingham, Ctr AIDS Res, 845 19th St South BBRB 256, Birmingham, AL 35294 USA.
EM msaag@uab.edu; hmasur@cc.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 0
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0891-5520
EI 1557-9824
J9 INFECT DIS CLIN N AM
JI Infect. Dis. Clin. North Am.
PD DEC
PY 2014
VL 28
IS 4
BP IX
EP X
DI 10.1016/j.idc.2014.09.001
PG 2
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AX1BC
UT WOS:000346682400001
PM 25455316
ER
PT J
AU Beekmann, SE
Henderson, DK
AF Beekmann, Susan E.
Henderson, David K.
TI Prevention of Human Immunodeficiency Virus and AIDS Postexposure
Prophylaxis (Including Health Care Workers)
SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA
LA English
DT Article
DE HIV; Postexposure prophylaxis; Occupational exposure; Nonoccupational
exposure; HIV PEP
ID TRANSMITTED DRUG-RESISTANCE; OCCUPATIONAL-EXPOSURE; NEEDLESTICK INJURY;
HIV SEROCONVERSION; SEXUAL EXPOSURE; UNITED-STATES; TRANSMISSION;
INFECTION; NEVIRAPINE; MACAQUES
AB Postexposure prophylaxis (PEP), which is designed to prevent human immunodeficiency virus (HIV) infection after an exposure, is one of several strategies for HIV prevention. PEP was first used after occupational HIV exposures in the late 1980s, with the Centers for Disease Control and Prevention issuing the first set of guidelines that included considerations regarding the use of antiretroviral agents for PEP after occupational HIV exposures in 1990. Use of PEP has been extended to nonoccupational exposures, including after sexual contact or injection-drug use. This article provides a rationale for PEP, assessment of the need for PEP, and details of its implementation.
C1 [Beekmann, Susan E.] Univ Iowa, Coll Med, Dept Internal Med, Iowa City, IA 52242 USA.
[Henderson, David K.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
RP Henderson, DK (reprint author), NIH, Ctr Clin, Bldg 10 CRC,Rm 6-2551, Bethesda, MD 20892 USA.
EM DHenderson@cc.nih.gov
FU Intramural NIH HHS [Z99 CL999999]
NR 55
TC 2
Z9 2
U1 0
U2 5
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0891-5520
EI 1557-9824
J9 INFECT DIS CLIN N AM
JI Infect. Dis. Clin. North Am.
PD DEC
PY 2014
VL 28
IS 4
BP 601
EP +
DI 10.1016/j.idc.2014.08.005
PG 14
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AX1BC
UT WOS:000346682400006
PM 25287589
ER
PT J
AU Fojo, T
Mailankody, S
Lo, A
AF Fojo, Tito
Mailankody, Sham
Lo, Andrew
TI Unintended Consequences of Expensive Cancer Therapeutics-The Pursuit of
Marginal Indications and a Me-Too Mentality That Stifles Innovation and
Creativity The John Conley Lecture
SO JAMA OTOLARYNGOLOGY-HEAD & NECK SURGERY
LA English
DT Article
ID CELL LUNG-CANCER; PHASE-III TRIAL; METASTATIC COLORECTAL-CANCER;
ADVANCED BREAST-CANCER; GASTROINTESTINAL STROMAL TUMORS; IXABEPILONE
PLUS CAPECITABINE; MEDULLARY-THYROID CANCER; PROSTATE-CANCER;
OPEN-LABEL; DOUBLE-BLIND
AB Cancer is expected to continue as a major health and economic problem worldwide. Several factors are contributing to the increasing economic burden imposed by cancer, with the cost of cancer drugs an undeniably important variable. The use of expensive therapies with marginal benefits for their approved indications and for unproven indications is contributing to the rising cost of cancer care. We believe that expensive therapies are stifling progress by (1) encouraging enormous expenditures of time, money, and resources on marginal therapeutic indications and (2) promoting a me-too mentality that is stifling innovation and creativity. The modest gains of Food and Drug Administration-approved therapies and the limited progress against major cancers is evidence of a lowering of the efficacy bar that, together with high drug prices, has inadvertently incentivized the pursuit of marginal outcomes and a me-too mentality evidenced by the duplication of effort and redundant pharmaceutical pipelines. We discuss the economic realities that are driving this process and provide suggestions for radical changes to reengineer our collective cancer ecosystem to achieve better outcomes for society.
C1 [Fojo, Tito; Mailankody, Sham] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Lo, Andrew] MIT, Sloan Sch Management, Cambridge, MA 02139 USA.
RP Fojo, T (reprint author), NCI, Ctr Canc Res, 9000 Rockville Pike,Bldg 10,Rm 12N226, Bethesda, MD 20892 USA.
EM fojot@mail.nih.gov
NR 113
TC 53
Z9 53
U1 3
U2 20
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6181
EI 2168-619X
J9 JAMA OTOLARYNGOL
JI JAMA Otolaryngol-Head Neck Surg.
PD DEC
PY 2014
VL 140
IS 12
BP 1225
EP 1236
DI 10.1001/jamaoto.2014.1570
PG 12
WC Otorhinolaryngology; Surgery
SC Otorhinolaryngology; Surgery
GA AX0JC
UT WOS:000346637700017
PM 25068501
ER
PT J
AU Fuhrman, BJ
Feigelson, HS
Flores, R
Gail, MH
Xu, X
Ravel, J
Goedert, JJ
AF Fuhrman, Barbara J.
Feigelson, Heather Spencer
Flores, Roberto
Gail, Mitchell H.
Xu, Xia
Ravel, Jacques
Goedert, James J.
TI Associations of the Fecal Microbiome With Urinary Estrogens and Estrogen
Metabolites in Postmenopausal Women
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID BREAST-CANCER RISK; MASS SPECTROMETRY METHOD; NECROSIS-FACTOR-ALPHA;
CORE GUT MICROBIOME; ESTRADIOL METABOLISM; MENOPAUSAL WOMEN; OBESITY;
HORMONES; DETERMINANTS; EXCRETION
AB Context: Thegut microbiota may influence the risk of breast cancer through effects on endogenous estrogens.
Objective: The objective of the study was to investigate whether urinary estrogens and estrogen metabolites are associated with the diversity and composition of the fecal microbiome.
Design and Setting: This was a cross-sectional study among women enrolled in Kaiser Permanente of Colorado.
Participants: A total of 60 women drawn from a random sample of healthy postmenopausal women (aged 55-69 y), without current or recent use of antibiotics or hormone therapy and no history of cancer or gastrointestinal disease participated in the study.
Outcome Measures and Methods: Creatinine-standardized urinary estrogens (estrone and estradiol) and 13 hydroxylated estrogen metabolites were measured in spot urines by liquid chromatography-tandem mass spectrometry. The fecal microbiome was assessed using pyrosequencing of 16S rRNA amplicons. General linear models were used to test for associations of diversity and composition of the fecal microbiome with parent estrogen (estrone + estradiol), total estrogens, and estrogen metabolites and the ratio of estrogen metabolites to parent estrogen, which has been predictive of postmenopausal breast cancer risk in previous studies.
Results: The ratio of metabolites to parents was directly associated with whole-tree phylogenetic diversity (R = 0.35, P = .01 ). Relative abundances of the order Clostridiales (R = 0.32, P = .02) and the genus Bacteroides (R = -0.30, P = .03) were also correlated with the ratio of metabolites to parents. Associations were independent of age, body mass index, and study design factors.
Conclusions: Ourdata suggest that women with a more diverse gut microbiome exhibit an elevated urinary ratio of hydroxylated estrogen metabolites to parent estrogen. Further research is warranted to confirm and relate these findings to clinical disease.
C1 [Fuhrman, Barbara J.] Univ Arkansas Med Sci, Fay W Boozman Coll Publ Hlth, Dept Epidemiol, Little Rock, AR 72205 USA.
[Fuhrman, Barbara J.; Flores, Roberto; Gail, Mitchell H.; Goedert, James J.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Flores, Roberto] NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Feigelson, Heather Spencer] Kaiser Permanente Colorado, Inst Hlth Res, Denver, CO 80231 USA.
[Xu, Xia] Leidos Biomed Res Inc, Canc Res Technol Program, Frederick Natl Lab Canc Res, Frederick, MD 21702 USA.
[Ravel, Jacques] Univ Maryland, Inst Genome Sci, Baltimore, MD 21201 USA.
RP Goedert, JJ (reprint author), NCI, Div Canc Epidemiol, NIH, Dept Hlth & Human Serv, 9609 Med Ctr Dr,Room 6E106,MSC 9767, Bethesda, MD 20892 USA.
EM goedertj@mail.nih.gov
OI Fuhrman, Barbara/0000-0002-1777-9888; Ravel, Jacques/0000-0002-0851-2233
FU Intramural Research Program of the NCI; National Institutes of Health;
National Cancer Institute Intramural Research Program
[HHSN261200800001E]
FX This research was supported by the Intramural Research Program of the
NCI, National Institutes of Health, but this support did not influence
the data analysis, manuscript preparation, or decision to submit for
publication.; This work was supported in whole or in part by federal
funds from the National Cancer Institute Intramural Research Program
under Contract HHSN261200800001E.
NR 40
TC 11
Z9 13
U1 7
U2 27
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD DEC
PY 2014
VL 99
IS 12
BP 4632
EP 4640
DI 10.1210/jc.2014-2222
PG 9
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AX1ZP
UT WOS:000346743300035
PM 25211668
ER
PT J
AU Crocker, MK
Gourgari, E
Lodish, M
Stratakis, CA
AF Crocker, Melissa K.
Gourgari, Evgenia
Lodish, Maya
Stratakis, Constantine A.
TI Use of Aromatase Inhibitors in Large Cell Calcifying Sertoli Cell
Tumors: Effects on Gynecomastia, Growth Velocity, and Bone Age
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID PEUTZ-JEGHERS-SYNDROME; PREPUBERTAL GYNECOMASTIA; CARNEY COMPLEX;
FEATURES; TESTIS
AB Context: Large cell calcifying Sertoli cell tumors (LCCSCT) present in isolation or, especially in children, in association with Carney Complex (CNC) or Peutz- Jeghers Syndrome (PJS). These tumors overexpress aromatase (CYP19A1), which leads to increased conversion of delta-4-androstenedi-one to estrone and testosterone to estradiol. Prepubertal boys may present with growth acceleration, advanced bone age, and gynecomastia.
Objective: To investigate the outcomes of aromatase inhibitor therapy (AIT) in prepubertal boys with LCCSCTs.
Design: Case series of a very rare tumor and chart review of cases treated at other institutions.
Setting: Tertiary care and referral center.
Patients: Six boys, five with PJS and one with CNC, were referred to the National Institutes of Health for treatment of LCCSCT. All patients had gynecomastia, testicular enlargement, and advanced bone ages, and were being treated by their referring physicians with AIT.
Interventions: Patients were treated for a total of 6-60 months on AIT.
Main Outcome Measures: Height, breast tissue mass, and testicular size were all followed; physical examination, scrotal ultrasounds, and bone ages were obtained, and hormonal concentrations and tumor markers were measured.
Results: Tumor markers were negative. All patients had decreases in breast tissue while on therapy. Height percentiles declined, and predicted adult height moved closer to midparental height as bone age advancement slowed. Testicular enlargement stabilized until entry into central puberty. Only one patient required unilateral orchiectomy.
Conclusions: Patients with LCCSCT benefit from AIT with reduction and/or elimination of gynecomastia and slowing of linear growth and bone age advancement. Further study of long-term outcomesandsafety monitoring areneededbut these preliminary data suggest thatmammoplasty and/or orchiectomy may be foregone in light of the availability of medical therapy.
C1 [Crocker, Melissa K.; Gourgari, Evgenia; Lodish, Maya; Stratakis, Constantine A.] NIH, Sect Endocrinol & Genet, Program Dev Endocrinol & Genet, Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD 20892 USA.
[Crocker, Melissa K.] Boston Childrens Hosp, Div Endocrinol, Boston, MA 02115 USA.
[Gourgari, Evgenia] Georgetown Univ, Div Pediat Endocrinol, Washington, DC 20007 USA.
RP Lodish, M (reprint author), Bg 10-CRC Room 1-3330,10 Ctr Dr, Bethesda, MD 20814 USA.
EM lodishma@mail.nih.gov
FU Intramural Research Programs of The Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD); National
Institutes of Health Clinical Center
FX This work was supported by The Intramural Research Programs of The
Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) and the National Institutes of Health Clinical
Center.
NR 21
TC 2
Z9 2
U1 0
U2 2
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD DEC
PY 2014
VL 99
IS 12
BP E2673
EP E2680
DI 10.1210/jc.2014-2530
PG 8
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AX1ZP
UT WOS:000346743300076
PM 25226294
ER
PT J
AU Ma, YHV
Schwartz, AV
Sigurdsson, S
Hue, TF
Lang, TF
Harris, TB
Rosen, CJ
Vittinghoff, E
Eiriksdottir, G
Hauksdottir, AM
Siggeirsdottir, K
Sigurdsson, G
Oskarsdottir, D
Napoli, N
Palermo, L
Gudnason, V
Li, XJ
AF Ma, Yu-Heng Vivian
Schwartz, Ann V.
Sigurdsson, Sigurdur
Hue, Trisha F.
Lang, Thomas F.
Harris, Tamara B.
Rosen, Clifford J.
Vittinghoff, Eric
Eiriksdottir, Gudny
Hauksdottir, Alda M.
Siggeirsdottir, Kristin
Sigurdsson, Gunnar
Oskarsdottir, Diana
Napoli, Nicola
Palermo, Lisa
Gudnason, Vilmundur
Li, Xiaojuan
TI Circulating Sclerostin Associated With Vertebral Bone Marrow Fat in
Older Men But Not Women
SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
LA English
DT Article
ID SERUM SCLEROSTIN; MINERAL DENSITY; POSTMENOPAUSAL WOMEN; FRACTURE;
ADULTS; MASS; ADIPOGENESIS; OSTEOPOROSIS; PERFUSION; STRENGTH
AB Context: Osteocyte activity is crucial to the maintenance of bone quality. Sclerostin, an osteocyte product, inhibits bone formation, yet higher circulating sclerostin is associated with higher bone density. Bone marrow fat (MF) is associated with osteoporosis, but little is known about the relationship between osteocyte activity and MF.
Objective: Our objective was to assess the relationships between circulating sclerostin, vertebral MF, volumetric bone mineral density (vBMD), and other fat depots in older adults.
Design, Setting, and Participants: We conducted a cross-sectional study in the Age Gene/Environment Susceptibility-Reykjavik cohort.
Main Outcome Measures: Outcome measures included vertebral MF (L1-L4) measured with magnetic resonance spectroscopy and vBMD (spine and hip) and abdominal fat measured with quantitative computed tomography.
Results: After excluding subjects with bone-active medication use (n = 50), inadequate serum (n = 2), or inadequate magnetic resonance spectroscopy (n = 1), analyses included 115 men and 134 women (mean age 79 y, mean body mass index 27.7 kg/m(2)). In men, but not women, vertebral MF was greater in those with higher serum sclerostin levels. MF was 52.2% in the lowest tertile of serum sclerostin and 56.3% in the highest tertile in men (P for trend <.01) in models adjusted for age, body mass index, and diabetes. Sclerostin was positively associated with cortical and trabecular total hip vBMD, weight in men and women, and total fat mass in men but was not associated with total lean mass or abdominal fat depots.
Conclusion: Circulating sclerostin levels are associated with higher vertebral marrow fat in men, suggesting a relationship between osteocyte function and marrow adipogenesis.
C1 [Ma, Yu-Heng Vivian; Schwartz, Ann V.; Hue, Trisha F.; Lang, Thomas F.; Vittinghoff, Eric; Palermo, Lisa; Li, Xiaojuan] Univ Calif San Francisco, San Francisco, CA 94107 USA.
[Sigurdsson, Sigurdur; Eiriksdottir, Gudny; Hauksdottir, Alda M.; Siggeirsdottir, Kristin; Oskarsdottir, Diana; Gudnason, Vilmundur] Iceland Heart Assoc, IS-201 Kopavogur, Iceland.
[Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Intramural Res Program, Bethesda, MD 20892 USA.
[Rosen, Clifford J.] Maine Med Ctr Res Inst, Scarborough, ME 04074 USA.
[Sigurdsson, Gunnar; Oskarsdottir, Diana; Gudnason, Vilmundur] Univ Iceland, Fac Med, IS-101 Reykjavik, Iceland.
[Sigurdsson, Gunnar] Landspitali Univ Hosp, Dept Endocrinol & Metab, IS-101 Reykjavik, Iceland.
[Napoli, Nicola] Univ Campus Bio Med, I-00128 Rome, Italy.
RP Schwartz, AV (reprint author), Univ Calif San Francisco, 185 Berry St,Lobby 5,Suite 5700, San Francisco, CA 94107 USA.
EM aschwartz@psg.ucsf.edu
RI Gudnason, Vilmundur/K-6885-2015;
OI Gudnason, Vilmundur/0000-0001-5696-0084; Napoli,
Nicola/0000-0002-3091-8205
FU National Institute of Arthritis and Musculoskeletal and Skin Diseases
[R01AR057819]; National Institutes of Health [N01-AG-12100]; National
Institute on Aging Intramural Research Program, Hjartavernd (The
Icelandic Heart Association); Althingi (The Icelandic Parliament);
National Institute of Diabetes and Digestive and Kidney Diseases
[R24DK092759]
FX The ancillary study was supported by the National Institute of Arthritis
and Musculoskeletal and Skin Diseases (Grant R01AR057819). The AGES
Reykjavik Study is supported by funding from the National Institutes of
Health (Contract N01-AG-12100), the National Institute on Aging
Intramural Research Program, Hjartavernd (The Icelandic Heart
Association), and the Althingi (The Icelandic Parliament). C.J.R.
received support from the National Institute of Diabetes and Digestive
and Kidney Diseases (Grant R24DK092759).
NR 31
TC 11
Z9 12
U1 1
U2 3
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0021-972X
EI 1945-7197
J9 J CLIN ENDOCR METAB
JI J. Clin. Endocrinol. Metab.
PD DEC
PY 2014
VL 99
IS 12
BP E2584
EP E2590
DI 10.1210/jc.2013-4493
PG 7
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AX1ZP
UT WOS:000346743300065
PM 25144629
ER
PT J
AU Moustgaard, H
Bello, S
Miller, FG
Hrobjartsson, A
AF Moustgaard, Helene
Bello, Segun
Miller, Franklin G.
Hrobjartsson, Asbjorn
TI Subjective and objective outcomes in randomized clinical trials:
definitions differed in methods publications and were often absent from
trial reports
SO JOURNAL OF CLINICAL EPIDEMIOLOGY
LA English
DT Review
DE Subjective outcomes; Objective outcomes; Types of outcomes; Endpoints;
Risk of bias; Randomized clinical trials
ID OBSERVER BIAS; ASSESSORS; AUTHORS
AB Objectives: The degree of bias in randomized clinical trials varies depending on whether the outcome is subjective or objective. Assessment of the risk of bias in a clinical trial will therefore often involve categorization of the type of outcome. Our primary aim was to examine how the concepts "subjective outcome" and "objective outcome" are defined in methodological publications and clinical trial reports. To put this examination into perspective, we also provide an overview of how outcomes are classified more broadly.
Study Design and Setting: A systematic review of methodological publications providing a classification of clinical trial outcomes and a descriptive study of how outcomes were classified in 200 PubMed indexed clinical trial reports published in 2012.
Results: We identified 90 methodological publications with some form of a classification of outcomes. Three distinct definitions were provided for subjective outcome: (1) dependent on assessor judgment, (2) patient-reported outcome, or (3) private phenomena (ie, phenomena only assessable by the patient). Of the 200 clinical trial reports, 12 used the term "subjective" and/or "objective" about outcomes, but no clinical trial reports explicitly defined the terms.
Conclusion: The terms "subjective" and "objective" are ambiguous when used to describe outcomes in randomized clinical trials. We suggest that the terms should be defined explicitly when used in connection with the assessment of risk of bias in a clinical trial, in meta-epidemiological research, and generally in the reporting of clinical trials. We also suggest that adding an explicit clarification of the terms in future versions of the Cochrane Handbook might further strengthen its important role in guiding review authors. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Moustgaard, Helene; Bello, Segun; Hrobjartsson, Asbjorn] Rigshosp, Nord Cochrane Ctr, DK-2100 Copenhagen O, Denmark.
[Miller, Franklin G.] NIH, Dept Bioeth, Bethesda, MD 20892 USA.
RP Moustgaard, H (reprint author), Rigshosp, Nord Cochrane Ctr, Dept 7811,Blegdamsvej 9, DK-2100 Copenhagen O, Denmark.
EM helene.moustgaard@gmail.com
NR 26
TC 5
Z9 5
U1 2
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0895-4356
EI 1878-5921
J9 J CLIN EPIDEMIOL
JI J. Clin. Epidemiol.
PD DEC
PY 2014
VL 67
IS 12
BP 1327
EP 1334
DI 10.1016/j.jclinepi.2014.06.020
PG 8
WC Health Care Sciences & Services; Public, Environmental & Occupational
Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
Health
GA AX4DI
UT WOS:000346883700008
PM 25263546
ER
PT J
AU Ning, J
Qin, J
Shen, Y
AF Ning, Jing
Qin, Jing
Shen, Yu
TI Score Estimating Equations from Embedded Likelihood Functions Under
Accelerated Failure Time Model
SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION
LA English
DT Article
DE Cox model; Length-biased data; Proportional odds model; Score equation
ID RIGHT-CENSORED DATA; LARGE-SAMPLE THEORY; LINEAR RANK-TESTS; EMPIRICAL
DISTRIBUTIONS; REGRESSION-ANALYSIS; PREVALENT COHORT; SURVIVAL;
INFERENCE
AB The semiparametric accelerated failure time (AFT) model is one of the most popular models for analyzing time-to-event outcomes. One appealing feature of the AFT model is that the observed failure time data can be transformed to identically independent distributed random variables without covariate effects. We describe a class of estimating equations based on the score functions for the transformed data, which are derived from the full likelihood function under commonly used semiparametric models such as the proportional hazards or proportional odds model. The methods of estimating regression parameters under the AFT model can be applied to traditional right-censored survival data as well as more complex time-to-event data subject to length-biased sampling. We establish the asymptotic properties and evaluate the small sample performance of the proposed estimators. We illustrate the proposed methods through applications in two examples.
C1 [Ning, Jing; Shen, Yu] Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
[Qin, Jing] NIAID, Biostat Res Branch, Bethesda, MD 20817 USA.
RP Ning, J (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Biostat, Houston, TX 77030 USA.
EM jning@mdanderson.edu; jingqin@niaid.nih.gov; yshen@mdanderson.org
FU National Institutes of Health [CA079466, CA016672]; Seniors'
Independence Research Program through the National Health Research and
Development Program of Health Canada [6606-3954-MC(S)]; Pfizer Canada
Incorporated through Medical Research Council/Pharmaceutical
Manufacturers Association of Canada Health Activity Program, NHRDP
[6603-1417-302(R)]; Bayer Incorporated; British Columbia Health Research
Foundation [38 (93-2), 34 (96-1)]
FX This work was supported in part by grants CA079466 and CA016672 from the
National Institutes of Health. The authors are grateful to Professor M.
Asgharian and investigators from the Canadian Study of Health and Aging
for providing us with the dementia data. The data reported in the
example were collected as part of the CSHA. The core study was funded by
the Seniors' Independence Research Program through the National Health
Research and Development Program of Health Canada (Project no.
6606-3954-MC(S)). Additional funding was provided by Pfizer Canada
Incorporated through the Medical Research Council/Pharmaceutical
Manufacturers Association of Canada Health Activity Program, NHRDP
Project 6603-1417-302(R), Bayer Incorporated, and the British Columbia
Health Research Foundation Projects 38 (93-2) and 34 (96-1). The study
was coordinated through the University of Ottawa and the Division of
Aging and Seniors, Health Canada.
NR 36
TC 2
Z9 2
U1 2
U2 7
PU AMER STATISTICAL ASSOC
PI ALEXANDRIA
PA 732 N WASHINGTON ST, ALEXANDRIA, VA 22314-1943 USA
SN 0162-1459
EI 1537-274X
J9 J AM STAT ASSOC
JI J. Am. Stat. Assoc.
PD DEC
PY 2014
VL 109
IS 508
BP 1625
EP 1635
DI 10.1080/01621459.2014.946034
PG 11
WC Statistics & Probability
SC Mathematics
GA AX2TI
UT WOS:000346797000024
PM 25663727
ER
PT J
AU Li, Y
Arao, Y
Hall, JM
Burkett, S
Liu, LW
Gerrish, K
Cavailles, V
Korach, KS
AF Li, Yin
Arao, Yukitomo
Hall, Julie M.
Burkett, Sandra
Liu, Liwen
Gerrish, Kevin
Cavailles, Vincent
Korach, Kenneth S.
TI Research Resource: STR DNA Profile and Gene Expression Comparisons of
Human BG-1 Cells and a BG-1/MCF-7 Clonal Variant
SO MOLECULAR ENDOCRINOLOGY
LA English
DT Article
ID OVARIAN-CANCER CELLS; ESTROGEN-RECEPTOR-BETA; ENDOCRINE DISRUPTING
CHEMICALS; MESSENGER-RIBONUCLEIC-ACID; HUMAN-BREAST-CANCER; ALPHA
ER-ALPHA; DOWN-REGULATION; LINE; FIBULIN-1; ESTRADIOL
AB Human ovarian cancer BG-1 cells are a valuable in vitro model that has enabled several laboratories to study the estrogenic responses of ovarian cancers. We recently discovered that there are two different BG-1 cell lines being used for experiments, denoted here as BG-1 FR and BG-1 NIEHS, which exhibit striking morphological differences. The objective of this study was to methodically analyze these two BG-1 variants and compare their characteristics. Short tandem repeat analysis revealed that the DNA profile of BG-1 FR cells was unique, yet the Short tandem repeat pattern of BG-1 NIEHS was identical with that of MCF-7 cells. From a cytogenetic analysis, it became apparent that the BG-1 FR line had the same profile as previously reported, whereas the BG-1 NIEHS and MCF-7 cells share a similar genetic display. A significant number of unique chromosomal translocations were observed between the BG-1 NIEHS and MCF-7 cells, suggesting that acquired genotypic differences resulted in the formation of two lines from a common origin. Although all cell types demonstrated a similar estrogen responsiveness in reporter gene assays, a microarray analysis revealed distinct estrogen-responsive gene expression patterns with surprisingly moderate to low overlap. We conclude that BG-1 FR is the original ovarian cancer cell line, whereas the BG-1 NIEHS is a variant from the MCF-7 cells. These findings provide much needed clarification of the identities and characteristics of key cell line models that are widely used to study estrogen action in female reproductive cancers.
C1 [Li, Yin; Arao, Yukitomo; Korach, Kenneth S.] NIEHS, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Liu, Liwen; Gerrish, Kevin] NIEHS, Mol Genom Core Facil, NIH, Res Triangle Pk, NC 27709 USA.
[Hall, Julie M.] Campbell Univ, Coll Pharm & Hlth Sci, Buies Creek, NC 27506 USA.
[Burkett, Sandra] NCI, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
[Cavailles, Vincent] Univ Montpellier I, Inst Rech Cancerol Montpellier, F-34298 Montpellier, France.
[Cavailles, Vincent] Univ Montpellier I, INSERM, Unite 896, F-34298 Montpellier, France.
RP Korach, KS (reprint author), NIEHS, Reprod & Dev Toxicol Lab, NIH, 111 Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA.
EM korach@niehs.nih.gov
OI Korach, Kenneth/0000-0002-7765-418X
FU Division of Intramural Research of the National Institute of
Environmental Health Sciences [Z01 ES70065]
FX This work was supported by the Division of Intramural Research of the
National Institute of Environmental Health Sciences through Grant Z01
ES70065 (to K.S.K.).
NR 48
TC 2
Z9 2
U1 2
U2 5
PU ENDOCRINE SOC
PI WASHINGTON
PA 2055 L ST NW, SUITE 600, WASHINGTON, DC 20036 USA
SN 0888-8809
J9 MOL ENDOCRINOL
JI Mol. Endocrinol.
PD DEC
PY 2014
VL 28
IS 12
BP 2072
EP 2081
DI 10.1210/me.2014-1229
PG 10
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA AX3KC
UT WOS:000346837200015
PM 25321415
ER
PT J
AU Polotow, TG
Vardaris, CV
Mihaliuc, AR
Goncalves, MS
Pereira, B
Ganini, D
Barros, MP
AF Polotow, Tatiana G.
Vardaris, Cristina V.
Mihaliuc, Andrea R.
Goncalves, Marina S.
Pereira, Benedito
Ganini, Douglas
Barros, Marcelo P.
TI Astaxanthin Supplementation Delays Physical Exhaustion and Prevents
Redox Imbalances in Plasma and Soleus Muscles of Wistar Rats
SO NUTRIENTS
LA English
DT Article
DE carotenoid; exercise; iron; uric acid; oxidative stress; mitochondria
ID OXIDATIVE STRESS; SKELETAL-MUSCLE; LIQUID-CHROMATOGRAPHY; TISSUE
DISTRIBUTION; LIPID-METABOLISM; FREE-RADICALS; HUMAN HEALTH; EXERCISE;
GLUTATHIONE; FATIGUE
AB Astaxanthin (ASTA) is a pinkish-orange carotenoid commonly found in marine organisms, especially salmon. ASTA is a powerful antioxidant and suggested to provide benefits for human health, including the inhibition of LDL oxidation, UV-photoprotection, and prophylaxis of bacterial stomach ulcers. Exercise is associated to overproduction of free radicals in muscles and plasma, with pivotal participation of iron ions and glutathione (GSH). Thus, ASTA was studied here as an auxiliary supplement to improve antioxidant defenses in soleus muscles and plasma against oxidative damage induced by exhaustive exercise. Long-term 1 mg ASTA/kg body weight (BW) supplementation in Wistar rats (for 45 days) significantly delayed time to exhaustion by 29% in a swimming test. ASTA supplementation increased scavenging/iron-chelating capacities (TEAC/FRAP) and limited exercise-induced iron overload and its related pro-oxidant effects in plasma of exercising animals. On the other hand, ASTA induced significant mitochondrial Mn-dependent superoxide dismutase and cytosolic glutathione peroxidase antioxidant responses in soleus muscles that, in turn, increased GSH content during exercise, limited oxidative stress, and delayed exhaustion. We also provided significant discussion about a putative "mitochondrial-targeted" action of ASTA based on previous publications and on the positive results found in the highly mitochondrial populated (oxidative-type) soleus muscles here.
C1 [Polotow, Tatiana G.; Vardaris, Cristina V.; Mihaliuc, Andrea R.; Goncalves, Marina S.; Ganini, Douglas; Barros, Marcelo P.] Univ Cruzeiro Sul, Inst Phys Act & Sports Sci ICAFE, BR-01506000 Sao Paulo, Brazil.
[Pereira, Benedito] Univ Sao Paulo, Sch Phys Educ & Sports EEFE, BR-05508900 Sao Paulo, Brazil.
[Ganini, Douglas] NIEHS, Free Rad Metab Grp, Lab Toxicol & Pharmacol, Durham, NC 27709 USA.
RP Barros, MP (reprint author), Univ Cruzeiro Sul, Inst Phys Act & Sports Sci ICAFE, BR-01506000 Sao Paulo, Brazil.
EM tatianapolotow@hotmail.com; crisvardaris@gmail.com;
andreamihaliuc@hotmail.com; masg_je@yahoo.com.br; benepe@usp.br;
douganini@uol.com.br; marcelo.barros@cruzeirodosul.edu.br
RI Barros, Marcelo/K-1410-2013
OI Barros, Marcelo/0000-0003-3565-8331
FU Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [FAPESP
2009/12342-8]; Conselho Nacional de Desenvolvimento Cientifico e
Tecnologico (Bolsa Produtividade em Pesquisa, Nivel 2, CNPq, Brazil)
[307474/2012-7]; Programa de Suporte a Pos-Graduacao de Instituicoes de
Ensino Particulares (PROSUP/CAPES); CYTED (Spain, EU) [112RT0445]
FX The authors are indebted to the Brazilian funding agencies Fundacao de
Amparo a Pesquisa do Estado de Sao Paulo (FAPESP 2009/12342-8), Conselho
Nacional de Desenvolvimento Cientifico e Tecnologico (Bolsa
Produtividade em Pesquisa, Nivel 2, #307474/2012-7, CNPq, Brazil), and
the Programa de Suporte a Pos-Graduacao de Instituicoes de Ensino
Particulares (PROSUP/CAPES). The authors, Tatiana G. Polotow, Cristina
V. Vardaris, and Marcelo P. Barros are members of the IBERCAROT network,
funded by CYTED (ref. 112RT0445, Spain, EU). The authors are also
indebted to Gustavo Egea Gallucci, Marilia Cerqueira Leite Seelaender
and Rui Curi, from Institute of Biological Sciences (ICB/USP),
University of Sao Paulo, and Etelvino J. H. Bechara, from Federal
University of Sao Paulo (UNIFESP-Diadema) for experimental and equipment
support. Marcelo Paes de Barros is also indebted to Ake Lignell, CEO and
Marketing Director of AstaReal AB (Gustavsberg, Sweden) for donating
astaxanthin-rich algal biomass for animal supplementation in our study.
NR 57
TC 4
Z9 7
U1 5
U2 23
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2072-6643
J9 NUTRIENTS
JI Nutrients
PD DEC
PY 2014
VL 6
IS 12
BP 5819
EP 5838
DI 10.3390/nu6125819
PG 20
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA AX2TA
UT WOS:000346796100028
PM 25514562
ER
PT J
AU Jacobson, KA
Costanzi, S
Paolettal, S
AF Jacobson, Kenneth A.
Costanzi, Stefano
Paolettal, Silvia
TI Computational studies to predict or explain G protein coupled receptor
polypharmacology
SO TRENDS IN PHARMACOLOGICAL SCIENCES
LA English
DT Review
DE G protein-coupled receptors; molecular modeling; bioinformatics;
chemoinformatics
ID STRUCTURE-BASED DISCOVERY; LIGAND DISCOVERY; DRUG DISCOVERY;
CRYSTAL-STRUCTURE; HOMOLOGY MODELS; IN-SILICO; ANTAGONISTS; DOCKING;
GENOME; CRYSTALLOGRAPHY
AB Since G protein-coupled receptors (GPCRs) belong to a very large superfamily of evolutionarily related receptors (>800 members in humans), and due to the rapid progress on their structural biology, they are ideal candidates for polypharmacology studies. Broad screening and bioinformatics/chemoinformatics have been applied to understanding off-target effects of GPCR ligands. It is now feasible to approach the question of GPCR polypharmacology using molecular modeling and the available X-ray GPCR structures. As an example, large and sterically constrained adenosine derivatives (potent adenosine receptor ligands with low conformational freedom and multiple extended substituents) were screened for binding at diverse receptors. Unanticipated off-target interactions, including at biogenic amine receptors, were then modeled using a structure-based approach to provide a consistent understanding of recognition. A conserved Asp in TM3 changed its role from counterion for biogenic amines to characteristic H-bonding to adenosine. The same systematic approach could potentially be applied to many GPCRs or other receptors using other sets of congeneric ligands.
C1 [Jacobson, Kenneth A.; Paolettal, Silvia] NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Costanzi, Stefano] Amer Univ, Dept Chem, Washington, DC 20016 USA.
[Costanzi, Stefano] Amer Univ, Ctr Behav Neurosci, Washington, DC 20016 USA.
RP Jacobson, KA (reprint author), NIDDK, Mol Recognit Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM kennethj@helix.nih.gov
RI Jacobson, Kenneth/A-1530-2009
OI Jacobson, Kenneth/0000-0001-8104-1493
FU Intramural NIH HHS [Z99 DK999999, ZIA DK031126-08]
NR 58
TC 11
Z9 11
U1 3
U2 21
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0165-6147
J9 TRENDS PHARMACOL SCI
JI Trends Pharmacol. Sci.
PD DEC
PY 2014
VL 35
IS 12
BP 658
EP 663
DI 10.1016/j.tips.2014.10.009
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AX4HS
UT WOS:000346894700008
PM 25458540
ER
PT J
AU Duignan, PJ
Van Bressem, MF
Baker, JD
Barbieri, M
Colegrove, KM
De Guise, S
de Swart, RL
Di Guardo, G
Dobson, A
Duprex, WP
Early, G
Fauquier, D
Goldstein, T
Goodman, SJ
Grenfell, B
Groch, KR
Gulland, F
Hall, A
Jensen, BA
Lamy, K
Matassa, K
Mazzariol, S
Morris, SE
Nielsen, O
Rotstein, D
Rowles, TK
Saliki, JT
Siebert, U
Waltzek, T
Wellehan, JFX
AF Duignan, Padraig J.
Van Bressem, Marie-Francoise
Baker, Jason D.
Barbieri, Michelle
Colegrove, Kathleen M.
De Guise, Sylvain
de Swart, Rik L.
Di Guardo, Giovanni
Dobson, Andrew
Duprex, W. Paul
Early, Greg
Fauquier, Deborah
Goldstein, Tracey
Goodman, Simon J.
Grenfell, Bryan
Groch, Katia R.
Gulland, Frances
Hall, Ailsa
Jensen, Brenda A.
Lamy, Karina
Matassa, Keith
Mazzariol, Sandro
Morris, Sinead E.
Nielsen, Ole
Rotstein, David
Rowles, Teresa K.
Saliki, Jeremy T.
Siebert, Ursula
Waltzek, Thomas
Wellehan, James F. X.
TI Phocine Distemper Virus: Current Knowledge and Future Directions
SO VIRUSES-BASEL
LA English
DT Review
DE Morbillivirus; pinnipeds; sea otter; CD150/SLAM; phylogeny; pathology;
epidemiology; immunity; vaccine
ID EUROPEAN HARBOR SEALS; OTTERS ENHYDRA-LUTRIS; SCOTTISH GREY SEALS;
HAWAIIAN MONK SEAL; CANINE-DISTEMPER; MEASLES-VIRUS; HALICHOERUS-GRYPUS;
MORBILLIVIRUS INFECTION; MASS MORTALITY; CETACEAN MORBILLIVIRUS
AB Phocine distemper virus (PDV) was first recognized in 1988 following a massive epidemic in harbor and grey seals in north-western Europe. Since then, the epidemiology of infection in North Atlantic and Arctic pinnipeds has been investigated. In the western North Atlantic endemic infection in harp and grey seals predates the European epidemic, with relatively small, localized mortality events occurring primarily in harbor seals. By contrast, PDV seems not to have become established in European harbor seals following the 1988 epidemic and a second event of similar magnitude and extent occurred in 2002. PDV is a distinct species within the Morbillivirus genus with minor sequence variation between outbreaks over time. There is now mounting evidence of PDV-like viruses in the North Pacific/Western Arctic with serological and molecular evidence of infection in pinnipeds and sea otters. However, despite the absence of associated mortality in the region, there is concern that the virus may infect the large Pacific harbor seal and northern elephant seal populations or the endangered Hawaiian monk seals. Here, we review the current state of knowledge on PDV with particular focus on developments in diagnostics, pathogenesis, immune response, vaccine development, phylogenetics and modeling over the past 20 years.
C1 [Duignan, Padraig J.; Lamy, Karina] Univ Calgary, Dept Ecosyst & Publ Hlth, Calgary, AB T2N 4Z6, Canada.
[Van Bressem, Marie-Francoise] Peruvian Ctr Cetacean Res CEPEC, Cetacean Conservat Med Grp CMED, Lima 20, Peru.
[Baker, Jason D.; Barbieri, Michelle] NOAA, Natl Marine Fisheries Serv, Pacific Isl Fisheries Sci Ctr, Honolulu, HI 96818 USA.
[Barbieri, Michelle; Gulland, Frances] Marine Mammal Ctr, Sausalito, CA 94965 USA.
[Colegrove, Kathleen M.] Univ Illinois, Coll Vet Med, Zool Pathol Program, Maywood, IL 60153 USA.
[De Guise, Sylvain] Univ Connecticut, Dept Pathobiol & Vet Sci, Storrs, CT 06269 USA.
[De Guise, Sylvain] Univ Connecticut, Connecticut Sea Grant Coll Program, Storrs, CT 06269 USA.
[de Swart, Rik L.] Erasmus MC, Dept Virosci, NL-3015 CN Rotterdam, Netherlands.
[Di Guardo, Giovanni] Univ Teramo, Fac Vet Med, I-64100 Teramo, Italy.
[Dobson, Andrew; Grenfell, Bryan; Morris, Sinead E.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Duprex, W. Paul] Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA.
[Early, Greg] Integrated Stat, Woods Hole, MA 02543 USA.
[Fauquier, Deborah; Rowles, Teresa K.] NOAA, Natl Marine Fisheries Serv, Marine Mammal Hlth & Stranding Response Program, Silver Spring, MD 20910 USA.
[Goldstein, Tracey] Univ Calif Davis, Sch Vet Med, Hlth Inst 1, Davis, CA 95616 USA.
[Goodman, Simon J.] Univ Leeds, Sch Biol, Leeds LS2 9JT, W Yorkshire, England.
[Grenfell, Bryan] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Groch, Katia R.] Univ Sao Paulo, Sch Vet Med & Anim Sci, Dept Pathol, BR-05508270 Sao Paulo, Brazil.
[Gulland, Frances] Marine Mammal Commiss, Bethesda, MD 20814 USA.
[Hall, Ailsa] Univ St Andrews, Scottish Oceans Inst, Sea Mammal Res Unit, St Andrews KY16 8LB, Fife, Scotland.
[Jensen, Brenda A.] Hawaii Pacific Univ, Dept Nat Sci, Kaneohe, HI 96744 USA.
[Matassa, Keith] Pacific Marine Mammal Ctr, Laguna Beach, CA 92651 USA.
[Mazzariol, Sandro] Univ Padua, Dept Comparat Biomed & Food Sci, I-35020 Legnaro Padua, Italy.
[Nielsen, Ole] Dept Fisheries & Oceans Canada, Winnipeg, MB R3T 2N6, Canada.
[Rotstein, David] Marine Mammal Pathol Serv, Olney, MD 20832 USA.
[Saliki, Jeremy T.] Univ Georgia, Coll Vet Med, Athens Vet Diagnost Lab, Athens, GA 30602 USA.
[Siebert, Ursula] Univ Vet Med, Inst Terr & Aquat Wildlife Res, D-30173 Hannover, Germany.
[Waltzek, Thomas] Univ Florida, Coll Vet Med, Dept Infect Dis & Pathol, Gainesville, FL 32611 USA.
[Wellehan, James F. X.] Univ Florida, Coll Vet Med, Dept Small Anim Clin Sci, Gainesville, FL 32610 USA.
RP Duignan, PJ (reprint author), Univ Calgary, Dept Ecosyst & Publ Hlth, Calgary, AB T2N 4Z6, Canada.
EM ppjduign@ucalgary.ca; mfb.cmed@gmail.com; Jason.Baker@noaa.gov;
michelle.barbieri@noaa.gov; katie.colegrove@gmail.com;
sylvain.deguise@uconn.edu; r.deswart@erasmusmc.nl; gdiguardo@unite.it;
dobson@princeton.edu; pduprex@bu.edu; greg.early@yahoo.com;
deborah.fauquier@noaa.gov; tgoldstein@ucdavis.edu;
s.j.goodman@leeds.ac.uk; grenfell@princeton.edu; katia.groch@gmail.com;
gullandf@tmmc.org; ajh7@st-andrews.ac.uk; bjensen@hpu.edu;
klamy@gmail.com; kmatassa@pacificmmc.org; sandro.mazzariol@unipd.it;
semorris@princeton.edu; ole.nielsen@dfo-mpo.gc.ca; drdrot@gmail.com;
teri.rowles@noaa.gov; jsaliki@uga.edu; ursula.siebert@tiho-hannover.de;
tomwaltzek@gmail.com; wellehanj@ufl.edu
OI Mazzariol, Sandro/0000-0002-4756-1871; De Swart, Rik/0000-0003-3599-8969
FU RAPIDD program of the Science and Technology Directorate, Department of
Homeland Security; Fogarty International Center, National Institutes of
Health
FX This review is the product of an international marine mammal
morbillivirus workshop held at Princeton University, USA, in August 2014
and funded by the RAPIDD program of the Science and Technology
Directorate, Department of Homeland Security and the Fogarty
International Center, National Institutes of Health.
NR 228
TC 7
Z9 7
U1 4
U2 50
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD DEC
PY 2014
VL 6
IS 12
BP 5093
EP 5134
DI 10.3390/v6125093
PG 42
WC Virology
SC Virology
GA AX3JA
UT WOS:000346834500015
PM 25533658
ER
PT J
AU Van Bressem, MF
Duignan, PJ
Banyard, A
Barbieri, M
Colegrove, KM
De Guise, S
Di Guardo, G
Dobson, A
Domingo, M
Fauquier, D
Fernandez, A
Goldstein, T
Grenfell, B
Groch, KR
Gulland, F
Jensen, BA
Jepson, PD
Hall, A
Kuiken, T
Mazzariol, S
Morris, SE
Nielsen, O
Raga, JA
Rowles, TK
Saliki, J
Sierra, E
Stephens, N
Stone, B
Tomo, I
Wang, J
Waltzek, T
Wellehan, JFX
AF Van Bressem, Marie-Francoise
Duignan, Padraig J.
Banyard, Ashley
Barbieri, Michelle
Colegrove, Kathleen M.
De Guise, Sylvain
Di Guardo, Giovanni
Dobson, Andrew
Domingo, Mariano
Fauquier, Deborah
Fernandez, Antonio
Goldstein, Tracey
Grenfell, Bryan
Groch, Katia R.
Gulland, Frances
Jensen, Brenda A.
Jepson, Paul D.
Hall, Ailsa
Kuiken, Thijs
Mazzariol, Sandro
Morris, Sinead E.
Nielsen, Ole
Raga, Juan A.
Rowles, Teresa K.
Saliki, Jeremy
Sierra, Eva
Stephens, Nahiid
Stone, Brett
Tomo, Ikuko
Wang, Jianning
Waltzek, Thomas
Wellehan, James F. X.
TI Cetacean Morbillivirus: Current Knowledge and Future Directions
SO VIRUSES-BASEL
LA English
DT Review
DE cetacean morbillivirus; epidemics; mass stranding; SLAM; phylogeny;
pathogenesis; diagnosis; endemic infections
ID DOLPHINS STENELLA-COERULEOALBA; CANINE-DISTEMPER-VIRUS; BOTTLE-NOSED
DOLPHINS; PORPOISES PHOCOENA-PHOCOENA; GULF-OF-MEXICO; SUBACUTE
SCLEROSING-PANENCEPHALITIS; POLYMERASE-CHAIN-REACTION; PETITS RUMINANTS
VIRUS; MEASLES-VIRUS; STRIPED DOLPHINS
AB We review the molecular and epidemiological characteristics of cetacean morbillivirus (CeMV) and the diagnosis and pathogenesis of associated disease, with six different strains detected in cetaceans worldwide. CeMV has caused epidemics with high mortality in odontocetes in Europe, the USA and Australia. It represents a distinct species within the Morbillivirus genus. Although most CeMV strains are phylogenetically closely related, recent data indicate that morbilliviruses recovered from Indo-Pacific bottlenose dolphins (Tursiops aduncus), from Western Australia, and a Guiana dolphin (Sotalia guianensis), from Brazil, are divergent. The signaling lymphocyte activation molecule (SLAM) cell receptor for CeMV has been characterized in cetaceans. It shares higher amino acid identity with the ruminant SLAM than with the receptors of carnivores or humans, reflecting the evolutionary history of these mammalian taxa. In Delphinidae, three amino acid substitutions may result in a higher affinity for the virus. Infection is diagnosed by histology, immunohistochemistry, virus isolation, RT-PCR, and serology. Classical CeMV-associated lesions include bronchointerstitial pneumonia, encephalitis, syncytia, and lymphoid depletion associated with immunosuppression. Cetaceans that survive the acute disease may develop fatal secondary infections and chronic encephalitis. Endemically infected, gregarious odontocetes probably serve as reservoirs and vectors. Transmission likely occurs through the inhalation of aerosolized virus but mother to fetus transmission was also reported.
C1 [Van Bressem, Marie-Francoise] Peruvian Ctr Cetacean Res CEPEC, Cetacean Conservat Med Grp CMED, Lima 20, Peru.
[Duignan, Padraig J.] Univ Calgary, Dept Ecosyst & Publ Hlth, Calgary, AB T2N 4Z6, Canada.
[Banyard, Ashley] APHA, Wildlife Zoonoses & Vector Borne Dis Res Grp, Weybridge KT15 3NB, Surrey, England.
[Barbieri, Michelle; Gulland, Frances] Marine Mammal Ctr, Sausalito, CA 94965 USA.
[Colegrove, Kathleen M.] Univ Illinois, Coll Vet Med, Zool Pathol Program, Maywood, IL 60153 USA.
[De Guise, Sylvain] Univ Connecticut, Dept Pathobiol & Vet Sci, Storrs, CT 06269 USA.
[De Guise, Sylvain] Univ Connecticut, Connecticut Sea Grant Coll Program, Storrs, CT 06269 USA.
[Di Guardo, Giovanni] Univ Teramo, Fac Vet Med, I-64100 Teramo, Italy.
[Dobson, Andrew; Grenfell, Bryan; Morris, Sinead E.] Princeton Univ, Dept Ecol & Evolutionary Biol, Princeton, NJ 08544 USA.
[Domingo, Mariano] Autonomous Univ Barcelona, Ctr Recerca Sanitat Anim CReSA, E-08193 Barcelona, Spain.
[Fauquier, Deborah; Rowles, Teresa K.] Natl Marine Fisheries Serv, Marine Mammal Hlth & Stranding Response Program, Silver Spring, MD 20910 USA.
[Fernandez, Antonio; Sierra, Eva] Univ Las Palmas Gran Canaria, Sch Vet, Inst Anim Hlth, Dept Vet Pathol, Las Palmas Gran Canaria 35413, Spain.
[Goldstein, Tracey] Univ Calif Davis, Sch Vet Med, Hlth Inst 1, Davis, CA 95616 USA.
[Grenfell, Bryan] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Groch, Katia R.] Univ Sao Paulo, Sch Vet Med & Anim Sci, Dept Pathol, BR-05508207 Sao Paulo, Brazil.
[Groch, Katia R.] Humpback Whale Inst, BR-45900000 Caravelas, Bahia, Brazil.
[Gulland, Frances] Marine Mammal Commiss, Bethesda, MD 20814 USA.
[Jensen, Brenda A.] Hawaii Pacific Univ, Dept Nat Sci, Kaneohe, HI 96744 USA.
[Jepson, Paul D.] Zool Soc London, Inst Zool, London NW1 4RY, England.
[Hall, Ailsa] Univ St Andrews, Scottish Oceans Inst, Sea Mammal Res Unit, St Andrews KY16 8LB, Fife, Scotland.
[Kuiken, Thijs] Erasmus MC, Dept Virosci, NL-3015 CN Rotterdam, Netherlands.
[Mazzariol, Sandro] Univ Padua, Dept Comparat Biomed & Food Sci, I-35020 Padua, Italy.
[Nielsen, Ole] Cent & Arctic Reg, Dept Fisheries & Oceans Canada, Winnipeg, MB R3T 2N6, Canada.
[Raga, Juan A.] Univ Valencia, Cavanilles Inst Biodivers & Evolutionary Biol, Marine Zool Unit, Valencia 22085, Spain.
[Saliki, Jeremy] Univ Georgia, Athens Vet Diagnost Lab, Coll Vet Med, Athens, GA 30602 USA.
[Stephens, Nahiid] Murdoch Univ, Sch Vet & Life Sci, Perth, WA 6150, Australia.
[Stone, Brett] QML Vetnost, Murarrie, Qld 4172, Australia.
[Tomo, Ikuko] S Australian Museum, Adelaide, SA 5000, Australia.
[Wang, Jianning] CSIRO, East Geelong, Vic 3220, Australia.
[Waltzek, Thomas] Univ Florida, Dept Infect Dis & Pathol, Coll Vet Med, Gainesville, FL 32611 USA.
[Wellehan, James F. X.] Univ Florida, Dept Small Anim Clin Sci, Coll Vet Med, Gainesville, FL 32611 USA.
RP Van Bressem, MF (reprint author), Peruvian Ctr Cetacean Res CEPEC, Cetacean Conservat Med Grp CMED, Lima 20, Peru.
EM mfb.cmed@gmail.com; ppjduign@ucalgary.ca;
ashley.banyard@apha.gsi.gov.uk; michelle.barbieri@noaa.gov;
katie.colegrove@gmail.com; sylvain.deguise@uconn.edu;
gdiguardo@unite.it; dobson@princeton.edu; Mariano.Domingo@cresa.uab.cat;
deborah.fauquier@noaa.gov; afernandez@dmor.ulpgc.es;
tgoldstein@ucdavis.edu; grenfell@princeton.edu; katia.groch@gmail.com;
gullandf@tmmc.org; bjensen@hpu.edu; paul.jepson@ioz.ac.uk;
ajh7@st-andrews.ac.uk; t.kuiken@erasmusmc.n1; sandro.mazzariol@unipd.it;
semorris@princeton.edu; ole.nielsen@dfo-mpo.gc.ca; raga@uv.es;
teri.rowles@noaa.gov; jsaliki@uga.edu; esierra@becarios.ulpgc.es;
n.stephens@murdoch.edu.au; brett.stone@qml.com.au;
ikuko.tomo@samuseum.sa.gov.au; Jianning.Wang@csiro.au;
tomwaltzek@gmail.com; wellehanj@ufl.edu
RI Banyard, Ashley/C-7998-2011; APHA, Staff publications/E-6082-2010;
Fernandez, Antonio/G-3448-2015; Sierra, Eva/H-9352-2015;
OI Banyard, Ashley/0000-0002-1286-9825; Fernandez,
Antonio/0000-0001-5281-0521; Sierra, Eva/0000-0003-3749-8845; Mazzariol,
Sandro/0000-0002-4756-1871; Raga, Juan Antonio/0000-0003-2687-2539
FU RAPIDD program of the Science and Technology Directorate, Department of
Homeland Security; Fogarty International Center, National Institutes of
Health; Swan River Trust; Department of Parks and Wildlife
FX We kindly thank Rik de Swart for inviting us to participate to this
special issue, K Van Waerebeek and Jason Baker for their constructive
comments on this manuscript, two anonymous reviewers for their useful
comments and suggestions and Rob Deaville for the image of a harbor
porpoise. This work emerged from a meeting funded by the RAPIDD program
of the Science and Technology Directorate, Department of Homeland
Security and the Fogarty International Center, National Institutes of
Health. N. Stephens thanks the Swan River Trust and the Department of
Parks and Wildlife for their support.
NR 162
TC 26
Z9 27
U1 6
U2 45
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1999-4915
J9 VIRUSES-BASEL
JI Viruses-Basel
PD DEC
PY 2014
VL 6
IS 12
BP 5145
EP 5181
DI 10.3390/v6125145
PG 37
WC Virology
SC Virology
GA AX3JA
UT WOS:000346834500017
PM 25533660
ER
PT J
AU Conde-Agudelo, A
Romero, R
AF Conde-Agudelo, Agustin
Romero, Roberto
TI Prediction of preterm birth in twin gestations using biophysical and
biochemical tests
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Review
DE cervical length; fetal fibronectin; predictive value of tests;
pregnancy; premature birth
ID TUMOR-NECROSIS-FACTOR; AMNIOTIC-FLUID INTERLEUKIN-6; MONOCYTE
CHEMOTACTIC PROTEIN-1; HUMAN CHORIONIC-GONADOTROPIN; ACTIVATING
PEPTIDE-1 INTERLEUKIN-8; SONOGRAPHIC CERVICAL LENGTH; FETAL GROWTH
RESTRICTION; BLOOD-CELL COUNT; MULTIPLE PREGNANCIES; MICROBIAL INVASION
AB The objective of this study was to determine the performance of biophysical and biochemical tests for the prediction of preterm birth in both asymptomatic and symptomatic women with twin gestations. We identified a total of 19 tests proposed to predict preterm birth, mainly in asymptomatic women. In these women, a single measurement of cervical length with transvaginal ultrasound before 25 weeks of gestation appears to be a good test to predict preterm birth. Its clinical potential is enhanced by the evidence that vaginal progesterone administration in asymptomatic women with twin gestations and a short cervix reduces neonatal morbidity and mortality associated with spontaneous preterm delivery. Other tests proposed for the early identification of asymptomatic women at increased risk of preterm birth showed minimal to moderate predictive accuracy. None of the tests evaluated in this review meet the criteria to be considered clinically useful to predict preterm birth among patients with an episode of preterm labor. However, a negative cervicovaginal fetal fibronectin test could be useful in identifying women who are not at risk for delivering within the next week, which could avoid unnecessary hospitalization and treatment. This review underscores the need to develop accurate tests for predicting preterm birth in twin gestations. Moreover, the use of interventions in these patients based on test results should be associated with the improvement of perinatal outcomes.
C1 [Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Detroit, MI USA.
[Romero, Roberto] Univ Michigan, Dept Obstet & Gynecol, Ann Arbor, MI 48109 USA.
[Romero, Roberto] Michigan State Univ, Dept Epidemiol & Biostat, E Lansing, MI 48824 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.
EM romeror@mail.nih.gov
FU 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
FX This research was supported by the Intramural Research Program of the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Department of Health and
Human Services.
NR 139
TC 13
Z9 13
U1 0
U2 12
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
EI 1097-6868
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 2014
VL 211
IS 6
BP 583
EP 595
DI 10.1016/j.ajog.2014.07.047
PG 13
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AW9NW
UT WOS:000346585300005
PM 25072736
ER
PT J
AU Parry, S
Zhang, HP
Biggio, J
Bukowski, R
Varner, M
Xu, YJ
Andrews, WW
Saade, GR
Esplin, MS
Leite, R
Ilekis, J
Reddy, UM
Sadovsky, Y
Blair, IA
AF Parry, Samuel
Zhang, Heping
Biggio, Joseph
Bukowski, Radek
Varner, Michael
Xu, Yaji
Andrews, William W.
Saade, George R.
Esplin, M. Sean
Leite, Rita
Ilekis, John
Reddy, Uma M.
Sadovsky, Yoel
Blair, Ian A.
CA Eunice Kennedy Shriver Natl Inst C
Genomic Proteomic Network Preterm
TI Maternal serum serpin B7 is associated with early spontaneous preterm
birth
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE preterm birth; proteomics; serine proteinase inhibitors
ID SPECTROMETRY-BASED PROTEOMICS; TANDEM MASS-SPECTROMETRY; AMNIOTIC-FLUID;
STATISTICAL-MODEL; IGA NEPHROPATHY; IDENTIFICATION; BIOMARKERS;
EXPRESSION; PROTEINS; MEGSIN
AB OBJECTIVE: We sought to identify serum biomarkers of early spontaneous preterm birth (SPTB) using semiquantitative proteomic analyses.
STUDY DESIGN: This was a nested case-control study of pregnant women with previous SPTB. Maternal serum was collected at 19-24 and 28-32 weeks' gestation, and analyzed by liquid chromatography-multiple reaction monitoring/mass spectrometry. Targeted and shotgun proteomics identified 31 candidate proteins that were differentially expressed in pooled serum samples from spontaneous preterm (cases [< 34 weeks]) and term (controls) deliveries. Candidate protein expression was compared in individual serum samples between cases and controls matched by age and race groups, and clinical site. Protein expression was verified by Western blot in the placenta and fetal membranes from cases and controls.
RESULTS: Serum samples were available for 35 cases and 35 controls at 19-24 weeks, and 16 cases and 16 controls at 28-32 weeks. One protein, serpin B7, yielded serum concentrations that differed between cases and controls. The mean concentration of serpin B7 at 28-32 weeks was 1.5-fold higher in women with subsequent preterm deliveries compared to controls; there was no difference at 19-24 weeks. Higher levels of serpin B7 at both gestational age windows were associated with a shorter interval to delivery, and higher levels of serpin B7 in samples from 28-32 weeks were associated with a lower gestational age at delivery. Western blotting identified serpin B7 protein in placenta, amnion, and chorion from cases and controls.
CONCLUSION: Targeted and shotgun serum proteomics analyses associated 1 protein, serpin B7, with early SPTB. Our results require validation in other cohorts and analysis of the possible mechanistic role of serpin B7 in parturition.
C1 [Parry, Samuel; Leite, Rita] Univ Penn, Sch Med, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
[Zhang, Heping; Xu, Yaji] Yale Univ, Sch Publ Hlth, Collaborat Ctr Stat Sci, New Haven, CT USA.
[Biggio, Joseph; Andrews, William W.] Univ Alabama Birmingham, Sch Med, Dept Obstet & Gynecol, Birmingham, AL USA.
[Bukowski, Radek; Saade, George R.] Univ Texas Med Branch, Dept Obstet & Gynecol, Div Maternal Fetal Med, Galveston, TX 77555 USA.
[Varner, Michael; Esplin, M. Sean] Univ Utah, Sch Med, Dept Obstet & Gynecol, Salt Lake City, UT 84132 USA.
[Ilekis, John; Reddy, Uma M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, Ctr Dev Biol & Perinatal Med, Bethesda, MD USA.
[Sadovsky, Yoel] Univ Pittsburgh, Magee Womens Res Inst, Sch Med, Pittsburgh, PA USA.
[Blair, Ian A.] Univ Penn, Sch Med, Ctr Canc Pharmacol, Philadelphia, PA 19104 USA.
RP Parry, S (reprint author), Univ Penn, Sch Med, Dept Obstet & Gynecol, Philadelphia, PA 19104 USA.
EM parry@mail.med.upenn.edu
RI Xu, Yaji/M-4985-2015; Varner, Michael/K-9890-2013
OI Varner, Michael/0000-0001-9455-3973
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
of Child Health and Human Development (NICHD); National Center for
Advancing Translational Sciences
FX The National Institutes of Health, the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (NICHD), and the
National Center for Advancing Translational Sciences provided grant
support for the NICHD Genomics and Proteomics Network for Preterm Birth
(GPN). While NICHD staff had input into the study design, conduct,
analysis, and manuscript drafting, the comments and views of the authors
do not necessarily represent the views of the NICHD.
NR 31
TC 2
Z9 2
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
EI 1097-6868
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD DEC
PY 2014
VL 211
IS 6
AR 678.e1
DI 10.1016/j.ajog.2014.06.035
PG 12
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AW9NW
UT WOS:000346585300031
PM 24954659
ER
PT J
AU Yao, JH
Taveira-DaSilva, AM
Jones, AM
Julien-Williams, P
Stylianou, M
Moss, J
AF Yao, Jianhua
Taveira-DaSilva, Angelo M.
Jones, Amanda M.
Julien-Williams, Patricia
Stylianou, Mario
Moss, Joel
TI Sustained Effects of Sirolimus on Lung Function and Cystic Lung Lesions
in Lymphangioleiomyomatosis
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE sirolimus; lung cystic destruction; LAM
ID TUBEROUS SCLEROSIS COMPLEX; PLACEBO-CONTROLLED TRIAL; GIANT-CELL
ASTROCYTOMAS; PULMONARY LYMPHANGIOLEIOMYOMATOSIS; MATRIX
METALLOPROTEINASES; TISSUE INHIBITORS; DOXYCYCLINE USE; GENE-PRODUCTS;
TSC2; ACTIVATION
AB Rationale: Sirolimus therapy stabilizes lung function and reduces the size of chylous effusions and lymphangioleiomyomas in patients with lymphangioleiomyomatosis.
Objectives: to determine whether sirolimus has beneficial effects on lung function, cystic areas, and adjacent lung parenchyma; whether these effects are sustained; and whether sirolimus is well tolerated by patients.
Methods: Lung function decline over time, lung volume occupied by cysts (cyst score), and lung tissue texture in the vicinity of the cysts were quantified with a computer-aided diagnosis system in 38 patients. Then we compared cyst scores from the last study on sirolimus with studies done on sirolimus therapy. In 12 patients, we evaluated rates of change in lung function and cyst scores off and on sirolimus.
Measurements and Main Results: Sirolimus reduced yearly declines in FEV1 (-2.3 +/- 0.1 vs. 1.0 +/- 0.3% predicted; P < 0.001) and diffusing capacity of carbon monoxide (-2.6 +/- 0.1 vs. 0.9 +/- 0.2% predicted; P < 0.001). Cyst scores 1.2 +/- 0.8 years (30.5 +/- 11.9%) and 2.5 +/- 2 years (29.7 +/- 12.1%) after initiating sirolimus were not significantly different from pretreatment values (28.4 +/- 12.5%). In 12 patients followed for 5 years, a significant reduction in rates of yearly decline in FEV1 (-1.4 +/- 0.2 vs. 0.3 +/- 0.4% predicted; P = 0.025) was observed. Analyses of 104 computed tomography scans showed a nonsignificant (P = 0.23) reduction in yearly rates of change of cyst scores (1.8 +/- 0.2 vs. 0.3 +/- 0.3%; P = 0.23) and lung texture features. Despite adverse events, most patients were able to continue sirolimus therapy.
Conclusions: Sirolimus therapy slowed down lung function decline and increase in cystic lesions. Most patients were able to tolerate sirolimus therapy.
C1 [Yao, Jianhua] NHLBI, Radiol & Imaging Sci Dept, NIH, Bethesda, MD 20892 USA.
[Taveira-DaSilva, Angelo M.; Jones, Amanda M.; Julien-Williams, Patricia; Moss, Joel] NHLBI, Cardiovasc & Pulm Branch, NIH, Bethesda, MD 20892 USA.
[Stylianou, Mario] NHLBI, Off Biostat Res, NIH, Bethesda, MD 20892 USA.
RP Taveira-DaSilva, AM (reprint author), NHLBI, Cardiovasc & Pulm Branch, NIH, Bldg 10,Room 6D03,MSC 1590, Bethesda, MD 20892 USA.
EM dasilvaa@nhlbi.nih.gov
FU Intramural Research Program, National Institutes of Health, NHLBI
[95-H-0186]
FX Supported by the Intramural Research Program, National Institutes of
Health, NHLBI (Protocol 95-H-0186, J.M.).
NR 47
TC 16
Z9 16
U1 0
U2 2
PU AMER THORACIC SOC
PI NEW YORK
PA 25 BROADWAY, 18 FL, NEW YORK, NY 10004 USA
SN 1073-449X
EI 1535-4970
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD DEC 1
PY 2014
VL 190
IS 11
BP 1273
EP 1282
DI 10.1164/rccm.201405-09180C
PG 10
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA AW5RF
UT WOS:000346331000011
PM 25329516
ER
PT J
AU Duncan, K
Sturke, R
AF Duncan, Kalina
Sturke, Rachel
TI NIH TOBACCO OR HEALTH RESEARCH AND CAPACITY BUILDING GRANT PROGRAM
REVIEW
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
C1 [Duncan, Kalina] NCI, Rockville, MD USA.
[Sturke, Rachel] Fogarty Int Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD DEC
PY 2014
VL 10
SU 9
SI SI
MA 304
BP 1
EP 2
PG 2
WC Oncology
SC Oncology
GA AW5XG
UT WOS:000346343700005
ER
PT J
AU Vinson, C
Stevens, L
Torode, J
Saraiya, M
Sutcliffe, S
Gospodacrowicz, M
Anderson, B
Adewole, I
Luciani, S
AF Vinson, Cynthia
Stevens, Lisa
Torode, Julie
Saraiya, Mona
Sutcliffe, Simon
Gospodacrowicz, Mary
Anderson, Benjamin
Adewole, Isaac
Luciani, Silvana
TI AN INTERNATIONAL PARTNERSHIP TO ALIGN CANCER CONTROL PLANNING EFFORTS
WITH GLOBAL NONCOMMUNICABLE DISEASE (NCD) CONTROL TARGETS
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
C1 [Vinson, Cynthia; Stevens, Lisa] NCI, Bethesda, MD 20892 USA.
[Torode, Julie] UICC, Geneva, Switzerland.
[Saraiya, Mona] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Sutcliffe, Simon] Int Canc Control Congress Assoc, Vancouver, BC, Canada.
[Gospodacrowicz, Mary] Univ Toronto, Princess Margaret Hosp, Toronto, ON, Canada.
[Anderson, Benjamin] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Adewole, Isaac] African Org Res & Training Canc, Ibadan, Nigeria.
[Luciani, Silvana] Pan Amer Hlth Org, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD DEC
PY 2014
VL 10
SU 9
SI SI
MA 326
BP 8
EP 8
PG 1
WC Oncology
SC Oncology
GA AW5XG
UT WOS:000346343700022
ER
PT J
AU Galassi, A
Burg, A
Schneider, J
Williams, M
Al-Ruzzieh, M
Bigirimana, JB
Buswell, L
Challinor, J
Cummings, G
Day, S
de Calvo, LEA
Houlihan, K
Nevidjon, B
Teahon, M
So, WN
Were, P
AF Galassi, Annette
Burg, Allison
Schneider, Julie
Williams, Makeda
Al-Ruzzieh, Majeda
Bigirimana, Jean Bosco
Buswell, Lori
Challinor, Julia
Cummings, Greta
Day, Sara
Esperanza Ayala de Calvo, Luz
Houlihan, Kathy
Nevidjon, Brenda
Teahon, Marina
So, Winnie
Were, Pamela
TI BUILDING CAPACITY FOR ONCOLOGY NURSING EDUCATION AND TRAINING IN LOW-
AND MIDDLE-INCOME COUNTRIES: A CALL TO ACTION
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
C1 [Galassi, Annette; Schneider, Julie; Williams, Makeda] NCI, Rockville, MD USA.
[Burg, Allison] Amer Soc Clin Oncol, Alexandria, VA USA.
[Al-Ruzzieh, Majeda] King Hussein Canc Ctr, Amman, Jordan.
[Bigirimana, Jean Bosco] Inshuti Mu Buzima, Rwinkwavu, Rwanda.
[Buswell, Lori; Houlihan, Kathy] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Challinor, Julia] Int Network Canc Treatment & Res, Brussels, Belgium.
[Cummings, Greta; Nevidjon, Brenda] Int Soc Nurses Canc Care, Vancouver, BC, Canada.
[Day, Sara] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
[Teahon, Marina] Union Int Canc Control, Geneva, Switzerland.
[So, Winnie] Chinese Univ Hong Kong, Shatin, Hong Kong, Peoples R China.
[Were, Pamela] Epidemiol Burkitt Lymphoma East African Children, Eldoret, Kenya.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD DEC
PY 2014
VL 10
SU 9
SI SI
MA 330
BP 9
EP 9
PG 1
WC Oncology
SC Oncology
GA AW5XG
UT WOS:000346343700026
ER
PT J
AU Cremer, M
Maza, M
Alfaro, K
Gage, J
Castle, P
Kim, J
AF Cremer, Miriam
Maza, Mauricio
Alfaro, Karla
Gage, Julia
Castle, Philip
Kim, Jane
TI INTRODUCING CAREHPV INTO A PUBLIC SECTOR SCREENING PROGRAM IN EL
SALVADOR
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
C1 [Cremer, Miriam] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
[Maza, Mauricio; Alfaro, Karla] Basic Hlth Int, San Salvador, El Salvador.
[Gage, Julia] NCI, Bethesda, MD 20892 USA.
[Kim, Jane] Harvard Univ, Sch Publ Hlth, Cambridge, MA 02138 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD DEC
PY 2014
VL 10
SU 9
SI SI
MA 341
BP 13
EP 13
PG 1
WC Oncology
SC Oncology
GA AW5XG
UT WOS:000346343700036
ER
PT J
AU Sun, L
Dickie, L
Adamo, P
Li, J
Houston, K
Su, J
AF Sun, Leon
Dickie, Lois
Adamo, Peggy
Li, Jun
Houston, Keisha
Su, Joseph
TI EPIDEMIOLOGICAL AND CLINICAL CHARACTERISTICS OF PROSTATE CANCER MEN WITH
MULTIPLE CANCERS
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
C1 [Sun, Leon; Dickie, Lois; Adamo, Peggy] NCI, NIH, Rockville, MD USA.
[Li, Jun] Ctr Dis Control & Prevent, Div Canc Prevent & Control, Atlanta, GA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD DEC
PY 2014
VL 10
SU 9
SI SI
MA 539
BP 56
EP 57
PG 2
WC Oncology
SC Oncology
GA AW5XG
UT WOS:000346343700163
ER
PT J
AU Duncan, K
Galassi, A
Williams, M
AF Duncan, Kalina
Galassi, Annette
Williams, Makeda
TI JOINING FORCES TO OVERCOME CANCER: THE KENYA CANCER RESEARCH AND CONTROL
STAKEHOLDER MEETING EXPERIENCE
SO ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Meeting Abstract
C1 [Duncan, Kalina; Galassi, Annette; Williams, Makeda] NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1743-7555
EI 1743-7563
J9 ASIA-PAC J CLIN ONCO
JI Asia-Pac. J. Clin. Oncol.
PD DEC
PY 2014
VL 10
SU 9
SI SI
MA 696
BP 104
EP 104
PG 1
WC Oncology
SC Oncology
GA AW5XG
UT WOS:000346343700310
ER
PT J
AU Khrushchinskii, AA
Kuten', SA
Minenko, VF
Zhukova, OM
Podgaiskaya, AA
Germenchuk, MG
Kukhta, TA
Vakulovskii, SM
Drozdovitch, VV
AF Khrushchinskii, A. A.
Kuten', S. A.
Minenko, V. F.
Zhukova, O. M.
Podgaiskaya, A. A.
Germenchuk, M. G.
Kukhta, T. A.
Vakulovskii, S. M.
Drozdovitch, V. V.
TI Radionuclide Ratios in Precipitation on the Territory of Belarus After
the Chernobyl Accident: Calculation from Gamma-Spectrometric
Measurements on Soil in May-July 1986
SO ATOMIC ENERGY
LA English
DT Article
AB The correlations between the fallout density and ratio of radionuclides in different regions of Belarus after the accident at the Chernobyl NPP are investigated using data obtained by means of gamma-spectrometric measurements performed on soil in May-July 1986. It is shown that the isotopes of cesium and/or ruthenium are most suitable for reconstructing the activity of I-131 in the fallout. Charts showing the isolines of the activity ratios I-131/Cs-137 and Cs-134/Cs-137 in the fallout are constructed. The geometric averages obtained for the log-normal distribution of the ratios Cs-134/Cs-137 and I-131/Cs-137 in terms of May 10, 1986 equal 0.47 and 5.4, respectively. The distribution of the activity ratio I-131/Cs-137 in the fallout and the correlation coefficients show that on the whole there is no consistent interrelation between the fallout indices of these radionuclides over the territory.
C1 [Khrushchinskii, A. A.; Kuten', S. A.; Minenko, V. F.] Belarusian State Univ, Res Inst Nucl Problems, Minsk 220050, Byelarus.
[Zhukova, O. M.; Podgaiskaya, A. A.; Germenchuk, M. G.] Minist Nat Resources Republ Belarus, Republican Ctr Radiat Control & Environm Monitori, Minsk, Byelarus.
[Kukhta, T. A.] Joint Inst Informat Problems, Minsk, Byelarus.
[Vakulovskii, S. M.] Taifun Sci Ind Assoc, Obninsk, Russia.
[Drozdovitch, V. V.] NCI, Bethesda, MD 20892 USA.
RP Khrushchinskii, AA (reprint author), Belarusian State Univ, Res Inst Nucl Problems, Minsk 220050, Byelarus.
RI Kuten, Semen/F-6699-2016
OI Kuten, Semen/0000-0003-0827-8421
FU International Scientific and Technical Center [MNTTs-B-488P,
MNTTS-3452]; National Cancer Institute (USA)
FX This work was performed as part of the projects MNTTs-B-488P and
MNTTS-3452 of the International Scientific and Technical Center with the
financial support from the National Cancer Institute (USA).
NR 16
TC 1
Z9 1
U1 2
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1063-4258
EI 1573-8205
J9 ATOM ENERGY+
JI Atom. Energy
PD DEC
PY 2014
VL 117
IS 2
BP 143
EP 148
DI 10.1007/s10512-014-9902-4
PG 6
WC Nuclear Science & Technology
SC Nuclear Science & Technology
GA AW4FF
UT WOS:000346235800011
ER
PT J
AU Buchanan, S
Noinaj, N
Kuszak, AJ
Gumbart, JC
Lukacik, P
Chang, H
Easley, NC
Lithgow, T
AF Buchanan, S.
Noinaj, N.
Kuszak, A. J.
Gumbart, J. C.
Lukacik, P.
Chang, H.
Easley, N. C.
Lithgow, T.
TI Structural insight into the biogenesis of beta-barrel membrane proteins
SO BIOCHEMISTRY AND CELL BIOLOGY-BIOCHIMIE ET BIOLOGIE CELLULAIRE
LA English
DT Meeting Abstract
C1 [Buchanan, S.; Noinaj, N.; Kuszak, A. J.; Chang, H.; Easley, N. C.] NIDDK, NIH, Bethesda, MD 20892 USA.
[Gumbart, J. C.] Georgia Inst Technol, Atlanta, GA 30332 USA.
[Lukacik, P.] Harwell Sci & Innovat Campus, Diamond Light Source, Didcot OX11 0QX, Oxon, England.
[Lithgow, T.] Monash Univ, Clayton, Vic 3800, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 4
PU CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
PI OTTAWA
PA 65 AURIGA DR, SUITE 203, OTTAWA, ON K2E 7W6, CANADA
SN 0829-8211
EI 1208-6002
J9 BIOCHEM CELL BIOL
JI Biochem. Cell Biol.
PD DEC
PY 2014
VL 92
IS 6
BP 597
EP 597
PG 1
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AW6FX
UT WOS:000346366200101
ER
PT J
AU Wentzensen, N
Fetterman, B
Tokugawa, D
Schiffman, M
Castle, PE
Wood, SN
Stiemerling, E
Poitras, N
Lorey, T
Kinney, W
AF Wentzensen, Nicolas
Fetterman, Barbara
Tokugawa, Diane
Schiffman, Mark
Castle, Philip E.
Wood, Shannon N.
Stiemerling, Eric
Poitras, Nancy
Lorey, Thomas
Kinney, Walter
TI Interobserver Reproducibility and Accuracy of p16/Ki-67 Dual-Stain
Cytology in Cervical Cancer Screening
SO CANCER CYTOPATHOLOGY
LA English
DT Article
DE cervical cancer screening; p16; Ki-67; human papillomavirus;
reproducibility; cytology; Papanicolaou test
ID HPV-POSITIVE WOMEN; INTRAEPITHELIAL NEOPLASIA; HUMAN-PAPILLOMAVIRUS;
TRIAGE; POPULATION; COLPOSCOPY; PRECURSORS; CELLS; ASCUS; RISK
AB BACKGROUNDDual-stain cytology for p16 and Ki-67 has been proposed as a biomarker in cervical cancer screening. The authors evaluated the reproducibility and accuracy of dual-stain cytology among 10 newly trained evaluators.
METHODSIn total, 480 p16/Ki-67-stained slides from human papillomavirus-positive women were evaluated in masked fashion by 10 evaluators. None of the evaluators had previous experience with p16 or p16/Ki-67 cytology. All participants underwent p16/Ki-67 training and subsequent proficiency testing. Reproducibility of dual-stain cytology was measured using the percentage agreement, individual and aggregate values, as well as McNemar statistics. Clinical performance for the detection of cervical intraepithelial neoplasia grade 2 or greater (CIN2+) was evaluated for each individual evaluator and for all evaluators combined compared with the reference evaluation by a cytotechnologist who had extensive experience with dual-stain cytology.
RESULTSThe percentage agreement of individual evaluators with the reference evaluation ranged from 83% to 91%, and the values ranged from 0.65 to 0.81. The combined value was 0.71 for all evaluators and 0.73 for cytotechnologists. The average sensitivity and specificity for the detection of CIN2+ among novice evaluators was 82% and 64%, respectively; whereas the reference evaluation had 84% sensitivity and 63% specificity, respectively. Agreement on dual-stain positivity increased with greater numbers of p16/Ki-67-positive cells on the slides.
CONCLUSIONSGood to excellent reproducibility of p16/Ki-67 dual-stain cytology was observed with almost identical clinical performance of novice evaluators compared with reference evaluations. The current findings suggest that p16/Ki-67 dual-stain evaluation can be implemented in routine cytology practice with limited training. Cancer (Cancer Cytopathol) 2014;122:914-920. (c) 2014 American Cancer Society.
The authors evaluate the reproducibility and accuracy of p16/Ki-67 dual-stain cytology among 10 newly trained evaluators. The results indicate that the evaluation of p16/Ki-67 dual staining on cytology slides can be implemented in routine cytology practice with limited training and good to excellent reproducibility.
C1 [Wentzensen, Nicolas; Schiffman, Mark; Wood, Shannon N.] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Fetterman, Barbara; Tokugawa, Diane; Stiemerling, Eric; Poitras, Nancy; Lorey, Thomas] Kaiser Permanente, Permanente Med Grp Reg Lab, Berkeley, CA USA.
[Castle, Philip E.] Global Coalit Cerv Canc, Arlington, VA USA.
[Kinney, Walter] Kaiser Permanente Med Care Program, Div Gynecol Oncol, Oakland, CA USA.
RP Wentzensen, N (reprint author), NCI, Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 7-E114, Bethesda, MD 20892 USA.
EM wentzenn@mail.nih.gov
FU Roche; BD; GE Healthcare; Cepheid; Hologic; Qiagen; ClearPath; Guided
Therapeutics
FX Dr. Wentzensen reports non-financial support from mtm Laboratories. Dr.
Schiffman reports that Roche has performed HPV tests at no cost for
NCI-sponsored studies; the results are published collaboratively. Dr.
Castle is compensated for serving on a Merck Data and Safety Monitoring
Board for HPV vaccines and has served as a paid consultant to Roche, BD,
GE Healthcare, Cepheid, and Hologic; he reports personal fees from
Qiagen, BD, ClearPath, Guided Therapeutics, Cepheid, and GE Healthcare
and non-financial support from Roche, Qiagen, Norchip, and mtm
Laboratories.
NR 16
TC 14
Z9 15
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1934-662X
EI 1934-6638
J9 CANCER CYTOPATHOL
JI Cancer Cytopathol.
PD DEC
PY 2014
VL 122
IS 12
BP 914
EP 920
DI 10.1002/cncy.21473
PG 7
WC Oncology; Pathology
SC Oncology; Pathology
GA AW5YY
UT WOS:000346348000011
PM 25132656
ER
PT J
AU Soto-Pantoja, DR
Terabe, M
Ghosh, A
Ridnour, LA
DeGraff, WG
Wink, DA
Berzofsky, JA
Roberts, DD
AF Soto-Pantoja, David R.
Terabe, Masaki
Ghosh, Arunima
Ridnour, Lisa A.
DeGraff, William G.
Wink, David A.
Berzofsky, Jay A.
Roberts, David D.
TI CD47 in the Tumor Microenvironment Limits Cooperation between Antitumor
T-cell Immunity and Radiotherapy
SO CANCER RESEARCH
LA English
DT Article
ID DENDRITIC CELLS; STEM-CELLS; THROMBOSPONDIN-1; ANTIBODY; PROTEIN;
CANCER; PHAGOCYTOSIS; INTEGRIN; MODEL; IMMUNOSURVEILLANCE
AB Although significant advances in radiotherapy have increased its effectiveness in many cancer settings, general strategies to widen the therapeutic window between normal tissue toxicity and malignant tumor destruction would still offer great value. CD47 blockade has been found to confer radioprotection to normal tissues while enhancing tumor radiosensitivity. Here, we report that CD47 blockade directly enhances tumor immunosurveillance by CD8(+) T cells. Combining CD47 blockade with irradiation did not affect fibrosarcoma growth in T cell-deficient mice, whereas adoptive transfer of tumor-specific CD8(+) T cells restored combinatorial efficacy. Furthermore, ablation of CD8(+) T cells abolished radiotherapeutic response in immunocompetent syngeneic hosts. CD47 blockade in either target cells or effector cells was sufficient to enhance antigen-dependent CD8(+) CTL-mediated tumor cell killing in vitro. In CD47-deficient syngeneic hosts, engrafted B16 melanomas were 50% more sensitive to irradiation, establishing that CD47 expression in the microenvironment was sufficient to limit tumor radiosensitivity. Mechanistic investigations revealed increased tumor infiltration by cytotoxic CD8(+) T cells in a CD47-deficient microenvironment, with an associated increase in T cell-dependent intratumoral expression of granzyme B. Correspondingly, an inverse correlation between CD8(+) T-cell infiltration and CD47 expression was observed in human melanomas. Our findings establish that blocking CD47 in the context of radiotherapy enhances antitumor immunity by directly stimulating CD8(+) cytotoxic T cells, with the potential to increase curative responses. (C) 2014 AACR.
C1 [Soto-Pantoja, David R.; Ghosh, Arunima; Roberts, David D.] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Terabe, Masaki; Berzofsky, Jay A.] NCI, Vaccine Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Ridnour, Lisa A.; DeGraff, William G.; Wink, David A.] NCI, Radiat Biol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Roberts, DD (reprint author), NCI, Pathol Lab, Ctr Canc Res, NIH, 10 Ctr Dr, Bethesda, MD 20892 USA.
EM dr9y@nih.gov
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
FU Intramural Research Program of the NIH/NCI
FX This work was supported by the Intramural Research Program of the
NIH/NCI (D.D. Roberts, D.A. Wink, and J.A. Berzofsky).
NR 55
TC 26
Z9 26
U1 2
U2 18
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD DEC 1
PY 2014
VL 74
IS 23
BP 6771
EP 6783
DI 10.1158/0008-5472.AN-14-0037-T
PG 13
WC Oncology
SC Oncology
GA AW6EN
UT WOS:000346362400005
PM 25297630
ER
PT J
AU Lapeire, L
Hendrix, A
Lambein, K
Van Bockstal, M
Braems, G
Van Den Broecke, R
Limame, R
Mestdagh, P
Vandesompele, J
Vanhove, C
Maynard, D
Lehuede, C
Muller, C
Valet, P
Gespach, CP
Bracke, M
Cocquyt, V
Denys, H
De Wever, O
AF Lapeire, Lore
Hendrix, An
Lambein, Kathleen
Van Bockstal, Mieke
Braems, Geert
Van Den Broecke, Rudy
Limame, Ridha
Mestdagh, Pieter
Vandesompele, Jo
Vanhove, Christian
Maynard, Dawn
Lehuede, Camille
Muller, Catherine
Valet, Philippe
Gespach, Christian P.
Bracke, Marc
Cocquyt, Veronique
Denys, Hannelore
De Wever, Olivier
TI Cancer-Associated Adipose Tissue Promotes Breast Cancer Progression by
Paracrine Oncostatin M and Jak/STAT3 Signaling
SO CANCER RESEARCH
LA English
DT Article
ID EPITHELIAL-CELLS; GENE-EXPRESSION; RHEUMATOID-ARTHRITIS; TUMOR
PROGRESSION; STROMAL CELLS; STEM-CELLS; IN-VIVO; DIFFERENTIATION;
INVASION; TUMORIGENESIS
AB Increasing evidence supports the critical roles played by adipose tissue in breast cancer progression. Yet, the mediators and mechanisms are poorly understood. Here, we show that breast cancer-associated adipose tissue from freshly isolated tumors promotes F-actin remodeling, cellular scattering, invasiveness, and spheroid reorganization of cultured breast cancer cells. A combination of techniques, including transcriptomics, proteomics, and kinomics enabled us to identify paracrine secretion of oncostatin M (OSM) by cancer-associated adipose tissue. Specifically, OSM, expressed by CD45(+) leucocytes in the stromal vascular fraction, induced phosphorylation of STAT3 (pSTAT3-) Y705 and S727 in breast cancer cells and transcription of several STAT3-dependent genes, including S100 family members S100A7, S100A8, and S100A9. Autocrine activation of STAT3 in MCF-7 cells ectopically expressing OSM-induced cellular scattering and peritumoral neovascularization of orthotopic xenografts. Conversely, selective inhibition of OSM by neutralizing antibody and Jak family kinases by tofacitinib inhibited STAT3 signaling, peritumoral angiogenesis, and cellular scattering. Importantly, nuclear staining of pSTAT3-Y705 identified at the tumor invasion front in ductal breast carcinomas correlates with increased lymphovascular invasion. Our work reveals the potential of novel therapeutic strategies targeting the OSM and STAT3 axis in patients with breast cancer harboring nuclear pSTAT3-Y705. (C) 2014 AACR.
C1 [Lapeire, Lore; Cocquyt, Veronique; Denys, Hannelore] Ghent Univ Hosp, Dept Med Oncol, B-9000 Ghent, Belgium.
[Hendrix, An; Bracke, Marc; De Wever, Olivier] Ghent Univ Hosp, Dept Radiat Oncol & Expt Canc Res, Lab Expt Canc Res, B-9000 Ghent, Belgium.
[Lambein, Kathleen; Van Bockstal, Mieke] Ghent Univ Hosp, Dept Pathol, B-9000 Ghent, Belgium.
[Braems, Geert; Van Den Broecke, Rudy] Ghent Univ Hosp, Dept Gynaecol, B-9000 Ghent, Belgium.
[Limame, Ridha] Univ Antwerp, Ctr Oncol Res CORE, B-2020 Antwerp, Belgium.
[Mestdagh, Pieter; Vandesompele, Jo] Ghent Univ Hosp, Ctr Med Genet, B-9000 Ghent, Belgium.
[Vanhove, Christian] Ghent Univ Hosp, Inst Biomed Technol, B-9000 Ghent, Belgium.
[Maynard, Dawn] NHGRI, Med Genet Branch, Bethesda, MD 20892 USA.
[Lehuede, Camille; Muller, Catherine] Univ Toulouse, UPS, Inst Pharmacol & Biol Struct, Toulouse, France.
[Valet, Philippe] Univ Toulouse 3, INSERM, U1048, F-31062 Toulouse, France.
[Gespach, Christian P.] Univ Paris 06, INSERM, U938, Paris, France.
RP De Wever, O (reprint author), Ghent Univ Hosp, Dept Radiat Oncol & Expt Canc Res, Lab Expt Canc Res, De Pintelaan 185, B-9000 Ghent, Belgium.
EM olivier.dewever@ugent.be
RI de wever, olivier/J-3094-2013; MULLER, Catherine/E-2060-2011
OI de wever, olivier/0000-0002-5453-760X;
FU Fund for Scientific Spearheads of Ghent University Hospital and Research
Council of Ghent University; National Cancer Plan [KPC_ 29_ 012];
"Bijzonder Onderzoeksfonds" (BOF) of Ghent University; Fund for
Scientific Research-Flanders
FX This research was supported by Fund for Scientific Spearheads of Ghent
University Hospital and Research Council of Ghent University, the
National Cancer Plan (KPC_ 29_ 012), a grant from the "Bijzonder
Onderzoeksfonds" (BOF) of Ghent University (to H. Denys), a postdoctoral
grant (to A. Hendrix), and a travel grant (L. Lapeire) from Fund for
Scientific Research-Flanders.
NR 53
TC 17
Z9 17
U1 1
U2 10
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD DEC 1
PY 2014
VL 74
IS 23
BP 6806
EP 6819
DI 10.1158/0008-5472.CAN-14-0160
PG 14
WC Oncology
SC Oncology
GA AW6EN
UT WOS:000346362400008
PM 25252914
ER
PT J
AU Josse, R
Martin, SE
Guha, R
Ormanoglu, P
Pfister, TD
Reaper, PM
Barnes, CS
Jones, J
Charlton, P
Pollard, JR
Morris, J
Doroshow, JH
Pommier, Y
AF Josse, Rozenn
Martin, Scott E.
Guha, Rajarshi
Ormanoglu, Pinar
Pfister, Thomas D.
Reaper, Philip M.
Barnes, Christopher S.
Jones, Julie
Charlton, Peter
Pollard, John R.
Morris, Joel
Doroshow, James H.
Pommier, Yves
TI ATR Inhibitors VE-821 and VX-970 Sensitize Cancer Cells to Topoisomerase
I Inhibitors by Disabling DNA Replication Initiation and Fork Elongation
Responses
SO CANCER RESEARCH
LA English
DT Article
ID S-PHASE CHECKPOINT; MULTIDRUG-RESISTANCE; DAMAGE RESPONSE;
PROTEIN-KINASE; SINGLE-CELL; ACTIVATION; CAMPTOTHECIN; ANTICANCER;
RADIATION; STRESS
AB Camptothecin and its derivatives, topotecan and irinotecan, are specific topoisomerase I (Top1) inhibitors and potent anticancer drugs killing cancer cells by producing replication-associated DNA double-strand breaks, and the indenoisoquinoline LMP-400 (indotecan) is a novel Top1 inhibitor in clinical trial. To develop novel drug combinations, we conducted a synthetic lethal siRNA screen using a library that targets nearly 7,000 human genes. Depletion of ATR, the main transducer of replication stress, came as a top candidate gene for camptothecin synthetic lethality. Validation studies using ATR siRNA and the ATR inhibitor VE-821 confirmed marked antiproliferative synergy with camptothecin and even greater synergy with LMP-400. Single-cell analyses and DNA fiber combing assays showed that VE-821 abrogates the S-phase replication elongation checkpoint and the replication origin-firing checkpoint induced by camptothecin and LMP-400. As expected, the combination of Top1 inhibitors with VE-821 inhibited the phosphorylation of ATR and Chk1; however, it strongly induced gamma H2AX. In cells treated with the combination, the gamma H2AX pattern changed over time from the well-defined Top1-induced damage foci to an intense peripheral and diffuse nuclear staining, which could be used as response biomarker. Finally, the clinical derivative of VE-821, VX-970, enhanced the in vivo tumor response to irinotecan without additional toxicity. A key implication of our work is the mechanistic rationale and proof of principle it provides to evaluate the combination of Top1 inhibitors with ATR inhibitors in clinical trials. (C) 2014 AACR.
C1 [Josse, Rozenn; Doroshow, James H.; Pommier, Yves] NCI, Dev Therapeut Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Josse, Rozenn; Doroshow, James H.; Pommier, Yves] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Martin, Scott E.; Guha, Rajarshi; Ormanoglu, Pinar] NIH, Natl Ctr Adv Translat Sci, Div Preclin Innovat, Rockville, MD USA.
[Pfister, Thomas D.] Leidos Biomed Res Inc, Natl Lab Canc Res, Lab Human Toxicol & Pharmacol, Appl Dev Res Directorate, Frederick, MD USA.
[Reaper, Philip M.; Barnes, Christopher S.; Jones, Julie; Charlton, Peter; Pollard, John R.] Vertex Pharmaceut Europe Ltd, Abingdon, Oxon, England.
[Morris, Joel; Doroshow, James H.] NCI, Drug Synth & Chem Branch, Div Canc Treatment, Div Canc Treatment & Diag DTP DCTD,NIH, Bethesda, MD 20892 USA.
RP Pommier, Y (reprint author), NCI, NIH, 37 Convent Dr,Bldg 37,Room 5068, Bethesda, MD 20892 USA.
EM pommier@nih.gov
FU NCI Intramural Program, Center for Cancer Research [Z01-BC006161,
Z01-BC006150]; Federal funds from NCI, NIH [HHSN261200800001E]; American
Recovery and Reinvestment Act funds
FX The studies were supported by the NCI Intramural Program, Center for
Cancer Research (Z01-BC006161 and Z01-BC006150), by the Federal funds
from the NCI, NIH under contract no. HHSN261200800001E, and in part by
the American Recovery and Reinvestment Act funds.
NR 50
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Z9 27
U1 2
U2 18
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD DEC 1
PY 2014
VL 74
IS 23
BP 6968
EP 6979
DI 10.1158/0008-5472.CAN-13-3369
PG 12
WC Oncology
SC Oncology
GA AW6EN
UT WOS:000346362400022
PM 25269479
ER
PT J
AU Gordon, MS
Robert, F
Matei, D
Mendelson, DS
Goldman, JW
Chiorean, EG
Strother, RM
Seon, BK
Figg, WD
Peer, CJ
Alvarez, D
Adams, BJ
Theuer, CP
Rosen, LS
AF Gordon, Michael S.
Robert, Francisco
Matei, Daniela
Mendelson, David S.
Goldman, Jonathan W.
Chiorean, E. Gabriela
Strother, Robert M.
Seon, Ben K.
Figg, William D.
Peer, Cody J.
Alvarez, Delia
Adams, Bonne J.
Theuer, Charles P.
Rosen, Lee S.
TI An Open-Label Phase Ib Dose-Escalation Study of TRC105 (Anti-Endoglin
Antibody) with Bevacizumab in Patients with Advanced Cancer
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID ENDOTHELIAL GROWTH-FACTOR; HEREDITARY HEMORRHAGIC TELANGIECTASIA;
MICROVESSEL DENSITY; CD105 EXPRESSION; HEPATOCELLULAR-CARCINOMA;
MONOCLONAL-ANTIBODY; PROGNOSTIC MARKERS; TUMOR VASCULATURE;
COLORECTAL-CANCER; THERAPY
AB Purpose: Endoglin, an endothelial cell membrane receptor expressed on angiogenic tumor vessels, is essential for angiogenesis and upregulated in the setting of VEGF inhibition. TRC105 is an anti-endoglin IgG1 monoclonal antibody that potentiates VEGF inhibitors in preclinical models. This study assessed safety, pharmacokinetics, and antitumor activity of TRC105 in combination with bevacizumab.
Experimental Design: Patients (n = 38) with advanced solid tumors, Eastern Cooperative Group performance status 0-1, and normal organ function were treated with escalating doses of TRC105 plus bevacizumab until disease progression or unacceptable toxicity using a standard 3 + 3 phase I design.
Results: TRC105 and bevacizumab were well tolerated at their recommended single-agent doses (10 mg/kg) when the initial dose of TRC105 was delayed by one week and divided over 2 days to limit the frequency of headache. The concurrent administration of bevacizumab and TRC105 did not otherwise potentiate known toxicities of TRC105 or bevacizumab. Hypertension and proteinuria were observed, though not at rates expected for single-agent bevacizumab. Several patients who had previously progressed on bevacizumab or VEGF receptor tyrosine kinase inhibitor (VEGFR TKI) treatment experienced reductions in tumor volume, including two partial responses by RECIST, and 6 remained without progression for longer periods than during their prior VEGF inhibitor therapy.
Conclusions: TRC105 was well tolerated with bevacizumab and clinical activity was observed in a VEGF inhibitor- refractory population. Ongoing clinical trials are testing TRC105 in combination with bevacizumab in glioblastoma and with VEGFR TKIs in renal cell carcinoma, hepatocellular carcinoma, and soft tissue sarcoma.
C1 [Gordon, Michael S.; Mendelson, David S.] Pinnacle Oncol Hematol, Scottsdale, AZ 85258 USA.
[Robert, Francisco] Univ Alabama Birmingham, Birmingham, AL USA.
[Matei, Daniela; Chiorean, E. Gabriela; Strother, Robert M.] Indiana Univ Sch Med, Indianapolis, IN 46202 USA.
[Goldman, Jonathan W.; Rosen, Lee S.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Chiorean, E. Gabriela] Univ Washington, Seattle, WA 98195 USA.
[Seon, Ben K.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Figg, William D.; Peer, Cody J.] NCI, Clin Pharmacol Program, Bethesda, MD 20892 USA.
[Alvarez, Delia; Adams, Bonne J.; Theuer, Charles P.] TRACON Pharmaceut, San Diego, CA USA.
RP Gordon, MS (reprint author), Pinnacle Oncol Hematol, 9055 E Del Camino,Suite 100, Scottsdale, AZ 85258 USA.
EM mgordon@azpoh.com
RI Figg Sr, William/M-2411-2016;
OI Strother, Robert Matthew/0000-0001-8118-8954
FU TRACON Pharmaceuticals Inc; Center for Cancer Research of the National
Cancer Institute; National Cancer Institute; NIH [HHSN261200800001E]
FX This research was supported by TRACON Pharmaceuticals Inc and the Center
for Cancer Research of the National Cancer Institute. This study has
also been funded in whole or in part with federal funds from the
National Cancer Institute, NIH, under contract number HHSN261200800001E.
NR 40
TC 17
Z9 18
U1 1
U2 11
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 1
PY 2014
VL 20
IS 23
BP 5918
EP 5926
DI 10.1158/1078-0432.CCR-14-1143
PG 9
WC Oncology
SC Oncology
GA AW7AS
UT WOS:000346417400009
PM 25261556
ER
PT J
AU Hassan, R
Kindler, HL
Jahan, T
Bazhenova, L
Reck, M
Thomas, A
Pastan, I
Parno, J
O'Shannessy, DJ
Fatato, P
Maltzman, JD
Wallin, BA
AF Hassan, Raffit
Kindler, Hedy L.
Jahan, Thierry
Bazhenova, Lyudmila
Reck, Martin
Thomas, Anish
Pastan, Ira
Parno, Jeff
O'Shannessy, Daniel J.
Fatato, Penny
Maltzman, Julia D.
Wallin, Bruce A.
TI Phase II Clinical Trial of Amatuximab, a Chimeric Antimesothelin
Antibody with Pemetrexed and Cisplatin in Advanced Unresectable Pleural
Mesothelioma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID MEGAKARYOCYTE POTENTIATING FACTOR; MALIGNANT MESOTHELIOMA;
MONOCLONAL-ANTIBODY; OVARIAN-CANCER; TUMOR-MARKER; SOLUBLE MESOTHELIN;
EXPRESSION; SERUM; ADENOCARCINOMAS; OSTEOPONTIN
AB Purpose: Amatuximab is a chimeric monoclonal antibody to mesothelin, a cell surface glycoprotein highly expressed in malignant pleural mesothelioma (MPM). On the basis of its synergy with chemotherapy in preclinical studies, we evaluated the antitumor activity of amatuximab plus pemetrexed and cisplatin in patients with unresectable MPM.
Experimental Design: In a single-arm phase II study, amatuximab (5 mg/kg) was administered on days 1 and 8 with pemetrexed (500 mg/m(2)) and cisplatin (75 mg/m(2)) on day 1 of 21-day cycles for up to six cycles. Patients with response or stable disease received amatuximab maintenance until disease progression. Primary endpoint was progression-free survival (PFS) at 6 months. Secondary endpoints were overall survival (OS), response rate, and safety.
Results: Eighty-nine patients were enrolled at 26 centers. Median of five cycles (range, 1-6) of combination treatment was administered, and 56 (63%) patients received amatuximab maintenance. Combination therapy resulted in no overlapping toxicities. Eleven patients (12.4%) had amatuximabrelated hypersensitivity reactions. Responses included partial responses in 33 (40%) and stable disease in 42 (51%). Six-month PFS rate was 51% [95% confidence interval (CI), 39.1-62.3)], median PFS was 6.1 months (95% CI, 5.8-6.4), and median OS was 14.8 months (95% CI, 12.4-18.5) with 29 patients alive at data cut-off.
Conclusions: Amatuximab with pemetrexed and cisplatin was well tolerated with objective tumor response or stable disease rate of 90% by independent radiologic review. Although PFS was not significantly different from historical controls, the median OS was 14.8 months with a third of patients alive and 5 continuing to receive amatuximab at the time of analysis.
C1 [Hassan, Raffit; Thomas, Anish] NCI, Thorac & GI Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kindler, Hedy L.] Univ Chicago, Chicago, IL 60637 USA.
[Jahan, Thierry] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Bazhenova, Lyudmila] Univ Calif San Diego, San Diego, CA 92103 USA.
[Reck, Martin] Lung Clin Grosshansdorf, Dept Thorac Oncol, Grosshansdorf, Stormarn, Germany.
[Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Parno, Jeff] United BioSource Corp, Blue Bell, PA USA.
[O'Shannessy, Daniel J.; Fatato, Penny; Maltzman, Julia D.; Wallin, Bruce A.] Morphotek Inc, Exton, PA USA.
RP Hassan, R (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM hassanr@mail.nih.gov
OI Thomas, Anish/0000-0003-3293-3115
FU Intramural Research Program of the NIH; National Cancer Institute;
Morphotek, Inc.; Cooperative Research and Development Agreement; NCI
FX This research was supported in part by the Intramural Research Program
of the NIH, National Cancer Institute, Center for Cancer Research, and
in part by Morphotek, Inc., under a Cooperative Research and Development
Agreement with the NCI.
NR 33
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Z9 30
U1 2
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 1
PY 2014
VL 20
IS 23
BP 5927
EP 5936
DI 10.1158/1078-0432.CCR-14-0804
PG 10
WC Oncology
SC Oncology
GA AW7AS
UT WOS:000346417400010
PM 25231400
ER
PT J
AU Kim, EJ
Sahai, V
Abel, EV
Griffith, KA
Greenson, JK
Takebe, N
Khan, GN
Blau, JL
Craig, R
Balis, UG
Zalupski, MM
Simeone, DM
AF Kim, Edward J.
Sahai, Vaibhav
Abel, Ethan V.
Griffith, Kent A.
Greenson, Joel K.
Takebe, Naoko
Khan, Gazala N.
Blau, John L.
Craig, Ronald
Balis, Ulysses G.
Zalupski, Mark M.
Simeone, Diane M.
TI Pilot Clinical Trial of Hedgehog Pathway Inhibitor GDC-0449 (Vismodegib)
in Combination with Gemcitabine in Patients with Metastatic Pancreatic
Adenocarcinoma
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID PHASE-III TRIAL; DUCTAL ADENOCARCINOMA; 1ST-LINE TREATMENT; PLUS
GEMCITABINE; ONCOLOGY-GROUP; CANCER; SURVIVAL; THERAPY; STROMA
AB Purpose: The hedgehog (HH) signaling pathway is a key regulator in tumorigenesis of pancreatic adenocarcinoma and is upregulated in pancreatic adenocarcinoma cancer stem cells (CSCs). GDC-0449 is an oral small-molecule inhibitor of the HH pathway. This study assessed the effect of GDC-0449-mediated HH inhibition in paired biopsies, followed by combined treatment with gemcitabine, in patients with metastatic pancreatic adenocarcinoma.
Experimental Design: Twenty-five patients were enrolled of which 23 underwent core biopsies at baseline and following 3 weeks of GDC-0449. On day 29, 23 patients started weekly gemcitabine while continuing GDC-0449. We evaluated GLI1 and PTCH1 inhibition, change in CSCs, Ki-67, fibrosis, and assessed tumor response, survival and toxicity.
Results: On pretreatment biopsy, 75% of patients had elevated sonic hedgehog (SHH) expression. On posttreatment biopsy, GLI1 and PTCH1 decreased in 95.6% and 82.6% of 23 patients, fibrosis decreased in 45.4% of 22, and Ki-67 in 52.9% of 17 evaluable patients. No significant changes were detected in CSCs pre-and postbiopsy. The median progression-free and overall survival for all treated patients were 2.8 and 5.3 months. The response and disease control rate was 21.7% and 65.2%. No significant correlation was noted between CSCs, fibrosis, SHH, Ki-67, GLI1, PTCH1 (baseline values or relative change on posttreatment biopsy), and survival. Grade >= 3 adverse events were noted in 56% of patients.
Conclusion: We show that GDC-0449 for 3 weeks leads to downmodulation of GLI1 and PTCH1, without significant changes in CSCs compared with baseline. GDC-0449 and gemcitabine were not superior to gemcitabine alone in the treatment of metastatic pancreatic cancer. (C) 2014 AACR.
C1 [Kim, Edward J.; Sahai, Vaibhav; Khan, Gazala N.; Zalupski, Mark M.] Univ Michigan, Div Hematol Oncol, Dept Internal Med, Ann Arbor, MI 48109 USA.
[Sahai, Vaibhav; Abel, Ethan V.; Simeone, Diane M.] Univ Michigan, Translat Oncol Program, Ann Arbor, MI 48109 USA.
[Griffith, Kent A.] Univ Michigan, Sch Publ Hlth, Ctr Canc Biostat, Ann Arbor, MI 48109 USA.
[Greenson, Joel K.; Blau, John L.; Craig, Ronald; Balis, Ulysses G.] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA.
[Takebe, Naoko] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Simeone, DM (reprint author), Univ Michigan, Translat Oncol Program, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM simeone@med.umich.edu
FU NIH through the University of Michigan's Cancer Center Support Grant [5
P30 CA046592]; Cancer Center Clinical Trials Office Core; Michigan
Institute for Clinical and Health Research Pilot Grant [ULRR024986]
FX This work was supported (in part) by the NIH through the University of
Michigan's Cancer Center Support Grant (5 P30 CA046592) by the use of
the Cancer Center Clinical Trials Office Core and also supported (in
part) by a Michigan Institute for Clinical and Health Research Pilot
Grant (ULRR024986).
NR 27
TC 48
Z9 49
U1 1
U2 16
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
EI 1557-3265
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD DEC 1
PY 2014
VL 20
IS 23
BP 5937
EP 5945
DI 10.1158/1078-0432.CCR-14-1269
PG 9
WC Oncology
SC Oncology
GA AW7AS
UT WOS:000346417400011
PM 25278454
ER
PT J
AU Huestis, MA
AF Huestis, Marilyn A.
TI Untitled
SO CLINICAL CHEMISTRY
LA English
DT Editorial Material
C1 [Huestis, Marilyn A.] NIDA, Baltimore, MD 21224 USA.
RP Huestis, MA (reprint author), NIDA, Biomed Res Ctr, 251 Bayview Blvd,Suite 200,Rm 05A-721, Baltimore, MD 21224 USA.
EM mhuestis@intra.nida.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER ASSOC CLINICAL CHEMISTRY
PI WASHINGTON
PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 USA
SN 0009-9147
EI 1530-8561
J9 CLIN CHEM
JI Clin. Chem.
PD DEC
PY 2014
VL 60
IS 12
BP 1484
EP 1485
DI 10.1373/clinchem.2014.224543
PG 3
WC Medical Laboratory Technology
SC Medical Laboratory Technology
GA AW7CS
UT WOS:000346422800008
PM 25432994
ER
PT J
AU Vuppalanchi, R
Jain, AK
Deppe, R
Yates, K
Comerford, M
Masuoka, HC
Neuschwander-Tetri, BA
Loomba, R
Brunt, EM
Kleiner, DE
Molleston, JP
Schwimmer, JB
Lavine, JE
Tonascia, J
Chalasani, N
AF Vuppalanchi, Raj
Jain, Ajay K.
Deppe, Ross
Yates, Katherine
Comerford, Megan
Masuoka, Howard C.
Neuschwander-Tetri, Brent A.
Loomba, Rohit
Brunt, Elizabeth M.
Kleiner, David E.
Molleston, Jean P.
Schwimmer, Jeffrey B.
Lavine, Joel E.
Tonascia, James
Chalasani, Naga
TI Relationship Between Changes in Serum Levels of Keratin 18 and Changes
in Liver Histology in Children and Adults With Nonalcoholic Fatty Liver
Disease
SO CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
LA English
DT Article
DE Serum K18; Noninvasive Biomarker; Nonalcoholic Steatohepatitis; PIVENS;
TONIC
ID VITAMIN-E; CYTOKERATIN-18 FRAGMENTS; PLASMA CYTOKERATIN-18; HEPATIC
STEATOSIS; STEATOHEPATITIS; PREVALENCE; APOPTOSIS; PIOGLITAZONE;
EPIDEMIOLOGY; POPULATION
AB BACKGROUND & AIMS: Cross-sectional studies have associated serum levels of the keratin 18 (K18) fragment with histologic features of liver in individuals with nonalcoholic fatty liver disease (NAFLD). We investigated the relationship between changes in serum levels of K18 and changes in liver histology in adults and children with NAFLD.
METHODS: We measured levels of K18 in stored serum samples collected at baseline and various time points from 231 adults with nonalcoholic steatohepatitis and 152 children with NAFLD who participated in 2 separate prospective randomized clinical trials. Liver biopsy specimens collected at baseline and week 96 were reviewed centrally.
RESULTS: There were greater decreases in serum levels of K18 in adults with histologic improvement at week 96 than in those without histologic improvement at week 16 (decrease, 193 +/- 293 vs 139 +/- 467 U/L; P < .001), week 48 (decrease, 232 +/- 360 vs 113 +/- 425 U/L; P < .001), or week 96 (decrease, 269 +/- 368 vs 97 +/- 400 U/L; P < .001). There were greater decreases in serum levels of K18 in children with histologic improvements than in those without histologic improvements at week 48 (decrease, 197 +/- 467 vs 47 +/- 350 U/L; P = .005) and week 96 (decrease, 206 +/- 432 vs 2 +/- 474 U/L; P < .001). However, reductions in serum levels of K18 were not better than reductions in levels of alanine aminotransferase in identifying adults with histologic improvement (area under the receiver operator characteristic [AUROC], 0.71; 95% confidence interval [CI], 0.63-0.80; vs AUROC, 0.68; 95% CI, 0.61-0.79; P = .34) or children (AUROC, 0.72; 95% CI, 0.63-0.81; vs AUROC, 0.79; 95% CI, 0.70-0.87; P = .42).
CONCLUSIONS: Decreases in serum levels of K18 are associated strongly with improved liver histologies in adults or children with NAFLD. However, reductions in K18 do not perform better than those in alanine aminotransferase level in identifying histologic changes in NAFLD.
C1 [Vuppalanchi, Raj; Deppe, Ross; Comerford, Megan; Masuoka, Howard C.; Molleston, Jean P.; Chalasani, Naga] Indiana Univ Sch Med, Dept Med, Indianapolis, IN 46202 USA.
[Jain, Ajay K.; Neuschwander-Tetri, Brent A.] St Louis Univ, St Louis, MO 63103 USA.
[Yates, Katherine; Tonascia, James] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Loomba, Rohit] Univ Calif San Diego, Div Gastroenterol, San Diego, CA 92103 USA.
[Schwimmer, Jeffrey B.] Univ Calif San Diego, Dept Pediat, San Diego, CA 92103 USA.
[Brunt, Elizabeth M.] Washington Univ, Sch Med, St Louis, MO USA.
[Kleiner, David E.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Schwimmer, Jeffrey B.] Rady Childrens Hosp, Dept Gastroenterol, San Diego, CA USA.
[Lavine, Joel E.] Columbia Univ, Dept Pediat, New York, NY 10027 USA.
RP Chalasani, N (reprint author), Indiana Univ Sch Med, Div Gastroenterol & Hepatol, 1050 Wishard Blvd,RG 4100, Indianapolis, IN 46202 USA.
EM nchalasa@iu.edu
OI Vuppalanchi, Raj/0000-0003-0637-1577
FU American Recovery and Reinvestment Act [3K24DK069290-05S1]
FX Supported in part by an award from the American Recovery and
Reinvestment Act of 2009 ( 3K24DK069290-05S1 to N.C.).
NR 33
TC 12
Z9 12
U1 0
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1542-3565
EI 1542-7714
J9 CLIN GASTROENTEROL H
JI Clin. Gastroenterol. Hepatol.
PD DEC
PY 2014
VL 12
IS 12
BP 2121
EP U416
DI 10.1016/j.cgh.2014.05.010
PG 12
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AW6FA
UT WOS:000346363600029
PM 24846279
ER
PT J
AU Lauer, MS
AF Lauer, Michael S.
TI Clinical trials in crisis: Four simple methodologic fixes Commentary
SO CLINICAL TRIALS
LA English
DT Editorial Material
ID HEALTH-CARE; GISSI; STORY; LUNG
C1 NHLBI, Div Cardiovasc Sci DCVS, Bethesda, MD 20892 USA.
RP Lauer, MS (reprint author), NHLBI, Div Cardiovasc Sci DCVS, Bldg 10, Bethesda, MD 20892 USA.
EM lauerm@nhlbi.nih.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 16
TC 0
Z9 0
U1 0
U2 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1740-7745
EI 1740-7753
J9 CLIN TRIALS
JI Clin. Trials
PD DEC
PY 2014
VL 11
IS 6
BP 622
EP 623
DI 10.1177/1740774514553482
PG 2
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AW6QU
UT WOS:000346394500002
PM 25389225
ER
PT J
AU Meert, K
Keele, L
Clark, A
AF Meert, Kathleen
Keele, Linda
Clark, Amy
CA Collaborative Pediat Critical Care
TI VARIABILITY IN END-OF-LIFE PRACTICE AMONG US TERTIARY CARE PEDIATRIC
INTENSIVE CARE UNITS (PICUS)
SO CRITICAL CARE MEDICINE
LA English
DT Meeting Abstract
C1 [Meert, Kathleen] Wayne State Univ, Detroit, MI USA.
[Keele, Linda; Clark, Amy] Univ Utah, Salt Lake City, UT USA.
[Collaborative Pediat Critical Care] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD DEC
PY 2014
VL 42
IS 12
SU S
MA 389
PG 1
WC Critical Care Medicine
SC General & Internal Medicine
GA AW3UP
UT WOS:000346211800354
ER
PT J
AU Pollack, M
Holubkov, R
Tomohiko, F
AF Pollack, Murray
Holubkov, Richard
Tomohiko, Funai
CA CPCCRN
TI SIMULTANEOUS PREDICTION OF MORBIDITY (M), MORTALITY (D), AND INTACT
SURVIVAL (S)
SO CRITICAL CARE MEDICINE
LA English
DT Meeting Abstract
C1 [Pollack, Murray] Childrens Natl Hlth Syst, Washington, DC USA.
[Holubkov, Richard; Tomohiko, Funai] Univ Utah, Salt Lake City, UT USA.
[CPCCRN] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0090-3493
EI 1530-0293
J9 CRIT CARE MED
JI Crit. Care Med.
PD DEC
PY 2014
VL 42
IS 12
SU S
MA 373
PG 1
WC Critical Care Medicine
SC General & Internal Medicine
GA AW3UP
UT WOS:000346211800338
ER
PT J
AU Kost, RG
Lee, LN
Yessis, JL
Wesley, R
Alfano, S
Alexander, SR
Kassis, SB
Cola, P
Dozier, A
Ford, DE
Harris, PA
Kim, E
Lee, SC
O'Riordan, G
Roth, MT
Schuff, K
Wasser, J
Henderson, DK
Coller, BS
AF Kost, Rhonda G.
Lee, Laura N.
Yessis, Jennifer L.
Wesley, Robert
Alfano, Sandra
Alexander, Steven R.
Kassis, Sylvia Baedorf
Cola, Philip
Dozier, Ann
Ford, Dan E.
Harris, Paul A.
Kim, Emmelyn
Lee, Simon Craddock
O'Riordan, Gerri
Roth, Mary-Tara
Schuff, Kathryn
Wasser, June
Henderson, David K.
Coller, Barry S.
TI Research Participant-Centered Outcomes at NIH-Supported Clinical
Research Centers
SO CTS-CLINICAL AND TRANSLATIONAL SCIENCE
LA English
DT Article
DE patient-centered outcomes research; translational research; patient
satisfaction; outcomes research; clinical trials
ID CARE-SYSTEM DISTRUST; HOSPITAL SURVEY; PERCEPTION; RETURN
AB BackgroundAlthough research participation is essential for clinical investigation, few quantitative outcome measures exist to assess participants' experiences. To address this, we developed and deployed a survey at 15 NIH-supported clinical research centers to assess participant-centered outcomes; we report responses from 4,961 participants.
MethodsSurvey questions addressed core aspects of the research participants' experience, including their overall rating, motivation, trust, and informed consent. We describe participant characteristics, responses to individual questions, and correlations among responses.
ResultsRespondents broadly represented the research population in sex, race, and ethnicity. Seventy-three percent awarded top ratings to their overall research experience and 94% reported no pressure to enroll. Top ratings correlated with feeling treated with respect, listened to, and having access to the research team (R-2 = 0.80-0.96). White participants trusted researchers more (88%) than did nonwhite participants collectively (80%; p < 0.0001). Many participants felt fully prepared by the informed consent process (67%) and wanted to receive research results (72%).
ConclusionsOur survey demonstrates that a majority of participants at NIH-supported clinical research centers rate their research experience very positively and that participant-centered outcome measures identify actionable items for improvement of participant's experiences, research protections, and the conduct of clinical investigation.
C1 [Kost, Rhonda G.; Coller, Barry S.] Rockefeller Univ, Ctr Clin Translat Sci, New York, NY 10021 USA.
[Lee, Laura N.; Wesley, Robert; Henderson, David K.] NIH, Off Deputy Director Clin Care, Ctr Clin, Bethesda, MD 20892 USA.
[Yessis, Jennifer L.] Univ Waterloo, Propel Ctr Populat Hlth, Waterloo, ON N2L 3G1, Canada.
[Alfano, Sandra] Yale Univ, Human Invest Comm, New Haven, CT USA.
[Alexander, Steven R.; O'Riordan, Gerri] Stanford Univ, Spectrum Stanford Univ Ctr Clin & Translat Educ &, Palo Alto, CA 94304 USA.
[Kassis, Sylvia Baedorf; Roth, Mary-Tara] Boston Univ, Clin & Translat Sci Inst, Boston, MA 02215 USA.
[Cola, Philip] Univ Hosp Case Med Ctr, Cleveland, OH USA.
[Cola, Philip] Case Western Reserve Univ, Sch Med, Cleveland, OH USA.
[Dozier, Ann] Univ Rochester, Rochester, NY USA.
[Ford, Dan E.] Johns Hopkins Inst Clin Translat Res, Baltimore, MD USA.
[Harris, Paul A.] Vanderbilt Univ, Vanderbilt Inst Clin & Translat Res, Nashville, TN 37235 USA.
[Kim, Emmelyn] North Shore LIJ Hlth Syst, Feinstein Inst Med Res, Manhasset, NY USA.
[Lee, Simon Craddock] Univ Texas SW Med Ctr Dallas, Dept Clin Sci, Dallas, TX 75390 USA.
[Schuff, Kathryn] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Wasser, June] Tufts Univ, Sch Med, Boston, MA 02111 USA.
RP Kost, RG (reprint author), Rockefeller Univ, Ctr Clin Translat Sci, 1230 York Ave, New York, NY 10021 USA.
EM kostr@rockefeller.edu
OI Lee, Simon J. Craddock/0000-0001-6345-1237
FU National Center for Research Resources (NCRR) [UL1TR000043, UL1TR000157,
UL1TR000128, UL1TR000093, 1-U54-AI108332-01, UL1TR000445, UL1TR001085,
UL1RR024143, UL1TR001064, UL1TR000073, UL1TR000439, UL1TR001105,
UL1RR024160, UL1RR024128, UL1TR00111]; National Center for Advancing
Translational Sciences (NCATS), National Institutes of Health
FX Supported in part by grants UL1TR000043, UL1TR000157, UL1TR000128,
UL1TR000093, 1-U54-AI108332-01, UL1TR000445, UL1TR001085, UL1RR024143,
UL1TR001064, UL1TR000073, UL1TR000439, UL1TR001105, UL1RR024160,
UL1RR024128, and UL1TR00111 from the National Center for Research
Resources (NCRR) and the National Center for Advancing Translational
Sciences (NCATS), National Institutes of Health.
NR 35
TC 1
Z9 1
U1 1
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1752-8054
EI 1752-8062
J9 CTS-CLIN TRANSL SCI
JI CTS-Clin. Transl. Sci.
PD DEC
PY 2014
VL 7
IS 6
BP 430
EP 440
DI 10.1111/cts.12167
PG 11
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AW5CD
UT WOS:000346292600002
PM 24842076
ER
PT J
AU Zhao, GH
Blackstone, C
AF Zhao, Guohua
Blackstone, Craig
TI ER Morphology: Sculpting with XendoU
SO CURRENT BIOLOGY
LA English
DT Editorial Material
ID ENDOPLASMIC-RETICULUM; NETWORK FORMATION; FAMILY
C1 [Zhao, Guohua; Blackstone, Craig] NINDS, Cell Biol Sect, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
RP Blackstone, C (reprint author), NINDS, Cell Biol Sect, Neurogenet Branch, NIH, Bldg 35,Room 2C-913,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM blackstc@ninds.nih.gov
NR 20
TC 0
Z9 0
U1 1
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD DEC
PY 2014
VL 24
IS 24
DI 10.1016/j.cub.2014.11.005
PG 4
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AW9ME
UT WOS:000346580700014
PM 25514011
ER
PT J
AU Burns, DN
Grossman, C
Turpin, J
Elharrar, V
Veronese, F
AF Burns, David N.
Grossman, Cynthia
Turpin, Jim
Elharrar, Vanessa
Veronese, Fulvia
TI Role of Oral Pre-exposure Prophylaxis (PrEP) in Current and Future HIV
Prevention Strategies
SO CURRENT HIV/AIDS REPORTS
LA English
DT Article
DE HIV/human immunodeficiency virus; Prevention; PrEP/pre-exposure
prophylaxis; ARVs/antiretrovirals
ID TENOFOVIR DISOPROXIL FUMARATE; FEMALE GENITAL-TRACT; UNITED-STATES;
COST-EFFECTIVENESS; ANTIRETROVIRAL THERAPY; TOPICAL MICROBICIDES;
MATHEMATICAL-MODELS; INTERIM GUIDANCE; HETEROSEXUAL MEN; DRUG-RESISTANCE
AB Treatment as prevention is expected to have a major role in reducing HIV incidence, but other prevention interventions will also be required to bring the epidemic under control, particularly among key populations. One or more forms of pre-exposure prophylaxis (PrEP) will likely play a critical role. Oral PrEP with emtricitabine-tenofovir (TruvadaA (R)) is currently available in the US and some other countries, but uptake has been slow. We review the concerns that have contributed to this slow uptake and discuss current and future research in this critical area of HIV prevention research.
C1 [Burns, David N.; Turpin, Jim; Elharrar, Vanessa; Veronese, Fulvia] NIAID, Div Aids, NIH, Bethesda, MD 20892 USA.
[Grossman, Cynthia] NIMH, Div Aids, NIH, Bethesda, MD 20892 USA.
RP Burns, DN (reprint author), NIAID, Div Aids, NIH, 5601 Fishers Lane,MSC 9831, Bethesda, MD 20892 USA.
EM burnsda@niaid.nih.gov
NR 81
TC 7
Z9 7
U1 3
U2 22
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1548-3568
EI 1548-3576
J9 CURR HIV-AIDS REP
JI Curr. Hiv/Aids Rep.
PD DEC
PY 2014
VL 11
IS 4
BP 393
EP 403
DI 10.1007/s11904-014-0234-8
PG 11
WC Infectious Diseases
SC Infectious Diseases
GA AW4IY
UT WOS:000346245800003
PM 25283184
ER
PT J
AU Bezrukov, SM
Schimansky-Geier, L
Schmid, G
AF Bezrukov, S. M.
Schimansky-Geier, L.
Schmid, G.
TI Brownian motion in confined geometries
SO EUROPEAN PHYSICAL JOURNAL-SPECIAL TOPICS
LA English
DT Editorial Material
ID DIFFUSION; TRANSPORT; CHANNEL
AB In a great number of technologically and biologically relevant cases, transport of micro- or nanosized objects is governed by both omnipresent thermal fluctuations and confining walls or constrictions limiting the available phase space. The present Topical Issue covers the most recent applications and theoretical findings devoted to studies of Brownian motion under confinement of channel-like geometries.
C1 [Bezrukov, S. M.] NICHD, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Schimansky-Geier, L.] Humboldt Univ, Inst Phys, D-12489 Berlin, Germany.
[Schmid, G.] Univ Augsburg, Inst Phys, D-86159 Augsburg, Germany.
RP Bezrukov, SM (reprint author), NICHD, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
EM bezrukos@mail.nih.gov; alsg@physik.hu-berlin.de;
Gerhard.Schmid@physik.uni-augsburg.de
NR 41
TC 1
Z9 1
U1 3
U2 24
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1951-6355
EI 1951-6401
J9 EUR PHYS J-SPEC TOP
JI Eur. Phys. J.-Spec. Top.
PD DEC
PY 2014
VL 223
IS 14
BP 3021
EP 3025
DI 10.1140/epjst/e2014-02316-6
PG 5
WC Physics, Multidisciplinary
SC Physics
GA AW7AI
UT WOS:000346416400001
ER
PT J
AU Berezhkovskii, AM
Bezrukov, SM
AF Berezhkovskii, A. M.
Bezrukov, S. M.
TI On the applicability of entropy potentials in transport problems
SO EUROPEAN PHYSICAL JOURNAL-SPECIAL TOPICS
LA English
DT Review
ID FACILITATED MEMBRANE-TRANSPORT; CHANNEL; DIFFUSION; VDAC; TUBULIN
AB Transport in confined structures of varying geometry has become the subject of growing attention in recent years since such structures are ubiquitous in biology and technology. In analyzing transport in systems of this type, the notion of entropy potentials is widely used. Entropy potentials naturally arise in one-dimensional description of equilibrium distributions in multidimensional confined structures. However, their application to transport problems requires some caution. In this article we discuss such applications and summarize the results of recent studies exploring the limits of applicability. We also consider an example of a transport problem in a system of varying geometry, where the conventional approach is inapplicable since the geometry changes abruptly. In addition, we demonstrate how the entropy potential can be used to analyze optimal transport through a three-dimensional cosine-shaped channel.
C1 [Berezhkovskii, A. M.; Bezrukov, S. M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Berezhkovskii, A. M.] NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Berezhkovskii, AM (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
FU NIH, Center for Information Technology; Eunice Kennedy Shriver National
Institute of Child Health and Human Development
FX This study was supported by the Intramural Research Program of the NIH,
Center for Information Technology and Eunice Kennedy Shriver National
Institute of Child Health and Human Development.
NR 36
TC 6
Z9 6
U1 1
U2 10
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1951-6355
EI 1951-6401
J9 EUR PHYS J-SPEC TOP
JI Eur. Phys. J.-Spec. Top.
PD DEC
PY 2014
VL 223
IS 14
BP 3063
EP 3077
DI 10.1140/epjst/e2014-02319-3
PG 15
WC Physics, Multidisciplinary
SC Physics
GA AW7AI
UT WOS:000346416400004
PM 26339466
ER
PT J
AU Liang, XY
Chen, LJ
Ng, TK
Tuo, J
Gao, JL
Tam, POS
Lai, TYY
Chan, CC
Pang, CP
AF Liang, X. Y.
Chen, L. J.
Ng, T. K.
Tuo, J.
Gao, J-L
Tam, P. O. S.
Lai, T. Y. Y.
Chan, C-C
Pang, C. P.
TI FPR1 interacts with CFH, HTRA1 and smoking in exudative age-related
macular degeneration and polypoidal choroidal vasculopathy
SO EYE
LA English
DT Article
ID FORMYL PEPTIDE RECEPTOR; PIGMENT EPITHELIAL-CELLS; FORMYLPEPTIDE
RECEPTOR; BRUCHS MEMBRANE; FUNCTIONAL DOMAINS; ALZHEIMERS-DISEASE;
ASSOCIATION; POLYMORPHISMS; INFLAMMATION; CHEMOTAXIS
AB Purpose To determine the genetic association of an inflammation-related gene, formyl peptide receptor 1 (FPR1), in exudative age-related macular degeneration (AMD) and polypoidal choroidal vasculopathy (PCV).
Methods The coding region of FPR1 gene was sequenced in 554 unrelated Chinese individuals: 155 exudative AMD patients, 179 PCV patients, and 220 controls. Interactions and combined effects of FPR1 with complement factor H (CFH), high temperature requirement factor A1 (HTRA1), and smoking were also investigated. Results A total of 28 polymorphisms in FPR1 were identified. Single nucleotide polymorphisms (SNP) rs78488639 increased the risk to exudative AMD (P = 0.043) and PCV (P = 0.016), whereas SNP rs867229 decreased the risk to exudative AMD (P = 0.0026), but not PCV. Homozygous G allele of rs1042229 was associated with exudative AMD (P = 0.0394, odds ratio (OR) = 2.27, 95% confident interval: 1.08-4.74), but not with PCV. Exudative AMD, but not PCV, was associated with the heterozygous genotypes of rs2070746 (P = 0.019, OR = 0.57) and rs867229 (P = 0.0082, OR = 0.54).
Significantly, interactions were identified among FPR1 rs78488639, CFH rs800292, and HTRA1 rs11200638 in both exudative AMD and PCV. Combined heterozygous risk alleles of CFH rs800292 GA and FPR1 rs78488639 CA were posed to PCV (P = 2.22 x 10(-4), OR = 10.47), but not exudative AMD. Furthermore, FPR1 rs78488639 CA combining with HTRA1 rs11200638 and smoking was also predisposed risks to exudative AMD and PCV.
Conclusion FPR1 is associated with exudative AMD and PCV in a Hong Kong Chinese cohort. FPR1 rs78488639 interacted with CFH rs800292, HTRA1 rs11200638, and smoking, enhancing risk to exudative AMD and PCV.
C1 [Liang, X. Y.; Chen, L. J.; Ng, T. K.; Tam, P. O. S.; Lai, T. Y. Y.; Pang, C. P.] Chinese Univ Hong Kong, Dept Ophthalmol & Visual Sci, Hong Kong Eye Hosp, Kowloon, Hong Kong, Peoples R China.
[Tuo, J.; Chan, C-C] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
[Gao, J-L] NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Pang, CP (reprint author), Chinese Univ Hong Kong, Dept Ophthalmol & Visual Sci, Hong Kong Eye Hosp, 4-F,147K Argyle St, Kowloon, Hong Kong, Peoples R China.
EM cppang@cuhk.edu.hk
OI Ng, Tsz Kin/0000-0001-7863-7229
FU Endowment Fund for Lim Por-Yen Eye Genetics Research Centre; Chinese
University of Hong Kong; General Research Fund from the Research Grants
Council, Hong Kong [473410]
FX We express our greatest appreciation to all the study participants. This
study was supported in part by the Endowment Fund for Lim Por-Yen Eye
Genetics Research Centre, the Chinese University of Hong Kong and the
General Research Fund from the Research Grants Council (grant number
473410), Hong Kong.
NR 51
TC 2
Z9 2
U1 1
U2 2
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-222X
EI 1476-5454
J9 EYE
JI Eye
PD DEC
PY 2014
VL 28
IS 12
BP 1502
EP 1510
DI 10.1038/eye.2014.226
PG 9
WC Ophthalmology
SC Ophthalmology
GA AW6FQ
UT WOS:000346365600015
PM 25277308
ER
PT J
AU Chen, J
Teixeira, PF
Glaser, E
Levine, RL
AF Chen, Jue
Teixeira, Pedro Filipe
Glaser, Elzbieta
Levine, Rodney L.
TI Mechanism of oxidative inactivation of human presequence protease by
hydrogen peroxide
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Presequence protease; Protein oxidation; Peptide degradation; Cysteine
oxidation; Methionine sulfoxide; Free radicals
ID METHIONINE SULFOXIDE REDUCTASE; METAL-CATALYZED OXIDATION;
ALZHEIMERS-DISEASE; ORGANELLAR PEPTIDASOME; PROTEINS; PREP; DEGRADATION;
MITOCHONDRIA; PEROXIREDOXINS; QUANTITATION
AB The mitochondrial presequence protease (PreP) is a member of the pitrilysin class of metalloproteases. It degrades the mitochondrial targeting presequences of mitochondria-localized proteins as well as unstructured peptides such as amyloid-beta peptide. The specific activity of PreP is reduced in Alzheimer patients and animal models of Alzheimer disease. The loss of activity can be mimicked in vitro by exposure to oxidizing conditions, and indirect evidence suggested that inactivation was due to methionine oxidation. We performed peptide mapping analyses to elucidate the mechanism of inactivation. None of the 24 methionine residues in recombinant human PreP was oxidized. We present evidence that inactivation is due to oxidation of cysteine residues and consequent oligomerization through intermolecular disulfide bonds. The most susceptible cysteine residues to oxidation are Cys34, Cys112, and Cys119. Most, but not all, of the activity loss is restored by the reducing agent dithiothreitol. These findings elucidate a redox mechanism for regulation of PreP and also provide a rational basis for therapeutic intervention in conditions characterized by excessive oxidation of PreP. Published by Elsevier Inc.
C1 [Chen, Jue; Levine, Rodney L.] Natl Heart Lung & Blood Inst, Biochem Lab, Bethesda, MD 20892 USA.
[Teixeira, Pedro Filipe; Glaser, Elzbieta] Stockholm Univ, Arrhenius Labs Nat Sci, Dept Biochem & Biophys, S-10691 Stockholm, Sweden.
RP Levine, RL (reprint author), Natl Heart Lung & Blood Inst, Biochem Lab, Bethesda, MD 20892 USA.
EM rlevine@nih.gov
RI Levine, Rodney/D-9885-2011
FU Intramural Research Program of the National Heart, Lung, and Blood
Institute; Swedish Research Council [621-2012-4713]; Swedish Alzheimer
Foundation [03-067]
FX This study was supported by the Intramural Research Program of the
National Heart, Lung, and Blood Institute (J.C., R.L.L.) and by grants
from the Swedish Research Council (621-2012-4713) and the Swedish
Alzheimer Foundation (03-067) (to E.G.).
NR 31
TC 1
Z9 1
U1 2
U2 5
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2014
VL 77
BP 57
EP 63
DI 10.1016/j.freeradbiomed.2014.08.016
PG 7
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA AW6QA
UT WOS:000346392500007
PM 25236746
ER
PT J
AU Ono, K
Akaike, T
Sawa, T
Kumagai, Y
Wink, DA
Tantillo, DJ
Hobbs, AJ
Nagy, P
Xian, M
Lin, J
Fukuto, JM
AF Ono, Katsuhiko
Akaike, Takaaki
Sawa, Tomohiro
Kumagai, Yoshito
Wink, David A.
Tantillo, Dean J.
Hobbs, Adrian J.
Nagy, Peter
Xian, Ming
Lin, Joseph
Fukuto, Jon M.
TI Redox chemistry and chemical biology of H2S, hydropersulfides, and
derived species: Implications of their possible biological activity and
utility
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Review
DE Hydrogen sulfide; Persulfides; Polysulfides; Thiols; Thiol redox
ID PECTINATA BACTERIA SYMBIOSIS; PROTEIN S-SULFHYDRATION; SPERM-WHALE
MYOGLOBIN; ANIMATION-LIKE STATE; HYDROGEN-SULFIDE; LUCINA-PECTINATA;
OXIDATIVE STRESS; HEMOGLOBIN-I; REDUCTION POTENTIALS; ALIPHATIC
DISULFIDES
AB Hydrogen sulfide (H2S) is an endogenously generated and putative signaling/effector molecule. Despite its numerous reported functions, the chemistry by which it elicits its functions is not understood. Moreover, recent studies allude to the existence of other sulfur species besides H2S that may play critical physiological roles. Herein, the basic chemical biology of H2S as well as other related or derived species is discussed and reviewed. This review particularly focuses on the per- and polysulfides which are likely in equilibrium with free H2S and which may be important biological effectors themselves. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Ono, Katsuhiko; Fukuto, Jon M.] Sonoma State Univ, Dept Chem, Rohnert Pk, CA 94928 USA.
[Akaike, Takaaki; Sawa, Tomohiro] Tohoku Univ, Grad Sch Med, Dept Environm Hlth Sci & Mol Toxicol, Sendai, Miyagi 9808575, Japan.
[Kumagai, Yoshito] Univ Tsukuba, Grad Sch Comprehens Human Sci, Doctoral Program Biomed Sci, Tsukuba, Ibaraki 3058575, Japan.
[Wink, David A.] NCI, Radiat Biol Branch, Tumor Biol Sect, Bethesda, MD 20892 USA.
[Tantillo, Dean J.] Univ Calif Davis, Dept Chem, Davis, CA 95616 USA.
[Hobbs, Adrian J.] Queen Mary Univ London, Bart & London Sch Med, William Harvey Res Inst, London EC1M 6BQ, England.
[Nagy, Peter] Natl Inst Oncol, Dept Mol Immunol & Toxicol, Budapest, Hungary.
[Xian, Ming] Washington State Univ, Dept Chem, Pullman, WA 99164 USA.
[Lin, Joseph] Sonoma State Univ, Dept Biol, Rohnert Pk, CA 94928 USA.
RP Fukuto, JM (reprint author), Sonoma State Univ, Dept Chem, Rohnert Pk, CA 94928 USA.
EM fukuto@sonoma.edu
RI Nagy, Peter/C-6768-2008
OI Nagy, Peter/0000-0003-3393-235X
FU Marie Curie International Reintegration Grant [PIRG08-GA-2010-277006]
FX P.N. is grateful for financial support from FP7-PEOPLE-2010-RG (Marie
Curie International Reintegration Grant PIRG08-GA-2010-277006) and The
Hungarian National Science Foundation (OTKA; Grant K109843). The authors
also acknowledge support from the NIH (HL106598 to J.M.F.; R01HL116571
to M.X.), NSF (CHE-1148641 to J.M.F.), and ACS-PRF (52801-ND4 to
D.J.T.). T.A., T.S., and Y.K. acknowledge support by Grants-in Aid for
Scientific Research from the Ministry of Education, Culture, Sports,
Sciences, and Technology (MEXT), Japan. P.N., J. M. F. and A. J. H. also
acknowledge COST action BM1005 for providing networking opportunities.
NR 100
TC 62
Z9 65
U1 11
U2 53
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2014
VL 77
BP 82
EP 94
DI 10.1016/j.freeradbiomed.2014.09.007
PG 13
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA AW6QA
UT WOS:000346392500010
PM 25229186
ER
PT J
AU Yun, JW
Son, MJ
Abdelmegeed, MA
Banerjee, A
Morgan, TR
Yoo, SH
Song, BJ
AF Yun, Jun-Won
Son, Min-Jeong
Abdelmegeed, Mohamed A.
Banerjee, Atrayee
Morgan, Timothy R.
Yoo, Seong-Ho
Song, Byoung-Joon
TI Binge alcohol promotes hypoxic liver injury through a CYP2E1-HIF-1
alpha-dependent apoptosis pathway in mice and humans
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Article
DE Binge ethanol; Alcohol-metabolizing enzymes; CYP2E1; Hypoxia; Protein
nitration; Apoptosis; Human liver injury; Free radicals
ID INDUCIBLE FACTOR 1-ALPHA; INDUCED MITOCHONDRIAL DYSFUNCTION; PROLYL
HYDROXYLASE-ACTIVITY; PROTEIN-TYROSINE NITRATION; NITRIC-OXIDE SYNTHASE;
FATTY LIVER; PROTEASOME ACTIVITY; OXYGEN-CONSUMPTION; CYTOCHROME
P4502E1; ETHANOL
AB Binge drinking, a common pattern of alcohol ingestion, is known to potentiate liver injury caused by chronic alcohol abuse. This study was aimed at investigating the effects of acute binge alcohol on hypoxia-inducible factor-la (HIF-1 alpha)-mediated liver injury and the roles of alcohol-metabolizing enzymes in alcohol-induced hypoxia and hepatotoxicity. Mice and human specimens assigned to binge or nonbinge groups were analyzed for blood alcohol concentration (BAC), alcohol-metabolizing enzymes, HIF-1 alpha-related protein nitration, and apoptosis. Binge alcohol promoted acute liver injury in mice with elevated levels of ethanol-inducible cytochrome P450 2E1 (CYP2E1) and hypoxia, both of which were colocalized in the centrilobular areas. We observed positive correlations among elevated BAC, CYP2E1, and HIF-1 alpha in mice and humans exposed to binge alcohol. The CYP2E1 protein levels (r = 0.629, p = 0.001) and activity (r = 0.641, p = 0.001) showed a significantly positive correlation with BAC in human livers. HIF-1 alpha levels were also positively correlated with BAC (r = 0.745, p < 0.001) or CYP2E1 activity (r = 0.792, p < 0.001) in humans. Binge alcohol promoted protein nitration and apoptosis with significant correlations observed between inducible nitric oxide synthase and BAC, CYP2E1, or HIF-1 alpha in human specimens. Binge-alcohol-induced HIF-1 alpha activation and subsequent protein nitration or apoptosis seen in wild type were significantly alleviated in the corresponding Cyp2e1-null mice, whereas pretreatment with an HIF-1 alpha inhibitor, PX-478, prevented HIF-1 alpha elevation with a trend of decreased levels of 3-nitrotyrosine and apoptosis, supporting the roles of CYP2E1 and HIF-1 alpha in binge-alcohol-mediated protein nitration and hepatotoxicity. Thus binge alcohol promotes acute liver injury in mice and humans at least partly through a CYP2E1-HIF-1 alpha-dependent apoptosis pathway. Published by Elsevier Inc.
C1 [Yun, Jun-Won; Abdelmegeed, Mohamed A.; Banerjee, Atrayee; Song, Byoung-Joon] NIAAA, Lab Membrane Biochem & Biophys, Bethesda, MD 20892 USA.
[Son, Min-Jeong; Yoo, Seong-Ho] Seoul Natl Univ, Coll Med, Inst Forens Med, Seoul, South Korea.
[Morgan, Timothy R.] Vet Adm Long Beach Healthcare Syst, Gastroenterol Serv, Long Beach, CA 90822 USA.
[Morgan, Timothy R.] Univ Calif Irvine, Div Gastroenterol, Irvine, CA 92697 USA.
RP Yoo, SH (reprint author), Seoul Natl Univ, Coll Med, Inst Forens Med, Seoul, South Korea.
EM yoosh@snu.ac.kr; bj.song@nih.gov
FU Intramural Program of the National Institute on Alcohol Abuse and
Alcoholism; National Research Foundation grant - Korean government
[800-20120365]
FX This research was supported by the Intramural Program of the National
Institute on Alcohol Abuse and Alcoholism and a National Research
Foundation grant funded by the Korean government (800-20120365 to
S.-H.Y.). We are also grateful to Dr. Klaus Gawrisch for his support.
NR 55
TC 7
Z9 8
U1 4
U2 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5849
EI 1873-4596
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD DEC
PY 2014
VL 77
BP 183
EP 194
DI 10.1016/j.freeradbiomed.2014.08.030
PG 12
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA AW6QA
UT WOS:000346392500018
PM 25236742
ER
PT J
AU Allen, AK
Nesmith, JE
Golden, A
AF Allen, Anna K.
Nesmith, Jessica E.
Golden, Andy
TI An RNAi-Based Suppressor Screen Identifies Interactors of the Myt1
Ortholog of Caenorhabditis elegans
SO G3-GENES GENOMES GENETICS
LA English
DT Article
DE WEE-1.3; fertility; suppressor; oocyte maturation; EGA
ID TO-EMBRYO TRANSITION; OOCYTE MEIOTIC MATURATION; YEAST NUCLEOLAR
PROTEIN; CELL-CYCLE PROGRESSION; LARGE GENE LISTS; C-ELEGANS;
ENDOPLASMIC-RETICULUM; FUNCTIONAL-ANALYSIS; HISTONE H3; KINASE
AB Oocyte maturation in all species is controlled by a protein complex termed the maturation promoting factor (MPF). MPF comprises a cyclin-dependent kinase (CDK) and its partner cyclin, and it is regulated by dueling regulatory phosphorylation events on the CDK. In Caenorhabditis elegans, the Wee1/Myt1 ortholog WEE-1.3 provides the inhibitory phosphorylations on CDK-1 that keep MPF inactive and halt meiosis. Prior work has shown that depletion of WEE-1.3 in C. elegans results in precocious oocyte maturation in vivo and a highly penetrant infertility phenotype. This study sought to further define the precocious maturation phenotype and to identify novel interactors with WEE-1.3. We found that WEE-1.3 is expressed throughout the germline and in developing embryos in a perinuclear pattern, and demonstrated that oocytes in WEE-1.3-depleted germlines have begun to transcribe embryonic genes and exhibit inappropriate expression of proteins normally restricted to fertilized eggs. In addition, we performed an RNAi suppressor screen of the infertile phenotype to identify novel factors that, when co-depleted with WEE-1.3, restore fertility to these animals. We screened similar to 1900 essential genes by RNAi feeding and identified 44 (similar to 2% of the tested genes) that are suppressors of the WEE-1.3 depletion phenotype. The suppressors include many previously unidentified players in the meiotic cell cycle and represent a pool of potential WEE-1.3 interacting proteins that function during C. elegans oocyte maturation and zygotic development.
C1 [Allen, Anna K.; Nesmith, Jessica E.; Golden, Andy] NIDDK, Lab Biochem & Genet, NIH, Bethesda, MD 20892 USA.
RP Allen, AK (reprint author), Howard Univ, EE Just Hall,Room 244, Washington, DC 20059 USA.
EM anna.allen@howard.edu
FU Intramural Research Program of the NIH, The National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK); NIH National Center
for Research Resources
FX We thank Daphna Joseph-Strauss and Orna Cohen-Fix for generating the EMB
RNAi library from the OpenBiosystems RNAi library, David Levine for
making the CBD-1::mCherry transgenic animal, John Hanover for help with
the DAVID analysis, and Aimee Jaramillo-Lambert, Michelle Bond, and
Harold Smith for advice and comments regarding the manuscript. We thank
members of the O'Connell and Golden laboratory for valuable discussions.
This research was supported by the Intramural Research Program of the
NIH, The National Institute of Diabetes and Digestive and Kidney
Diseases (NIDDK). Some nematode strains used in this work were provided
by the Caenorhabditis Genetics Center, which is funded by the NIH
National Center for Research Resources.
NR 64
TC 2
Z9 2
U1 2
U2 6
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 2160-1836
J9 G3-GENES GENOM GENET
JI G3-Genes Genomes Genet.
PD DEC 1
PY 2014
VL 4
IS 12
BP 2329
EP 2343
DI 10.1534/g3.114.013649
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA AW5WJ
UT WOS:000346341500004
PM 25298536
ER
PT J
AU Jansen, M
Scholvinck, DW
Kushima, R
Sekine, S
Weusten, BLAM
Wang, GQQ
Fleischer, DE
Yoshinaga, S
Dawsey, SM
Meijer, SL
Bergman, JJGHM
Oda, I
AF Jansen, Marnix
Scholvinck, Dirk W.
Kushima, Ryoji
Sekine, Shigeki
Weusten, Bas L. A. M.
Wang, Guiqi Q.
Fleischer, David E.
Yoshinaga, Shigetaka
Dawsey, Sanford M.
Meijer, Sybren L.
Bergman, Jacques J. G. H. M.
Oda, Ichiro
TI Is it justified to ablate flat-type esophageal squamous cancer? An
analysis of endoscopic submucosal dissection specimens of lesions
meeting the selection criteria of radio frequency studies
SO GASTROINTESTINAL ENDOSCOPY
LA English
DT Article
ID CELL CARCINOMA; RADIOFREQUENCY ABLATION; MUCOSAL RESECTION; METASTASIS;
PREVALENCE; EPITHELIUM; NEOPLASIA; DEVICE
AB Background: Endoscopic radiofrequency ablation (RFA) appears to be a safe and effective treatment for flat-type noninvasive squamous neoplasia of the esophagus. However, if RFA is applied to lesions containing invasive cancer (esophageal squamous cell carcinoma [ESCC]), histological features associated with lymph node metastases may remain undetected. In addition, extension of neoplasia down the ducts of esophageal submucosal glands (SMGs) may create a sheltered "niche" beyond the reach of ablation.
Objective: To determine the RFA eligibility of flat-type ESCC.
Design: Retrospective analysis of prospectively collected data of ESCC patients.
Setting: National Cancer Center Hospital, Tokyo, Japan.
Patients: Patients with flat-type ESCC larger than 3 cm removed by endoscopic submucosal dissection (ESD).
Interventions: Three endoscopists involved in RFA studies in China reviewed endoscopic images to select lesions eligible for RFA. Corresponding ESD resection specimens were histologically examined.
Main Outcome Measurements: The presence of poor histological features (ie, invasion in m3 or deeper, poor tumor differentiation, or lymphovascular invasion) and the number of involved esophageal SMGs and ducts.
Results: Sixty-five lesions were included, 17 (26%) of which qualified as RFA eligible by RFA endoscopists. Interobserver agreement for this assessment was poor (k = 0.09). Six of the 17 specimens (35%) showed relevant disease: 4 lesions invaded in the muscularis mucosae, 1 of which also showed lymphovascular invasion; 2 lesions showed extension of neoplasia into SMGs.
Limitations: Limited number of cases. RFA eligibility status was based on analysis of still images.
Conclusions: One third of flat-type ESCC, deemed eligible for RFA, demonstrated histological features that are considered (relative) contraindications to endoscopic treatment. Because it appears difficult for endoscopists to identify low-risk ESCC, conservative use of RFA for flat-type ESCC is advocated until long-term follow-up data are available.
C1 [Jansen, Marnix; Meijer, Sybren L.] Univ Amsterdam, Acad Med Ctr, Dept Pathol, NL-1105 AZ Amsterdam, Netherlands.
[Scholvinck, Dirk W.; Bergman, Jacques J. G. H. M.] Univ Amsterdam, Acad Med Ctr, Dept Gastroenterol & Hepatol, NL-1105 AZ Amsterdam, Netherlands.
[Scholvinck, Dirk W.; Weusten, Bas L. A. M.] St Antonius Hosp, Dept Gastroenterol & Hepatol, Nieuwegein, Netherlands.
[Kushima, Ryoji; Sekine, Shigeki] Natl Canc Ctr, Div Pathol, Tokyo, Japan.
[Yoshinaga, Shigetaka; Oda, Ichiro] Natl Canc Ctr, Endoscopy Div, Tokyo, Japan.
[Wang, Guiqi Q.] Chinese Acad Med Sci, Peking Union Med Coll, Dept Endoscopy, Canc Inst & Hosp, Beijing 100730, Peoples R China.
[Fleischer, David E.] Mayo Clin, Dept Gastroenterol & Hepatol, Scottsdale, AZ USA.
[Dawsey, Sanford M.] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
RP Bergman, JJGHM (reprint author), Univ Amsterdam, Acad Med Ctr, Dept Gastroenterol & Hepatol, Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands.
NR 24
TC 3
Z9 3
U1 0
U2 2
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0016-5107
EI 1097-6779
J9 GASTROINTEST ENDOSC
JI Gastrointest. Endosc.
PD DEC
PY 2014
VL 80
IS 6
BP 995
EP 1002
DI 10.1016/j.gie.2014.09.004
PG 8
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA AW7JY
UT WOS:000346441600009
PM 25434658
ER
PT J
AU Ma, BY
Kolb, S
Diprima, M
Karna, M
Tosato, G
Yang, QQ
Huang, Q
Nussinov, R
AF Ma, Buyong
Kolb, Stephanie
Diprima, Michael
Karna, Molleshree
Tosato, Giovanna
Yang, Qiqi
Huang, Qiang
Nussinov, Ruth
TI Investigation of the interactions between the EphB2 receptor and SNEW
peptide variants
SO GROWTH FACTORS
LA English
DT Article
DE EphB2 receptor; ephrin ligands; inhibitor design; molecular dynamics
simulations; protein stability; protein dynamics
ID MOLECULAR-DYNAMICS; EPHA4 RECEPTOR; TUMOR SUPPRESSION; PROTEIN DYNAMICS;
CELL; EPHRINS; BINDING; CANCER; PROLIFERATION; SIMULATION
AB EphB2 interacts with cell surface-bound ephrin ligands to relay bidirectional signals. Overexpression of the EphB2 receptor protein has been linked to different types of cancer. The SNEW (SNEWIQPRLPQH) peptide binds with high selectivity and moderate affinity to EphB2, inhibiting Eph-ephrin interactions by competing with ephrin ligands for the EphB2 high-affinity pocket. We used rigorous free energy perturbation (FEP) calculations to re-evaluate the binding interactions of SNEW peptide with the EphB2 receptor, followed by experimental testing of the computational results. Our results provide insight into dynamic interactions of EphB2 with SNEW peptide. While the first four residues of the SNEW peptide are already highly optimized, change of the C-terminal end of the peptide has the potential to improve SNEW-binding affinity. We identified a PXSPY motif that can be similarly aligned with several other EphB2-binding peptides.
C1 [Ma, Buyong; Kolb, Stephanie; Nussinov, Ruth] NCI, Basic Sci Program, Leidos Biomed Res Inc, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Diprima, Michael; Karna, Molleshree; Tosato, Giovanna] NCI, Cellular Oncol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Yang, Qiqi; Huang, Qiang] Fudan Univ, Sch Life Sci, State Key Lab Genet Engn, Shanghai 200433, Peoples R China.
[Nussinov, Ruth] Tel Aviv Univ, Sackler Sch Med, Sackler Inst Mol Med, Dept Human Genet & Mol Med, IL-69978 Tel Aviv, Israel.
RP Ma, BY (reprint author), NCI, Basic Sci Program, Leidos Biomed Res Inc, Canc & Inflammat Program, Frederick, MD 21702 USA.
EM mabuyong@-mail.nih.gov; NussinoR@helix.nih.gov
RI Ma, Buyong/F-9491-2011
OI Ma, Buyong/0000-0002-7383-719X
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; CCR/NCI; NIBIB/NIH Biomedical Engineering Summer
Internship Program (BESIP); Hi-tech Research and Development Program of
China [2008AA02Z311]; Shanghai Natural Science Foundation [13ZR1402400];
Shanghai Leading Academic Discipline Project [B111]
FX The authors report no declarations of interest. 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. This work was also supported by the intramural
program of the CCR/NCI. M. K. was supported by the NIBIB/NIH Biomedical
Engineering Summer Internship Program (BESIP). Q. Huang was supported in
part by the grants from the Hi-tech Research and Development Program of
China (No. 2008AA02Z311), the Shanghai Natural Science Foundation (No.
13ZR1402400), and the Shanghai Leading Academic Discipline Project
(B111).
NR 53
TC 3
Z9 3
U1 1
U2 5
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0897-7194
EI 1029-2292
J9 GROWTH FACTORS
JI Growth Factors
PD DEC
PY 2014
VL 32
IS 6
BP 236
EP 246
DI 10.3109/08977194.2014.985786
PG 11
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA AW5FZ
UT WOS:000346302600009
PM 25410963
ER
PT J
AU Maroun, MC
Olivero, O
Lipovich, L
Stark, A
Tait, L
Bandyopadhyay, S
Burke, M
Zarbo, R
Chitale, D
Nathanson, SD
Long, M
Peebles, C
Madrid, FF
AF Maroun, Marie-Claire
Olivero, Ofelia
Lipovich, Leonard
Stark, Azadeh
Tait, Larry
Bandyopadhyay, Sudeshna
Burke, Matthew
Zarbo, Richard
Chitale, Dhananjay
Nathanson, S. David
Long, Mike
Peebles, Carol
Madrid, Felix Fernandez
TI Anti-centrosome antibodies in breast cancer are the expression of
autoimmunity
SO IMMUNOLOGIC RESEARCH
LA English
DT Article
DE Breast cancer; Centrosome proteins; Autoimmunity; Chromosomal
instability
ID UBIQUITIN-PROTEASOME PATHWAY; DUCTAL CARCINOMA; STATHMIN;
AUTOANTIBODIES; KINASE; TUMORS; ACTIN; ONCOPROTEIN-18; OVEREXPRESSION;
INSTABILITY
AB Centrosome abnormalities have been observed in nearly all human solid tumors, but their role in tumorigenesis is unclear. We have demonstrated that autoantibodies reacting with antigens in centrosomes are frequently found in BC sera. In this work, we attempted to characterize the centrosome antigens associated with BC. We immunoscreened a T7 cDNA library of BC proteins with BC sera, and the autoantigens identified were printed as a microarray and hybridized with BC and control sera. We used immunohistochemistry (IHC) to investigate the expression of the cloned autoantigens in BC tissue. Immunoscreening with BC sera led to the cloning of autoantibodies recognizing epitopes developing in a family of proteins located on centrosomes such as peri-centriolar material-1, isomorph CRA, stathmin1, HS actin gamma1, SUMO/sentrin peptidase 2, and ubiquitin-conjugating enzyme E2 variant 1. Antibody reactivity to these proteins that are associated with centrosome assembly and/or microtubule function was highly associated with the diagnosis of BC. IHC staining of formalin-fixed paraffin-embedded sections with specific antibodies showed that aurora and stathmin are expressed in BC. The discovery of autoantibodies to important centrosome antigens associated with BC suggests that this immune reactivity could be related to autoimmunity developing in BC. Our finding that some of these antibodies are also present in a group of healthy women suggests that breakdown of tolerance to centrosome proteins may occur early in breast carcinogenesis and that autoantibodies to centrosome antigens might be biomarkers of early BC.
C1 [Maroun, Marie-Claire; Madrid, Felix Fernandez] Wayne State Univ, Sch Med, Dept Internal Med, Div Rheumatol, Detroit, MI 48201 USA.
[Olivero, Ofelia] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
[Lipovich, Leonard; Madrid, Felix Fernandez] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI 48201 USA.
[Stark, Azadeh] Henry Ford Hlth Syst, Dept Pathol, Detroit, MI 48202 USA.
[Tait, Larry; Madrid, Felix Fernandez] Karmanos Canc Inst, Detroit, MI 48201 USA.
[Bandyopadhyay, Sudeshna] Wayne State Univ, Dept Pathol, Detroit, MI 48202 USA.
[Burke, Matthew] Henry Ford Hosp & Hlth Network, Dept Diagnost Radiol, Detroit, MI 48202 USA.
[Zarbo, Richard; Chitale, Dhananjay] Henry Ford Hosp, Detroit, MI 48202 USA.
[Nathanson, S. David] Henry Ford Hlth Syst, Dept Surg, Detroit, MI 48202 USA.
[Long, Mike] Childrens Hosp Michigan, Wayne State Sch Med, Dept Pathol, Detroit, MI USA.
[Peebles, Carol] INOVA Diagnost Inc, San Diego, CA 92131 USA.
RP Maroun, MC (reprint author), Wayne State Univ, Sch Med, Dept Internal Med, Div Rheumatol, 540 Canfield, Detroit, MI 48201 USA.
EM mmaroun@med.wayne.edu
FU NIH NCI [R01 122277]
FX This work was done with the partial support of NIH NCI R01 122277. We
thank the technical work of Naimei Tang and Xinbo Zhang in several
aspects of this project.
NR 57
TC 3
Z9 3
U1 0
U2 3
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0257-277X
EI 1559-0755
J9 IMMUNOL RES
JI Immunol. Res.
PD DEC
PY 2014
VL 60
IS 2-3
SI SI
BP 339
EP 347
DI 10.1007/s12026-014-8582-4
PG 9
WC Immunology
SC Immunology
GA AW6YT
UT WOS:000346412300022
PM 25420961
ER
PT J
AU Courcoulas, AP
Yanovski, SZ
Bonds, D
Eggerman, TL
Horlick, M
Staten, MA
Arterburn, DE
AF Courcoulas, Anita P.
Yanovski, Susan Z.
Bonds, Denise
Eggerman, Thomas L.
Horlick, Mary
Staten, Myrlene A.
Arterburn, David E.
TI Long-term Outcomes of Bariatric Surgery A National Institutes of Health
Symposium
SO JAMA SURGERY
LA English
DT Article
ID SWEDISH OBESE SUBJECTS; GASTRIC BYPASS-SURGERY; HIGH-RISK PATIENTS;
CONTROLLED INTERVENTION; LONGITUDINAL ASSESSMENT; CARDIOVASCULAR EVENTS;
SLEEVE GASTRECTOMY; MEDICAL THERAPY; TRIAL; ATTITUDES
AB IMPORTANCE The clinical evidence base demonstrating bariatric surgery's health benefits is much larger than it was when the National Institutes of Health last held a consensus panel in 1991. Still, it remains unclear whether ongoing studies will address critical questions about long-term complication rates and the sustainability of weight loss and comorbidity control.
OBJECTIVE To summarize findings from a multidisciplinary workshop convened in May 2013 by the National Institute of Diabetes and Digestive and Kidney Diseases and the National Heart, Lung, and Blood Institute. The workshop aimed to summarize the current state of knowledge of bariatric surgery, review research findings on the long-term outcomes of bariatric surgery, and establish priorities for future research directions.
EVIDENCE REVIEW The evidence presented at the workshop was selected by the planning committee for both its quality and duration of follow-up. The data review emphasized randomized clinical trials and large observational studies with long-term follow-up, with or without a control group.
FINDINGS Several small randomized clinical trials showed greater weight loss and type 2 diabetes mellitus remission compared with nonsurgical treatments within the first 2 years of follow-up after bariatric surgery. Large, long-term observational studies have shown durable (>5 years) weight loss, diabetes, and lipid improvements with bariatric surgery. Still unclear are predictors of outcomes, long-term complications, long-term survival, microvascular and macrovascular events, mental health outcomes, and costs. The studies needed to address these knowledge gaps would be expensive and logistically difficult to perform.
CONCLUSIONS AND RELEVANCE High-quality evidence shows that bariatric surgical procedures result in greater weight loss than nonsurgical treatments and are more effective at inducing initial type 2 diabetes mellitus remission in obese patients. More information is needed about the long-term durability of comorbidity control and complications after bariatric procedures and this evidence will most likely come from carefully designed observational studies.
C1 [Courcoulas, Anita P.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA 15213 USA.
[Yanovski, Susan Z.; Horlick, Mary] NIDDK, Div Digest Dis & Nutr, NIH, Bethesda, MD 20892 USA.
[Bonds, Denise] NHLBI, Div Cardiovasc Sci, NIH, Bethesda, MD 20892 USA.
[Eggerman, Thomas L.; Staten, Myrlene A.] NIDDK, Div Diabet, NIH, Bethesda, MD 20892 USA.
[Arterburn, David E.] Grp Hlth Cooperat Puget Sound, Grp Hlth Res Inst, Seattle, WA USA.
RP Courcoulas, AP (reprint author), Univ Pittsburgh, Med Ctr, 3380 Blvd Allies,Ste 390, Pittsburgh, PA 15213 USA.
EM courcoulasap@upmc.edu
FU National Institutes of Health (NIH)-National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK); Covidien; EndoGastric Solutions;
Nutrisystem; J&J Ethicon Scientific; NIH; Informed Medical Decisions
Foundation; Department of Veterans Affairs; Agency for Healthcare
Research and Quality
FX Dr Courcoulas has received grants from the National Institutes of Health
(NIH)-National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), Covidien, EndoGastric Solutions, and Nutrisystem, and advisory
board and personal fees from J&J Ethicon Scientific outside of the
submitted work. Dr Arterburn has received grants from the NIH, grants
and nonfinancial support from the Informed Medical Decisions Foundation,
grants from the Department of Veterans Affairs, and grants from the
Agency for Healthcare Research and Quality outside of the submitted
work. No other disclosures were reported.
NR 47
TC 46
Z9 46
U1 2
U2 13
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6254
EI 2168-6262
J9 JAMA SURG
JI JAMA Surg.
PD DEC
PY 2014
VL 149
IS 12
BP 1323
EP 1329
DI 10.1001/jamasurg.2014.2440
PG 7
WC Surgery
SC Surgery
GA AW7YK
UT WOS:000346477400025
PM 25271405
ER
PT J
AU Thorpe, RJ
McCleary, R
Smolen, JR
Whitfield, KE
Simonsick, EM
LaVeist, T
AF Thorpe, Roland J., Jr.
McCleary, Rachael
Smolen, Jenny R.
Whitfield, Keith E.
Simonsick, Eleanor M.
LaVeist, Thomas
TI Racial Disparities in Disability Among Older Adults: Finding From the
Exploring Health Disparities in Integrated Communities Study
SO JOURNAL OF AGING AND HEALTH
LA English
DT Article
DE disability; older adults; racial disparities; African Americans; EHDIC
ID INCIDENT MOBILITY LIMITATION; LOWER-EXTREMITY FUNCTION; BLACK-WHITE
DIFFERENCES; SOCIOECONOMIC-STATUS; RESIDENTIAL SEGREGATION; RACE
DISPARITIES; NEIGHBORHOOD CHARACTERISTICS; AFRICAN-AMERICANS; PHYSICAL
FUNCTION; SOCIAL-CONTEXT
AB Objective: Persistent and consistently observed racial disparities in physical functioning likely stem from racial differences in social resources and environmental conditions. Method: We examined the association between race and reported difficulty performing instrumental activities of daily living (IADL) in 347 African American (45.5%) and Whites aged 50 or above in the Exploring Health Disparities in Integrated Communities-Southwest Baltimore, Maryland Study (EHDIC-SWB). Results: Contrary to previous studies, African Americans had lower rates of disability (women: 25.6% vs. 44.6%, p = .006; men: 15.7% vs. 32.9%; p = .017) than Whites. After adjusting for sociodemographics, health behaviors, and comorbidities, African American women (odds ratio [OR] = 0.32, 95% confidence interval [CI] = [0.14, 0.70]) and African American men (OR = 0.34, 95% CI = [0.13, 0.90]) retained their functional advantage compared with White women and men, respectively. Conclusion: These findings within an integrated, low-income urban sample support efforts to ameliorate health disparities by focusing on the social context in which people live.
C1 [Thorpe, Roland J., Jr.; McCleary, Rachael; Smolen, Jenny R.; LaVeist, Thomas] Johns Hopkins Bloomberg Sch Publ Hlth, Hopkins Ctr Hlth Dispar Solut, Baltimore, MD 21205 USA.
[Thorpe, Roland J., Jr.; Whitfield, Keith E.] Duke Univ, Ctr Biobehav Hlth Dispar Res, Durham, NC USA.
[Simonsick, Eleanor M.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Simonsick, Eleanor M.] NIA, Baltimore, MD 21224 USA.
RP Thorpe, RJ (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Hopkins Ctr Hlth Dispar Solut, 624 N Broadway,Ste 708, Baltimore, MD 21205 USA.
EM rthorpe@jhu.edu
FU NIMHD NIH HHS [P60MD000214, P60 MD000217, P60 MD000214]
NR 73
TC 2
Z9 2
U1 2
U2 13
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0898-2643
EI 1552-6887
J9 J AGING HEALTH
JI J. Aging Health
PD DEC
PY 2014
VL 26
IS 8
SI SI
BP 1261
EP 1279
DI 10.1177/0898264314534892
PG 19
WC Gerontology; Health Policy & Services
SC Geriatrics & Gerontology; Health Care Sciences & Services
GA AW4PD
UT WOS:000346262200002
PM 25502241
ER
PT J
AU Yeboah, J
Bluemke, DA
Hundley, WG
Rodriguez, CJ
Lima, JAC
Herrington, DM
AF Yeboah, Joseph
Bluemke, David A.
Hundley, W. Gregory
Rodriguez, Carlos J.
Lima, Joao A. C.
Herrington, David M.
TI Left Ventricular Dilation and Incident Congestive Heart Failure in
Asymptomatic Adults Without Cardiovascular Disease: Multi-Ethnic Study
of Atherosclerosis (MESA)
SO JOURNAL OF CARDIAC FAILURE
LA English
DT Article
DE Left ventricular dilation; left ventricular remodeling; heart failure;
risk factors; left ventricular ejection fraction
ID MYOCARDIAL-INFARCTION; SYSTOLIC DYSFUNCTION; MORTALITY; SURVIVAL
AB Background: Limited data exist on the association between left ventricular (LV) dilation/remodeling and incident heart failure (I-IF), especially in adults without prior myocardial infarction (MI) and valvular heart disease. We assessed the association between LV dilation and remodeling and incident HF in a multiethnic cohort.
Methods and Results: A total of 4,974 of 6,814 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) had cardiac magnetic resonance imaging and complete data. Kaplan-Meier and Cox proportional hazard analyses were used to assess the association between LV end-diastolic diameter (LVEDD) and adjudicated HF. During the 12 years of follow-up (mean 9.4 y), 177 (3.6%) HF events occurred, 126(71.2%) in HF with reduced ejection fraction (EF) and 51(28.8%) in HF with preserved EF. LV dilation (LVEDD >52 mm or > 95th percentile) was associated with HF in univariate (hazard ratio [HR] 1.21, 95% confidence interval [CI] 1.08-1.46; P = .007) and multivariable Cox models (HR 1.28, 95% CI 1.09-1.57; P = .01) adjusting for traditional risk factors, medication use, LV EF, and interim MI. We found a significant multiplicative interaction between LVEDD and LV EF in our full multivariable models. Participants with dilated LV and preserved EF had increased risk [HR 2.22, 95% CI 1.46-3.37; P = .006) and those with dilated LV and reduced EF had worse prognosis (HR 7.35, 95% CI 2.36-22.85; P = .0006) compared with normal-size LV and preserved EF. A high proportion of participants with LV dilation had eccentric remodeling, a risk factor for HF. Concentric hypertrophy, also a risk factor for HF, was common in the normal-size LV group.
Conclusions: LV dilation predicts incident HF independently from risk factors, LV EF, and interim MI.
C1 [Yeboah, Joseph; Hundley, W. Gregory; Rodriguez, Carlos J.; Herrington, David M.] Wake Forest Univ, Bowman Gray Sch Med, Dept Internal Med, Winston Salem, NC 27103 USA.
[Yeboah, Joseph; Hundley, W. Gregory; Rodriguez, Carlos J.; Herrington, David M.] Wake Forest Univ, Bowman Gray Sch Med, Dept Cardiol, Winston Salem, NC USA.
[Yeboah, Joseph; Rodriguez, Carlos J.; Herrington, David M.] Wake Forest Sch Med, Dept Epidemiol & Prevent, Winston Salem, NC 27157 USA.
[Bluemke, David A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Lima, Joao A. C.] Johns Hopkins Univ, Baltimore, MD USA.
RP Yeboah, J (reprint author), Wake Forest Sch Med, Dept Internal Med Cardiol, Med Ctr Blvd, Winston Salem, NC 27157 USA.
EM jyeboah@wakehealth.edu
OI Bluemke, David/0000-0002-8323-8086
FU NIH/NHLBI [N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162,
N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167];
[R01HL098445]
FX NIH/NHLBI contracts N01-HC-95159 through N01-HC-95167 and a Diversity
Supplement to R01HL098445.
NR 20
TC 3
Z9 3
U1 0
U2 1
PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
PI PHILADELPHIA
PA CURTIS CENTER, INDEPENDENCE SQUARE WEST, PHILADELPHIA, PA 19106-3399 USA
SN 1071-9164
EI 1532-8414
J9 J CARD FAIL
JI J. Card. Fail.
PD DEC
PY 2014
VL 20
IS 12
BP 905
EP 911
DI 10.1016/j.cardfail.2014.09.002
PG 7
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA AW4CP
UT WOS:000346229300006
PM 25225112
ER
PT J
AU Murthy, SB
Moradiya, Y
Shah, S
Naval, NS
AF Murthy, Santosh B.
Moradiya, Yogesh
Shah, Shreyansh
Naval, Neeraj S.
TI In-hospital outcomes of aneurysmal subarachnoid hemorrhage associated
with cocaine use in the USA
SO JOURNAL OF CLINICAL NEUROSCIENCE
LA English
DT Article
DE Cocaine use; Intracranial aneurysms; Nationwide Inpatient Sample;
Subarachnoid hemorrhage
ID VASOSPASM; ABUSE
AB Cocaine use is associated with higher mortality in small retrospective studies of brain-injured patients. We aimed to explore in-hospital outcomes in a large population based study of aneurysmal subarachnoid hemorrhage (aSAH) with cocaine use. aSAH patients were identified from the 2007-2010 USA Nationwide Inpatient Sample using International Classification of Disease, Ninth Revision codes. Demographics, comorbidities and surgical procedures were compared between cocaine users and non-users. The primary outcomes were in-hospital mortality and home discharge/self-care. Secondary outcomes were vasospasm treated with angioplasty, hydrocephalus, gastrostomy and tracheostomy. There were 103,876 patients with aSAH. The cocaine group were younger (45.8 +/- 9.8 versus 58.4 +/- 15.8, p < 0.001), predominantly male (53.3% versus 38.5%, p < 0.001) and had a higher proportion of black patients (36.9% versus 11.5%, p < 0.001). The incidence of seizures was higher among cocaine users (16.2% versus 11.1%, p < 0.001). Endovascular coiling of intracranial aneurysms (24% versus 18.5%, p < 0.001) was more frequent in cocaine users. The univariate analysis showed higher rates of in-hospital mortality and vasospasm treated with angioplasty, but lower home discharge in the cocaine group. In the multivariate analysis, the cocaine cohort had higher in-hospital mortality (odds ratio [OR] 1.43, 95% confidence interval [CI] 1.27-1.61, p < 0.001) and lower home discharge rates (OR 0.79, 95% CI 0.69-0.87, p < 0.001) after adjusting for confounders. Rates of vasospasm treated with angioplasty however were similar between the two groups. Cocaine use was found to be independently associated with poor outcomes, particularly higher mortality and lower home discharge rates. Cocaine use however, was not associated with vasospasm that required treatment with angioplasty. Prospective confirmation is warranted. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Murthy, Santosh B.; Moradiya, Yogesh; Naval, Neeraj S.] Johns Hopkins Univ, Sch Med, Div Neurosci Crit Care, Baltimore, MD 21287 USA.
[Shah, Shreyansh] NIH, Dept Vasc Neurol, Bethesda, MD 20892 USA.
RP Murthy, SB (reprint author), Johns Hopkins Univ, Sch Med, Div Neurosci Crit Care, 600 N Wolfe St,Phipps 455, Baltimore, MD 21287 USA.
EM santoshbmurthy@gmail.com
NR 18
TC 6
Z9 6
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0967-5868
EI 1532-2653
J9 J CLIN NEUROSCI
JI J. Clin. Neurosci.
PD DEC
PY 2014
VL 21
IS 12
BP 2088
EP 2091
DI 10.1016/j.jocn.2014.05.012
PG 4
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AX0DF
UT WOS:000346622900006
PM 24998859
ER
PT J
AU Kim, S
Yang, JY
Jung, ES
Lee, J
Heo, NJ
Lee, JW
Na, KY
Han, JS
AF Kim, Sejoong
Yang, Jin Young
Jung, Eun Sook
Lee, Jeonghwan
Heo, Nam Ju
Lee, Jae Wook
Na, Ki Young
Han, Jin Suk
TI Effects of Sodium Citrate on Salt Sensitivity and Kidney Injury in
Chronic Renal Failure
SO JOURNAL OF KOREAN MEDICAL SCIENCE
LA English
DT Article
DE Kidney Failure, Chronic; Citrates; Acidosis; Natriuresis
ID GLOMERULAR-FILTRATION-RATE; METABOLIC-ACIDOSIS; ESSENTIAL-HYPERTENSION;
ENDOTHELIN; DECLINE; TRANSPORTERS; PROGRESSION; RATS; GFR
AB Metabolic acidosis, which is observed in salt-sensitive hypertension, is also associated with kidney injury. Alkali therapy in chronic renal failure (CRF) may ameliorate the progression of kidney disease; however, few studies have examined the effects of alkali therapy on salt sensitivity and kidney injury in CRF. We randomly administered standard diet (SD), sodium chloride with 20% casein diet (NACL), or sodium citrate with 20% casein diet (NACT) to Sprague-Dawley rats after a CRF or a sham operation. Four weeks after 5/6 nephrectomy, serum bicarbonate levels were higher in the NACT-treated group. On the pressure-natriuresis curve, NACT-treated CRF rats were more salt-resistant than NACL-treated CRF rats. Additionally, the NACT-treated CRF group showed less tubulointerstitial damage than the NACL-treated CRF group. The expression and immunoreactivity of NHE3 in the kidney in the NACT-treated CRF group were lower than those in the NACL-treated CRF group. We observed that dietary NACT as alkali therapy in CRF might improve the altered salt-sensitivity and ameliorate the progression of kidney injury compared to the NACL diet, which may be related to reduced renal NHE3 expression.
C1 [Kim, Sejoong; Yang, Jin Young; Na, Ki Young] Seoul Natl Univ, Bundang Hosp, Dept Internal Med, Songnam, South Korea.
[Kim, Sejoong; Jung, Eun Sook; Heo, Nam Ju; Na, Ki Young; Han, Jin Suk] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 151, South Korea.
[Lee, Jeonghwan] Hallym Univ, Hangang Sacred Heart Hosp, Dept Internal Med, Seoul, South Korea.
[Heo, Nam Ju] Seoul Natl Univ Hosp, Dept Internal Med, Healthcare Syst Gangnam Ctr, Seoul 110744, South Korea.
[Lee, Jae Wook] NHLBI, Epithelial Syst Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Han, JS (reprint author), Seoul Natl Univ Hosp, Dept Internal Med, 103 Daehak Ro, Seoul 110744, South Korea.
EM jshan@snu.ac.kr
OI Lee, Jae Wook/0000-0003-0120-8164
FU Seoul National University Bundang Hospital Research Fund [03-2012-020];
National Research Foundation of Korea [2013R1A1A1012689]
FX This work was supported by grant from the Seoul National University
Bundang Hospital Research Fund (No. 03-2012-020) and grant (No.
2013R1A1A1012689) from the National Research Foundation of Korea.
NR 25
TC 1
Z9 2
U1 1
U2 7
PU KOREAN ACAD MEDICAL SCIENCES
PI SEOUL
PA 302 75 DONG DU ICHON, DONG YONGSAN KU, SEOUL 140 031, SOUTH KOREA
SN 1011-8934
EI 1598-6357
J9 J KOREAN MED SCI
JI J. Korean Med. Sci.
PD DEC
PY 2014
VL 29
IS 12
BP 1658
EP 1664
DI 10.3346/jkms.2014.29.12.1658
PG 7
WC Medicine, General & Internal
SC General & Internal Medicine
GA AW8JF
UT WOS:000346507200012
PM 25469066
ER
PT J
AU Yaniv, Y
Lyashkov, AE
Sirenko, S
Okamoto, Y
Guiriba, TR
Ziman, BD
Morrell, CH
Lakatta, EG
AF Yaniv, Yael
Lyashkov, Alexey E.
Sirenko, Syevda
Okamoto, Yosuke
Guiriba, Toni-Rose
Ziman, Bruce D.
Morrell, Christopher H.
Lakatta, Edward G.
TI Stochasticity intrinsic to coupled-clock mechanisms underlies
beat-to-beat variability of spontaneous action potential firing in
sinoatrial node pacemaker cells
SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
LA English
DT Article
DE Ca2+ cycling; Ion channels; Physiology; Sarcoplasmic reticulum;
Sinoatrial nodal pacemaker cells
ID HEART-RATE-VARIABILITY; RECTIFIER K+ CURRENT; CYCLOPIAZONIC ACID; RABBIT
SINOATRIAL; IVABRADINE; SYNCHRONIZATION; AUTOMATICITY; MODULATION;
KINETICS; CURRENTS
AB Recent evidence indicates that the spontaneous action potential (AP) of isolated sinoatrial node cells (SANCs) is regulated by a system of stochastic mechanisms embodied within two clocks: ryanodine receptors of the "Ca2+ clock" within the sarcoplasmic reticulum, spontaneously activate during diastole and discharge local Ca2+ releases (LCRs) beneath the cell surface membrane; clock crosstalk occurs as LCRs activate an inward Na+/Ca2+ exchanger current (I-NCX), which together with I-f and decay of K+ channels prompts the "M clock," the ensemble of sarcolemmal-electrogenic molecules, to generate APs. Prolongation of the average LCR period accompanies prolongation of the average AP beating interval (BI). Moreover, the prolongation of the average AP BI accompanies increased AP BI variability. We hypothesized that both the average AP Bland AP BI variability are dependent upon stochasticity of clock mechanisms reported by the variability of LCR period.
We perturbed the coupled-clock system by directly inhibiting the M clock by ivabradine (IVA) or the Ca2+ clock by cyclopiazonic acid (CPA). When either clock is perturbed by IVA (3, 10 and 30 mu M), which has no direct effect on Ca2+ cycling, or CPA (0.5 and 5 mu M), which has no direct effect on the M clock ion channels, the clock system failed to achieve the basal AP Bland both AP BI and AP BI variability increased. The changes in average LCR period and its variability in response to perturbations of the coupled-clock system were correlated with changes in AP beating interval and AP beating interval variability. We conclude that the stochasticity within the coupled-clock system affects and is affected by the AP BI firing rate and rhythm via modulation of the effectiveness of clock coupling. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Yaniv, Yael; Sirenko, Syevda; Okamoto, Yosuke; Guiriba, Toni-Rose; Ziman, Bruce D.; Morrell, Christopher H.; Lakatta, Edward G.] NIA, Lab Cardiovasc Sci, Biomed Res Ctr, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
[Yaniv, Yael] Technion Israel Inst Technol, Biomed Engn Fac, Haifa, Israel.
[Lyashkov, Alexey E.] NIA, Biomed Res Ctr, Translat Gerontol Branch, Intramural Res Program,NIH, Baltimore, MD 21224 USA.
[Morrell, Christopher H.] Loyola Univ, Dept Math & Stat, Baltimore, MD USA.
RP Yaniv, Y (reprint author), Technion Israel Inst Technol, Biomed Engn Fac, Haifa, Israel.
EM yaely@bm.technion.ac.il; lakattae@grc.nia.nih.gov
RI Yaniv, Yael/B-3311-2015
OI Yaniv, Yael/0000-0002-5183-6284
FU National Institute on Aging, National Institutes of Health; Technion
V.P.R. Fund -Krbling Biomedical Engineering Research Fund
FX The work was supported in part by the Intramural Research Program of the
National Institute on Aging, National Institutes of Health and by the
Technion V.P.R. Fund -Krbling Biomedical Engineering Research Fund
(Y.Y.).
NR 34
TC 9
Z9 9
U1 1
U2 15
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2828
EI 1095-8584
J9 J MOL CELL CARDIOL
JI J. Mol. Cell. Cardiol.
PD DEC
PY 2014
VL 77
BP 1
EP 10
DI 10.1016/j.yjmcc.2014.09.008
PG 10
WC Cardiac & Cardiovascular Systems; Cell Biology
SC Cardiovascular System & Cardiology; Cell Biology
GA AW7QQ
UT WOS:000346460100001
PM 25257916
ER
PT J
AU Meulendyke, KA
Queen, SE
Engle, EL
Shirk, EN
Liu, JY
Steiner, JP
Nath, A
Tarwater, PM
Graham, DR
Mankowski, JL
Zink, MC
AF Meulendyke, Kelly A.
Queen, Suzanne E.
Engle, Elizabeth L.
Shirk, Erin N.
Liu, Jiayang
Steiner, Joseph P.
Nath, Avindra
Tarwater, Patrick M.
Graham, David R.
Mankowski, Joseph L.
Zink, M. Christine
TI Combination fluconazole/paroxetine treatment is neuroprotective despite
ongoing neuroinflammation and viral replication in an SIV model of HIV
neurological disease
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Article
DE HIV; SIV; Fluconazole; Paroxetine; Selective serotonin reuptake
inhibitor; CNS
ID CENTRAL-NERVOUS-SYSTEM; IMMUNODEFICIENCY VIRUS ENCEPHALITIS;
BETA-AMYLOID PRECURSOR; NEUROCOGNITIVE DISORDERS; CEREBROSPINAL-FLUID;
OXIDATIVE STRESS; NEUROFILAMENT PROTEIN; NEURONAL PLASTICITY; BEHAVIORAL
DEFICITS; MACAQUE MODEL
AB Effective combined antiretroviral therapy (cART) in HIV-infected patients has made HIV a treatable infection; however, debilitating HIV-associated neurocognitive disorders (HAND) can still affect approximately 50 % of HIV-infected individuals even under cART. While cART has greatly reduced the prevalence of the most severe form of HAND, milder forms have increased in prevalence, leaving the total proportion of HIV-infected individuals suffering from HAND relatively unchanged. In this study, an in vitro drug screen identified fluconazole and paroxetine as protective compounds against HIV gp120 and Tat neurotoxicity. Using an accelerated, consistent SIV/macaque model of HIV-associated CNS disease, we tested the in vivo neuroprotective capabilities of combination fluconazole/paroxetine (FluPar) treatment. FluPar treatment protected macaques from SIV-induced neurodegeneration, as measured by neurofilament light chain in the CSF, APP accumulation in axons, and CaMKII alpha in the frontal cortex, but did not significantly reduce markers of neuroinflammation or plasma or CNS viral loads. Since HIV and SIV neurodegeneration is often attributed to accompanying neuroinflammation, this study provides proof of concept that neuroprotection can be achieved even in the face of ongoing neuroinflammation and viral replication.
C1 [Meulendyke, Kelly A.; Queen, Suzanne E.; Engle, Elizabeth L.; Shirk, Erin N.; Graham, David R.; Mankowski, Joseph L.; Zink, M. Christine] Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, Baltimore, MD 21205 USA.
[Liu, Jiayang; Tarwater, Patrick M.] Texas Tech Univ, Hlth Sci Ctr, Foster Sch Med, Dept Biostat & Epidemiol, El Paso, TX USA.
[Steiner, Joseph P.] NINDS, Translat Neurosci Ctr, NIH, Bethesda, MD 20892 USA.
[Nath, Avindra] NINDS, Sect Infect Nervous Syst, NIH, Bethesda, MD 20892 USA.
RP Zink, MC (reprint author), Johns Hopkins Univ, Sch Med, Dept Mol & Comparat Pathobiol, 733 North Broadway St,MRB 819, Baltimore, MD 21205 USA.
EM mczink@jhmi.edu
FU National Institutes of Health [P30 MH075673, R01 MH087233, R01 MH085554,
P01 MH070306, P40 OD013117]
FX These studies were funded by the National Institutes of Health (grants
P30 MH075673, R01 MH087233, R01 MH085554, P01 MH070306, and P40
OD013117).
NR 60
TC 5
Z9 5
U1 0
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD DEC
PY 2014
VL 20
IS 6
BP 591
EP 602
DI 10.1007/s13365-014-0283-1
PG 12
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA AW4FX
UT WOS:000346237700005
PM 25227932
ER
PT J
AU Sacktor, N
Miyahara, S
Evans, S
Schifitto, G
Cohen, B
Haughey, N
Drewes, JL
Graham, D
Zink, MC
Anderson, C
Nath, A
Pardo, CA
McCarthy, S
Hosey, L
Clifford, D
AF Sacktor, Ned
Miyahara, Sachiko
Evans, Scott
Schifitto, Giovanni
Cohen, Bruce
Haughey, Norman
Drewes, Julia L.
Graham, David
Zink, M. Christine
Anderson, Caroline
Nath, Avindra
Pardo, Carlos A.
McCarthy, Sean
Hosey, Lara
Clifford, David
CA ACTG A5235 Team
TI Impact of minocycline on cerebrospinal fluid markers of oxidative
stress, neuronal injury, and inflammation in HIV-seropositive
individuals with cognitive impairment
SO JOURNAL OF NEUROVIROLOGY
LA English
DT Article
DE Minocycline; HIV; Cognitive; Oxidative; Stress; Biomarker
ID NERVOUS-SYSTEM; DEMENTIA; CERAMIDE; METABOLISM; INFECTION; TRIAL; BRAIN
AB Elevated cerebrospinal fluid (CSF) levels of markers of oxidative stress, neuronal injury, and inflammation and decreased neurotransmitter levels have been reported in HIV-associated neurocognitive disorders (HAND). Minocycline may have a neuroprotective effect by inhibiting inducible nitric oxide synthase, which produces nitric oxide, a compound that induces oxygen free radical production. In A5235, "Phase II, Randomized, Placebo-Controlled, Double-Blind Study of Minocycline in the Treatment of HIV-Associated Cognitive Impairment," minocycline was not associated with cognitive improvement, but the effect on the above CSF measures was not examined previously. The objective of this study was to examine the effect of minocycline on markers of oxidative stress, neuronal injury, neurotransmitter levels, and inflammation from CSF in participants in A5235. One hundred seven HIV+ individuals received either minocycline 100 mg or placebo orally every 12 h for 24 weeks. Twenty-one HIV+ individuals received the optional lumbar punctures. Lipid and protein markers of oxidative stress (e.g., ceramides and protein carbonyls), glutamate, neurotransmitter precursors, kynurenine metabolites, neurofilament heavy chain, and inflammatory cytokines were measured in the CSF before and after treatment. The 24-week change in ceramides was larger in a beneficial direction in the minocycline group compared to the placebo group. The two groups did not differ in the 24-week changes for other markers.
These results suggest that minocycline may decrease lipid markers of oxidative stress (ceramides) in individuals with HAND; however, an effect of minocycline on other CSF markers was not observed. A larger sample size is needed to further validate these results.
C1 [Sacktor, Ned; Haughey, Norman; Drewes, Julia L.; Graham, David; Zink, M. Christine; Pardo, Carlos A.] Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA.
[Miyahara, Sachiko; Evans, Scott] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Schifitto, Giovanni] Univ Rochester, Rochester, NY USA.
[Cohen, Bruce] Northwestern Univ, Chicago, IL 60611 USA.
[Anderson, Caroline; Nath, Avindra] NIH, Bethesda, MD 20892 USA.
[McCarthy, Sean; Hosey, Lara] AIDS Clin Trials Grp ACTG Operat Ctr, Silver Spring, MD USA.
[Clifford, David] Washington Univ, St Louis, MO USA.
RP Sacktor, N (reprint author), Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA.
EM sacktor@jhmi.edu
FU AIDS Clinical Trials Group (ACTG) - NIAID [AI38858, AI38855, AI27670,
AI27668, AI27658, AI34853, AI127660, AI27664, AI27659, AI25903, AI25915,
AI046376, AI46370, AI46381, AI50410, AI25868, AI46386, CFAR AI 127757];
AIDS Clinical Trials Group (ACTG) - Neurologic AIDS Research Consortium
[NS32228, NS081196, NS055628, MH075673, MH64409, AI 068634]; GCRC Units
- National Center for Research Resources (NCRR) [RR00052, RR00044,
RR00046]; University of California, San Diego Antiviral Research CTU
[AI069432]; Johns Hopkins University CTU [AI069465]; CTSA [UL1
RR025005]; UCLA School of Medicine CTU [AI069424]; Washington University
(St. Louis) CTU [AI069495]; Research & Education Group-Portland CRS CTU
[AI069503]; Henry Ford Hospital CRS CTU [AI069503]; Massachusetts
General Hospital CTU [AI069472]; NYU/NYC HHC at Bellevue CTU [AI069532];
Univ. of Colorado Hospital CTU [AI069450]; Northwestern University CTU
[AI069471]; Virginia Commonwealth University Medical Center CRS CTU
[AI069503]; University of Washington (Seattle) CTU [AI069434];
University of North Carolina CTU [AI069423]; University of Rochester
Medical Center CTU [AI069511]; Emory University, The Ponce de Leon
Center CTU [AI069452]; University of Pennsylvania, Philadelphia CTU
[AI069467-04]; National Institute of Allergy and Infectious Diseases,
National Institute of Mental Health (NIMH) [AI068636]; National
Institute of Dental and Craniofacial Research (NIDCR)
FX The authors would like to thank Marie Sonderman for administrative
support. The statistical analysis was carried out by S. Miyahara. This
study was supported in part by the AIDS Clinical Trials Group (ACTG)
funded by the following: NIAID, AI38858, AI38855, AI27670, AI27668,
AI27658, AI34853, AI127660, AI27664, AI27659, AI25903, AI25915,
AI046376, AI46370, AI46381, AI50410, AI25868, AI46386, CFAR AI 127757,
the Neurologic AIDS Research Consortium, NS32228, NS081196, NS055628,
MH075673, MH64409, AI 068634 and GCRC Units funded by the National
Center for Research Resources (NCRR), RR00052, RR00044, RR00046. The NCT
number for this study is NCT 00361257. This study is registered in
Clinical Trials.gov. Participating site ACTG Clinical Trials Unit (CTU)
grant numbers include the following:; University of California, San
Diego Antiviral Research CTU Grant AI069432; Johns Hopkins University
CTU Grant AI069465; CTSA Grant UL1 RR025005; UCLA School of Medicine CTU
Grant AI069424; Washington University (St. Louis) CTU Grant AI069495;
The Research & Education Group-Portland CRS CTU Grant AI069503; Henry
Ford Hospital CRS CTU Grant AI069503; Massachusetts General Hospital CTU
Grant AI069472; NYU/NYC HHC at Bellevue CTU Grant AI069532; Univ. of
Colorado Hospital CTU Grant AI069450; Northwestern University CTU Grant
AI069471; Virginia Commonwealth University Medical Center CRS CTU Grant
AI069503; University of Washington (Seattle) CTU Grant AI069434;
University of North Carolina CTU Grant AI069423; University of Rochester
Medical Center CTU Grant AI069511; Emory University, The Ponce de Leon
Center CTU Grant AI069452; and University of Pennsylvania, Philadelphia
CTU Grant AI069467-04.; The project described was supported by Award
Number AI068636 from the National Institute of Allergy and Infectious
Diseases, National Institute of Mental Health (NIMH), and National
Institute of Dental and Craniofacial Research (NIDCR). The content is
solely the responsibility of the authors and does not necessarily
represent the official views of the National Institute of Allergy and
Infectious Diseases or the National Institutes of Health.
NR 22
TC 8
Z9 8
U1 0
U2 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1355-0284
EI 1538-2443
J9 J NEUROVIROL
JI J. Neurovirol.
PD DEC
PY 2014
VL 20
IS 6
BP 620
EP 626
DI 10.1007/s13365-014-0292-0
PG 7
WC Neurosciences; Virology
SC Neurosciences & Neurology; Virology
GA AW4FX
UT WOS:000346237700008
PM 25377444
ER
PT J
AU Ward, RE
Boudreau, RM
Caserotti, P
Harris, TB
Zivkovic, S
Goodpaster, BH
Satterfield, S
Kritchevsky, SB
Schwartz, AV
Vinik, AI
Cauley, JA
Simonsick, EM
Newman, AB
Strotmeyer, ES
AF Ward, Rachel E.
Boudreau, Robert M.
Caserotti, Paolo
Harris, Tamara B.
Zivkovic, Sasa
Goodpaster, Bret H.
Satterfield, Suzanne
Kritchevsky, Stephen B.
Schwartz, Ann V.
Vinik, Aaron I.
Cauley, Jane A.
Simonsick, Eleanor M.
Newman, Anne B.
Strotmeyer, Elsa S.
CA Hlth Aging Body Composition Study
TI Sensory and Motor Peripheral Nerve Function and Incident Mobility
Disability
SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY
LA English
DT Article
DE peripheral nerve function; disability; older adults; longitudinal
analysis; muscle strength
ID MUSCLE STRENGTH; OLDER-ADULTS; BODY-COMPOSITION; PHYSICAL PERFORMANCE;
DIABETIC-NEUROPATHY; WOMENS HEALTH; AGE; CONDUCTION; BLACK; DEGENERATION
AB ObjectivesTo assess the relationship between sensorimotor nerve function and incident mobility disability over 10years.
DesignProspective cohort study with longitudinal analysis.
SettingTwo U.S. clinical sites.
ParticipantsPopulation-based sample of community-dwelling older adults with no mobility disability at 2000/01 examination (N=1,680; mean age SD 76.52.9, body mass index 27.14.6; 50.2% female, 36.6% black, 10.7% with diabetes mellitus).
MeasurementsMotor nerve conduction amplitude (poor <1 mV) and velocity (poor <40m/s) were measured on the deep peroneal nerve. Sensory nerve function was measured using 10- and 1.4-g monofilaments and vibration detection threshold at the toe. Lower extremity symptoms included numbness or tingling and aching or burning pain. Incident mobility disability assessed semiannually over 8.5years (interquartile range 4.5-9.6years) was defined as two consecutive self-reports of a lot of difficulty or inability to walk one-quarter of a mile or climb 10 steps.
ResultsNerve impairments were detected in 55% of participants, and 30% developed mobility disability. Worse motor amplitude (HR=1.29 per SD, 95% CI=1.16-1.44), vibration detection threshold (HR=1.13 per SD, 95% CI=1.04-1.23), symptoms (HR=1.65, 95% CI=1.26-2.17), two motor impairments (HR=2.10, 95% CI=1.43-3.09), two sensory impairments (HR=1.91, 95% CI=1.37-2.68), and three or more nerve impairments (HR=2.33, 95% CI=1.54-3.53) predicted incident mobility disability after adjustment. Quadriceps strength mediated relationships between certain nerve impairments and mobility disability, although most remained significant.
ConclusionPoor sensorimotor nerve function independently predicted mobility disability. Future work should investigate modifiable risk factors and interventions such as strength training for preventing disability and improving function in older adults with poor nerve function.
C1 [Ward, Rachel E.] Spaulding Rehabil Hosp, Cambridge, England.
[Ward, Rachel E.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Boudreau, Robert M.; Cauley, Jane A.; Newman, Anne B.; Strotmeyer, Elsa S.] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Epidemiol, Pittsburgh, PA 15213 USA.
[Caserotti, Paolo] Univ Southern Denmark, Inst Sports Sci & Clin Biomech, Odense, Denmark.
[Harris, Tamara B.] NIA, Lab Epidemiol Biometry & Demog, NIH, Bethesda, MD USA.
[Zivkovic, Sasa] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA.
[Zivkovic, Sasa] Vet Affairs Pittsburgh Hlth Care Syst, Pittsburgh, PA USA.
[Goodpaster, Bret H.] Univ Pittsburgh, Sch Med, Dept Med, Pittsburgh, PA 15213 USA.
[Satterfield, Suzanne] Univ Tennessee, Dept Prevent Med, Memphis, TN USA.
[Kritchevsky, Stephen B.] Wake Forest, Div Gerontol & Geriatr Med, Dept Internal Med, Winston Salem, NC USA.
[Schwartz, Ann V.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Vinik, Aaron I.] Eastern Virginia Med Sch, Dept Neurobiol, Norfolk, VA 23501 USA.
[Simonsick, Eleanor M.] NIA, Translat Gerontol Branch, NIH, Baltimore, MD 21224 USA.
RP Strotmeyer, ES (reprint author), Univ Pittsburgh, Dept Epidemiol, 130 N Bellefield Ave,Rm 515, Pittsburgh, PA 15213 USA.
EM StrotmeyerE@edc.pitt.edu
RI Cauley, Jane/N-4836-2015; Newman, Anne B./C-6408-2013;
OI Cauley, Jane/0000-0003-0752-4408; Newman, Anne B./0000-0002-0106-1150;
Strotmeyer, Elsa/0000-0002-4093-6036; Boudreau,
Robert/0000-0003-0162-5187
FU National Institute on Aging [N01-AG-6-2101, N01-AG-6-2103,
N01-AG-6-2106, 1-R01-AG 028050]; National Institute of Nursing Research
Grant [R01-NR012459]; Intramural Research Program of the National
Institutes of Health, National Institute on Aging; University of
Pittsburgh Claude D. Pepper Older Americans Independence Center
[P30-AG024827]; American Diabetes Association [1-04-JF-46]
FX This research was supported by National Institute on Aging Contracts
N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106 and Grant 1-R01-AG
028050 (to ESS) and National Institute of Nursing Research Grant
R01-NR012459 and supported in part by the Intramural Research Program of
the National Institutes of Health, National Institute on Aging, the
University of Pittsburgh Claude D. Pepper Older Americans Independence
Center (P30-AG024827) Pilot Grant (to ESS), and the American Diabetes
Association (1-04-JF-46 to ESS).
NR 33
TC 10
Z9 10
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0002-8614
EI 1532-5415
J9 J AM GERIATR SOC
JI J. Am. Geriatr. Soc.
PD DEC
PY 2014
VL 62
IS 12
BP 2273
EP 2279
DI 10.1111/jgs.13152
PG 7
WC Geriatrics & Gerontology; Gerontology
SC Geriatrics & Gerontology
GA AW8FX
UT WOS:000346497600005
PM 25482096
ER
PT J
AU Wang, WD
Qiu, LR
Howard, A
Solis, N
Li, CL
Wang, XX
Kopp, JB
Levi, M
AF Wang, Weidong
Qiu, Liru
Howard, Allison
Solis, Nathaniel
Li, Chunling
Wang, Xiaoxin
Kopp, Jeffrey B.
Levi, Moshe
TI Protective effects of aliskiren and valsartan in mice with diabetic
nephropathy
SO JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
LA English
DT Article
DE Albuminuria; renin inhibition; lipid metabolism; ER stress; diabetic
nephropathy
ID RENIN-ANGIOTENSIN SYSTEM; RENAL LIPID-METABOLISM;
ENDOPLASMIC-RETICULUM-STRESS; CARDIORENAL END-POINTS; MESANGIAL CELLS;
KIDNEY-DISEASE; ALDOSTERONE SYSTEM; GLUCOSE-METABOLISM;
INSULIN-RESISTANCE; ACE-INHIBITION
AB Aim: We investigated whether aliskiren, a direct renin inhibitor, provided protection in a model of diabetic nephropathy in mice and compared its protective effects to valsartan, an angiotensin II type 1 receptor blocker.
Materials and methods: Hyperglycemia was induced with streptozotocin (STZ, 40 mg/kg/day x 5 days) injection in DBA/2J mice fed on a high fat diet. Mice were treated with either aliskiren (25 mg/kg/day) or valsartan (8 mg/kg/day) for 6 weeks.
Results: Aliskiren and/or valsartan treatment significantly attenuated albuminuria, urinary nephrin excretion and glomerulosclerosis. Aliskiren and/or valsartan prevented reduction of podocin and WT1 protein abundance in diabetic mice. Aliskiren and/or valsartan significantly prevented increased expression of profibrotic growth factors (TGF, CTGF and PAI-1), proinflammatory cytokines (MCP-1, TNF and IL-1), endoplasmic reticulum (ER) stress markers (CHOP and XBP-1) and lipid accumulation in the kidney of diabetic animals. Aliskiren showed similar efficacy compared to valsartan therapy and dual treatment in some aspects has synergistic protective effects.
Conclusion: Our study indicates that aliskiren and/or valsartan protects against diabetic kidney disease through multiple mechanisms, including decreasing podocyte injury, activation of profibrotic growth factors and proinflammatory cytokines, ER stress and accumulation of lipids.
C1 [Wang, Weidong; Qiu, Liru; Howard, Allison; Solis, Nathaniel; Wang, Xiaoxin; Levi, Moshe] Univ Colorado, Dept Med, Div Renal Dis & Hypertens, Boulder, CO 80309 USA.
[Wang, Weidong; Li, Chunling] Sun Yat Sen Univ, Zhongshan Sch Med, Inst Hypertens & Kidney Res, Guangzhou 510080, Guangdong, Peoples R China.
[Kopp, Jeffrey B.] NIDDK, Kidney Dis Sect, NIH, Bethesda, MD 20892 USA.
RP Wang, WD (reprint author), Sun Yat Sen Univ, Zhongshan Sch Med, Inst Hypertens & Kidney Res, 74 Zhongshan Er Rd, Guangzhou 510080, Guangdong, Peoples R China.
EM wangwd6@mail.sysu.edu.cn
OI Kopp, Jeffrey/0000-0001-9052-186X
FU Novartis Medical School IISS; NIH [R01 AG026529]; Novartis grants;
Natural Science Foundation of China [81370822]; Guangdong Nature Science
Foundation [S2013010015499]
FX This work was supported by grants from Grants from Novartis Medical
School IISS and NIH R01 AG026529. WW was supported by Novartis grants.
This work was also supported by the Natural Science Foundation of China
(Grant No. 81370822) and Guangdong Nature Science Foundation (Grant No.
S2013010015499).
NR 54
TC 13
Z9 14
U1 3
U2 6
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1470-3203
EI 1752-8976
J9 J RENIN-ANGIO-ALDO S
JI J. Renin-Angiotensin-Aldosterone Syst.
PD DEC
PY 2014
VL 15
IS 4
BP 384
EP 395
DI 10.1177/1470320313507123
PG 12
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA AW4SA
UT WOS:000346269600007
PM 25031296
ER
PT J
AU Blumenfeld, YJ
Momirova, V
Rouse, DJ
Caritis, SN
Sciscione, A
Peaceman, AM
Reddy, UM
Varner, MW
Malone, FD
Iams, JD
Mercer, BM
Thorp, JM
Sorokin, Y
Carpenter, MW
Lo, J
Ramin, SM
Harper, M
AF Blumenfeld, Yair J.
Momirova, Valerija
Rouse, Dwight J.
Caritis, Steve N.
Sciscione, Anthony
Peaceman, Alan M.
Reddy, Uma M.
Varner, Michael W.
Malone, Fergal D.
Iams, Jay D.
Mercer, Brian M.
Thorp, John M., Jr.
Sorokin, Yoram
Carpenter, Marshall W.
Lo, Julie
Ramin, Susan M.
Harper, Margaret
CA Eunice Kennedy Shriver Natl Inst
TI Accuracy of Sonographic Chorionicity Classification in Twin Gestations
SO JOURNAL OF ULTRASOUND IN MEDICINE
LA English
DT Article
DE accuracy; chorionicity; obstetric ultrasound; sonography; twins
ID PREGNANT-WOMEN; AMNIONICITY; PREDICTION; STILLBIRTH; ULTRASOUND;
DIAGNOSIS; COHORT; RISK
AB Objectives-To evaluate the accuracy of sonographic classification of chorionicity in a large cohort of twins and investigate which factors maybe associated with sonographic accuracy.
Methods-We conducted a secondary analysis of a randomized trial of preterm birth prevention in twins. Sonographic classification of chorionicity was compared with pathologic examination of the placenta. Maternal (age, body mass index, diabetes, and hypertension), obstetric (prior cesarean delivery, gestational age at the first sonographic examination, and antepartum bleeding), and sonographic (oligohydramnios, polyhydramnios, and twin-twin transfusion syndrome) factors were assessed for their possible association with accuracy.
Results-A total of 545 twin sets in which chorionicity was classified by sonography before 20 weeks' gestation were included; 455 were dichorionic and 90 were monochorionic based on pathologic examination. Sonography misclassified 35 of 545 twin pregnancies (6.4%): 18 of 455 dichorionic twins (4.0%) and 17 of 90 monochorionic twins (19.0%). The sensitivity and specificity of sonographic diagnosis of monochorionicity were 81.1% and 96.0%, respectively. In a multivariable analysis, pregnancies with initial sonographic examinations before 14 weeks' gestation were less likely to have misclassified chorionicity than those with sonographic examinations at 15 to 20 weeks (odds ratio [On 0.47; 95% confidence interval [CI], 0.23-0.96). For each week increase in gestational age, the odds of misclassification rose by 10% (OR, 1.10; 95% CI, 1.01-1.2). In the multivariable analysis, maternal age, body mass index, parity, and prior cesarean delivery were not associated with sonographic accuracy.
Conclusions-Sonography before 20 weeks incorrectly classified chorionicity in 6.4% of twin gestations. Those with first sonographic examinations performed at earlier gestational ages had improved chorionicity diagnosis.
C1 [Blumenfeld, Yair J.] Stanford Univ, Sch Med, Dept Obstet & Gynecol, Stanford, CA 94305 USA.
[Momirova, Valerija] George Washington Univ, Ctr Biostat, Washington, DC USA.
[Rouse, Dwight J.] Univ Alabama Birmingham, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
[Caritis, Steve N.] Univ Pittsburgh, Pittsburgh, PA USA.
[Sciscione, Anthony] Drexel Univ, Philadelphia, PA 19104 USA.
[Peaceman, Alan M.] Northwestern Univ, Chicago, IL 60611 USA.
[Reddy, Uma M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Varner, Michael W.] Univ Utah, Salt Lake City, UT USA.
[Malone, Fergal D.] Columbia Univ, New York, NY USA.
[Iams, Jay D.] Ohio State Univ, Columbus, OH 43210 USA.
[Mercer, Brian M.] Case Western Reserve Univ, Metrohlth Med Ctr, Cleveland, OH USA.
[Thorp, John M., Jr.] Univ N Carolina, Chapel Hill, NC USA.
[Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
[Carpenter, Marshall W.] Brown Univ, Providence, RI 02912 USA.
[Lo, Julie] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Ramin, Susan M.] Univ Texas Hlth Sci Ctr Houston, Houston, TX 77030 USA.
[Harper, Margaret] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
RP Blumenfeld, YJ (reprint author), Stanford Univ, Sch Med, Dept Obstet & Gynecol, Div Maternal Fetal Med, 300 Pasteur Dr,Room HH333, Stanford, CA 94305 USA.
EM yairb@stanford.edu
RI Varner, Michael/K-9890-2013
OI Varner, Michael/0000-0001-9455-3973
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development (NICHD) [HD27869, HD21410, HD40512, HD34136, HD34208,
HD40485, HD27915, HD40544, HD40560, HD27917, HD40500, HD34116, HD40545,
HD27860, HD36801]; National Center for Research Resources [M01 RR00080,
UL1 RR024989]
FX We thank the following subcommittee members who participated in protocol
development and coordination between clinical research centers (Margaret
Cotroneo, RN, and Allison T. Northen, MSN, RN), protocol/data management
and statistical analysis (Elizabeth Thom, PhD), and protocol development
and oversight (Catherine Y. Spong, MD). This project was supported by
grants from the Eunice Kennedy Shriver National Institute of Child
Health and Human Development (NICHD; HD27869, HD21410, HD40512, HD34136,
HD34208, HD40485, HD27915, HD40544, HD40560, HD27917, HD40500, HD34116,
HD40545, HD27860, and HD36801) and the National Center for Research
Resources (M01 RR00080 and UL1 RR024989); its contents do not
necessarily represent the official view of the NICHD, National Heart,
Lung, and Blood Institute, National Center for Research Resources, or
National Institutes of Health. Source of the study: NICHD Maternal-Fetal
Medicine Units Network Trial of Progesterone in Twins and Triplets to
Prevent Preterm Birth study (clinicaltrials.gov number NCT00099164). The
study was presented at the 2013 American Institute of Ultrasound in
Medicine Annual Convention; April 6-10, 2013; New York, New York.
NR 20
TC 8
Z9 8
U1 0
U2 2
PU AMER INST ULTRASOUND MEDICINE
PI LAUREL
PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906
USA
SN 0278-4297
EI 1550-9613
J9 J ULTRAS MED
JI J. Ultrasound Med.
PD DEC
PY 2014
VL 33
IS 12
BP 2187
EP 2192
DI 10.7863/ultra.33.12.2187
PG 6
WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging
GA AW4DY
UT WOS:000346232600017
PM 25425377
ER
PT J
AU Eudy, AM
Vines, AI
Dooley, MA
Cooper, GS
Parks, CG
AF Eudy, A. M.
Vines, A. I.
Dooley, M. A.
Cooper, G. S.
Parks, C. G.
TI Elevated C-reactive protein and self-reported disease activity in
systemic lupus erythematosus
SO LUPUS
LA English
DT Article
DE Systemic lupus erythematosus; C-reactive protein; flares; socioeconomic
factors
ID ERYTHROCYTE SEDIMENTATION-RATE; SOUTHEASTERN UNITED-STATES;
RHEUMATOID-ARTHRITIS; ACTIVITY QUESTIONNAIRE; SOCIOECONOMIC-STATUS;
REVISED CRITERIA; HEALTH; DAMAGE; VALIDATION; AMERICAN
AB C-reactive protein (CRP), a biomarker of inflammation, has been associated with increased disease activity in rheumatoid arthritis. However, the association in systemic lupus erythematosus (SLE) remains unclear. We examined the association of CRP with self-reported disease activity in the Carolina Lupus Study and described differences by sociodemographic characteristics. The study included baseline and three-year follow-up data on 107 African-American and 69 Caucasian SLE patients enrolled at a median 13 months since diagnosis. Models estimated prevalence differences in the association of baseline CRP with self-reported flares, adjusting for age, sex, race and education. Active disease or flare was reported by 59% at baseline and 58% at follow-up. Higher CRP (> 10 mu g/ml vs. <3 mu g/ml) was associated with a 17% (95% confidence interval (CI): -20, 53%) higher prevalence of flare at baseline and a 26% (95% CI: -9, 62%) higher prevalence of flare at follow-up. These CRP-flare associations were notably stronger in patients with lower education at baseline and in African-Americans at follow-up. These findings suggest that CRP may be a useful marker in studies of SLE health disparities.
C1 [Eudy, A. M.; Vines, A. I.] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27599 USA.
[Dooley, M. A.] Univ N Carolina, Chapel Hill, NC 27599 USA.
[Cooper, G. S.] US EPA, Natl Ctr Environm Assessment, Washington, DC 20460 USA.
[Parks, C. G.] NIEHS, Epidemiol Branch, NIH, DHHS, Durham, NC USA.
RP Eudy, AM (reprint author), Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Campus Box 7435, Chapel Hill, NC 27599 USA.
EM aeudy@email.unc.edu
OI Eudy, Amanda/0000-0002-3107-5545; Parks, Christine/0000-0002-5734-3456
FU Intramural Research Program of the NIEHS; National Center for Minority
Health and Health Disparities of the NIH
FX This work was supported by the Intramural Research Program of the NIEHS
and the National Center for Minority Health and Health Disparities of
the NIH.
NR 36
TC 3
Z9 3
U1 1
U2 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0961-2033
EI 1477-0962
J9 LUPUS
JI Lupus
PD DEC
PY 2014
VL 23
IS 14
BP 1460
EP 1467
DI 10.1177/0961203314543915
PG 8
WC Rheumatology
SC Rheumatology
GA AW3HK
UT WOS:000346177000003
PM 25057037
ER
PT J
AU Lee, M
Dworkin, AM
Lichtenberg, J
Patel, SJ
Trivedi, NS
Gildea, D
Bodine, DM
Crawford, NPS
AF Lee, Minnkyong
Dworkin, Amy M.
Lichtenberg, Jens
Patel, Shashank J.
Trivedi, Niraj S.
Gildea, Derek
Bodine, David M.
Crawford, Nigel P. S.
TI Metastasis-Associated Protein Ribosomal RNA Processing 1 Homolog B
(RRP1B) Modulates Metastasis through Regulation of Histone Methylation
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID ZINC-FINGER PROTEINS; BREAST-CANCER; TRANSCRIPTIONAL REPRESSION; C-MYC;
GENOME; EXPRESSION; SIGNATURE; INTERACTS; SURVIVAL; DATABASE
AB Overexpression of ribosomal RNA processing 1 homolog B (RRP1B) induces a transcriptional profile that accurately predicts patient outcome in breast cancer. However, the mechanism by which RRP1B modulates transcription is unclear. Here, the chromatin-binding properties of RRP1B were examined to define how it regulates metastasis-associated transcription. To identify genome-wide RRP1B-binding sites, high-throughput ChIP-seq was performed in the human breast cancer cell line MDA-MB-231 and HeLa cells using antibodies against endogenous RRP1B. Global changes in repressive marks such as histone H3 lysine 9 trimethylation (H3K9me3) were also examined by ChIP-seq. Analysis of these samples identified 339 binding regions in MDA-MB-231 cells and 689 RRP1B-binding regions in HeLa cells. Among these, 136 regions were common to both cell lines. Gene expression analyses of these RRP1B-binding regions revealed that transcriptional repression is the primary result of RRP1B binding to chromatin. ChIP-reChIP assays demonstrated that RRP1B co-occupies loci with decreased gene expression with the heterochromatin-associated proteins, tripartite motif-containing protein 28 (TRIM28/KAP1), and heterochromatin protein 1-alpha (CBX5/HP1 alpha). RRP1B occupancy at these loci was also associated with higher H3K9me3 levels, indicative of heterochromatinization mediated by the TRIM28/HP1 alpha complex. In addition, RRP1B upregulation, which is associated with metastasis suppression, induced globalchanges in histone methylation. (C) 2014 AACR.
C1 [Lee, Minnkyong; Dworkin, Amy M.; Lichtenberg, Jens; Patel, Shashank J.; Bodine, David M.; Crawford, Nigel P. S.] NHGRI, Genet & Mol Biol Branch, NIH, Bethesda, MD 20892 USA.
[Trivedi, Niraj S.; Gildea, Derek] NHGRI, Genome Technol Branch, NIH, Bethesda, MD 20892 USA.
RP Crawford, NPS (reprint author), NHGRI, NIH, 50 South Dr Rm 5154, Bethesda, MD 20892 USA.
EM crawforn@mail.nih.gov
FU Intramural Research Program of the National Human Genome Research
Institute, NIH
FX This work was supported by the Intramural Research Program of the
National Human Genome Research Institute, NIH.
NR 37
TC 5
Z9 5
U1 0
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
EI 1557-3125
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD DEC
PY 2014
VL 12
IS 12
BP 1818
EP 1828
DI 10.1158/1541-7786.MCR-14-0167
PG 11
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA AW9EN
UT WOS:000346560400011
PM 25092915
ER
PT J
AU Johnson, IRD
Parkinson-Lawrence, EJ
Shandala, T
Weigert, R
Butler, LM
Brooks, DA
AF Johnson, Ian R. D.
Parkinson-Lawrence, Emma J.
Shandala, Tetyana
Weigert, Roberto
Butler, Lisa M.
Brooks, Doug A.
TI Altered Endosome Biogenesis in Prostate Cancer Has Biomarker Potential
SO MOLECULAR CANCER RESEARCH
LA English
DT Article
ID CATHEPSIN-B; CELL-LINES; ACID-PHOSPHATASE; ADAPTER PROTEIN; RAB
PROTEINS; TRAFFICKING; PROGRESSION; STATISTICS; MORPHOLOGY; SECRETION
AB Prostate cancer is the second most common form of cancer in males, affecting one in eight men by the time they reach the age of 70 years. Current diagnostic tests for prostate cancer have significant problems with both false negatives and false positives, necessitating the search for new molecular markers. A recent investigation of endosomal and lysosomal proteins revealed that the critical process of endosomal biogenesis might be altered in prostate cancer. Here, a panel of endosomal markers was evaluated in prostate cancer and nonmalignant cells and a significant increase in gene and protein expression was found for early, but not late endosomal proteins. There was also a differential distribution of early endosomes, and altered endosomal traffic and signaling of the transferrin receptors (TFRC and TFR2) in prostate cancer cells. These findings support the concept that endosome biogenesis and function are altered in prostate cancer. Microarray analysis of a clinical cohort confirmed the altered endosomal gene expression observed in cultured prostate cancer cells. Furthermore, in prostate cancer patient tissue specimens, the early endosomal marker and adaptor protein APPL1 showed consistently altered basement membrane histology in the vicinity of tumors and concentrated staining within tumor masses. These novel observations on altered early endosome biogenesis provide a new avenue for prostate cancer biomarker investigation and suggest new methods for the early diagnosis and accurate prognosis of prostate cancer. (C) 2014 AACR.
C1 [Johnson, Ian R. D.; Parkinson-Lawrence, Emma J.; Shandala, Tetyana; Brooks, Doug A.] Univ S Australia, Sch Pharm & Med Sci, Sansom Inst Hlth Res, Mech Cell Biol & Dis Res Grp Leader, Adelaide, SA 5001, Australia.
[Weigert, Roberto] NIDCR, NIH, Bethesda, MD USA.
[Butler, Lisa M.] Univ Adelaide, Sch Med, Dame Roma Mitchell Canc Res Lab, Adelaide, SA, Australia.
[Butler, Lisa M.] Univ Adelaide, Sch Med, Adelaide Prostate Canc Res Ctr, Adelaide, SA, Australia.
RP Brooks, DA (reprint author), Univ S Australia, Sch Pharm & Med Sci, Sansom Inst Hlth Res, Mech Cell Biol & Dis Res Grp Leader, GPO Box 2471, Adelaide, SA 5001, Australia.
EM Doug.Brooks@unisa.edu.au
RI Brooks, Doug/K-6714-2012; di Ronza, Alberto/H-7674-2016;
OI di Ronza, Alberto/0000-0002-9813-5143; Johnson, Ian/0000-0001-7875-3510
FU University of South Australia Presidents Scholarship; University of
South Australia Postgraduate Award; University of South Australia
Research SA Seeding Funds
FX This project was funded by a University of South Australia Presidents
Scholarship and a University of South Australia Postgraduate Award,
together with additional support from University of South Australia
Research SA Seeding Funds.
NR 51
TC 5
Z9 5
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1541-7786
EI 1557-3125
J9 MOL CANCER RES
JI Mol. Cancer Res.
PD DEC
PY 2014
VL 12
IS 12
BP 1851
EP 1862
DI 10.1158/1541-7786.MCR-14-0074
PG 12
WC Oncology; Cell Biology
SC Oncology; Cell Biology
GA AW9EN
UT WOS:000346560400014
PM 25080433
ER
PT J
AU Haddad, MR
Patel, KD
Sullivan, PH
Goldstein, DS
Murphy, KM
Centeno, JA
Kaler, SG
AF Haddad, Marie Reine
Patel, Keyur D.
Sullivan, Patricia H.
Goldstein, David S.
Murphy, Kevin M.
Centeno, Jose A.
Kaler, Stephen G.
TI Molecular and biochemical characterization of Mottled-dappled, an
embryonic lethal Menkes disease mouse model
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE Copper; Mottled-dappled; Menkes disease; Atp7a
ID NEUROCHEMICAL ABNORMALITIES; NEONATAL DIAGNOSIS; ATP7A GENE; TRANSPORT;
PLASMA; LOCALIZATION; TRAFFICKING; DELETION; PATTERN; PROTEIN
AB Mottled-dappled (Mo-dp) is a mouse model of Menkes disease caused by a large, previously uncharacterized deletion in the 5' region of Atp7a, the mouse ortholog of ATP7A. Affected mutants die in utero at embryonic day 17, and show bending and thickening of the ribs and distortion of the pectoral and pelvic girdles and limbs. To characterize this allele, we designed a custom 4x180K microarray on the mouse X chromosome and performed comparative genomic hybridization using extracted DNA from normal and carrier Mo-dp females, and identified an approximately 9 kb deletion. We used PCR to fine-map the breakpoints and amplify a junction fragment of 630 bp. Sequencing of the junction fragment disclosed the exact breakpoint locations and that the Mo-dp deletion is precisely 8990 bp, including approximately 2 kb in the promoter region of Atp7a. Western blot analysis of Mo-dp heterozygous brains showed diminished amounts of Atp7a protein, consistent with reduced expression due to the promoter region deletion on one allele. In heterozygous females, brain copper levels tended to be lower compared to wild type whereas neurochemical analyses revealed higher dihydroxyphenylacetic acid: dihydroxyphenylglycol (DOPAC:DHPG) and dopamine:norepinephrine (DA:NE) ratios compared to normal (P = 0.002 and 0.029, respectively), consistent with partial deficiency of dopamine-beta-hydroxylase, a copper-dependent enzyme. Heterozygous females showed no significant differences in body weight compared to wild type females. Our results delineate the molecular details of the Mo-dp mutation for the first time and define novel biochemical findings in heterozygous female carriers of this allele. Published by Elsevier Inc.
C1 [Haddad, Marie Reine; Patel, Keyur D.; Kaler, Stephen G.] NICHD, Sect Translat Neurosci, Program Mol Med, NIH, Bethesda, MD 20892 USA.
[Sullivan, Patricia H.; Goldstein, David S.] NINDS, Clin Neurocardiol Sect, Clin Neurosci Program, NIH, Bethesda, MD 20892 USA.
[Murphy, Kevin M.; Centeno, Jose A.] Andrews Air Force Base, Malcolm Grow Med Clin, Joint Pathol Ctr, Div Biophys Toxicol, Camp Springs, MD 20762 USA.
RP Kaler, SG (reprint author), NICHD, Sect Translat Neurosci, Program Mol Med, NIH, 35A Convent Dr,Bldg 35A,Room 2D971,MSC 3754, Bethesda, MD 20892 USA.
EM reina.haddad@nih.gov; keyur.patel19@gmail.com; psullivanl@ninds.nih.gov;
goldsteind@ninds.nih.gov; kevin.m.murphy2@navy.mil;
jose.centeno@afncr.af.mil; kalers@mail.nih.gov
FU Intramural Research Program of the National Institutes of Health [Z01
HD008768]
FX We thank Daniel Abebe, Lynn Holtzclaw, and Matt Schech for animal care
support and assistance and Diego Martinelli for helpful discussions and
comments. We also wish to acknowledge the late David Newsom (Nationwide
Children's Hospital, Columbus, OH) for very helpful discussions and
planning for array CGH. This work was supported by the Intramural
Research Program of the National Institutes of Health Grant No. Z01
HD008768 (Disorders of Copper Transport).
NR 27
TC 1
Z9 1
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 1096-7192
EI 1096-7206
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD DEC
PY 2014
VL 113
IS 4
BP 294
EP 300
DI 10.1016/j.ymgme.2014.10.001
PG 7
WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research &
Experimental
SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental
Medicine
GA AX0DG
UT WOS:000346623000010
PM 25456742
ER
PT J
AU Kramar, CP
Barbano, MF
Medina, JH
AF Kramar, Cecilia P.
Flavia Barbano, M.
Medina, Jorge H.
TI Dopamine D1/D5 receptors in the dorsal hippocampus are required for the
acquisition and expression of a single trial cocaine-associated memory
SO NEUROBIOLOGY OF LEARNING AND MEMORY
LA English
DT Article
DE Cocaine; Memory; Dopamine; Hippocampus; One-pairing CPP
ID LONG-TERM-MEMORY; CONDITIONED PLACE PREFERENCE; NUCLEUS-ACCUMBENS CORE;
MEDIAL PREFRONTAL CORTEX; REWARD MEMORY; BASOLATERAL AMYGDALA; SYNAPTIC
PLASTICITY; SEEKING BEHAVIOR; D-1 RECEPTOR; CONSOLIDATION
AB The role of the hippocampus in memory supporting associative learning between contexts and unconditioned stimuli is well documented. Hippocampal dopamine neurotransmission modulates synaptic plasticity and memory processing of fear-motivated and spatial learning tasks. Much less is known about the involvement of the hippocampus and its D1/D5 dopamine receptors in the acquisition, consolidation and expression of memories for drug-associated experiences, more particularly, in the processing of single pairing cocaine conditioned place preference (CPP) training. To determine the temporal dynamics of cocaine CPP memory formation, we trained rats in a one-pairing CPP paradigm and tested them at different time intervals after conditioning. The cocaine-associated memory lasted 24 h but not 72 h. Then, we bilaterally infused the dorsal hippocampus with the GABA A receptor agonist muscimol or the D1/D5 dopamine receptor antagonist SCH 23390 at different stages to evaluate the mechanisms involved in the acquisition, consolidation or expression of cocaine CPP memory. Blockade of D1/D5 dopamine receptors at the moment of training impaired the acquisition of cocaine CPP memories, without having any effect when administered immediately or 12 h after training. The expression of cocaine CPP memory was also affected by the administration of SCH 23390 at the moment of the test. Conversely, muscimol impaired the consolidation of cocaine CPP memory only when administered 12 h post conditioning. These findings suggests that dopaminergic inputs to the dorsal hippocampus are required for the acquisition and expression of one trial cocaine-associated memory while neural activity of this structure is required for the late consolidation of these types of memories. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Kramar, Cecilia P.; Flavia Barbano, M.; Medina, Jorge H.] Univ Buenos Aires, Fac Med, Inst Biol Celular & Neurociencias, CONICET UBA, Buenos Aires, DF, Argentina.
[Flavia Barbano, M.] NIDA, Neuronal Networks Sect, NIH, Baltimore, MD USA.
[Medina, Jorge H.] Univ Buenos Aires, Fac Med, Dept Fisiol, Buenos Aires, DF, Argentina.
RP Medina, JH (reprint author), Univ Buenos Aires, Fac Med, Inst Biol Celular & Neurociencias, Paraguay 2155 3rd Floor,C1121ABG, Buenos Aires, DF, Argentina.
EM jmedina@fmed.uba.ar
FU CONICET, Argentina; CONICET [PIP 11420110100282]; UBA; Foncyt [PICT
2010-1169, PICT 2011-1941]
FX We gratefully acknowledge Verardo y Cia. laboratory for their kind
donation of cocaine hydrochloride. We would also like to thank Carolina
Gonzalez and Fernando Castillo Diaz for excellent technical help and
Pedro Bekinschtein for the revision of the manuscript. CP Kramar was
supported by a doctoral fellowship from CONICET, Argentina. This work
was supported by CONICET (Grant PIP 11420110100282 to Dr. Barbano), UBA
and Foncyt (Grants PICT 2010-1169 to Dr. Medina and PICT 2011-1941 to
Dr. Barbano). The authors declare no conflict of interests.
NR 67
TC 6
Z9 6
U1 0
U2 7
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1074-7427
EI 1095-9564
J9 NEUROBIOL LEARN MEM
JI Neurobiol. Learn. Mem.
PD DEC
PY 2014
VL 116
BP 172
EP 180
DI 10.1016/j.nlm.2014.10.004
PG 9
WC Behavioral Sciences; Neurosciences; Psychology; Psychology,
Multidisciplinary
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA AW6QN
UT WOS:000346393800019
PM 25452086
ER
PT J
AU Grimes, CL
Lukacz, ES
Gantz, MG
Warren, LK
Brubaker, L
Zyczynski, HM
Richter, HE
Jelovsek, JE
Cundiff, G
Fine, P
Visco, AG
Zhang, M
Meikle, S
AF Grimes, Cara L.
Lukacz, Emily S.
Gantz, Marie G.
Warren, Lauren Klein
Brubaker, Linda
Zyczynski, Halina M.
Richter, Holly E.
Jelovsek, John Eric
Cundiff, Geoffrey
Fine, Paul
Visco, Anthony G.
Zhang, Min
Meikle, Susan
CA NICHD Pelvic Floor Disorders
TI What Happens to the Posterior Compartment and Bowel Symptoms After
Sacrocolpopexy?: Evaluation of 5-Year Outcomes From E-CARE
SO OBSTETRICAL & GYNECOLOGICAL SURVEY
LA English
DT Editorial Material
AB Posterior pelvic organ prolapse (pPOP) commonly occurs with apical prolapse, other vaginal compartment defects, and symptoms of defecatory dysfunction including obstructed defecation (OD). The indication for concomitant posterior repair (PR) during apical prolapse repair may be based on the presence or absence of symptoms. Some surgeons do not perform PR during repair of apical prolapse in the absence of symptoms. The Extended Colpopexy and Urinary Reduction Efforts (E-CARE) trial assessed the progression of posterior compartment prolapse and symptoms of OD after open abdominal sacrocolpopexy (ASC). Data from that study have been published in the primary article (Nygaard, JAMA 2013;309:2016). This secondary analysis of E-CARE data assessed the occurrence of pPOP and symptoms of OD in patients 5 years after open ASC. The study was designed to determine whether PR is necessary at the time of ASC. Participants with baseline and 5-year outcome data were divided into 3 groups using baseline posterior Pelvic Organ Prolapse Quantification points and concomitant PR: (1) no PR, Ap < 0; (2) no PR, Ap 0; and (3) +PR. Decision for concomitant PR was performed at the surgeon's discretion and included posterior colporrhaphy, perineorrhaphy, or sacrocolpoperineopexy. Five-year outcomes were dichotomized into presence/absence of pPOP (Ap > 0) and OD symptoms of moderate or greater bother (2) on 1 or more Pelvic Floor Distress Inventory questions about digital assistance, excessive straining, or incomplete evacuation. Composite failure during the 5-year interval was defined by both pPOP and OD symptoms or pPOP reoperation. Completed baseline and 5-year outcomes were available for 90 participants (60%); mean (SD) follow-up was 7.1 (1.0) years. At 5 years, only 2 women (6%) with no PR (AP < 0) developed de novo pPOP with OD symptoms; 1 of these underwent subsequent PR. Without PR repair, nearly all participants (23/24; 96%) demonstrated sustained resolution of pPOP, and none underwent PR within 5 years. Obstructed defecation symptoms improved in all groups after ASC with or without PR, although OD symptoms were still present at 5 years, with rates ranging from 17% to 19%. Regardless of concomitant PR, symptomatic pPOP is common 5 years after ASC. Obstructed defecation symptoms may improve after ASC with or without PR. Additional studies are needed to define criteria for performing PR at the time of planned ASC.
C1 [Grimes, Cara L.] Columbia Univ, Med Ctr, Dept Obstet & Gynecol, New York, NY 10027 USA.
[Lukacz, Emily S.] UC San Diego Hlth Syst, Dept Reprod Med, San Diego, CA USA.
[Gantz, Marie G.; Warren, Lauren Klein] RTI Int, Res Triangle Pk, NC USA.
[Brubaker, Linda] Loyola Univ, Stritch Sch Med, Dept Obstet & Gynecol, Chicago, IL 60611 USA.
[Brubaker, Linda] Loyola Univ, Stritch Sch Med, Dept Urol, Chicago, IL 60611 USA.
[Zyczynski, Halina M.] Univ Pittsburgh, Dept Obstet Gynecol & Reprod Sci, Pittsburgh, PA USA.
[Richter, Holly E.] Univ Alabama Birmingham, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
[Jelovsek, John Eric] Cleveland Clin, Obstet Gynecol & Womens Hlth Inst, Cleveland, OH 44106 USA.
[Cundiff, Geoffrey] Univ British Columbia, Dept Obstet & Gynaecol, Vancouver, BC V5Z 1M9, Canada.
[Fine, Paul] Baylor Coll Med, Dept Obstet & Gynecol, Houston, TX 77030 USA.
[Visco, Anthony G.] Duke Univ, Med Ctr, Dept Obstet & Gynecol, Durham, NC 27710 USA.
[Zhang, Min] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Meikle, Susan] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
RP Grimes, CL (reprint author), Columbia Univ, Med Ctr, Dept Obstet & Gynecol, New York, NY 10027 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0029-7828
EI 1533-9866
J9 OBSTET GYNECOL SURV
JI Obstet. Gynecol. Surv.
PD DEC
PY 2014
VL 69
IS 12
BP 734
EP 735
DI 10.1097/OGX.0000000000000131
PG 2
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA AW4XM
UT WOS:000346280900011
ER
PT J
AU Alstott, J
Panzarasa, P
Rubinov, M
Bullmore, ET
Vertes, PE
AF Alstott, Jeff
Panzarasa, Pietro
Rubinov, Mikail
Bullmore, Edward T.
Vertes, Petra E.
TI A Unifying Framework for Measuring Weighted Rich Clubs
SO SCIENTIFIC REPORTS
LA English
DT Article
ID COMMUNITY STRUCTURE; COMPLEX NETWORKS; ORGANIZATION; CONNECTOME;
CENTRALITY
AB Network analysis can help uncover meaningful regularities in the organization of complex systems. Among these, rich clubs are a functionally important property of a variety of social, technological and biological networks. Rich clubs emerge when nodes that are somehow prominent or 'rich' (e.g., highly connected) interact preferentially with one another. The identification of rich clubs is non-trivial, especially in weighted networks, and to this end multiple distinct metrics have been proposed. Here we describe a unifying framework for detecting rich clubs which intuitively generalizes various metrics into a single integrated method. This generalization rests upon the explicit incorporation of randomized control networks into the measurement process. We apply this framework to real-life examples, and show that, depending on the selection of randomized controls, different kinds of rich-club structures can be detected, such as topological and weighted rich clubs.
C1 [Alstott, Jeff; Rubinov, Mikail; Bullmore, Edward T.; Vertes, Petra E.] Univ Cambridge, Dept Psychiat, Behav & Clin Neurosci Inst, Cambridge CB2 0SZ, England.
[Alstott, Jeff] NIMH, Sect Crit Brain Dynam, Bethesda, MD 20892 USA.
[Panzarasa, Pietro] Queen Mary Univ London, Sch Business & Management, London E1 4NS, England.
[Rubinov, Mikail] Univ Cambridge, Churchill Coll, Cambridge CB2 0SZ, England.
RP Alstott, J (reprint author), Univ Cambridge, Dept Psychiat, Behav & Clin Neurosci Inst, Cambridge CB2 0SZ, England.
EM jja34@cam.ac.uk
OI Vertes, Petra E./0000-0002-0992-3210; Bullmore,
Edward/0000-0002-8955-8283
FU NIH-Oxford-Cambridge Scholarship Program; NARSAD Young Investigator
grant; Isaac Newton Trust grant; Medical Research Council [MR/K020706/1]
FX We would like to extend our gratitude to Vittoria Colizza for her
comments and suggestions on the development of this paper. We would like
to thank Tore Opsahl and Martijn van den Heuvel for making their data
easily accessible. J.A. is supported by the NIH-Oxford-Cambridge
Scholarship Program. P.P. is employed by Queen Mary University of
London. M.R. is supported by the NARSAD Young Investigator and Isaac
Newton Trust grants. E.T.B. is employed half-time by the University of
Cambridge, UK, and half-time by GlaxoSmithKline (GSK). P.E.V. is
supported by the Medical Research Council (grant number MR/K020706/1).
NR 28
TC 5
Z9 5
U1 1
U2 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD DEC 1
PY 2014
VL 4
AR 7258
DI 10.1038/srep07258
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA AW4NK
UT WOS:000346257700006
PM 25435201
ER
PT J
AU Behar, SM
Carpenter, SM
Booty, MG
Barber, DL
Jayaraman, P
AF Behar, Samuel M.
Carpenter, Stephen M.
Booty, Matthew G.
Barber, Daniel L.
Jayaraman, Pushpa
TI Orchestration of pulmonary T cell immunity during Mycobacterium
tuberculosis infection: Immunity interruptus
SO SEMINARS IN IMMUNOLOGY
LA English
DT Review
DE Tuberculosis; T cell; Priming; Cytokine; Exhaustion; Memory
ID CHRONIC VIRAL-INFECTION; NITRIC-OXIDE SYNTHASE; TUMOR-NECROSIS-FACTOR;
IFN-GAMMA PRODUCTION; CD8(+) T; ACTIVE TUBERCULOSIS; PROTECTIVE
IMMUNITY; IN-VIVO; INTERFERON-GAMMA; LATENT TUBERCULOSIS
AB Despite the introduction almost a century ago of Mycobacterium bovis BCG (BCG), an attenuated form of M. bovis that is used as a vaccine against Mycobacterium tuberculosis, tuberculosis remains a global health threat and kills more than 1.5 million people each year. This is mostly because BCG fails to prevent pulmonary disease - the contagious form of tuberculosis. Although there have been significant advances in understanding how the immune system responds to infection, the qualities that define protective immunity against M. tuberculosis remain poorly characterized. The ability to predict who will maintain control over the infection and who will succumb to clinical disease would revolutionize our approach to surveillance, control, and treatment. Here we review the current understanding of pulmonary T cell responses following M. tuberculosis infection. While infection elicits a strong immune response that contains infection, M. tuberculosis evades eradication. Traditionally, its intracellular lifestyle and alteration of macrophage function are viewed as the dominant mechanisms of evasion. Now we appreciate that chronic inflammation leads to T cell dysfunction. While this may arise as the host balances the goals of bacterial sterilization and avoidance of tissue damage, it is becoming clear that T cell dysfunction impairs host resistance. Defining the mechanisms that lead to T cell dysfunction is crucial as memory T cell responses are likely to be subject to the same subject to the same pressures. Thus, success of T cell based vaccines is predicated on memory T cells avoiding exhaustion while at the same time not promoting overt tissue damage. (C) 2014 Elsevier Ltd. All rights reserved.
C1 [Behar, Samuel M.; Carpenter, Stephen M.; Booty, Matthew G.; Jayaraman, Pushpa] Univ Massachusetts, Sch Med, Dept Microbiol & Physiol Syst, Worcester, MA 01655 USA.
[Carpenter, Stephen M.] Univ Massachusetts, Sch Med, Millennium Program, Grad Sch Biomed Sci, Worcester, MA 01605 USA.
[Carpenter, Stephen M.] Univ Massachusetts, Sch Med, Dept Med, Div Infect Dis & Immunol, Worcester, MA 01605 USA.
[Carpenter, Stephen M.] Brigham & Womens Hosp, Div Infect Dis, Dept Med, Boston, MA 02115 USA.
[Booty, Matthew G.] Harvard Univ, Div Med Sci, Program Immunol, Sch Med, Boston, MA 02115 USA.
[Barber, Daniel L.] NIAID, Lymphocyte Biol Unit T, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
RP Behar, SM (reprint author), Univ Massachusetts, Sch Med, Dept Microbiol & Physiol Syst, Sherman Ctr 8th Floor,55 Lake Ave North, Worcester, MA 01655 USA.
EM samuel.behar@umassmed.edu
OI Booty, Matthew/0000-0002-0835-3439; Behar, Samuel/0000-0002-3374-6699
FU Intramural Research Program of the NIH/NIAID; NIH [AI106725, AI098637,
AI085669, AI100766]
FX D.L.B. is supported by the Intramural Research Program of the NIH/NIAID.
S.M.B. is supported by the following NIH grants: AI106725, AI098637,
AI085669, and AI100766.
NR 247
TC 18
Z9 18
U1 1
U2 5
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 1044-5323
J9 SEMIN IMMUNOL
JI Semin. Immunol.
PD DEC
PY 2014
VL 26
IS 6
BP 559
EP 577
DI 10.1016/j.smim.2014.09.003
PG 19
WC Immunology
SC Immunology
GA AW5RE
UT WOS:000346330900013
PM 25311810
ER
PT J
AU Zeng, XM
Hunsberger, JG
Simeonov, A
Malik, N
Pei, Y
Rao, M
AF Zeng, Xianmin
Hunsberger, Joshua G.
Simeonov, Anton
Malik, Nasir
Pei, Ying
Rao, Mahendra
TI Concise Review: Modeling Central Nervous System Diseases Using Induced
Pluripotent Stem Cells
SO STEM CELLS TRANSLATIONAL MEDICINE
LA English
DT Review
DE Central nervous system disease; iPSC; Cell-based screening; Genetic
engineering
ID FATTY-ACID-COMPOSITION; BLOOD-BRAIN-BARRIER; IN-VITRO MODELS;
ALZHEIMERS-DISEASE; IPS CELLS; DOCOSAHEXAENOIC ACID;
DOPAMINERGIC-NEURONS; DRUG DISCOVERY; SMALL-MOLECULE; RETT-SYNDROME
AB Induced pluripotent stem cells (iPSCs) offer an opportunity to delve into the mechanisms underlying development while also affording the potential to take advantage of a number of naturally occurring mutations that contribute to either disease susceptibility or resistance. Just as with any new field, several models of screening are being explored, and innovators are working on the most efficient methods to overcome the inherent limitations of primary cell screens using iPSCs. In the present review, we provide a background regarding why iPSCs represent a paradigm shift for central nervous system (CNS) disease modeling. We describe the efforts in the field to develop more biologically relevant CNS disease models, which should provide screening assays useful for the pharmaceutical industry. We also provide some examples of successful uses for iPSC-based screens and suggest that additional development could revolutionize the field of drug discovery. The development and implementation of these advanced iPSC-based screens will create a more efficient disease-specific process underpinned by the biological mechanism in a patient- and disease-specific manner rather than by trial-and-error. Moreover, with careful and strategic planning, shared resources can be developed that will enable exponential advances in the field. This will undoubtedly lead to more sensitive and accurate screens for early diagnosis and allow the identification of patient-specific therapies, thus, paving the way to personalized medicine.
C1 [Zeng, Xianmin] XCell Sci Inc, Novato, CA USA.
[Zeng, Xianmin; Pei, Ying] Buck Inst Res Aging, Novato, CA 94945 USA.
[Hunsberger, Joshua G.; Malik, Nasir; Rao, Mahendra] Ctr Regenerat Med, Lab Stem Cell Biol, NIH, Bethesda, MD USA.
[Simeonov, Anton] Natl Ctr Adv Translat Sci, NIH, Bethesda, MD USA.
[Rao, Mahendra] New York Stem Cell Fdn, New York, NY USA.
RP Zeng, XM (reprint author), Buck Inst Res Aging, 8001 Redwood Blvd, Novato, CA 94945 USA.
EM xzeng@xcellscience.com
NR 67
TC 8
Z9 9
U1 2
U2 17
PU ALPHAMED PRESS
PI DURHAM
PA 318 BLACKWELL ST, STE 260, DURHAM, NC 27701-2884 USA
SN 2157-6564
EI 2157-6580
J9 STEM CELL TRANSL MED
JI Stem Cells Transl. Med.
PD DEC
PY 2014
VL 3
IS 12
BP 1418
EP 1428
DI 10.5966/sctm.2014-0102
PG 11
WC Cell & Tissue Engineering
SC Cell Biology
GA AW7QZ
UT WOS:000346460900017
PM 25368377
ER
PT J
AU Desai, VG
Kwekel, JC
Vijay, V
Moland, CL
Herman, EH
Lee, T
Han, T
Lewis, SM
Davis, KJ
Muskhelishvili, L
Kerr, S
Fuscoe, JC
AF Desai, Varsha G.
Kwekel, Joshua C.
Vijay, Vikrant
Moland, Carrie L.
Herman, Eugene H.
Lee, Taewon
Han, Tao
Lewis, Sherry M.
Davis, Kelly J.
Muskhelishvili, Levan
Kerr, Susan
Fuscoe, James C.
TI Early biomarkers of doxorubicin-induced heart injury in a mouse model
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE Doxorubicin; Heart; MicroRNA profiling; Biomarker; Mouse
ID CARDIAC TROPONIN-T; MYOCARDIAL-INFARCTION; INDUCED CARDIOTOXICITY;
CARDIOVASCULAR-DISEASE; INDUCED CARDIOMYOPATHY; MOLECULAR-MECHANISMS;
GENE-EXPRESSION; MUSCLE CELLS; MICRORNAS; FAILURE
AB Cardiac troponins, which are used as myocardial injury markers, are released in plasma only after tissue damage has occurred. Therefore, there is a need for identification of biomarkers of earlier events in cardiac injury to limit the extent of damage. To accomplish this, expression profiling of 1179 unique microRNAs (miRNAs) was performed in a chronic cardiotoxicity mouse model developed in our laboratory. Male B6C3F(1) mice were injected intravenously with 3 mg/kg doxorubicin (DOX; an anti-cancer drug), or saline once a week for 2, 3, 4, 6, and 8 weeks, resulting in cumulative DOX doses of 6, 9, 12, 18, and 24 mg/kg, respectively. Mice were euthanized a week after the last dose. Cardiac injury was evidenced in mice exposed to 18 mg/kg and higher cumulative DOX dose whereas examination of hearts by light microscopy revealed cardiac lesions at 24 mg/kg DOX. Also, 24 miRNAs were differentially expressed in mouse hearts, with the expression of 1, 1, 2, 8, and 21 miRNAs altered at 6, 9, 12, 18, and 24 mg/kg DOX, respectively. A pro-apoptotic miR-34a was the only miRNA that was upregulated at all cumulative DOX doses and showed a significant dose-related response. Up-regulation of miR-34a at 6 mg/kg DOX may suggest apoptosis as an early molecular change in the hearts of DOX-treated mice. At 12 mg/kg DOX, up-regulation of miR-34a was associated with down-regulation of hypertrophy-related miR-150; changes observed before cardiac injury. These findings may lead to the development of biomarkers of earlier events in DOX-induced cardiotoxicity that occur before the release of cardiac troponins. Published by Elsevier Inc.
C1 [Desai, Varsha G.; Kwekel, Joshua C.; Vijay, Vikrant; Moland, Carrie L.; Han, Tao; Fuscoe, James C.] US FDA, Personalized Med Branch, Div Syst Biol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
[Herman, Eugene H.] NCI, Toxicol & Pharmacol Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Rockville, MD 20850 USA.
[Lee, Taewon] Korea Univ, Dept Math, Sejong 339700, Chungnam, South Korea.
[Lewis, Sherry M.] US FDA, Off Sci Coordinat, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
[Davis, Kelly J.; Muskhelishvili, Levan] Natl Ctr Toxicol Res, Toxicol Pathol Associates, Jefferson, AR 72079 USA.
[Kerr, Susan] Arkansas Heart Hosp, Little Rock, AR 72211 USA.
RP Desai, VG (reprint author), US FDA, Personalized Med Branch, Div Syst Biol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA.
EM varsha.desai@fda.hhs.gov
RI Vijay, Vikrant/E-7651-2010
OI Vijay, Vikrant/0000-0001-8425-1285
NR 63
TC 20
Z9 21
U1 2
U2 13
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD DEC 1
PY 2014
VL 281
IS 2
BP 221
EP 229
DI 10.1016/j.taap.2014.10.006
PG 9
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA AW4BR
UT WOS:000346227000008
PM 25448438
ER
PT J
AU Ennis, RC
Asico, LD
Armando, I
Yang, J
Feranil, JB
Jurgens, JA
Escano, CS
Yu, PY
Wang, XY
Sibley, DR
Jose, PA
Villar, VAM
AF Ennis, Riley Charles
Asico, Laureano D.
Armando, Ines
Yang, Jian
Feranil, Jun B.
Jurgens, Julie A.
Escano, Crisanto S., Jr.
Yu, Peiying
Wang, Xiaoyan
Sibley, David R.
Jose, Pedro A.
Villar, Van Anthony M.
TI Dopamine D-1-like receptors regulate the alpha(1A)-adrenergic receptor
in human renal proximal tubule cells and D-1-like dopamine receptor
knockout mice
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE adrenergic receptor; dopamine receptor; knockout mice; renal proximal
tubule cells; sodium transport
ID ANGIOTENSIN-II TYPE-1; NA-K-ATPASE; EPITHELIAL-CELLS; NA+,K+-ATPASE
ACTIVITY; SODIUM-TRANSPORT; ALPHA-1-ADRENERGIC RECEPTOR; BIDIRECTIONAL
REGULATION; ADRENERGIC-STIMULATION; CAVEOLAE MICRODOMAINS; INTRARENAL
DOPAMINE
AB Thehomeostatic control of blood pressure hinges upon the delicate balance between prohypertensinogenic and antihypertensinogenic systems. D-1-like dopamine receptors [dopamine D-1 and D-5 receptors (D(1)Rs and D(5)Rs, respectively)] and the alpha(1A)-adrenergic receptor (alpha(1A)-AR) are expressed in the renal proximal tubule and engender opposing effects on Na+ transport, i.e., natriuresis (via D(1)Rs and D(5)Rs) or antinatriuresis (via alpha(1A)-ARs). We tested the hypothesis that the D1R/D5R regulates the alpha(1A)-AR. D-1-like dopamine receptors coimmunoprecipitated, colocalized, and cofractionated with alpha(1A)-ARs in lipid rafts in immortalized human renal proximal tubule cells. Long-term treatment with the D1R/D5R agonist fenoldopam resulted in decreased D1R and D5R expression but increased alpha(1A)-AR abundance in the plasma membrane. Short-term fenoldopam treatment stimulated the translocation of Na+-K+-ATPase from the plasma membrane to the cytosol that was partially reversed by an alpha(1A)-AR agonist, which by itself induced Na+-K+-ATPase translocation from the cytosol to the plasma membrane. The alpha(1A)-AR-specific agonist A610603 also minimized the ability of fenoldopam to inhibit Na+ K+-ATPase activity. To determine the interaction among D(1)Rs, D(5)Rs, and alpha(1A)-ARs in vivo, we used phenylephrine and A610603 to decrease Na+ excretion in several D1-like dopamine receptor knockout mouse strains. Phenylephrine and A61603 treatment resulted in a partial reduction of urinary Na+ excretion in wild-type mice and its abolition in D1R knockout, D5R knockout, and D1R-D5R double-knockout mice. Our results demonstrate the ability of the D-1-like dopamine receptors to regulate the expression and activity of alpha(1A)-AR. Elucidating the intricacies of the interaction among these receptors is crucial for a better understanding of the crosstalk between anti-and pro-hypertensive systems.
C1 [Ennis, Riley Charles] Thomas Jefferson High Sch Sci & Technol, Alexandria, VA USA.
[Asico, Laureano D.; Armando, Ines; Yang, Jian; Feranil, Jun B.; Jurgens, Julie A.; Escano, Crisanto S., Jr.; Yu, Peiying; Wang, Xiaoyan; Jose, Pedro A.; Villar, Van Anthony M.] Univ Maryland, Sch Med, Dept Med, Div Nephrol, Baltimore, MD 21201 USA.
[Sibley, David R.] NINDS, Mol Neuropharmacol Sect, NIH, Bethesda, MD 20892 USA.
[Jose, Pedro A.] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
RP Villar, VAM (reprint author), Univ Maryland, Sch Med, 20 Penn St,HSF 2,Suite S003C, Baltimore, MD 21201 USA.
EM vvillar@medicine.umaryland.edu
FU National Institutes of Health [R01-DK-039308, R01-HL-092196,
R37-HL-023081, R01-DK-090918]
FX This work was supported, in part, by National Institutes of Health
Grants R01-DK-039308, R01-HL-092196, R37-HL-023081, and R01-DK-090918.
NR 77
TC 0
Z9 0
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
EI 1522-1466
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD DEC 1
PY 2014
VL 307
IS 11
BP F1238
EP F1248
DI 10.1152/ajprenal.00119.2014
PG 11
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA AW0YW
UT WOS:000346018200009
PM 25339698
ER
PT J
AU Tan, FCC
Hutchison, ER
Eitan, E
Mattson, MP
AF Tan, Florence C. C.
Hutchison, Emmette R.
Eitan, Erez
Mattson, Mark P.
TI Are there roles for brain cell senescence in aging and neurodegenerative
disorders?
SO BIOGERONTOLOGY
LA English
DT Review
DE Senescence; Neurons; Neurodegeneration; Astrocytes
ID DNA-DAMAGE RESPONSE; NEURAL STEM-CELLS; LYSOSOMAL BETA-GALACTOSIDASE;
AMYLOID PRECURSOR PROTEIN; SPINAL GANGLION NEURONS; FIBROBLASTS
IN-VITRO; N-TERMINAL KINASE; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE;
REPLICATIVE SENESCENCE
AB The term cellular senescence was introduced more than five decades ago to describe the state of growth arrest observed in aging cells. Since this initial discovery, the phenotypes associated with cellular senescence have expanded beyond growth arrest to include alterations in cellular metabolism, secreted cytokines, epigenetic regulation and protein expression. Recently, senescence has been shown to play an important role in vivo not only in relation to aging, but also during embryonic development. Thus, cellular senescence serves different purposes and comprises a wide range of distinct phenotypes across multiple cell types. Whether all cell types, including post-mitotic neurons, are capable of entering into a senescent state remains unclear. In this review we examine recent data that suggest that cellular senescence plays a role in brain aging and, notably, may not be limited to glia but also neurons. We suggest that there is a high level of similarity between some of the pathological changes that occur in the brain in Alzheimer's and Parkinson's diseases and those phenotypes observed in cellular senescence, leading us to propose that neurons and glia can exhibit hallmarks of senescence previously documented in peripheral tissues.
C1 [Tan, Florence C. C.; Hutchison, Emmette R.; Eitan, Erez; Mattson, Mark P.] NIA, Lab Neurosci, Intramural Res Program, Baltimore, MD 21224 USA.
RP Hutchison, ER (reprint author), NIA, Lab Neurosci, Intramural Res Program, Baltimore, MD 21224 USA.
EM hutchisone@mail.nih.gov; erez.eitan@nih.gov
FU Intramural Research Program of the NIH, National Institute on Aging
FX This research was supported by the Intramural Research Program of the
NIH, National Institute on Aging.
NR 190
TC 8
Z9 9
U1 1
U2 18
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1389-5729
EI 1573-6768
J9 BIOGERONTOLOGY
JI Biogerontology
PD DEC
PY 2014
VL 15
IS 6
SI SI
BP 643
EP 660
DI 10.1007/s10522-014-9532-1
PG 18
WC Geriatrics & Gerontology
SC Geriatrics & Gerontology
GA AW3EH
UT WOS:000346168100008
PM 25305051
ER
PT J
AU Roy, AK
Benson, BE
Degnan, KA
Perez-Edgar, K
Pine, DS
Fox, NA
Ernst, M
AF Roy, Amy Krain
Benson, Brenda E.
Degnan, Kathryn A.
Perez-Edgar, Koraly
Pine, Daniel S.
Fox, Nathan A.
Ernst, Monique
TI Alterations in amygdala functional connectivity reflect early
temperament
SO BIOLOGICAL PSYCHOLOGY
LA English
DT Article
DE Behavioral inhibition; Functional connectivity; Amygdala; Temperament;
Anxiety; fMRI
ID GENERALIZED ANXIETY DISORDER; BEHAVIORAL-INHIBITION; ANXIOUS
TEMPERAMENT; RISK-FACTOR; CORTEX; ADOLESCENTS; CHILDHOOD; CEREBELLUM;
RESPONSES; FACES
AB Behavioral inhibition (BI) is a temperament identified early in life that is associated with increased risk for anxiety disorders. Amygdala hyperresponsivity, found both in behaviorally inhibited and anxious individuals, suggests that amygdala dysfunction may represent a marker of anxiety risk. However, broader amygdala networks have not been examined in individuals with a history of childhood BI. This study uses resting state fMRI to assess amygdala intrinsic functional connectivity (iFC) in 38 healthy young adults (19 with a history of BI, 19 with no history of BI) selected from a longitudinal study. Centromedial, basolateral, and superficial amygdala iFCs were compared between groups and examined in relation to self-report measures of anxiety. Group differences were observed in amygdala iFC with prefrontal cortex, striatum, anterior insula, and cerebellum. Adults characterized with BI in childhood endorsed greater state anxiety prior to entering the scanner, which was associated with several of the group differences. Findings support enduring effects of BI on amygdala circuitry, even in the absence of current psychopathology. (C) 2014 Elsevier B.V. All rights reserved.
C1 [Roy, Amy Krain] Fordham Univ, Dept Psychol, Bronx, NY 10458 USA.
[Benson, Brenda E.; Pine, Daniel S.; Ernst, Monique] NIMH, Sect Dev & Affect Neurosci, Bethesda, MD 20892 USA.
[Degnan, Kathryn A.; Fox, Nathan A.] Univ Maryland, Dept Human Dev & Quantitat Methodol, College Pk, MD 20742 USA.
[Perez-Edgar, Koraly] Penn State Univ, Dept Psychol, University Pk, PA 16802 USA.
RP Roy, AK (reprint author), Fordham Univ, Dept Psychol, 441 East Fordham Rd, Bronx, NY 10458 USA.
EM aroy3@fordham.edu
OI Perez-Edgar, Koraly/0000-0003-4051-9563
FU National Institute of Mental Health [5U01MH093349-02, 3U01MH093349-02S1,
K01-MH073569]
FX This research was supported by the National Institute of Mental Health
(5U01MH093349-02; 3U01MH093349-02S1 [PI: N.A. Fox]; K01-MH073569 [PI: K.
Perez-Edgar]).
NR 41
TC 9
Z9 9
U1 5
U2 16
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0301-0511
EI 1873-6246
J9 BIOL PSYCHOL
JI Biol. Psychol.
PD DEC
PY 2014
VL 103
BP 248
EP 254
DI 10.1016/j.biopsycho.2014.09.007
PG 7
WC Psychology, Biological; Behavioral Sciences; Psychology; Psychology,
Experimental
SC Psychology; Behavioral Sciences
GA AW0HF
UT WOS:000345971200031
PM 25261727
ER
PT J
AU Zhu, C
Pinsky, P
Huang, WY
Purdue, M
AF Zhu, Claire
Pinsky, Paul
Huang, Wen-Yi
Purdue, Mark
TI Laboratory Detective Work Identifies a Mishandling Problem in Sample
Aliquoting
SO BIOPRESERVATION AND BIOBANKING
LA English
DT Article
ID CANCER SCREENING TRIAL; OVARIAN-CANCER; PROSTATE; LUNG
AB Data from a recent ovarian cancer biomarker study using serum aliquots from the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial Biorepository showed that CA125II concentrations in these aliquots were significantly lower than those previously measured in the same subjects from the same blood draw. We designed an experiment to investigate whether samples used in the study (reference study) were compromised during the aliquoting process. We measured CA125II in the "sister" vials created during the same aliquoting process as the reference study aliquot, and in "cousin" vials newly aliquoted from another parent vial from the same blood draw, from 15 healthy controls in the study. Because the sister vials were created in a specific order, we also assessed whether there was a CA125II concentration gradient among the sisters. The Wilcoxon signed-rank test was used to test the statistical significance of the observed differences. Mean CA125II concentration (volume-averaged) was greater in the sisters than the cousins in all 15 subjects (p<0.001). The mean coefficient of variation was 0.25 (range: 0.12-0.43) in the sisters and 0.11 (range: 0.-1.1) in the cousins (p<0.008). The mean ratio of CA125II in the 5(th) aliquoted versus the 3(rd) aliquoted sister vial was 1.66 (1.25-2.5, p<0.001). These data suggest that the parent vials were not adequately mixed before they were aliquoted. CA125II in serum can partially precipitate to form a concentration gradient in long-term storage. Rigorous vortexing after thawing and before aliquoting is thus critical.
C1 [Zhu, Claire; Pinsky, Paul] NCI, Canc Prevent Div, Bethesda, MD 20892 USA.
[Huang, Wen-Yi; Purdue, Mark] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Zhu, C (reprint author), NCI, Early Detect Res Grp, Canc Prevent Div, 9609 Med Ctr Dr,Room 5E106 MSC 9790, Bethesda, MD 20892 USA.
EM zhucla@mail.nih.gov
NR 5
TC 0
Z9 0
U1 2
U2 2
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1947-5535
EI 1947-5543
J9 BIOPRESERV BIOBANK
JI Biopreserv. Biobank.
PD DEC 1
PY 2014
VL 12
IS 6
BP 430
EP 432
DI 10.1089/bio.2014.0046
PG 3
WC Cell Biology; Chemistry, Applied; Medical Laboratory Technology
SC Cell Biology; Chemistry; Medical Laboratory Technology
GA AW5SY
UT WOS:000346335300012
PM 25496156
ER
PT J
AU Modi, HR
Basselin, M
Rapoport, SI
AF Modi, Hiren R.
Basselin, Mireille
Rapoport, Stanley I.
TI Valnoctamide, a non-teratogenic amide derivative of valproic acid,
inhibits arachidonic acid activation in vitro by recombinant acyl-CoA
synthetase-4
SO BIPOLAR DISORDERS
LA English
DT Article
DE acyl-CoA synthetase 4; anticonvulsant; arachidonic acid; bipolar
disorder; brain; cascade; enzyme; inhibition; metabolism;
Michaelis-Menten kinetics; mood stabilizer; rat; valnoctamide; valproate
ID STEREOSELECTIVE PHARMACOKINETIC ANALYSIS; BIPOLAR DISORDER;
HEALTHY-SUBJECTS; LIGASE 4; BRAIN; ISOMER; DRUG; RATS; ANTICONVULSANT;
EXPRESSION
AB ObjectiveValproic acid (VPA), a mood stabilizer used for treating bipolar disorder (BD), uncompetitively inhibits acylation of arachidonic acid (AA) by recombinant AA-selective acyl-CoA synthetase 4 (Acsl4) at an enzyme inhibition constant (K-i) of 25mM. Inhibition may account for VPA's ability to reduce AA turnover in brain phospholipids of unanesthetized rats and to be therapeutic in BD. However, VPA is teratogenic. We tested whether valnoctamide (VCD), a non-teratogenic amide derivative of a VPA chiral isomer, which had antimanic potency in a phase III BD trial, also inhibits recombinant Acsl4.
MethodsRat Acsl4-flag protein was expressed in Escherichia coli. We used Michaelis-Menten kinetics to characterize and quantify the ability of VCD to inhibit conversion of AA to AA-CoA by recombinant Acsl4 in vitro.
ResultsAcsl4-mediated activation of AA to AA-CoA by Acsl4 was inhibited uncompetitively by VCD, with a K-i of 6.38mM.
ConclusionsVCD's ability to uncompetitively inhibit AA activation to AA-CoA by Acsl4, at a lower K-i than VPA, suggests that, like VPA, VCD may reduce AA turnover in rat brain phospholipids. If so, VCD and other non-teratogenic Acsl4 inhibitors might be considered further for treating BD.
C1 [Modi, Hiren R.; Basselin, Mireille; Rapoport, Stanley I.] NIA, Brain Physiol & Metab Sect, Lab Neurosci, NIH, Bethesda, MD 20892 USA.
RP Modi, HR (reprint author), NIA, Brain Physiol & Metab Sect, Lab Neurosci, NIH, 9000 Rockville Pike Bldg 9,Room 1S126, Bethesda, MD 20892 USA.
EM hirumodi@gmail.com
FU Intramural Research Program of the National Institute on Aging, National
Institute of Health
FX This work was supported by the Intramural Research Program of the
National Institute on Aging, National Institute of Health. We thank the
Chemical Synthesis and Drug Supply Program of the National Institute of
Mental Health (Research Triangle Park, NC, USA) for supplying us with
valnoctamide.
NR 39
TC 1
Z9 1
U1 3
U2 4
PU WILEY
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1398-5647
EI 1399-5618
J9 BIPOLAR DISORD
JI Bipolar Disord.
PD DEC
PY 2014
VL 16
IS 8
BP 875
EP 880
DI 10.1111/bdi.12220
PG 6
WC Clinical Neurology; Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA AW0KK
UT WOS:000345980900010
PM 25041123
ER
PT J
AU Fuhrman, BJ
Xu, X
Falk, RT
Dallal, CM
Veenstra, TD
Keefer, LK
Graubard, BI
Brinton, LA
Ziegler, RG
Gierach, GL
AF Fuhrman, Barbara J.
Xu, Xia
Falk, Roni T.
Dallal, Cher M.
Veenstra, Timothy D.
Keefer, Larry K.
Graubard, Barry I.
Brinton, Louise A.
Ziegler, Regina G.
Gierach, Gretchen L.
TI Assay Reproducibility and Interindividual Variation for 15 Serum
Estrogens and Estrogen Metabolites Measured by Liquid
Chromatography-Tandem Mass Spectrometry
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BREAST-CANCER RISK; POSTMENOPAUSAL WOMEN; URINARY ESTROGENS;
HORMONE-LEVELS; ESTRADIOL
AB Background: Interindividual differences in estrogen metabolism may partially account for differences in risks of estrogen-responsive cancers. Weconducted a proof-of-performance study to assess the reproducibility of a LC/MS-MS method for measurement of 15 serum estrogens and metabolites (all 15 termed EM) in total (conjugated+unconjugated) and unconjugated forms and describe interindividual variation.
Methods: Interindividual variation in serum EM profiles was evaluated for 20 premenopausal women, 15 postmenopausal women, and 10 men. Replicate aliquots from 10 premenopausal women, 5 postmenopausal women, and 5 men were assayed eight times over 4 weeks. Components of variance were used to calculate coefficients of variation (CV) and intraclass correlation coefficients (ICC).
Results: In postmenopausal women and men, median EM concentrations were similar and substantially lower than that in premenopausal women. Within each sex/menopausal group, the sum of all EM varied 5- to 7-fold across extreme deciles. Some EM had greater variation; total estrone varied approximately 12-fold in premenopausal and postmenopausal women. Unconjugated estradiol varied 17-fold in postmenopausal women but only 5- fold in premenopausal women and men. CVs reflecting variation across replicate measures for individuals were <5% for most EM, but higher in some individuals with a low EM concentration. Overall laboratory CVs for all but one EM were <2% and ICCs were >99% for all EM in each group.
Conclusions: The serum EM assay has excellent laboratory reproducibility. In premenopausal women, postmenopausal women, and men, interindividual variation in EM measures is substantially greater than laboratory variation.
Impact: The serum EM assay is suitable for epidemiologic application. (C) 2014 AACR.
C1 [Fuhrman, Barbara J.; Falk, Roni T.; Dallal, Cher M.; Graubard, Barry I.; Brinton, Louise A.; Ziegler, Regina G.; Gierach, Gretchen L.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Xu, Xia; Veenstra, Timothy D.] Leidos Biomed Res Inc, Lab Analyt Technol, Canc Res Technol Program, Frederick Natl Lab Canc Res, Frederick, MD USA.
[Keefer, Larry K.] NCI, Biol Chem Lab, Ctr Canc Res, Frederick, MD 21701 USA.
RP Fuhrman, BJ (reprint author), Univ Arkansas Med Sci, Fay Boozman Coll Publ Hlth, Dept Epidemiol, 4301 W Markham St 820, Little Rock, AR 72205 USA.
EM bjfuhrman@uams.edu
RI Keefer, Larry/N-3247-2014; Brinton, Louise/G-7486-2015; Gierach,
Gretchen/E-1817-2016;
OI Keefer, Larry/0000-0001-7489-9555; Brinton, Louise/0000-0003-3853-8562;
Gierach, Gretchen/0000-0002-0165-5522; Fuhrman,
Barbara/0000-0002-1777-9888
FU Intramural Research Program of the Division of Cancer Epidemiology and
Genetics of the National Cancer Institute; National Cancer Institute
federal funds [HHSN261200800001E]
FX This work was supported by the Intramural Research Program of the
Division of Cancer Epidemiology and Genetics of the National Cancer
Institute and National Cancer Institute federal funds awarded under
Contract HHSN261200800001E to SAIC-Frederick, Inc.
NR 18
TC 11
Z9 11
U1 0
U2 7
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 DEC
PY 2014
VL 23
IS 12
BP 2649
EP 2657
DI 10.1158/1055-9965.EPI-14-0438
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300005
PM 25472673
ER
PT J
AU Altekruse, SF
Rosenfeld, GE
Carrick, DM
Pressman, EJ
Schully, SD
Mechanic, LE
Cronin, KA
Hernandez, BY
Lynch, CF
Cozen, W
Khoury, MJ
Penberthy, LT
AF Altekruse, Sean F.
Rosenfeld, Gabriel E.
Carrick, Danielle M.
Pressman, Emilee J.
Schully, Sheri D.
Mechanic, Leah E.
Cronin, Kathleen A.
Hernandez, Brenda Y.
Lynch, Charles F.
Cozen, Wendy
Khoury, Muin J.
Penberthy, Lynne T.
TI SEER Cancer Registry Biospecimen Research: Yesterday and Tomorrow
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID PARAFFIN-EMBEDDED TISSUES; EPITHELIAL HISTOPATHOLOGIC MARKERS;
HUMAN-PAPILLOMAVIRUS TYPES; PRE-RITUXIMAB ERA; B-CELL LYMPHOMA;
UNITED-STATES; PROTEIN EXPRESSION; COLORECTAL-CANCER; VACCINE
INTRODUCTION; DNA METHYLATION
AB The National Cancer Institute's (NCI) Surveillance, Epidemiology, and End Results (SEER) registries have been a source of biospecimens for cancer research for decades. Recently, registry-based biospecimen studies have become more practical, with the expansion of electronic networks for pathology and medical record reporting. Formalin-fixed paraffin-embedded specimens are now used for next-generation sequencing and other molecular techniques. These developments create new opportunities for SEER biospecimen research. We evaluated 31 research articles published during 2005 to 2013 based on authors' confirmation that these studies involved linkage of SEER data to biospecimens. Rather than providing an exhaustive review of all possible articles, our intent was to indicate the breadth of research made possible by such a resource. We also summarize responses to a 2012 questionnaire that was broadly distributed to the NCI intra- and extramural biospecimen research community. This included responses from 30 investigators who had used SEER biospecimens in their research. The survey was not intended to be a systematic sample, but instead to provide anecdotal insight on strengths, limitations, and the future of SEER biospecimen research. Identified strengths of this research resource include biospecimen availability, cost, and annotation of data, including demographic information, stage, and survival. Shortcomings include limited annotation of clinical attributes such as detailed chemotherapy history and recurrence, and timeliness of turnaround following biospecimen requests. A review of selected SEER biospecimen articles, investigator feedback, and technological advances reinforced our view that SEER biospecimen resources should be developed. This would advance cancer biology, etiology, and personalized therapy research. (C) 2014 AACR.
C1 [Altekruse, Sean F.; Rosenfeld, Gabriel E.; Carrick, Danielle M.; Pressman, Emilee J.; Schully, Sheri D.; Mechanic, Leah E.; Cronin, Kathleen A.; Khoury, Muin J.; Penberthy, Lynne T.] NCI, Div Canc Control & Populat Sci, NIH, Rockville, MD 20850 USA.
[Hernandez, Brenda Y.] Univ Hawaii, Ctr Canc, Honolulu, HI 96822 USA.
[Lynch, Charles F.] Univ Iowa, Dept Epidemiol, Coll Publ Hlth, Iowa City, IA USA.
[Cozen, Wendy] Univ So Calif, Dept Prevent Med, Keck Sch Med, USC Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Cozen, Wendy] Univ So Calif, Dept Pathol, Keck Sch Med, USC Norris Comprehens Canc Ctr, Los Angeles, CA USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Gen, Atlanta, GA USA.
RP Altekruse, SF (reprint author), NCI, Div Canc Control & Populat Sci, 9609 Med Ctr Dr,Room 4E536, Rockville, MD 20850 USA.
EM altekrusesf@mail.nih.gov
FU Intramural NIH HHS [Z99 CA999999]
NR 46
TC 3
Z9 3
U1 1
U2 4
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 DEC
PY 2014
VL 23
IS 12
BP 2681
EP 2687
DI 10.1158/1055-9965.EPI-14-0490
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300009
PM 25472677
ER
PT J
AU Khodr, ZG
Sherman, ME
Pfeiffer, RM
Gierach, GL
Brinton, LA
Falk, RT
Patel, DA
Linville, LM
Papathomas, D
Clare, SE
Visscher, DW
Mies, C
Hewitt, SM
Storniolo, AMV
Rosebrock, A
Caban, JJ
Figueroa, JD
AF Khodr, Zeina G.
Sherman, Mark E.
Pfeiffer, Ruth M.
Gierach, Gretchen L.
Brinton, Louise A.
Falk, Roni T.
Patel, Deesha A.
Linville, Laura M.
Papathomas, Daphne
Clare, Susan E.
Visscher, Daniel W.
Mies, Carolyn
Hewitt, Stephen M.
Storniolo, Anna Maria V.
Rosebrock, Adrian
Caban, Jesus J.
Figueroa, Jonine D.
TI Circulating Sex Hormones and Terminal Duct Lobular Unit Involution of
the Normal Breast
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID PLASMA PROLACTIN CONCENTRATIONS; CANCER RISK; POSTMENOPAUSAL WOMEN;
PREMENOPAUSAL WOMEN; EPIC COHORT; SERUM; PROGESTERONE; TESTOSTERONE;
ESTROGEN; AGE
AB Background: Terminal duct lobular units (TDLU) are the predominant source of breast cancers. Lesser degrees of age-related TDLU involution have been associated with increased breast cancer risk, but factors that influence involution are largely unknown. We assessed whether circulating hormones, implicated in breast cancer risk, are associated with levels of TDLU involution using data from the Susan G. Komen Tissue Bank (KTB) at the Indiana University Simon Cancer Center (2009-2011).
Methods: Weevaluated three highly reproducible measures of TDLU involution, using normal breast tissue samples from the KTB (n = 390): TDLU counts, median TDLU span, and median acini counts per TDLU. RRs (for continuous measures), ORs (for categorical measures), 95% confidence intervals (95% CI), and P-trends were calculated to assess the association between tertiles of estradiol, testosterone, sex hormone-binding globulin (SHBG), progesterone, and prolactin with TDLU measures. All models were stratified by menopausal status and adjusted for confounders.
Results: Among premenopausal women, higher prolactin levels were associated with higher TDLU counts (RRT3vsT1:1.18; 95% CI: 1.07-1.31; P-trend = 0.0005), but higher progesterone was associated with lower TDLU counts (RRT3vsT1:0.80; 95% CI: 0.72-0.89; P-trend < 0.0001). Among postmenopausal women, higher levels of estradiol (RRT3vsT1:1.61; 95% CI: 1.32-1.97; P-trend < 0.0001) and testosterone (RRT3vsT1: 1.32; 95% CI: 1.09-1.59; P-trend = 0.0043) were associated with higher TDLU counts.
Conclusions: These data suggest that select hormones may influence breast cancer risk potentially through delaying TDLU involution.
Impact: Increased understanding of the relationship between circulating markers and TDLU involution may offer new insights into breast carcinogenesis. (C) 2014 AACR.
C1 [Khodr, Zeina G.; Sherman, Mark E.; Pfeiffer, Ruth M.; Gierach, Gretchen L.; Brinton, Louise A.; Falk, Roni T.; Patel, Deesha A.; Papathomas, Daphne; Figueroa, Jonine D.] NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Sherman, Mark E.] NCI, Canc Prevent Div, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Linville, Laura M.] George Washington Univ, Sch Med & Hlth Sci, Washington, DC 20052 USA.
[Clare, Susan E.] Northwestern Univ, Dept Surg, Feinberg Sch Med, Chicago, IL 60611 USA.
[Visscher, Daniel W.] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Mies, Carolyn] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Hewitt, Stephen M.] NCI, Appl Mol Pathol Lab, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Storniolo, Anna Maria V.] Indiana Univ, Susan G Komen Tissue Bank, Simon Canc Ctr, Indianapolis, IN 46204 USA.
[Rosebrock, Adrian] Univ Maryland, Dept Comp Sci & Elect Engn, Baltimore, MD 21201 USA.
[Caban, Jesus J.] Walter Reed Natl Mil Med Ctr, Natl Intrepid Ctr Excellence, Bethesda, MD USA.
RP Figueroa, JD (reprint author), NCI, 9609 Med Ctr Dr,7E-122,MSC 9774, Bethesda, MD 20892 USA.
EM FigueroaJ@mail.nih.gov
RI Brinton, Louise/G-7486-2015; Gierach, Gretchen/E-1817-2016;
OI Brinton, Louise/0000-0003-3853-8562; Gierach,
Gretchen/0000-0002-0165-5522; Hewitt, Stephen/0000-0001-8283-1788
FU Division of Cancer Epidemiology and Genetics at the National Cancer
Institute; Breast Cancer Research Foundation, Oracle Giving; Catherine
Peachey Fund, Inc.; National Cancer Institute, Intramural Research
Program; Susan G. Komen
FX This study was supported by intramural funds from the Division of Cancer
Epidemiology and Genetics at the National Cancer Institute. S. Clare and
A. Storniolo are supported by Susan G. Komen, the Breast Cancer Research
Foundation, Oracle Giving, and the Catherine Peachey Fund, Inc. Z.
Khodr, M. Sherman, R. Pfeiffer, G. Gierach, L. Brinton, R. Falk, D.
Patel, L. Linvile, D. Papathomas, S. Hewitt, and J. Figueroa are
supported by funds from the National Cancer Institute, Intramural
Research Program.
NR 53
TC 8
Z9 8
U1 1
U2 3
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 DEC
PY 2014
VL 23
IS 12
BP 2765
EP 2773
DI 10.1158/1055-9965.EPI-14-0667
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300018
PM 25472681
ER
PT J
AU Sun, XZ
Sandhu, R
Figueroa, JD
Gierach, GL
Sherman, ME
Troester, MA
AF Sun, Xuezheng
Sandhu, Rupninder
Figueroa, Jonine D.
Gierach, Gretchen L.
Sherman, Mark E.
Troester, Melissa A.
TI Benign Breast Tissue Composition in Breast Cancer Patients: Association
with Risk Factors, Clinical Variables, and Gene Expression
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID MAMMARY-GLAND DEVELOPMENT; TUMOR-STROMA RATIO; MAMMOGRAPHIC DENSITY;
PROGNOSTIC-SIGNIFICANCE; BASAL-LIKE; MICROENVIRONMENT; PROGRESSION;
INVOLUTION; PATTERNS; SUBTYPES
AB Background: Breast tissue composition (epithelium, non-fatty stroma, and adipose) changes qualitatively and quantitatively throughout the lifespan, and may mediate relationships between risk factors and breast cancer initiation. We sought to identify relationships between tissue composition, risk factors, tumor characteristics, and gene expression.
Methods: Participants were 146 patients from the Polish Breast Cancer Study, with data on risk factor and clinicopathological characteristics. Benign breast tissue composition was evaluated using digital image analysis of histologic sections. Whole-genome microarrays were performed on the same tissue blocks.
Results: Mean epithelial, non-fatty stromal, and adipose proportions were 8.4% (SD = 4.9%), 27.7% (SD = 24.0%), and 64.0% (SD = 24.0%), respectively. Among women <50 years old, stroma proportion decreased and adipose proportion increased with age, with approximately 2% difference per year (P < 0.01). The variation in epithelial proportion with age was modest (0.1% per year). Higher epithelial proportion was associated with obesity (7.6% in nonobese vs. 10.1% in obese; P = 0.02) and with poorly differentiated tumors (7.8% in well/moderate vs. 9.9% in poor; P = 0.05). Gene expression signatures associated with epithelial and stromal proportion were identified and validated. Stroma-associated genes were in metabolism and stem cell maintenance pathways, whereas epithelial genes were enriched for cytokine and immune response pathways.
Conclusions: Breast tissue composition was associated with age, body mass index, and tumor grade, with consequences for breast gene expression.
Impact: Breast tissue morphologic factors may influence breast cancer etiology. Composition and gene expression may act as biomarkers of breast cancer risk and progression. (C) 2014 AACR.
C1 [Sun, Xuezheng; Troester, Melissa A.] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC 27599 USA.
[Sandhu, Rupninder; Troester, Melissa A.] Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
[Figueroa, Jonine D.; Gierach, Gretchen L.; Sherman, Mark E.] NCI, Hormonal & Reprod Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Sherman, Mark E.] NCI, Breast & Gynecol Canc Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Troester, MA (reprint author), Univ N Carolina, Dept Epidemiol, CB 7435, Chapel Hill, NC 27599 USA.
EM troester@unc.edu
RI Gierach, Gretchen/E-1817-2016
OI Gierach, Gretchen/0000-0002-0165-5522
FU National Cancer Institute [U01-ES019472, R01-CA138255]; Breast SPORE
Project [P50CA058223]; Avon Foundation; Intramural Research Program of
the NIH, National Cancer Institute
FX This work was supported by grants from the National Cancer Institute
(U01-ES019472 and R01-CA138255 to M.A. Troester), a Breast SPORE Project
(grant P50CA058223, H.S. Earp PI), and a grant from the Avon Foundation
(to M.A. Troester). This work was supported (in part) by the Intramural
Research Program of the NIH, National Cancer Institute.
NR 43
TC 5
Z9 5
U1 0
U2 5
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 DEC
PY 2014
VL 23
IS 12
BP 2810
EP 2818
DI 10.1158/1055-9965.EPI-14-0507
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300022
PM 25249325
ER
PT J
AU Kitahara, CM
Trabert, B
Katki, HA
Chaturvedi, AK
Kemp, TJ
Pinto, LA
Moore, SC
Purdue, MP
Wentzensen, N
Hildesheim, A
Shiels, MS
AF Kitahara, Cari M.
Trabert, Britton
Katki, Hormuzd A.
Chaturvedi, Anil K.
Kemp, Troy J.
Pinto, Ligia A.
Moore, Steven C.
Purdue, Mark P.
Wentzensen, Nicolas
Hildesheim, Allan
Shiels, Meredith S.
TI Body Mass Index, Physical Activity, and Serum Markers of Inflammation,
Immunity, and Insulin Resistance
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID C-REACTIVE PROTEIN; ENDOMETRIAL CANCER-RISK; ADIPOSE-TISSUE;
BREAST-CANCER; OBESITY; WOMEN; COHORT; MECHANISMS; BIOMARKERS; LEPTIN
AB Background: Epidemiologic studies examining circulating levels of inflammatory markers in relation to obesity and physical inactivity may aid in our understanding of the role of inflammation in obesity-related cancers. However, previous studies on this topic have focused on a limited set of markers.
Methods: We evaluated associations between body mass index (BMI) and vigorous physical activity level, based on self-report, and serum levels of 78 inflammation-related markers. Markers were measured using a bead-based multiplex method among 1,703 men and women, ages 55-74 years, and with no prior history of cancer at blood draw, and selected for case-control studies nested within the Prostate, Lung, Ovarian, and Colorectal Cancer Screening Trial. Analyses were adjusted for age, sex, smoking, case-control study, physical activity, and BMI.
Results: Twelve markers were positively associated with BMI after FDR correction. ORs and 95% confidence interval (CI) for highest versus lowest levels of CCL2/MCP-1, CXCL5/ENA-78, sTNFRII, CXCL10/IP-10, CXCL6/GCP2, CCL13/MCP-4, amylin, CRP, C-peptide, CCL19/MIP-3b, insulin, and leptin were: 1.50 (1.14-1.98), 1.52 (1.12-2.05), 1.61 (1.17-2.20), 1.69 (1.25-2.28), 1.74 (1.24-2.44), 1.75 (1.22-2.50), 1.91 (1.31-2.78), 2.41 (1.36-4.25), 2.78 (1.83-4.24), 3.30 (2.28-4.78), 4.05 (2.51-6.55), and 50.03 (19.87-125.99) per 5 kg/m(2), respectively. Only CXCL12/SDF-1a was associated with physical activity (>= 3 vs. <1 h/wk; OR, 3.28; 95% CI, 1.55-6.94) after FDR correction.
Conclusions: BMI was associated with a wide range of circulating markers involved in the inflammatory response.
Impact: This cross-sectional analysis identified serum markers could be considered in future studies aimed at understanding the underlying mechanisms linking inflammation with obesity and obesity-related cancers. (C) 2014 AACR.
C1 [Kitahara, Cari M.; Trabert, Britton; Katki, Hormuzd A.; Chaturvedi, Anil K.; Moore, Steven C.; Purdue, Mark P.; Wentzensen, Nicolas; Hildesheim, Allan; Shiels, Meredith S.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Kemp, Troy J.; Pinto, Ligia A.] Leidos Biomed Res Inc, Frederick Natl Lab Canc Res, HPV Immunol Lab, Frederick, MD USA.
RP Kitahara, CM (reprint author), Div Canc Epidemiol & Genet, 9609 Med Ctr Dr,Room 7E 566, Bethesda, MD 20892 USA.
EM meinholdc@mail.nih.gov
RI Katki, Hormuzd/B-4003-2015; Hildesheim, Allan/B-9760-2015; Purdue,
Mark/C-9228-2016; Trabert, Britton/F-8051-2015; Moore,
Steven/D-8760-2016; Chaturvedi, Anil/J-2024-2015; Kitahara,
Cari/R-8267-2016
OI Hildesheim, Allan/0000-0003-0257-2363; Purdue, Mark/0000-0003-1177-3108;
Moore, Steven/0000-0002-8169-1661; Chaturvedi, Anil/0000-0003-2696-8899;
FU Intramural Research Program of the National Cancer Institute, NIH,
Bethesda, Maryland
FX This work was supported in part by the Intramural Research Program of
the National Cancer Institute, NIH, Bethesda, Maryland.
NR 34
TC 19
Z9 19
U1 0
U2 13
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 DEC
PY 2014
VL 23
IS 12
BP 2840
EP 2849
DI 10.1158/1055-9965.EPI-14-0699-T
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300025
PM 25249326
ER
PT J
AU Cui, Y
Shu, XO
Gao, YT
Cai, QY
Ji, BT
Li, HL
Rothman, N
Wu, J
Yang, G
Xiang, YB
Zheng, W
AF Cui, Yong
Shu, Xiao-Ou
Gao, Yu-Tang
Cai, Qiuyin
Ji, Bu-Tian
Li, Hong-Lan
Rothman, Nathaniel
Wu, Jie
Yang, Gong
Xiang, Yong-Bing
Zheng, Wei
TI Urinary Prostaglandin E-2 Metabolite and Breast Cancer Risk
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID CARCINOMA IN-SITU; ELEVATED AROMATASE EXPRESSION; CYCLOOXYGENASE-2
EXPRESSION; ASPIRIN USE; INFLAMMATION; OBESITY; TUMORIGENESIS;
METAANALYSIS; ASSOCIATION; INHIBITORS
AB Background: Levels of the cyclooxygenase 2 (COX2) enzyme are elevated in breast cancer tissue, and most COX2 effects are believed to be mediated through overproduction of prostaglandin E2 (PGE2). We evaluated associations between the primary urinary metabolite of PGE2 (PGE-M) and breast cancer risk.
Methods: A nested case-control study of 504 cases and 1,082 controls was conducted using data from the Shanghai Women's Health Study, a large population-based prospective cohort study of 74,941 Chinese women. Urinary PGE-M was measured using a liquid chromatography/tandem mass spectrometric method. Logistic regression estimated odds ratios (OR) and 95% confidence intervals (95% CI) with adjustment for potential confounders.
Results: Overall, no association between urinary PGE-M and breast cancer was detected. However, a suggestive positive association was found among postmenopausal women. In particular, a clear dose-response relationship between urinary PGE-M and breast cancer was observed among postmenopausal women with a body mass index (BMI) < 25 kg/m(2) (P-linear trend = 0.005). Among these women, risk of breast cancer increased from 1.00 (reference) to 1.06 (95% CI, 0.56-1.99), 1.50 (95% CI, 0.79-2.83), and 2.32 (95% CI, 1.24-4.41) for the lowest to highest quartiles of PGE-M, and such associations were stronger among those who were diagnosed with cancer within the first four years of sample collection. No apparent association was observed among overweight postmenopausal women (BMI >= 25 kg/m(2)).
Conclusion: High urinary PGE-M level was associated with elevated risk of breast cancer among normal weight, postmenopausal women.
Impact: Urinary PGE-M level may be useful for breast cancer risk assessment among normal weight, postmenopausal women. (C) 2014 AACR.
C1 [Cui, Yong; Shu, Xiao-Ou; Cai, Qiuyin; Wu, Jie; Yang, Gong; Zheng, Wei] Vanderbilt Univ, Vanderbilt Epidemiol Ctr, Vanderbilt Ingram Canc Ctr, Sch Med,Dept Med,Div Epidemiol, Nashville, TN 37203 USA.
[Gao, Yu-Tang; Li, Hong-Lan; Xiang, Yong-Bing] Shanghai Jiao Tong Univ, Renji Hosp, Sch Med, Shanghai Canc Inst,Dept Epidemiol, Shanghai 200030, Peoples R China.
[Ji, Bu-Tian; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, NIH, Rockville, MD USA.
[Gao, Yu-Tang; Li, Hong-Lan; Xiang, Yong-Bing] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
RP Zheng, W (reprint author), Vanderbilt Univ, Vanderbilt Epidemiol Ctr, Sch Med, 2525 West End Ave,8th Floor, Nashville, TN 37203 USA.
EM wei.zheng@vanderbilt.edu
FU U.S. NIH [R37 CA070867]
FX This study was supported by grant number R37 CA070867 (to W. Zheng) from
the U.S. NIH.
NR 38
TC 7
Z9 7
U1 0
U2 6
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 DEC
PY 2014
VL 23
IS 12
BP 2866
EP 2873
DI 10.1158/1055-9965.EPI-14-0685
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300028
PM 25214156
ER
PT J
AU Tasevska, N
Midthune, D
Tinker, LF
Potischman, N
Lampe, JW
Neuhouser, ML
Beasley, JM
van Horn, L
Prentice, RL
Kipnis, V
AF Tasevska, Natasha
Midthune, Douglas
Tinker, Lesley F.
Potischman, Nancy
Lampe, Johanna W.
Neuhouser, Marian L.
Beasley, Jeannette M.
van Horn, Linda
Prentice, Ross L.
Kipnis, Victor
TI Use of a Urinary Sugars Biomarker to Assess Measurement Error in
Self-Reported Sugars Intake in the Nutrition and Physical Activity
Assessment Study (NPAAS)
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID FOOD FREQUENCY QUESTIONNAIRE; DOUBLY LABELED WATER; RECOVERY BIOMARKERS;
ENERGY-EXPENDITURE; EPIDEMIOLOGIC ASSESSMENT; CALIBRATION EQUATIONS;
OBSERVING PROTEIN; HEALTH; CONSUMPTION; RELIABILITY
AB Background: Measurement error in self- reported sugars intake may be obscuring the association between sugars and cancer risk in nutritional epidemiologic studies.
Methods: We used 24-hour urinary sucrose and fructose as a predictive biomarker for total sugars, to assess measurement error in self-reported sugars intake. The Nutrition and Physical Activity Assessment Study (NPAAS) is a biomarker study within the Women's Health Initiative (WHI) Observational Study that includes 450 postmenopausal women ages 60 to 91 years. Food Frequency Questionnaires (FFQ), four-day food records (4DFR), and three 24-hour dietaryrecalls (24HRs) were collected along with sugars and energy dietary biomarkers.
Results: Using the biomarker, we found self-reported sugars to be substantially and roughly equally misreported across the FFQ, 4DFR, and 24HR. All instruments were associated with considerable intake-and person-specific bias. Three 24HRs would provide the least attenuated risk estimate for sugars (attenuation factor, AF = 0.57), followed by FFQ (AF = 0.48) and 4DFR (AF = 0.32), in studies of energy-adjusted sugars and disease risk. In calibration models, self-reports explained little variation in true intake (5%-6% for absolute sugars and 7%-18% for sugars density). Adding participants' characteristics somewhat improved the percentage variation explained (16%-18% for absolute sugars and 29%-40% for sugars density).
Conclusions: None of the self-report instruments provided a good estimate of sugars intake, although overall 24HRs seemed to perform the best.
Impact: Assuming the calibrated sugars biomarker is unbiased, this analysis suggests that measuring the biomarker in a subsample of the study population for calibration purposes may be necessary for obtaining unbiased risk estimates in cancer association studies. (C) 2014 AACR.
C1 [Tasevska, Natasha; Midthune, Douglas; Potischman, Nancy; Kipnis, Victor] NCI, Bethesda, MD 20892 USA.
[Tasevska, Natasha] Arizona State Univ, Sch Nutr & Hlth Promot, Phoenix, AZ 85004 USA.
[Tinker, Lesley F.; Lampe, Johanna W.; Neuhouser, Marian L.; Prentice, Ross L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98104 USA.
[Beasley, Jeannette M.] Albert Einstein Coll Med, Dept Epidemiol & Populat Sci, Bronx, NY 10467 USA.
[van Horn, Linda] Northwestern Univ, Dept Prevent Med, Chicago, IL 60611 USA.
RP Tasevska, N (reprint author), Arizona State Univ, Sch Nutr & Hlth Promot, 500 North 3rd St, Phoenix, AZ 85004 USA.
EM natasha.tasevska@asu.edu
OI Beasley, Jeannette/0000-0002-9343-6895
FU Intramural Research Program of the National Cancer Institute, NIH;
National Cancer Institute [R01 CA119171-04A1]; National Heart, Lung, and
Blood Institute, NIH; U.S. Department of Health and Human Services
[HHSN268201100046C, HHSN268201100001C, HHSN268201100002C,
HHSN268201100003C, HHSN268201100004C, HHSN271201100004C]
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, NIH, U.S. Department of Health and Human
Services. The NPAAS was supported by the National Cancer Institute grant
R01 CA119171-04A1 (L.F. Tinker, J.W. Lampe, M.L. Neuhouser, and R.L.
Prentice). The WHI program is funded by the National Heart, Lung, and
Blood Institute, NIH, U.S. Department of Health and Human Services
through contracts HHSN268201100046C, HHSN268201100001C,
HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and
HHSN271201100004C.
NR 35
TC 8
Z9 8
U1 2
U2 8
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 DEC
PY 2014
VL 23
IS 12
BP 2874
EP 2883
DI 10.1158/1055-9965.EPI-14-0594
PG 10
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300029
PM 25234237
ER
PT J
AU Okayama, H
Schetter, AJ
Ishigame, T
Robles, AI
Kohno, T
Yokota, J
Takenoshita, S
Harris, CC
AF Okayama, Hirokazu
Schetter, Aaron J.
Ishigame, Teruhide
Robles, Ana I.
Kohno, Takashi
Yokota, Jun
Takenoshita, Seiichi
Harris, Curtis C.
TI The Expression of Four Genes as a Prognostic Classifier for Stage I Lung
Adenocarcinoma in 12 Independent Cohorts
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; ADJUVANT CHEMOTHERAPY; SURVIVAL PREDICTION;
CANCER PATIENTS; BREAST-CANCER; SIGNATURES; VALIDATION; METAANALYSES;
ASSAY
AB Background: We previously developed a prognostic classifier using the expression levels of BRCA1, HIF1A, DLC1, and XPO1 that identified stage I lung adenocarcinoma patients with a high risk of relapse. That study evaluated patients in five independent cohorts from various regions of the world. In an attempt to further validate the classifier, we have used a meta-analysis-based approach to study 12 cohorts consisting of 1,069 tumor-node-metastasis stage I lung adenocarcinoma patients from every suitable, publically available dataset.
Methods: Cohorts were obtained through a systematic search of public gene expression datasets. These data were used to calculate the risk score using the previously published 4-gene risk model. A fixed effect metaanalysis model was used to generate a pooled estimate for all cohorts.
Results: The classifier was associated with prognosis in 10 of the 12 cohorts (P < 0.05). This association was highly consistent regardless of the ethnic diversity or microarray platform. The pooled estimate demonstrated that patients classified as high risk had worse overall survival for all stage I [HR, 2.66; 95% confidence interval (CI), 1.93-3.67; P < 0.0001] patients and in stratified analyses of stage IA (HR, 2.69; 95% CI, 1.66-4.35; P < 0.0001) and stage IB (HR, 2.69; 95% CI, 1.74-4.16; P < 0.0001) patients.
Conclusions: The 4-gene classifier provides independent prognostic stratification of stage IA and stage IB patients beyond conventional clinical factors.
Impact: Our results suggest that the 4-gene classifier may assist clinicians in decisions about the postoperative management of early-stage lung adenocarcinoma patients. (C) 2014 AACR.
C1 [Okayama, Hirokazu; Schetter, Aaron J.; Ishigame, Teruhide; Robles, Ana I.; Harris, Curtis C.] NCI, Ctr Canc Res, Human Carcinogenesis Lab, NIH, Bethesda, MD 20892 USA.
[Kohno, Takashi] Natl Canc Ctr, Res Inst, Div Genome Biol, Tokyo 104, Japan.
[Yokota, Jun] Inst Predict & Personalized Med Canc, Genom & Epigenom Canc Predict Program, Barcelona, Spain.
[Takenoshita, Seiichi] Fukushima Med Univ, Sch Med, Dept Organ Regulatory Surg, Fukushima, Japan.
RP Harris, CC (reprint author), NCI, Human Carcinogenesis Lab, NIH, 37 Convent Dr MSC4258,Bldg 37,Room 3068A, Bethesda, MD 20892 USA.
EM Curtis_Harris@nih.gov
FU Intramural Research Program of the National Cancer Institute, NIH;
Department of Defense Congressionally Directed Medical Research Program
[PR093793]
FX This work was supported by the Intramural Research Program of the
National Cancer Institute, NIH and Department of Defense Congressionally
Directed Medical Research Program Grant PR093793.
NR 44
TC 12
Z9 12
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
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 2014
VL 23
IS 12
BP 2884
EP 2894
DI 10.1158/1055-9965.EPI-14-0182
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300030
PM 25242053
ER
PT J
AU Arnold, KB
Hermos, JA
Anderson, KB
Minasian, L
Tangen, CM
Probstfield, JF
Cook, ED
AF Arnold, Kathryn B.
Hermos, John A.
Anderson, Karen B.
Minasian, Lori
Tangen, Catherine M.
Probstfield, Jeffrey F.
Cook, Elise D.
TI Retention of Black and White Participants in the Selenium and Vitamin E
Cancer Prevention Trial (SWOG-Coordinated Intergroup Study S0000)
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID AFRICAN-AMERICAN MEN; FOLLOW-UP; CLINICAL-TRIALS; PROSTATE-CANCER;
MINORITY RECRUITMENT; SCREENING TRIAL; COLORECTAL-CANCER; RISK; HEALTH;
SELECT
AB Background: Disproportionally low retention of minority populations can adversely affect the generalizability of clinical research trials. We determine the overall retention rates for White and Black participants from the Selenium and Vitamin E Cancer Prevention Trial (SELECT) and explore participant and site characteristics associated with retention failure (study disengagement) for these groups.
Methods: A secondary analysis of 28,118 White (age >= 55), and 4,322 Black (age >= 50) SELECT participants used multivariate Cox regression to estimate overall retention rates and to calculate HRs and 95% confidence intervals (CI).
Results: Blacks had higher age-adjusted risk of disengagement than Whites (HR, 1.92; 95% CI, 1.77-2.08). Among Black participants, those ages 50 to 54 were at three times the risk of disengagement than those >= 65 years of age (HR, 3.61; 95% CI, 2.41-5.41). Blacks age >= 65 had 1.6 times the risk of disengagement than Whites age >= 65 (HR, 1.60; 95% CI, 1.38-1.87). By 6 years after randomization, 84% of Whites and 69% of Blacks remained engaged in the study. Current smoking status was an independent risk factor for study disengagement for both White and Black participants. For both groups, sites whose staffs missed SELECT training sessions or who received SELECT Retention and Adherence grants were associated with increased and decreased disengagement risks, respectively.
Conclusions: SELECT retention was disproportionately lower for Blacks than for Whites.
Impact: The observed difference in retention rates for Blacks and Whites and factors identified by race for study disengagement in SELECT may inform retention efforts for future long-term, cancer prevention trials. (C) 2014 AACR.
C1 [Arnold, Kathryn B.; Tangen, Catherine M.] Fred Hutchinson Canc Res Ctr, SWOG Stat Ctr, Seattle, WA 98109 USA.
[Hermos, John A.] VA Boston Healthcare Syst, VA Cooperat Studies Program, Coordinating Ctr, Boston, MA USA.
[Anderson, Karen B.] SWOG Data Management Canc Res & Biostat, Seattle, WA USA.
[Minasian, Lori] NCI, Div Canc Prevent, Rockville, MD USA.
[Probstfield, Jeffrey F.] Univ Washington, Dept Med, Clin Trials Serv Unit, Seattle, WA USA.
[Cook, Elise D.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
RP Arnold, KB (reprint author), Fred Hutchinson Canc Res Ctr, SWOG Stat Ctr, 1100 Fairview Ave North,M3-C102,POB 19024, Seattle, WA 98109 USA.
EM karnold@fhcrc.org
FU Public Health Service Cooperative Agreement, National Cancer Institute,
NIH, Department of Health and Human Services [CA37429]; National Center
for Complementary and Alternative Medicine (NIH)
FX This research was supported in part by Public Health Service Cooperative
Agreement grant CA37429 (to K.B. Arnold, K.B. Anderson, C.M. Tangen; and
PI, C. Blanke) awarded by the National Cancer Institute, NIH, Department
of Health and Human Services, and in part by the National Center for
Complementary and Alternative Medicine (NIH). Study agents and packaging
were provided by Perrigo Company (Allegan, MI), Sabinsa Corporation
(Piscataway, NJ), Tishcon Corporation (Westbury, NY), and DSM
Nutritional Products Inc.
NR 46
TC 2
Z9 2
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
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 2014
VL 23
IS 12
BP 2895
EP 2905
DI 10.1158/1055-9965.EPI-14-0724
PG 11
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300031
PM 25242051
ER
PT J
AU Han, PKJ
Williams, AE
Haskins, A
Gutheil, C
Lucas, FL
Klein, WMP
Mazor, KM
AF Han, Paul K. J.
Williams, Andrew E.
Haskins, Amy
Gutheil, Caitlin
Lucas, F. Lee
Klein, William M. P.
Mazor, Kathleen M.
TI Individual Differences in Aversion to Ambiguity Regarding Medical Tests
and Treatments: Association with Cancer Screening Cognitions
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID PREFERENCES; UNCERTAINTY; RISK; LITERACY; CARE
AB Background: Aversion to "ambiguity"-uncertainty about the reliability, credibility, or adequacy of information-about medical tests and treatments is an important psychological response that varies among individuals, but little is known about its nature and extent. The purpose of this study was to examine how individual-level ambiguity aversion relates to important health cognitions related to different cancer screening tests.
Methods: A survey of 1,074 adults, ages 40 to 70 years, was conducted in four integrated U.S. healthcare systems. The Ambiguity Aversion in Medicine (AA-Med) scale, a measure of individual differences in aversion to ambiguity (AA) about medical tests and treatments, was administered along with measures of several cancer screening-related cognitions: perceived benefits and harms of colonoscopy, mammography, and PSA screening, and ambivalence and future intentions regarding these tests. Multivariable analyses were conducted to assess the associations between AA-Med scores and cancer screening cognitions.
Results: Individual-level AA as assessed by the AA-Med scale was significantly associated (P < 0.05) with lower perceived benefits, greater perceived harms, and greater ambivalence about all three screening tests, and lower intentions for colonoscopy but not mammography or PSA screening.
Conclusion: Individual-level AA is broadly and simultaneously associated with various pessimistic cognitive appraisals of multiple cancer screening tests. The breadth of these associations suggests that the influence of individual-level AA is insensitive to the degree and nonspecific with respect to the causes of ambiguity.
Impact: Individual-level AA constitutes a measurable, wide-ranging cognitive bias against medical intervention, and more research is needed to elucidate its mechanisms and effects. (C) 2014 AACR.
C1 [Han, Paul K. J.; Williams, Andrew E.; Haskins, Amy; Gutheil, Caitlin; Lucas, F. Lee] Maine Med Ctr, Ctr Outcomes Res Evaluat, Portland, ME 04101 USA.
[Klein, William M. P.] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Mazor, Kathleen M.] Univ Massachusetts, Sch Med, Meyers Primary Care Inst, Worcester, MA USA.
RP Han, PKJ (reprint author), Maine Med Ctr, Ctr Outcomes Res Evaluat, 509 Forest Ave, Portland, ME 04101 USA.
EM hanp@mmc.org
OI Han, Paul/0000-0003-0165-1940
FU National Cancer Institute [U19 CA079689]
FX This work was supported by the National Cancer Institute (grant U19
CA079689; to K.M. Mazor, A.E. Williams, and P.K.J. Han).
NR 18
TC 3
Z9 3
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
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 2014
VL 23
IS 12
BP 2916
EP 2923
DI 10.1158/1055-9965.EPI-14-0872
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300033
PM 25258015
ER
PT J
AU Du, MM
Zhang, XH
Hoffmeister, M
Schoen, RE
Baron, JA
Berndt, SI
Brenner, H
Carlson, CS
Casey, G
Chan, AT
Curtis, KR
Duggan, D
Gauderman, WJ
Giovannucci, EL
Gong, J
Harrison, TA
Hayes, RB
Henderson, BE
Hopper, JL
Hsu, L
Hudson, TJ
Hutter, CM
Jenkins, MA
Jiao, S
Kocarnik, JM
Kolonel, LN
Le Marchand, L
Lin, Y
Newcomb, PA
Rudolph, A
Seminara, D
Thornquist, MD
Ulrich, CM
White, E
Wu, K
Zanke, BW
Campbell, PT
Slattery, ML
Peters, U
Chang-Claude, J
Potter, JD
AF Du, Mengmeng
Zhang, Xuehong
Hoffmeister, Michael
Schoen, Robert E.
Baron, John A.
Berndt, Sonja I.
Brenner, Hermann
Carlson, Christopher S.
Casey, Graham
Chan, Andrew T.
Curtis, Keith R.
Duggan, David
Gauderman, W. James
Giovannucci, Edward L.
Gong, Jian
Harrison, Tabitha A.
Hayes, Richard B.
Henderson, Brian E.
Hopper, John L.
Hsu, Li
Hudson, Thomas J.
Hutter, Carolyn M.
Jenkins, Mark A.
Jiao, Shuo
Kocarnik, Jonathan M.
Kolonel, Laurence N.
Le Marchand, Loic
Lin, Yi
Newcomb, Polly A.
Rudolph, Anja
Seminara, Daniela
Thornquist, Mark D.
Ulrich, Cornelia M.
White, Emily
Wu, Kana
Zanke, Brent W.
Campbell, Peter T.
Slattery, Martha L.
Peters, Ulrike
Chang-Claude, Jenny
Potter, John D.
CA Colon Canc Family Registry Geneti
TI No Evidence of Gene-Calcium Interactions from Genome-Wide Analysis of
Colorectal Cancer Risk
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID ENVIRONMENT INTERACTIONS; SUSCEPTIBILITY LOCI; METAANALYSIS
AB Background: Calcium intake may reduce risk of colorectal cancer, but the mechanisms remain unclear. Studies of interaction between calcium intake and SNPs in calcium-related pathways have yielded inconsistent results.
Methods: To identify gene-calcium interactions, we tested interactions between approximately 2.7 million SNPs across the genome with self-reported calcium intake (from dietary or supplemental sources) in 9,006 colorectal cancer cases and 9,503 controls of European ancestry. To test for multiplicative interactions, we used multivariable logistic regression and defined statistical significance using the conventional genome-wide alpha = 5E-08.
Results: After accounting for multiple comparisons, there were no statistically significant SNP interactions with total, dietary, or supplemental calcium intake.
Conclusions: We found no evidence of SNP interactions with calcium intake for colorectal cancer risk in a large population of 18,509 individuals.
Impact: These results suggest that in genome-wide analysis common genetic variants do not strongly modify the association between calcium intake and colorectal cancer in European populations. (C) 2014 AACR.
C1 [Du, Mengmeng; Carlson, Christopher S.; Curtis, Keith R.; Gong, Jian; Harrison, Tabitha A.; Hsu, Li; Hutter, Carolyn M.; Jiao, Shuo; Kocarnik, Jonathan M.; Lin, Yi; Newcomb, Polly A.; Thornquist, Mark D.; Ulrich, Cornelia M.; White, Emily; Peters, Ulrike; Potter, John D.] Fred Hutchinson Canc Res Ctr, Publ Hlth Sci Div, Seattle, WA 98109 USA.
[Du, Mengmeng; Kocarnik, Jonathan M.; Newcomb, Polly A.; Ulrich, Cornelia M.; White, Emily; Peters, Ulrike; Potter, John D.] Univ Washington, Sch Publ Hlth, Seattle, WA 98195 USA.
[Du, Mengmeng; Zhang, Xuehong; Chan, Andrew T.; Giovannucci, Edward L.] Brigham & Womens Hosp, Channing Div Network Med, Boston, MA 02115 USA.
[Du, Mengmeng; Zhang, Xuehong; Chan, Andrew T.; Giovannucci, Edward L.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Hoffmeister, Michael; Brenner, Hermann] German Canc Res Ctr, Div Clin Epidemiol & Aging Res, Heidelberg, Germany.
[Schoen, Robert E.] Univ Pittsburgh, Med Ctr, Dept Med & Epidemiol, Pittsburgh, PA USA.
[Baron, John A.] Univ N Carolina, Sch Med, Dept Med, Chapel Hill, NC USA.
[Berndt, Sonja I.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Brenner, Hermann] German Canc Consortium DKTK, Heidelberg, Germany.
[Casey, Graham] Univ So Calif, Dept Prevent Med, Los Angeles, CA 90089 USA.
[Chan, Andrew T.] Massachusetts Gen Hosp, Div Gastroenterol, Boston, MA 02114 USA.
[Chan, Andrew T.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Duggan, David] Genet Basis Human Dis Translat Genom Res Inst TGe, Phoenix, AZ USA.
[Gauderman, W. James] Univ So Calif, Keck Sch Med, Los Angeles, CA 90033 USA.
[Giovannucci, Edward L.; Wu, Kana] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Giovannucci, Edward L.] Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
[Hayes, Richard B.; Jenkins, Mark A.] NYU, Sch Med, Dept Populat Hlth, Div Epidemiol, New York, NY USA.
[Hopper, John L.; Jenkins, Mark A.] Univ Melbourne, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.
[Hudson, Thomas J.] Ontario Inst Canc Res, Toronto, ON, Canada.
[Hudson, Thomas J.] Univ Toronto, Dept Med Biophys, Toronto, ON, Canada.
[Hudson, Thomas J.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
[Hutter, Carolyn M.; Seminara, Daniela; Chang-Claude, Jenny] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
[Kolonel, Laurence N.; Le Marchand, Loic] Univ Hawaii, Ctr Canc, Program Epidemiol, Honolulu, HI 96822 USA.
[Rudolph, Anja] German Canc Res Ctr, Div Canc Epidemiol, Unit Genet Epidemiol, Heidelberg, Germany.
[Ulrich, Cornelia M.] Natl Ctr Tumor Dis NCT, Heidelberg, Germany.
[Zanke, Brent W.] Univ Ottawa, Fac Med, Div Hematol, Ottawa, ON, Canada.
[Campbell, Peter T.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
[Slattery, Martha L.] Univ Utah, Hlth Sci Ctr, Dept Internal Med, Salt Lake City, UT USA.
[Potter, John D.] Massey Univ, Ctr Publ Hlth Res, Wellington, New Zealand.
RP Du, MM (reprint author), Fred Hutchinson Canc Res Ctr, Canc Prevent Program, 1100 Fairview Ave North,M4-B402, Seattle, WA 98109 USA.
EM mdu@fhcrc.org
RI Hoffmeister, Michael/B-5745-2012; Brenner, Hermann/B-4627-2017; Jenkins,
Mark/P-7803-2015;
OI Hoffmeister, Michael/0000-0002-8307-3197; Brenner,
Hermann/0000-0002-6129-1572; Potter, John/0000-0001-5439-1500; Jenkins,
Mark/0000-0002-8964-6160; Hayes, Richard/0000-0002-0918-661X
FU National Cancer Institute, NIH, U.S. Department of Health and Human
Services [U01 CA137088, R01 CA059045]; NIH [R01 CA60987, R01 CA48998,
P01 CA 055075, UM1 CA167552, R01 137178, P50 CA127003, R01 CA137178, P01
CA 087969, P50 CA 127003, R01 CA42182, R37 CA54281, P01 CA033619, R01
CA63464, U01 CA074783, U01 HG004446, R01 CA076366]; NIH (RFA)
[CA-95011]; National Cancer Institute, NIH [U01 CA122839, R25 CA94880];
NIH: Australasian Colorectal Cancer Family Registry [U01 CA097735];
Ontario Registry for Studies of Familial Colorectal Cancer [U01
CA074783]; Seattle Colorectal Cancer Family Registry [U01 CA074794];
German Research Council (Deutsche Forschungsgemeinschaft) [BR 17046-1,
BR 17046-3, BR 17046-4, CH1171-1]; German Federal Ministry of Education
and Research [01KH0404, 01ER0814]; Ontario Research Fund; Canadian
Institutes of Health Research; Ontario Institute for Cancer Research,
through Ontario Ministry of Research and Innovation; Intramural Research
Program of the Division of Cancer Epidemiology and Genetics; Division of
Cancer Prevention, National Cancer Institute, NIH, DHHS; National
Institutes of Health (NIH) Genes, Environment, and Health Initiative
(GEI) [Z01 CP 010200]; NIH GEI [U01 HG 004438]; NIH from the National
Cancer Institute [K05 CA154337]; NIH from the Office of Dietary
Supplements; ACS; GECCO [R01 CA059045]; National Institutes of
Environmental Health Sciences [ES020801]; National Heart, Lung, and
Blood Institute, NIH, U.S. Department of Health and Human Services
[HHSN268201100046C, HHSN268201100001C, HHSN268201100002C,
HHSN268201100003C, HHSN268201100004C, HHSN271201100004C]; [U19
CA148107]
FX C.S. Carlson, K.R. Curtis, M. Du, J. Gong, T. A. Harrison, L. Hsu, C.M.
Hutter, J.M. Kocarnik, S. Jiao, Y. Lin, U. Peters, M.D. Thornquist, and
C.M. Ulrich are affiliated with GECCO, which is supported by the
following grants from the National Cancer Institute, NIH, U.S.
Department of Health and Human Services: U01 CA137088 and R01 CA059045.;
L. Le Marchand is affiliated with COLO2& 3, which is supported by the
NIH (R01 CA60987).; J.A. Baron, G. Casey, J.L. Hopper, M.A. Jenkins, and
P.A. Newcomb are affiliated with CCFR, which is supported by the NIH
(RFA # CA-95011) 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, NIH by U01 CA122839. The
following Colon CFR centers contributed data to this article and were
supported by NIH: Australasian Colorectal Cancer Family Registry (U01
CA097735), Ontario Registry for Studies of Familial Colorectal Cancer
(U01 CA074783), and Seattle Colorectal Cancer Family Registry (U01
CA074794).; H. Brenner, J. Chang-Claude, M. Hoffmeister, and A. Rudolph
are affiliated with DACHS, which was supported by grants from the German
Research Council (Deutsche Forschungsgemeinschaft, BR 17046-1, BR
17046-3, BR 17046-4 and CH1171-1), and the German Federal Ministry of
Education and Research (01KH0404 and 01ER0814).; J.D. Potter and M.L.
Slattery are affiliated with DALS, which was supported by the NIH (R01
CA48998 to M.L. Slattery). A.T. Chan, E.L. Giovannucci, K. Wu, and X.
Zhang are affiliated with HPFS, NHS, and PHS. HPFS was supported by the
NIH (P01 CA 055075, UM1 CA167552, R01 137178, and P50 CA127003), NHS by
the NIH (R01 CA137178, P01 CA 087969, and P50 CA 127003), and PHS by the
NIH (R01 CA42182).; B.E. Henderson, L.N. Kolonel, and L. Le Marchand are
affiliated with MEC, which is supported by the following grants from the
NIH: R37 CA54281, P01 CA033619, and R01 CA63464.; T.J. Hudson and B.W.
Zanke are affiliated with OFCCR, which is supported by the NIH, through
funding allocated to the Ontario Registry for Studies of Familial
Colorectal Cancer (U01 CA074783); see CCFR section above. Additional
funding toward genetic analyses of OFCCR includes the Ontario Research
Fund, the Canadian Institutes of Health Research, and the Ontario
Institute for Cancer Research, through generous support from the Ontario
Ministry of Research and Innovation.; S.I. Berndt, R.B. Hayes, and R.E.
Schoen are affiliated with PLCO, which 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, NIH, DHHS. In addition, a subset of control samples
were genotyped as part of the Cancer Genetic Markers of Susceptibility
(CGEMS) Prostate Cancer GWAS (Yeager, M and colleagues Genome-wide
association study of prostate cancer identifies a second risk locus at
8q24. Nat Genet. 2007 May; 39(5): 645-9), Colon CGEMS pancreatic cancer
scan (PanScan; Amundadottir, L and colleagues Genome-wide association
study identifies variants in the ABO locus associated with
susceptibility to pancreatic cancer. Nat Genet. 2009 Sep;41(9):986-90,
and Petersen, GM and colleagues A genome-wide association study
identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1,
1q32.1 and 5p15.33. Nat Genet. 2010 Mar;42(3):224-8), and the Lung
Cancer and Smoking study (Landi MT, and colleagues A genome-wide
association study of lung cancer identifies a region of chromosome 5p15
associated with risk for adenocarcinoma. Am J Hum Genet. 2009
Nov;85(5):679-91). The prostate and PanScan study datasets were accessed
with appropriate approval through the dbGaP online resource
(http://cgems.cancer.gov/data/) accession numbers phs000207.v1.p1 and
phs000206.v3.p2, respectively, and the lung datasets were accessed from
the dbGaP website (http://www.ncbi.nlm.nih.gov/gap) through accession
number phs000093.v2.p2. Funding for the Lung Cancer and Smoking study
was provided by National Institutes of Health (NIH), Genes, Environment,
and Health Initiative (GEI) Z01 CP 010200, NIH U01 HG004446, and NIH GEI
U01 HG 004438. For the lung study, the GENEVA Coordinating Center
provided assistance with genotype cleaning and general study
coordination, and the Johns Hopkins University Center for Inherited
Disease Research conducted genotyping.; P.A. Newcomb is affiliated with
PMH, which is supported by the NIH (R01 CA076366 to P.A. Newcomb). E.
White is affiliated with VITAL, which is supported in part by the NIH
(K05 CA154337) from the National Cancer Institute and Office of Dietary
Supplements.; P.T. Campbell is at the American Cancer Society (ACS) and
funded through ACS.; M. Du is supported by the National Cancer
Institute, NIH (R25 CA94880).; D. Duggan is affiliated with TGEN and
funded through a subaward with GECCO (R01 CA059045).; W.J. Gauderman is
affiliated with Colorectal Transdisciplinary Study (CORECT), which is
funded through U19 CA148107, and by the National Institutes of
Environmental Health Sciences (ES020801).; D. Seminara is a Senior
Scientist and Consortia Coordinator at the Epidemiology and Genetics
Research Program, Division of Cancer Control and Population Sciences,
National Cancer Institute, NIH.; The WHI program is funded by the
National Heart, Lung, and Blood Institute, NIH, U.S. Department of
Health and Human Services through contracts HHSN268201100046C,
HHSN268201100001C, HHSN268201100002C, HHSN268201100003C,
HHSN268201100004C, and HHSN271201100004C.
NR 8
TC 1
Z9 1
U1 0
U2 3
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 DEC
PY 2014
VL 23
IS 12
BP 2971
EP 2976
DI 10.1158/1055-9965.EPI-14-0893
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300040
PM 25192705
ER
PT J
AU Kim, C
Bassig, BA
Seow, WJ
Hu, W
Purdue, MP
Shu, XO
Huang, WY
Liu, CS
Cheng, WL
Lin, TT
Xiang, YB
Ji, BT
Gao, YT
Chow, WH
Mannisto, S
Weinstein, SJ
Albanes, D
Zheng, W
Hosgood, HD
Lim, U
Rothman, N
Lan, Q
AF Kim, Christopher
Bassig, Bryan A.
Seow, Wei Jie
Hu, Wei
Purdue, Mark P.
Shu, Xiao-Ou
Huang, Wen-Yi
Liu, Chin-San
Cheng, Wen-Ling
Lin, Ta-Tsung
Xiang, Yong-Bing
Ji, Bu-Tian
Gao, Yu-Tang
Chow, Wong-Ho
Maennistoe, Satu
Weinstein, Stephanie J.
Albanes, Demetrius
Zheng, Wei
Hosgood, H. Dean
Lim, Unhee
Rothman, Nathaniel
Lan, Qing
TI Pooled Analysis of Mitochondrial DNA Copy Number and Lung Cancer Risk in
Three Prospective Studies
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID OXIDATIVE STRESS
AB Background: We previously reported that higher levels of mitochondrial DNA copy number (mtDNA CN) were associated with lung cancer risk among male heavy smokers (i.e., >= 20 cigarettes per day) in the Alpha-Tocopherol Beta-Carotene (ATBC) study. Here, we present two additional prospective investigations nested in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cancer screening trial and the Shanghai Women's Health Study (SWHS), and pooled with previously published data from ATBC.
Materials: All DNA were extracted from peripheral whole blood samples using the phenol-chloroform method, and mtDNA CN was assayed by fluorescence-based qPCR. Multivariate unconditional logistic regression models were used to estimate ORs and 95% confidence intervals for the association of mtDNA CN and lung cancer risk.
Results: Overall, mtDNA CN was not associated with lung cancer risk in the PLCO, SWHS, or pooled populations (all P trends > 0.42, P heterogeneity = 0.0001), and mtDNA CN was inversely associated with lung cancer risk among male smokers in PLCO, the opposite direction observed in ATBC. In addition, the mtDNA CN association observed among male heavy smokers in ATBC was the opposite direction in PLCO.
Conclusions: mtDNA CN was not consistently associated with lung cancer risk across three prospective study populations from Europe, Asia, and the United States.
Impact: This pooled study suggests no consistent association between prediagnostic mtDNA CN levels and lung cancer risk across several populations. (C) 2014 AACR.
C1 [Kim, Christopher; Bassig, Bryan A.; Seow, Wei Jie; Hu, Wei; Purdue, Mark P.; Huang, Wen-Yi; Ji, Bu-Tian; Weinstein, Stephanie J.; Albanes, Demetrius; Rothman, Nathaniel; Lan, Qing] NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Shu, Xiao-Ou; Zheng, Wei] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Liu, Chin-San; Cheng, Wen-Ling; Lin, Ta-Tsung] Changhua Christian Hosp, Neurol & Vasc & Genom Ctr, Changhua, Taiwan.
[Xiang, Yong-Bing] Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, Shanghai Canc Inst, Shanghai 200030, Peoples R China.
[Gao, Yu-Tang] Shanghai Canc Inst, Shanghai, Peoples R China.
[Chow, Wong-Ho] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Maennistoe, Satu] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
[Hosgood, H. Dean] Yeshiva Univ Albert Einstein Coll Med, Bronx, NY 10461 USA.
[Lim, Unhee] Univ Hawaii, Ctr Canc, Program Epidemiol, Honolulu, HI 96822 USA.
RP Kim, C (reprint author), NCI, NIH, 9609 Med Ctr Dr,MSSC 9771, Bethesda, MD 20892 USA.
EM christopher.kim@nih.gov
RI Albanes, Demetrius/B-9749-2015; Purdue, Mark/C-9228-2016;
OI Purdue, Mark/0000-0003-1177-3108; Mannisto, Satu/0000-0002-8668-3046
FU NIH intramural research program
FX This study was supported by NIH intramural research program.
NR 8
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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
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD DEC
PY 2014
VL 23
IS 12
BP 2977
EP 2980
DI 10.1158/1055-9965.EPI-14-1070
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA AW0FU
UT WOS:000345967300041
PM 25293879
ER
PT J
AU Tucker, JA
Jochems, C
Boyerinas, B
Fallon, J
Greiner, JW
Palena, C
Rodell, TC
Schlom, J
Tsang, KY
AF Tucker, Jo A.
Jochems, Caroline
Boyerinas, Benjamin
Fallon, Jonathan
Greiner, John W.
Palena, Claudia
Rodell, Timothy C.
Schlom, Jeffrey
Tsang, Kwong-Yok
TI Identification and characterization of a cytotoxic T-lymphocyte agonist
epitope of brachyury, a transcription factor involved in epithelial to
mesenchymal transition and metastasis
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Agonist epitope; Brachyury; Cytotoxic T lymphocytes (CTL); Epithelial to
mesenchymal transition (EMT); Immunotherapy; Saccharomyces cerevisiae
vector
ID PROSTATE-SPECIFIC ANTIGEN; CARCINOEMBRYONIC ANTIGEN; TUMOR-CELLS;
VACCINE; CANCER; PROGRESSION; EXPRESSION; RESISTANCE; REGULATOR; TARGET
AB The transcription factor brachyury is a major driver of epithelial to mesenchymal transition in human carcinoma cells. It is overexpressed in several human tumor types versus normal adult tissues, except for testes and thyroid. Overexpression is associated with drug resistance and poor prognosis. Previous studies identified a brachyury HLA-A2 cytotoxic T-lymphocyte epitope. The studies reported here describe an enhancer epitope of brachyury. Compared to the native epitope, the agonist epitope: (a) has enhanced binding to MHC class I, (b) increased the IFN-gamma production from brachyury-specific T cells, (c) generated brachyury-specific T cells with greater levels of perforin and increased proliferation, (d) generated T cells more proficient at lysing human carcinoma cells endogenously expressing the native epitope, and (e) achieved greater brachyury-specific T-cell responses in vivo in HLA-A2 transgenic mice. These studies also report the generation of a heat-killed recombinant Saccharomyces cerevisiae (yeast) vector expressing the full-length brachyury gene encoding the agonist epitope. Compared to yeast-brachyury (native) devoid of the agonist epitope, the yeast-brachyury (agonist) enhanced the activation of brachyury-specific T cells, which efficiently lysed human carcinoma cells. In addition to providing the rationale for the recombinant yeast-brachyury (agonist) as a potential vaccine in cancer therapy, these studies also provide the rationale for the use of the agonist in (a) dendritic cell (DC) vaccines, (b) adjuvant or liposomal vaccines, (c) recombinant viral and/or bacterial vaccines, (d) protein/polypeptide vaccines, (e) activation of T cells ex vivo in adoptive therapy protocols, and (f) generation of genetically engineered targeted T cells.
C1 [Tucker, Jo A.; Jochems, Caroline; Boyerinas, Benjamin; Fallon, Jonathan; Greiner, John W.; Palena, Claudia; Schlom, Jeffrey; Tsang, Kwong-Yok] NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Rodell, Timothy C.] GlobeImmune Inc, Louisville, CO 80027 USA.
RP Schlom, J (reprint author), NCI, Lab Tumor Immunol & Biol, Ctr Canc Res, NIH, 10 Ctr Dr,Room 8B09,MSC 1750, Bethesda, MD 20892 USA.
EM js141c@nih.gov
FU Intramural Research Program of the Center for Cancer Research, National
Cancer Institute, National Institutes of Health; National Cancer
Institute; GlobeImmune, Inc.
FX Grant support was provided by the Intramural Research Program of the
Center for Cancer Research, National Cancer Institute, National
Institutes of Health, and a Cooperative Research and Development
Agreement between the National Cancer Institute and GlobeImmune, Inc.
The authors thank Diane J. Poole, Garland Davis and Curtis Randolph for
technical assistance and Debra Weingarten for editorial assistance in
the preparation of this manuscript.
NR 39
TC 15
Z9 15
U1 1
U2 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-7004
EI 1432-0851
J9 CANCER IMMUNOL IMMUN
JI Cancer Immunol. Immunother.
PD DEC
PY 2014
VL 63
IS 12
BP 1307
EP 1317
DI 10.1007/s00262-014-1603-2
PG 11
WC Oncology; Immunology
SC Oncology; Immunology
GA AW0EK
UT WOS:000345963000007
PM 25186612
ER
PT J
AU Brown, AW
Hall, KD
Thomas, D
Dhurandhar, NV
Heymsfield, SB
Allison, DB
AF Brown, Andrew W.
Hall, Kevin D.
Thomas, Diana
Dhurandhar, Nikhil V.
Heymsfield, Steven B.
Allison, David B.
TI Order of Magnitude Misestimation of Weight Effects of Children's Meal
Policy Proposals
SO CHILDHOOD OBESITY
LA English
DT Letter
ID POUND; RULE
C1 [Brown, Andrew W.; Allison, David B.] Univ Alabama Birmingham, Off Energet, Nutr & Obes Res Ctr, Birmingham, AL 35294 USA.
[Hall, Kevin D.] NIDDKD, Lab Biol Modeling, NIH, Bethesda, MD USA.
[Thomas, Diana] Montclair State Univ, Ctr Quantitat Obes Res, Montclair, NJ USA.
[Dhurandhar, Nikhil V.; Heymsfield, Steven B.] Louisiana State Univ Syst, Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Allison, David B.] Univ Alabama Birmingham, Dept Nutr Sci, Birmingham, AL 35294 USA.
RP Brown, AW (reprint author), Univ Alabama Birmingham, Off Energet, Nutr & Obes Res Ctr, 435 Lister Hall Lib, Birmingham, AL 35294 USA.
EM awbrown@uab.edu
OI Allison, David/0000-0003-3566-9399; Brown, Andrew/0000-0002-1758-8205
FU NIDDK NIH HHS [P30 DK056336]
NR 16
TC 4
Z9 4
U1 0
U2 1
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 2153-2168
EI 2153-2176
J9 CHILD OBES
JI Child Obes.
PD DEC 1
PY 2014
VL 10
IS 6
BP 542
EP 544
DI 10.1089/chi.2014.0081
PG 3
WC Pediatrics
SC Pediatrics
GA AW1SN
UT WOS:000346070300012
PM 25496036
ER
PT J
AU Luo, FR
Ding, J
Chen, HX
Liu, H
Fung, MC
Koehler, M
Armand, JP
Jiang, L
Xu, X
Zhang, G
Xu, L
Qian, P
Yan, L
AF Luo, Feng Roger
Ding, Jian
Chen, Helen X.
Liu, Hao
Fung, Man-Cheong
Koehler, Maria
Armand, Jean Pierre
Jiang, Lei
Xu, Xiao
Zhang, Ge
Xu, Li
Qian, Pascal
Yan, Li
TI Breakthrough cancer medicine and its impact on novel drug development in
China: report of the US Chinese Anti-Cancer Association (USCACA) and
Chinese Society of Clinical Oncology (CSCO) Joint Session at the 17th
CSCO Annual Meeting
SO CHINESE JOURNAL OF CANCER
LA English
DT Review
DE Breakthrough; clinical trial; cancer medicine
ID CELL LUNG-CANCER; GASTRIC-CANCER; BREAST-CANCER; INHIBITOR; PCI-32765;
IBRUTINIB
AB The US Chinese Anti-Cancer Association (USCACA) teamed up with Chinese Society of Clinical Oncology (CSCO) to host a joint session at the 17th CSCO Annual Meeting on September 20th, 2014 in Xiamen, China. With a focus on breakthrough cancer medicines, the session featured innovative approaches to evaluate breakthrough agents and established a platform to interactively share successful experiences from case studies of 6 novel agents from both the United States and China. The goal of the session is to inspire scientific and practical considerations for clinical trial design and strategy to expedite cancer drug development in China. A panel discussion further provided in-depth advice on advancing both early and full development of novel cancer medicines in China.
C1 [Luo, Feng Roger; Chen, Helen X.; Xu, Xiao; Xu, Li; Qian, Pascal; Yan, Li] US Chinese Anticanc Assoc, Martinez, CA 94553 USA.
[Luo, Feng Roger; Fung, Man-Cheong] Janssen Res & Dev LLC, Dept Oncol, Raritan, NJ 08869 USA.
[Ding, Jian; Jiang, Lei] Chinese Acad Sci, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China.
[Chen, Helen X.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Liu, Hao; Qian, Pascal] Novartis Pharmaceut China Oncol, Beijing 10004, Peoples R China.
[Koehler, Maria] Pfizer Oncol, New York, NY 10017 USA.
[Armand, Jean Pierre] Inst Gustave Roussy, F-94805 Villejuif, France.
[Xu, Xiao] ACEA Biosci Inc, San Diego, CA 92121 USA.
[Zhang, Ge; Xu, Li] Jiangsu Hengrui Med Co Ltd, Shanghai 200122, Peoples R China.
[Yan, Li] Peking Univ, Beijing Canc Hosp & Inst, Sch Oncol, Beijing 100142, Peoples R China.
RP Luo, FR (reprint author), US Chinese Anticanc Assoc, Martinez, CA 94553 USA.
EM Rluo1@its.jnj.com; ynyinternational@yahoo.com
NR 24
TC 0
Z9 0
U1 4
U2 7
PU SUN YAT SEN UNIV MED SCI WHO
PI GUANGZHOU
PA 651 DONGFENG RD E, GUANGZHOU, GUANGDONG 510060, PEOPLES R CHINA
SN 1000-467X
EI 1944-446X
J9 CHIN J CANCER
JI Chin. J. Cancer
PD DEC
PY 2014
VL 33
IS 12
BP 620
EP 624
DI 10.5732/cjc.014.10246
PG 5
WC Oncology
SC Oncology
GA AW4CH
UT WOS:000346228500007
PM 25418191
ER
PT J
AU Berkowitz, JL
Janik, JE
Stewart, DM
Jaffe, ES
Stetler-Stevenson, M
Shih, JH
Fleisher, TA
Turner, M
Urquhart, NE
Wharfe, GH
Figg, WD
Peer, CJ
Goldman, CK
Waldmann, TA
Morris, JC
AF Berkowitz, Jonathan L.
Janik, John E.
Stewart, Donn M.
Jaffe, Elaine S.
Stetler-Stevenson, Maryalice
Shih, Joanna H.
Fleisher, Thomas A.
Turner, Maria
Urquhart, Nicole E.
Wharfe, Gillian H.
Figg, William D.
Peer, Cody J.
Goldman, Carolyn K.
Waldmann, Thomas A.
Morris, John C.
TI Safety, efficacy, and pharmacokinetics/pharmacodynamics of daclizumab
(anti-CD25) in patients with adult T-cell leukemia/lymphoma
SO CLINICAL IMMUNOLOGY
LA English
DT Article
DE Adult T-cell leukemia/lymphoma; Daclizumab; Human T-cell leukemia virus
1 (HTLV-1) associated ATL; Interleukin-2 receptor alpha; Monoclonal
antibody
ID LEUKEMIA-LYMPHOMA VIRUS; AND/OR PARACRINE GROWTH; HUMANIZED ANTI-TAC;
RENAL-TRANSPLANTATION; MULTIPLE-SCLEROSIS; CLINICAL-TRIALS; IL-2
RECEPTOR; THERAPY; INTERLEUKIN-2-RECEPTOR; BLOCKADE
AB Interleukin-2 receptor a chain (CD25) is overexpressed in human T-cell leukemia virus 1 associated adult T-cell leukemia! lymphoma (ATL). Daclizumab a humanized monoclonal antibody blocks IL-2 binding by recognizing the interleukin-2 receptor a chain (CD25). We conducted a phase I/II trial of daclizumab in 34 patients with ATL. Saturation of surface CD25 on circulating ATL cells was achieved at all doses; however saturation on ATL cells in lymph nodes required 8 mg/kg. Up to 8 mg/kg of daclizumab administered every 3 weeks was well tolerated. No responses were observed in 18 patients with acute or lymphoma ATL; however, 6 partial responses were observed in 16 chronic and smoldering ATL patients. The pharmacokinetics/ pharmacodynamics of daclizumab suggest that high-dose daclizumab would be more effective than low-dose daclizumab in treatment of lymphoid malignancies and autoimmune diseases (e.g., multiple sclerosis) since high-dose daclizumab is required to saturate IL-2R alpha in extravascular sites. Published by Elsevier Inc.
C1 [Berkowitz, Jonathan L.; Janik, John E.; Stewart, Donn M.; Goldman, Carolyn K.; Waldmann, Thomas A.; Morris, John C.] NCI, Lymphoid Malignancies Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Jaffe, Elaine S.; Stetler-Stevenson, Maryalice] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Shih, Joanna H.] NCI, Biometr Res Branch, NIH, Bethesda, MD 20892 USA.
[Fleisher, Thomas A.] NIH, Dept Clin Pathol, Bethesda, MD 20892 USA.
[Turner, Maria] NCI, Dermatol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Urquhart, Nicole E.; Wharfe, Gillian H.] Univ W Indies, Dept Haematol & Pathol, Jamaica, NY USA.
[Figg, William D.; Peer, Cody J.] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Waldmann, TA (reprint author), NIH, Ctr Canc Res, Lymphoid Malignancies Branch, 10 Ctr Dr,Bldg 10,Room 4N115, Bethesda, MD 20892 USA.
EM tawald@helix.nih.gov
RI Figg Sr, William/M-2411-2016
FU Intramural Research Program of the National Cancer Institute, Center for
Cancer Research, National Institutes of Health
FX The work was supported by the Intramural Research Program of the
National Cancer Institute, Center for Cancer Research, National
Institutes of Health.
NR 44
TC 16
Z9 18
U1 2
U2 14
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1521-6616
EI 1521-7035
J9 CLIN IMMUNOL
JI Clin. Immunol.
PD DEC
PY 2014
VL 155
IS 2
BP 176
EP 187
DI 10.1016/j.clim.2014.09.012
PG 12
WC Immunology
SC Immunology
GA AW2JQ
UT WOS:000346114300003
PM 25267440
ER
PT J
AU Symonds, JM
Hoffman, MP
AF Symonds, Jennifer M.
Hoffman, Matthew P.
TI Luminal Signaling: It's What's on the Inside that Counts
SO DEVELOPMENTAL CELL
LA English
DT Editorial Material
ID MORPHOGENESIS; TISSUE
AB During organogenesis, FGFs are diffusible communication signals that allow cells to coordinate morphogenesis and establish tissue architecture. Recently in Nature, Durdu et al. (2014) show that epithelial cell clusters secrete FGFs into a microlumen, restricting FGF localization so that participating cells coordinate differentiation and collective migration via luminal signaling.
C1 [Symonds, Jennifer M.; Hoffman, Matthew P.] NIDCR, Matrix & Morphogenesis Sect, NIH, Bethesda, MD 20892 USA.
RP Hoffman, MP (reprint author), NIDCR, Matrix & Morphogenesis Sect, NIH, Bethesda, MD 20892 USA.
EM mhoffman@mail.nih.gov
FU Intramural NIH HHS
NR 7
TC 0
Z9 0
U1 0
U2 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1534-5807
EI 1878-1551
J9 DEV CELL
JI Dev. Cell
PD DEC
PY 2014
VL 31
IS 5
BP 519
EP 520
DI 10.1016/j.devcel.2014.11.019
PG 2
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA AW2JB
UT WOS:000346112800002
PM 25490261
ER
PT J
AU Kindberg, AA
Bendriem, RM
Spivak, CE
Chen, J
Handreck, A
Lupica, CR
Liu, J
Freed, WJ
Lee, CT
AF Kindberg, Abigail A.
Bendriem, Raphael M.
Spivak, Charles E.
Chen, Jia
Handreck, Annelie
Lupica, Carl R.
Liu, Jinny
Freed, William J.
Lee, Chun-Ting
TI An in vitro model of human neocortical development using pluripotent
stem cells: cocaine-induced cytoarchitectural alterations
SO DISEASE MODELS & MECHANISMS
LA English
DT Article
DE Neocortical development; Dorsal forebrain model; hPSCs; Cocaine;
Premature neuronal differentiation
ID DEVELOPING CEREBRAL-CORTEX; NEUROTROPHIC FACTOR; SIGMA-1 RECEPTOR;
LAMINAR FATE; INTERNEURONS; NEURONS; PROLIFERATION; INHIBITION; MONKEY;
MOUSE
AB Neocortical development involves ordered specification of forebrain cortical progenitors to various neuronal subtypes, ultimately forming the layered cortical structure. Modeling of this process using human pluripotent stem cells (hPSCs) would enable mechanistic studies of human neocortical development, while providing new avenues for exploration of developmental neocortical abnormalities. Here, we show that preserving hPSCs aggregates - allowing embryoid body formation - while adding basic fibroblast growth factor (bFGF) during neuroepithelial development generates neural rosettes showing dorsal forebrain identity, including Mash1(+) dorsal telencephalic GABAergic progenitors. Structures that mirrored the organization of the cerebral cortex formed after rosettes were seeded and cultured for 3 weeks in the presence of FGF18, BDNF and NT3. Neurons migrated along radial glia scaffolding, with deep-layer CTIP2(+) cortical neurons appearing after 1 week and upper-layer SATB2(+) cortical neurons forming during the second and third weeks. At the end of differentiation, these structures contained both glutamatergic and GABAergic neurons, with glutamatergic neurons being most abundant. Thus, this differentiation protocol generated an hPSC-based model that exhibits temporal patterning and a neuronal subtype ratio similar to that of the developing human neocortex. This model was used to examine the effects of cocaine during neocorticogenesis. Cocaine caused premature neuronal differentiation and enhanced neurogenesis of various cortical neuronal subtypes. These cocaine-induced changes were inhibited by the cytochrome P450 inhibitor cimetidine. This in vitro model enables mechanistic studies of neocorticogenesis, and can be used to examine the mechanisms through which cocaine alters the development of the human neocortex.
C1 [Kindberg, Abigail A.; Bendriem, Raphael M.; Spivak, Charles E.; Chen, Jia; Lupica, Carl R.; Freed, William J.; Lee, Chun-Ting] NIDA, Cellular Neurobiol Res Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Baltimore, MD 21244 USA.
[Handreck, Annelie] Univ Vet Med, Dept Pharmacol Toxicol & Pharm, D-30173 Hannover, Germany.
[Liu, Jinny] US Naval Res Lab, Center Bio Mol Sci & Engn, Washington, DC 20375 USA.
RP Lee, CT (reprint author), NIDA, Cellular Neurobiol Res Branch, Intramural Res Program, NIH,Dept Hlth & Human Serv, Baltimore, MD 21244 USA.
EM clee@mail.nih.gov
FU National Institute on Drug Abuse Intramural Research Program (NIDA IRP)
FX This work was funded by the National Institute on Drug Abuse Intramural
Research Program (NIDA IRP).
NR 35
TC 3
Z9 3
U1 2
U2 20
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 1754-8403
EI 1754-8411
J9 DIS MODEL MECH
JI Dis. Model. Mech.
PD DEC
PY 2014
VL 7
IS 12
BP 1397
EP 1405
DI 10.1242/dmm.017251
PG 9
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA AW2AL
UT WOS:000346090500009
PM 25288682
ER
PT J
AU Chowell, G
Blumberg, S
Simonsen, L
Miller, MA
Viboud, C
AF Chowell, Gerardo
Blumberg, Seth
Simonsen, Lone
Miller, Mark A.
Viboud, Cecile
TI Synthesizing data and models for the spread of MERS-CoV, 2013: Key role
of index cases and hospital transmission
SO EPIDEMICS
LA English
DT Article
DE Middle East respiratory syndrome; Reproduction number; Epidemic
modeling; Index cases; Community; Hospital
ID RESPIRATORY SYNDROME CORONAVIRUS; HONG-KONG; DROMEDARY CAMELS; SYNDROME
SARS; SAUDI-ARABIA; INFECTIOUS-DISEASES; EPIDEMIC; OUTBREAK; SINGAPORE;
DYNAMICS
AB The outbreak of Middle East respiratory syndrome coronavirus (MERS-CoV) has caused 209 deaths and 699 laboratory-confirmed cases in the Arabian Peninsula as of June 11, 2014. Preparedness efforts are hampered by considerable uncertainty about the nature and intensity of human-to-human transmission, with previous reproduction number estimates ranging from 0.4 to 1.5. Here we synthesize epidemiological data and transmission models for the MERS-CoV outbreak during April-October 2013 to resolve uncertainties in epidemic risk, while considering the impact of observation bias. We match the progression of MERS-CoV cases in 2013 to a dynamic transmission model that incorporates community and hospital compartments, and distinguishes transmission by zoonotic (index) cases and secondary cases. When observation bias is assumed to account for the fact that all reported zoonotic cases are severe, but only similar to 57% of secondary cases are symptomatic, the average reproduction number of MERS-CoV is estimated to be 0.45 (95% CI: 0.29-0.61). Alternatively, if these epidemiological observations are taken at face value, index cases are estimated to transmit substantially more effectively than secondary cases, (R-i=0.84 (0.58-1.20) vs R-s=0.36 (0.24-0.51)). In both scenarios the relative contribution of hospital-based transmission is over four times higher than that of community transmission, indicating that disease control should be focused on hospitalized patients.
Adjusting previously published estimates for observation bias confirms a strong support for the average R < 1 in the first stage of the outbreak in 2013 and thus, transmissibility of secondary cases of MERS-CoV remained well below the epidemic threshold. More information on the observation process is needed to clarify whether MERS-CoV is intrinsically weakly transmissible between people or whether existing control measures have contributed meaningfully to reducing the transmissibility of secondary cases. Our results could help evaluate the progression of MERS-CoV in recent months in response to changes in disease surveillance, control interventions, or viral adaptation. (C) 2014 The Authors. Published by Elsevier B.V.
C1 [Chowell, Gerardo; Blumberg, Seth; Simonsen, Lone; Miller, Mark A.; Viboud, Cecile] NIH, Div Int Epidemiol & Populat Studies, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Chowell, Gerardo] Arizona State Univ, Sch Human Evolut & Social Change, Ctr Global Hlth, Tempe, AZ USA.
[Chowell, Gerardo] Arizona State Univ, Sch Human Evolut & Social Change, Math Computat & Modeling Sci Ctr, Tempe, AZ USA.
[Blumberg, Seth] Univ Calif San Francisco, Francis I Proctor Fdn, San Francisco, CA 94143 USA.
[Simonsen, Lone] George Washington Univ, Sch Publ Hlth & Hlth Serv, Dept Global Hlth, Washington, DC USA.
RP Chowell, G (reprint author), Arizona State Univ, POB 872402, Tempe, AZ 85287 USA.
EM gchowell@asu.edu
OI Simonsen, Lone/0000-0003-1535-8526
FU RAPIDD program of the Science & Technology Directorate, Department of
Homeland Security; Office of Global Affairs' International Influenza
Unit in the Office of the Secretary of the Department of Health and
Human Services; RAPIDD program of the Science and Technology
Directorate, Department of Homeland Security; Fogarty International
Center; National Institutes of Health; National Institute of Health
MIDAS program (Modeling Infectious Disease Agent Study) [NIH NIGMS
1-U01-GM08778]
FX This research was conducted in the context of the Multinational
Influenza Seasonal Mortality Study (MISMS), an on-going international
collaborative effort to understand influenza epidemiological and
evolutionary patterns, led by the Fogarty International Center, National
Institutes of Health (http://www.origem.info/misms/index.php). Funding
for this project comes in part (LS) from the RAPIDD program of the
Science & Technology Directorate, Department of Homeland Security, and
from the Office of Global Affairs' International Influenza Unit in the
Office of the Secretary of the Department of Health and Human Services.
SB acknowledges financial support from RAPIDD program of the Science and
Technology Directorate, Department of Homeland Security, the Fogarty
International Center, National Institutes of Health, and the National
Institute of Health MIDAS program (Modeling Infectious Disease Agent
Study, grant number NIH NIGMS 1-U01-GM08778].
NR 52
TC 30
Z9 31
U1 6
U2 21
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1755-4365
J9 EPIDEMICS-NETH
JI Epidemics
PD DEC
PY 2014
VL 9
BP 40
EP 51
DI 10.1016/j.epidem.2014.09.011
PG 12
WC Infectious Diseases
SC Infectious Diseases
GA AW0TN
UT WOS:000346006500005
PM 25480133
ER
PT J
AU Camacho, A
Kucharski, AJ
Funk, S
Breman, J
Piot, P
Edmunds, WJ
AF Camacho, A.
Kucharski, A. J.
Funk, S.
Breman, J.
Piot, P.
Edmunds, W. J.
TI Potential for large outbreaks of Ebola virus disease
SO EPIDEMICS
LA English
DT Article
DE Ebola; 1976 Zaire outbreak; Mathematical model; Basic reproduction
number
ID HEMORRHAGIC-FEVER; REPRODUCTIVE NUMBER; RISK-FACTORS; EPIDEMIC; UGANDA;
CONGO; TRANSMISSION; INFERENCE; ZAIRE
AB Outbreaks of Ebola virus can cause substantial morbidity and mortality in affected regions. The largest outbreak of Ebola to date is currently underway in West Africa, with 3944 cases reported as of 5th September 2014. To develop a better understanding of Ebola transmission dynamics, we revisited data from the first known Ebola outbreak, which occurred in 1976 in Zaire (now Democratic Republic of Congo). By fitting a mathematical model to time series stratified by disease onset, outcome and source of infection, we were able to estimate several epidemiological quantities that have previously proved challenging to measure, including the contribution of hospital and community infection to transmission. We found evidence that transmission decreased considerably before the closure of the hospital, suggesting that the decline of the outbreak was most likely the result of changes in host behaviour. Our analysis suggests that the person-to-person reproduction number was 1.34 (95% CI: 0.92-2.11) in the early part of the outbreak. Using stochastic simulations we demonstrate that the same epidemiological conditions that were present in 1976 could have generated a large outbreak purely by chance. At the same time, the relatively high person-to-person basic reproduction number suggests that Ebola would have been difficult to control through hospital-based infection control measures alone. (C) 2014 The Authors. Published by Elsevier B.V.
C1 [Camacho, A.; Kucharski, A. J.; Funk, S.; Edmunds, W. J.] London Sch Hyg & Trop Med, Ctr Math Modelling Infect Dis, Dept Infect Dis Epidemiol, London WC1, England.
[Breman, J.] NIH, Fogarty Int Ctr, Bethesda, MD USA.
[Piot, P.] London Sch Hyg & Trop Med, London WC1, England.
RP Camacho, A (reprint author), London Sch Hyg & Trop Med, Ctr Math Modelling Infect Dis, Dept Infect Dis Epidemiol, London WC1, England.
EM anton.camacho@lshtm.ac.uk; adam.kucharski@lshtm.ac.uk
FU Medical Research Council [MR/J01432X/1, MR/K021524/1, MR/K021680/1];
Region Ile-de-France through the scientific program DIM MALINF
FX This work was supported by the Medical Research Council (AC, fellowship
MR/J01432X/1; AJK, fellowship MR/K021524/1; SF, fellowship
MR/K021680/1). We thank Prof. Bernard Cazelles for access to the
computational resources used in this work, which were funded by an
investment grant from the Region Ile-de-France through the scientific
program DIM MALINF.
NR 28
TC 32
Z9 34
U1 3
U2 71
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1755-4365
J9 EPIDEMICS-NETH
JI Epidemics
PD DEC
PY 2014
VL 9
BP 70
EP 78
DI 10.1016/j.epidem.2014.09.003
PG 9
WC Infectious Diseases
SC Infectious Diseases
GA AW0TN
UT WOS:000346006500008
PM 25480136
ER
PT J
AU Robert, MA
Okamoto, KW
Gould, F
Lloyd, AL
AF Robert, Michael A.
Okamoto, Kenichi W.
Gould, Fred
Lloyd, Alun L.
TI Antipathogen genes and the replacement of disease-vectoring mosquito
populations: a model-based evaluation
SO EVOLUTIONARY APPLICATIONS
LA English
DT Article
DE Aedes aegypti; antipathogen genes; dengue fever; female-killing;
ordinary differential equation model; reduce and replace
ID AEDES-AEGYPTI DIPTERA; GENETICALLY-MODIFIED MOSQUITOS; BORNE DISEASES;
DENGUE TRANSMISSION; ENGINEERED UNDERDOMINANCE; INTRODUCING TRANSGENES;
THEORETICAL-ANALYSIS; INSECT POPULATIONS; DENSITY-DEPENDENCE; AUTOCIDAL
CONTROL
AB Recently, genetic strategies aimed at controlling populations of disease-vectoring mosquitoes have received considerable attention as alternatives to traditional measures. Theoretical studies have shown that female-killing (FK), antipathogen (AP), and reduce and replace (R&R) strategies can each decrease the number competent vectors. In this study, we utilize a mathematical model to evaluate impacts on competent Aedes aegypti populations of FK, AP, and R&R releases as well as hybrid strategies that result from combinations of these three approaches. We show that while the ordering of efficacy of these strategies depends upon population life history parameters, sex ratio of releases, and switch time in combination strategies, AP-only and R&R/AP releases typically lead to the greatest long-term reduction in competent vectors. R&R-only releases are often less effective at long-term reduction of competent vectors than AP-only releases or R&R/AP releases. Furthermore, the reduction in competent vectors caused by AP-only releases is easier to maintain than that caused by FK-only or R&R-only releases even when the AP gene confers a fitness cost. We discuss the roles that density dependence and inclusion of females play in the order of efficacy of the strategies. We anticipate that our results will provide added impetus to continue developing AP strategies.
C1 [Robert, Michael A.; Lloyd, Alun L.] N Carolina State Univ, Dept Math, Raleigh, NC 27695 USA.
[Robert, Michael A.; Lloyd, Alun L.] N Carolina State Univ, Biomath Grad Program, Raleigh, NC 27695 USA.
[Robert, Michael A.] Univ New Mexico, Dept Biol, Albuquerque, NM 87131 USA.
[Robert, Michael A.] Univ New Mexico, Dept Math & Stat, Albuquerque, NM 87131 USA.
[Okamoto, Kenichi W.; Gould, Fred] N Carolina State Univ, Dept Entomol, Raleigh, NC 27695 USA.
[Gould, Fred; Lloyd, Alun L.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Robert, MA (reprint author), Univ New Mexico, Dept Biol, Albuquerque, NM 87131 USA.
EM marobert@unm.edu
FU National Institutes of Health (NIH) [R01AI091980]; Foundation for the
NIH through the Bill and Melinda Gates Foundation Grand Challenges in
Global Health initiative; W.M. Keck Foundation; University of
Pretoria-North Carolina State University Strategic Collaboration Seed
Grant; Isaac Newton Institute for Mathematical Sciences, Cambridge, UK,
as part of their Infectious Disease Dynamics program; NIH [U01GM097661]
FX We are grateful to Tim Antonelli, Kevin Gross, and two anonymous
reviewers for comments that improved the content of this paper. This
work benefitted from discussion fostered by the Research and Policy for
Infectious Disease Dynamics (RAPIDD) program of the Science and
Technology Directory, Department of Homeland Security, and Fogarty
International Center, NIH. This work was funded in part by National
Institutes of Health (NIH) grant R01AI091980, a grant to the Regents of
the University of California from the Foundation for the NIH through the
Bill and Melinda Gates Foundation Grand Challenges in Global Health
initiative and a grant from the W.M. Keck Foundation. A.L. Lloyd also
acknowledges support from a University of Pretoria-North Carolina State
University Strategic Collaboration Seed Grant and from the Isaac Newton
Institute for Mathematical Sciences, Cambridge, UK, as part of their
Infectious Disease Dynamics program (August-September 2013). M. A.
Robert was also partially supported by NIH grant U01GM097661.
NR 64
TC 1
Z9 2
U1 3
U2 24
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1752-4571
J9 EVOL APPL
JI Evol. Appl.
PD DEC
PY 2014
VL 7
IS 10
BP 1238
EP 1251
DI 10.1111/eva.12219
PG 14
WC Evolutionary Biology
SC Evolutionary Biology
GA AW1WO
UT WOS:000346079400008
PM 25558284
ER
PT J
AU Paix, A
Wang, YM
Smith, HE
Lee, CYS
Calidas, D
Lu, T
Smith, J
Schmidt, H
Krause, MW
Seydoux, G
AF Paix, Alexandre
Wang, Yuemeng
Smith, Harold E.
Lee, Chih-Yung S.
Calidas, Deepika
Lu, Tu
Smith, Jarrett
Schmidt, Helen
Krause, Michael W.
Seydoux, Geraldine
TI Scalable and Versatile Genome Editing Using Linear DNAs with
Microhomology to Cas9 Sites in Caenorhabditis elegans
SO GENETICS
LA English
DT Article
ID HOMOLOGOUS RECOMBINATION; CRISPR-CAS; C-ELEGANS; DROSOPHILA; IMMUNITY;
SYSTEMS
AB Homology-directed repair (HDR) of double-strand DNA breaks is a promising method for genome editing, but is thought to be less efficient than error-prone nonhomologous end joining in most cell types. We have investigated HDR of double-strand breaks induced by CRISPR-associated protein 9 (Cas9) in Caenorhabditis elegans. We find that HDR is very robust in the C. elegans germline. Linear repair templates with short (similar to 30-60 bases) homology arms support the integration of base and gene-sized edits with high efficiency, bypassing the need for selection. Based on these findings, we developed a systematic method to mutate, tag, or delete any gene in the C. elegans genome without the use of co-integrated markers or long homology arms. We generated 23 unique edits at 11 genes, including premature stops, whole-gene deletions, and protein fusions to antigenic peptides and GFP. Whole-genome sequencing of five edited strains revealed the presence of passenger variants, but no mutations at predicted off-target sites. The method is scalable for multi-gene editing projects and could be applied to other animals with an accessible germline.
C1 [Paix, Alexandre; Wang, Yuemeng; Lee, Chih-Yung S.; Calidas, Deepika; Lu, Tu; Smith, Jarrett; Schmidt, Helen; Seydoux, Geraldine] Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, Baltimore, MD 21205 USA.
[Smith, Harold E.; Krause, Michael W.] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Seydoux, G (reprint author), Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, PCTB 706, Baltimore, MD 21205 USA.
EM gseydoux@jhmi.edu
RI Paix, Alexandre/E-9137-2011;
OI Wang, Yuemeng/0000-0003-3928-6926; Paix, Alexandre/0000-0002-8080-7546;
Seydoux, Geraldine/0000-0001-8257-0493; Krause,
Michael/0000-0001-6127-3940; Schmidt, Helen/0000-0002-3449-2790
FU National Institutes of Health (NIH) [R01HD37047]; Intramural Research
Program of the NIH; National Institute of Diabetes and Digestive and
Kidney Diseases
FX We thank Craig Mello for sharing results prior to publication, Mario de
Bono for reagents, Bram Lambrus for sgRNA cloning assistance, Dominique
Rasoloson for strain archival, and Andrew Folkmann and Dan Dickinson for
discussion and comments on the manuscript. This work was supported by
National Institutes of Health (NIH) grant R01HD37047, by the Intramural
Research Program of the NIH, and the National Institute of Diabetes and
Digestive and Kidney Diseases. G.S. is an investigator of the Howard
Hughes Medical Institute.
NR 27
TC 50
Z9 51
U1 2
U2 21
PU GENETICS SOCIETY AMERICA
PI BETHESDA
PA 9650 ROCKVILLE AVE, BETHESDA, MD 20814 USA
SN 0016-6731
EI 1943-2631
J9 GENETICS
JI Genetics
PD DEC
PY 2014
VL 198
IS 4
BP 1347
EP +
DI 10.1534/genetics.114.170423
PG 25
WC Genetics & Heredity
SC Genetics & Heredity
GA AW1OQ
UT WOS:000346059300001
PM 25249454
ER
PT J
AU Teutsch, SM
Fielding, JE
Khoury, MJ
Evans, JP
AF Teutsch, Steven M.
Fielding, Jonathan E.
Khoury, Muin J.
Evans, James P.
TI Utility before business
SO GENETICS IN MEDICINE
LA English
DT Editorial Material
ID MEDICINE; COST
C1 [Teutsch, Steven M.; Fielding, Jonathan E.] Dept Publ Hlth, Los Angeles, CA 90082 USA.
[Fielding, Jonathan E.] Univ Calif Los Angeles, Fielding Sch Publ Hlth, Los Angeles, CA USA.
[Fielding, Jonathan E.] Univ Calif Los Angeles, Sch Med, Los Angeles, CA USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA USA.
[Khoury, Muin J.] NIH, Epidemiol & Genom Res Program, Bethesda, MD 20892 USA.
[Evans, James P.] Univ N Carolina, Sch Med, Chapel Hill, NC USA.
RP Teutsch, SM (reprint author), Dept Publ Hlth, Los Angeles, CA 90082 USA.
EM steventeutsch@gmail.com; jfielding@ph.lacounty.gov
FU Intramural CDC HHS [CC999999]; NHGRI NIH HHS [U01 HG006487]
NR 12
TC 2
Z9 2
U1 0
U2 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2014
VL 16
IS 12
BP 869
EP 870
DI 10.1038/gim.2014.71
PG 2
WC Genetics & Heredity
SC Genetics & Heredity
GA AW1HN
UT WOS:000346040900002
PM 25010054
ER
PT J
AU Feero, WG
Manolio, TA
Khoury, MJ
AF Feero, W. Gregory
Manolio, Teri A.
Khoury, Muin J.
TI Translational research is a key to nongeneticist physicians' genomics
education
SO GENETICS IN MEDICINE
LA English
DT Editorial Material
ID GENETICS
C1 [Feero, W. Gregory] Maine Dartmouth Family Med Residency Program, Augusta, ME 04332 USA.
[Manolio, Teri A.] NHGRI, Div Genom Med, NIH, Bethesda, MD 20892 USA.
[Khoury, Muin J.] Ctr Dis Control & Prevent, Off Publ Hlth Genom, Atlanta, GA USA.
[Khoury, Muin J.] NCI, Epidemiol & Genom Res Program, Div Canc Control & Populat Sci, NIH, Rockville, MD USA.
RP Feero, WG (reprint author), Maine Dartmouth Family Med Residency Program, Augusta, ME 04332 USA.
EM wfeero@mainegeneral.org
FU Intramural CDC HHS [CC999999]
NR 8
TC 10
Z9 10
U1 0
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2014
VL 16
IS 12
BP 871
EP 873
DI 10.1038/gim.2014.67
PG 3
WC Genetics & Heredity
SC Genetics & Heredity
GA AW1HN
UT WOS:000346040900003
PM 24875299
ER
PT J
AU Biesecker, BB
Klein, W
Lewis, KL
Fisher, TC
Wright, MF
Biesecker, LG
Han, PK
AF Biesecker, Barbara B.
Klein, William
Lewis, Katie L.
Fisher, Tyler C.
Wright, Martha Frances
Biesecker, Leslie G.
Han, Paul K.
TI How do research participants perceive "uncertainty" in genome
sequencing?
SO GENETICS IN MEDICINE
LA English
DT Article
DE epistemological beliefs; expectations; genome sequencing; informed
choice; uncertainty
ID DECISION-MAKING; CHILDREN; CLINSEQ
AB Purpose: The scope of uncertainty in genome sequence information has no rival in health-care delivery. We present data from adults participating in a National Institutes of Health study using this technology, in which perceptions of uncertainty are hypothesized to be key in predicting decisions to learn and act on genome health information.
Methods: We conducted six professionally moderated focus groups with 39 randomly selected ClinSeq participants varying on whether they had coronary heart disease and had received prior sequence results. We elicited perceptions of the uncertainties associated with genome sequencing using written prompts.
Results: Participants perceived uncertainty as a quality of genome information. The majority of participants characterized uncertainty of sequencing information as "changing, fluid, developing, or ground breaking" These responses led to anticipation of more optimistic future outcomes. Fewer participants described uncertainty as, "questionable; less accurate, limited, or poorly understood." These; perceptions seemed to undermine participants' faith in genome information, leading to feelings of disillusionment.
Conclusion: Our findings suggest that perceptions Of uncertainty are related to epistemological beliefs that inform expectations for the information. Interventions that promote realistic expectations of genome sequencing may mitigate negative responses to uncertainty.
C1 [Biesecker, Barbara B.; Fisher, Tyler C.] NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA.
[Klein, William] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Lewis, Katie L.; Wright, Martha Frances; Biesecker, Leslie G.] NHGRI, Genet Dis Res Branch, NIH, Bethesda, MD 20892 USA.
[Han, Paul K.] Ctr Outcomes Res & Evaluat, Maine Med Ctr, Res Inst, Scarborough, ME USA.
RP Biesecker, BB (reprint author), NHGRI, Social & Behav Res Branch, NIH, Bethesda, MD 20892 USA.
EM barbarab@mail.nih.gov
OI Han, Paul/0000-0003-0165-1940
FU National Human Genome Research Institute, National Institutes of Health
FX We thank the focus group participants; Chanza Baytop and Barbara
Rosenthal for moderating the groups; and Chris Anderson for help with
the references. The Intramural Research Program of the National Human
Genome Research Institute, National Institutes of Health, funded this
research.
NR 15
TC 9
Z9 9
U1 2
U2 3
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD DEC
PY 2014
VL 16
IS 12
BP 977
EP 980
DI 10.1038/gim.2014.57
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA AW1HN
UT WOS:000346040900017
PM 24875302
ER
PT J
AU Lin, HH
Joehanes, R
Pilling, LC
Dupuis, J
Lunetta, KL
Ying, SX
Benjamin, EJ
Hernandez, D
Singleton, A
Melzer, D
Munson, PJ
Levy, D
Ferrucci, L
Murabito, JM
AF Lin, Honghuang
Joehanes, Roby
Pilling, Luke C.
Dupuis, Josee
Lunetta, Kathryn L.
Ying, Sai-Xia
Benjamin, Emelia J.
Hernandez, Dena
Singleton, Andrew
Melzer, David
Munson, Peter J.
Levy, Daniel
Ferrucci, Luigi
Murabito, Joanne M.
TI Whole blood gene expression and interleukin-6 levels
SO GENOMICS
LA English
DT Article
DE Inflammation; Gene expression; Interleukin-6; Epidemiology
ID CORONARY-HEART-DISEASE; C-REACTIVE PROTEIN; FRAIL MOUSE MODEL; ANDROGEN
RECEPTOR; INFLAMMATORY BIOMARKERS; OLDER PERSONS; FRAMINGHAM; CELLS;
RISK; AGE
AB Background: Circulating interleukin-6 levels increase with advancing age and are a risk factor for various diseases and mortality. The characterization of gene expression profiles associated with interleukin-6 levels might suggest important molecular events underlying its regulation.
Methods and results: We studied the association of transcriptional profiles with interleukin-6 levels in 2422 participants from the Framingham Heart Study Offspring Cohort using Affymetrix Human Exon 1.0 ST Array. We identified 4139 genes that were significantly associated with interleukin-6 levels (FDR < 0.05) after adjusting for age, sex and blood cell components. We then replicated 807 genes in the InCHIANTI study with 694 participants. Many of the top genes are involved in inflammation-related pathways or erythrocyte function, including JAK/Stat signaling pathway and interleukin-10 signaling pathway.
Conclusion: We identified and replicated 807 genes that were associated with circulating interleukin-6 levels. Future characterization of interleukin-6 regulation networks may facilitate the identification of additional potential targets for treating inflammation-related diseases. (C) 2014 Elsevier Inc. All rights reserved.
C1 [Lin, Honghuang] Boston Univ, Sch Med, Dept Med, Sect Computat Biomed, Boston, MA 02118 USA.
[Lin, Honghuang; Joehanes, Roby; Dupuis, Josee; Lunetta, Kathryn L.; Benjamin, Emelia J.; Munson, Peter J.; Levy, Daniel; Murabito, Joanne M.] NHLBI, Framingham, MA USA.
[Lin, Honghuang; Joehanes, Roby; Dupuis, Josee; Lunetta, Kathryn L.; Benjamin, Emelia J.; Munson, Peter J.; Levy, Daniel; Murabito, Joanne M.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Joehanes, Roby; Ying, Sai-Xia; Munson, Peter J.] NIH, Ctr Informat Technol, Math & Stat Comp Lab, Bethesda, MD 20892 USA.
[Joehanes, Roby; Munson, Peter J.; Levy, Daniel] NHLBI, Populat Sci Branch, Bethesda, MD 20892 USA.
[Pilling, Luke C.; Melzer, David] Univ Exeter, Sch Med, Exeter EX1 2LU, Devon, England.
NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Dupuis, Josee; Lunetta, Kathryn L.] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Benjamin, Emelia J.] Boston Univ, Sch Med, Dept Med, Sect Cardiovasc Med & Prevent Med, Boston, MA 02118 USA.
[Benjamin, Emelia J.] Boston Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA USA.
[Ferrucci, Luigi] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Murabito, Joanne M.] Boston Univ, Sch Med, Dept Med, Gen Internal Med Sect, Boston, MA 02118 USA.
RP Lin, HH (reprint author), Boston Univ, Sch Med, Dept Med, Sect Computat Biomed, 72 East Concord St,B-616, Boston, MA 02118 USA.
EM hhlin@bu.edu; murabito@bu.edu
RI Singleton, Andrew/C-3010-2009;
OI Pilling, Luke/0000-0002-3332-8454; Lin, Honghuang/0000-0003-3043-3942;
Benjamin, Emelia/0000-0003-4076-2336; Melzer, David/0000-0002-0170-3838
FU Division of Intramural Research; National Heart, Lung, and Blood
Institute, National Institutes of Health, Bethesda, MD.; NIH [1R01
HL64753, R01AG028321, R01AG029451]; Intramural Research Program,
National Institute on Aging (Ferrucci); Wellcome Trust grant; plus
internal medical school funding (Melzer); National Heart, Lung, and
Blood Institute [N01-HC-25195]; [R01 HL 064753]; [R01 HL076784]
FX FHS gene expression profiling was funded through the Division of
Intramural Research (Principal Investigator, Daniel Levy), National
Heart, Lung, and Blood Institute, National Institutes of Health,
Bethesda, MD. Measurement of interleukin-6 was funded through R01 HL
064753 and R01 HL076784. This work is supported by NIH grants 1R01
HL64753 (Benjamin), R01AG028321 (Benjamin), and R01AG029451 (Murabito).
This study was supported in part by the Intramural Research Program,
National Institute on Aging (Ferrucci). UK based work was supported by a
Wellcome Trust grant to the University of Exeter, plus internal medical
school funding (Melzer). The Framingham Heart Study is supported by the
National Heart, Lung, and Blood Institute contract N01-HC-25195.
NR 61
TC 5
Z9 5
U1 0
U2 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0888-7543
EI 1089-8646
J9 GENOMICS
JI Genomics
PD DEC
PY 2014
VL 104
IS 6
BP 490
EP 495
DI 10.1016/j.ygeno.2014.10.003
PN B
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA AW1OT
UT WOS:000346059600007
PM 25311648
ER
PT J
AU Marangoni, D
Wu, ZJ
Wiley, HE
Zeiss, CJ
Vijayasarathy, C
Zeng, Y
Hiriyanna, S
Bush, RA
Wei, LL
Colosi, P
Sieving, PA
AF Marangoni, Dario
Wu, Zhijian
Wiley, Henry E.
Zeiss, Caroline J.
Vijayasarathy, Camasamudram
Zeng, Yong
Hiriyanna, Suja
Bush, Ronald A.
Wei, Lisa L.
Colosi, Peter
Sieving, Paul A.
TI Preclinical Safety Evaluation of a Recombinant AAV8 Vector for X-Linked
Retinoschisis After Intravitreal Administration in Rabbits
SO HUMAN GENE THERAPY CLINICAL DEVELOPMENT
LA English
DT Article
ID HUMAN GENE-THERAPY; LEBERS CONGENITAL AMAUROSIS; RETINAL TOXICITY;
CLINICAL-TRIAL; DELIVERY; TRIAMCINOLONE; TRANSDUCTION; EXPRESSION;
KNOCKOUT; EFFICACY
AB X-linked retinoschisis (XLRS) is a retinal disease caused by mutations in the gene encoding the protein retinoschisin (RS1) and one of the most common causes of macular degeneration in young men. Currently, no FDA-approved treatments are available for XLRS and a replacement gene therapy could provide a promising strategy. We have developed a novel gene therapy approach for XLRS, based on the administration of AAV8-scRS/IRBPhRS, an adeno-associated viral vector coding the human RS1 protein, via the intravitreal route. On the basis of our prior study in an Rs1-KO mouse, this construct transduces efficiently all the retinal layers, resulting in an RS1 expression similar to that observed in the wild-type and improving retinal structure and function. In support of a clinical trial, we carried out a study to evaluate the ocular safety of intravitreal administration of AAV8-scRS/IRBPhRS into 39 New Zealand White rabbits. Two dose levels of vector, 2e(10) and 2e(11) vector genomes per eye (vg/eye), were tested and ocular inflammation was monitored over a 12-week period by serial ophthalmological and histopathological analysis. A mild ocular inflammatory reaction, consisting mainly of vitreous infiltrates, was observed within 4 weeks from injection, in both 2e(10) and 2e(11) vg/eye groups and was likely driven by the AAV8 capsid. At 12-week follow-up, ophthalmological examination revealed no clinical signs of vitreitis in either of the dose groups. However, while vitreous inflammatory infiltrate was significantly reduced in the 2e(10) vg/eye group at 12 weeks, some rabbits in the higher dose group still showed persistence of inflammatory cells, histologically. In conclusion, intravitreal administration of AAV8-scRS/IRBPhRS into the rabbit eye produces a mild and transient intraocular inflammation that resolves, at a 2e(10) vg/eye dose, within 3 months, and does not cause irreversible tissue damages. These data support the initiation of a clinical trial of intravitreal administration of AAV8-scRS/IRBPhRS in XLRS patients.
C1 [Marangoni, Dario; Vijayasarathy, Camasamudram; Zeng, Yong; Bush, Ronald A.; Sieving, Paul A.] Natl Inst Deafness & Other Commun Disorders, NIH, Bethesda, MD 20892 USA.
[Wu, Zhijian; Wiley, Henry E.; Hiriyanna, Suja; Wei, Lisa L.; Colosi, Peter; Sieving, Paul A.] NEI, NIH, Bethesda, MD 20892 USA.
[Marangoni, Dario] Univ Aquila, Dept Biotechnol & Appl Clin Sci, I-67100 Laquila, Italy.
[Zeiss, Caroline J.] Yale Univ, Sch Med, Comparat Med Sect, New Haven, CT 06520 USA.
RP Sieving, PA (reprint author), NEI, NIH, 31 Ctr Dr,Room 6A03, Bethesda, MD 20892 USA.
EM pas@nei.nih.gov
FU National Institutes of Health, National Institute on Deafness and Other
Communication Disorders; National Eye Institute
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute on Deafness and Other
Communication Disorders, and the National Eye Institute.
NR 41
TC 6
Z9 7
U1 0
U2 7
PU MARY ANN LIEBERT, INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 2324-8637
EI 2324-8645
J9 HUM GENE THER CL DEV
JI Hum. Gene Ther. Clin. Dev.
PD DEC 1
PY 2014
VL 25
IS 4
BP 202
EP 211
DI 10.1089/humc.2014.067
PG 10
WC Biotechnology & Applied Microbiology; Critical Care Medicine; Medicine,
Research & Experimental
SC Biotechnology & Applied Microbiology; General & Internal Medicine;
Research & Experimental Medicine
GA AW5TG
UT WOS:000346336100002
PM 25211193
ER
PT J
AU Nagaraja, N
Warach, S
Hsia, AW
Adams, HP
Auh, S
Latour, LL
Merino, JG
AF Nagaraja, Nandakumar
Warach, Steven
Hsia, Amie W.
Adams, Harold P., Jr.
Auh, Sungyoung
Latour, Lawrence L.
Merino, Jose G.
TI Association Between Neurologic Improvement With Decline in Blood
Pressure and Recanalization in Stroke
SO JAMA NEUROLOGY
LA English
DT Article
ID VENTRICULAR RESPONSE; ATRIAL-FIBRILLATION; ISCHEMIC-STROKE; THROMBOLYSIS
AB IMPORTANCE Patients with stroke often have a decline in blood pressure after thrombolysis. Neurologic improvement could result from recanalization or better collateral flow despite persistent occlusion. We hypothesized that neurologic improvement with concurrent decline in blood pressure may be a clinical sign of recanalization after intravenous tissue plasminogen activator.
OBSERVATIONS Patients treated with intravenous tissue plasminogen activator at Suburban Hospital, Bethesda, Maryland, and MedStar Washington Hospital Center, Washington, DC, from 1999 to 2009 were included in the study if they had pretreatment and 24-hour magnetic resonance angiographic scans, National Institutes of Health Stroke Scale scores at those times, and proximal middle cerebral artery occlusion demonstrated prior to treatment. The recanalization status on 24-hour magnetic resonance angiography was classified as none, partial, or complete. Seventeen patients met study criteria. On 24-hour magnetic resonance angiography, 3 patients had no recanalization, 8 had partial recanalization, and 6 had complete recanalization. At 24 hours after thrombolysis, neurologic improvement with concurrent decline in systolic blood pressure of 20 mm Hg or greater was seen in 4 patients with partial recanalization, 4 patients with complete recanalization, and none of the patients with no recanalization.
CONCLUSIONS AND RELEVANCE Neurologic improvement with concurrent decline in systolic blood pressure of 20 mm Hg or greater after intravenous tissue plasminogen activator may be a clinical sign of recanalization. This observation needs confirmation in a larger cohort.
C1 [Nagaraja, Nandakumar; Hsia, Amie W.; Latour, Lawrence L.; Merino, Jose G.] NINDS, Stroke Diagnost & Therapeut Sect, Bethesda, MD 20892 USA.
[Nagaraja, Nandakumar; Adams, Harold P., Jr.] Univ Iowa, Iowa City, IA 52242 USA.
[Warach, Steven] Univ Texas SW Med Ctr, Austin, TX USA.
[Hsia, Amie W.] MedStar Washington Hosp Ctr, Washington, DC USA.
[Auh, Sungyoung] NINDS, Bethesda, MD 20892 USA.
[Merino, Jose G.] Johns Hopkins Community Phys, Bethesda, MD USA.
RP Nagaraja, N (reprint author), Univ Iowa, 200 Hawkins Dr,2149 RCP, Iowa City, IA 52242 USA.
EM nandakumar-nagaraja@uiowa.edu
OI Merino, Jose/0000-0002-6676-0008
FU Intramural Research Program of the National Institutes of Health,
National Institute of Neurological Disorders and Stroke; National
Institute of Neurological Disorders and Stroke
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Neurological
Disorders and Stroke. Dr Adams has grant support from the National
Institute of Neurological Disorders and Stroke.
NR 6
TC 3
Z9 4
U1 0
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6149
EI 2168-6157
J9 JAMA NEUROL
JI JAMA Neurol.
PD DEC
PY 2014
VL 71
IS 12
BP 1555
EP 1558
DI 10.1001/jamaneurol.2014.2036
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA AW1YA
UT WOS:000346083500015
PM 25330362
ER
PT J
AU Pandey, S
Byler, DL
Hallett, M
AF Pandey, Sanjay
Byler, Debra L.
Hallett, Mark
TI HemidystoniaWith One Eye-of-the-Tiger Sign
SO JAMA NEUROLOGY
LA English
DT Editorial Material
C1 [Pandey, Sanjay; Hallett, Mark] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
[Pandey, Sanjay] Govind Ballabh Pant Hosp, Dept Neurol, New Delhi, India.
[Byler, Debra L.] Penn State Coll Med, Dept Neurol, Hershey, PA USA.
[Byler, Debra L.] Penn State Coll Med, Dept Pediat, Hershey, PA USA.
RP Hallett, M (reprint author), NINDS, Human Motor Control Sect, NIH, 10 Ctr Dr,MSC 1428,Bldg 10,Room 7D37, Bethesda, MD 20892 USA.
EM hallettm@ninds.nih.gov
FU Intramural NIH HHS
NR 3
TC 2
Z9 2
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6149
EI 2168-6157
J9 JAMA NEUROL
JI JAMA Neurol.
PD DEC
PY 2014
VL 71
IS 12
BP 1574
EP 1575
DI 10.1001/jamaneurol.2014.1077
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA AW1YA
UT WOS:000346083500019
PM 25347119
ER
PT J
AU Janssen, E
Morbach, H
Ullas, S
Bannock, JM
Massad, C
Menard, L
Barlan, I
Lefranc, G
Su, H
Dasouki, M
Al-Herz, W
Keles, S
Chatila, T
Geha, RS
Meffre, E
AF Janssen, Erin
Morbach, Henner
Ullas, Sumana
Bannock, Jason M.
Massad, Christopher
Menard, Laurence
Barlan, Isil
Lefranc, Gerard
Su, Helen
Dasouki, Majed
Al-Herz, Waleed
Keles, Sevgi
Chatila, Talal
Geha, Raif S.
Meffre, Eric
TI Dedicator of cytokinesis 8-deficient patients have a breakdown in
peripheral B-cell tolerance and defective regulatory T cells
SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
LA English
DT Article
DE Dedicator of cytokinesis 8; autoimmunity; B-cell tolerance; regulatory T
cells
ID HYPER-IGE SYNDROME; DOCK8 DEFICIENCY; AUTOANTIBODY PRODUCTION;
TRANSPLANTATION; HUMANS; ACTIVATION; EXPRESSION; MUTATIONS; LIGAND;
LUPUS
AB Background: Dedicator of cytokinesis 8 (DOCK8) deficiency is typified by recurrent infections, increased serum IgE levels, eosinophilia, and a high incidence of allergic and autoimmune manifestations.
Objective: We sought to determine the role of DOCK8 in the establishment and maintenance of human B-cell tolerance.
Methods: Autoantibodies were measured in the plasma of DOCK8-deficient patients. The antibody-coding genes from new emigrant/transitional and mature naive B cells were cloned and assessed for their ability to bind self-antigens. RegulatoryT(Treg) cells in the blood were analyzed by means of flow cytometry, and their function was tested by examining their capacity to inhibit the proliferation of CD4(+)CD25(-) effector T cells.
Results: DOCK8-deficient patients had increased levels of autoantibodies in their plasma. We determined that central B-cell tolerance did not require DOCK8, as evidenced by the normally low frequency of polyreactive new emigrant/transitional B cells in DOCK8-deficient patients. In contrast, autoreactive B cells were enriched in the mature naive B-cell compartment, revealing a defective peripheral B-cell tolerance checkpoint. In addition, we found that Treg cells were decreased and exhibited impaired suppressive activity in DOCK8-deficient patients.
Conclusions: Our data support a critical role for DOCK8 in Treg cell homeostasis and function and the enforcement of peripheral B-cell tolerance.
C1 [Janssen, Erin; Ullas, Sumana; Keles, Sevgi; Chatila, Talal; Geha, Raif S.] Boston Childrens Hosp, Div Immunol, Boston, MA 02115 USA.
[Janssen, Erin; Chatila, Talal; Geha, Raif S.] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Morbach, Henner; Bannock, Jason M.; Massad, Christopher; Menard, Laurence; Meffre, Eric] Yale Univ, Sch Med, Dept Immunobiol, New Haven, CT USA.
[Barlan, Isil] Marmara Univ, Istanbul, Turkey.
[Lefranc, Gerard] Univ Montpellier, IMGT, F-34059 Montpellier, France.
[Lefranc, Gerard] CNRS, Inst Human Genet, Montpellier, France.
[Su, Helen] NIH, Human Immunol Dis Unit, Bethesda, MD 20892 USA.
[Dasouki, Majed] Univ Kansas, Med Ctr, Div Genet Endocrinol & Metab, Dept Pediat, Kansas City, MO USA.
[Dasouki, Majed] Univ Kansas, Med Ctr, Div Genet Endocrinol & Metab, Dept Internal Med, Kansas City, MO USA.
[Al-Herz, Waleed] Kuwait Univ, Fac Med, Dept Pediat, Safat 13060, Kuwait.
[Keles, Sevgi] Necmettin Erbakan Univ, Meram Med Fac, Div Pediat Immunol & Allergy, Konya, Turkey.
RP Geha, RS (reprint author), Boston Childrens Hosp, One Blackfan St, Boston, MA 02115 USA.
EM raif.geha@childrens.harvard.edu; eric.meffre@yale.edu
RI Su, Helen/H-9541-2015
OI Su, Helen/0000-0002-5582-9110
FU National Institutes of Health (NIH)/National Institute of Allergy and
Infectious Diseases (NIAID) [AI061093, AI071087, AI082713, AI095848,
AI100315, HL059561, 5K 12HD052896]; Manton Foundation; German Research
Foundation [DFG MO2160/2-1]; Dubai-Harvard Foundation for Medical
Research; Jeffrey Modell Foundation; Intramural Research Program of the
NIH; NIAID; Kuwait Foundation for the Advancement of Sciences
[2010-1302-05]
FX Supported by National Institutes of Health (NIH)/National Institute of
Allergy and Infectious Diseases (NIAID) grants AI061093, AI071087,
AI082713, and AI095848 (to E.M.); AI100315 and HL059561 (to R.S.G.); and
5K 12HD052896 (to E.J.), as well as by grants from the Manton Foundation
(to E.J.), German Research Foundation grant DFG MO2160/2-1 (to H.M.),
the Dubai-Harvard Foundation for Medical Research and the Jeffrey Modell
Foundation (to R.S.G.), the Intramural Research Program of the NIH,
NIAID (to H.S.), and the Kuwait Foundation for the Advancement of
Sciences 2010-1302-05 (to W.A.-H.).
NR 48
TC 22
Z9 22
U1 0
U2 8
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0091-6749
EI 1097-6825
J9 J ALLERGY CLIN IMMUN
JI J. Allergy Clin. Immunol.
PD DEC
PY 2014
VL 134
IS 6
BP 1365
EP 1374
DI 10.1016/j.jaci.2014.07.042
PG 10
WC Allergy; Immunology
SC Allergy; Immunology
GA AW1UG
UT WOS:000346075400019
PM 25218284
ER
PT J
AU Cookson, MR
AF Cookson, Mark R.
TI Lardy brains make Parkinson's disease mice worse
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Editorial Material
AB Read the full article Diet-induced obesity accelerates the onset of terminal phenotypes in -synuclein transgenic mice' on page 848.
C1 NIA, Cell Biol & Gene Express Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
RP Cookson, MR (reprint author), NIA, Cell Biol & Gene Express Sect, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
EM cookson@mail.nih.gov
FU Intramural NIH HHS [ZIA AG000939-07]
NR 7
TC 1
Z9 1
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
EI 1471-4159
J9 J NEUROCHEM
JI J. Neurochem.
PD DEC
PY 2014
VL 131
IS 6
BP 697
EP 698
DI 10.1111/jnc.12843
PG 2
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AW2ZX
UT WOS:000346156200001
PM 25142063
ER
PT J
AU Shpyleva, S
Pogribna, M
Cozart, C
Bryant, MS
Muskhelishvili, L
Tryndyak, VP
Ross, SA
Beland, FA
Pogribny, IP
AF Shpyleva, Svitlana
Pogribna, Marta
Cozart, Christy
Bryant, Matthew S.
Muskhelishvili, Levan
Tryndyak, Volodymyr P.
Ross, Sharon A.
Beland, Frederick A.
Pogribny, Igor P.
TI Interstrain differences in the progression of nonalcoholic
steatohepatitis to fibrosis in mice are associated with altered hepatic
iron metabolism
SO JOURNAL OF NUTRITIONAL BIOCHEMISTRY
LA English
DT Article
DE NAFLD; Methyl-deficient diet; Liver fibrogenesis; Iron metabolism; IRP1;
miR-200a
ID FATTY LIVER-DISEASE; FOLATE-DEFICIENT DIET; ENDOPLASMIC-RETICULUM
STRESS; REGULATORY PROTEINS; LIPID-METABOLISM; OXIDATIVE STRESS;
STELLATE CELLS; FERRITIN; CHOLINE; INJURY
AB Nonalcoholic fatty liver disease (NAFLD) is a major health problem worldwide. Currently, there is a lack of conclusive information to clarify the molecular events and mechanisms responsible for the progression of NAFLD to fibrosis and cirrhosis and, more importantly, for differences in interindividual disease severity. The aim of this study was to investigate a role of interindividual differences in iron metabolism among inbred mouse strains in the pathogenesis and severity of fibrosis in a model of NAFLD. Feeding male A/J, 129S1/SvImJ and WSB/EiJ mice a choline- and folate-deficient diet caused NAFLD-associated liver injury and iron metabolism abnormalities, especially in WSB/EiJ mice. NAFLD-associated fibrogenesis was correlated with a marked strain- and injury-dependent increase in the expression of iron metabolism genes, especially transferrin receptor (Tfrc), ferritin heavy chain (Fth1), and solute carrier family 40 (iron-regulated transporter), member 1 (Slc40a1, Fpn1) and their related proteins, and pronounced down-regulation of the iron regulatory protein 1 (IRP1), with the magnitude being A/J<129S1/SvImJ 1.5, whereas this was seen in none of the controls (p < 0.0001). At time of the first positive qPCR for JCV DNA, 11 of 20 (55%) patients with natalizumab-associated PML had an AI(JCV) > 1.5. JCV DNA levels of <100 copies/ml were seen in 14 (70%) of these 20 patients, of whom 8 (57%) demonstrated an AI(JCV) > 1.5.
InterpretationDetermination of the AI(JCV) could be an added tool in the diagnostic workup for PML and should be included in the case definition of natalizumab-associated PML. Ann Neurol 2014;76:792-801
C1 [Warnke, Clemens; Dehmel, Thomas; Hartung, Hans-Peter; Kieseier, Bernd C.] Univ Dusseldorf, Dept Neurol, Fac Med, D-40225 Dusseldorf, Germany.
[von Geldern, Gloria; Major, Eugene] NINDS, NIH, Bethesda, MD 20892 USA.
[Markwerth, Philipp; Adams, Ortwin] Univ Dusseldorf, Inst Virol, D-40225 Dusseldorf, Germany.
[Hoepner, Robert; Gold, Ralf] Ruhr Univ Bochum, Dept Neurol, Bochum, Germany.
[Pawlita, Michael] German Canc Res Ctr, Res Program Infect & Canc, Heidelberg, Germany.
[Kuempfel, Tania; Hohlfeld, Reinhard] Univ Munich, Inst Clin Neuroimmunol, Munich, Germany.
[Kuempfel, Tania; Hohlfeld, Reinhard] Munich Cluster Syst Neurol SyNergy, Munich, Germany.
[Maeurer, Mathias] Caritas Hosp, Dept Neurol, Bad Mergentheim, Germany.
[Stangel, Martin; Wegner, Florian] Hannover Med Sch, Dept Neurol, Hannover, Germany.
[Straeten, Vera] Johannes Wesling Hosp Minden, Dept Neurol, Minden, Germany.
[Limmroth, Volker] Merheim Hosp, Dept Neurol, Cologne, Germany.
[Weber, Thomas] Marienhosp Hamburg, Dept Neurol, Hamburg, Germany.
[Hermsen, Derik] Univ Hosp Dusseldorf, Inst Clin Chem & Lab Diagnost, Dusseldorf, Germany.
[Kleinschnitz, Christoph] Univ Wurzburg, Dept Neurol, Wurzburg, Germany.
[Wattjes, Mike P.] Vrije Univ Amsterdam, Med Ctr, MS Ctr Amsterdam, Amsterdam, Netherlands.
[Wattjes, Mike P.] Vrije Univ Amsterdam, Med Ctr, Dept Radiol, Amsterdam, Netherlands.
[Svenningson, Anders] Umea Univ Hosp, Dept Pharmacol & Clin Neurosci, S-90185 Umea, Sweden.
[Olsson, Tomas] Karolinska Inst, Ctr Mol Med, Dept Neurol, Stockholm, Sweden.
RP Warnke, C (reprint author), Univ Dusseldorf, Dept Neurol, Moorenstr 5, D-40225 Dusseldorf, Germany.
EM clemens.warnke@med.uni-duesseldorf.de
RI Waterboer, Tim/G-1252-2010;
OI Svenningsson, Anders/0000-0003-0663-2220; Pawlita,
Michael/0000-0002-4720-8306
FU Research Commission of Heinrich Heine University, Dusseldorf [HHU];
German Ministry for Education and Research (BMBF; German Competence
Network MS [KKNMS], Natalizumab Pharmacovigilance Study) [01GI1002];
European Committee for Treatment and Research; European Union [115303];
European Federation of Pharmaceutical Industries and Associations
companies; Walter and Ilse Rose Foundation; German Research Foundation
[DFG CRC TRR128]; BMBF (KKNMS); Niedersachsen Research Network on
Neuroinfectiology of the Ministry of Science and Culture of Lower Saxony
FX This work was supported by a local faculty grant (Research Commission of
Heinrich Heine University, Dusseldorf [HHU]; O.A.) and a grant from the
German Ministry for Education and Research (BMBF; German Competence
Network MS [KKNMS], Natalizumab Pharmacovigilance Study, 01GI1002;
B.C.K.). C.W. was supported by a European Committee for Treatment and
Research in MS fellowship stipend. The research leading to these results
received support from the Innovative Medicines Initiative Joint
Undertaking under grant agreement No. 115303, resources of which are
composed of a financial contribution from the European Union's Seventh
Framework Program (FP7/2007-2013) and European Federation of
Pharmaceutical Industries and Associations companies' in-kind
contribution (to H.P.H., B.C.K, C.W.). The MS Center at the Department
of Neurology, HHU is supported by the Walter and Ilse Rose Foundation.
R.Hoh. was supported by the German Research Foundation (DFG CRC TRR128,
Z2) and BMBF (KKNMS). M.S. is supported by the Niedersachsen Research
Network on Neuroinfectiology of the Ministry of Science and Culture of
Lower Saxony.
NR 39
TC 30
Z9 30
U1 0
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD DEC
PY 2014
VL 76
IS 6
BP 792
EP 801
DI 10.1002/ana.24153
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA AU6BN
UT WOS:000345687600004
PM 24729444
ER
PT J
AU Zhou, YF
Wang, SN
Yu, ZX
Hoyt, RF
Hunt, T
Kindzelski, B
Shou, D
Xie, W
Du, YB
Liu, CY
Horvath, KA
AF Zhou, Yifu
Wang, Suna
Yu, Zuxi
Hoyt, Robert F., Jr.
Hunt, Timothy
Kindzelski, Bogdan
Shou, David
Xie, Wen
Du, Yubin
Liu, Chengyu
Horvath, Keith A.
TI Induced Pluripotent Stem Cell Transplantation in the Treatment of
Porcine Chronic Myocardial Ischemia
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID CORONARY-ARTERY-DISEASE; EPIGENETIC MEMORY; SOMATIC-CELLS; TOPCARE-AMI;
INFARCTION; DIFFERENTIATION; PARACRINE; REGENERATION; DELIVERY; KIDNEY
AB Background. This study was designed to test the effects of induced pluripotent stem cell (iPSC) in the treatment of chronic myocardial ischemia.
Methods. The reprogramming of passage 3 myocardial fibroblasts was performed by using the lentiviral vector containing 4 human factors: OCT4, SOX2, KLF4, and c-MYC. The iPSC colonies at P12-17 were allogeneically transplanted into ischemic myocardium of 10 swine by direct injection. Cohorts of 2 animals were sacrificed at 2, 4, 6, 8, and 12 weeks after injection.
Results. No signs of graft versus host disease were evident at any time points. At 2 weeks, clusters of SSEA-4-positive iPSCs were detected in the injected area. At 4 to 8 weeks, these cells started to proliferate into small spheres surrounded by thin capsules. At 12 weeks the cell clusters still existed, but decreased in size and numbers. The cells inside these masses were homogeneous with no sign of differentiation into any specific lineage. Increased smooth muscle actin or vWF positive cells were found inside and around the iPSC clusters, compared with non-injected areas. By real-time polymerase chain reaction, the levels of VEGF, basic FGF, and ANRT expression were significantly higher in the iPSC-treated myocardium compared with untreated areas. These results suggest that iPSCs contributed to angiogenesis.
Conclusions. Allogeneically transplanted pig iPSCs proliferated despite an ischemic environment in the first 2 months and survived for at least 3 months in immunocompetent hosts. Transplanted iPSCs were also proangiogenic and thus might have beneficial effects on the ischemic heart diseases. (C) 2014 by The Society of Thoracic Surgeons
C1 [Zhou, Yifu; Wang, Suna; Yu, Zuxi; Hoyt, Robert F., Jr.; Hunt, Timothy; Kindzelski, Bogdan; Shou, David; Xie, Wen; Du, Yubin; Liu, Chengyu; Horvath, Keith A.] NHLBI, Cellular Biol Sect, Cardiothorac Surg Res Program, NIH, Bethesda, MD 20892 USA.
RP Zhou, YF (reprint author), NHLBI, Cellular Biol Sect, Cardiothorac Surg Res Program, NIH, 10 Ctr Dr,MSC 1550,Bldg 10,Rm B1-D47, Bethesda, MD 20892 USA.
EM zhouyifu@mail.nih.gov
FU Intramural NIH HHS [Z99 HL999999]
NR 27
TC 3
Z9 6
U1 0
U2 9
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
EI 1552-6259
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD DEC
PY 2014
VL 98
IS 6
BP 2130
EP 2137
DI 10.1016/j.athoracsur.2014.07.008
PG 8
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA AU6WX
UT WOS:000345743200045
PM 25443017
ER
PT J
AU Kindzelski, BA
Li, M
Mazilu, D
Hunt, T
Horvath, KA
AF Kindzelski, Bogdan A.
Li, Ming
Mazilu, Dumitru
Hunt, Timothy
Horvath, Keith A.
TI Real-Time Magnetic Resonance-Guided Aortic Valve Replacement Using
Engager Valve
SO ANNALS OF THORACIC SURGERY
LA English
DT Article
ID IMPLANTATION
AB Purpose. New-generation stented bioprostheses coupled with better imaging modalities are expanding the clinical utility of transcatheter aortic valve replacement (TAVR). This study aimed at evaluating the feasibility of real-time cardiovascular magnetic resonance (rtCMR) -guided TAVR using the Medtronic Engager aortic valve system in a preclinical model.
Description. The Engager delivery device was slightly modified to make it CMR-compatible. Ten Yucatan swine underwent rtCMR-guided transapical TAVR. Postplacement phase-contrast and first-pass perfusion CMR sequences were used to evaluate for aortic regurgitation and myocardial perfusion, respectively.
Evaluation. Real-time CMR provided excellent visualization of cardiac anatomy during TAVR. Nine of 10 animals had proper valve placement in the aortic annulus as determined by CMR and confirmed by necropsy inspection. Postplacement phase-contrast scans confirmed no intravalvular or paravalvular leaks. Perfusion scans demonstrated sufficient coronary flow. Roentgenographs confirmed proper placement of the prostheses.
Conclusions. The Engager valve can be implanted transapically under rtCMR guidance with a modified, CMR-compatible delivery device in a preclinical model. Cardiovascular magnetic resonance allowed for accurate preplacement evaluation, real-time guidance, and postplacement functional assessment. (C) 2014 by The Society of Thoracic Surgeons.
C1 [Kindzelski, Bogdan A.; Li, Ming; Mazilu, Dumitru; Hunt, Timothy; Horvath, Keith A.] NHLBI, Cardiothorac Surg Res Program, NIH, Bethesda, MD 20892 USA.
RP Horvath, KA (reprint author), NHLBI, Cardiothorac Surg Res Program, NIH, Bldg 10,Rm B1D47,10 Ctr Dr, Bethesda, MD 20892 USA.
EM horvathka@mail.nih.gov
FU National Heart, Lung, and Blood Institute, NIH; NIH Medical Research
Scholars Program; NIH; DHHS
FX This research was made possible by funding from the Intramural Research
Program of the National Heart, Lung, and Blood Institute, NIH, DHHS, and
the NIH Medical Research Scholars Program, a public-private partnership
supported jointly by the NIH and generous contributions to the
Foundation for the NIH from Pfizer Inc, The Doris Duke Charitable
Foundation, The Alexandria Real Estate Equities, Inc and Mr. and Mrs.
Joel S. Marcus, and the Howard Hughes Medical Institute, as well as
other private donors. The authors would like to thank Medtronic for
generously providing the Engager valves and delivery devices for the
rtCMR-guided experiments. The authors had full freedom of investigation.
NR 10
TC 2
Z9 2
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
EI 1552-6259
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD DEC
PY 2014
VL 98
IS 6
BP 2194
EP 2199
DI 10.1016/j.athoracsur.2014.09.017
PG 6
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA AU6WX
UT WOS:000345743200055
PM 25468087
ER
PT J
AU Hendrickx, DM
Boyles, RR
Kleinjans, JCS
Dearry, A
AF Hendrickx, Diana M.
Boyles, Rebecca R.
Kleinjans, Jos C. S.
Dearry, Allen
TI Workshop report: Identifying opportunities for global integration of
toxicogenomics databases, 26-27 June 2013, Research Triangle Park, NC,
USA
SO ARCHIVES OF TOXICOLOGY
LA English
DT Article
DE Databases; Data sharing; Hazard identification; Human; Omics
technologies; Risk assessment
ID BIOLOGICAL-SYSTEMS; TOXICITY DATA; IN-VITRO; MICROARRAY; TOXICOLOGY;
PROJECT; DISCOVERY; SCIENCE; DISEASE; DESIGN
AB A joint US-EU workshop on enhancing data sharing and exchange in toxicogenomics was held at the National Institute for Environmental Health Sciences. Currently, efficient reuse of data is hampered by problems related to public data availability, data quality, database interoperability (the ability to exchange information), standardization and sustainability. At the workshop, experts from universities and research institutes presented databases, studies, organizations and tools that attempt to deal with these problems. Furthermore, a case study showing that combining toxicogenomics data from multiple resources leads to more accurate predictions in risk assessment was presented. All participants agreed that there is a need for a web portal describing the diverse, heterogeneous data resources relevant for toxicogenomics research. Furthermore, there was agreement that linking more data resources would improve toxicogenomics data analysis. To outline a roadmap to enhance interoperability between data resources, the participants recommend collecting user stories from the toxicogenomics research community on barriers in data sharing and exchange currently hampering answering to certain research questions. These user stories may guide the prioritization of steps to be taken for enhancing integration of toxicogenomics databases.
C1 [Hendrickx, Diana M.; Kleinjans, Jos C. S.] Maastricht Univ, Dept Toxicogen, NL-6229 ER Maastricht, Netherlands.
[Boyles, Rebecca R.; Dearry, Allen] NIEHS, Dept Hlth & Human Serv, NIH, Res Triangle Pk, NC 27709 USA.
RP Hendrickx, DM (reprint author), Maastricht Univ, Dept Toxicogen, Univ Singel 40, NL-6229 ER Maastricht, Netherlands.
EM d.hendrickx@maastrichtuniversity.nl
RI Kleinjans, Jos/E-7241-2015;
OI Hendrickx, Diana/0000-0001-7225-4307; Boyles,
Rebecca/0000-0003-0073-6854
FU Research Data Alliance (RDA) Europe (European Union); NIEHS; NIH,
National Institute of Environmental Health Sciences
FX This report is based on the "Workshop on Identifying Opportunities for
Global Integration of Toxicogenomics Databases", 26-27 June 2013, hosted
at the National Institute of Environmental Health Sciences (NIEHS) and
sponsored by Research Data Alliance (RDA) Europe (the European Union's
Seventh Framework Programme) and the NIEHS. The paper reflects a
consensus view of the participants of the workshop. This work was
supported in part by the NIH, National Institute of Environmental Health
Sciences. The views in this article are those of the authors and do not
necessarily reflect the views of the NIEHS or the European Union. The
authors like to thank the other participants of the workshop: Beth Plale
(Indiana University, USA), Jennifer Fostel (NIEHS, USA), Ugis Sarkans
(EMBL-EBI, UK), Caroline Mattingly (North Carolina State University,
USA), Aravind Subramanian (Broad Institute, USA), Florian Caiment
(Maastricht University, The Netherlands), Weida Tong (FDA, USA), Stephen
Edwards (EPA, USA), Scott Auerbach (NIEHS, USA) and Anne Hersey
(EMBL-EBI, UK).
NR 33
TC 3
Z9 3
U1 0
U2 6
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0340-5761
EI 1432-0738
J9 ARCH TOXICOL
JI Arch. Toxicol.
PD DEC
PY 2014
VL 88
IS 12
BP 2323
EP 2332
DI 10.1007/s00204-014-1387-3
PG 10
WC Toxicology
SC Toxicology
GA AU6GG
UT WOS:000345701100021
PM 25326818
ER
PT J
AU Fleischer, SJ
Giesecke, C
Mei, HE
Lipsky, PE
Daridon, C
Dorner, T
AF Fleischer, Sarah J.
Giesecke, Claudia
Mei, Henrik E.
Lipsky, Peter E.
Daridon, Capucine
Doerner, Thomas
TI Increased Frequency of a Unique Spleen Tyrosine Kinase Bright Memory B
Cell Population in Systemic Lupus Erythematosus
SO ARTHRITIS & RHEUMATOLOGY
LA English
DT Article
ID TRANSCRIPTION FACTOR BRIGHT; AUTOANTIBODY PRODUCTION; REVISED CRITERIA;
DISEASE-ACTIVITY; TRANSGENIC MICE; CLASSIFICATION; PATHOGENESIS;
EXPRESSION; NEPHRITIS; ARTHRITIS
AB Objective. Systemic lupus erythematosus (SLE) is characterized by B cell hyperactivity and autoantibody production. As spleen tyrosine kinase (Syk) is pivotal in B cell activation, these experiments aimed to examine the extent to which Syk was abnormally expressed in SLE B cells and the nature of the B cell subset that differently expressed Syk. Methods. B cells from healthy donors and SLE patients were analyzed by flow cytometry to assess basal expression of Syk and phosphorylated Syk. B cell subsets expressing higher levels of Syk were found, and their detailed phenotype, in vitro differentiation into plasmablasts/ plasma cells, and Syk induction by cytokines were determined. Results. Syk expression was higher in CD27 memory B cells than in naive B cells from SLE patients. However, a significantly increased frequency of CD27 B cells with bright expression of Syk (Syk ) was found in SLE patients. CD27 Syk B cells showed enhanced basal expression of p-Syk and stronger Syk phosphorylation upon B cell receptor (BCR) engagement as compared to CD27 Syk B cells. CD27 Syk B cells were CD38 as well as CD19 , CD20 , and mainly CD21 , with decreased ABCB1 transporter activity. In contrast to CD27 Syk B cells, CD27 Syk B cells exhibited enhanced differentiation into CD27 IgG-secreting cells and expressed somatically mutated BCR gene rearrangements. Syk B cells were inducible in vitro by stimulation with interferon-, lipopolysaccharide, or tumor necrosis factor . Conclusion. SLE patients exhibit an increased frequency of hitherto unknown CD27 Syk memorylike B cells, indicating that intracellular Syk density could distinguish CD27 memory B cells from truly naive B cell subsets. Furthermore, the CD27 Syk subset is a candidate for a source of increased plasma cells in SLE.
C1 [Fleischer, Sarah J.; Giesecke, Claudia; Mei, Henrik E.; Daridon, Capucine; Doerner, Thomas] Charite, D-13353 Berlin, Germany.
[Fleischer, Sarah J.; Giesecke, Claudia; Mei, Henrik E.; Daridon, Capucine; Doerner, Thomas] German Rheumatism Res Ctr Berlin, Berlin, Germany.
[Lipsky, Peter E.] NIAMSD, NIH, Bethesda, MD 20892 USA.
RP Dorner, T (reprint author), Charite, Dept Med Rheumatol & Clin Immunol, Charitepl 01, D-10098 Berlin, Germany.
EM thomas.doerner@charite.de
FU DFG [SFB650, SFB633 A14, SPP ImmunoBone DFG Do491/8-2, Do491/7-3]
FX Supported by the DFG (SFB650 project TP16, SFB633 A14, SPP ImmunoBone
DFG Do491/8-2, and DFG project Do491/7-3).
NR 35
TC 14
Z9 14
U1 0
U2 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2326-5191
EI 2326-5205
J9 ARTHRITIS RHEUMATOL
JI Arthritis Rheumatol.
PD DEC
PY 2014
VL 66
IS 12
BP 3424
EP 3435
DI 10.1002/art.38854
PG 12
WC Rheumatology
SC Rheumatology
GA AU4HK
UT WOS:000345571200020
PM 25156507
ER
PT J
AU Galski, H
Oved-Gelber, T
Simanovsky, M
Lazarovici, P
Gottesman, MM
Nagler, A
AF Galski, Hanan
Oved-Gelber, Tamar
Simanovsky, Masha
Lazarovici, Philip
Gottesman, Michael M.
Nagler, Arnon
TI P-glycoprotein-dependent resistance of cancer cells toward the extrinsic
TRAIL apoptosis signaling pathway (vol 86, pg 584, 2013)
SO BIOCHEMICAL PHARMACOLOGY
LA English
DT Correction
C1 [Galski, Hanan; Oved-Gelber, Tamar; Simanovsky, Masha; Nagler, Arnon] Chaim Sheba Med Ctr, Div Hematol, Lab Mol Immunol, IL-52621 Tel Hashomer, Israel.
[Lazarovici, Philip] Hebrew Univ Jerusalem, Inst Drug Sci, Sch Pharm, IL-91905 Jerusalem, Israel.
[Gottesman, Michael M.] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Galski, H (reprint author), Chaim Sheba Med Ctr, Lab Mol Immunobiol, IL-52621 Ramat Gan, Israel.
EM Hanan.Galski@sheba.health.gov.il
NR 1
TC 0
Z9 0
U1 1
U2 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0006-2952
EI 1873-2968
J9 BIOCHEM PHARMACOL
JI Biochem. Pharmacol.
PD DEC 1
PY 2014
VL 92
IS 3
BP 518
EP 518
DI 10.1016/j.bcp.2014.08.020
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AW0BM
UT WOS:000345955400014
ER
PT J
AU Qin, J
Follmann, DA
AF Qin, Jing
Follmann, Dean A.
TI Semiparametric maximum likelihood inference by using failed contact
attempts to adjust for nonignorable nonresponse
SO BIOMETRIKA
LA English
DT Article
DE Call-back in survey; Nonignorable nonresponse data; Semiparametric
maximum likelihood estimation
AB In marketing research, social science and epidemiological studies, call-back of nonrespondents is standard. If respondents and nonrespondents tend to give different answers, the missing data are called non-ignorable, and using them alone may produce biased results. To extend earlier work on nonresponse in the presence of call-backs, Alho (1990) proposed modelling the probability of response at each attempt through logistic regression, where outcomes of interest and covariates are explanatory variables. In this paper we propose a semiparametric maximum likelihood approach, and discuss large-sample properties and the semiparametric likelihood ratio statistic used to test whether the data are missing completely at random. Simulations are conducted to evaluate this approach and a modification of the method of Alho (1990). Data from the National Health Interview Survey are used for illustration.
C1 [Qin, Jing; Follmann, Dean A.] NIAID, Biostat Res Branch, Bethesda, MD 20892 USA.
RP Qin, J (reprint author), NIAID, Biostat Res Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM jingqin@niaid.nih.gov; DFollmann@niaid.nih.gov
NR 5
TC 0
Z9 0
U1 2
U2 4
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-3444
EI 1464-3510
J9 BIOMETRIKA
JI Biometrika
PD DEC
PY 2014
VL 101
IS 4
BP 985
EP 991
DI 10.1093/biomet/asu046
PG 7
WC Biology; Mathematical & Computational Biology; Statistics & Probability
SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational
Biology; Mathematics
GA AU8DZ
UT WOS:000345827900018
ER
PT J
AU Curtis, LM
Grkovic, L
Mitchell, SA
Steinberg, SM
Cowen, EW
Datiles, MB
Mays, J
Bassim, C
Joe, G
Comis, LE
Berger, A
Avila, D
Taylor, T
Pulanic, D
Cole, K
Baruffaldi, J
Fowler, DH
Gress, RE
Pavletic, SZ
AF Curtis, L. M.
Grkovic, L.
Mitchell, S. A.
Steinberg, S. M.
Cowen, E. W.
Datiles, M. B.
Mays, J.
Bassim, C.
Joe, G.
Comis, L. E.
Berger, A.
Avila, D.
Taylor, T.
Pulanic, D.
Cole, K.
Baruffaldi, J.
Fowler, D. H.
Gress, R. E.
Pavletic, S. Z.
TI NIH response criteria measures are associated with important parameters
of disease severity in patients with chronic GVHD
SO BONE MARROW TRANSPLANTATION
LA English
DT Article
ID VERSUS-HOST-DISEASE; CONSENSUS DEVELOPMENT PROJECT; WORKING
GROUP-REPORT; CLINICAL-TRIALS; VALIDATION; SCALES
AB Lack of standardized criteria measuring therapeutic response remains an obstacle to the development of better treatments for chronic GVHD (cGVHD). This cross-sectional prospective study examined the concurrent and predictive validity of 18 clinician-reported ('Form A') and 8 patient-reported ('Form B') response measures proposed by NIH criteria. Concurrent parameters of interest were NIH global score, cGVHD activity, Lee symptom score and SF36 PCS. Patient cohort included 193 adults with moderate-to-severe cGVHD. Measures associated with the highest number of outcomes were lung function score (LFS), 2-min walk, grip strength, 4-point health-care provider (HCP) and patient global scores, 11-point clinician- and patient-reported global symptom severity scores, and Karnofsky performance score (KPS). Measures associated with survival in univariate analyses led to a Cox model containing skin erythema, LFS, KPS, eosinophil count and interval from cGVHD diagnosis to enrollment as jointly associated with survival. In conclusion, 4-point HCP and patient global scores and 11-point clinician- and patient-reported global symptom severity scores are associated with the majority of concurrent outcomes. Skin erythema is a potentially reversible sign of cGVHD that is associated with survival. These results define a subset of measures that should be prioritized for evaluation in future studies.
C1 [Curtis, L. M.] NCI, Med Oncol Serv, NIH, Bethesda, MD 20892 USA.
[Curtis, L. M.; Grkovic, L.; Avila, D.; Taylor, T.; Cole, K.; Baruffaldi, J.; Fowler, D. H.; Gress, R. E.; Pavletic, S. Z.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Grkovic, L.; Pulanic, D.] Univ Zagreb, Clin Hosp Ctr Zagreb, Dept Hematol, Zagreb 41000, Croatia.
[Mitchell, S. A.] NCI, Outcomes Branch, Bethesda, MD 20892 USA.
[Mitchell, S. A.] NCI, Div Canc Control & Populat Sci, NIH, Bethesda, MD 20892 USA.
[Steinberg, S. M.] NCI, Biostat & Data Management Sect, NIH, Rockville, MD USA.
[Cowen, E. W.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Datiles, M. B.] NEI, NIH, Bethesda, MD 20892 USA.
[Mays, J.; Bassim, C.] Natl Inst Dent & Craniofacial Res, Bethesda, MD USA.
[Joe, G.; Comis, L. E.] NIH, Ctr Clin, Dept Rehabil Med, Bethesda, MD 20892 USA.
[Berger, A.] NIH, Ctr Clin, Pain & Palliat Care Med Dept, Bethesda, MD 20892 USA.
RP Pavletic, SZ (reprint author), NCI, Ctr Canc Res, NIH, Bldg 10,Room CRC 3-3330, Bethesda, MD 20892 USA.
EM pavletis@mail.nih.gov
OI Datiles, Manuel III B./0000-0003-4660-1664
FU National Institutes of Health, Clinical Center, Nursing and Patient Care
Services; Research Program of the National Institutes of Health (NIH),
National Cancer Institute, Center for Cancer Research
FX This research was also supported also by National Institutes of Health,
Clinical Center, Nursing and Patient Care Services. We thank all
patients and their families who participated in the natural history of
cGVHD protocol. This research was supported by the Intramural Research
Program of the National Institutes of Health (NIH), National Cancer
Institute, Center for Cancer Research. The authors are employees of the
United States Government, and, as such, this work was carried out in
that capacity. The views expressed do not necessarily represent the
views of the National Institutes of Health or the United States
Government.
NR 21
TC 6
Z9 6
U1 1
U2 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0268-3369
EI 1476-5365
J9 BONE MARROW TRANSPL
JI Bone Marrow Transplant.
PD DEC
PY 2014
VL 49
IS 12
BP 1513
EP 1520
DI 10.1038/bmt.2014.188
PG 8
WC Biophysics; Oncology; Hematology; Immunology; Transplantation
SC Biophysics; Oncology; Hematology; Immunology; Transplantation
GA AU9IM
UT WOS:000345905300011
PM 25153693
ER
PT J
AU Pinsky, PF
Nath, PH
Gierada, DS
Sonavane, S
Szabo, E
AF Pinsky, Paul F.
Nath, P. Hrudaya
Gierada, David S.
Sonavane, Sushil
Szabo, Eva
TI Short- and Long-term Lung Cancer Risk Associated with Noncalcified
Nodules Observed on Low-Dose CT
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID GROUND-GLASS OPACITY; COMPUTED-TOMOGRAPHY; SCREENING CT; MORTALITY;
SMOKERS; TRIAL; SCAN
AB Chemoprevention is an important potential tool in reducing lung cancer incidence. Noncalcified nodules (NCN) observed on low-dose computed tomography (LDCT) have been proposed as intermediate endpoints in chemoprevention trials, but whether NCNs represent cancer precursors is unclear. We analyzed data from subjects in the LDCT arm of the National Lung Screening Trial (NLST) to examine short- and long-term lung cancer risks associated with NCNs and to elucidate whether some NCNs may be cancer precursors. NLST subjects received a baseline and two additional LDCT screens and were followed for a median of 6.5 years. We examined lung cancer incidence over three distinct periods from baseline-0-23 months (short-term), 24-59 months (medium-term), and 60-84 months (long-term)-in relation to baseline NCN characteristics. Spatially, lung cancer incidence was analyzed at the person, lung, and lobe levels relative to NCN location. A total of 26,272 subjects received the baseline LDCT screen, with 468, 413, and 190 lung cancers observed in the three periods. The presence of an NCN gave significantly elevated long-term lung cancer risk ratios (RR) of 1.8, 2.4, and 3.5 at the person, lung, and lobe levels; corresponding short-term RRs were 10.3, 16.8, and 38.0. Ground-glass attenuation was positively associated with long-term lung cancer risk but inversely associated with short-term risk; NCN size was positively associated with short-term risk but not significantly associated with long-term risk. That NCNs convey significantly elevated excess long-term of lung cancer lends evidence to the hypothesis that some NCNs may be cancer precursors. (C)2014 AACR.
C1 [Pinsky, Paul F.; Szabo, Eva] NCI, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Nath, P. Hrudaya; Sonavane, Sushil] Univ Alabama Birmingham, Birmingham, AL USA.
[Gierada, David S.] Washington Univ, Sch Med, St Louis, MO USA.
RP Pinsky, PF (reprint author), NCI, 9609 Med Ctr Dr, Bethesda, MD 20892 USA.
EM pp4f@nih.gov
FU National Cancer Institute
FX This study was supported by contracts from the National Cancer
Institute.
NR 15
TC 8
Z9 8
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
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2014
VL 7
IS 12
BP 1179
EP 1185
DI 10.1158/1940-6207.CAPR-13-0438
PG 7
WC Oncology
SC Oncology
GA AU6WP
UT WOS:000345742400002
PM 24755313
ER
PT J
AU Mohammed, A
Janakiram, NB
Madka, V
Ritchie, RL
Brewer, M
Biddick, L
Patlolla, JMR
Sadeghi, M
Lightfoot, S
Steele, VE
Rao, CV
AF Mohammed, Altaf
Janakiram, Naveena B.
Madka, Venkateshwar
Ritchie, Rebekah L.
Brewer, Misty
Biddick, Laura
Patlolla, Jagan Mohan R.
Sadeghi, Michael
Lightfoot, Stan
Steele, Vernon E.
Rao, Chinthalapally V.
TI Eflornithine (DFMO) Prevents Progression of Pancreatic Cancer by
Modulating Ornithine Decarboxylase Signaling
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID ENGINEERED MOUSE MODELS; ALPHA-DIFLUOROMETHYLORNITHINE; C-MYC; PROSTATE
CARCINOGENESIS; POLYAMINE BIOSYNTHESIS; DUCTAL ADENOCARCINOMA;
CELL-PROLIFERATION; DOUBLE-BLIND; SKIN-CANCER; CHEMOPREVENTION
AB Ornithine decarboxylase (ODC) is the key rate-limiting enzyme in the polyamine synthesis pathway and it is overexpressed in a variety of cancers. We found that polyamine synthesis and modulation of ODC signaling occurs at early stages of pancreatic precursor lesions and increases as the tumor progresses in Krasactivated p48(Cre/+) -LSL-Kras(G12D/+) mice. Interest in use of the ODC inhibitor eflornithine (DFMO) as a cancer chemopreventive agent has increased in recent years since ODC was shown to be transactivated by the c-myc oncogene and to cooperate with the ras oncogene in malignant transformation of epithelial tissues. We tested the effects of DFMO on pancreatic intraepithelial neoplasias (PanIN) and their progression to pancreatic ductal adenocarcinoma (PDAC) in genetically engineered Kras mice. The Kras(G12D/+) mice fed DFMO at 0.1% and 0.2% in the diet showed a significant inhibition (P < 0.0001) of PDAC incidence compared with mice fed control diet. Pancreatic tumor weights were decreased by 31% to 43% (P < 0.03-0.001) with both doses of DFMO. DFMO at 0.1% and 0.2% caused a significant suppression (27% and 31%; P < 0.02-0.004) of PanIN 3 lesions (carcinoma in situ). DFMO-treated pancreas exhibited modulated ODC pathway components along with decreased proliferation and increased expression of p21/p27 as compared with pancreatic tissues derived from mice fed control diet. In summary, our preclinical data indicate that DFMO has potential for chemoprevention of pancreatic cancer and should be evaluated in other PDAC models and in combination with other drugs in anticipation of future clinical trials. (C)2014 AACR.
C1 [Mohammed, Altaf; Janakiram, Naveena B.; Madka, Venkateshwar; Ritchie, Rebekah L.; Brewer, Misty; Biddick, Laura; Patlolla, Jagan Mohan R.; Sadeghi, Michael; Lightfoot, Stan; Rao, Chinthalapally V.] Univ Oklahoma, Hlth Sci Ctr, Ctr Canc Prevent & Drug Dev, Dept Med,Hem Onc Sect, Oklahoma City, OK 73104 USA.
[Steele, Vernon E.] NCI, Canc Prevent Div, Chemoprevent Agent Dev Res Grp, Bethesda, MD 20892 USA.
RP Rao, CV (reprint author), Univ Oklahoma, Hlth Sci Ctr, Ctr Canc Prevent & Drug Dev, 975 NE 10th St,BRC 2,Room 1203, Oklahoma City, OK 73104 USA.
EM altaf-mohammed@ouhsc.edu; cv-rao@ouhsc.edu
FU National Cancer Institute [N01-CN-53300]
FX This work was supported by the National Cancer Institute N01-CN-53300 to
C.V. Rao.
NR 50
TC 10
Z9 11
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
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2014
VL 7
IS 12
BP 1198
EP 1209
DI 10.1158/1940-6207.CAPR-14-0176
PG 12
WC Oncology
SC Oncology
GA AU6WP
UT WOS:000345742400004
PM 25248858
ER
PT J
AU Robles, AI
Yang, P
Jen, J
McClary, AC
Calhoun, K
Bowman, ED
Vahakangas, K
Greathouse, KL
Wang, Y
Olivo-Marston, S
Wenzlaff, AS
Deng, B
Schwartz, AG
Ryan, BM
AF Robles, Ana I.
Yang, Ping
Jen, Jin
McClary, Andrew C.
Calhoun, Kara
Bowman, Elise D.
Vahakangas, Kirsi
Greathouse, K. Leigh
Wang, Yi
Olivo-Marston, Susan
Wenzlaff, Angela S.
Deng, Bo
Schwartz, Ann G.
Ryan, Brid M.
TI A DRD1 Polymorphism Predisposes to Lung Cancer among Those Exposed to
Secondhand Smoke during Childhood
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID DOPAMINE D1 RECEPTOR; CD4+AND CD8+T CELLS; TOBACCO-SMOKE; GENOME-WIDE;
SUSCEPTIBILITY LOCUS; PARKINSONS-DISEASE; NICOTINE DEPENDENCE;
CIGARETTE-SMOKING; TUMOR-GROWTH; IN-VITRO
AB Lung cancer has a familial component which suggests a genetic contribution to its etiology. Given the strong evidence linking smoking with lung cancer, we studied miRNA-related loci in genes associated with smoking behavior. CHRNA, CHRNB gene families, CYP2A6, and DRD1 (dopamine receptor D1) were mined for SNPs that fell within the seed region of miRNA binding sites and then tested for associations with risk in a three-stage validation approach. A 3'UTR (untranslated region) SNP in DRD1 was associated with a lower risk of lung cancer among individuals exposed to secondhand smoke during childhood [OR, 0.69; 95% confidence interval (CI), 0.60-0.79; P < 0.0001]. This relationship was evident in both ever (OR, 0.74; 95% CI, 0.62-0.88; P = 0.001) and never smokers (OR, 0.61; 95% CI, 0.47-0.79; P < 0.0001), European American (OR, 0.65; 95% CI, 0.53-0.80; P < 0.0001), and African American (OR, 0.73; 95% CI, 0.62-0.88; P = 0.001) populations. Although much remains undefined about the long-term risks associated with exposure to secondhand smoke and heterogeneity between individuals in regard to their susceptibility to the effects of secondhand smoke, our data show an interaction between an SNP in the 3'UTR of DRD1 and exposure to secondhand smoke during childhood. Further work is needed to explore the mechanistic underpinnings of this SNP and the nature of the interaction between DRD1 and exposure to secondhand smoke during childhood. (C)2014 AACR.
C1 [Robles, Ana I.; McClary, Andrew C.; Calhoun, Kara; Bowman, Elise D.; Greathouse, K. Leigh; Ryan, Brid M.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Yang, Ping] Mayo Clin, Dept Hlth Sci Res, Rochester, MN USA.
[Jen, Jin] Mayo Clin, Dept Lab Med & Pathol, Rochester, MN USA.
[Jen, Jin] Mayo Clin, Div Pulm & Crit Care Med, Rochester, MN USA.
[McClary, Andrew C.] Stanford Univ Hosp & Clin, Dept Pathol, Stanford, CA USA.
[Vahakangas, Kirsi] Univ Eastern Finland, Sch Pharm Toxicol, Fac Hlth Sci, Kuopio, Finland.
[Wang, Yi] Wenzhou Med Univ, Sch Environm Sci & Publ Hlth, Div Prevent Med, Wenzhou, Zhejiang, Peoples R China.
[Wang, Yi; Deng, Bo] Mayo Clin, Div Epidemiol, Rochester, MN USA.
[Olivo-Marston, Susan] Ohio State Univ, Coll Publ Hlth, Div Epidemiol, Columbus, OH 43210 USA.
[Wenzlaff, Angela S.; Schwartz, Ann G.] Wayne State Univ, Sch Med, Dept Oncol, Karmanos Canc Inst, Detroit, MI USA.
[Deng, Bo] Third Mil Med Univ, Inst Surg Res, Daping Hosp, Dept Thorac Surg, Chongqing, Peoples R China.
RP Ryan, BM (reprint author), NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
EM ryanb@mail.nih.gov
FU Intramural Program of the Centre for Cancer Research, National Cancer
Institute; NIH [R01 CA060691, P30 CA022453, HHSN26120100028C,
NIH-R01-CA80127, NIH-R01-CA84354, NIH-R01-CA115857]; American Cancer
Society; Mayo Clinic Cancer Center; Center for Individualized Medicine;
Mayo Clinic Foundation
FX This work was supported by the Intramural Program of the Centre for
Cancer Research, National Cancer Institute (to A.I. Robles and B.M.
Ryan), NIH R01 CA060691 (to A.G. Schwartz), contracts HHSN26120100028C
(to A.G. Schwartz), NIH P30 CA022453 (to A.G. Schwartz), NIH-R01-CA80127
(to P. Yang), NIH-R01-CA84354 (to P. Yang), and NIH-R01-CA115857 (to P.
Yang). J. Jen is a recipient of the New Investigator Award from the
American Cancer Society and supported by funding from Mayo Clinic Cancer
Center and the Center for Individualized Medicine. P. Yang, J. Jen, and
Y. Wang received support from The Mayo Clinic Foundation.
NR 61
TC 6
Z9 6
U1 7
U2 16
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2014
VL 7
IS 12
BP 1210
EP 1218
DI 10.1158/1940-6207.CAPR-14-0158
PG 9
WC Oncology
SC Oncology
GA AU6WP
UT WOS:000345742400005
PM 25281486
ER
PT J
AU Barry, KH
Moore, LE
Sampson, J
Yan, LY
Meyer, A
Oler, AJ
Chung, CC
Wang, ZM
Yeager, M
Amundadottir, L
Berndt, SI
AF Barry, Kathryn Hughes
Moore, Lee E.
Sampson, Joshua
Yan, Liying
Meyer, Ann
Oler, Andrew J.
Chung, Charles C.
Wang, Zhaoming
Yeager, Meredith
Amundadottir, Laufey
Berndt, Sonja I.
TI DNA Methylation Levels at Chromosome 8q24 in Peripheral Blood Are
Associated with 8q24 Cancer Susceptibility Loci
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SINGLE-NUCLEOTIDE POLYMORPHISM; LONG-RANGE
INTERACTION; PROSTATE-CANCER; COLORECTAL-CANCER; BLADDER-CANCER; RISK
LOCI; GENETIC-VARIANTS; OVARIAN-CANCER; NONCODING RNA
AB Chromosome 8q24 has emerged as an important region for genetic susceptibility to various cancers, but little is known about the contribution of DNA methylation at 8q24. To evaluate variability in DNA methylation levels at 8q24 and the relationship with cancer susceptibility single nucleotide polymorphisms (SNPs) in this region, we quantified DNA methylation levels in peripheral blood at 145 CpG sites nearby 8q24 cancer susceptibility SNPs or MYC using pyrosequencing among 80 Caucasian men in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. For the 60 CpG sites meeting quality control, which also demonstrated temporal stability over a 5-year period, we calculated pairwise Spearman correlations for DNA methylation levels at each CpG site with 42 8q24 cancer susceptibility SNPs. To account for multiple testing, we adjusted P values into q values reflecting the false discovery rate (FDR). In contrast to the MYC CpG sites, most sites nearby the SNPs demonstrated good reproducibility, high methylation levels, and moderate-high between-individual variation. We observed 10 statistically significant (FDR<0.05) CpG site-SNP correlations. These included correlations between an intergenic CpG site at Chr8: 128393157 and the prostate cancer SNP rs16902094 (rho = -0.54; P = 9.7 x 10(-7); q = 0.002), a PRNCR1 CpG site at Chr8: 128167809 and the prostate cancer SNP rs1456315 (rho = 0.52; P = 1.4 x 10(-6); q = 0.002), and two POU5F1B CpG sites and several prostate/colorectal cancer SNPs (for Chr8: 128498051 and rs6983267, rho = 0.46; P = 2.0 x 10(-5); q = 0.01). This is the first report of correlations between blood DNA methylation levels and cancer susceptibility SNPs at 8q24, suggesting that DNA methylation at this important susceptibility locus may contribute to cancer risk. (C)2014 AACR.
C1 [Barry, Kathryn Hughes; Moore, Lee E.; Berndt, Sonja I.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Sampson, Joshua] NCI, Biostat Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Yan, Liying; Meyer, Ann] EpigenDx Inc, Hopkinton, MA USA.
[Oler, Andrew J.] NIAID, Bioinformat & Computat Biosci Branch, Off Cyber Infrastruct & Computat Biol, Bethesda, MD 20892 USA.
[Chung, Charles C.; Wang, Zhaoming; Yeager, Meredith] NCI, Canc Genom Res Lab, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Amundadottir, Laufey] NCI, Lab Translat Genom, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
RP Barry, KH (reprint author), NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, 9609 Med Ctr Dr,Room 6E618 MSC 9771, Bethesda, MD 20892 USA.
EM barrykh@mail.nih.gov
RI Amundadottir, Laufey/L-7656-2016
OI Amundadottir, Laufey/0000-0003-1859-8971
FU Intramural Research Program of the National Cancer Institute; National
Institute of Allergy and Infectious Diseases, NIH
FX This research was supported by the Intramural Research Program of the
National Cancer Institute and in part by the National Institute of
Allergy and Infectious Diseases, NIH (to A. Oler).
NR 49
TC 3
Z9 4
U1 0
U2 3
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
EI 1940-6215
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD DEC
PY 2014
VL 7
IS 12
BP 1282
EP 1292
DI 10.1158/1940-6207.CAPR-14-0132
PG 11
WC Oncology
SC Oncology
GA AU6WP
UT WOS:000345742400012
PM 25315430
ER
PT J
AU Brenerman, BM
Illuzzi, JL
Wilson, DM
AF Brenerman, Boris M.
Illuzzi, Jennifer L.
Wilson, David M., III
TI Base excision repair capacity in informing healthspan
SO CARCINOGENESIS
LA English
DT Review
ID DNA-POLYMERASE-BETA; PERFORMANCE LIQUID-CHROMATOGRAPHY; SINGLE-STRAND
BREAKS; ABASIC SITES; APURINIC/APYRIMIDINIC-ENDONUCLEASE; COLON
CARCINOGENESIS; HETEROZYGOUS MICE; OXIDATIVE STRESS; MOUSE MODELS;
LUNG-CANCER
AB Base excision repair (BER) is a frontline defense mechanism for dealing with many common forms of endogenous DNA damage, several of which can drive mutagenic or cell death outcomes. The pathway engages proteins such as glycosylases, abasic endonucleases, polymerases and ligases to remove substrate modifications from DNA and restore the genome back to its original state. Inherited mutations in genes related to BER can give rise to disorders involving cancer, immunodeficiency and neurodegeneration. Studies employing genetically defined heterozygous (haploinsufficient) mouse models indicate that partial reduction in BER capacity can increase vulnerability to both spontaneous and exposure-dependent pathologies. In humans, measurement of BER variation has been imperfect to this point, yet tools to assess BER in epidemiological surveys are steadily evolving. We provide herein an overview of the BER pathway and discuss the current efforts toward defining the relationship of BER defects with disease susceptibility.
C1 [Brenerman, Boris M.; Illuzzi, Jennifer L.; Wilson, David M., III] NIA, Lab Mol Gerontol, Intramural Res Program, Natl Inst Hlth, Baltimore, MD 21224 USA.
RP Wilson, DM (reprint author), NIA, Lab Mol Gerontol, Intramural Res Program, Natl Inst Hlth, Baltimore, MD 21224 USA.
EM wilsonda@mail.nih.gov
FU National Institutes of Health, National Institute on Aging [Z01
AG000750]
FX Intramural Research Program at the National Institutes of Health,
National Institute on Aging (Z01 AG000750).
NR 111
TC 8
Z9 8
U1 0
U2 12
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 DEC
PY 2014
VL 35
IS 12
BP 2643
EP 2652
DI 10.1093/carcin/bgu225
PG 10
WC Oncology
SC Oncology
GA AU8HC
UT WOS:000345836200002
PM 25355293
ER
PT J
AU Hoskins, JW
Jia, JP
Flandez, M
Parikh, H
Xiao, WM
Collins, I
Emmanuel, MA
Ibrahim, A
Powell, J
Zhang, L
Malats, N
Bamlet, WR
Petersen, GM
Real, FX
Amundadottir, LT
AF Hoskins, Jason W.
Jia, Jinping
Flandez, Marta
Parikh, Hemang
Xiao, Wenming
Collins, Irene
Emmanuel, Mickey A.
Ibrahim, Abdisamad
Powell, John
Zhang, Lizhi
Malats, Nuria
Bamlet, William R.
Petersen, Gloria M.
Real, Francisco X.
Amundadottir, Laufey T.
TI Transcriptome analysis of pancreatic cancer reveals a tumor suppressor
function for HNF1A
SO CARCINOGENESIS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COHORT-CONSORTIUM; GENE-EXPRESSION;
POOLED-ANALYSIS; INTRAEPITHELIAL NEOPLASIA; DUCTAL ADENOCARCINOMA;
CIGARETTE-SMOKING; NUCLEAR FACTOR; SUSCEPTIBILITY; CELLS
AB Pancreatic ductal adenocarcinoma (PDAC) is driven by the accumulation of somatic mutations, epigenetic modifications and changes in the micro-environment. New approaches to investigating disruptions of gene expression networks promise to uncover key regulators and pathways in carcinogenesis. We performed messenger RNA-sequencing in pancreatic normal (n = 10) and tumor (n = 8) derived tissue samples, as well as in pancreatic cancer cell lines (n = 9), to determine differential gene expression (DE) patterns. Sub-network enrichment analyses identified HNF1A as the regulator of the most significantly and consistently dysregulated expression sub-network in pancreatic tumor tissues and cells (median P = 7.56 x 10(-7), median rank = 1, range = 1-25). To explore the effects of HNF1A expression in pancreatic tumor-derived cells, we generated stable HNF1A-inducible clones in two pancreatic cancer cell lines (PANC-1 and MIA PaCa-2) and observed growth inhibition (5.3-fold, P = 4.5 x 10(-5) for MIA PaCa-2 clones; 7.2-fold, P = 2.2 x 10(-5) for PANC-1 clones), and a G(0)/G(1) cell cycle arrest and apoptosis upon induction. These effects correlated with HNF1A-induced down-regulation of 51 of 84 cell cycle genes (e. g. E2F1, CDK2, CDK4, MCM2/3/4/5, SKP2 and CCND1), decreased expression of anti-apoptotic genes (e. g. BIRC2/5/6 and AKT) and increased expression of pro-apoptotic genes (e. g. CASP4/9/10 and APAF1). In light of the established role of HNF1A in the regulation of pancreatic development and homeostasis, our data suggest that it also functions as an important tumor suppressor in the pancreas.
C1 [Hoskins, Jason W.; Jia, Jinping; Parikh, Hemang; Collins, Irene; Emmanuel, Mickey A.; Ibrahim, Abdisamad; Amundadottir, Laufey T.] NIH, Lab Translat Gen, Div Canc Epidemiol & Genet, Natl Canc Inst, Bethesda, MD 20892 USA.
[Flandez, Marta; Malats, Nuria; Real, Francisco X.] CNIO Spanish Natl Canc Res Ctr, Epithelial Carcinogenesis Grp, E-28029 Madrid, Spain.
[Xiao, Wenming] NIH, Lymphoid Malignancies Branch, Ctr Canc Res, Natl Canc Inst, Bethesda, MD 20892 USA.
[Powell, John] NIH, Bioinformat & Mol Anal Sect, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA.
[Zhang, Lizhi] Dept Lab Med & Pathol, Rochester, MN 55905 USA.
[Bamlet, William R.; Petersen, Gloria M.] Dept Hlth Sci Res, Div Epidemiol, Mayo Clin, Rochester, MN 55905 USA.
[Real, Francisco X.] Univ Pompeu Fabra, Dept Ciencies Expt Salut, Barcelona 08003, Spain.
RP Amundadottir, LT (reprint author), NIH, Lab Translat Gen, Div Canc Epidemiol & Genet, Natl Canc Inst, Bldg 10, Bethesda, MD 20892 USA.
EM amundadottirl@mail.nih.gov
RI Malats, Nuria/H-7041-2015; Real Arribas, Francisco/H-5275-2015;
Amundadottir, Laufey/L-7656-2016;
OI Malats, Nuria/0000-0003-2538-3784; Real Arribas,
Francisco/0000-0001-9501-498X; Amundadottir, Laufey/0000-0003-1859-8971;
Hoskins, Jason/0000-0001-6944-1996
FU Intramural Research Program of the Division of Cancer Epidemiology and
Genetics; National Cancer Institute; National Institutes of Health
[HHSN261200800001E]
FX Intramural Research Program of the Division of Cancer Epidemiology and
Genetics; National Cancer Institute; National Institutes of Health
(HHSN261200800001E).
NR 50
TC 9
Z9 9
U1 1
U2 8
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 DEC
PY 2014
VL 35
IS 12
BP 2670
EP 2678
DI 10.1093/carcin/bgu193
PG 9
WC Oncology
SC Oncology
GA AU8HC
UT WOS:000345836200005
PM 25233928
ER
PT J
AU Li, WQ
Pfeiffer, RM
Hyland, PL
Shi, JX
Gu, FY
Wang, ZM
Bhattacharjee, S
Luo, J
Xiong, XQ
Yeager, M
Deng, X
Hu, N
Taylor, PR
Albanes, D
Caporaso, NE
Gapstur, SM
Amundadottir, L
Chanock, SJ
Chatterjee, N
Landi, MT
Tucker, MA
Goldstein, AM
Yang, XHR
AF Li, Wen-Qing y
Pfeiffer, Ruth M.
Hyland, Paula L.
Shi, Jianxin
Gu, Fangyi
Wang, Zhaoming
Bhattacharjee, Samsiddhi
Luo, Jun
Xiong, Xiaoqin
Yeager, Meredith
Deng, Xiang
Hu, Nan
Taylor, Philip R.
Albanes, Demetrius
Caporaso, Neil E.
Gapstur, Susan M.
Amundadottir, Laufey
Chanock, Stephen J.
Chatterjee, Nilanjan
Landi, Maria Teresa
Tucker, Margaret A.
Goldstein, Alisa M.
Yang, Xiaohong R.
TI Genetic polymorphisms in the 9p21 region associated with risk of
multiple cancers
SO CARCINOGENESIS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; SQUAMOUS-CELL CARCINOMA; SUSCEPTIBILITY LOCI;
PANCREATIC-CANCER; BREAST-CANCER; GASTRIC ADENOCARCINOMA; CHINESE
POPULATION; CDKN2A MUTATIONS; IDENTIFIES 5; VARIANTS
AB The chromosome 9p21 region has been implicated in the pathogenesis of multiple cancers. We analyzed 9p21 single nucleotide polymorphisms (SNPs) from eight genome-wide association studies (GWAS) with data deposited in dbGaP, including studies of esophageal squamous cell carcinoma (ESCC), gastric cancer (GC), pancreatic cancer, renal cell carcinoma (RCC), lung cancer (LC), breast cancer (BrC), bladder cancer (BC) and prostate cancer (PrC). The number of subjects ranged from 2252 (PrC) to 7619 (LC). SNP-level analyses for each cancer were conducted by logistic regression or random-effects meta-analysis. A subset-based statistical approach (ASSET) was performed to combine SNP-level P values across multiple cancers. We calculated gene-level P values using the adaptive rank truncated product method. We identified that rs1063192 and rs2157719 in the CDKN2A/2B region were significantly associated with ESCC and rs2764736 (3' of TUSC1) was associated with BC (P = 2.59 x 10(-6)). ASSET analyses identified four SNPs significantly associated with multiple cancers: rs3731239 (CDKN2A intronic) with ESCC, GC and BC (P = 3.96 x 10(-4)); rs10811474 (3' of IFNW1) with RCC and BrC (P = 0.001); rs12683422 (LINGO2 intronic) with RCC and BC (P = 5.93 x 10(-4)) and rs10511729 (3' of ELAVL2) with LC and BrC (P = 8.63 x 10(-4)). At gene level, CDKN2B, CDKN2A and CDKN2B-AS1 were significantly associated with ESCC (P = 4.70 x 10(-5)). Rs10511729 and rs10811474 were associated with cis-expression of 9p21 genes in corresponding cancer tissues in the expression quantitative trait loci analysis. In conclusion, we identified several genetic variants in the 9p21 region associated with the risk of multiple cancers, suggesting that this region may contribute to a shared susceptibility across different cancer types.
C1 [Li, Wen-Qing y; Pfeiffer, Ruth M.; Hyland, Paula L.; Shi, Jianxin; Gu, Fangyi; Wang, Zhaoming; Yeager, Meredith; Deng, Xiang; Hu, Nan; Taylor, Philip R.; Albanes, Demetrius; Caporaso, Neil E.; Amundadottir, Laufey; Chanock, Stephen J.; Chatterjee, Nilanjan; Landi, Maria Teresa; Tucker, Margaret A.; Goldstein, Alisa M.; Yang, Xiaohong R.] NIH, Div Canc Epidemiol & Genet, NCI, Bethesda, MD 20892 USA.
[Li, Wen-Qing y] Brown Univ, Dept Dermatol, Warren Alpert Med Sch, Providence, RI 02912 USA.
[Wang, Zhaoming; Yeager, Meredith; Deng, Xiang] SAIC Frederick Inc, NCI Frederick, Can Genom Res Lab, Frederick, MD USA.
[Bhattacharjee, Samsiddhi] Nat Inst Biomed Gen, Kalyani, W Bengal, India.
[Xiong, Xiaoqin] Informat Management Serv Inc, Calverton, MD USA.
[Gapstur, Susan M.] Amer Canc Soc, Epidemiol Res Program, Atlanta, GA 30329 USA.
RP Li, WQ (reprint author), NIH, Div Canc Epidemiol & Genet, NCI, Bldg 10, Bethesda, MD 20892 USA.
EM wen-qing_li@brown.edu; royang@mail.nih.gov
RI Tucker, Margaret/B-4297-2015; Albanes, Demetrius/B-9749-2015;
Amundadottir, Laufey/L-7656-2016
OI Amundadottir, Laufey/0000-0003-1859-8971
FU Intramural Research Program of the National Institute of Health (NIH);
National Cancer Institute; Division of Cancer Epidemiology and Genetics
FX Intramural Research Program of the National Institute of Health (NIH);
National Cancer Institute; Division of Cancer Epidemiology and Genetics.
NR 44
TC 19
Z9 19
U1 1
U2 15
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 DEC
PY 2014
VL 35
IS 12
BP 2698
EP 2705
DI 10.1093/carcin/bgu203
PG 8
WC Oncology
SC Oncology
GA AU8HC
UT WOS:000345836200008
PM 25239644
ER
PT J
AU Saud, SM
Li, WD
Morris, NL
Matter, MS
Colburn, NH
Kim, YS
Young, MR
AF Saud, Shakir M.
Li, Weidong
Morris, Nicole L.
Matter, Matthias S.
Colburn, Nancy H.
Kim, Young S.
Young, Matthew R.
TI Resveratrol prevents tumorigenesis in mouse model of Kras activated
sporadic colorectal cancer by suppressing oncogenic Kras expression
SO CARCINOGENESIS
LA English
DT Article
ID FAMILIAL ADENOMATOUS POLYPOSIS; K-RAS; TUMOR-SUPPRESSOR; COLON; CELLS;
GENE; PROGRESSION; MUTATIONS; CARCINOMA; APC
AB Sporadic and non-hereditary mutations account for the majority of colorectal cancers (CRC). After the loss of adenomatous polyposis coli (APC) function and activation of the beta-catenin/LEF signaling pathway, activating mutations in Kras are major drivers of sporadic CRC. Preventing the outgrowth of cells that develop sporadic mutations will decrease CRC. Resveratrol, a naturally occurring polyphenolic compound has anti-inflammatory, anti-oxidant and anti-cancer activities. We used a genetically engineered mouse model for sporadic CRC where the APC locus is knocked out and Kras is activated specifically in the distal colon to determine the effects of resveratrol on preventing and treating CRC. Feeding mice a diet supplemented with 150 or 300 ppm resveratrol (105 and 210 mg daily human equivalent dose, respectively) before tumors were visible by colonoscopy resulted in a 60% inhibition of tumor production. In the 40% of mice that did develop tumors Kras expression was lost in the tumors. In a therapeutic assay where tumors were allowed to develop prior to treatment, feeding tumor bearing mice with resveratrol resulted in a complete remission in 33% of the mice and a 97% decrease in tumor size in the remaining mice. Analysis of miRNA expression in non-tumoral and tumoral colonic tissue of resveratrol treated mice showed an increased expression of miR-96, a miRNA previously shown to regulate Kras translation. These data indicate that resveratrol can prevent the formation and growth of colorectal tumors by downregulating Kras expression.
C1 [Saud, Shakir M.; Kim, Young S.] NCI, Nutr Sci Res Grp, Canc Prevent Div, Rockville, MD USA.
[Saud, Shakir M.; Li, Weidong; Young, Matthew R.] NCI, Lab Canc Prevent, Ctr Canc Res, Frederick, MD 21701 USA.
[Li, Weidong] China Acad Chinese Med Sci, Dept Oncol, Guanganmen Hosp, Beijing, Peoples R China.
[Morris, Nicole L.] Leidos Biomed Res Inc, Lab Anim Sci Program, Frederick, MD USA.
[Matter, Matthias S.] NCI, Expt Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Young, MR (reprint author), NCI, 1050 Boyles St, Ft Detrick, MD 21702 USA.
EM youngma@mail.nih.gov
FU Office of Dietary Supplements, Office of the Director; Division of
Cancer Prevention; Intramural Research Program, National Cancer
Institute; Department of Health and Human Services (DHHS), National
Institutes of Health, Bethesda, MD [ZIA BC 010025]
FX The Office of Dietary Supplements, Office of the Director; the Division
of Cancer Prevention and the Intramural Research Program, National
Cancer Institute; Department of Health and Human Services (DHHS),
National Institutes of Health, Bethesda, MD (ZIA BC 010025).
NR 41
TC 14
Z9 16
U1 0
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 DEC
PY 2014
VL 35
IS 12
BP 2778
EP 2786
DI 10.1093/carcin/bgu209
PG 9
WC Oncology
SC Oncology
GA AU8HC
UT WOS:000345836200018
PM 25280562
ER
PT J
AU Benabentos, R
Ray, P
Kumar, D
AF Benabentos, Rocio
Ray, Payal
Kumar, Deepak
TI Addressing Health Disparities in the Undergraduate Curriculum: An
Approach to Develop a Knowledgeable Biomedical Workforce
SO CBE-LIFE SCIENCES EDUCATION
LA English
DT Article
ID MEDICAL-EDUCATION; CARE DISPARITIES; IMPROVE CARE; PHYSICIANS
AB Disparities in health and healthcare are a major concern in the United States and worldwide. Approaches to alleviate these disparities must be multifaceted and should include initiatives that touch upon the diverse areas that influence the healthcare system. Developing a strong biomedical workforce with an awareness of the issues concerning health disparities is crucial for addressing this issue. Establishing undergraduate health disparities courses that are accessible to undergraduate students in the life sciences is necessary to increase students' understanding and awareness of these issues and motivate them to address these disparities during their careers. The majority of universities do not include courses related to health disparities in their curricula, and only a few universities manage them from their life sciences departments. The figures are especially low for minority-serving institutions, which serve students from communities disproportionally affected by health disparities. Universities should consider several possible approaches to infuse their undergraduate curricula with health disparities courses or activities. Eliminating health disparities will require efforts from diverse stakeholders. Undergraduate institutions can play an important role in developing an aware biomedical workforce and helping to close the gap in health outcomes.
C1 [Benabentos, Rocio] Natl Sci Fdn, Div Human Resource Dev, Directorate Educ & Human Resources, Arlington, VA 22230 USA.
[Ray, Payal] NICHHD, NIH, Bethesda, MD 20892 USA.
[Benabentos, Rocio; Ray, Payal; Kumar, Deepak] Univ Dist Columbia, Coll Arts & Sci, Dept Biol Chem & Phys, Washington, DC 20008 USA.
RP Kumar, D (reprint author), Univ Dist Columbia, Coll Arts & Sci, Dept Biol Chem & Phys, Washington, DC 20008 USA.
EM dkumar@udc.edu
FU CDMPRP Prostate Cancer Research Program [PC073564, PC131862, PC111314];
National Cancer Institute Center to Reduce Cancer Health Disparities
[CA162264]
FX The authors thank Shifali Arora, Oni Celestin, Sharmi Das, Patricia
Forcinito, Natasha Lugo-Escobar, Steve Schultz, and Susan Singer for
insightful comments and suggestions. R.B. thanks Beth Mitchneck and
Sylvia James for support of this work. Any opinions, findings, and
conclusions or recommendations expressed in this material are those of
the authors alone and do not necessarily reflect the views of the
National Science Foundation, NIH, AAAS, or any other organizations with
which the authors are affiliated. D.K. gratefully acknowledges the
support from the CDMPRP Prostate Cancer Research Program (PC073564,
PC131862, PC111314) and the National Cancer Institute Center to Reduce
Cancer Health Disparities (CA162264).
NR 29
TC 0
Z9 0
U1 2
U2 4
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1931-7913
J9 CBE-LIFE SCI EDUC
JI CBE-Life Sci. Educ.
PD DEC 1
PY 2014
VL 13
IS 4
BP 636
EP 640
DI 10.1187/cbe.14-06-0101
PG 5
WC Education, Scientific Disciplines
SC Education & Educational Research
GA AU7FR
UT WOS:000345766800010
PM 25452486
ER
PT J
AU Akinkugbe, A
Iafolla, T
Chattopadhyay, A
Garcia, I
Adams, A
Kingman, A
AF Akinkugbe, Aderonke
Iafolla, Timothy
Chattopadhyay, Amit
Garcia, Isabel
Adams, Amy
Kingman, Albert
TI The role of partial recording protocols in reporting prevalence and
severity of dental fluorosis
SO COMMUNITY DENTISTRY AND ORAL EPIDEMIOLOGY
LA English
DT Article
DE bias; correction factor; dental fluorosis; fluorosis; negative
predictive value; partial recording protocols; sensitivity; subset of
teeth
ID PERIODONTAL-DISEASE; DRINKING-WATER; FLUORIDE; INDEX; COMMUNITIES;
PATTERNS
AB ObjectivesTo evaluate the role of partial recording protocols (PRPs) in reporting prevalence and severity of dental fluorosis and assess whether prevalence/severity estimates derived from PRPs differ by race/ethnicity.
MethodsData from the National Health and Nutrition Examination Survey (NHANES) for the years 1999-2004 were analyzed with Stata((R)) v.11. Prevalence of dental fluorosis obtained from a full-mouth examination (28 teeth gold standard) was compared with estimates derived from four subsets of teeth (maxillary canine-to-canine; maxillary first-premolar-to-first-premolar; all-premolars; all-molars). Sensitivity, negative predictive value (NPV), absolute bias, and correction factors were calculated against gold standard estimate. Analysis was stratified according to race/ethnicity to assess differences in estimates derived from PRPs.
ResultsAll subsets underestimated prevalence albeit to varying degrees. Two subsets (all-premolars and all-molars) had prevalence and severity estimates closest to gold standard estimates. The all-molars subset (eight teeth) recorded the highest sensitivity (84.5%) and the lowest absolute bias (3.5%) of all subsets relative to gold standard. Subsets derived from esthetically relevant teeth produced the lowest fluorosis prevalence. For instance, the maxillary canine-to-canine subset underestimated prevalence by 9.5%; incorporating the maxillary first premolars in the span improved prevalence estimate by 31%. Among non-Hispanic Whites, the all-premolars subset produced estimates closest to gold standard while the all-molars subset produced estimates closest to the gold standard among non-Hispanic Blacks and Hispanics.
ConclusionWhile the majority of dental fluorosis in the United States is very mild, concerns regarding its growing prevalence underscore the need for careful monitoring. The use of PRPs offers an alternative method of assessment, with validity of reported prevalence and severity dependent on choice of subset.
C1 [Akinkugbe, Aderonke] Univ N Carolina, Dept Epidemiol, Chapel Hill, NC USA.
[Iafolla, Timothy; Chattopadhyay, Amit; Adams, Amy; Kingman, Albert] NIDCR, Off Sci Policy & Anal, NIH, Bethesda, MD 20892 USA.
[Garcia, Isabel] NIDCR, NIH, Bethesda, MD 20892 USA.
RP Chattopadhyay, A (reprint author), NIDCR, NIH, 31 Ctr Dr,5B55 MSC 2190, Bethesda, MD 20892 USA.
EM Amit.Chattopadhyay@nih.gov
FU NIDCR's Dental Public Health Residency Program; NIH/NIDCR Training Grant
[R90 DE022527]
FX The authors gratefully acknowledge Drs. Eugenio Beltran-Aguilar and
Bruce Dye for providing very useful historical perspectives about the
NHANES and the dental examination portion of the NHANES. This work was
supported by NIDCR's Dental Public Health Residency Program. Dr.
Akinkugbe's work was partly supported by the NIH/NIDCR Training Grant
R90 DE022527.
NR 27
TC 0
Z9 0
U1 2
U2 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0301-5661
EI 1600-0528
J9 COMMUNITY DENT ORAL
JI Community Dentist. Oral Epidemiol.
PD DEC
PY 2014
VL 42
IS 6
BP 563
EP 571
DI 10.1111/cdoe.12115
PG 9
WC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
SC Dentistry, Oral Surgery & Medicine; Public, Environmental & Occupational
Health
GA AU6EE
UT WOS:000345695000009
PM 24995860
ER
PT J
AU Scott, BH
Mishkin, M
Yin, PB
AF Scott, Brian H.
Mishkin, Mortimer
Yin, Pingbo
TI Neural Correlates of Auditory Short-Term Memory in Rostral Superior
Temporal Cortex
SO CURRENT BIOLOGY
LA English
DT Article
ID SINGLE-UNIT-ACTIVITY; PREFRONTAL CORTEX; RECOGNITION MEMORY;
WORKING-MEMORY; BEHAVIORAL DEPENDENCY; RHESUS-MONKEYS; VISUAL MEMORY;
TASK; INFORMATION; PITCH
AB Background: Auditory short-term memory (STM) in the monkey is less robust than visual STM and may depend on a retained sensory trace, which is likely to reside in the higher-order cortical areas of the auditory ventral stream.
Results: We recorded from the rostral superior temporal cortex as monkeys performed serial auditory delayed match-to-sample (DMS). A subset of neurons exhibited modulations of their firing rate during the delay between sounds, during the sensory response, or during both. This distributed subpopulation carried a predominantly sensory signal modulated by the mnemonic context of the stimulus. Excitatory and suppressive effects on match responses were dissociable in their timing and in their resistance to sounds intervening between the sample and match.
Conclusions: Like the monkeys' behavioral performance, these neuronal effects differ from those reported in the same species during visual DMS, suggesting different neural mechanisms for retaining dynamic sounds and static images in STM.
C1 [Scott, Brian H.; Mishkin, Mortimer; Yin, Pingbo] NIMH, Neuropsychol Lab, NIH, Bethesda, MD 20892 USA.
[Yin, Pingbo] Univ Maryland, Syst Res Inst, Neural Syst Lab, College Pk, MD 20742 USA.
RP Scott, BH (reprint author), NIMH, Neuropsychol Lab, NIH, Bldg 9, Bethesda, MD 20892 USA.
EM brianscott@mail.nih.gov
FU Intramural Research Program of the NIMH/NIH/DHHS
FX We thank H. Tak, M. Munoz-Lopez, K. Moorhead, P. Sergo, A. Kloth, and H.
Vinal for assistance with animal training and data collection and R.C.
Saunders and M. Malloy for providing technical expertise. This research
was supported by the Intramural Research Program of the NIMH/NIH/DHHS.
NR 48
TC 6
Z9 6
U1 0
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD DEC 1
PY 2014
VL 24
IS 23
BP 2767
EP 2775
DI 10.1016/j.cub.2014.10.004
PG 9
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AU7WH
UT WOS:000345808700017
PM 25456448
ER
PT J
AU Feldblum, JT
Wroblewski, EE
Rudicell, RS
Hahn, BH
Paiva, T
Cetinkaya-Rundel, M
Pusey, AE
Gilby, IC
AF Feldblum, Joseph T.
Wroblewski, Emily E.
Rudicell, Rebecca S.
Hahn, Beatrice H.
Paiva, Thais
Cetinkaya-Rundel, Mine
Pusey, Anne E.
Gilby, Ian C.
TI Sexually Coercive Male Chimpanzees Sire More Offspring
SO CURRENT BIOLOGY
LA English
DT Article
ID PAN-TROGLODYTES-SCHWEINFURTHII; KIBALE NATIONAL-PARK; FEMALE CHOICE;
WILD CHIMPANZEES; GENETIC-MARKERS; COTE-DIVOIRE; AGGRESSION; DOMINANCE;
VERUS; PRIMATES
AB In sexually reproducing animals, male and female reproductive strategies often conflict [1]. In some species, males use aggression to overcome female choice [2, 3], but debate persists over the extent to which this strategy is successful. Previous studies of male aggression toward females among wild chimpanzees have yielded contradictory results about the relationship between aggression and mating behavior [4-11]. Critically, however, copulation frequency in primates is not always predictive of reproductive success [12]. We analyzed a 17-year sample of behavioral and genetic data from the Kasekela chimpanzee (Pan troglodytes schweinfurthii)community in Gombe National Park, Tanzania, to test the hypothesis that male aggression toward females increases male reproductive success. We examined the effect of male aggression toward females during ovarian cycling, including periods when the females were sexually receptive (swollen) and periods when they were not. We found that, after controlling for confounding factors, male aggression during a female's swollen periods was positively correlated with copulation frequency. However, aggression toward swollen females was not predictive of paternity. Instead, aggression by high-ranking males toward females during their nonswollen periods was positively associated with likelihood of paternity. This indicates that long-term patterns of intimidation allow high-ranking males to increase their reproductive success, supporting the sexual coercion hypothesis. To our knowledge, this is the first study to present genetic evidence of sexual coercion as an adaptive strategy in a social mammal.
C1 [Feldblum, Joseph T.; Pusey, Anne E.] Duke Univ, Dept Evolutionary Anthropol, Durham, NC 27708 USA.
[Wroblewski, Emily E.] Stanford Univ, Sch Med, Dept Biol Struct, Stanford, CA 94305 USA.
[Rudicell, Rebecca S.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Rudicell, Rebecca S.] Sanofi, Cambridge, MA 02139 USA.
[Hahn, Beatrice H.] Univ Penn, Perelman Sch Med, Dept Med, Philadelphia, PA 19104 USA.
[Hahn, Beatrice H.] Univ Penn, Perelman Sch Med, Dept Microbiol, Philadelphia, PA 19104 USA.
[Paiva, Thais; Cetinkaya-Rundel, Mine] Duke Univ, Dept Stat Sci, Durham, NC 27708 USA.
[Gilby, Ian C.] Arizona State Univ, Sch Human Evolut & Social Change, Tempe, AZ 85287 USA.
RP Feldblum, JT (reprint author), Duke Univ, Dept Evolutionary Anthropol, Durham, NC 27708 USA.
EM jtf9@duke.edu
FU National Science Foundation (NSF) [LTREB-1052693]; National Institutes
of Health (NIH) [R01 AI 058715]; NSF [LTREB-1052693, DBS-9021946,
SBR-9319909, BCS-0452315, BCS-0648481]; NIH [R01 AI 058715]; University
of Minnesota; Harris Steel Group; Windibrow Foundation; JGI; Carnegie
Corporation; Duke University
FX Data collection was supported primarily by the Jane Goodall Institute
(JGI), with additional support from the National Science Foundation
(NSF) (LTREB-1052693) and the National Institutes of Health (NIH) (R01
AI 058715). Digitization and analysis of behavioral and genetic data
were supported by grants from the NSF (DBS-9021946, SBR-9319909,
BCS-0452315, BCS-0648481, and LTREB-1052693), the NIH (R01 AI 058715),
the University of Minnesota, the Harris Steel Group, the Windibrow
Foundation, JGI, the Carnegie Corporation, and Duke University. We thank
Jane Goodall for permission to work with the long-term data and the
Tanzania National Parks, Tanzania Wildlife Research Institute, and
Tanzania Commission for Science and Technology for permission to work in
Gombe National Park. All data collection was approved by these Tanzanian
bodies and the Duke University Institutional Animal Care and Use
Committee. We are very grateful to the wonderful Gombe Stream Research
Center staff for their heroic data collection; Esther Collins for
translation; Joann Schumacher-Stankey for data extraction; and Kara
Schroepfer-Walker, Emily Boehm, Steffen Foerster, Susan Alberts, Mathias
Franz, Amanda Lea, Sammy Feldblum, and Amelia O'Rourke-Owens for
thoughtful comments and invaluable technical advice.
NR 40
TC 16
Z9 16
U1 15
U2 65
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD DEC 1
PY 2014
VL 24
IS 23
BP 2855
EP 2860
DI 10.1016/j.cub.2014.10.039
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AU7WH
UT WOS:000345808700031
PM 25454788
ER
PT J
AU Walters, AD
May, CK
Dauster, ES
Cinquin, BP
Smith, EA
Robellet, X
D'Amours, D
Larabell, CA
Cohen-Fix, O
AF Walters, Alison D.
May, Christopher K.
Dauster, Emma S.
Cinquin, Bertrand P.
Smith, Elizabeth A.
Robellet, Xavier
D'Amours, Damien
Larabell, Carolyn A.
Cohen-Fix, Orna
TI The Yeast Polo Kinase Cdc5 Regulates the Shape of the Mitotic Nucleus
SO CURRENT BIOLOGY
LA English
DT Article
ID SISTER-CHROMATID SEPARATION; CHROMOSOME CONDENSATION; BUDDING-YEAST;
SACCHAROMYCES-CEREVISIAE; GENOME STABILITY; IN-VIVO; ENVELOPE; EXIT;
PHOSPHORYLATION; NETWORK
AB Abnormal nuclear size and shape are hallmarks of aging and cancer [1, 2]. However, the mechanisms regulating nuclear morphology and nuclear envelope (NE) expansion are poorly understood. In metazoans, the NE disassembles prior to chromosome segregation and reassembles at the end of mitosis [3]. In budding yeast, the NE remains intact. The nucleus elongates as chromosomes segregate and then divides at the end of mitosis to form two daughter nuclei without NE disassembly. The budding yeast nucleus also undergoes remodeling during a mitotic arrest; the NE continues to expand despite the pause in chromosome segregation, forming a nuclear extension, or "flare," that encompasses the nucleolus [4]. The distinct nucleolar localization of the mitotic flare indicates that the NE is compartmentalized and that there is a mechanism by which NE expansion is confined to the region adjacent to the nucleolus. Here we show that mitotic flare formation is dependent on the yeast polo kinase Cdc5. This function of Cdc5 is independent of its known mitotic roles, including rDNA condensation. High-resolution imaging revealed that following Cdc5 inactivation, nuclei expand isometrically rather than forming a flare, indicating that Cdc5 is needed for NE compartmentalization. Even in an uninterrupted cell cycle, a small NE expansion occurs adjacent to the nucleolus prior to anaphase in a Cdc5-dependent manner. Our data provide the first evidence that polo kinase, a key regulator of mitosis [5], plays a role in regulating nuclear morphology and NE expansion.
C1 [Walters, Alison D.; May, Christopher K.; Dauster, Emma S.; Cohen-Fix, Orna] NIDDK, Mol & Cellular Biol Lab, NIH, Bethesda, MD 20892 USA.
[Cinquin, Bertrand P.; Smith, Elizabeth A.; Larabell, Carolyn A.] Univ Calif San Francisco, Dept Anat, San Francisco, CA 94158 USA.
[Cinquin, Bertrand P.; Smith, Elizabeth A.; Larabell, Carolyn A.] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Phys Biosci Div, Berkeley, CA 94720 USA.
[Robellet, Xavier; D'Amours, Damien] Univ Montreal, Inst Res Immunol & Canc, Montreal, PQ H3C 3J7, Canada.
[Robellet, Xavier; D'Amours, Damien] Univ Montreal, Dept Pathol & Biol Cellulaire, Montreal, PQ H3C 3J7, Canada.
RP Cohen-Fix, O (reprint author), NIDDK, Mol & Cellular Biol Lab, NIH, Bethesda, MD 20892 USA.
EM ornac@helix.nih.gov
FU National Institute of Diabetes and Digestive and Kidney Diseases;
National Institute of General Medical Science of the NIH [P41GM103445];
U.S. Department of Energy, Office of Biological and Environmental
Research [DE-AC02-05CH11231]; Canadian Institutes of Health Research
[MOP 82912, MOP 136788]; Canada Research Chair in Cell Cycle Regulation
and Genomic Integrity
FX We thank D. Reynolds, A. Hoyt, T. Eng, D. Koshland, A. Amon, S.
Lacefield, and J. Diffley for yeast strains and plasmids and M. Lichten,
W. Prinz, F. Chang, and members of the O.C.-F. laboratory for
discussions on the manuscript. A.D.W., C.K.M., E.S.D., and O.C.-F. are
funded by an intramural National Institute of Diabetes and Digestive and
Kidney Diseases grant. C.A.L., B.P.C., and E.A.S. are funded by the
National Institute of General Medical Science of the NIH (P41GM103445)
and the U.S. Department of Energy, Office of Biological and
Environmental Research (DE-AC02-05CH11231). Research in D.D.'s
laboratory is supported by the Canadian Institutes of Health Research
(MOP 82912 and MOP 136788). D.D. is a recipient of a Tier II Canada
Research Chair in Cell Cycle Regulation and Genomic Integrity.
NR 31
TC 7
Z9 7
U1 2
U2 9
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
EI 1879-0445
J9 CURR BIOL
JI Curr. Biol.
PD DEC 1
PY 2014
VL 24
IS 23
BP 2861
EP 2867
DI 10.1016/j.cub.2014.10.029
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA AU7WH
UT WOS:000345808700032
PM 25454593
ER
PT J
AU Heffner, KM
Hizal, DB
Kumar, A
Shiloach, J
Zhu, J
Bowen, MA
Betenbaugh, MJ
AF Heffner, Kelley M.
Hizal, Deniz Baycin
Kumar, Amit
Shiloach, Joseph
Zhu, Jie
Bowen, Michael A.
Betenbaugh, Michael J.
TI Exploiting the proteomics revolution in biotechnology: from disease and
antibody targets to optimizing bioprocess development
SO CURRENT OPINION IN BIOTECHNOLOGY
LA English
DT Review
ID HAMSTER OVARY CELLS; ESCHERICHIA-COLI; MONOCLONAL-ANTIBODIES; SHOTGUN
PROTEOMICS; PROTEIN; IDENTIFICATION; CULTURE; GENOME; SERUM; CLEAVAGE
AB Recent advancements in proteomics have enabled the generation of high-quality data sets useful for applications ranging from target and monoclonal antibody (mAB) discovery to bioprocess optimization. Comparative proteomics approaches have recently been used to identify novel disease targets in oncology and other disease conditions. Proteomics has also been applied as a new avenue for mAb discovery. Finally, CHO and Escherichia coli cells represent the dominant production hosts for biopharmaceutical development, yet the physiology of these cells types has yet to be fully established. Proteomics approaches can provide new insights into these cell types, aiding in recombinant protein production, cell growth regulation, and medium formulation. Optimization of sample preparations and protein database developments are enhancing the quantity and accuracy of proteomic results. In these ways, innovations in proteomics are enriching biotechnology and bioprocessing research across a wide spectrum of applications.
C1 [Heffner, Kelley M.; Kumar, Amit; Betenbaugh, Michael J.] Johns Hopkins Univ, Baltimore, MD 21218 USA.
[Hizal, Deniz Baycin; Zhu, Jie; Bowen, Michael A.] MedImmune LLC, Antibody Discovery & Prot Engn, Gaithersburg, MD 20878 USA.
[Kumar, Amit; Shiloach, Joseph] NIDDK, NIH, Bethesda, MD 20892 USA.
RP Heffner, KM (reprint author), Johns Hopkins Univ, Baltimore, MD 21218 USA.
FU National Science Foundation [DGE-1232825]
FX This material is based upon work supported by the National Science
Foundation Graduate Research Fellowship Program under Grant No.
DGE-1232825. Any opinions, findings, and conclusions or recommendations
expressed in this material are those of the author(s) and do not
necessarily reflect the views of the National Science Foundation.
NR 44
TC 8
Z9 9
U1 2
U2 32
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0958-1669
EI 1879-0429
J9 CURR OPIN BIOTECH
JI Curr. Opin. Biotechnol.
PD DEC
PY 2014
VL 30
BP 80
EP 86
DI 10.1016/j.copbio.2014.06.006
PG 7
WC Biochemical Research Methods; Biotechnology & Applied Microbiology
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology
GA AU8BS
UT WOS:000345822300014
PM 24997444
ER
PT J
AU Adney, DR
van Doremalen, N
Brown, VR
Bushmaker, T
Scott, D
de Wit, E
Bowen, RA
Munster, VJ
AF Adney, Danielle R.
van Doremalen, Neeltje
Brown, Vienna R.
Bushmaker, Trenton
Scott, Dana
de Wit, Emmie
Bowen, Richard A.
Munster, Vincent J.
TI Replication and Shedding of MERS-CoV in Upper Respiratory Tract of
Inoculated Dromedary Camels
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID SYNDROME CORONAVIRUS; SAUDI-ARABIA; INFECTION; ANTIBODIES; LIVESTOCK;
JUNE
AB In 2012, a novel coronavirus associated with severe respiratory disease in humans emerged in the Middle East. Epidemiologic investigations identified dromedary camels as the likely source of zoonotic transmission of Middle East respiratory syndrome coronavirus (MERS-CoV). Here we provide experimental support for camels as a reservoir for MERS-CoV. We inoculated 3 adult camels with a human isolate of MERS-CoV and a transient, primarily upper respiratory tract infection developed in each of the 3 animals. Clinical signs of the MERS-CoV infection were benign, but each of the camels shed large quantities of virus from the upper respiratory tract. We detected infectious virus in nasal secretions through 7 days postinoculation, and viral RNA up to 35 days postinoculation. The pattern of shedding and propensity for the upper respiratory tract infection in dromedary camels may help explain the lack of systemic illness among naturally infected camels and the means of efficient camel-to-camel and camel-to-human transmission.
C1 [Adney, Danielle R.; Brown, Vienna R.; Bowen, Richard A.] Colorado State Univ, Ft Collins, CO 80523 USA.
[van Doremalen, Neeltje; Bushmaker, Trenton; Scott, Dana; de Wit, Emmie; Munster, Vincent J.] NIH, Hamilton, MT USA.
RP Bowen, RA (reprint author), Colorado State Univ, Dept Biomed Sci, W113 ARBL Bldg,Foothills Campus, Ft Collins, CO 80523 USA.
EM Richard.Bowen@colostate.edu
OI de Wit, Emmie/0000-0002-9763-7758; Munster, Vincent/0000-0002-2288-3196
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health; Animal Models Core at Colorado State University;
Colorado State University
FX This work was supported by the Intramural Research Program of the
National Institute of Allergy and Infectious Diseases, National
Institutes of Health, and the Animal Models Core at Colorado State
University. D.R.A. was supported through the Infectious Disease:
Translational Research Training Program at Colorado State University.
NR 29
TC 70
Z9 71
U1 2
U2 19
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD DEC
PY 2014
VL 20
IS 12
BP 1999
EP 2005
DI 10.3201/eid2012.141280
PG 7
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AU6RP
UT WOS:000345729900004
PM 25418529
ER
PT J
AU Yondon, M
Zayat, B
Nelson, MI
Heil, GL
Anderson, BD
Lin, XD
Halpin, RA
McKenzie, PP
White, SK
Wentworth, DE
Gray, GC
AF Yondon, Myagmarsukh
Zayat, Batsukh
Nelson, Martha I.
Heil, Gary L.
Anderson, Benjamin D.
Lin, Xudong
Halpin, Rebecca A.
McKenzie, Pamela P.
White, Sarah K.
Wentworth, David E.
Gray, Gregory C.
TI Equine Influenza A(H3N8) Virus Isolated from Bactrian Camel, Mongolia
SO EMERGING INFECTIOUS DISEASES
LA English
DT Article
ID A VIRUS; H1N1
AB Because little is known about the ecology of influenza viruses in camels, 460 nasal swab specimens were collected from healthy (no overt illness) Bactrian camels in Mongolia during 2012. One specimen was positive for influenza A virus (A/camel/Mongolia/335/2012[H3N8]), which is phylogenetically related to equine influenza A(H3N8) viruses and probably represents natural horse-to-camel transmission.
C1 [Yondon, Myagmarsukh; Zayat, Batsukh] Inst Vet Med, Ulaanbaatar, Mongol Peo Rep.
[Nelson, Martha I.] NIH, Bethesda, MD 20892 USA.
[Heil, Gary L.; Anderson, Benjamin D.; White, Sarah K.; Gray, Gregory C.] Univ Florida, Gainesville, FL USA.
[Lin, Xudong; Halpin, Rebecca A.; Wentworth, David E.] J Craig Venter Inst, Rockville, MD USA.
[McKenzie, Pamela P.] St Jude Childrens Res Hosp, Memphis, TN 38105 USA.
RP Gray, GC (reprint author), Univ Florida, Coll Publ Hlth & Hlth Profess, Box 100188, Gainesville, FL 32610 USA.
EM gcgray@phhp.ufl.edu
OI Wentworth, David/0000-0002-5190-980X
FU National Institute of Allergy and Infectious Diseases, National
Institutes of Health, Department of Health and Human Services, USA
[HH-SN266200700005C, HHSN272200900007C]; National Institute of Allergy
and Infectious Diseases [R01 AI068803-ARRA]; US Department of Defense
Armed Forces Health Surveillance Center, Global Emerging Infections
Surveillance and Response Program; Office of Global Affairs at the
Department of Health and Human Services
FX This research was supported by multiple grants: contracts
HH-SN266200700005C (St. Jude Children's Research Hospital) and
HHSN272200900007C (J. Craig Venter Institute) from the National
Institute of Allergy and Infectious Diseases, National Institutes of
Health, Department of Health and Human Services, USA; R01 AI068803-ARRA
supplement (G.C.G.) from the National Institute of Allergy and
Infectious Diseases; and multiple grants (G.C.G.) from the US Department
of Defense Armed Forces Health Surveillance Center, Global Emerging
Infections Surveillance and Response Program. This research was
conducted within the context of the Multinational Influenza Seasonal
Mortality Study, an ongoing international collaborative effort to
understand influenza epidemiology and evolution, led by the Fogarty
International Center, National Institutes of Health, with funding from
the Office of Global Affairs at the Department of Health and Human
Services (M.I.N.).
NR 15
TC 6
Z9 7
U1 0
U2 6
PU CENTERS DISEASE CONTROL
PI ATLANTA
PA 1600 CLIFTON RD, ATLANTA, GA 30333 USA
SN 1080-6040
EI 1080-6059
J9 EMERG INFECT DIS
JI Emerg. Infect. Dis
PD DEC
PY 2014
VL 20
IS 12
BP 2144
EP 2147
DI 10.3201/eid2012.140435
PG 4
WC Immunology; Infectious Diseases
SC Immunology; Infectious Diseases
GA AU6RP
UT WOS:000345729900033
PM 25418532
ER
PT J
AU Wall, EH
Hewitt, SC
Case, LK
Lin, CY
Korach, KS
Teuscher, C
AF Wall, Emma H.
Hewitt, Sylvia C.
Case, Laure K.
Lin, Chin-Yo
Korach, Kenneth S.
Teuscher, Cory
TI The role of genetics in estrogen responses: a critical piece of an
intricate puzzle
SO FASEB JOURNAL
LA English
DT Review
DE genotype; reproductive tissue
ID MAMMARY-GLAND DEVELOPMENT; ESTRADIOL-REGULATED RESPONSES; QUANTITATIVE
TRAIT LOCI; BREAST-CANCER CELLS; X ACI INTERCROSS; RECEPTOR-ALPHA;
FEMALE MICE; IN-VIVO; OPPOSITE-SEX; BISPHENOL-A
AB The estrogens are female sex hormones that are involved in a variety of physiological processes, including reproductive development and function, wound healing, and bone growth. They are mainly known for their roles in reproductive tissues-specifically, 17 beta-estradiol (E-2), the primary estrogen, which is secreted by the ovaries and induces cellular proliferation and growth of the uterus and mammary glands. In addition to the role of estrogens in promoting tissue growth and development during normal physiological states, they have a well-established role in determining susceptibility to disease, particularly cancer, in reproductive tissues. The responsiveness of various tissues to estrogen is genetically controlled, with marked quantitative variation observed across multiple species, including humans. This variation presents both researchers and clinicians with a veritable physiological puzzle, the pieces of which-many of them unknown-are complex and difficult to fit together. Although genetics is known to play a major role in determining sensitivity to estrogens, there are other factors, including parent of origin and the maternal environment, that are intimately linked to heritable phenotypes but do not represent genotype, per se. The objectives of this review article were to summarize the current knowledge of the role of genotype, and uterine and neonatal environments, in phenotypic variation in the response to estrogens; to discuss recent findings and the potential mechanisms involved; and to highlight exciting research opportunities for the future.
C1 [Wall, Emma H.; Case, Laure K.; Teuscher, Cory] Univ Vermont, Dept Med & Pathol, Burlington, VT 05405 USA.
[Hewitt, Sylvia C.; Korach, Kenneth S.] US Natl Inst Hlth, Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
[Lin, Chin-Yo] Univ Houston, Ctr Nucl Receptors & Cell Signaling, Houston, TX USA.
RP Teuscher, C (reprint author), Univ Vermont, C331 Given Med Bldg, Burlington, VT 05405 USA.
EM c.teuscher@uvm.edu
OI Korach, Kenneth/0000-0002-7765-418X
FU Intramural Research Program of the U.S. National Institutes of Health,
National Institute of Environmental Health Sciences grant [Z01ES70065]
FX This research was supported, in part, by the Intramural Research Program
of the U.S. National Institutes of Health, National Institute of
Environmental Health Sciences grant Z01ES70065.
NR 137
TC 4
Z9 4
U1 0
U2 7
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
EI 1530-6860
J9 FASEB J
JI Faseb J.
PD DEC
PY 2014
VL 28
IS 12
BP 5042
EP 5054
DI 10.1096/fj.14-260307
PG 13
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
Topics; Cell Biology
GA AU9EN
UT WOS:000345894500003
PM 25212221
ER
PT J
AU Usadi, RS
Alvero, R
Armstrong, AY
Rebar, RW
DeCherney, AH
Maddox, YT
AF Usadi, Rebecca S.
Alvero, Ruben
Armstrong, Alicia Y.
Rebar, Robert W.
DeCherney, Alan H.
Maddox, Yvonne T.
TI Keeping clinicians in research: the Clinical Research/Reproductive
Scientist Training Program (CREST) strategy, 2006-2012
SO FERTILITY AND STERILITY
LA English
DT Editorial Material
C1 [Usadi, Rebecca S.] North Carolinas Healthcare Syst, Carolinas Healthcare Reprod Med & Infertil, Charlotte, NC 28204 USA.
[Alvero, Ruben] Univ Colorado, Dept Obstet & Gynecol, Div Reprod Endocrinol & Infertil, Denver, CO 80202 USA.
[Armstrong, Alicia Y.; DeCherney, Alan H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Bethesda, MD USA.
[Rebar, Robert W.] Western Michigan Univ, Homer Stryker MD Sch Med, Dept Obstet & Gynecol, Kalamazoo, MI 49008 USA.
[Rebar, Robert W.] Michigan State Univ, Coll Human Med, Dept Obstet Gynecol & Reprod Biol, Grand Rapids, MI USA.
[Rebar, Robert W.] Univ Alabama Birmingham, Dept Obstet & Gynecol, Birmingham, AL 35294 USA.
[Maddox, Yvonne T.] Natl Inst Minor Hlth & Hlth Dispar, NIH, Bethesda, MD USA.
RP Usadi, RS (reprint author), North Carolinas Healthcare Syst, Carolinas Healthcare Reprod Med & Infertil, Charlotte, NC 28204 USA.
NR 5
TC 0
Z9 0
U1 0
U2 3
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0015-0282
EI 1556-5653
J9 FERTIL STERIL
JI Fertil. Steril.
PD DEC
PY 2014
VL 102
IS 6
BP 1542
EP 1544
DI 10.1016/j.fertnstert.2014.09.002
PG 3
WC Obstetrics & Gynecology; Reproductive Biology
SC Obstetrics & Gynecology; Reproductive Biology
GA AU4YF
UT WOS:000345613600008
PM 25439798
ER
PT J
AU Cote, LR
Bornstein, MH
AF Cote, Linda R.
Bornstein, Marc H.
TI Productive vocabulary among three groups of bilingual American children:
Comparison and prediction
SO FIRST LANGUAGE
LA English
DT Article
DE Bilingual; development; English; immigrant; Japanese; Korean; language;
Spanish; toddlers; vocabulary
ID DUAL LANGUAGE EXPOSURE; EXPRESSIVE VOCABULARY; FIT INDEXES; TODDLERS;
VALIDITY; ENGLISH; SPANISH; INFANTS; PARENT; INPUT
AB The importance of input factors for bilingual children's vocabulary development was investigated. Forty-seven Argentine, 42 South Korean, 51 European American, 29 Latino immigrant, 26 Japanese immigrant, and 35 Korean immigrant mothers completed checklists of their 20-month-old children's productive vocabularies. Bilingual children's vocabulary sizes in each language separately were consistently smaller than their monolingual peers but only Latino bilingual children had smaller total vocabularies than monolingual children. Bilingual children's vocabulary sizes were similar to each other. Maternal acculturation predicted the amount of input in each language, which then predicted children's vocabulary size in each language. Maternal acculturation also predicted children's English-language vocabulary size directly.
C1 [Cote, Linda R.] Marymount Univ, Arlington, VA 22207 USA.
[Cote, Linda R.; Bornstein, Marc H.] NIH, Bethesda, MD USA.
RP Cote, LR (reprint author), Marymount Univ, Dept Psychol, 2807 N Glebe Rd, Arlington, VA 22207 USA.
EM linda.cote-reilly@marymount.edu
FU Intramural NIH HHS [ZIA HD001119-27]
NR 58
TC 4
Z9 4
U1 1
U2 9
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0142-7237
EI 1740-2344
J9 FIRST LANG
JI First Lang.
PD DEC
PY 2014
VL 34
IS 6
BP 467
EP 485
DI 10.1177/0142723714560178
PG 19
WC Psychology, Developmental; Linguistics; Language & Linguistics
SC Psychology; Linguistics
GA AU9NX
UT WOS:000345922000001
PM 25620820
ER
PT J
AU Steinberg, KM
Schneider, VA
Graves-Lindsay, TA
Fulton, RS
Agarwala, R
Huddleston, J
Shiryev, SA
Morgulis, A
Surti, U
Warren, WC
Church, DM
Eichler, EE
Wilson, RK
AF Steinberg, Karyn Meltz
Schneider, Valerie A.
Graves-Lindsay, Tina A.
Fulton, Robert S.
Agarwala, Richa
Huddleston, John
Shiryev, Sergey A.
Morgulis, Aleksandr
Surti, Urvashi
Warren, Wesley C.
Church, Deanna M.
Eichler, Evan E.
Wilson, Richard K.
TI Single haplotype assembly of the human genome from a hydatidiform mole
SO GENOME RESEARCH
LA English
DT Article
ID COPY-NUMBER VARIATION; SEGMENTAL DUPLICATIONS; STRUCTURAL VARIATION;
BREAKPOINT REGION; SEQUENCE; MAP; DIVERSITY; EVOLUTION; GENES;
ISOCHROMOSOME
AB A complete reference assembly is essential for accurately interpreting individual genomes and associating variation with phenotypes. While the current human reference genome sequence is of very high quality, gaps and misassemblies remain due to biological and technical complexities. Large repetitive sequences and complex allelic diversity are the two main drivers of assembly error. Although increasing the length of sequence reads and library fragments can improve assembly, even the longest available reads do not resolve all regions. In order to overcome the issue of allelic diversity, we used genomic DNA from an essentially haploid hydatidiform mole, CHM1. We utilized several resources from this DNA including a set of end-sequenced and indexed BAC clones and 100x Illumina whole-genome shotgun (WGS) sequence coverage. We used the WGS sequence and the GRCh37 reference assembly to create an assembly of the CHM1 genome. We subsequently incorporated 382 finished BAC clone sequences to generate a draft assembly, CHM_11.1(NCBI AssemblyDB GCA_000306695.2). Analysis of gene, repetitive element, and segmental duplication content show this assembly to be of excellent quality and contiguity. However, comparison to assembly-independent resources, such as BAC clone end sequences and PacBio long reads, indicate misassembled regions. Most of these regions are enriched for structural variation and segmental duplication, and can be resolved in the future. This publicly available assembly will be integrated into the Genome Reference Consortium curation framework for further improvement, with the ultimate goal being a completely finished gap-free assembly.
C1 [Steinberg, Karyn Meltz; Graves-Lindsay, Tina A.; Fulton, Robert S.; Warren, Wesley C.; Wilson, Richard K.] Washington Univ, Genome Inst, St Louis, MO 63108 USA.
[Schneider, Valerie A.; Agarwala, Richa; Shiryev, Sergey A.; Morgulis, Aleksandr] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
[Huddleston, John; Eichler, Evan E.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA.
[Huddleston, John; Eichler, Evan E.] Univ Washington, Howard Hughes Med Inst, Seattle, WA 98795 USA.
[Surti, Urvashi] Univ Pittsburgh, Dept Pathol & Human Genet, Pittsburgh, PA 15260 USA.
[Church, Deanna M.] Personalis Inc, Menlo Pk, CA 94025 USA.
RP Wilson, RK (reprint author), Washington Univ, Genome Inst, St Louis, MO 63108 USA.
EM rwilson@genome.wustl.edu
OI Meltz Steinberg, Karyn/0000-0002-8676-3337
FU NIH [2R01HG002385, 5P01HG004120]
FX We thank Pieter de Jong for the creation of the CHORI-17 BAG library
used extensively in this project. We acknowledge Nathan Bouk for his
expertise in sequence alignment and insightful discussions of alignment
data. We acknowledge the efforts of the production and finishing groups
at The Genome Institute, particularly Aye Wollom, Susie Rock, Milinn
Kremitzki, and Derek Albrecht. We are greatly appreciative of BioNano
Genomics and Dr. Pui Kwok for generously sharing the genomic map and
alignments to the CHM1_1.1 assembly. E.E.E. is an investigator of the
Howard Hughes Medical Institute. This work was supported by NIH Grants
2R01HG002385 and 5P01HG004120 to E.E.E.
NR 49
TC 17
Z9 17
U1 1
U2 8
PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
PI COLD SPRING HARBOR
PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA
SN 1088-9051
EI 1549-5469
J9 GENOME RES
JI Genome Res.
PD DEC
PY 2014
VL 24
IS 12
BP 2066
EP 2076
DI 10.1101/gr.180893.114
PG 11
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Genetics & Heredity
GA AU7XB
UT WOS:000345810600015
PM 25373144
ER
PT J
AU Aka, P
Emmanuel, B
Vila, MC
Jariwala, A
Nkrumah, F
Periago, MV
Neequaye, J
Kiruthu, C
Levine, PH
Biggar, RJ
Bhatia, K
Bethony, JM
Mbulaiteye, SM
AF Aka, Peter
Emmanuel, Benjamin
Vila, Maria Candida
Jariwala, Amar
Nkrumah, Francis
Periago, Maria V.
Neequaye, Janet
Kiruthu, Christine
Levine, Paul H.
Biggar, Robert J.
Bhatia, Kishor
Bethony, Jeffrey M.
Mbulaiteye, Sam M.
TI Elevated serum levels of interleukin-6 in endemic Burkitt lymphoma in
Ghana
SO HEMATOLOGICAL ONCOLOGY
LA English
DT Letter
ID EPSTEIN-BARR-VIRUS; MALARIA
C1 [Aka, Peter; Emmanuel, Benjamin; Kiruthu, Christine; Bhatia, Kishor; Mbulaiteye, Sam M.] NCI, Div Canc Epidemiol & Genet, DCEG, Bethesda, MD 20892 USA.
[Vila, Maria Candida; Jariwala, Amar; Periago, Maria V.; Levine, Paul H.; Bethony, Jeffrey M.] George Washington Univ, Dept Microbiol & Trop Med, Washington, DC USA.
[Nkrumah, Francis] Noguchi Mem Inst, Accra, Ghana.
[Neequaye, Janet] Korle Bu Univ, Teaching Hosp Accra, Dept Child Hlth, Accra, Ghana.
[Biggar, Robert J.] Queensland Univ Technol, Inst Hlth & Biotechnol, Brisbane, Qld 4001, Australia.
RP Aka, P (reprint author), NCI, Div Canc Epidemiol & Genet, DCEG, Bethesda, MD 20892 USA.
EM mbulaits@mail.nih.gov
OI Periago, Maria Victoria/0000-0002-1470-5146
FU Intramural NIH HHS [Z99 CA999999]; NCI NIH HHS [N01CO12400,
N01-CO-12400]
NR 13
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0278-0232
EI 1099-1069
J9 HEMATOL ONCOL
JI Hematol. Oncol.
PD DEC
PY 2014
VL 32
IS 4
BP 218
EP 220
DI 10.1002/hon.2121
PG 3
WC Oncology; Hematology
SC Oncology; Hematology
GA AU9LL
UT WOS:000345914200009
PM 24493366
ER
PT J
AU Hou, YA
Wu, XM
Hallett, M
Chan, P
Wu, T
AF Hou, Yanan
Wu, Xuemin
Hallett, Mark
Chan, Piu
Wu, Tao
TI Frequency-Dependent Neural Activity in Parkinson's Disease
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE functional MRI; amplitude of low frequency fluctuation; frequency band;
midbrain; basal ganglia
ID EXTERNALLY TRIGGERED MOVEMENTS; SPONTANEOUS BRAIN ACTIVITY; STATE
FUNCTIONAL MRI; CEREBRAL-BLOOD-FLOW; BASAL GANGLIA; REGIONAL
HOMOGENEITY; RED NUCLEUS; PREFRONTAL CORTEX; SUBSTANTIA-NIGRA; PYRAMIDAL
TRACT
AB The brainstem and basal ganglia are important in the pathophysiology of Parkinson's disease (PD). Reliable and sensitive detection of neural activity changes in these regions should be helpful in scientific and clinical research on PD. In this study, we used resting state functional MRI and amplitude of low frequency fluctuation (ALFF) methods to examine spontaneous neural activity in 109 patients with PD. We examined activity in two frequency bands, slow-4 (between 0.027 and 0.073 Hz) and slow-5 (0.010-0.027 Hz). Patients had decreased ALFF in the striatum and increased ALFF in the midbrain, and changes were more significant in slow-4. Additionally, changes in slow-4 in both basal ganglia and midbrain correlated with the severity of the parkinsonism. The ALFF in the caudate nucleus positively correlated with the dose of levodopa, while the ALFF in the putamen negatively correlated with the disease duration in both slow-4 and slow-5 bands. In addition, the ALFF in the rostral supplementary motor area negatively correlated with bradykinesia subscale scores. Our findings show that with a large cohort of patients and distinguishing frequency bands, neural modulations in the brainstem and striatum in PD can be detected and may have clinical relevance. The physiological interpretation of these changes needs to be determined. Hum Brain Mapp 35:5815-5833, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [Hou, Yanan; Wu, Xuemin; Chan, Piu; Wu, Tao] Capital Med Univ, Dept Neurobiol, Key Lab Neurodegenerat Disorders, Minist Educ,Beijing Inst Geriatr,Xuanwu Hosp, Beijing 100053, Peoples R China.
[Hou, Yanan; Wu, Xuemin; Chan, Piu; Wu, Tao] Beijing Inst Brain Disorders, Beijing Key Lab Parkinsons Dis, Parkinson Dis Ctr, Beijing, Peoples R China.
[Hallett, Mark] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA.
RP Wu, T (reprint author), Capital Med Univ, Dept Neurobiol, Key Lab Neurodegenerat Disorders, Minist Educ,Beijing Inst Geriatr,Xuanwu Hosp, Beijing 100053, Peoples R China.
EM wutao69@gmail.com
FU National Science Foundation of China [30870693, 81071012, 81271429];
NINDS Intramural Program
FX Contract grant sponsor: National Science Foundation of China; Contract
grant numbers: 30870693; 81071012; and 81271429; Contract grant sponsor:
NINDS Intramural Program (to Dr. Hallett).
NR 63
TC 14
Z9 16
U1 1
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD DEC
PY 2014
VL 35
IS 12
BP 5815
EP 5833
DI 10.1002/hbm.22587
PG 19
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AS6WA
UT WOS:000344398900007
PM 25045127
ER
PT J
AU Tinaz, S
Belluscio, BA
Malone, P
van der Veen, JW
Hallett, M
Horovitz, SG
AF Tinaz, Sule
Belluscio, Beth A.
Malone, Patrick
van der Veen, Jan Willem
Hallett, Mark
Horovitz, Silvina G.
TI Role of the Sensorimotor Cortex in Tourette Syndrome using Multimodal
Imaging
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE gamma-aminobutyric acid; magnetic resonance spectroscopy; functional
magnetic resonance imaging; magnetoencephalography; resting state;
functional connectivity; beta oscillations
ID IN-VIVO NEUROCHEMISTRY; HUMAN CEREBRAL-CORTEX; TIC GENERATION; INSULA;
SYSTEM; DISORDER; SCALE; BODY; INDIVIDUALS; ABNORMALITY
AB Tourette syndrome (TS) is a neuropsychiatric disorder characterized by motor and vocal tics. Most patients describe uncomfortable premonitory sensations preceding the tics and a subjective experience of increased sensitivity to tactile stimuli. These reports indicate that a sensory processing disturbance is an important component of TS together with motor phenomena. Thus, we focused our investigation on the role of the sensorimotor cortex (SMC) in TS using multimodal neuroimaging techniques. We measured the gamma-aminobutyric acid (GABA)+/Creatine (Cre) ratio in the SMC using GABA H-1 magnetic resonance spectroscopy. We recorded the baseline beta activity in the SMC using magnetoencephalography and correlated GABA+/Cre ratio with baseline beta band power. Finally, we examined the resting state functional connectivity (FC) pattern of the SMC using functional magnetic resonance imaging (fMRI). GABA+/Cre ratio in the SMC did not differ between patients and controls. Correlation between the baseline beta band power and GABA+/Cre ratio was abnormal in patients. The anterior insula showed increased FC with the SMC in patients. These findings suggest that altered limbic input to the SMC and abnormal GABA-mediated beta oscillations in the SMC may underpin some of the sensorimotor processing disturbances in TS and contribute to tic generation. Hum Brain Mapp 35:5834-5846, 2014. Published 2014. This article is a U.S. Government work and is in the public domain in the USA.
C1 [Tinaz, Sule; Belluscio, Beth A.; Malone, Patrick; Hallett, Mark; Horovitz, Silvina G.] NINDS, Human Motor Control Sect, NIH, Bethesda, MD 20892 USA.
[van der Veen, Jan Willem] NIMH, Magnet Resonance Spect Core, NIH, Bethesda, MD 20892 USA.
RP Tinaz, S (reprint author), 10 Ctr Dr MSC 1428,Bldg 10,Room 7D42, Bethesda, MD 20892 USA.
EM aysesule.tinaz@nih.gov
FU NINDS
FX Contract grant sponsor: NINDS Intramural Research Program
NR 48
TC 15
Z9 15
U1 2
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD DEC
PY 2014
VL 35
IS 12
BP 5834
EP 5846
DI 10.1002/hbm.22588
PG 13
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AS6WA
UT WOS:000344398900008
PM 25044024
ER
PT J
AU Hamann, JM
Dayan, E
Hummel, FC
Cohen, LG
AF Hamann, Janne M.
Dayan, Eran
Hummel, Friedhelm C.
Cohen, Leonardo G.
TI Baseline Frontostriatal-Limbic Connectivity Predicts Reward-Based Memory
Formation
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE reward learning; brain connectivity; learning; memory; resting state
functional magnetic resonance imaging; ventral striatum
ID INTRINSIC FUNCTIONAL CONNECTIVITY; HUMAN NUCLEUS-ACCUMBENS; DEFAULT-MODE
NETWORK; RESTING STATE FMRI; LONG-TERM-MEMORY; MOTOR SKILL;
CORRELATION-COEFFICIENT; DOPAMINERGIC MIDBRAIN; NEURAL MECHANISMS;
MONETARY REWARD
AB Reward mediates the acquisition and long-term retention of procedural skills in humans. Yet, learning under rewarded conditions is highly variable across individuals and the mechanisms that determine interindividual variability in rewarded learning are not known. We postulated that baseline functional connectivity in a large-scale frontostriatal-limbic network could predict subsequent interindividual variability in rewarded learning. Resting-state functional MRI was acquired in two groups of subjects (n=30) who then trained on a visuomotor procedural learning task with or without reward feedback. We then tested whether baseline functional connectivity within the frontostriatal-limbic network predicted memory strength measured immediately, 24 h and 1 month after training in both groups. We found that connectivity in the frontostriatal-limbic network predicted interindividual variability in the rewarded but not in the unrewarded learning group. Prediction was strongest for long-term memory. Similar links between connectivity and reward-based memory were absent in two control networks, a fronto-parieto-temporal language network and the dorsal attention network. The results indicate that baseline functional connectivity within the frontostriatal-limbic network successfully predicts long-term retention of rewarded learning. Hum Brain Mapp 35:5921-5931, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [Hamann, Janne M.; Dayan, Eran; Cohen, Leonardo G.] NINDS, Human Cort Physiol & Neurorehabil Sect, NIH, Bethesda, MD 20892 USA.
[Hamann, Janne M.; Hummel, Friedhelm C.] Univ Med Ctr Hamburg Eppendorf, BrainImaging & NeuroStimulat BINS Lab, D-20251 Hamburg, Germany.
RP Dayan, E (reprint author), NINDS, Human Cort Physiol & Neurorehabil Sect, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM dayane@ninds.nih.gov
OI Dayan, Eran/0000-0001-9710-9210
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke at the National Institutes of Health and by the
Mentoring Program for Excellent Students of the University Medical
Center Hamburg-Eppendorf; Scholarship from Claussen-Simon Stiftung
FX Contract grant sponsor(s): Intramural Research Program of the National
Institute of Neurological Disorders and Stroke at the National
Institutes of Health and by the Mentoring Program for Excellent Students
of the University Medical Center Hamburg-Eppendorf (to JMH); Scholarship
from Claussen-Simon Stiftung (to JMH).
NR 85
TC 2
Z9 2
U1 2
U2 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD DEC
PY 2014
VL 35
IS 12
BP 5921
EP 5931
DI 10.1002/hbm.22594
PG 11
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AS6WA
UT WOS:000344398900014
PM 25078102
ER
PT J
AU Eddin, AS
Wang, J
Wu, WS
Sargolzaei, S
Bjornson, B
Jones, RA
Gaillard, WD
Adjouadi, M
AF Eddin, Anas Salah
Wang, Jin
Wu, Wensong
Sargolzaei, Saman
Bjornson, Bruce
Jones, Richard A.
Gaillard, William D.
Adjouadi, Malek
TI The Effects of Pediatric Epilepsy on a Language Connectome
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE functional network; language network; graph theory; functional magnetic
resonance imaging; independent component analysis
ID TEMPORAL-LOBE EPILEPSY; INDEPENDENT COMPONENT ANALYSIS;
LOCALIZATION-RELATED EPILEPSY; SMALL-WORLD ORGANIZATION; DEFAULT-MODE
NETWORK; FUNCTIONAL CONNECTIVITY; RESTING-STATE; BRAIN NETWORKS;
IMPAIRED ATTENTION; ATYPICAL LANGUAGE
AB This study introduces a new approach for assessing the effects of pediatric epilepsy on a language connectome. Two novel data-driven network construction approaches are presented. These methods rely on connecting different brain regions using either extent or intensity of language related activations as identified by independent component analysis of fMRI. An auditory word definition decision task paradigm was used to activate the language network for 29 patients and 30 controls. Evaluations illustrated that pediatric epilepsy is associated with a network efficiency reduction. Patients showed a propensity to inefficiently use the whole brain network to perform the language task; whereas, controls seemed to efficiently use smaller segregated network components to achieve the same task. To explain the causes of the decreased efficiency, graph theoretical analysis was performed. The analysis revealed substantial global network feature differences between the patients and controls for the extent of activation network. It also showed that for both subject groups the language network exhibited small-world characteristics; however, the patient's extent of activation network showed a tendency toward randomness. It was also shown that the intensity of activation network displayed ipsilateral hub reorganization on the local level. We finally showed that a clustering scheme was able to fairly separate the subjects into their respective patient or control groups. The clustering was initiated using local and global nodal measurements. Compared to the intensity of activation network, the extent of activation network clustering demonstrated better precision. This ascertained that the network differences presented by the networks were associated with pediatric epilepsy. Hum Brain Mapp 35:5996-6010, 2014. (c) 2014 Wiley Periodicals, Inc.
C1 [Eddin, Anas Salah] Florida Polytech Univ, Dept Comp Sci & Informat Technol, Lakeland, FL USA.
[Eddin, Anas Salah; Wang, Jin; Sargolzaei, Saman; Adjouadi, Malek] Florida Int Univ, Dept Elect & Comp Engn, Miami, FL 33174 USA.
[Wu, Wensong] Florida Int Univ, Dept Math & Stat, Miami, FL 33174 USA.
[Bjornson, Bruce] British Columbia Childrens Hosp, Div Neurol, Vancouver, BC V6H 3V4, Canada.
[Jones, Richard A.] Childrens Healthcare Atlanta, Dept Radiol, Atlanta, GA USA.
[Jones, Richard A.] Emory Univ, Dept Radiol, Atlanta, GA 30322 USA.
[Gaillard, William D.] George Washington Univ, Childrens Natl Med Ctr, Dept Neurosci, Washington, DC USA.
[Gaillard, William D.] NINDS, Clin Epilepsy Sect, NIH, Bethesda, MD 20892 USA.
[Adjouadi, Malek] Florida Int Univ, Dept Biomed Engn, Miami, FL 33174 USA.
RP Adjouadi, M (reprint author), Florida Int Univ, Coll Engn & Comp, 10555 W Flagler St,EC 2672, Miami, FL 33174 USA.
EM adjouadi@fiu.edu
RI Bjornson, Bruce/A-8616-2010
OI Bjornson, Bruce/0000-0002-1465-6196
FU National Science Foundation [CNS-0959985, CNS-1042341, HRD-0833093,
IIP-1230661]; National Institutes of Health [NINDS R01 NS44280, NCRR
M01RR020359]; Intellectual and Developmental Research Center
[HD040677-07]; Ware Foundation; joint Neuro-Engineering Program; Miami
Children's Hospital
FX Contract grant sponsor: National Science Foundation; Contract grant
numbers: CNS-0959985; CNS-1042341; HRD-0833093; and IIP-1230661;
Contract grant sponsor: National Institutes of Health; Contract grant
numbers: NINDS R01 NS44280; NCRR M01RR020359; Contract grant sponsor:
Intellectual and Developmental Research Center; Contract grant number:
HD040677-07; Contract grant sponsor: Ware Foundation and the joint
Neuro-Engineering Program with Miami Children's Hospital.
NR 82
TC 1
Z9 1
U1 1
U2 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD DEC
PY 2014
VL 35
IS 12
BP 5996
EP 6010
DI 10.1002/hbm.22600
PG 15
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA AS6WA
UT WOS:000344398900020
PM 25082062
ER
PT J
AU Mansoor, A
Bagci, U
Xu, ZY
Foster, B
Olivier, KN
Elinoff, JM
Suffredini, AF
Udupa, JK
Mollura, DJ
AF Mansoor, Awais
Bagci, Ulas
Xu, Ziyue
Foster, Brent
Olivier, Kenneth N.
Elinoff, Jason M.
Suffredini, Anthony F.
Udupa, Jayaram K.
Mollura, Daniel J.
TI A Generic Approach to Pathological Lung Segmentation
SO IEEE TRANSACTIONS ON MEDICAL IMAGING
LA English
DT Article
DE Anatomy-guided segmentation; computed tomography; fuzzy connectedness;
pathological lung segmentation; random forest
ID COMPUTER-AIDED DIAGNOSIS; CT IMAGES; FUZZY CONNECTEDNESS; THORACIC CT;
AUTOMATIC SEGMENTATION; ATTENUATION VALUES; LOBE SEGMENTATION;
GROUND-GLASS; ATLAS; CLASSIFICATION
AB In this study, we propose a novel pathological lung segmentation method that takes into account neighbor prior constraints and a novel pathology recognition system. Our proposed framework has two stages; during stage one, we adapted the fuzzy connectedness (FC) image segmentation algorithm to perform initial lung parenchyma extraction. In parallel, we estimate the lung volume using rib-cage information without explicitly delineating lungs. This rudimentary, but intelligent lung volume estimation system allows comparison of volume differences between rib cage and FC based lung volume measurements. Significant volume difference indicates the presence of pathology, which invokes the second stage of the proposed framework for the refinement of segmented lung. In stage two, texture-based features are utilized to detect abnormal imaging patterns (consolidations, ground glass, interstitial thickening, tree-inbud, honeycombing, nodules, and micro-nodules) that might have been missed during the first stage of the algorithm. This refinement stage is further completed by a novel neighboring anatomy-guided segmentation approach to include abnormalities with weak textures, and pleura regions. We evaluated the accuracy and efficiency of the proposed method on more than 400 CT scans with the presence of a wide spectrum of abnormalities. To our best of knowledge, this is the first study to evaluate all abnormal imaging patterns in a single segmentation framework. The quantitative results show that our pathological lung segmentation method improves on current standards because of its high sensitivity and specificity and may have considerable potential to enhance the performance of routine clinical tasks.
C1 [Mansoor, Awais; Bagci, Ulas; Xu, Ziyue; Foster, Brent; Mollura, Daniel J.] NIH, Dept Radiol & Imaging Sci, Bethesda, MD 20892 USA.
[Elinoff, Jason M.; Suffredini, Anthony F.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Olivier, Kenneth N.] NIAID, Immunopathogenesis Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Udupa, Jayaram K.] Univ Penn, Dept Radiol, Philadelphia, PA 19104 USA.
RP Mansoor, A (reprint author), NIH, Dept Radiol & Imaging Sci, Bldg 10, Bethesda, MD 20892 USA.
EM ulasbagci@gmail.com
OI Bagci, Ulas/0000-0001-7379-6829
FU Center for Infectious Disease Imaging (CIDI); National Institute of
Allergy and Infectious Diseases (NIAID); National Institute of
Biomedical Imaging and Bioengineering (NIBIB)
FX This work was supported by Center for Infectious Disease Imaging (CIDI),
the intramural research program of the National Institute of Allergy and
Infectious Diseases (NIAID), and the National Institute of Biomedical
Imaging and Bioengineering (NIBIB). Asterisk indicates corresponding
author.
NR 61
TC 21
Z9 22
U1 4
U2 24
PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC
PI PISCATAWAY
PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA
SN 0278-0062
EI 1558-254X
J9 IEEE T MED IMAGING
JI IEEE Trans. Med. Imaging
PD DEC
PY 2014
VL 33
IS 12
BP 2293
EP 2310
DI 10.1109/TMI.2014.2337057
PG 18
WC Computer Science, Interdisciplinary Applications; Engineering,
Biomedical; Engineering, Electrical & Electronic; Imaging Science &
Photographic Technology; Radiology, Nuclear Medicine & Medical Imaging
SC Computer Science; Engineering; Imaging Science & Photographic
Technology; Radiology, Nuclear Medicine & Medical Imaging
GA AU9JC
UT WOS:000345907400006
PM 25020069
ER
PT J
AU Trinchieri, G
AF Trinchieri, G.
TI Cancer as a disease of the metaorganism
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Trinchieri, G.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 93
BP 13
EP 13
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600030
ER
PT J
AU Ombrello, MJ
AF Ombrello, M. J.
TI Genetically-complex autoinflammatory diseases: Still's disease and
Behcet's disease
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Ombrello, M. J.] NIAMSD, Translat Genet & Genom Unit, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 109
BP 34
EP 34
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600076
ER
PT J
AU Kolev, M
Dimeloe, S
Le Friec, G
Arbore, G
Povoleri, GA
Fischer, M
Razik, L
Watson, J
Couzi, L
Afzali, B
Lavender, P
Hess, C
Kemper, C
AF Kolev, M.
Dimeloe, S.
Le Friec, G.
Arbore, G.
Povoleri, G. A.
Fischer, M.
Razik, L.
Watson, J.
Couzi, L.
Afzali, B.
Lavender, P.
Hess, C.
Kemper, C.
TI CD46 links complement and metabolic reprogramming in human Th1 responses
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Kolev, M.; Le Friec, G.; Arbore, G.; Povoleri, G. A.; Afzali, B.; Kemper, C.] Kings Coll London, MRC, Ctr Transplantat, Div Transplant Immunol & Mucosal Biol, London, England.
[Dimeloe, S.; Fischer, M.; Razik, L.; Hess, C.] Univ Basel, Dept Biomed, Basel, Switzerland.
[Povoleri, G. A.; Afzali, B.] Kings Hlth Partners, Biomed Res Ctr, London, England.
[Watson, J.; Lavender, P.] Kings Coll London, MRC, London, England.
[Watson, J.; Lavender, P.] Kings Coll London, Asthma UK Ctr Allerg Mech Asthma, London, England.
[Couzi, L.] CHU Bordeaux, Hosp Pellegrin, CNRS, UMR 1564, Bordeaux, France.
[Afzali, B.] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
RI Kemper, Claudia/B-1502-2015; kolev, mihail/D-1476-2015
OI kolev, mihail/0000-0002-5226-4759
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 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 613
BP 49
EP 49
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600110
ER
PT J
AU Galloway, A
Hodson, D
Bell, L
Saveliev, A
Lukasiak, S
Turner, M
AF Galloway, A.
Hodson, D.
Bell, L.
Saveliev, A.
Lukasiak, S.
Turner, M.
TI The RNA-binding proteins ZFP36L1 and ZFP36L2 are essential for the
development of B lymphocytes
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Galloway, A.; Bell, L.; Saveliev, A.; Lukasiak, S.; Turner, M.] Babraham Inst, LLSD, Cambridge, England.
[Hodson, D.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 489
BP 73
EP 73
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600186
ER
PT J
AU Dutzan, N
Abusleme, L
Bouladoux, N
Greenwell-Wild, T
Betts, K
Belkaid, Y
Moutsopoulos, N
Konkel, JE
AF Dutzan, N.
Abusleme, L.
Bouladoux, N.
Greenwell-Wild, T.
Betts, K.
Belkaid, Y.
Moutsopoulos, N.
Konkel, J. E.
TI Tissue-specific control of immune responses in the oral mucosa
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Dutzan, N.; Abusleme, L.; Greenwell-Wild, T.; Betts, K.; Moutsopoulos, N.] NIDCR, NIH, Bethesda, MD USA.
[Bouladoux, N.; Belkaid, Y.] NIAID, NIH, Bethesda, MD 20892 USA.
[Konkel, J. E.] Univ Manchester, Manchester, Lancs, England.
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 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 560
BP 75
EP 75
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600193
ER
PT J
AU Whibley, N
Mamo, A
Coleman, B
Conti, H
Traggiai, E
Kolbinger, F
Vogel, B
Kammuller, M
Siebenlist, U
Iwakura, Y
Gaffen, S
AF Whibley, N.
Mamo, A.
Coleman, B.
Conti, H.
Traggiai, E.
Kolbinger, F.
Vogel, B.
Kammuller, M.
Siebenlist, U.
Iwakura, Y.
Gaffen, S.
TI Differential requirements of IL-17 family cytokines in anti-fungal
immunity against oral candidiasis
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Whibley, N.; Mamo, A.; Coleman, B.; Conti, H.; Gaffen, S.] Univ Pittsburgh, Pittsburgh, PA USA.
[Traggiai, E.; Kolbinger, F.; Vogel, B.; Kammuller, M.] Novartis Inst Biomed Res, Basel, Switzerland.
[Siebenlist, U.] NIAID, NIH, Bethesda, MD 20892 USA.
[Iwakura, Y.] Tokyo Univ Sci, Chiba, Japan.
RI Iwakura, Yoichiro/E-5457-2011
OI Iwakura, Yoichiro/0000-0002-9934-5775
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 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 433
BP 86
EP 86
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600232
ER
PT J
AU Askenase, MH
Byrd, AL
Bouladoux, N
da Fonseca, DM
Konkel, JE
Belkaid, Y
Grainger, JR
AF Askenase, M. H.
Byrd, A. L.
Bouladoux, N.
da Fonseca, D. Morais
Konkel, J. E.
Belkaid, Y.
Grainger, J. R.
TI Education of monocyte precursors instructs for regulatory function at
barrier sites during infection
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Askenase, M. H.; Byrd, A. L.; Bouladoux, N.; da Fonseca, D. Morais; Belkaid, Y.; Grainger, J. R.] NIAID, Program Barrier Immun & Repair, Mucosal Immunol Sect, LPD,NIH, Bethesda, MD 20892 USA.
Univ Penn, Immunol Grad Grp, Philadelphia, PA 19104 USA.
NHGRI, Translat & Funct Genom Branch, NIH, Bethesda, MD 20892 USA.
[Konkel, J. E.] MCCIR, Manchester, Lancs, England.
Univ Manchester, Fac Life Sci, Manchester, Lancs, England.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 532
BP 104
EP 104
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600295
ER
PT J
AU Sansom, DM
Schubert, D
Bode, C
Kenefeck, R
Hou, T
Wing, J
Kennedy, A
Unger, S
Bulashevska, A
Gruning, B
Petersen, B
Schaffer, A
Frede, N
Dueckers, G
Seneviratne, S
Kanariou, M
Rensing-Ehl, A
Salzer, U
Warnatz, K
Cathomen, T
Emmerich, F
Fisch, P
Rakhmanov, M
Franke, A
Sakaguchi, S
Walker, LS
Grimbacher, B
AF Sansom, D. M.
Schubert, D.
Bode, C.
Kenefeck, R.
Hou, T.
Wing, J.
Kennedy, A.
Unger, S.
Bulashevska, A.
Gruning, B.
Petersen, B.
Schaffer, A.
Frede, N.
Dueckers, G.
Seneviratne, S.
Kanariou, M.
Rensing-Ehl, A.
Salzer, U.
Warnatz, K.
Cathomen, T.
Emmerich, F.
Fisch, P.
Rakhmanov, M.
Franke, A.
Sakaguchi, S.
Walker, L. S.
Grimbacher, B.
TI Heterozygous mutations in CTLA-4 are associated with defective
regulatory T-cell function, causing an immune dysregulation syndrome in
humans
SO IMMUNOLOGY
LA English
DT Meeting Abstract
CT Annual Congress of the British-Society-for-Immunology
CY DEC 01-04, 2014
CL Brighton, ENGLAND
SP British Soc Immunol
C1 [Sansom, D. M.; Schubert, D.; Bode, C.; Kenefeck, R.; Hou, T.; Kennedy, A.; Kanariou, M.; Emmerich, F.; Fisch, P.; Walker, L. S.; Grimbacher, B.] UCL, Inst Immun & Transplantat, London, 20892, England.
[Unger, S.; Bulashevska, A.; Frede, N.; Rensing-Ehl, A.; Salzer, U.; Warnatz, K.; Cathomen, T.; Rakhmanov, M.] Univ Med Ctr, Ctr Chron Immunodeficiency, Freiburg, Germany.
Univ Freiburg, Spemann Grad Sch Biol & Med, Freiburg NW3 2QG, Germany.
[Wing, J.; Sakaguchi, S.] Osaka Univ, Dept Expt Immunol, Osaka, Japan.
[Gruning, B.] Univ Freiburg, Dept Comp Sci, Freiburg, Germany.
[Petersen, B.; Franke, A.] Univ Kiel, Inst Clin Mol Biol, Kiel, Germany.
[Schaffer, A.] NIH, Bethesda, MD USA.
[Dueckers, G.] Childrens Hosp Krefeld, Krefeld, Germany.
[Seneviratne, S.] Royal Free Hosp, Dept Immunol, London, England.
AS Childrens Hosp, Dept Immunol & Histocompatibil, Athens, Greece.
Univ Med Ctr, Dept Transfus Med, Freiburg, Germany.
Univ Med Ctr, Dept Pathol, Freiburg, Germany.
RI HOU, TIEZHENG/B-4848-2015
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 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 329
BP 155
EP 155
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600470
ER
PT J
AU Williams, EL
Dhanda, A
Liu, B
Lait, PJP
Schewitz-Bowers, LP
Collins, P
Dick, AD
Nussenblatt, RB
Lee, RWJ
AF Williams, E. L.
Dhanda, A.
Liu, B.
Lait, P. J. P.
Schewitz-Bowers, L. P.
Collins, P.
Dick, A. D.
Nussenblatt, R. B.
Lee, R. W. J.
CA UNITE Human Ocular Immunology
TI CD14(++)CD16(+) monocytes are enriched in inflammatory diseases and
promote the sensitivity of T-cells to corticosteroids
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Williams, E. L.; Dhanda, A.; Lait, P. J. P.; Schewitz-Bowers, L. P.; Dick, A. D.; Lee, R. W. J.] Univ Bristol, Sch Clin Sci, Bristol, Avon, England.
Moorfields Eye Hosp, Natl Inst Hlth Res NIHR Biomed Res Ctr, London, England.
UCL, Inst Ophthalmol, London, England.
[Collins, P.] Univ Hosp Bristol NHS Fdn Trust, Bristol, Avon, England.
[Liu, B.; Nussenblatt, R. B.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
NIH, Ctr Human Immunol Autoimmun & Inflammat, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 357
BP 157
EP 158
PG 2
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600477
ER
PT J
AU Lait, PJP
Schewitz-Bowers, LP
Copland, DA
Chen, P
Vistica, B
Dhanda, A
Liu, B
Jawad, S
Li, Z
Hirani, S
Wu, W
Sen, HN
Conway-Campbell, B
Wei, L
Gery, I
Dick, AD
Lee, RWJ
Nussenblatt, RB
AF Lait, P. J. P.
Schewitz-Bowers, L. P.
Copland, D. A.
Chen, P.
Vistica, B.
Dhanda, A.
Liu, B.
Jawad, S.
Li, Z.
Hirani, S.
Wu, W.
Sen, H. Nida
Conway-Campbell, B.
Wei, L.
Gery, I.
Dick, A. D.
Lee, R. W. J.
Nussenblatt, R. B.
CA UNITE Human Ocular Immunolgy Cons
TI Corticosteroid resistant Th17 cells are sensitive to calcineurin
inhibition
SO IMMUNOLOGY
LA English
DT Meeting Abstract
C1 [Lait, P. J. P.; Schewitz-Bowers, L. P.; Copland, D. A.; Dhanda, A.; Conway-Campbell, B.; Dick, A. D.; Lee, R. W. J.] Univ Bristol, Sch Clin Sci, Bristol, Avon, England.
Moorfields Eye Hosp, Natl Inst Hlth Res, Biomed Res Ctr, London, England.
UCL, Inst Ophthalmol, London, England.
[Chen, P.; Vistica, B.; Liu, B.; Jawad, S.; Li, Z.; Hirani, S.; Wu, W.; Sen, H. Nida; Wei, L.; Gery, I.; Nussenblatt, R. B.] NEI, Immunol Lab, NIH, Bethesda, MD 20892 USA.
Univ Hosp Bristol NHS Fdn Trust, Bristol, Avon, England.
NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
NIH, Ctr Human Immunol Autoimmun & Inflammat, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0019-2805
EI 1365-2567
J9 IMMUNOLOGY
JI Immunology
PD DEC
PY 2014
VL 143
SU 2
SI SI
MA 428
BP 161
EP 161
PG 1
WC Immunology
SC Immunology
GA AU6GT
UT WOS:000345702600490
ER
PT J
AU Persaud, D
Patel, K
Karalius, B
Rainwater-Lovett, K
Ziemniak, C
Ellis, A
Chen, YH
Richman, D
Siberry, GK
Van Dyke, RB
Burchett, S
Seage, GR
Luzuriaga, K
AF Persaud, Deborah
Patel, Kunjal
Karalius, Brad
Rainwater-Lovett, Kaitlin
Ziemniak, Carrie
Ellis, Angela
Chen, Ya Hui
Richman, Douglas
Siberry, George K.
Van Dyke, Russell B.
Burchett, Sandra
Seage, George R., III
Luzuriaga, Katherine
CA Pediat HIV AIDS Cohort Study
TI Influence of Age at Virologic Control on Peripheral Blood Human
Immunodeficiency Virus Reservoir Size and Serostatus in Perinatally
Infected Adolescents
SO JAMA PEDIATRICS
LA English
DT Article
ID PRIMARY HIV-1 INFECTION; ACTIVE ANTIRETROVIRAL THERAPY; HIV-1-INFECTED
CHILDREN; MICROBIAL TRANSLOCATION; GASTROINTESTINAL-TRACT; IMMUNE
ACTIVATION; VIRAL RESERVOIRS; SOLUBLE CD14; INFANTS; PERSISTENCE
AB IMPORTANCE Combination antiretroviral therapy initiated within several weeks of human immunodeficiency virus (HIV) infection in adults limits proviral reservoirs that preclude HIV cure. Biomarkers of restricted proviral reservoirs may aid in the monitoring of HIV remission or cure.
OBJECTIVES To quantify peripheral blood proviral reservoir size in perinatally HIV-infected (PHIV+) adolescents and to identify correlates of limited proviral reservoirs.
DESIGN, SETTING, AND PARTICIPANTS A cross-sectional study including 144 PHIV+ youths (median age, 14.3 years) enrolled in the United States-based Pediatric HIV/AIDS Cohort Study and receiving durable (median duration, 10.2 years) combination antiretroviral therapy, stratified by age at virologic control.
MAIN OUTCOMES AND MEASURES The primary end pointwas peripheral blood mononuclear cell (PBMC) proviral load after virologic control at different ages. Correlations between proviral load and markers of active HIV production (ie, HIV-specific antibodies, 2-long terminal repeat circles) and markers of immune activation and inflammation were also assessed.
RESULTS Proviral reservoir size was markedly reduced in the PHIV+ youth who achieved virologic control before 1 year of age (4.2 [interquartile range, 2.6-8.6] copies per 1 million PBMCs) compared with those who achieved virologic control at 1 to 5 years of age (19.4 [interquartile range, 5.5-99.8] copies per 1 million PBMCs) or after 5 years of age (70.7 [interquartile range, 23.2-209.4] copies per 1 million PBMCs; P < .001). A proviral burden of less than 10 copies per 1 million PBMCs in PHIV+ youth was measured in 11 (79%), 20 (40%), and 13 (18%) participants with virologic control before 1 year, at 1 to 5 years, and after 5 years of age, respectively (P < .001). Lower proviral load was associated with undetectable 2-long terminal repeat circles (P < .001) and HIV-negative or indeterminate serostatus (P < .001) but not with concentrations of soluble immune activation markers CD14 and CD163.
CONCLUSIONS AND RELEVANCE Early effective combination antiretroviral therapy with prolonged virologic suppression after perinatal HIV infection leads to negligible peripheral blood proviral reservoirs in adolescence and is associated with negative or indeterminate HIV serostatus. These findings highlight the long-term effect of early effective control of HIV replication on biomarkers of HIV persistence in perinatal infection and the utility of HIV serostatus as a biomarker for small proviral reservoir size, although not necessarily for cure.
C1 [Persaud, Deborah; Rainwater-Lovett, Kaitlin; Ziemniak, Carrie; Chen, Ya Hui] Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA.
[Patel, Kunjal; Karalius, Brad; Seage, George R., III] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Patel, Kunjal; Karalius, Brad; Seage, George R., III] Harvard Univ, Sch Publ Hlth, Ctr Biostat AIDS Res, Boston, MA 02115 USA.
[Ellis, Angela] Frontier Sci & Technol Res Fdn Inc, Buffalo, NY USA.
[Richman, Douglas] Univ Calif San Diego, Dept Pathol, La Jolla, CA 92093 USA.
[Richman, Douglas] Vet Affairs San Diego Healthcare Syst, San Diego, CA USA.
[Siberry, George K.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Maternal & Pediat Infect Dis Branch, Bethesda, MD USA.
[Van Dyke, Russell B.] Tulane Univ, Sch Med, Dept Pediat, New Orleans, LA 70112 USA.
[Burchett, Sandra] Boston Childrens Hosp, Div Infect Dis, Boston, MA USA.
[Luzuriaga, Katherine] Univ Massachusetts, Sch Med, Dept Pediat, Program Mol Med, Worcester, MA USA.
[Luzuriaga, Katherine] Univ Massachusetts, Sch Med, Ctr Clin & Translat Sci, Worcester, MA USA.
RP Persaud, D (reprint author), Johns Hopkins Univ, Sch Med, Dept Pediat, 720 Rutland Ave,Ross Bldg,Room 1170, Baltimore, MD 21287 USA.
EM dpers@jhmi.edu
FU National Institutes of Health (NIH) [R01HD080474, R21AI100656]; American
Foundation for AIDS Research; International Maternal Pediatric
Adolescent AIDS Clinical Trials Network (Dr Persaud) [UO1-AI-068632];
Johns Hopkins University Center for AIDS Research [P30-AI094189]; Eunice
Kennedy Shriver National Institute of Child Health and Human
Development; National Institute on Drug Abuse; National Institute of
Allergy and Infectious Diseases; Office of AIDS Research; National
Institute of Mental Health; National Institute of Neurological and
Communicative Disorders and Stroke; National Institute on Deafness and
Other Communication Disorders; National Heart, Lung, and Blood
Institute; National Institute of Dental and Craniofacial Research;
National Institute on Alcohol Abuse and Alcoholism [HD052102, 3 U01
HD052102-05S1, 3 U01 HD052102-06S3]; Harvard School of Public Health;
Tulane University School of Medicine [HD052104, 3U01 HD052104-06S1];
Collaboratory for AIDS Research on Eradication (CARE) [U19 AI096113];
University of California; San Diego; Center for AIDS Research; James
Pendleton Charitable Trust
FX The laboratory studies were supported by grants R01HD080474 and
R21AI100656 from the National Institutes of Health (NIH) (Dr Persaud);
by funding from the American Foundation for AIDS Research (Drs Persaud
and Luzuriaga); and by grants U01-AI-068632 from the International
Maternal Pediatric Adolescent AIDS Clinical Trials Network (Dr Persaud)
and P30-AI094189 from the Johns Hopkins University Center for AIDS
Research (Dr Persaud). The study was also supported by the Eunice
Kennedy Shriver National Institute of Child Health and Human Development
with cofunding from the National Institute on Drug Abuse, the National
Institute of Allergy and Infectious Diseases, the Office of AIDS
Research, the National Institute of Mental Health, the National
Institute of Neurological and Communicative Disorders and Stroke, the
National Institute on Deafness and Other Communication Disorders, the
National Heart, Lung, and Blood Institute, the National Institute of
Dental and Craniofacial Research, and the National Institute on Alcohol
Abuse and Alcoholism through cooperative agreements HD052102, 3 U01
HD052102-05S1, and 3 U01 HD052102-06S3 with the Harvard School of Public
Health (principal investigator [PI], George R. Seage III, DSc, MPH;
project director, Julie Alperen, DrPH) and HD052104 and 3U01
HD052104-06S1 from the Tulane University School of Medicine (PI, Russell
B. Van Dyke, MD; co-PI, Kenneth Rich, MD; project director, Patrick
Davis, BS). Dr Richman was supported by grant U19 AI096113 from the
Collaboratory for AIDS Research on Eradication (CARE), grant AI306214
from the University of California, San Diego, Center for AIDS Research,
and the James Pendleton Charitable Trust. Data management services were
provided by Frontier Science and Technology Research Foundation (PI,
Suzanne Siminski, MS, MBA), and regulatory services and logistical
support were provided byWestat, Inc (PI, Julie Davidson, MSN).
NR 39
TC 17
Z9 17
U1 1
U2 5
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD DEC
PY 2014
VL 168
IS 12
BP 1138
EP 1146
DI 10.1001/jamapediatrics.2014.1560
PG 9
WC Pediatrics
SC Pediatrics
GA AU9GO
UT WOS:000345900000012
PM 25286283
ER
PT J
AU Vanicek, T
Spies, M
Rami-Mark, C
Savli, M
Hoflich, A
Kranz, GS
Hahn, A
Kutzelnigg, A
Traub-Weidinger, T
Mitterhauser, M
Wadsak, W
Hacker, M
Volkow, ND
Kasper, S
Lanzenberger, R
AF Vanicek, Thomas
Spies, Marie
Rami-Mark, Christina
Savli, Markus
Hoeflich, Anna
Kranz, Georg S.
Hahn, Andreas
Kutzelnigg, Alexandra
Traub-Weidinger, Tatjana
Mitterhauser, Markus
Wadsak, Wolfgang
Hacker, Marcus
Volkow, Nora D.
Kasper, Siegfried
Lanzenberger, Rupert
TI The Norepinephrine Transporter in Attention-Deficit/Hyperactivity
Disorder Investigated With Positron Emission Tomography
SO JAMA PSYCHIATRY
LA English
DT Article
ID DEFICIT-HYPERACTIVITY DISORDER; NONHUMAN PRIMATE BRAIN; DOPAMINE
TRANSPORTER; EXTRACELLULAR DOPAMINE; PREFRONTAL CORTEX; IN-VIVO; ORAL
METHYLPHENIDATE; LOCUS-COERULEUS; NAIVE ADULTS; PET
AB IMPORTANCE Attention-deficit/hyperactivity disorder (ADHD) research has long focused on the dopaminergic system's contribution to pathogenesis, although the results have been inconclusive. However, a case has been made for the involvement of the noradrenergic system, which modulates cognitive processes, such as arousal, working memory, and response inhibition, all of which are typically affected in ADHD. Furthermore, the norepinephrine transporter (NET) is an important target for frequently prescribed medication in ADHD. Therefore, the NET is suggested to play a critical role in ADHD.
OBJECTIVE To explore the differences in NET nondisplaceable binding potential (NET BPND) using positron emission tomography and the highly selective radioligand (S,S)-[F-18]FMeNER-D-2 [(S,S)-2-(alpha-(2-[F-18]fluoro[H-2(2)]methoxyphenoxy)benzyl)morpholine] between adults with ADHD and healthy volunteers serving as controls.
DESIGN, SETTING, AND PARTICIPANTS Twenty-two medication-free patients with ADHD (mean [SD] age, 30.7[10.4] years; 15[68%] men) without psychiatric comorbidities and 22 age-and sex-matched healthy controls (30.9[10.6] years; 15[68%] men) underwent positron emission tomography once. A linear mixed model was used to compare NET BPND between groups.
MAIN OUTCOMES AND MEASURES The NET BPND in selected regions of interest relevant for ADHD, including the hippocampus, putamen, pallidum, thalamus, midbrain with pons (comprising a region of interest that includes the locus coeruleus), and cerebellum. In addition, the NET BPND was evaluated in thalamic subnuclei (13 atlas-based regions of interest).
RESULTS We found no significant differences in NET availability or regional distribution between patients with ADHD and healthy controls in all investigated brain regions (F-1,F-41 < 0.01; P = .96). Furthermore, we identified no significant association between ADHD symptom severity and regional NET availability. Neither sex nor smoking status influenced NET availability. We determined a significant negative correlation between age and NET availability in the thalamus (R-2 = 0.29; P < .01 corrected) and midbrain with pons, including the locus coeruleus (R-2 = 0.18; P < .01 corrected), which corroborates prior findings of a decrease in NET availability with aging in the human brain.
CONCLUSIONS AND RELEVANCE Our results do not indicate involvement of changes in brain NET availability or distribution in the pathogenesis of ADHD. However, the noradrenergic transmitter system may be affected on a different level, such as in cortical regions, which cannot be reliably quantified with this positron emission tomography ligand. Alternatively, different key proteins of noradrenergic neurotransmission might be affected.
C1 [Vanicek, Thomas; Spies, Marie; Savli, Markus; Hoeflich, Anna; Kranz, Georg S.; Hahn, Andreas; Kutzelnigg, Alexandra; Kasper, Siegfried; Lanzenberger, Rupert] Med Univ Vienna, Dept Psychiat & Psychotherapy, A-1090 Vienna, Austria.
[Rami-Mark, Christina; Traub-Weidinger, Tatjana; Mitterhauser, Markus; Wadsak, Wolfgang; Hacker, Marcus] Med Univ Vienna, Dept Biomed Imaging & Image Guided Therapy, Div Nucl Med, A-1090 Vienna, Austria.
[Volkow, Nora D.] NIAAA, NIH, Bethesda, MD USA.
RP Lanzenberger, R (reprint author), Med Univ Vienna, Dept Psychiat & Psychotherapy, Funct Mol & Translat Neuroimaging Lab, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
EM rupert.lanzenberger@meduniwien.ac.at
OI Hahn, Andreas/0000-0001-9727-7580
FU Austrian Science Fund (FWF) [P22981]
FX This research was supported by grant P22981 from the Austrian Science
Fund (FWF) (Dr Lanzenberger).
NR 76
TC 10
Z9 10
U1 5
U2 13
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-622X
EI 2168-6238
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD DEC
PY 2014
VL 71
IS 12
BP 1340
EP 1349
DI 10.1001/jamapsychiatry.2014.1226
PG 10
WC Psychiatry
SC Psychiatry
GA AU9MQ
UT WOS:000345917900006
PM 25338091
ER
PT J
AU Correll, CU
Robinson, DG
Schooler, NR
Brunette, MF
Mueser, KT
Rosenheck, RA
Marcy, P
Addington, J
Estroff, SE
Robinson, J
Penn, DL
Azrin, S
Goldstein, A
Severe, J
Heinssen, R
Kane, JM
AF Correll, Christoph U.
Robinson, Delbert G.
Schooler, Nina R.
Brunette, Mary F.
Mueser, Kim T.
Rosenheck, Robert A.
Marcy, Patricia
Addington, Jean
Estroff, Sue E.
Robinson, James
Penn, David L.
Azrin, Susan
Goldstein, Amy
Severe, Joanne
Heinssen, Robert
Kane, John M.
TI Cardiometabolic Risk in Patients With First-Episode Schizophrenia
Spectrum Disorders Baseline Results From the RAISE-ETP Study
SO JAMA PSYCHIATRY
LA English
DT Article
ID NUTRITION EXAMINATION SURVEY; 3RD NATIONAL-HEALTH; DENSITY-LIPOPROTEIN
CHOLESTEROL; RANDOMIZED CLINICAL-TRIAL; FASTING PLASMA-GLUCOSE;
UNITED-STATES; METABOLIC SYNDROME; MENTAL-ILLNESS; ANTIPSYCHOTIC-DRUGS;
SCHIZOAFFECTIVE DISORDER
AB IMPORTANCE The fact that individuals with schizophrenia have high cardiovascular morbidity and mortality is well established. However, risk status and moderators or mediators in the earliest stages of illness are less clear. OBJECTIVE To assess cardiometabolic risk in first-episode schizophrenia spectrum disorders (FES) and its relationship to illness duration, antipsychotic treatment duration and type, sex, and race/ethnicity.
DESIGN, SETTING, AND PARTICIPANTS Baseline results of the Recovery After an Initial Schizophrenia Episode (RAISE) study, collected between July 22, 2010, and July 5, 2012, from 34 community mental health facilities without major research, teaching, or clinical FES programs. Patients were aged 15 to 40 years, had research-confirmed diagnoses of FES, and had less than 6 months of lifetime antipsychotic treatment.
EXPOSURE Prebaseline antipsychotic treatment was based on the community clinician's and/or patient's decision.
MAIN OUTCOMES AND MEASURES Body composition and fasting lipid, glucose, and insulin parameters.
RESULTS In 394 of 404 patients with cardiometabolic data (mean [SD] age, 23.6 [5.0] years; mean [SD] lifetime antipsychotic treatment, 47.3 [46.1] days), 48.3% were obese or overweight, 50.8% smoked, 56.5% had dyslipidemia, 39.9% had prehypertension, 10.0% had hypertension, and 13.2% had metabolic syndrome. Prediabetes (glucose based, 4.0%; hemoglobin A(1c) based, 15.4%) and diabetes (glucose based, 3.0%; hemoglobin A1c based, 2.9%) were less frequent. Total psychiatric illness duration correlated significantly with higher body mass index, fat mass, fat percentage, and waist circumference (all P < .01) but not elevated metabolic parameters (except triglycerides to HDL-C ratio [P = .04]). Conversely, antipsychotic treatment duration correlated significantly with higher non-HDL-C, triglycerides, and triglycerides to HDL-C ratio and lower HDL-C and systolic blood pressure (all P <= .01). Olanzapine was significantly associated with higher triglycerides, insulin, and insulin resistance, whereas quetiapine fumarate was associated with significantly higher triglycerides to HDL-C ratio (all P <= .02).
CONCLUSIONS AND RELEVANCE In patients with FES, cardiometabolic risk factors and abnormalities are present early in the illness and likely related to the underlying illness, unhealthy lifestyle, and antipsychotic medications, which interact with each other. Prevention of and early interventions for psychiatric illness and treatment with lower-risk agents, routine antipsychotic adverse effect monitoring, and smoking cessation interventions are needed from the earliest illness phases.
C1 [Correll, Christoph U.; Robinson, Delbert G.; Schooler, Nina R.; Marcy, Patricia; Kane, John M.] Zucker Hillside Hosp, North Shore LIJ Hlth Syst, Div Psychiat Res, Glen Oaks, NY 11004 USA.
[Correll, Christoph U.; Robinson, Delbert G.; Marcy, Patricia; Kane, John M.] Feinstein Inst Med Res, Manhasset, NY USA.
[Correll, Christoph U.; Robinson, Delbert G.; Robinson, James; Kane, John M.] Hofstra North Shore LIJ Sch Med, Hempstead, NY USA.
[Correll, Christoph U.; Robinson, Delbert G.; Kane, John M.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Schooler, Nina R.] Suny Downstate Med Ctr, New York, NY USA.
[Brunette, Mary F.] Geisel Sch Med Dartmouth, Hanover, NH USA.
[Brunette, Mary F.] Dept Hlth & Human Serv, Bur Behav Hlth, Hanover, NH USA.
[Mueser, Kim T.] Boston Univ, Ctr Psychiat Rehabil, Dept Occupat Therapy, Boston, MA 02215 USA.
[Mueser, Kim T.] Boston Univ, Ctr Psychiat Rehabil, Dept Psychiat, Boston, MA 02215 USA.
[Mueser, Kim T.] Boston Univ, Ctr Psychiat Rehabil, Dept Psychol, Boston, MA 02215 USA.
[Rosenheck, Robert A.] Yale Univ, Dept Psychiat & Epidemiol, Princeton, NJ USA.
[Rosenheck, Robert A.] Yale Univ, Dept Publ Hlth, Princeton, NJ USA.
[Addington, Jean] Univ Calgary, Hotchkiss Brain Inst, Dept Psychiat, Calgary, AB, Canada.
[Estroff, Sue E.] Univ N Carolina, Dept Social Med, Chapel Hill, NC USA.
[Robinson, James] Nathan S Kline Inst Psychiat Res, Orangeburg, NY USA.
[Penn, David L.] Univ N Carolina, Dept Psychol, Chapel Hill, NC USA.
[Azrin, Susan; Goldstein, Amy; Severe, Joanne; Heinssen, Robert] NIMH, Bethesda, MD 20892 USA.
RP Correll, CU (reprint author), Zucker Hillside Hosp, North Shore LIJ Hlth Syst, Div Psychiat Res, 75-59 263rd St, Glen Oaks, NY 11004 USA.
EM ccorrell@lij.edu
FU National Institute of Mental Health [HHSN-271-2009-00019C]; American
Recovery and Reinvestment Act
FX This work was supported in part by grant HHSN-271-2009-00019C from the
National Institute of Mental Health (Dr Kane) and by federal funds from
the American Recovery and Reinvestment Act.
NR 79
TC 71
Z9 73
U1 7
U2 22
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 2168-622X
EI 2168-6238
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD DEC
PY 2014
VL 71
IS 12
BP 1350
EP 1363
DI 10.1001/jamapsychiatry.2014.1314
PG 14
WC Psychiatry
SC Psychiatry
GA AU9MQ
UT WOS:000345917900007
PM 25321337
ER
PT J
AU Duverger, O
Ohara, T
Shaffer, JR
Donahue, D
Zerfas, P
Dullnig, A
Crecelius, C
Beniash, E
Marazita, ML
Morasso, MI
AF Duverger, Olivier
Ohara, Takahiro
Shaffer, John R.
Donahue, Danielle
Zerfas, Patricia
Dullnig, Andrew
Crecelius, Christopher
Beniash, Elia
Marazita, Mary L.
Morasso, Maria I.
TI Hair keratin mutations in tooth enamel increase dental decay risk
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID TUFT PROTEIN; CARIES; MATRIX; MORPHOGENESIS; DETERMINANTS; DISORDER;
TEETH; K6HF
AB Tooth enamel is the hardest substance in the human body and has a unique combination of hardness and fracture toughness that protects teeth from dental caries, the most common chronic disease worldwide. In addition to a high mineral content, tooth enamel comprises organic material that is important for mechanical performance and influences the initiation and progression of caries; however, the protein composition of tooth enamel has not been fully characterized. Here, we determined that epithelial hair keratins, which are crucial for maintaining the integrity of the sheaths that support the hair shaft, are expressed in the enamel organ and are essential organic components of mature enamel. Using genetic and intraoral examination data from 386 children and 706 adults, we found that individuals harboring known hair disorder-associated polymorphisms in the gene encoding keratin 75 (KRT75), KRT75(A161T) and KRT75(E337K), are prone to increased dental caries. Analysis of teeth from individuals carrying the KRT75(A161T) variant revealed an altered enamel structure and a marked reduction of enamel hardness, suggesting that a functional keratin network is required for the mechanical stability of tooth enamel. Taken together, our results identify a genetic locus that influences enamel structure and establish a connection between hair disorders and susceptibility to dental caries.
C1 [Duverger, Olivier; Ohara, Takahiro; Morasso, Maria I.] NIAMSD, Skin Biol Lab, NIAMS, NIH, Bethesda, MD USA.
[Shaffer, John R.; Marazita, Mary L.] Univ Pittsburgh, Dept Human Genet, Pittsburgh, PA USA.
[Donahue, Danielle] NINDS, Mouse Imaging Facil, NIH, Bethesda, MD 20892 USA.
[Zerfas, Patricia] NIH, Off Res Serv, Div Vet Resources, Bethesda, MD 20892 USA.
[Dullnig, Andrew; Crecelius, Christopher] Walter Reed Natl Mil Med Ctr, Natl Capital Consortium Oral & Maxillofacial Surg, Bethesda, MD USA.
[Beniash, Elia; Marazita, Mary L.] Univ Pittsburgh, Dept Oral Biol, Pittsburgh, PA USA.
[Beniash, Elia] Univ Pittsburgh, Ctr Craniofacial Regenerat, Pittsburgh, PA USA.
[Marazita, Mary L.] Univ Pittsburgh, Ctr Craniofacial & Dent Genet, Pittsburgh, PA USA.
[Marazita, Mary L.] Univ Pittsburgh, Clin & Translat Sci Inst, Pittsburgh, PA USA.
RP Morasso, MI (reprint author), Skin Biol Lab, 50 South Dr,Room 1523, Bethesda, MD 20892 USA.
EM morasso@nih.gov
FU Intramural Research Program of NIAMS [ZIA AR041171-07]; National
Institute of Dental and Craniofacial Research [R01-DE014899,
U01-DE018903, R56-DE016703]
FX This work was supported by the Intramural Research Program of NIAMS (ZIA
AR041171-07 to M.I. Morasso) and by grants from the National Institute
of Dental and Craniofacial Research (R01-DE014899 and U01-DE018903 to
M.L. Marazita and R56-DE016703 to E. Beniash). We thank Paul Bible,
Meghan Kellett, Julie Erthal, and Juliane Lessard from the Laboratory of
Skin Biology. We thank members of NIAMS: Martha Somerman, Leon Nesti,
Gustavo Gutierrez-Cruz, Hong-Wei Sun, and the Light Imaging Facility. We
thank Glen Imamura and the residents at the Walter Reed National
Military Medical Center; Yang Xu, Toshiki Soejima, and Robert J. Weyant
from the University of Pittsburgh; Daniel W. McNeil and Richard Crout
from West Virginia University; Jiang Chen and Dennis Roop from the
University of Colorado Denver. We would like to express our gratitude to
the COHRA participants and field research teams whose contributions made
this work possible.
NR 32
TC 5
Z9 5
U1 1
U2 22
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2014
VL 124
IS 12
BP 5219
EP 5224
DI 10.1172/JCI78272
PG 6
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AU5XP
UT WOS:000345677200015
PM 25347471
ER
PT J
AU Chang, J
Lee, S
Blackstone, C
AF Chang, Jaerak
Lee, Seongju
Blackstone, Craig
TI Spastic paraplegia proteins spastizin and spatacsin mediate autophagic
lysosome reformation
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID NEURODEGENERATIVE DISEASE; SPG11; LOCALIZATION; CYTOKINESIS; BIOGENESIS;
MECHANISM; ENDOSOME; MTOR; MICE
AB Autophagy allows cells to adapt to changes in their environment by coordinating the degradation and recycling of cellular components and organelles to maintain homeostasis. Lysosomes are organelles critical for terminating autophagy via their fusion with mature autophagosomes to generate autolysosomes that degrade autophagic materials; therefore, maintenance of the lysosomal population is essential for autophagy-dependent cellular clearance. Here, we have demonstrated that the two most common autosomal recessive hereditary spastic paraplegia gene products, the SPG15 protein spastizin and the SPG11 protein spatacsin, are pivotal for autophagic lysosome reformation (ALR), a pathway that generates new lysosomes. Lysosomal targeting of spastizin required an intact FYVE domain, which binds phosphatidylinositol 3-phosphate. Loss of spastizin or spatacsin resulted in depletion of free lysosomes, which are competent to fuse with autophagosomes, and an accumulation of autolysosomes, reflecting a failure in ALR. Moreover, spastizin and spatacsin were essential components for the initiation of lysosomal tubulation. Together, these results link dysfunction of the autophagy/lysosomal biogenesis machinery to neurodegeneration.
C1 [Chang, Jaerak; Lee, Seongju; Blackstone, Craig] NINDS, Cell Biol Sect, Neurogenet Branch, NIH, Bethesda, MD 20892 USA.
RP Blackstone, C (reprint author), NINDS, Neurogenet Branch, NIH Bldg 35,Room 2C-913,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM blackstc@ninds.nih.gov
FU Intramural Research Program of the National Institute of Neurological
Disorders and Stroke, NIH
FX This work was supported by the Intramural Research Program of the
National Institute of Neurological Disorders and Stroke, NIH.
NR 41
TC 26
Z9 26
U1 0
U2 8
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2014
VL 124
IS 12
BP 5249
EP 5262
DI 10.1172/JCI77598
PG 14
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AU5XP
UT WOS:000345677200018
PM 25365221
ER
PT J
AU Sungalee, S
Mamessier, E
Morgado, E
Gregoire, E
Brohawn, PZ
Morehouse, CA
Jouve, N
Monvoisin, C
Menard, C
Debroas, G
Faroudi, M
Mechin, V
Navarro, JM
Drevet, C
Eberle, FC
Chasson, L
Baudimont, F
Mancini, SJ
Tellier, J
Picquenot, JM
Kelly, R
Vineis, P
Ruminy, P
Chetaille, B
Jaffe, ES
Schiff, C
Hardwigsen, J
Tice, DA
Higgs, BW
Tarte, K
Nadel, B
Roulland, S
AF Sungalee, Stephanie
Mamessier, Emilie
Morgado, Ester
Gregoire, Emilie
Brohawn, Philip Z.
Morehouse, Christopher A.
Jouve, Nathalie
Monvoisin, Celine
Menard, Cedric
Debroas, Guilhaume
Faroudi, Mustapha
Mechin, Violaine
Navarro, Jean-Marc
Drevet, Charlotte
Eberle, Franziska C.
Chasson, Lionel
Baudimont, Fannie
Mancini, Stephane J.
Tellier, Julie
Picquenot, Jean-Michel
Kelly, Rachel
Vineis, Paolo
Ruminy, Philippe
Chetaille, Bruno
Jaffe, Elaine S.
Schiff, Claudine
Hardwigsen, Jean
Tice, David A.
Higgs, Brandon W.
Tarte, Karin
Nadel, Bertrand
Roulland, Sandrine
TI Germinal center reentries of BCL2-overexpressing B cells drive
follicular lymphoma progression
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Article
ID CLASS SWITCH RECOMBINATION; HEALTHY-INDIVIDUALS; T(14/18) TRANSLOCATION;
IN-SITU; MEMORY; STEP; TRANSFORMATION; HYPERMUTATION; PATHOGENESIS;
ACTIVATION
AB It has recently been demonstrated that memory B cells can reenter and reengage germinal center (GC) reactions, opening the possibility that multi-hit lymphomagenesis gradually occurs throughout life during successive immunological challenges. Here, we investigated this scenario in follicular lymphoma (FL), an indolent GC-derived malignancy. We developed a mouse model that recapitulates the FL hallmark t(14;18) translocation, which results in constitutive activation of antiapoptotic protein B cell lymphoma 2 (BCL2) in a subset of B cells, and applied a combination of molecular and immunofluorescence approaches to track normal and t(14;18)(+) memory B cells in human and BCL2-overexpressing B cells in murine lymphoid tissues. BCL2-overexpressing B cells required multiple GC transits before acquiring FL-associated developmental arrest and presenting as GCB cells with constitutive activation-induced cytidine deaminase (AID) mutator activity. Moreover, multiple reentries into the GC were necessary for the progression to advanced precursor stages of FL. Together, our results demonstrate that protracted subversion of immune dynamics contributes to early dissemination and progression of t(14;18)(+) precursors and shapes the systemic presentation of FL patients.
C1 [Sungalee, Stephanie; Mamessier, Emilie; Morgado, Ester; Jouve, Nathalie; Debroas, Guilhaume; Faroudi, Mustapha; Mechin, Violaine; Navarro, Jean-Marc; Drevet, Charlotte; Chasson, Lionel; Baudimont, Fannie; Mancini, Stephane J.; Tellier, Julie; Schiff, Claudine; Nadel, Bertrand; Roulland, Sandrine] Aix Marseille Univ, Ctr Immunol Marseille Luminy, F-13288 Marseille 9, France.
[Sungalee, Stephanie; Mamessier, Emilie; Morgado, Ester; Jouve, Nathalie; Debroas, Guilhaume; Faroudi, Mustapha; Mechin, Violaine; Navarro, Jean-Marc; Drevet, Charlotte; Chasson, Lionel; Baudimont, Fannie; Mancini, Stephane J.; Tellier, Julie; Schiff, Claudine; Nadel, Bertrand; Roulland, Sandrine] INSERM, U1104, F-13258 Marseille, France.
[Sungalee, Stephanie; Mamessier, Emilie; Morgado, Ester; Jouve, Nathalie; Debroas, Guilhaume; Faroudi, Mustapha; Mechin, Violaine; Navarro, Jean-Marc; Drevet, Charlotte; Chasson, Lionel; Baudimont, Fannie; Mancini, Stephane J.; Tellier, Julie; Schiff, Claudine; Nadel, Bertrand; Roulland, Sandrine] CNRS, UMR7280, Marseille, France.
[Gregoire, Emilie; Hardwigsen, Jean] Hop Conception, AP HM, Dept Surg & Liver Transplantat, Marseille, France.
[Brohawn, Philip Z.; Morehouse, Christopher A.; Tice, David A.; Higgs, Brandon W.] MedImmune, Translat Sci, Gaithersburg, MD USA.
[Monvoisin, Celine; Menard, Cedric; Tarte, Karin] Univ Rennes 1, EFS Bretagne, INSERM U917, Rennes, France.
[Eberle, Franziska C.; Jaffe, Elaine S.] NCI, Hematopathol Sect, Pathol Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Picquenot, Jean-Michel; Ruminy, Philippe] Ctr Henri Becquerel, Dept Pathol, INSERM U918, F-76038 Rouen, France.
[Kelly, Rachel; Vineis, Paolo] Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, MRC HPA Ctr Environm & Hlth, London, England.
[Chetaille, Bruno] Inst J Paoli I Calmettes, Dept Pathol, F-13009 Marseille, France.
RP Roulland, S (reprint author), Aix Marseille Univ, Ctr Immunol Marseille Luminy, F-13288 Marseille 9, France.
EM nadel@ciml.univ-mrs.fr; roulland@ciml.univ-mrs.fr
RI Jaffe, Elaine/G-8984-2014; Nadel, Bertrand/J-2197-2014; Mancini,
Stephane/R-4109-2016; jouve, nathalie/D-5098-2017;
OI Jaffe, Elaine/0000-0003-4632-0301; Mancini,
Stephane/0000-0001-9255-4606; Sungalee, Stephanie/0000-0001-5633-8826
FU Institut National du Cancer (INCa); Association pour la Recherche sur le
Cancer (ARC); MedImmune Strategic Collaboration to Fund; Conduct Medical
Science Research program; INSERM; CNRS; French Ministry of Research
(MRT); Fondation pour la Recherche Medicale (FRM)
FX This work was funded by grants from the Institut National du Cancer
(INCa); the Association pour la Recherche sur le Cancer (ARC); the
MedImmune Strategic Collaboration to Fund and Conduct Medical Science
Research program; INSERM; and CNRS. S. Sungalee was supported by a
fellowship from the French Ministry of Research (MRT) and the Fondation
pour la Recherche Medicale (FRM). We thank B. Malissen for providing the
LatY136F mice. We thank A. Anginot for help with mice
immunization and analysis and R. Fara, A. Camerlot, and D. Novero for
providing paired organ donor samples. We thank M. Bajenoff, M. Cogne,
and B. Reina-San-Martin for critical reading of the manuscript and C.J.
van Noesel for helpful discussions.
NR 43
TC 15
Z9 15
U1 1
U2 16
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD DEC
PY 2014
VL 124
IS 12
BP 5337
EP 5351
DI 10.1172/JCI72415
PG 15
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA AU5XP
UT WOS:000345677200025
PM 25384217
ER
PT J
AU Blanch-Hartigan, D
Nekhlyudov, L
Smith, T
Alfano, CM
Rowland, JH
Forsythe, LP
Ganz, PA
AF Blanch-Hartigan, Danielle
Nekhlyudov, Larissa
Smith, Tenbroeck
Alfano, Catherine M.
Rowland, Julia H.
Forsythe, Laura P.
Ganz, Patricia A.
TI Survivorship Care Plans: A Change of Perspective or a Failure Reply
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Letter
ID CANCER SURVIVORS
C1 [Blanch-Hartigan, Danielle] Bentley Univ, Waltham, MA 02452 USA.
[Nekhlyudov, Larissa] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Nekhlyudov, Larissa] Harvard Vanguard Med Associates, Boston, MA 02115 USA.
[Smith, Tenbroeck] Amer Canc Soc, Atlanta, GA 30329 USA.
[Alfano, Catherine M.; Rowland, Julia H.] Natl Canc Inst, Bethesda, MD USA.
[Forsythe, Laura P.] Patient Centered Outcomes Res Inst, Washington, DC USA.
[Ganz, Patricia A.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90024 USA.
RP Blanch-Hartigan, D (reprint author), Bentley Univ, Waltham, MA 02452 USA.
FU PHS HHS [HHSN261200700068C]
NR 10
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
EI 1527-7755
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD DEC 1
PY 2014
VL 32
IS 34
BP 3905
EP 3906
DI 10.1200/JCO.2014.58.1348
PG 2
WC Oncology
SC Oncology
GA AU9ID
UT WOS:000345904300025
PM 25245438
ER
PT J
AU Schuster, DM
Nanni, C
Fanti, S
Oka, S
Okudaira, H
Inoue, Y
Sorensen, J
Owenius, R
Choyke, P
Turkbey, B
Bogsrud, TV
Bach-Gansmo, T
Halkar, RK
Nye, JA
Odewole, OA
Savir-Baruch, B
Goodman, MM
AF Schuster, David M.
Nanni, Cristina
Fanti, Stefano
Oka, Shuntaro
Okudaira, Hiroyuki
Inoue, Yusuke
Sorensen, Jens
Owenius, Rikard
Choyke, Peter
Turkbey, Baris
Bogsrud, Trond V.
Bach-Gansmo, Tore
Halkar, Raghuveer K.
Nye, Jonathon A.
Odewole, Oluwaseun A.
Savir-Baruch, Bital
Goodman, Mark M.
TI Anti-1-Amino-3-F-18-Fluorocyclobutane-1-Carboxylic Acid: Physiologic
Uptake Patterns, Incidental Findings, and Variants That May Simulate
Disease
SO JOURNAL OF NUCLEAR MEDICINE
LA English
DT Article
DE F-18-FACBC; physiologic uptake; positron emission tomography
ID RECURRENT PROSTATE CARCINOMA; RADIOLABELED AMINO-ACIDS; TRANSPORT
MECHANISMS; RADIATION-DOSIMETRY; CANCER; PET/CT; BIODISTRIBUTION;
RADIOTRACER; AGENT; CELLS
AB Anti-1-amino-3-F-18-fluorocyclobutane-1-carboxylic acid (F-18-FACBC) is a synthetic amino acid analog PET radiotracer undergoing clinical trials for the evaluation of prostate and other cancers. We aimed to describe common physiologic uptake patterns, incidental findings, and variants in patients who had undergone F-18-FACBC PET. Methods: Sixteen clinical trials involving 611 F-18-FACBC studies from 6 centers, which included dosimetry studies on 12 healthy volunteers, were reviewed. Qualitative observations of common physiologic patterns, incidental uptake, and variants that could simulate disease were recorded and compared with similar observations in studies of the healthy volunteers. Quantitative analysis of select data and review of prior published reports and observations were also made. Results: The liver and pancreas demonstrated the most intense uptake. Moderate salivary and pituitary uptake and variable mild to moderate bowel activity were commonly visualized. Moderate bone marrow and mild muscle activity were present on early images, with marrow activity decreasing and muscle activity increasing with time. Brain and lungs demonstrated activity less than blood pool. Though F-18-FACBC exhibited little renal excretion or bladder uptake during the clinically useful early imaging time window, mild to moderate activity might accumulate in the bladder and interfere with evaluation of adjacent prostate bed and seminal vesicles in 5%-10% of patients. Uptake might also occur from benign processes such as infection, inflammation, prostatic hyperplasia, and metabolically active benign bone lesions such as osteoid osteoma. Conclusion: Common physiologic uptake patterns were similar to those noted in healthy volunteers. The activity in organs followed the presence of amino acid transport and metabolism described with other amino acid-based PET radiotracers. As with other PET radiotracers such as F-18-FDG, focal nonphysiologic uptake may represent incidental malignancy. Uptake due to benign etiologies distinct from physiologic background also occurred and could lead to misinterpretations if the reader is unaware of them.
C1 [Schuster, David M.; Halkar, Raghuveer K.; Nye, Jonathon A.; Odewole, Oluwaseun A.; Savir-Baruch, Bital; Goodman, Mark M.] Emory Univ Hosp, Dept Radiol & Imaging Sci, Atlanta, GA 30322 USA.
[Nanni, Cristina; Fanti, Stefano] Univ Bologna, Dept Nucl Med, Policlin S Orsola, Bologna, Italy.
[Oka, Shuntaro; Okudaira, Hiroyuki] Nihon Mediphys Co Ltd, Res Ctr, Chiba, Japan.
[Inoue, Yusuke] Kitasato Univ, Dept Diagnost Radiol, Sch Med, Kitasato, Japan.
[Sorensen, Jens] Uppsala Univ, Dept Radiol Oncol & Radiat Sci, Uppsala, Sweden.
[Owenius, Rikard] GE Healthcare, Imaging R&D, Uppsala, Sweden.
[Choyke, Peter; Turkbey, Baris] NCI, Mol Imaging Program, Bethesda, MD 20892 USA.
[Bogsrud, Trond V.; Bach-Gansmo, Tore] Oslo Univ Hosp, Dept Radiol & Nucl Med, Oslo, Norway.
[Bogsrud, Trond V.] Aarhus Univ Hosp, Dept Nucl Med, DK-8000 Aarhus, Denmark.
[Bogsrud, Trond V.] Aarhus Univ Hosp, PET Ctr, DK-8000 Aarhus, Denmark.
RP Schuster, DM (reprint author), Emory Univ Hosp, Div Nucl Med & Mol Imaging, Dept Radiol & Imaging Sci, Room E152,1364 Clifton Rd, Atlanta, GA 30322 USA.
EM dschust@emory.edu
RI Schuster, David/D-6156-2011
OI Schuster, David/0000-0003-3077-742X
FU National Institutes of Health [5R01CA129356, P50 CA 128301]; Society of
Nuclear Medicine and Molecular Imaging Research and Education
Foundation; Nihon Medi-Physics Co., Ltd.; GE Healthcare; Blue Earth
Diagnostics Limited; Glenn Family Breast Center Award, Winship Cancer
Institute of Emory University; Programma di Ricerca Regione (Emilia
Romagna)-Universita, Bando Giovani Ricercatori; Georgia Cancer Coalition
FX The costs of publication of this article were defrayed in part by the
payment of page charges. Therefore, and solely to indicate this fact,
this article is hereby marked "advertisement" in accordance with 18 USC
section 1734. Support was provided by the National Institutes of Health
(5R01CA129356 and P50 CA 128301); Society of Nuclear Medicine and
Molecular Imaging Research and Education Foundation; Nihon Medi-Physics
Co., Ltd.; GE Healthcare; Blue Earth Diagnostics Limited; Glenn Family
Breast Center Award, Winship Cancer Institute of Emory University;
Georgia Cancer Coalition; and Programma di Ricerca Regione (Emilia
Romagna)-Universita 2010-2012, Bando Giovani Ricercatori. Emory
University and Dr. Mark Goodman are eligible to receive royalties for
18F-FACBC. Dr. Schuster participates in sponsored research
involving 18F-FACBC and other radiotracers. No other
potential conflict of interest relevant to this article was reported.
NR 36
TC 11
Z9 11
U1 1
U2 5
PU SOC NUCLEAR MEDICINE INC
PI RESTON
PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA
SN 0161-5505
EI 1535-5667
J9 J NUCL MED
JI J. Nucl. Med.
PD DEC
PY 2014
VL 55
IS 12
BP 1986
EP 1992
DI 10.2967/jnumed.114.143628
PG 7
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA AU8EC
UT WOS:000345828300015
PM 25453047
ER
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