FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Wilson, WH
O'Connor, OA
Czuczman, MS
LaCasce, A
Gerecitano, J
Leonard, JP
Tulpule, A
Xiong, H
Chiu, YL
Busman, T
Enschede, S
Krivoshik, A
Humerickhouse, R
AF Wilson, Wyndham H.
O'Connor, Owen A.
Czuczman, Myron S.
LaCasce, Ann
Gerecitano, John
Leonard, John P.
Tulpule, Anil
Xiong, Hao
Chiu, Yi-Lin
Busman, Todd
Enschede, Sari
Krivoshik, Andrew
Humerickhouse, Rod
TI Phase 1/2a Study of ABT-263 in Relapsed or Refractory Lymphoid
Malignancies.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Wilson, Wyndham H.] NCI, CCR, NIH, Bethesda, MD 20892 USA.
[O'Connor, Owen A.] NYU, Langone Med Ctr, Inst Canc, New York, NY USA.
[Czuczman, Myron S.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[LaCasce, Ann] Dana Farber Canc Inst, Boston, MA 02115 USA.
[Gerecitano, John] Mem Sloan Kettering Canc Ctr, Lymphoma Serv, New York, NY 10021 USA.
[Leonard, John P.] Weill Cornell Med Coll, New York, NY USA.
[Tulpule, Anil] USC, Sch Med, Norris Canc Ctr, Los Angeles, CA USA.
[Xiong, Hao; Chiu, Yi-Lin; Busman, Todd; Enschede, Sari; Krivoshik, Andrew; Humerickhouse, Rod] Abbott Labs, Abbott Pk, IL 60064 USA.
NR 0
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 682
EP 682
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802079
ER
PT J
AU Katzmann, J
Clark, R
Dispenzieri, A
Kyle, R
Landgren, O
Bradwell, A
Rajkumar, SV
AF Katzmann, Jerry
Clark, Raynell
Dispenzieri, Angela
Kyle, Robert
Landgren, Ola
Bradwell, Arthur
Rajkumar, S. Vincent
TI Isotype-Specific Heavy/Light Chain (HLC) Suppression as a Predictor of
Myeloma Development in Monoclonal Gammopathy of Undetermined
Significance (MGUS).
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Katzmann, Jerry; Clark, Raynell; Dispenzieri, Angela; Kyle, Robert; Rajkumar, S. Vincent] Mayo Clin, Rochester, MN USA.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Bradwell, Arthur] Univ Birmingham, Sch Med, Dept Immunol, Birmingham B15 2TT, W Midlands, England.
NR 0
TC 1
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 711
EP 711
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802156
ER
PT J
AU Landgren, O
Devesa, S
Mink, P
Anderson, WF
Weiss, B
Kristinsson, SY
McGlynn, K
AF Landgren, Ola
Devesa, Susan
Mink, Pamela
Anderson, William F.
Weiss, Brendan
Kristinsson, Sigurdur Y.
McGlynn, Katherine
TI African-American Multiple Myeloma Patients Have a Better Survival Than
Caucasian Patients: a Population-Based Study Including 28,636 Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Devesa, Susan; Anderson, William F.; McGlynn, Katherine] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Mink, Pamela] Emory Univ, Atlanta, GA 30322 USA.
[Weiss, Brendan] Walter Reed Army Med Ctr, Washington, DC 20307 USA.
[Kristinsson, Sigurdur Y.] Karolinska Univ Hosp & Inst, Div Hematol, Dept Med, Stockholm, Sweden.
RI Kristinsson, Sigurdur /M-2910-2015
OI Kristinsson, Sigurdur /0000-0002-4964-7476
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 727
EP 727
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802200
ER
PT J
AU Kristinsson, SY
Pfeiffer, R
Bjorkhohm, M
Goldin, LR
Schulman, S
Blimark, C
Mellqvist, UH
Wahlin, A
Turesson, I
Landgren, O
AF Kristinsson, Sigurdur Y.
Pfeiffer, Ruth
Bjorkhohm, Magnus
Goldin, Lynn R.
Schulman, Sam
Blimark, Cecilie
Mellqvist, Ulf-Henrik
Wahlin, Anders
Turesson, Ingemar
Landgren, Ola
TI Arterial and Venous Thrombosis in Monoclonal Gammopathy of Undetermined
Significance and Multiple Myeloma: A Population-Based Study
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Kristinsson, Sigurdur Y.; Bjorkhohm, Magnus] Karolinska Univ Hosp, Dept Med, Div Hematol, Stockholm, Sweden.
[Kristinsson, Sigurdur Y.; Bjorkhohm, Magnus] Karolinska Inst, Stockholm, Sweden.
[Pfeiffer, Ruth] NCI, Biostat Branch, NIH, Bethesda, MD 20892 USA.
[Goldin, Lynn R.] NCI, Genet Epidemiol Branch, NIH, Bethesda, MD 20892 USA.
[Schulman, Sam] McMaster Univ, Dept Med, Hamilton, ON, Canada.
[Blimark, Cecilie; Mellqvist, Ulf-Henrik] Sahlgrens Univ Hosp, Dept Med, Sect Hematol & Coagulat, S-41345 Gothenburg, Sweden.
[Wahlin, Anders] Umea Univ Hosp, S-90185 Umea, Sweden.
[Turesson, Ingemar] Malmo Univ Hosp, Dept Med, Malmo, Sweden.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
RI Pfeiffer, Ruth /F-4748-2011; Wahlin, Anders/F-6043-2013; Kristinsson,
Sigurdur /M-2910-2015
OI Wahlin, Anders/0000-0001-6402-0463; Kristinsson, Sigurdur
/0000-0002-4964-7476
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 743
EP 743
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802240
ER
PT J
AU Miasnikova, GY
Niu, XM
Nouraie, M
Sergueeva, AI
Okhotin, DJ
Ammosova, T
Nekhai, S
Aliyu, Z
Sable, C
Dham, N
Gordeuk, VR
AF Miasnikova, Galina Y.
Niu, Xiaomei
Nouraie, Mehdi
Sergueeva, Adelina I.
Okhotin, Daniel J.
Ammosova, Tatiana
Nekhai, Sergei
Aliyu, Zakari
Sable, Craig
Dham, Niti
Gordeuk, Victor R.
TI Effect of Phlebotomy Therapy On Hemoglobin Concentration and Tricuspid
Regurgitation Velocity in Chuvash Polycythemia
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Miasnikova, Galina Y.] Chuvash Republ Clin Hosp 1, Chuvashia, Russia.
[Nouraie, Mehdi; Ammosova, Tatiana] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Sergueeva, Adelina I.] Cheboksary Childrens Hosp, Cheboksary, Russia.
[Okhotin, Daniel J.] Russian Res Serv Corp, Vancouver, WA USA.
[Aliyu, Zakari] NIH, Catonsville, MD USA.
[Sable, Craig; Dham, Niti] Childrens Natl Med Ctr, Washington, DC 20010 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 753
EP 753
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802265
ER
PT J
AU Elliott, NE
Cleveland, S
Grann, V
Janik, JE
Dave, UP
AF Elliott, Natalina E.
Cleveland, Susan
Grann, Victor
Janik, John E.
Dave, Utpal P.
TI The Role of JAK3 mutations in Adult T-Cell Leukemia/Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Elliott, Natalina E.; Cleveland, Susan; Dave, Utpal P.] Vanderbilt Univ, Ctr Med, Nashville, TN 37232 USA.
[Grann, Victor] Columbia Univ, Herbert Irving Comprehens Canc Ctr, New York, NY USA.
[Janik, John E.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 769
EP 769
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802308
ER
PT J
AU Bonzheim, I
Irmler, M
Anastasov, N
Klier-Richter, M
Schaefer, S
Beckers, J
Pittaluga, S
Fend, F
Raffeld, M
Quintanilla-Martinez, L
AF Bonzheim, Irina
Irmler, Martin
Anastasov, Natasa
Klier-Richter, Margit
Schaefer, Sabine
Beckers, Johannes
Pittaluga, Stefania
Fend, Falko
Raffeld, Mark
Quintanilla-Martinez, Leticia
TI Identification of Genes Which Play a Crucial Role in C/EBP beta
Downstream Signalling in ALK(+) ALCL Cell Lines
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting and Exposition of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Bonzheim, Irina; Klier-Richter, Margit; Schaefer, Sabine; Fend, Falko; Quintanilla-Martinez, Leticia] Univ Tubingen, Univ Tubingen Hosp, Tubingen, Germany.
[Irmler, Martin; Beckers, Johannes] German Res Ctr Environm Hlth, Helmholtz Ctr Munich, Inst Expt Genet, Neuherberg, Germany.
[Pittaluga, Stefania] NCI, NIH, Bethesda, MD 20892 USA.
[Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RI Irmler, Martin/B-3317-2013; Anastasov, Natasa/M-9848-2014
OI Irmler, Martin/0000-0003-3169-479X; Anastasov,
Natasa/0000-0002-4088-1119
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 770
EP 770
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802311
ER
PT J
AU Cardesa-Salzmann, TM
Colomo, L
Climent, F
Gonzalez-Barca, E
Lopez-Guillermo, A
Gutierrez, G
Mercadal, S
Gascoyne, RD
Connors, JM
Rimsza, LM
Braziel, RM
Cook, JR
Tubbs, RR
Rosenwald, A
Ott, G
Mate, JL
Ribera, JM
Arenillas, L
Serrano, S
Combalia, N
Delabie, J
Lenz, G
Wright, G
Jaffe, ES
Staudt, LM
Chan, WC
Weissenburger, D
Campo, E
AF Cardesa-Salzmann, Teresa M.
Colomo, Luis
Climent, Fina
Gonzalez-Barca, Eva
Lopez-Guillermo, Armando
Gutierrez, Gonzalo
Mercadal, Santiago
Gascoyne, Randy D.
Connors, Joseph M.
Rimsza, Lisa M.
Braziel, Rita M.
Cook, James R.
Tubbs, Raymond R.
Rosenwald, Andreas
Ott, German
Luis Mate, Jose
Ribera, Josep-Maria
Arenillas, Leonor
Serrano, Sergi
Combalia, Neus
Delabie, Jan
Lenz, Georg
Wright, George
Jaffe, Elaine S.
Staudt, Louis M.
Chan, Wing C.
Weissenburger, Dennis
Campo, Elias
TI High Microvascular Density Correlates with Poor Outcome in Patients with
Diffuse Large B-Cell Lymphoma (DLBCL) Treated with Rituximab Plus
Chemotherapy (R-CT).
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Cardesa-Salzmann, Teresa M.; Colomo, Luis; Lopez-Guillermo, Armando; Gutierrez, Gonzalo; Campo, Elias] Hosp Clin Barcelona, Barcelona, Spain.
[Climent, Fina] Hosp Univ Bellvitge, Barcelona, Spain.
[Gonzalez-Barca, Eva] Hosp Univ Bellvitge, Lhospitalet De Llobregat, Spain.
[Mercadal, Santiago] Inst Catala Oncol, Lhospitalet De Llobregat, Spain.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Dept Pathol, CTAG Lab, Vancouver, BC V5Z 4E6, Canada.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Dept Lab Med, CTAG Lab, Vancouver, BC V5Z 4E6, Canada.
[Rimsza, Lisa M.] Univ Arizona, Tucson, AZ USA.
[Braziel, Rita M.] Oregon Hlth & Sci Univ, Portland, OR 97201 USA.
[Cook, James R.] Cleveland Clin Fdn, Cleveland, OH 44195 USA.
[Tubbs, Raymond R.] Cleveland Clin, Cleveland, OH 44106 USA.
[Rosenwald, Andreas] Univ Wurzburg, Wurzburg, Germany.
[Ott, German] LLMPP, Wurzburg, Germany.
[Luis Mate, Jose] Hosp Badalona Germans Trias & Pujol, Badalona, Spain.
[Ribera, Josep-Maria] Hosp Badalona Germans Trias & Pujol, ICO, Barcelona, Spain.
[Arenillas, Leonor] Hosp del Mar, Pathol GRETNHE, IMIM, Barcelona, Spain.
[Serrano, Sergi] Hosp del Mar, Dept Pathol, Barcelona, Spain.
[Combalia, Neus] Hosp Parc Tauli, Sabadell, Spain.
[Delabie, Jan] Norwegian Radium Hosp, Oslo, Norway.
[Wright, George; Staudt, Louis M.] NCI, Metab Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Chan, Wing C.; Weissenburger, Dennis] Univ Nebraska Med Ctr, Omaha, NE USA.
RI Colomo, Luis/A-2259-2016
OI Colomo, Luis/0000-0001-5236-5085
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 772
EP 772
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802316
ER
PT J
AU Greenberg, KE
Li, L
Huso, D
Wolff, L
Small, D
AF Greenberg, Kathleen E.
Li, Li
Huso, David
Wolff, Linda
Small, Donald
TI Retroviral Insertional Mutagenesis Reveals Genes That Cooperate with
FLT3-ITD in Leukemogenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Li, Li; Huso, David] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Wolff, Linda] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 776
EP 777
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802328
ER
PT J
AU Odenike, O
Curran, E
Iyengar, N
Popplewell, L
Kirschbaum, M
Erba, HP
Green, M
Poire, X
Ihonor, P
Diaz-Flores, E
Shannon, K
Atallah, E
Wade, JL
Perdekamp, M
Nattam, S
Thomas, SP
Smith, SE
Doyle, LA
Rich, ES
Larson, RA
Stock, W
AF Odenike, Olatoyosi
Curran, Emily
Iyengar, Neil
Popplewell, Leslie
Kirschbaum, Mark
Erba, Harry P.
Green, Margaret
Poire, Xavier
Ihonor, Pamela
Diaz-Flores, Ernesto
Shannon, Kevin
Atallah, Ehab
Wade, James L., III
Perdekamp, Maria
Nattam, Sreenivasa
Thomas, Sachdev P.
Smith, Scott E.
Doyle, L. Austin
Rich, Elizabeth Shima
Larson, Richard A.
Stock, Wendy
TI Phase II Study of the Oral MEK Inhibitor AZD6244 in Advanced Acute
Myeloid Leukemia (AML)
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Odenike, Olatoyosi; Curran, Emily; Iyengar, Neil; Green, Margaret; Poire, Xavier; Ihonor, Pamela; Rich, Elizabeth Shima; Larson, Richard A.; Stock, Wendy] Univ Chicago, Chicago, IL 60637 USA.
[Popplewell, Leslie; Kirschbaum, Mark] City Hope Natl Med Ctr, Duarte, CA USA.
[Erba, Harry P.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Atallah, Ehab] Med Coll Wisconsin, Milwaukee, WI 53226 USA.
[Diaz-Flores, Ernesto; Shannon, Kevin] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Wade, James L., III; Perdekamp, Maria] Decatur Mem Hosp, Decatur, IL USA.
[Nattam, Sreenivasa] Ft Wayne Med Oncol & Hematol Inc, Ft Wayne, IN USA.
[Thomas, Sachdev P.] Oncol Hematol Associates, Peoria, IL USA.
[Smith, Scott E.] Loyola Univ, Med Ctr, Maywood, IL 60153 USA.
[Doyle, L. Austin] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 821
EP 822
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802449
ER
PT J
AU Pulanic, D
Liewehr, D
Steinberg, S
Mitchell, SA
Baird, K
Cowen, EW
Joe, G
Williams, KM
Avila, D
Salit, RB
Atlam, N
Carpenter, A
Hakim, F
Bishop, M
Gress, RE
Pavletic, SZ
AF Pulanic, Drazen
Liewehr, David
Steinberg, Seth
Mitchell, Sandra A.
Baird, Kristin
Cowen, Edward W.
Joe, Galen
Williams, Kirsten M.
Avila, Daniele
Salit, Rachel B.
Atlam, Niveen
Carpenter, Ashley
Hakim, Fran
Bishop, Michael
Gress, Ronald E.
Pavletic, Steven Z.
TI Determinants of Platelet Counts in Patients with Chronic Graft Versus
Host Disease
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Pulanic, Drazen; Williams, Kirsten M.; Avila, Daniele; Salit, Rachel B.; Carpenter, Ashley; Hakim, Fran; Bishop, Michael; Gress, Ronald E.; Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Liewehr, David; Steinberg, Seth; Atlam, Niveen] NCI, Biostat & Data Management Sect, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Mitchell, Sandra A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Baird, Kristin] NCI, Pediat Oncol Branch, NIH, Bethesda, MD 20892 USA.
[Cowen, Edward W.] NCI, Dermatol Branch, NIH, Bethesda, MD 20892 USA.
[Joe, Galen] NIH, Ctr Clin, Dept Rehabil Med, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 884
EP 884
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802611
ER
PT J
AU Foglietta, M
Neelapu, S
Fowler, DH
Steinberg, SM
Kwak, LW
Bishop, MR
AF Foglietta, Myriam
Neelapu, Sattva
Fowler, Daniel H.
Steinberg, Seth M.
Kwak, Larry W.
Bishop, Michael R.
TI Analysis of Antigen-Specific T-Cell Responses and Regulatory T Cells
Following Sibling Donor Immunization with Patient-Derived Idiotype
Vaccine Prior to Non-Myeloablative Allogeneic Stem Cell Transplantation
for Multiple Myeloma
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Foglietta, Myriam] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma & Myeloma, Houston, TX 77030 USA.
[Fowler, Daniel H.; Steinberg, Seth M.; Bishop, Michael R.] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 887
EP 887
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802618
ER
PT J
AU Jacobsohn, D
Chai, XY
Kurland, B
Arai, S
Arora, M
Cutler, C
Jagasia, M
Pavletic, SZ
Vogelsang, G
Lee, SJ
Flowers, MED
AF Jacobsohn, David
Chai, Xiaoyu
Kurland, Brenda
Arai, Sally
Arora, Mukta
Cutler, Corey
Jagasia, Madan
Pavletic, Steven Z.
Vogelsang, Georgia
Lee, Stephanie J.
Flowers, Mary E. D.
TI Correlation of the NIH and Vienna Skin Scores with Provider and
Patient-Reported Skin Changes in Chronic Graft-Versus-Host Disease
(GVHD)
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Jacobsohn, David] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Chai, Xiaoyu; Kurland, Brenda; Lee, Stephanie J.; Flowers, Mary E. D.] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
[Arai, Sally] Stanford Univ, Med Ctr, Stanford, CA 94305 USA.
[Arora, Mukta] Univ Minnesota, Minneapolis, MN USA.
[Cutler, Corey] Dana Farber Canc Inst, Div Hematol Malignancies, Boston, MA 02115 USA.
[Jagasia, Madan] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Vogelsang, Georgia] Johns Hopkins Univ, Baltimore, MD 21218 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 889
EP 889
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802624
ER
PT J
AU Stringaris, K
Adams, S
Uribe, M
Eniafe, R
Wu, C
Savani, BN
Barrett, AJ
AF Stringaris, Kate
Adams, Sharon
Uribe, Marcela
Eniafe, Rhoda
Wu, Colin
Savani, Bipin N.
Barrett, A. John
TI A Reduced Rate of Leukaemia Relapse After HLA-Identical Sibling Stem
Cell Transplantation for Acute Myeloid Leukaemia but Not Other
Haematological Malignancies Is Associated with Donor KIR Genes 2DL5A,
2DS1 and 3DS1
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Stringaris, Kate; Eniafe, Rhoda; Wu, Colin] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Savani, Bipin N.] Vanderbilt Univ, Nashville, TN USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 899
EP 900
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802650
ER
PT J
AU Liu, WL
Lee, HW
Rodgers, GP
AF Liu, Wenli
Lee, Hyun W.
Rodgers, Griffin P.
TI Olfactomedin 4 Mediates All-Trans Retinoic Acid Induced Growth
Inhibition, Differentiation and Apoptosis in Myeloid Leukemia Cells and
Inhibits 4E-BP1 Phosphorylation
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Liu, Wenli; Lee, Hyun W.; Rodgers, Griffin P.] NHLBI, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 946
EP 946
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802763
ER
PT J
AU Visconte, V
de Latour, RP
Calado, RT
Desierto, M
Chen, JC
Young, NS
AF Visconte, Valeria
de Latour, Regis Peffault
Calado, Rodrigo T.
Desierto, Marie
Chen, Jichun
Young, Neal S.
TI Reduced Hematopoietic Stem Cell Function in a Mouse Model with
Conditional Pig-a Gene Deletion.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Visconte, Valeria; de Latour, Regis Peffault; Calado, Rodrigo T.; Desierto, Marie; Chen, Jichun; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 958
EP 959
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802796
ER
PT J
AU Melenhorst, JJ
Scheinberg, P
Williams, A
Keyvanfar, K
Smith, M
McCoy, JP
Hensel, NF
Barrett, AJ
AF Melenhorst, J. Joseph
Scheinberg, Phillip
Williams, Ann
Keyvanfar, Keyvan
Smith, Melody
McCoy, J. Philip, Jr.
Hensel, Nancy F.
Barrett, A. John
TI Both Naive and Memory T-Cell Subsets Participate in Alloresponses to
HLA-Mismatched Targets - Implications for Adoptive Transfer of Viral
Antigen-Specific T Cells.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Melenhorst, J. Joseph; Williams, Ann; Keyvanfar, Keyvan; Hensel, Nancy F.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RI Scheinberg, Phillip/H-5251-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 963
EP 963
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802807
ER
PT J
AU Kato, K
Cui, SAY
Kuick, R
Mineishi, S
Hexner, E
Ferrara, JLM
Marquez, VE
Emerson, SG
Zhang, Y
AF Kato, Koji
Cui, Shuaiying
Kuick, Rork
Mineishi, Shin
Hexner, Elizabeth
Ferrara, James L. M.
Marquez, Victor E.
Emerson, Stephen G.
Zhang, Yi
TI Alloreactive CD8(+) Effector T Cells Proliferate and Persist Upon
Chronic Exposure to Alloantigens through Reactivation of Stem Cell
Transcriptional Programs.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting and Exposition of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Kato, Koji; Cui, Shuaiying; Mineishi, Shin; Ferrara, James L. M.] Univ Michigan, Blood & Marrow Transplant Program, Ann Arbor, MI 48109 USA.
[Kuick, Rork] Univ Michigan, Comprehens Canc Ctr Biostat Core, Ann Arbor, MI 48109 USA.
[Hexner, Elizabeth] Univ Penn, Philadelphia, PA 19104 USA.
[Marquez, Victor E.] NIH, Med Chem Lab, Frederick, MD USA.
[Emerson, Stephen G.] Haverford Coll, Haverford, PA 19041 USA.
[Zhang, Yi] Univ Michigan, Sch Med, Ann Arbor, MI USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 964
EP 964
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725802812
ER
PT J
AU Amarnath, S
Costanzo, CM
Foley, J
Mariotti, J
Konecki, DM
Gangopadhyay, A
Eckhaus, M
Wong, S
Levine, B
June, CH
Fowler, DH
AF Amarnath, Shoba
Costanzo, Carliann M.
Foley, Jason
Mariotti, Jacopo
Konecki, Daniel M.
Gangopadhyay, Anu
Eckhaus, Michael
Wong, Susan
Levine, Bruce
June, Carl H.
Fowler, Daniel H.
TI Rapamycin-Induced Autophagy Generates Anti-Apoptotic Th1/Tc1 Cells That
Mediate Increased Xenogeneic Gvhd.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Amarnath, Shoba; Costanzo, Carliann M.; Konecki, Daniel M.; Gangopadhyay, Anu; Eckhaus, Michael] NCI, Expt Transplantat Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Foley, Jason] Jason Foley, Expt Transplantat & Immunol, Bethesda, MD USA.
[Mariotti, Jacopo] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Wong, Susan] NHLBI, Hematol Branch, Bethesda, MD 20892 USA.
[Levine, Bruce; June, Carl H.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RI Levine, Bruce/D-1688-2009
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 969
EP 969
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803012
ER
PT J
AU Ballas, SK
Bauserman, RL
McCarthy, WF
Waclawiw, MA
Barton, BA
AF Ballas, Samir K.
Bauserman, Robert L.
McCarthy, William F.
Waclawiw, Myron A.
Barton, Bruce A.
TI Impact of Hydroxyurea On Employment Among Patients with Sickle Cell
Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Ballas, Samir K.] Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[Bauserman, Robert L.; McCarthy, William F.; Barton, Bruce A.] Maryland Med Res Inst, Baltimore, MD USA.
[Waclawiw, Myron A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 980
EP 980
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803041
ER
PT J
AU Hsieh, MM
Duan, ZG
Wright, EC
Tisdale, JF
Rodgers, GP
AF Hsieh, Matthew M.
Duan, Zhigang
Wright, Elizabeth C.
Tisdale, John F.
Rodgers, Griffin P.
TI There Is No Difference in the Prevalence of Neutropenia or Fever in
Hospitalized African-Americans and Caucasians with Cancer in the
SEER-Medicare Database
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Rodgers, Griffin P.] NIDDK, Mol & Clin Hematol Branch, NIH, Bethesda, MD USA.
[Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 986
EP 986
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803055
ER
PT J
AU Allen, RS
Jin, P
North, T
Goessling, W
Tian, Y
Metzger, ME
Bonifacino, AC
Stroncek, D
Zon, LI
Donahue, RE
AF Allen, Robyn S.
Jin, Ping
North, Trista
Goessling, Wolfram
Tian, Yu
Metzger, Mark E.
Bonifacino, Aylin C.
Stroncek, David
Zon, Leonard I.
Donahue, Robert E.
TI Global Gene Expression Signatures in CD34+Hematopoietic Cells Following
Exposure to 16,16-Dimethylprostaglandin E2
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Allen, Robyn S.; Tian, Yu; Metzger, Mark E.; Bonifacino, Aylin C.; Donahue, Robert E.] NHLBI, Hematol Branch, Rockville, MD USA.
[Jin, Ping; Stroncek, David] NIH, Bethesda, MD 20892 USA.
[North, Trista] Harvard Univ, Sch Med, Dept Pathol, Beth Israel Deaconess Med Ctr, Boston, MA USA.
[Goessling, Wolfram] Harvard Univ, Brigham & Womens Hosp, Div Genet, Sch Med, Boston, MA 02115 USA.
[Goessling, Wolfram] Harvard Univ, Brigham & Womens Hosp, Div Gastroenterol, Sch Med, Boston, MA 02115 USA.
[Goessling, Wolfram] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
[Zon, Leonard I.] Harvard Stem Cell Inst, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 994
EP 994
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803079
ER
PT J
AU Meier, ER
Byrnes, C
Weissman, M
Noel, P
Luban, NLC
Miller, JL
AF Meier, Emily Riehm
Byrnes, Colleen
Weissman, Maxine
Noel, Pierre
Luban, Naomi L. C.
Miller, Jeffery L.
TI Combining Fetal Hemoglobin and Reticulocytosis to Index Clinical
Severity of Sickle Cell Disease in Children.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Meier, Emily Riehm] NIDDK, Div Hematol, Childrens Natl Med Ctr, NIH, Washington, DC USA.
[Meier, Emily Riehm] NIDDK, Mol Med Branch, NIH, Washington, DC USA.
[Byrnes, Colleen; Miller, Jeffery L.] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
[Weissman, Maxine; Noel, Pierre] NIH, Serv Hematol, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Luban, Naomi L. C.] George Washington Univ, Childrens Natl Med Ctr, Div Hematol, Med Ctr, Washington, DC USA.
[Luban, Naomi L. C.] George Washington Univ, Dept Pediat, Med Ctr, Washington, DC 20052 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1003
EP 1004
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803112
ER
PT J
AU Klings, ES
Dworkis, DA
Sedgewick, A
Hartley, SW
Allison, AK
Telen, MJ
Kato, GJ
Gladwin, M
Sebastiani, P
Baldwin, CT
Steinberg, MH
AF Klings, Elizabeth S.
Dworkis, Daniel A.
Sedgewick, Amanda
Hartley, Stephen W.
Allison, Ashley-Koch
Telen, Marilyn J.
Kato, Gregory J.
Gladwin, Mark
Sebastiani, Paola
Baldwin, Clinton T.
Steinberg, Martin H.
TI Genetic Polymorphisms in NEDD4L Are Associated with Pulmonary
Hypertension of Sickle Cell Anemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Klings, Elizabeth S.] Boston Univ, Sch Med, Ctr Pulm, Boston, MA 02118 USA.
[Sedgewick, Amanda; Hartley, Stephen W.; Sebastiani, Paola] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Allison, Ashley-Koch] Duke Univ, Dept Med, Durham, NC USA.
[Telen, Marilyn J.] Duke Univ, Med Ctr, Durham, NC USA.
[Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Gladwin, Mark] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
[Dworkis, Daniel A.; Baldwin, Clinton T.] Boston Univ, Sch Med, Ctr Human Genet, Boston, MA 02118 USA.
[Steinberg, Martin H.] Boston Univ, Sch Med, Dept Med, Div Hematol & Oncol, Boston, MA 02118 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1006
EP 1006
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803118
ER
PT J
AU Hsu, LL
Noguchi, AC
Noguchi, C
Wood, KC
Taylor, JG
Kato, GJ
Gladwin, M
Diwan, B
AF Hsu, Lewis L.
Noguchi, Audrey C.
Noguchi, Constance
Wood, Katherine C.
Taylor, James G.
Kato, Gregory J.
Gladwin, Mark
Diwan, Bhalchandra
TI Liver Hypoxia and Tissue Injury Are Specific to Sickle Cell Mice in An
Experimental Model of Sickle Cell Vaso-Occlusion
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Noguchi, Audrey C.] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
[Noguchi, Constance] NIDDK, Mol Med Branch, NIH, Bethesda, MD USA.
[Wood, Katherine C.; Taylor, James G.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Gladwin, Mark] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
[Diwan, Bhalchandra] NCI, Basic Sci Program, SAIC Frederick, Frederick, MD 21701 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1008
EP 1009
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803125
ER
PT J
AU Castro, OL
Nouraie, M
Luchtman-Jones, L
Niu, XM
Minniti, C
Campbell, AD
Rana, SR
Kato, GJ
Gladwin, M
Gordeuk, VR
AF Castro, Oswaldo L.
Nouraie, Mehdi
Luchtman-Jones, Lori
Niu, Xiaomei
Minniti, Caterina
Campbell, Andrew D.
Rana, Sohail R.
Kato, Gregory J.
Gladwin, Mark
Gordeuk, Victor R.
TI Lower Ferritin Concentrations Are Associated with Decreased Hemolysis in
Sickle Cell Disease Children without Iron Overload
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Castro, Oswaldo L.; Nouraie, Mehdi; Niu, Xiaomei; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Luchtman-Jones, Lori] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Minniti, Caterina] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
[Campbell, Andrew D.] Univ Michigan, Med Ctr, Ann Arbor, MI USA.
[Rana, Sohail R.] Howard Univ Hosp, Dept Pediat & Child Hlth, Washington, DC USA.
[Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
[Gladwin, Mark] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1009
EP 1009
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803127
ER
PT J
AU Ballas, SK
McCarthy, WF
Bauseman, RI
Castro, OL
Swerdlow, PS
Smith, W
Waclawiw, MA
Barton, BA
AF Ballas, Samir K.
McCarthy, William F.
Bauseman, Robert I.
Castro, Oswaldo L.
Swerdlow, Paul S.
Smith, Wally
Waclawiw, Myron A.
Barton, Bruce A.
TI Patterns of Analgesic Utilization in the Multicenter Study of
Hydroxyurea (MSH)
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Ballas, Samir K.] Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[McCarthy, William F.; Bauseman, Robert I.; Barton, Bruce A.] Maryland Med Res Inst, Baltimore, MD USA.
[Castro, Oswaldo L.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
[Swerdlow, Paul S.] Wayne State Univ, Barbara Ann Karmanos Canc Inst, Detroit, MI USA.
[Smith, Wally] Virginia Commonwealth Univ, Richmond, VA USA.
[Waclawiw, Myron A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1011
EP 1012
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803133
ER
PT J
AU Ballas, SK
McCarthy, WF
Bauserman, RL
Castro, OL
Waclawiw, MA
Barton, BA
AF Ballas, Samir K.
McCarthy, William F.
Bauserman, Robert L.
Castro, Oswaldo L.
Waclawiw, Myron A.
Barton, Bruce A.
TI Sickle Cell Genetic Markers: Geographic Distribution and Relation to
Pain Outcomes in Multicenter Study of Hydroxyurea in Sickle Cell Anemia
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[McCarthy, William F.; Bauserman, Robert L.; Barton, Bruce A.] Maryland Med Res Inst, Baltimore, MD USA.
[Castro, Oswaldo L.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC USA.
[Waclawiw, Myron A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1013
EP 1014
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803138
ER
PT J
AU Minniti, CP
Hildesheim, M
Sachdev, V
Allen, D
Castro, O
Taylor, JG
Kato, GJ
AF Minniti, Caterina P.
Hildesheim, Mariana
Sachdev, Vandana
Allen, Darlene
Castro, Oswaldo
Taylor, James G.
Kato, Gregory J.
TI Sickle Cell Leg Ulcers Are Associated with Hyperuricemia, Hemolysis,
Pulmonary Hypertension and Death
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Minniti, Caterina P.] NIH, Chevy Chase, MD USA.
[Hildesheim, Mariana; Allen, Darlene; Taylor, James G.; Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, NIH, Bethesda, MD 20892 USA.
[Sachdev, Vandana] NIH, Translat Med Branch, Bethesda, MD 20892 USA.
[Castro, Oswaldo] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20059 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1014
EP 1014
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803139
ER
PT J
AU Betal, SG
Kato, GJ
Lawrence, MP
Seamon, C
Setty, Y
Stuart, MJ
Krishnan, S
AF Betal, Suhita Gayen
Kato, Gregory J.
Lawrence, Marlene Peters
Seamon, Catherine
Setty, Yamaja
Stuart, Marie J.
Krishnan, Suba
TI Thrombin Generation in Sickle Cell Disease: Insights From Computerized
Automated Thrombography
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Betal, Suhita Gayen; Setty, Yamaja; Stuart, Marie J.; Krishnan, Suba] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Kato, Gregory J.; Lawrence, Marlene Peters] NHLBI, Vasc Med Branch, Bethesda, MD 20892 USA.
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
NR 0
TC 2
Z9 2
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1015
EP 1016
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803142
ER
PT J
AU Chen, CL
Janik, JE
Kaucic, K
Roskos, L
Jallal, B
Robbie, GJ
AF Chen, Chunlin
Janik, John E.
Kaucic, Karen
Roskos, Lorin
Jallal, Bahija
Robbie, Gabriel J.
TI Population Pharmacokinetics of Siplizumab (MEDI-507), a Humanized
Anti-CD2 Monoclonal Antibody, in Cancer Patients.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Chen, Chunlin] Medimmune Inc, Translat Sci, Gaithersburg, MD USA.
[Janik, John E.] NCI, Canc Res Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1046
EP 1046
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803225
ER
PT J
AU Buckstein, R
Kuruvilla, J
Chua, N
Lee, C
Macdonald, DA
Al-Tourah, AJ
Foo, A
Walsh, W
Ivy, SP
Crump, M
Eisenhauer, E
AF Buckstein, Rena
Kuruvilla, John
Chua, Neil
Lee, Christina
Macdonald, David A.
Al-Tourah, Abdulwahab J.
Foo, Alison
Walsh, Wendy
Ivy, S. Percy
Crump, Michael
Eisenhauer, Elizabeth
TI Sunitinib in Relapsed or Refractory Diffuse Large B Cell Lymphoma:
Results of a Phase II Multi-Center Study of the NCIC Clinical Trials
Group.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Buckstein, Rena; Lee, Christina] Sunnybrook Hlth Sci Ctr, Toronto, ON M4N 3M5, Canada.
[Kuruvilla, John; Crump, Michael] Princess Margaret Hosp, Univ Hlth Network, Dept Med Oncol & Hematol, Toronto, ON M4X 1K9, Canada.
[Chua, Neil] Cross Canc Inst, Edmonton, AB T6G 1Z2, Canada.
[Macdonald, David A.] QEII Hlth Sci Ctr, Halifax, NS, Canada.
[Al-Tourah, Abdulwahab J.] BC Canc Ctr Fraser Valley Ctr, Surrey, BC, Canada.
[Foo, Alison; Walsh, Wendy; Eisenhauer, Elizabeth] NCIC, Clin Trials Grp, Kingston, ON, Canada.
[Ivy, S. Percy] NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1068
EP 1068
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803284
ER
PT J
AU Zoppoli, G
Cea, M
Fruscione, F
Bruzzone, S
Soncini, D
Bedognetti, D
Moran, E
Balleari, E
Bruzzone, A
Garuti, A
Cirmena, G
Rocco, I
Gobbi, M
Ghio, R
Pommier, Y
Carella, AM
Ballestrero, A
Parodi, S
Patrone, F
Nencioni, A
AF Zoppoli, Gabriele
Cea, Michele
Fruscione, Floriana
Bruzzone, Santina
Soncini, Debora
Bedognetti, Davide
Moran, Eva
Balleari, Enrico
Bruzzone, Andrea
Garuti, Anna
Cirmena, Gabriella
Rocco, Ilaria
Gobbi, Marco
Ghio, Riccardo
Pommier, Yves
Carella, Angelo Michele
Ballestrero, Alberto
Parodi, Silvio
Patrone, Franco
Nencioni, Alessio
TI Potent Synergistic Activity of the NAD plus Synthesis Inhibitor APO866
and of the Apoptosis Inducer TRAIL in in Vitro and Ex Vivo Cellular
Models of Non Hodgkin's Lymphoma and Chronic Lymphocytic Leukemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Zoppoli, Gabriele; Gobbi, Marco; Pommier, Yves] NCI, Mol Pharmacol Lab, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Zoppoli, Gabriele; Cea, Michele; Soncini, Debora; Moran, Eva; Balleari, Enrico; Bruzzone, Andrea; Garuti, Anna; Cirmena, Gabriella; Rocco, Ilaria; Gobbi, Marco; Ghio, Riccardo; Ballestrero, Alberto; Patrone, Franco; Nencioni, Alessio] Univ Genoa, Dept Internal Med, I-16126 Genoa, Italy.
[Fruscione, Floriana; Bruzzone, Santina] Univ Genoa, Dipartimento Med Sperimentale, Biochem Sect, I-16126 Genoa, Italy.
[Bedognetti, Davide] Univ Study Genova, Dept Transfus Med, Genoa, Italy.
[Carella, Angelo Michele] Univ San Martino, Azienda Osped, Div Hematol, BMT Unit, Genoa, Italy.
[Parodi, Silvio] Univ Genoa, Dept Oncol Biol & Genet DOBIG, Genoa, Italy.
RI Bedognetti, Davide/A-9090-2012; Bruzzone, Santina/A-4264-2015; Balleari,
Enrico/R-3119-2016
OI Bruzzone, Santina/0000-0003-2034-3716; Balleari,
Enrico/0000-0003-2186-8012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1069
EP 1069
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803288
ER
PT J
AU Rau, RE
McIntyre, E
Kaufmann, SH
Espinoza-Delgado, I
Karp, J
Brown, P
AF Rau, Rachel E.
McIntyre, Emily
Kaufmann, Scott H.
Espinoza-Delgado, Igor
Karp, Judith
Brown, Patrick
TI Combinations of the Histone Deacetylase Inhibitor Entinostat (SNDX-275,
MS-275) and Imatinib Have Divergent Effects in Imatinib-Sensitive Vs.
Imatinib-Resistant p210-(BCR/ABL) Expressing Cell Lines.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting and Exposition of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Rau, Rachel E.; McIntyre, Emily; Brown, Patrick] Johns Hopkins Univ, Baltimore, MD USA.
[Kaufmann, Scott H.] Mayo Clin, Rochester, MN USA.
[Espinoza-Delgado, Igor] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
[Karp, Judith] Johns Hopkins Univ SOM, Div Hematol, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1072
EP 1073
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803297
ER
PT J
AU Gough, SM
Chung, YJ
Aplan, PD
AF Gough, Sheryl M.
Chung, Yang Jo
Aplan, Peter D.
TI Rag1 Deficiency Does Not Affect Myelodysplasia but Leads to More Rapid
Leukemic Transformation in a Mouse Model of MDS.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Gough, Sheryl M.; Chung, Yang Jo; Aplan, Peter D.] NCI, Genet Branch, CCR, Bethesda, MD 20892 USA.
RI Aplan, Peter/K-9064-2016
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1089
EP 1089
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803339
ER
PT J
AU Weiss, B
Minter, A
Laquer, M
Howard, R
Abadie, J
Ascencao, J
Schechter, GP
Kuehl, M
Landgren, O
AF Weiss, Brendan
Minter, Alex
Laquer, Matthew
Howard, Robin
Abadie, Jude
Ascencao, Joao
Schechter, Geraldine P.
Kuehl, Michael
Landgren, Ola
TI Patterns of Monoclonal Immunoglobulins and Serum Free Light Chains Are
Significantly Different in African-American Compared to Caucasian MGUS
Patients
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Weiss, Brendan; Minter, Alex] Walter Reed Army Med Ctr, Hematol Oncol Serv, Washington, DC 20307 USA.
[Abadie, Jude] Walter Reed Army Med Ctr, Pathol & Area Lab Serv, Washington, DC 20307 USA.
[Ascencao, Joao] Washington DC Vet Affairs Med Ctr, Hematol Serv, Washington, DC USA.
[Schechter, Geraldine P.] Washington VA Med Ctr, Washington, DC USA.
[Schechter, Geraldine P.] George Washington Univ, Washington, DC USA.
[Kuehl, Michael] NCI, Genet Branch, Canc Res Ctr, Bethesda, MD 20892 USA.
[Landgren, Ola] NCI, Med Oncol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1108
EP 1109
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803393
ER
PT J
AU Deffenbacher, KE
Iqbal, J
Liu, ZF
Perkins, SL
Lim, MS
Fu, K
Shen, YL
Staudt, LM
Rimsza, LM
Jaffe, ES
Rosenwald, A
Ott, G
Delabie, J
Campo, E
Gascoyne, RD
Weisenburger, DD
Greiner, TC
Gross, T
Chan, WC
AF Deffenbacher, Karen E.
Iqbal, Javeed
Liu, Zhongfeng
Perkins, Sherrie L.
Lim, Megan S.
Fu, Kai
Shen, Yulei
Staudt, Louis M.
Rimsza, Lisa M.
Jaffe, Elaine S.
Rosenwald, Andreas
Ott, German
Delabie, Jan
Campo, Elias
Gascoyne, Randy D.
Weisenburger, Dennis D.
Greiner, Timothy C.
Gross, Thomas
Chan, Wing C.
TI Chromosomal Alterations in Gene Expression-Defined Pediatric Aggressive
B-Cell Non-Hodgkin Lymphoma (B-NHL)
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Deffenbacher, Karen E.; Iqbal, Javeed; Liu, Zhongfeng; Fu, Kai; Shen, Yulei; Weisenburger, Dennis D.; Greiner, Timothy C.; Chan, Wing C.] Univ Nebraska Med Ctr, Omaha, NE USA.
[Perkins, Sherrie L.] ARUP Labs, Hematopathol Off, Salt Lake City, UT USA.
[Lim, Megan S.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Staudt, Louis M.] NCI, Metab Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA.
[Rimsza, Lisa M.] Univ Arizona, Tucson, AZ USA.
[Rosenwald, Andreas; Ott, German] Univ Wurzburg, Wurzburg, Germany.
[Campo, Elias] Hosp Clin Barcelona, Barcelona, Spain.
[Delabie, Jan] Norwegian Radium Hosp, Oslo, Norway.
[Gascoyne, Randy D.] British Columbia Canc Agcy, Vancouver, BC V5Z 4E6, Canada.
[Gross, Thomas] Ohio State Univ, Nationwide Childrens Hosp, Columbus, OH 43210 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1142
EP 1142
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803477
ER
PT J
AU Rudelius, M
Pittaluga, S
Sebasigari, D
Davies-Hill, T
Klier, M
Quintanilla-Martinez, L
Fend, F
Tabe, Y
Raffeld, M
AF Rudelius, Martina
Pittaluga, Stefania
Sebasigari, Denise
Davies-Hill, Theresa
Klier, Margit
Quintanilla-Martinez, Leticia
Fend, Falko
Tabe, Yoko
Raffeld, Mark
TI PTEN Regulates SYK-Directed AKT Activation in MCL.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Rudelius, Martina] Tech Univ Munich, Inst Pathol, Munich, Germany.
[Pittaluga, Stefania; Sebasigari, Denise; Davies-Hill, Theresa; Tabe, Yoko; Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Klier, Margit; Quintanilla-Martinez, Leticia; Fend, Falko] Univ Tubingen, Univ Tubingen Hosp, Tubingen, Germany.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1149
EP 1149
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803496
ER
PT J
AU Metais, JY
Winkler, T
Calado, RT
Dunbar, CE
AF Metais, Jean-Yves
Winkler, Thomas
Calado, Rodrigo T.
Dunbar, Cynthia E.
TI BCL2A1 Is a Survival and Immortalization Factor for Primitive
Hematopoietic Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Metais, Jean-Yves; Winkler, Thomas; Calado, Rodrigo T.; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1155
EP 1155
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803512
ER
PT J
AU Greenblatt, SM
Li, L
Slape, C
Huso, D
Aplan, PD
Small, D
AF Greenblatt, Sarah M.
Li, Li
Slape, Christopher
Huso, David
Aplan, Peter D.
Small, Donald
TI Knock-in of a FLT3 Internal Tandem Duplication Mutation Cooperates with
a NUP98-HOXD13 Fusion to Generate Acute Leukemia in a Mouse Model.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Li, Li; Huso, David] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
[Slape, Christopher] Royal Melbourne Hosp, Bone Marrow Res Lab, Parkville, MD USA.
[Aplan, Peter D.] NCI, Genet Branch, NIH, CCR, Bethesda, MD 20892 USA.
RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016
OI Slape, Christopher/0000-0002-8407-3092;
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1156
EP 1157
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803516
ER
PT J
AU Visconte, V
de Latour, RP
Raghavachari, N
Liu, DL
Keyvanfar, K
Nunez, O
Young, NS
AF Visconte, Valeria
de Latour, Regis Peffault
Raghavachari, Nalini
Liu, Delong
Keyvanfar, Keyvan
Nunez, Olga
Young, Neal S.
TI Differential Gene Expression Profile in the T Cell Compartment Between
Classic PNH and Aplastic Anemia/PNH Syndrome
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Visconte, Valeria; de Latour, Regis Peffault; Raghavachari, Nalini; Keyvanfar, Keyvan; Nunez, Olga; Young, Neal S.] NHLBI, Hematol Branch, NIH, Genom Core Facil, Bethesda, MD 20892 USA.
[Liu, Delong] CIT, Math & Stat Comp Lab, DCB, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1173
EP 1173
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803566
ER
PT J
AU Zhang, H
Levine, B
Voong, N
Wayne, AS
June, CH
Mackall, CL
AF Zhang, Hua
Levine, Bruce
Voong, Nga
Wayne, Alan S.
June, Carl H.
Mackall, Crystal L.
TI Artificial Antigen Presenting Cells (aAPC) Expanded NK-Mediated Enhanced
Lysis of Allogeneic Tumor Cells Regardless of HLA Class I/KIR Mismatch
and Its Implication of Use in Eradicating Acute Lymphoblastic Leukemia
(ALL)
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Zhang, Hua; Mackall, Crystal L.] NCI, Pediat Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Levine, Bruce; June, Carl H.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
[Voong, Nga] NCI, Expt Transplantat & Immunol Branch, Bethesda, MD 20892 USA.
[Wayne, Alan S.] NCI, NIH, Bethesda, MD 20892 USA.
RI Levine, Bruce/D-1688-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1178
EP 1178
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803578
ER
PT J
AU Dhall, G
Jones, T
Radvinsky, D
Robison, N
Butturini, A
Rubin, JI
Gaynon, PS
Panosyan, EH
Avramis, IA
Avramis, VI
Ettinger, LJ
Seibel, NL
AF Dhall, Girish
Jones, Tamekia
Radvinsky, David
Robison, Nathan
Butturini, Anna
Rubin, Joan I.
Gaynon, Paul S.
Panosyan, Eduard H.
Avramis, Ioannis A.
Avramis, Vassilios I.
Ettinger, Lawrence J.
Seibel, Nita L.
TI Adverse Reactions to PEG and Erwinia Asparaginase and Correlation with
Anti-Asparaginase Antibody Data and Survival in Children with Acute
Lymphoblastic Leukemia (ALL): A Report From the Children's Oncology
Group Study CCG 1961
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Dhall, Girish] Univ So Calif, Childrens Hosp Los Angeles, Los Angeles, CA USA.
[Jones, Tamekia] Childrens Oncol Grp, Dept Epidemiol & Hlth Policy Res, Gainesville, FL USA.
[Radvinsky, David; Robison, Nathan; Butturini, Anna; Gaynon, Paul S.; Panosyan, Eduard H.; Avramis, Ioannis A.; Avramis, Vassilios I.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Rubin, Joan I.] St Peters Univ Hosp, New Brunswick, NJ USA.
[Ettinger, Lawrence J.] Univ S Florida, All Childrens Hosp, St Petersburg, FL 33701 USA.
[Seibel, Nita L.] NCI, Canc Therapy Evaluat Program, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1197
EP 1197
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803632
ER
PT J
AU Olnes, MJ
Leitman, S
Biancotto, A
McCoy, JP
Miranda, S
Tucker, Z
Pfannes, L
Furnari, M
Young, NS
Sloand, EM
AF Olnes, Matthew J.
Leitman, Susan
Biancotto, Angelique
McCoy, J. Philip, Jr.
Miranda, Susan
Tucker, Zachary
Pfannes, Loretta
Furnari, Megan
Young, Neal S.
Sloand, Elaine M.
TI Effects of Granulocyte Colony Stimulating Factor (G-CSF) On Monosomy 7
Aneuploidy and T Cell Subsets in Healthy Donors
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Olnes, Matthew J.; Tucker, Zachary; Pfannes, Loretta; Furnari, Megan] NIH, Hematol Branch, Bethesda, MD 20892 USA.
[Leitman, Susan] NIH, Blood Serv Sect, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[McCoy, J. Philip, Jr.] NHLBI, Flow Cytometry Core Facil, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1222
EP 1222
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803702
ER
PT J
AU Giri, N
Maric, I
Wesley, R
Arthur, DC
Noel, P
Savage, SA
Alter, BP
AF Giri, Neelam
Maric, Irina
Wesley, Robert
Arthur, Diane C.
Noel, Pierre
Savage, Sharon A.
Alter, Blanche P.
TI Bone Marrow Fibrosis in Patients with Inherited Bone Marrow Failure
Syndromes
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Giri, Neelam; Alter, Blanche P.] NCI, Clin Genet Branch, Rockville, MD USA.
[Maric, Irina] NIH, DLM, CC, Bethesda, MD 20892 USA.
[Arthur, Diane C.] NCI, LP, NIH, Bethesda, MD 20892 USA.
[Wesley, Robert] NIH, OD, CC, Bethesda, MD 20892 USA.
[Noel, Pierre] NIH, Hematol Serv, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
[Savage, Sharon A.] NCI, Div Canc Epidemiol & Gene, Bethesda, MD 20892 USA.
RI Savage, Sharon/B-9747-2015
OI Savage, Sharon/0000-0001-6006-0740
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1236
EP 1237
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803747
ER
PT J
AU Hutson, S
Han, P
Al-Rahawan, MM
Anand, S
Rife, S
Alter, BP
AF Hutson, Sadie
Han, Paul
Al-Rahawan, Mohamad M.
Anand, Sheeba
Rife, Sean
Alter, Blanche P.
TI Stem Cell Transplanation for Fanconi Anemia: A Survey of Decision-Making
among Families in the US and Canada.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Hutson, Sadie] E Tennessee State Univ, Div Grad Studies, Johnson City, TN 37614 USA.
[Hutson, Sadie] E Tennessee State Univ, Coll Nursing, Johnson City, TN 37614 USA.
[Han, Paul] Maine Med Ctr, Ctr Outcomes Res & Evaluat, Portland, ME 04102 USA.
[Al-Rahawan, Mohamad M.] Univ Illinois, Coll Med, Peoria, IL 61656 USA.
[Al-Rahawan, Mohamad M.] St Jude Midwest Affiliate, Peoria, IL USA.
[Rife, Sean] Kent State Univ, Social Relationships & Hlth Lab, Kent, OH 44242 USA.
[Alter, Blanche P.] NCI, Clin Genet Branch, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1242
EP 1243
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803762
ER
PT J
AU Rosenberg, PS
Zeidler, C
Bolyard, AA
Alter, BP
Bonilla, MA
Dror, Y
Kinsey, SE
Link, DC
Shimamura, A
Newburger, PE
Boxer, LA
Welte, K
Dale, DC
AF Rosenberg, Philip S.
Zeidler, Cornelia
Bolyard, Audrey Anna
Alter, Blanche P.
Bonilla, Mary Ann
Dror, Yigal
Kinsey, Sally E.
Link, Daniel C.
Shimamura, Akiko
Newburger, Peter E.
Boxer, Laurence A.
Welte, Karl
Dale, David C.
TI Stable Long-Term Risk of Leukemia in Patients with Severe Congenital
Neutropenia Maintained On G-CSF Therapy.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Alter, Blanche P.] NCI, Clin Genet Branch, Rockville, MD USA.
[Zeidler, Cornelia] Hannover Med Sch, SCNIR, D-3000 Hannover, Germany.
[Bolyard, Audrey Anna] Univ Washington, Severe Chron Neutropenia Int Registry, Seattle, WA 98195 USA.
[Bonilla, Mary Ann] St Josephs Childrens Hosp, Paterson, NJ USA.
[Dror, Yigal] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Kinsey, Sally E.] St James Univ Hosp, Leeds LS9 7TF, W Yorkshire, England.
[Link, Daniel C.] Washington Univ, Sch Med, St Louis, MO USA.
[Shimamura, Akiko] Washington Univ, Fred Hutchinson Canc Res Ctr, Seattle Childrens Hosp, St Louis, MO USA.
[Newburger, Peter E.] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Boxer, Laurence A.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Welte, Karl] Hannover Med Sch, Dept Pediat Hematol Oncol, D-3000 Hannover, Germany.
[Dale, David C.] Univ Washington, Seattle, WA 98195 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1242
EP 1242
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803761
ER
PT J
AU Calado, RT
Cooper, JN
Scheinberg, P
Wu, C
Zago, MA
Padilla-Nash, H
Ried, T
Sloand, EM
Young, NS
AF Calado, Rodrigo T.
Cooper, James N.
Scheinberg, Phillip
Wu, Colin
Zago, Marco A.
Padilla-Nash, Hesed
Ried, Thomas
Sloand, Elaine M.
Young, Neal S.
TI Telomere Shortening Promotes Chromosomal Instability and Predicts
Malignant Clonal Evolution in Aplastic Anemia.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Calado, Rodrigo T.; Cooper, James N.; Scheinberg, Phillip; Wu, Colin; Sloand, Elaine M.; Young, Neal S.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Zago, Marco A.] Univ Sao Paulo, Sch Med, Dept Internal Med, BR-14049 Ribeirao Preto, Brazil.
[Padilla-Nash, Hesed; Ried, Thomas] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA.
RI Calado, Rodrigo/G-2619-2011; Scheinberg, Phillip/H-5251-2012
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1243
EP 1243
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803763
ER
PT J
AU Zhu, BM
Wickre, M
Na, R
Klover, P
Martin, C
Kimura, A
Hennighausen, L
AF Zhu, Bing-Mei
Wickre, Mark
Na, Risu
Klover, Peter
Martin, Cyril
Kimura, Akiko
Hennighausen, Lothar
TI Stat5 Is Essential for BCR-ABL-Transformed Chronic Myeloid Leukemia
(CML) Associated with Increased CCN3 Gene Expression.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Zhu, Bing-Mei; Wickre, Mark; Na, Risu; Klover, Peter; Martin, Cyril; Kimura, Akiko; Hennighausen, Lothar] NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1266
EP 1266
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803826
ER
PT J
AU Klemm, L
Duy, C
Iacobucci, I
von Levetzow, G
Feldhahn, N
Kim, YM
Hofmann, WK
Jumaa, H
Groffen, J
Heisterkamp, N
Martinelli, G
Lieber, MR
Casellas, R
Muschen, M
AF Klemm, Lars
Duy, Cihangir
Iacobucci, Ilaria
von Levetzow, Gregor
Feldhahn, Niklas
Kim, Yong-mi
Hofmann, Wolf-Karsten
Jumaa, Hassan
Groffen, John
Heisterkamp, Nora
Martinelli, Giovanni
Lieber, Michael R.
Casellas, Rafael
Mueschen, Markus
TI The B Cell Mutator AID Promotes B Lymphoid Blast Crisis and
Drug-Resistance in Chronic Myeloid Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Klemm, Lars; Duy, Cihangir; von Levetzow, Gregor; Groffen, John; Heisterkamp, Nora; Mueschen, Markus] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Leukemia & Lymphoma Program, Los Angeles, CA 90033 USA.
[Iacobucci, Ilaria] Univ Bologna, Seragnoli Inst, Dept Hematol & Oncol Sci, Bologna, Italy.
[Feldhahn, Niklas] Rockefeller Univ, New York, NY 10021 USA.
[Kim, Yong-mi] Childrens Hosp Los Angeles, Leukemia Res Program, Los Angeles, CA 90027 USA.
[Hofmann, Wolf-Karsten] Univ Hosp Mannheim, Dept Hematol & Oncol, Mannheim, Germany.
[Jumaa, Hassan] Max Planck Inst Immunobiol, D-7800 Freiburg, Germany.
[Casellas, Rafael] NIAMS, Natl Inst Hlth Genom Integr & Immun, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1267
EP 1268
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803829
ER
PT J
AU Le, RQ
Bevans, M
Savani, BN
Mitchell, S
Stringaris, K
Koklanaris, EK
Barrett, AJ
AF Le, Robert Quan
Bevans, Margaret
Savani, Bipin N.
Mitchell, Sandra
Stringaris, Kate
Koklanaris, Eleftheria K.
Barrett, A. John
TI Favorable Outcome and Quality of Life in Patients Surviving 5 or More
Years After Allogeneic Hematopoietic Stem Cell Transplantation for
Hematologic Malignancies
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Le, Robert Quan; Stringaris, Kate; Koklanaris, Eleftheria K.; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Bevans, Margaret; Mitchell, Sandra] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Savani, Bipin N.] Vanderbilt Univ, Med Ctr, Hematol & Stem Cell Transplantat Sect, Div Hematol Oncol,Dept Med, Nashville, TN USA.
[Savani, Bipin N.] Vet Affairs Med Ctr, Nashville, TN 37212 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1284
EP 1284
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803867
ER
PT J
AU Pusic, I
DiPersio, JF
Goran, SL
Romvari, EM
Bauer, SL
Comer, HS
Abboud, CN
Cashen, AF
Gale, RP
Pavletic, SZ
AF Pusic, Iskra
DiPersio, John F.
Goran, Stefanie L.
Romvari, Edie M.
Bauer, Stephanie L.
Comer, Holly S.
Abboud, Camille N.
Cashen, Amanda F.
Gale, Robert Peter
Pavletic, Steven Z.
TI Phase-2 Study of Pomalidomide in Advanced Corticosteroid-Resistant
Chronic Graft-Versus-Host Disease (cGVHD)
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Pusic, Iskra; DiPersio, John F.; Goran, Stefanie L.; Romvari, Edie M.; Bauer, Stephanie L.; Comer, Holly S.; Abboud, Camille N.; Cashen, Amanda F.] Washington Univ, Sch Med, Siteman Canc Ctr, St Louis, MO USA.
[Gale, Robert Peter] Celgene Corp, Summit, NJ USA.
[Pavletic, Steven Z.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1290
EP 1290
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725803881
ER
PT J
AU Aue, G
Soto, S
Valdez, J
Arthur, DC
Roschewski, M
Wiestner, A
AF Aue, Georg
Soto, Susan
Valdez, Janet
Arthur, Diane C.
Roschewski, Mark
Wiestner, Adrian
TI A Phase II Trial of Pulse Dosing Lenalidomide: 3 Weeks On 3 Weeks off in
Previously Treated Chronic Lymphocytic Leukemia/Small Lymphocytic
Lymphoma.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Aue, Georg; Soto, Susan; Valdez, Janet; Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Arthur, Diane C.] NCI, Pathol Lab, Bethesda, MD 20892 USA.
[Roschewski, Mark] Walter Reed Army Med Ctr, Washington, DC 20307 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1331
EP 1331
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804092
ER
PT J
AU Kreitman, RJ
Wilson, WH
Stetler-Stevenson, M
Noel, P
FitzGerald, DJ
Pastan, I
AF Kreitman, Robert J.
Wilson, Wyndham H.
Stetler-Stevenson, Maryalice
Noel, Pierre
FitzGerald, David J.
Pastan, Ira
TI Long Term Results of BL22 (CAT-3888) in Multiply Relapsed Hairy Cell
Leukemia
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Kreitman, Robert J.; FitzGerald, David J.; Pastan, Ira] NCI, Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Stetler-Stevenson, Maryalice] NCI, Pathol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Noel, Pierre] NIH, Hematol Serv, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1337
EP 1337
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804107
ER
PT J
AU Cooper, N
Rao, VK
Fleisher, T
Bussel, JB
AF Cooper, Nichola
Rao, V. Koneti
Fleisher, Thomas
Bussel, James B.
TI Lymphocyte Homeostasis FAS Pathway Is Altered in Some Patients with
Immune Thrombocytopenia.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Cooper, Nichola] Hammersmith Hosp, Imperial Hlth Care NHS Trust, London, England.
[Rao, V. Koneti] NIAID, ALPS Unit, LCID, NIH, Bethesda, MD 20892 USA.
[Bussel, James B.] Weill Cornell Med Coll, Div Pediat Hematol Oncol, Platelet Disorders Ctr, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1363
EP 1363
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804179
ER
PT J
AU Larochelle, A
Savona, M
Wiggins, M
Anderson, S
Morrison, SJ
Dunbar, CE
AF Larochelle, Andre
Savona, Michael
Wiggins, Michael
Anderson, Stephanie
Morrison, Sean J.
Dunbar, Cynthia E.
TI Human and Rhesus Macaque Hematopoietic Stem Cells Are Not Enriched in
the CD150+CD48-SLAM Population
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Larochelle, Andre; Dunbar, Cynthia E.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Savona, Michael; Wiggins, Michael; Anderson, Stephanie] San Antonio Mil Med Ctr, Dept Hematol Oncol, San Antonio, TX USA.
[Morrison, Sean J.] Howard Hughes Med Inst, Dept Internal Med, Ann Arbor, MI USA.
[Morrison, Sean J.] Howard Hughes Med Inst, Ctr Stem Cell Biol & Life Sci, Ann Arbor, MI USA.
[Morrison, Sean J.] Univ Michigan, Ann Arbor, MI 48109 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1370
EP 1370
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804196
ER
PT J
AU Fitzhugh, C
Hsieh, MM
Phang, O
Madison, C
Luznik, L
Powell, J
Tisdale, JF
AF Fitzhugh, Courtney
Hsieh, Matthew M.
Phang, Oswald
Madison, Camille
Luznik, Leo
Powell, Jonathan
Tisdale, John F.
TI Post-Transplant Cyclophosphamide and Sirolimus Are Synergistic in
Preventing Rejection and Inducing Stable Mixed Chimerism Independently
of Regulatory T Cells
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Fitzhugh, Courtney; Hsieh, Matthew M.; Phang, Oswald; Madison, Camille; Tisdale, John F.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Luznik, Leo; Powell, Jonathan] Johns Hopkins Univ, Baltimore, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1373
EP 1374
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804205
ER
PT J
AU Mariotti, J
Ryan, K
Massey, P
Buxhoeveden, N
Foley, J
Fowler, D
AF Mariotti, Jacopo
Ryan, Kaitlyn
Massey, Paul
Buxhoeveden, Nicole
Foley, Jason
Fowler, Daniel
TI Pentostatin Facilitates Fully MHC-Disparate Murine Mini-Transplantation
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Mariotti, Jacopo; Ryan, Kaitlyn; Massey, Paul; Buxhoeveden, Nicole] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Foley, Jason] Jason Foley, Expt Transplantat & Immunol, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1373
EP 1373
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804204
ER
PT J
AU Bartelmez, S
Bhatwadekar, A
Iversen, P
Ruscetti, FW
Grant, M
AF Bartelmez, Stephen
Bhatwadekar, Ashay
Iversen, Patrick
Ruscetti, Francis W.
Grant, Maria
TI Transient Inhibition of Transforming Growth Factor-beta 1 in Human
Blood-Derived CD34+Cells Enhances Survival and Proliferation in Vitro
and Vascular Reparative functions In Vivo
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Bartelmez, Stephen] BetaStem Therapeut, Stem Cells, San Francisco, CA USA.
[Bhatwadekar, Ashay; Grant, Maria] Univ Florida, Gainesville, FL USA.
[Iversen, Patrick] AVI BioPharma, Biol, Corvallis, OR USA.
[Ruscetti, Francis W.] NCI, Expt Immunol Lab, NIH, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1376
EP 1376
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804211
ER
PT J
AU Harrow, FJ
Cline, AP
Seidel, NE
Persons, D
Gallagher, PG
Bodine, DM
AF Harrow, Faith J.
Cline, Amanda P.
Seidel, Nancy E.
Persons, Derek
Gallagher, Patrick G.
Bodine, David M.
TI A Modified ANK-1 Promoter Directs Uniform, Copy Number Dependent Gamma
Globin Gene Expression at Therapeutic Levels of a in a Lentivirus
Vector.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Harrow, Faith J.; Cline, Amanda P.; Seidel, Nancy E.; Bodine, David M.] NHGRI, Genet & Mol Biol Branch, Bethesda, MD 20892 USA.
[Persons, Derek] St Jude Childrens Hosp, Memphis, TN 38105 USA.
[Gallagher, Patrick G.] Yale Univ, Sch Med, New Haven, CT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1382
EP 1382
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804230
ER
PT J
AU Uchida, N
Washington, K
Hsieh, MM
Tisdale, JF
AF Uchida, Naoya
Washington, Kareem
Hsieh, Matthew M.
Tisdale, John F.
TI Chicken HS4 Insulators Have Minimal Functions in Human Hematopoietic
Cells That Were Transduced with An HIV1-Based Lentiviral Vector.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Uchida, Naoya; Washington, Kareem; Tisdale, John F.] NHLBI, MCHB, NIH, Bethesda, MD 20892 USA.
[Hsieh, Matthew M.] NIDDK, NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1384
EP 1384
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804235
ER
PT J
AU Staber, JM
Burnight, E
Sarvida, ME
McCaffrey, A
Kaminski, J
McCray, P
AF Staber, Janice M.
Burnight, Erin
Sarvida, Marie-Ellen
McCaffrey, Anton
Kaminski, Joseph
McCray, Paul
TI Gene Transfer Targeting Hepatocytes Using the PiggyBac Transposon
System: An Approach towards Hemophilia A Correction and Long Term
Expression of Factor VIII.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Staber, Janice M.; Burnight, Erin; McCaffrey, Anton; McCray, Paul] Univ Iowa Hosp & Clin, Iowa City, IA 52242 USA.
[Sarvida, Marie-Ellen] Loyola Univ Hlth Syst, Maywood, IL USA.
[Kaminski, Joseph] NIH, Med Coll Georgia, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1385
EP 1385
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804240
ER
PT J
AU Amarnath, S
Wang, JCM
Massey, PR
Riley, JL
Levine, B
June, CH
Medin, JA
Fowler, D
AF Amarnath, Shoba
Wang, James C. M.
Massey, Paul R.
Riley, James L.
Levine, Bruce
June, Carl H.
Medin, Jeffrey A.
Fowler, Daniel
TI PD-L1 Immuno-Gene Therapy Under Cell Fate Control: Persistence of
Cellular Delivery Vehicle and Transgene Expression
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Amarnath, Shoba] NCI, Expt Transplantat Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Medin, Jeffrey A.] Univ Hlth Network, Ontario Canc Inst, Toronto, ON, Canada.
[Massey, Paul R.] NCI, Expt Transplantat & Immunol Branch, NIH, Bethesda, MD 20892 USA.
[Riley, James L.; Levine, Bruce; June, Carl H.] Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
RI Levine, Bruce/D-1688-2009
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1387
EP 1387
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804245
ER
PT J
AU Dejesus, CE
Egen, JG
Alvarez, X
Metzger, ME
Combs, CA
Malide, DA
Yu, ZX
Donahue, RE
AF Dejesus, Catherine E.
Egen, Jackson G.
Alvarez, Xavier
Metzger, Mark E.
Combs, Christian A.
Malide, Daniela A.
Yu, Zu Xi
Donahue, Robert E.
TI The Transient Neutropenia Following G-CSF Administration Is Associated
with An Accumulation of Neutrophils in the Pulmonary and Splenic
Vasculature
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Dejesus, Catherine E.; Metzger, Mark E.; Donahue, Robert E.] NHLBI, Hematol Branch, Rockville, MD USA.
[Egen, Jackson G.] NIAID, Lymphocyte Biol Sect, Bethesda, MD 20892 USA.
[Alvarez, Xavier] Tulane Natl Primate Res Ctr, Div Comparat Pathol, Covington, LA USA.
[Combs, Christian A.; Malide, Daniela A.] NHLBI, Light Microscopy Core Facil, Bethesda, MD 20892 USA.
[Yu, Zu Xi] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1389
EP 1389
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804251
ER
PT J
AU Tuschong, L
Dejesus, CE
Adams, M
Bonifacino, AC
Hickstein, DD
Donahue, RE
AF Tuschong, Laura
Dejesus, Catherine E.
Adams, Meredith
Bonifacino, Aylin C.
Hickstein, Dennis D.
Donahue, Robert E.
TI Leukocyte Integrin CD18 Expression Mediates Transient Neutropenia
Following G-CSF Administration
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Tuschong, Laura; Hickstein, Dennis D.] NCI, Expt Transplantat & Immunol Ctr Canc Res, Bethesda, MD 20892 USA.
[Dejesus, Catherine E.; Adams, Meredith; Bonifacino, Aylin C.; Donahue, Robert E.] NHLBI, Hematol Branch, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1389
EP 1390
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804252
ER
PT J
AU Aerbajinai, W
Chin, K
Zhu, JQ
Hyun, L
Kumkhaek, C
Rodgers, GP
AF Aerbajinai, Wulin
Chin, Kyung
Zhu, Jianqiong
Hyun, Lee
Kumkhaek, Chutima
Rodgers, Griffin P.
TI Glia Maturation Factor-Gamma Mediates Lipopolysaccharide-Induced
Inflammation Via p38 MAPK and NF-Kappab
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Chin, Kyung; Hyun, Lee] NHLBI, Mol & Clin Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Rodgers, Griffin P.] NIDDK, Mol & Clin Hematol Branch, NIH, Bethesda, MD USA.
[Kumkhaek, Chutima] NIDDK, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1393
EP 1393
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804263
ER
PT J
AU Whittaker, S
Kim, EJ
Prince, M
Demierre, MF
Giver, C
Lonial, S
Pickarz, R
Kim, YH
Nichols, J
Nix, D
Bates, S
AF Whittaker, Sean
Kim, Ellen J.
Prince, Miles
Demierre, Marie France
Giver, Cynthia
Lonial, Sagar
Pickarz, Richard
Kim, Youn H.
Nichols, Jean
Nix, Darrell
Bates, Susan
TI Characterization of Cyclic Hematologic Changes Observed in Patients with
Cutaneous T-Cell Lymphoma (CTCL) Receiving Romidepsin, a Novel Histone
Deacetylase (HDAC) Inhibitor
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Whittaker, Sean] St Thomas Hosp, St Johns Inst Dermatol, London, England.
[Kim, Ellen J.] Univ Penn, Philadelphia, PA 19104 USA.
[Prince, Miles] Peter MacCallum Canc Ctr, Melbourne, Australia.
[Demierre, Marie France] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Giver, Cynthia; Lonial, Sagar] Emory Univ, Winship Canc Ctr, Atlanta, GA 30322 USA.
[Pickarz, Richard; Bates, Susan] NCI, Bethesda, MD 20892 USA.
[Kim, Youn H.] Stanford Univ, Stanford, CA 94305 USA.
[Nix, Darrell] Gloucester Pharmaceut, Drug Dev, Cambridge, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1425
EP 1425
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804365
ER
PT J
AU Cabell, C
Bates, S
Piekarz, R
Whittaker, S
Kim, YH
Currie, M
Godfrey, CJ
Schoonmaker, C
Nichols, J
Nix, D
Burris, HA
AF Cabell, Christopher
Bates, Susan
Piekarz, Richard
Whittaker, Sean
Kim, Youn H.
Currie, Michelle
Godfrey, C. J.
Schoonmaker, Christopher
Nichols, Jean
Nix, Darrell
Burris, Howard A.
TI Systematic Assessment of Potential Cardiac Effects of the Novel Histone
Deacetylase (HDAC) Inhibitor Romidepsin.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Cabell, Christopher] Quintiles Transnat, Durham, NC USA.
[Bates, Susan; Piekarz, Richard] NCI, Bethesda, MD 20892 USA.
[Whittaker, Sean] St Thomas Hosp, St Johns Inst Dermatol, London, England.
[Kim, Youn H.] Stanford Univ, Stanford, CA 94305 USA.
[Currie, Michelle; Schoonmaker, Christopher] Veristat Inc, Holliston, MA USA.
[Godfrey, C. J.] Anoixis Corp, Natick, MA USA.
[Nix, Darrell] Gloucester Pharmaceut, Drug Dev, Cambridge, MA USA.
[Burris, Howard A.] Sarah Cannon Res Inst, Nashville, TN USA.
NR 0
TC 2
Z9 2
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1428
EP 1429
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804373
ER
PT J
AU Younes, A
Copeland, AR
Romaguera, J
Fayad, L
Fanale, M
Faria, SD
Medeiros, LJ
Ivy, SP
AF Younes, Anas
Copeland, Amanda R.
Romaguera, Jorge
Fayad, Luis
Fanale, Michelle
Faria, Silvana de Castro
Medeiros, L. Jeffrey
Ivy, S. Percy
TI Clinical and Biologic Activity of the Heat Shock Protein-90 (HSP-90)
Inhibitor 17-AAG in Patients with Relapsed Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Younes, Anas; Copeland, Amanda R.] Univ Texas MD Anderson Canc Ctr, Dept Lymphoma Myeloma, Houston, TX 77030 USA.
[Ivy, S. Percy] NCI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 2
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1441
EP 1441
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804408
ER
PT J
AU Klier-Richter, M
Irmler, M
Bonzheim, I
Schaefer, S
Beckers, J
Fend, F
Raffeld, M
Quintanilla-Martinez, L
AF Klier-Richter, Margit
Irmler, Martin
Bonzheim, Irina
Schaefer, Sabine
Beckers, Johannes
Fend, Falko
Raffeld, Mark
Quintanilla-Martinez, Leticia
TI Identification of Cyclin D1-Dependent Genes by Gene Expression Profiling
in MCL Cell Lines and Primary Cases.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Klier-Richter, Margit; Bonzheim, Irina; Schaefer, Sabine; Fend, Falko; Quintanilla-Martinez, Leticia] Univ Tubingen, Univ Tubingen Hosp, Tubingen, Germany.
[Irmler, Martin; Beckers, Johannes] German Res Ctr Environm Hlth, Helmholtz Ctr Munich, Inst Expt Genet, Neuherberg, Germany.
[Raffeld, Mark] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RI Irmler, Martin/B-3317-2013
OI Irmler, Martin/0000-0003-3169-479X
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1513
EP 1513
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804600
ER
PT J
AU Sasaki, D
Imaizumi, Y
Hasegawa, H
Osaka, A
Tsuruda, K
Tsukasaki, K
Iwanaga, M
Miyazaki, Y
Yanagihara, K
Marquez, V
Kamihira, S
Yamada, Y
AF Sasaki, Daisuke
Imaizumi, Yoshitaka
Hasegawa, Hiroo
Osaka, Akemi
Tsuruda, Kazuto
Tsukasaki, Kunihiro
Iwanaga, Masako
Miyazaki, Yasushi
Yanagihara, Katsunori
Marquez, Victor
Kamihira, Shimeru
Yamada, Yasuaki
TI The Overexpression of Enhancer of Zeste Homologue 2 Is Associated with
Tumor Proliferation and Aggressive Behavior in Adult T-Cell
Leukemia/Lymphoma
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Sasaki, Daisuke; Imaizumi, Yoshitaka; Hasegawa, Hiroo; Osaka, Akemi; Tsuruda, Kazuto; Tsukasaki, Kunihiro; Iwanaga, Masako; Miyazaki, Yasushi; Yanagihara, Katsunori; Kamihira, Shimeru; Yamada, Yasuaki] Nagasaki Univ, Grad Sch Biomed Sci, Nagasaki 852, Japan.
[Marquez, Victor] NCI, Med Chem Lab, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1522
EP 1522
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804623
ER
PT J
AU Bergerson, RJ
Collier, LS
Lugthart, S
Allaei, R
Nixon, MJ
Silverstein, KAT
Sarver, A
Fan, DF
Lamblin, AFJ
Wolff, L
Kersey, JH
O'Sullivan, G
Delwel, R
Kogan, SC
Adams, DJ
Largaespada, D
AF Bergerson, Rachel Joy
Collier, Lara S.
Lugthart, Sanne
Allaei, Raha
Nixon, Molly J.
Silverstein, Kevin A. T.
Sarver, Aaron
Fan, Danhua Flora
Lamblin, Anne-Francoise J.
Wolff, Linda
Kersey, John H.
O'Sullivan, Gerard
Delwel, Ruud
Kogan, Scott C.
Adams, David J.
Largaespada, David
TI An Insertional Mutagenesis Screen for Genes That Cooperate with Mll-AF9
in Leukemogenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Bergerson, Rachel Joy; Allaei, Raha; Nixon, Molly J.; Silverstein, Kevin A. T.; Sarver, Aaron; Fan, Danhua Flora; O'Sullivan, Gerard; Largaespada, David] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN USA.
[Collier, Lara S.] Univ Wisconsin, Sch Pharm, Div Pharmaceut Sci, Madison, WI 53706 USA.
[Lugthart, Sanne; Delwel, Ruud] Erasmus Univ, Med Ctr, Rotterdam, Netherlands.
[Lamblin, Anne-Francoise J.] Univ Minnesota, Off Vice President Res, St Paul, MN 55108 USA.
[Wolff, Linda] NCI, NIH, Bethesda, MD 20892 USA.
[Kersey, John H.] Univ Minnesota, Lab Med & Pathol, Minneapolis, MN USA.
[Kogan, Scott C.] Univ Calif San Francisco, Lab Med, San Francisco, CA 94143 USA.
[Adams, David J.] Wellcome Trust Sanger Inst, Hinxton, England.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1523
EP 1524
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804626
ER
PT J
AU Aue, G
Du, Y
Cleveland, S
Smith, S
Dave, UP
Jenkins, N
Copeland, NG
Dunbar, C
AF Aue, Georg
Du, Yang
Cleveland, Susan
Smith, Stephen
Dave, Utpal P.
Jenkins, Nancy
Copeland, Neal G.
Dunbar, Cynthia
TI Sox4 Downregulates Pu.1 Gene Expression by Binding to An Upper
Regulatory Element of Pu.1, a Mechanism Contributing to Leukemogenesis
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Aue, Georg; Dunbar, Cynthia] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Du, Yang] Uniformed Serv Univ Hlth Sci, Bethesda, MD 20814 USA.
[Cleveland, Susan; Dave, Utpal P.] Vanderbilt Univ, Med Ctr, Nashville, TN USA.
[Smith, Stephen] Vanderbilt Univ, Sch Med, Nashville, TN USA.
[Jenkins, Nancy; Copeland, Neal G.] Inst Mol & Cellular Biol, Singapore, Singapore.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1529
EP 1529
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804643
ER
PT J
AU Luetkhoff, LK
Albisetti, M
Bernard, TJ
Bonduel, M
Brandao, LR
Chabrier, S
Chan, A
Fiedler, B
Fullerton, HJ
Ganesan, V
Goldenberg, NA
Golomb, M
Grabowski, EF
Heller, C
Holzhauer, S
Iorio, A
Journeycake, J
Kenet, G
Kirkham, FJ
Kurnik, K
Lynch, JK
Male, C
Manco-Johnson, MJ
Mesters, R
Monagle, P
van Ommen, HC
Raffini, L
Simioni, P
Straeter, R
Young, G
Nowak-Gottl, U
AF Luetkhoff, Lisa K.
Albisetti, Manuela
Bernard, Timothy J.
Bonduel, Mariana
Brandao, Leonardo R.
Chabrier, Stephanie
Chan, Anthony
Fiedler, Barbara
Fullerton, Heather J.
Ganesan, Vijeja
Goldenberg, Neil A.
Golomb, Meredith
Grabowski, Eric F.
Heller, Christine
Holzhauer, Susanne
Iorio, Alfonso
Journeycake, Janna
Kenet, Gili
Kirkham, Fenella J.
Kurnik, Karin
Lynch, John K.
Male, Christoph
Manco-Johnson, Marilyn J.
Mesters, Rolf
Monagle, Paul
van Ommen, Heleen C.
Raffini, Leslie
Simioni, Paolo
Straeter, Ronald
Young, Guy
Nowak-Gottl, Ulrike
TI Impact of Thrombophilia On Arterial Ischemic Stroke or Cerebral Venous
Sinus Thromboses in Children: A Systematic Review & Meta-Analysis of
Observational Studies
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Luetkhoff, Lisa K.; Fiedler, Barbara; Straeter, Ronald] Univ Childrens Hosp Munster, Munster, Germany.
[Albisetti, Manuela] Univ Childrens Hosp Zurich, Zurich, Switzerland.
[Bernard, Timothy J.] Univ Colorado, Dept Pediat, Sect Hem Onc BMT, Aurora, CO USA.
[Bernard, Timothy J.] Univ Colorado, Mt States Reg Hemophilia & Thrombosis Ctr, Aurora, CO USA.
[Bernard, Timothy J.; Goldenberg, Neil A.; Manco-Johnson, Marilyn J.] Childrens Hosp, Aurora, CO USA.
[Bonduel, Mariana] Hosp Pediat Prof Dr JP Garrahan, Serv Hematol & Oncol, Buenos Aires, DF, Argentina.
[Brandao, Leonardo R.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Chabrier, Stephanie] Ctr Hosp Univ, Unit Neonatol & Reanimat Pediat, St Etienne, France.
[Chan, Anthony] McMaster Univ, Hamilton, ON, Canada.
[Fullerton, Heather J.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Fullerton, Heather J.] UCSF Childrens Hosp, San Francisco, CA USA.
[Ganesan, Vijeja; Kirkham, Fenella J.] UCL, Neurosci Unit 11, Inst Child Hlth, London, England.
[Goldenberg, Neil A.] Univ Colorado Denver, Pediat & Mt States Reg Hemophilia & Thrombosis Ct, Aurora, CO USA.
[Golomb, Meredith] Indiana Univ, Sch Med, Indianapolis, IN USA.
[Grabowski, Eric F.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Grabowski, Eric F.] Harvard Univ, Sch Med, Boston, MA USA.
[Heller, Christine] Univ Hosp Frankfurt, Frankfurt, Germany.
[Holzhauer, Susanne] Charite, Berlin, Germany.
[Iorio, Alfonso] Univ Perugia, I-06100 Perugia, Italy.
[Journeycake, Janna] Childrens Med Ctr Dallas, Dept Pediat 17, Dallas, TX USA.
[Kenet, Gili] Chaim Sheba Med Ctr, Thrombosis Unit, IL-52621 Tel Hashomer, Israel.
[Kurnik, Karin] Dr V Hauners Childrens Univ Hosp, Pediat Hemophilia Ctr, Munich, Germany.
[Lynch, John K.] Natl Inst Neurol Disorders & Stroke, Div Stroke Diagnost & Therapeut 21, Bethesda, MD USA.
[Male, Christoph] Med Univ Vienna, Dept Pediat, Vienna, Austria.
[Mesters, Rolf] Univ Munster, Dept Internal Med, D-4400 Munster, Germany.
[Monagle, Paul] Univ Melbourne, Dept Paediat, Parkville, Vic 3052, Australia.
[van Ommen, Heleen C.] Emma Childrens Hosp AMC, Dept Pediat Hematol 25, Amsterdam, Netherlands.
[Raffini, Leslie] Childrens Hosp Philadelphia, Dept Pediat, Div Hematol 27, Philadelphia, PA 19104 USA.
[Simioni, Paolo] Univ Padua, Sch Med, Padua, Italy.
[Young, Guy] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[Nowak-Gottl, Ulrike] Univ Childrens Hosp, Dept Pediat Hem Onc, Munster, Germany.
RI Kirkham, Fenella/C-2442-2009;
OI Kirkham, Fenella/0000-0002-2443-7958; Young, Guy/0000-0001-6013-1254
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1534
EP 1535
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804657
ER
PT J
AU Tanno, T
Sripichai, O
Noh, SJ
Byrnes, C
Meier, ER
Lee, YT
Miller, JL
AF Tanno, Toshihiko
Sripichai, Orapan
Noh, Seung-Jae
Byrnes, Colleen
Meier, Emily Riehm
Lee, Y. Terry
Miller, Jeffery L.
TI Ineffective Erythropoiesis Caused by Phenylhydrazine Activates the
Expression of GDF15 in Maturing Erythroblasts
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Tanno, Toshihiko; Sripichai, Orapan; Noh, Seung-Jae; Byrnes, Colleen; Meier, Emily Riehm; Lee, Y. Terry; Miller, Jeffery L.] NIDDKD, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1547
EP 1547
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804696
ER
PT J
AU Wynne, E
Perkins, K
Price, S
Louie, A
Rao, VK
AF Wynne, Elisabeth
Perkins, Katie
Price, Susan
Louie, Adeline
Rao, V. Koneti
TI CT Scan Enumeration of Altered Spleen Status and Pulmonary Artery Size
in Patients with Autoimmune Lymphoproliferative Syndrome (ALPS)
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Wynne, Elisabeth] UVA Sch Med, Charlottesville, VA USA.
[Perkins, Katie; Price, Susan; Rao, V. Koneti] NIAID, ALPS Unit, LCID, NIH, Bethesda, MD 20892 USA.
[Louie, Adeline] NIH, Dept Radiol, Ctr Clin, Bethesda, MD 20892 USA.
NR 4
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1548
EP 1548
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804698
ER
PT J
AU Tanno, T
Rabel, A
Lee, YT
Leitman, S
Miller, JL
AF Tanno, Toshihiko
Rabel, Antoinett
Lee, Y. Terry
Leitman, Susan
Miller, Jeffery L.
TI A Comparison of Serum Hepcidin and GDF15 Expression in Cases of Iron
Depletion Due to Blood Loss
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Tanno, Toshihiko; Rabel, Antoinett; Lee, Y. Terry; Miller, Jeffery L.] NIDDKD, Mol Med Branch, NIH, Bethesda, MD 20892 USA.
[Leitman, Susan] NIH, Blood Serv Sect, Warren Grant Magnuson Clin Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1550
EP 1551
PG 2
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804706
ER
PT J
AU Falkenburg, WJJ
Melenhorst, JJ
Kester, MGD
Hombrink, P
Heemskerk, MHM
Gostick, E
Price, DA
Falkenburg, JHF
Barrett, AJ
Jedema, I
AF Falkenburg, Willem J. J.
Melenhorst, J. Joseph
Kester, Michel G. D.
Hombrink, Pleun
Heemskerk, Mirjam H. M.
Gostick, Emma
Price, David A.
Falkenburg, J. H. Frederik
Barrett, A. John
Jedema, Inge
TI Allogeneic HLA-A2-Restricted WT1-Specific T Cells From Mismatched Donors
Are Highly Reactive but Show Potentially Hazardous Promiscuity
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Falkenburg, Willem J. J.; Melenhorst, J. Joseph; Barrett, A. John] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Kester, Michel G. D.; Hombrink, Pleun; Heemskerk, Mirjam H. M.; Falkenburg, J. H. Frederik; Jedema, Inge] Leiden Univ, Med Ctr, Dept Hematol, Leiden, Netherlands.
[Gostick, Emma; Price, David A.] Cardiff Univ, Sch Med, Cardiff, S Glam, Wales.
RI Price, David/C-7876-2013
OI Price, David/0000-0001-9416-2737
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1565
EP 1565
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804744
ER
PT J
AU Lundqvist, A
Berg, M
Smith, A
Cook, L
Goodwin, R
Ramos, C
Vasu, S
Pantin, J
Lopez, R
Khuu, H
Fellowes, V
Stroncek, D
Donohue, T
Childs, R
AF Lundqvist, Andreas
Berg, M.
Smith, A.
Cook, L.
Goodwin, R.
Ramos, C.
Vasu, S.
Pantin, J.
Lopez, R.
Khuu, H.
Fellowes, V.
Stroncek, D.
Donohue, T.
Childs, R.
TI Adoptive Infusion of Ex Vivo Expanded Autologous Natural Killer (NK)
Cells in Cancer Patients Treated with Bortezomib to Sensitize to
NK-TRAIL Cytotoxicity
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Lundqvist, Andreas; Berg, M.; Smith, A.; Cook, L.; Goodwin, R.; Ramos, C.; Vasu, S.; Pantin, J.; Lopez, R.; Donohue, T.; Childs, R.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Khuu, H.] NIH, Cell Proc Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1565
EP 1565
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804743
ER
PT J
AU Rezvani, K
Yong, ASM
Mielke, S
Jafarpour, B
Savani, BN
Le, Q
Eniafe, R
Boss, C
Kurlander, RJ
Barrett, AJ
AF Rezvani, Katayoun
Yong, Agnes S. M.
Mielke, Stephan
Jafarpour, Behnam
Savani, Bipin N.
Le, Quan
Eniafe, Rhoda
Boss, Carol
Kurlander, Roger J.
Barrett, A. John
TI The Response to Repeated Vaccination with PR1 and WT1 Peptides Admixed
in Montanide Adjuvant Is Transient and Fails to Induce Sustained
Anti-Leukemia Responses in Patients with Myeloid Malignancies.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Rezvani, Katayoun] Univ London Imperial Coll Sci Technol & Med, Dept Haematol, London, England.
[Yong, Agnes S. M.; Jafarpour, Behnam; Le, Quan; Eniafe, Rhoda] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
[Mielke, Stephan] Univ Wurzburg, Wurzburg, Germany.
[Savani, Bipin N.] Vanderbilt Univ, Nashville, TN USA.
[Kurlander, Roger J.] NIH, Dept Lab Med, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1571
EP 1571
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804759
ER
PT J
AU Mattson, MP
AF Mattson, Mark P.
TI Mitochondria in Neuroplasticity, Neurologic Disease and Aging.
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Mattson, Mark P.] NIA, Neurosci Lab, NIH, Baltimore, MD 21224 USA.
RI Mattson, Mark/F-6038-2012
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1575
EP 1575
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804762
ER
PT J
AU Wiestner, A
AF Wiestner, Adrian
TI Biology and Treatment of Mantle Cell Lymphoma in the Genomic Era
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Wiestner, Adrian] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1581
EP 1581
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804788
ER
PT J
AU Stroncek, D
AF Stroncek, David
TI TRALI Pathophysiology
SO BLOOD
LA English
DT Meeting Abstract
CT 51st Annual Meeting of the American-Society-of-Hematology
CY DEC 05-08, 2009
CL New Orleans, LA
SP Amer Soc Hematol
C1 [Stroncek, David] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 20
PY 2009
VL 114
IS 22
BP 1586
EP 1586
PG 1
WC Hematology
SC Hematology
GA 532DS
UT WOS:000272725804808
ER
PT J
AU Blume, A
Torner, L
Liu, Y
Subburaju, S
Aguilera, G
Neumann, ID
AF Blume, Annegret
Torner, Luz
Liu, Ying
Subburaju, Sivan
Aguilera, Greti
Neumann, Inga D.
TI Prolactin induces Egr-1 gene expression in cultured hypothalamic cells
and in the rat hypothalamus
SO BRAIN RESEARCH
LA English
DT Article
DE Signaling; Neuroplasticity; Stress; Hypothalamo-pituitary-adrenal axis;
Transcription factor; Lactation
ID TRANSCRIPTION FACTOR ZIF268/EGR-1; CORTICOTROPIN-RELEASING HORMONE;
IMMEDIATE-EARLY GENE; NERVOUS-SYSTEM; MESSENGER-RNA;
HYPOTHALAMONEUROHYPOPHYSEAL SYSTEM; STIMULATED NEUROGENESIS;
GROWTH-FACTOR; LONG FORM; RECEPTOR
AB Prolactin (PRL), the major lactogenic hormone, acts also as neuromodulator and regulator of neuronal and glial plasticity in the brain. There is an increase in synthesis and release of PRL within the hypothalamus during peripartum and in response to stress. To identify mechanisms by which PRL induces neuroplasticity, we studied the ability of PRL to induce the transcription factor Egr-1 in the hypothalamic cell line, 4B, in vitro, and in specific neuronal cell types of the hypothalamus in vivo. PAL induced Egr-1 mRNA expression in 4B cells, an effect which was prevented by the MEK inhibitor, U0126. In vivo, intracerebroventricular PRL (1 mu g) increased Egr-1 mRNA levels in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON) of female rats. The increase in mRNA paralleled elevated Egr-1 protein expression in the PVN and SON. Double staining immunohistochemistry revealed Egr-1 localization in oxytocin neurons of the PVN and SON, but not in vasopressin neurons in these regions. In the dorsomedial PVN, a population of non-oxytocin or vasopressin cells localized in a region corresponding to corticotropin-releasing hormone neurons also showed marked Egr-1 immunoreactivity. The data suggest that PRL modulates plasticity in oxytocinergic neurons, through MAP kinase-dependent induction of Egr-1. Published by Elsevier B.V.
C1 [Liu, Ying; Subburaju, Sivan; Aguilera, Greti] NICHHD, Sect Endocrine Physiol, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
[Blume, Annegret; Torner, Luz; Neumann, Inga D.] Univ Regensburg, Inst Zool, Dept Behav & Mol Neuroendocrinol, D-8400 Regensburg, Germany.
[Torner, Luz] IMSS, Biochem Res Ctr Michoacan, Morelia, Michoacan, Mexico.
RP Aguilera, G (reprint author), NICHHD, Sect Endocrine Physiol, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
EM Greti_Aguilera@nih.gov
FU Intramural Research program of the NIH/NICHD; Bayerische
Forschungsstiftung; Deutsche Forschungsgemeinschaft; VolkswagenStiftung
FX The authors thank Luxiola Gonzalez and Remco Bredewold for expert
technical assistance. This work was partially supported by the
Intramural Research program of the NIH/NICHD (GA), by the Bayerische
Forschungsstiftung (AB+IDN), the Deutsche Forschungsgemeinschaft (IDN)
and the VolkswagenStiftung (IDN).
NR 48
TC 7
Z9 7
U1 1
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 20
PY 2009
VL 1302
BP 34
EP 41
DI 10.1016/j.brainres.2009.09.047
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 523KH
UT WOS:000272071600004
PM 19769948
ER
PT J
AU Luo, Y
Sarabi, SA
Backman, C
Shan, LF
Hoffer, B
Federoff, H
AF Luo, Yu
Sarabi, Sara Arezou
Backman, Cristina
Shan, Lufei
Hoffer, Barry
Federoff, Howard
TI Expression pattern of NuIP gene in adult mouse brain
SO BRAIN RESEARCH
LA English
DT Article
DE Nurr1; Protein interactor; G protein
ID NUCLEAR RECEPTOR NURR1; NGFI-B; CELLS; NEURONS; MICE; IDENTIFICATION;
PROTEIN; MEMORY; NUR77; RAS
AB We previously reported the identification of the Nurr1 interacting protein (NuIP) that was demonstrated to modulate the transcriptional activity of Nurr1, the orphan nuclear receptor required for midbrain dopaminergic neuron differentiation. NuIP was also cloned by others and referred to as a small G protein signaling modulators. The open reading frame of NuIP predicts a protein with an N-terminal RUN domain (RPIP8, UNC-14, and NESCA) and a C-terminal TBC domain (Tre-2, Bub2, and Cdc16) both of which are found in proteins of the GTPase activating protein (GAP) family, involved in the GTPase signaling pathway. To characterize the NuIP gene product, we developed a polyclonal antibody. Since NuIP gene is expressed most abundantly in adult and the level of expression during development is below the detection limit of immunohistochemistry, we now report the expression pattern of NuIP in adult mouse brain compared with the expression pattern of Nurr1 protein. Many regions co-expressed Nurr1 and NuIP including cortex, hippocampus, substantia nigra, and the cerebellum. However, there are also regions that exclusively express NuIP such as striatum, septum, globus pallidus, and the reticular thalamic nucleus. We also find that NuIP protein expresses mainly in NeuN-positive (neuronal nuclei) neurons but can be detected in GFAP-positive (glial fibrillary acidic protein) glial cells in hippocampus. Interestingly, NuIP is expressed in high levels in midbrain dopaminergic neurons including ventral tegmental area (VTA) and substantia nigra (SN) dopaminergic neurons but is not expressed or expressed in low levels in other dopaminergic neurons such as olfactory bulb and hypothalamus. Overall, the expression pattern of NuIP in adult mouse brain suggests that it may be involved in motor activity control in basal ganglia as well as higher central nervous system (CNS) functions such as cognition and memory in cortex and hippocampus. Published by Elsevier B.V.
C1 [Luo, Yu; Sarabi, Sara Arezou; Backman, Cristina; Shan, Lufei; Hoffer, Barry] NIDA, Intramural Res Program, Baltimore, MD 21224 USA.
[Federoff, Howard] Georgetown Univ, Dept Neurol, Washington, DC 20057 USA.
RP Hoffer, B (reprint author), NIDA, Intramural Res Program, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM bhoffer@mail.nih.gov
RI luo, Yu (Agnes)/E-4446-2010; backman, cristina/C-1276-2013
NR 25
TC 2
Z9 2
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 20
PY 2009
VL 1302
BP 42
EP 53
DI 10.1016/j.brainres.2009.09.026
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 523KH
UT WOS:000272071600005
PM 19765553
ER
PT J
AU Ma, XF
Takeda, K
Singh, A
Yu, ZX
Zerfas, P
Blount, A
Liu, CY
Towbin, JA
Schneider, MD
Adelstein, RS
Wei, QZ
AF Ma, Xuefei
Takeda, Kazuyo
Singh, Aman
Yu, Zu-Xi
Zerfas, Patricia
Blount, Anthony
Liu, Chengyu
Towbin, Jeffrey A.
Schneider, Michael D.
Adelstein, Robert S.
Wei, Qize
TI Conditional Ablation of Nonmuscle Myosin II-B Delineates Heart Defects
in Adult Mice
SO CIRCULATION RESEARCH
LA English
DT Article
DE nonmuscle myosin II-B; cardiomyopathy; intercalated discs
ID INTERCALATED DISK PROTEIN; HEAVY-CHAIN; CARDIAC-HYPERTROPHY; CONDUCTION
DEFECTS; CELL-ADHESION; MXIN-ALPHA; GENE; CARDIOMYOPATHY; MIGRATION;
CADHERIN
AB Rationale: Germline ablation of the cytoskeletal protein nonmuscle myosin II (NMII)-B results in embryonic lethality, with defects in both the brain and heart. Tissue-specific ablation of NMII-B by a Cre recombinase strategy should prevent embryonic lethality and permit study of the function of NMII-B in adult hearts.
Objective: We sought to understand the function of NMII-B in adult mouse hearts and to see whether the brain defects found in germline-ablated mice influence cardiac development.
Methods and Results: We used a loxP/Cre recombinase strategy to specifically ablate NMII-B in the brains or hearts of mice. Mice ablated for NMII-B in neural tissues die between postnatal day 12 and 22 without showing cardiac defects. Mice deficient in NMII-B only in cardiac myocytes (B(alpha MHC)/B(alpha MHC) mice) do not show brain defects. However, B(alpha MHC)/B(alpha MHC) mice display novel cardiac defects not seen in NMII-B germline-ablated mice. Most of the B(alpha MHC)/B(alpha MHC) mice are born with enlarged cardiac myocytes, some of which are multinucleated, reflecting a defect in cytokinesis. Between 6 to 10 months, they develop a cardiomyopathy that includes interstitial fibrosis and infiltration of the myocardium and pericardium with inflammatory cells. Four of 5 B(alpha MHC)/B(alpha MHC) hearts develop marked widening of intercalated discs.
Conclusions: By avoiding the embryonic lethality found in germline-ablated mice, we were able to study the function of NMII-B in adult mice and show that absence of NMII-B in cardiac myocytes results in cardiomyopathy in the adult heart. We also define a role for NMII-B in maintaining the integrity of intercalated discs. (Circ Res. 2009; 105: 1102-1109.)
C1 [Ma, Xuefei; Takeda, Kazuyo; Singh, Aman; Blount, Anthony; Adelstein, Robert S.; Wei, Qize] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
[Yu, Zu-Xi] NHLBI, Pathol Core Facil, NIH, Bethesda, MD 20892 USA.
[Liu, Chengyu] NHLBI, Transgen Mouse Core Facil, NIH, Bethesda, MD 20892 USA.
[Zerfas, Patricia] NIH, Div Vet Resources, Bethesda, MD 20892 USA.
[Towbin, Jeffrey A.] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA.
[Schneider, Michael D.] Univ London Imperial Coll Sci Technol & Med, Natl Heart & Lung Inst, London, England.
RP Adelstein, RS (reprint author), NHLBI, Mol Cardiol Lab, NIH, Bldg 10,Room 6C-103,10 Ctr Dr,MSC-1583, Bethesda, MD 20892 USA.
EM adelster@mail.nih.gov
OI Schneider, Michael/0000-0001-9645-1938; Adelstein,
Robert/0000-0002-8683-2144
FU Division of Intramural Research; National Heart, Lung, and Blood
Institute, NIH
FX This work was supported by the Division of Intramural Research, National
Heart, Lung, and Blood Institute, NIH.
NR 26
TC 16
Z9 17
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7330
J9 CIRC RES
JI Circ.Res.
PD NOV 20
PY 2009
VL 105
IS 11
BP 1102
EP U128
DI 10.1161/CIRCRESAHA.109.200303
PG 15
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA 521UC
UT WOS:000271948900008
PM 19815823
ER
PT J
AU Oldenhove, G
Bouladoux, N
Wohlfert, EA
Hall, JA
Chou, D
Dos Santos, L
O'Brien, S
Blank, R
Lamb, E
Natarajan, S
Kastenmayer, R
Hunter, C
Grigg, ME
Belkaid, Y
AF Oldenhove, Guillaume
Bouladoux, Nicolas
Wohlfert, Elizabeth A.
Hall, Jason A.
Chou, David
Dos Santos, Liliane
O'Brien, Shaun
Blank, Rebecca
Lamb, Erika
Natarajan, Sundar
Kastenmayer, Robin
Hunter, Christopher
Grigg, Michael E.
Belkaid, Yasmine
TI Decrease of Foxp3(+) Treg Cell Number and Acquisition of Effector Cell
Phenotype during Lethal Infection
SO IMMUNITY
LA English
DT Article
ID REGULATORY T-CELLS; TOXOPLASMA-GONDII; DENDRITIC CELLS; RETINOIC-ACID;
IFN-GAMMA; TGF-BETA; IN-VIVO; INTESTINAL INFLAMMATION; PERORAL
INFECTION; C57BL/6 MICE
AB Using a model of lethal oral infection with Toxoplasma gondii, we examined the fate of both induced and natural regulatory T (Treg) cells in the face of strong inflammatory responses occurring in a tolerogenicprone environment. We found that during highly T helper 1 (Th1) cell-polarized mucosal immune responses, Treg cell numbers collapsed via multiple pathways, including blockade of Treg cell induction and disruption of endogenous Treg cell homeostasis. In particular, shutdown of interleukin 2 (IL-2) in the highly Th1 cell-polarized environment triggered by infection directly contributes to Treg cell incapacity to suppress effector responses and eventually leads to immunopathogenesis. Furthermore, we found that environmental cues provided by both local dendritic cells and effector T cells can induce the expression of T-bet transcription factor and IFN-gamma by Treg cells. These data reveal a mechanism for Th1 cell pathogenicity that extends beyond their proinflammatory program to limit Treg cell survival.
C1 [Oldenhove, Guillaume; Bouladoux, Nicolas; Wohlfert, Elizabeth A.; Hall, Jason A.; Chou, David; Dos Santos, Liliane; Blank, Rebecca; Belkaid, Yasmine] NIAID, Mucosal Immunol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Kastenmayer, Robin] NIAID, Comparat Med Branch, Bill Young Ctr Biodefense & Emerging Infect Dis, NIH, Bethesda, MD 20892 USA.
[Lamb, Erika; Natarajan, Sundar; Grigg, Michael E.] NIAID, Mol Parasitol Unit, NIH, Bethesda, MD 20892 USA.
[Hunter, Christopher] Univ Penn, Sch Vet Med, Dept Pathobiol, Philadelphia, PA 19104 USA.
[Hall, Jason A.; O'Brien, Shaun] Univ Penn, Immunol Grad Grp, Philadelphia, PA 19104 USA.
RP Belkaid, Y (reprint author), NIAID, Mucosal Immunol Unit, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
EM ybelkaid@niaid.nih.gov
RI dos Santos, Liliane/D-1551-2010; Hunter, Christopher/H-1970-2011
FU Division of Intramural Research; National Institute of Allergy and
Infectious Diseases; National Institutes of Health
FX This work was supported by the Division of Intramural Research, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health. We would like to thank the students of the Biology of Parasitism
Course (Woods hole MBL 2008-2009) for contributing to some of the
experiments. We thank Dr. F. Torres for help with pathological
evaluation of samples. We thank Dr. K. Holmes and the MAID sorting
facility and K. Beacht for technical assistance. We thank A. O'Hara
(University of Pennsylvania, Immunology Graduate Program) for help with
the parasite and Dr. G. Yap for helpful suggestions. We thank Drs. F.A.
Sher and D. Jankovic for critical reading of the manuscript.
NR 58
TC 297
Z9 302
U1 1
U2 8
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
EI 1097-4180
J9 IMMUNITY
JI Immunity
PD NOV 20
PY 2009
VL 31
IS 5
BP 772
EP 786
DI 10.1016/j.immuni.2009.10.001
PG 15
WC Immunology
SC Immunology
GA 523TQ
UT WOS:000272097900012
PM 19896394
ER
PT J
AU Martin-Orozco, N
Muranski, P
Chung, Y
Yang, XXO
Yamazaki, T
Lu, SJ
Hwu, P
Restifo, NP
Overwijk, WW
Dong, C
AF Martin-Orozco, Natalia
Muranski, Pawel
Chung, Yeonseok
Yang, Xuexian O.
Yamazaki, Tomohide
Lu, Sijie
Hwu, Patrick
Restifo, Nicholas P.
Overwijk, Willem W.
Dong, Chen
TI T Helper 17 Cells Promote Cytotoxic T Cell Activation in Tumor Immunity
SO IMMUNITY
LA English
DT Article
ID POTENT ANTITUMOR IMMUNITY; DENDRITIC CELLS; IN-VIVO; TH17 CELLS;
CROSS-PRESENTATION; LYMPHOPENIC HOSTS; CUTTING EDGE; CANCER;
INTERLEUKIN-17; MELANOMA
AB Although T helper 17 (Th17) cells have been found in tumor tissues, their function in cancer immunity is unclear. We found that interleukin-17A (IL-17A)-deficient mice were more susceptible to developing lung melanoma. Conversely, adoptive T cell therapy with tumor-specific Th17 cells prevented tumor development. Importantly, the Th17 cells retained their cytokine signature and exhibited stronger therapeutic efficacy than Th1 cells. Unexpectedly, therapy using Th17 cells elicited a remarkable activation of tumor-specific CD8(+) T cells, which were necessary for the antitumor effect. Th17 cells promoted dendritic cell recruitment into the tumor tissues and in draining lymph nodes increased CD8 alpha(+) dendritic cells containing tumor material. Moreover, Th17 cells promoted CCL20 chemokine production by tumor tissues, and tumor-bearing CCR6-deficient mice did not respond to Th17 cell therapy. Thus, 17 cells elicited a protective inflammation that promotes the activation of tumor-specific CD8(+) T cells. These findings have important implications in antitumor immunotherapies.
C1 [Martin-Orozco, Natalia; Chung, Yeonseok; Yang, Xuexian O.; Yamazaki, Tomohide; Dong, Chen] Univ Texas Houston, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA.
[Lu, Sijie] Univ Texas Houston, MD Anderson Canc Ctr, Dept Stem Cell Transplantat & Cell Therapy, Houston, TX 77030 USA.
[Hwu, Patrick; Overwijk, Willem W.] Univ Texas Houston, MD Anderson Canc Ctr, Dept Melanoma Med Oncol, Houston, TX 77030 USA.
[Muranski, Pawel; Restifo, Nicholas P.] NCI, NIH, Bethesda, MD 20892 USA.
RP Dong, C (reprint author), Univ Texas Houston, MD Anderson Canc Ctr, Dept Immunol, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM cdong@mdanderson.org
RI dong, chen /B-3181-2009; Restifo, Nicholas/A-5713-2008; Martin Orozco,
Natalia/E-4794-2010; Muranski, Pawel/E-5572-2010;
OI dong, chen /0000-0002-0084-9130; Restifo, Nicholas
P./0000-0003-4229-4580; Chung, Yeonseok/0000-0001-5780-4841
FU National Institute of Health; Targeted Therapy of MID Anderson Cancer
Center; Leukemia and Lymphoma Society Scholar award; MD Anderson Cancer
Center
FX We thank the entire Dong lab for their help and discussion. This work is
supported in part by grants from the National Institute of Health (to
W.W.O. and C.D.) and a grant from the Center for Targeted Therapy of MID
Anderson Cancer Center (to C.D. and N.M.O.). C.D. received a Leukemia
and Lymphoma Society Scholar award and a Trust Fellowship of the MD
Anderson Cancer Center.
NR 40
TC 334
Z9 353
U1 4
U2 27
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1074-7613
J9 IMMUNITY
JI Immunity
PD NOV 20
PY 2009
VL 31
IS 5
BP 787
EP 798
DI 10.1016/j.immuni.2009.09.014
PG 12
WC Immunology
SC Immunology
GA 523TQ
UT WOS:000272097900013
PM 19879162
ER
PT J
AU Shim, MS
Kim, JY
Jung, HK
Lee, KH
Xu, XM
Carlson, BA
Kim, KW
Kim, IY
Hatfield, DL
Lee, BJ
AF Shim, Myoung Sup
Kim, Jin Young
Jung, Hee Kyoung
Lee, Kwang Hee
Xu, Xue-Ming
Carlson, Bradley A.
Kim, Ki Woo
Kim, Ick Young
Hatfield, Dolph L.
Lee, Byeong Jae
TI Elevation of Glutamine Level by Selenophosphate Synthetase 1 Knockdown
Induces Megamitochondrial Formation in Drosophila Cells
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SELENOPROTEIN SYNTHESIS; INDUCED APOPTOSIS; ESCHERICHIA-COLI;
TRANSFER-RNA; SELENIUM; SELENOCYSTEINE; PROTEIN; GENE; MELANOGASTER;
METABOLISM
AB Although selenophosphate synthetase 1 (SPS1/SelD) is an essential gene in Drosophila, its function has not been determined. To elucidate its intracellular role, we targeted the removal of SPS1/SelD mRNA in Drosophila SL2 cells using RNA interference technology that led to the formation of vacuole-like globular structures. Surprisingly, these structures were identified as megamitochondria, and only depolarized mitochondria developed into megamitochondria. The mRNA levels of l(2) 01810 and glutamine synthetase 1 (GS1) were increased by SPS1/SelD knockdown. Blocking the expression of GS1 and l(2) 01810 completely inhibited the formation of megamitochondria induced by loss of SPS1/SelD activity and decreased the intracellular levels of glutamine to those of control cells suggesting that the elevated level of glutamine is responsible for megamitochondrial formation. Overexpression of GS1 and l(2) 01810 had a synergistic effect on the induction of megamitochondrial formation and on the synthesis of glutamine suggesting that l(2) 01810 is involved in glutamine synthesis presumably by activating GS1. Our results indicate that, in Drosophila, SPS1/SelD regulates the intracellular glutamine by inhibiting GS1 and l(2) 01810 expression and that elevated levels of glutamine lead to a nutritional stress that provides a signal for megamitochondrial formation.
C1 [Shim, Myoung Sup; Kim, Jin Young; Jung, Hee Kyoung; Lee, Kwang Hee; Lee, Byeong Jae] Seoul Natl Univ, Sch Biol Sci, Inst Mol Biol & Genet, Lab Mol Genet & Genom, Seoul 151742, South Korea.
[Xu, Xue-Ming; Carlson, Bradley A.; Hatfield, Dolph L.] NCI, Lab Canc Prevent, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kim, Ki Woo] Seoul Natl Univ, Coll Agr & Life Sci, Natl Instrumentat Ctr Environm Management, Seoul 151742, South Korea.
[Kim, Ick Young] Korea Univ, Sch Life Sci & Biotechnol, Lab Cellular & Mol Biochem, Seoul 136701, South Korea.
RP Lee, BJ (reprint author), Seoul Natl Univ, Sch Biol Sci, Inst Mol Biol & Genet, Lab Mol Genet & Genom, Bldg 504,Rm 523, Seoul 151742, South Korea.
EM imbglmg@snu.ac.kr
FU Korean Government [KRF-2005-070-C00086, KRF-2008-005-J00201]; NCI,
Center for Cancer Research
FX This work was supported by Korea Research Foundation Grants
KRF-2005-070-C00086 and KRF-2008-005-J00201 funded by the Korean
Government (Ministry of Education, Science, and Technology) (to B. J.
L.). This work was also supported in part by a National Institutes of
Health Intramural Research Program grant from NCI, Center for Cancer
Research.
NR 57
TC 16
Z9 18
U1 0
U2 4
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 20
PY 2009
VL 284
IS 47
BP 32881
EP 32894
DI 10.1074/jbc.M109.026492
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 522VR
UT WOS:000272028400072
PM 19755423
ER
PT J
AU Matulonis, UA
Berlin, S
Ivy, P
Tyburski, K
Krasner, C
Zarwan, C
Berkenblit, A
Campos, S
Horowitz, N
Cannistra, SA
Lee, H
Lee, J
Roche, M
Hill, M
Whalen, C
Sullivan, L
Tran, C
Humphreys, BD
Penson, RT
AF Matulonis, Ursula A.
Berlin, Suzanne
Ivy, Percy
Tyburski, Karin
Krasner, Carolyn
Zarwan, Corrine
Berkenblit, Anna
Campos, Susana
Horowitz, Neil
Cannistra, Stephen A.
Lee, Hang
Lee, Julie
Roche, Maria
Hill, Margaret
Whalen, Christin
Sullivan, Laura
Tran, Chau
Humphreys, Benjamin D.
Penson, Richard T.
TI Cediranib, an Oral Inhibitor of Vascular Endothelial Growth Factor
Receptor Kinases, Is an Active Drug in Recurrent Epithelial Ovarian,
Fallopian Tube, and Peritoneal Cancer
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID GYNECOLOGIC-ONCOLOGY-GROUP; SOLID TUMORS; PHASE-I; COLORECTAL-CANCER;
BEVACIZUMAB; PACLITAXEL; GUIDELINES; EVALUATE; AZD2171;
LYMPHANGIOGENESIS
AB Purpose
Angiogenesis is important for epithelial ovarian cancer (EOC) growth, and blocking angiogenesis can lead to EOC regression. Cediranib is an oral tyrosine kinase inhibitor (TKI) of vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2, VEGFR-3, and c-kit.
Patients and Methods
We conducted a phase II study of cediranib for recurrent EOC or peritoneal or fallopian tube cancer; cediranib was administered as a daily oral dose, and the original dose was 45 mg daily. Because of toxicities observed in the first 11 patients, the dose was lowered to 30 mg. Eligibility included <= two lines of chemotherapy for recurrence. End points included response rate (via Response Evaluation Criteria in Solid Tumors [RECIST] or modified Gynecological Cancer Inter-group CA-125), toxicity, progression-free survival (PFS), and overall survival (OS).
Results
Forty-seven patients were enrolled; 46 were treated. Clinical benefit rate (defined as complete response [CR] or partial response [PR], stable disease [SD] > 16 weeks, or CA-125 nonprogression > 16 weeks), which was the primary end point, was 30%; eight patients (17%; 95% CI, 7.6% to 30.8%) had a PR, six patients (13%; 95% CI, 4.8% to 25.7%) had SD, and there were no CRs. Eleven patients (23%) were removed from study because of toxicities before two cycles. Grade 3 toxicities (> 20% of patients) included hypertension (46%), fatigue (24%), and diarrhea (13%). Grade 2 hypothyroidism occurred in 43% of patients. Grade 4 toxicities included CNS hemorrhage (n = 1), hypertriglyceridemia/hypercholesterolemia/elevated lipase (n = 1), and dehydration/elevated creatinine (n = 1). No bowel perforations or fistulas occurred. Median PFS was 5.2 months, and median OS has not been reached; median follow-up time is 10.7 months.
Conclusion
Cediranib has activity in recurrent EOC, tubal cancer, and peritoneal cancer with predictable toxicities observed with other TKIs.
C1 [Matulonis, Ursula A.] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02115 USA.
Massachusetts Gen Hosp, Dept Hematol & Oncol, Boston, MA 02114 USA.
Massachusetts Gen Hosp, Ctr Biostat, Boston, MA 02114 USA.
Brigham & Womens Hosp, Div Gynecol Oncol, Boston, MA 02115 USA.
Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
Beth Israel Deaconess Med Ctr, Dept Hematol & Oncol, Boston, MA 02215 USA.
Lahey Clin Fdn, Dept Hematol & Oncol, Burlington, MA USA.
Wyeth Pharmaceut, Cambridge, MA USA.
NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Matulonis, UA (reprint author), Dana Farber Canc Inst, Dept Med Oncol, 44 Binney St, Boston, MA 02115 USA.
EM Ursula_matulonis@dfci.harvard.edu
FU Madeline Franchi Ovarian Cancer Fund; Ovations for the Cure
FX Supported in part by donations made by the Madeline Franchi Ovarian
Cancer Fund and Ovations for the Cure.
NR 26
TC 150
Z9 155
U1 0
U2 4
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2009
VL 27
IS 33
BP 5601
EP 5606
DI 10.1200/JCO.2009.23.2777
PG 6
WC Oncology
SC Oncology
GA 521VS
UT WOS:000271954200019
PM 19826113
ER
PT J
AU Philip, PA
Mooney, M
Jaffe, D
Eckhardt, G
Moore, M
Meropol, N
Emens, L
O'Reilly, E
Korc, M
Ellis, L
Benedetti, J
Rothenberg, M
Willett, C
Tempero, M
Lowy, A
Abbruzzese, J
Simeone, D
Hingorani, S
Berlin, J
Tepper, J
AF Philip, Philip A.
Mooney, Margaret
Jaffe, Deborah
Eckhardt, Gail
Moore, Malcolm
Meropol, Neal
Emens, Leisha
O'Reilly, Eileen
Korc, Murray
Ellis, Lee
Benedetti, Jacqueline
Rothenberg, Mace
Willett, Christopher
Tempero, Margaret
Lowy, Andrew
Abbruzzese, James
Simeone, Diane
Hingorani, Sunil
Berlin, Jordan
Tepper, Joel
TI Consensus Report of the National Cancer Institute Clinical Trials
Planning Meeting on Pancreas Cancer Treatment
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID FACTOR RECEPTOR INHIBITION; PHASE-II TRIALS; K-RAS; STEM-CELLS; DUCTAL
ADENOCARCINOMA; MESENCHYMAL TRANSITION; CHRONIC INFLAMMATION;
TUMOR-GROWTH; GEMCITABINE; FARNESYLTRANSFERASE
AB Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer mortality, despite significant improvements in diagnostic imaging and operative mortality rates. The 5-year survival rate remains less than 5% because of microscopic or gross metastatic disease at time of diagnosis. The Clinical Trials Planning Meeting in pancreatic cancer was convened by the National Cancer Institute's Gastrointestinal Cancer Steering Committee to discuss the integration of basic and clinical knowledge in the design of clinical trials in PDAC. Major emphasis was placed on the enhancement of research to identify and validate the relevant targets and molecular pathways in PDAC, cancer stem cells, and the microenvironment. Emphasis was also placed on developing rational combinations of targeted agents and the development of predictive biomarkers to assist selection of patient subsets. The development of preclinical tumor models that are better predictive of human PDAC must be supported with wider availability to the research community. Phase III clinical trials should be implemented only if there is a meaningful clinical signal of efficacy and safety in the phase II setting. The emphasis must therefore be on performing well-designed phase II studies with uniform sets of basic entry and evaluation criteria with survival as a primary endpoint. Patients with either metastatic or locally advanced PDAC must be studied separately.
C1 [Philip, Philip A.] Wayne State Univ, Karmanos Canc Inst, Detroit, MI 48201 USA.
NCI, NIH, Bethesda, MD 20892 USA.
Univ Colorado, Denver, CO 80202 USA.
Princess Margaret Hosp, Toronto, ON M4X 1K9, Canada.
Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
Mem Sloan Kettering Canc Ctr, New York, NY 10021 USA.
Norris Cotton Canc Ctr, Lebanon, NH USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
SW Oncol Grp, Ctr Stat, Seattle, WA USA.
Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
Pfizer Oncol, New York, NY USA.
Univ Calif San Diego, San Diego, CA 92103 USA.
Univ Calif San Francisco, Med Ctr, San Francisco, CA 94143 USA.
Duke Univ, Med Ctr, Durham, NC 27706 USA.
Univ N Carolina, Lineberger Comprehens Canc Ctr, Chapel Hill, NC 27599 USA.
Univ Michigan, Ann Arbor, MI 48109 USA.
RP Philip, PA (reprint author), Wayne State Univ, Karmanos Canc Inst, 4 Hudson Weber Canc Res Ctr,4100 John R St, Detroit, MI 48201 USA.
EM philipp@karmanos.org
FU Pfizer; OSI Pharmaceuticals; Genentech; Response Genetics; OncoMed
Pharmaceuticals Expert Testimony
FX Philip A. Philip, sanofi-aventis, Bristol-Myers Squibb, Pfizer; Malcolm
Moore, OSI Pharmaceuticals; Leisha Emens, Genentech; Lee Ellis,
sanofi-aventis; Margaret Tempero, Response Genetics; Diane Simeone,
OncoMed Pharmaceuticals Expert Testimony: None Other Remuneration:
Jordan Berlin, Pfizer
NR 61
TC 131
Z9 135
U1 1
U2 6
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 20
PY 2009
VL 27
IS 33
BP 5660
EP 5669
DI 10.1200/JCO.2009.21.9022
PG 10
WC Oncology
SC Oncology
GA 521VS
UT WOS:000271954200027
PM 19858397
ER
PT J
AU Patnaik, S
Dietz, HC
Zheng, W
Austin, C
Marugan, JJ
AF Patnaik, Samarjit
Dietz, Harry C.
Zheng, Wei
Austin, Christopher
Marugan, Juan J.
TI Multi-Gram Scale Synthesis of FR180204
SO JOURNAL OF ORGANIC CHEMISTRY
LA English
DT Article
ID ERK; INHIBITORS; PATHWAY; RAS
AB A concise synthesis of the ERK inhibitor FR180204 has been developed. The synthesis consists of six operationally simple steps and can be utilized to make multi-gram quantities of FR180204.
C1 [Patnaik, Samarjit; Zheng, Wei; Austin, Christopher; Marugan, Juan J.] NIH, Chem Genom Ctr, Rockville, MD 20850 USA.
[Dietz, Harry C.] Johns Hopkins Univ, Sch Med, Baltimore, MD 21205 USA.
RP Patnaik, S (reprint author), NIH, Chem Genom Ctr, 9800 Med Ctr Dr, Rockville, MD 20850 USA.
EM patnaiks@mail.nih.gov
OI Zheng, Wei/0000-0003-1034-0757
FU Intramural NIH HHS [Z99 HG999999]
NR 15
TC 8
Z9 8
U1 0
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-3263
J9 J ORG CHEM
JI J. Org. Chem.
PD NOV 20
PY 2009
VL 74
IS 22
BP 8870
EP 8873
DI 10.1021/jo901835m
PG 4
WC Chemistry, Organic
SC Chemistry
GA 518AR
UT WOS:000271662500055
PM 19852504
ER
PT J
AU Jaworski, CJ
Aryankalayil-John, M
Campos, MM
Fariss, RN
Rowsey, J
Agarwalla, N
Reid, TW
Dushku, N
Cox, CA
Carper, D
Wistow, G
AF Jaworski, C. J.
Aryankalayil-John, M.
Campos, M. M.
Fariss, R. N.
Rowsey, J.
Agarwalla, N.
Reid, T. W.
Dushku, N.
Cox, C. A.
Carper, D.
Wistow, G.
TI Expression analysis of human pterygium shows a predominance of
conjunctival and limbal markers and genes associated with cell migration
SO MOLECULAR VISION
LA English
DT Article
ID BRONCHIAL EPITHELIAL-CELLS; INDUCED CORNEAL ASTIGMATISM; BETAIG-H3 GENE;
MESENCHYMAL TRANSITION; POLYAMINE ANALOGS; DOWN-REGULATION;
BREAST-CANCER; BASAL CELLS; STEM-CELLS; HUMAN-EYE
AB Purpose: Pterygium is a vision-impairing fibrovascular lesion that grows across the corneal surface and is associated with sunlight exposure. To increase our understanding of the cells types involved in pterygium, we have used expressed sequence tag analysis to examine the transcriptional repertoire of isolated pterygium and to identify marker genes for tissue origin and cell migration.
Methods: An unnormalized unamplified cDNA library was prepared from 15 pooled specimens of surgically removed pterygia as part of the NEIBank project. Gene expression patterns were compared with existing data for human cornea, limbus, and conjunctiva, and expression of selected genes was verified by immunofluorescence localization in normal eye ocular surface and in pterygium.
Results: Sequence analysis of 2,976 randomly selected clones produced over 1,800 unique clusters, potentially representing single genes. The most abundant complementary DNAs from pterygium include clusterin, keratins 13 (Krt13) and 4 (Krt4), S100A9/calgranulin B, and spermidine/spermine N1-acetyltransferase (SAT1). Markers for both conjunctiva (such as keratin 13/4 and AQP3) and corneal epithelium (such as keratin 12/3 and AQP5) were present. Immunofluorescence of Krt12 and 13 in the normal ocular surface showed specificity of Krt12 in cornea and Krt13 in conjunctival and limbal epithelia, with a fairly sharp boundary at the limbal-corneal border. In the pterygium there was a patchy distribution of both Krt12 and 13 up to a normal corneal epithelial region specific for Krt12. Immunoglobulins were also among the prominently expressed transcripts. Several of the genes expressed most abundantly in excised pterygium, particularly S100A9 and SAT1, have roles in cell migration. SAT1 exerts its effects through control of polyamine levels. IPENSpm, a polyamine analogue, showed a significant ability to reduce migration in primary cultures of pterygium. A number of genes highly expressed in cornea were not found in pterygium (several small leucine-rich proteoglycan family members) or were expressed at considerably lower levels (ALDH3A1 and decorin).
Conclusions: The expression pattern of keratins and other markers in pterygium most closely resemble those of conjunctival and limbal cells; some corneal markers are present, notably Krt12, but at lower levels than equivalent conjunctival markers. Our data are consistent with the model of pterygium developing from the migration of conjunctivaland limbal-like cells into corneal epithelium. Identification of genes with roles in cell migration suggests potential therapeutic targets. In particular, the ability of polyamine analogues to reduce migration in primary cultures of pterygium presents a possible approach to slowing pterygium growth.
C1 [Jaworski, C. J.] NEI, Sect Mol Therapeut, LRCMB, NIH, Bethesda, MD 20892 USA.
[Aryankalayil-John, M.] NCI, Bethesda, MD 20892 USA.
[Dushku, N.] Kaiser Permanente Med Ctr, Sacramento, CA USA.
[Reid, T. W.] Texas Tech Univ, Hlth Sci Ctr, Lubbock, TX 79430 USA.
[Campos, M. M.; Fariss, R. N.] NEI, NEI Biol Imaging Core, NIH, Bethesda, MD 20892 USA.
[Wistow, G.] NEI, Sect Mol Struct & Funct Genom, NIH, Bethesda, MD 20892 USA.
[Cox, C. A.] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96822 USA.
RP Jaworski, CJ (reprint author), NEI, Sect Mol Therapeut, LRCMB, NIH, Bldg 7,Room 202, Bethesda, MD 20892 USA.
EM Jaworski@helix.nih.gov
NR 72
TC 20
Z9 21
U1 0
U2 2
PU MOLECULAR VISION
PI ATLANTA
PA C/O JEFF BOATRIGHT, LAB B, 5500 EMORY EYE CENTER, 1327 CLIFTON RD, N E,
ATLANTA, GA 30322 USA
SN 1090-0535
J9 MOL VIS
JI Mol. Vis.
PD NOV 20
PY 2009
VL 15
IS 256-59
BP 2421
EP 2434
PG 14
WC Biochemistry & Molecular Biology; Ophthalmology
SC Biochemistry & Molecular Biology; Ophthalmology
GA 528VP
UT WOS:000272475400003
PM 19956562
ER
PT J
AU Calado, RT
Regal, JA
Kleiner, DE
Schrump, DS
Peterson, NR
Pons, V
Chanock, SJ
Lansdorp, PM
Young, NS
AF Calado, Rodrigo T.
Regal, Joshua A.
Kleiner, David E.
Schrump, David S.
Peterson, Nathan R.
Pons, Veronica
Chanock, Stephen J.
Lansdorp, Peter M.
Young, Neal S.
TI A Spectrum of Severe Familial Liver Disorders Associate with Telomerase
Mutations
SO PLOS ONE
LA English
DT Article
ID IDIOPATHIC PULMONARY-FIBROSIS; NODULAR REGENERATIVE HYPERPLASIA;
DOMINANT DYSKERATOSIS-CONGENITA; APLASTIC-ANEMIA; REVERSE-TRANSCRIPTASE;
CANCER; GENE; RNA; VARIANTS; 5P15.33
AB Background: Telomerase is an enzyme specialized in maintaining telomere lengths in highly proliferative cells. Loss-of-function mutations cause critical telomere shortening and are associated with the bone marrow failure syndromes dyskeratosis congenita and aplastic anemia and with idiopathic pulmonary fibrosis. Here, we sought to determine the spectrum of clinical manifestations associated with telomerase loss-of-function mutations.
Methodology/Principal Findings: Sixty-nine individuals from five unrelated families with a variety of hematologic, hepatic, and autoimmune disorders were screened for telomerase complex gene mutations; leukocyte telomere length was measured by flow fluorescence in situ hybridization in mutation carriers and some non-carriers; the effects of the identified mutations on telomerase activity were determined; and genetic and clinical data were correlated. In six generations of a large family, a loss-of-function mutation in the telomerase enzyme gene TERT associated with severe telomere shortening and a range of hematologic manifestations, from macrocytosis to acute myeloid leukemia, with severe liver diseases marked by fibrosis and inflammation, and one case of idiopathic pulmonary fibrosis but not with autoimmune disorders. Additionally, we identified four unrelated families in which loss-of-function TERC or TERT gene mutations tracked with marrow failure, pulmonary fibrosis, and a spectrum of liver disorders.
Conclusions/Significance: These results indicate that heterozygous telomerase loss-of-function mutations associate with but are not determinant of a large spectrum of hematologic and liver abnormalities, with the latter sometimes occurring in the absence of marrow failure. Our findings, along with the link between pulmonary fibrosis and telomerase mutations, also suggest a common pathogenic mechanism for fibrotic diseases in which defective telomere repair plays important role.
RP Calado, RT (reprint author), NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
EM calador@nhlbi.nih.gov
RI Calado, Rodrigo/G-2619-2011;
OI Kleiner, David/0000-0003-3442-4453
FU Canadian Institutes of Health Research [GMH79042, MOP38075]; Intramural
NIH HHS
NR 36
TC 83
Z9 83
U1 0
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2009
VL 4
IS 11
AR e7926
DI 10.1371/journal.pone.0007926
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 522NL
UT WOS:000272004800008
PM 19936245
ER
PT J
AU Ma, WX
Zhao, L
Fontainhas, AM
Fariss, RN
Wong, WT
AF Ma, Wenxin
Zhao, Lian
Fontainhas, Aurora M.
Fariss, Robert N.
Wong, Wai T.
TI Microglia in the Mouse Retina Alter the Structure and Function of
Retinal Pigmented Epithelial Cells: A Potential Cellular Interaction
Relevant to AMD
SO PLOS ONE
LA English
DT Article
ID MACULAR DEGENERATION; CHOROIDAL NEOVASCULARIZATION; SUBRETINAL
MICROGLIA; FRACTALKINE RECEPTOR; UNITED-STATES; IMMUNE-SYSTEM;
NITRIC-OXIDE; IN-VITRO; DRUSEN; INFLAMMATION
AB Background: Age-related macular degeneration (AMD) is a leading cause of legal blindness in the elderly in the industrialized word. While the immune system in the retina is likely to be important in AMD pathogenesis, the cell biology underlying the disease is incompletely understood. Clinical and basic science studies have implicated alterations in the retinal pigment epithelium (RPE) layer as a locus of early change. Also, retinal microglia, the resident immune cells of the retina, have been observed to translocate from their normal position in the inner retina to accumulate in the subretinal space close to the RPE layer in AMD eyes and in animal models of AMD.
Methodology/Principal Findings: In this study, we examined the effects of retinal microglia on RPE cells using 1) an in vitro model where activated retinal microglia are co-cultured with primary RPE cells, and 2) an in vivo mouse model where retinal microglia are transplanted into the subretinal space. We found that retinal microglia induced in RPE cells 1) changes in RPE structure and distribution, 2) increased expression and secretion of pro-inflammatory, chemotactic, and pro-angiogenic molecules, and 3) increased extent of in vivo choroidal neovascularization in the subretinal space.
Conclusions/Significance: These findings share similarities with important pathological features found in AMD and suggest the relevance of microglia-RPE interactions in AMD pathogenesis. We speculate that the migration of retinal microglia into the subretinal space in early stages of the disease induces significant changes in RPE cells that perpetuate further microglial accumulation, increase inflammation in the outer retina, and fosters an environment conducive for the formation of neovascular changes responsible for much of vision loss in advanced AMD.
RP Ma, WX (reprint author), NEI, Unit Neuron Glia Interact Retinal Dis, NIH, Bethesda, MD 20892 USA.
EM wongw@nei.nih.gov
RI Wong, Wai/B-6118-2017
OI Wong, Wai/0000-0003-0681-4016
FU Intramural NIH HHS
NR 61
TC 84
Z9 90
U1 1
U2 15
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2009
VL 4
IS 11
AR e7945
DI 10.1371/journal.pone.0007945
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 522NL
UT WOS:000272004800021
PM 19936204
ER
PT J
AU Chen, L
Kwon, YD
Zhou, TQ
Wu, XL
O'Dell, S
Cavacini, L
Hessell, AJ
Pancera, M
Tang, M
Xu, L
Yang, ZY
Zhang, MY
Arthos, J
Burton, DR
Dimitrov, DS
Nabel, GJ
Posner, MR
Sodroski, J
Wyatt, R
Mascola, JR
Kwong, PD
AF Chen, Lei
Kwon, Young Do
Zhou, Tongqing
Wu, Xueling
O'Dell, Sijy
Cavacini, Lisa
Hessell, Ann J.
Pancera, Marie
Tang, Min
Xu, Ling
Yang, Zhi-Yong
Zhang, Mei-Yun
Arthos, James
Burton, Dennis R.
Dimitrov, Dimiter S.
Nabel, Gary J.
Posner, Marshall R.
Sodroski, Joseph
Wyatt, Richard
Mascola, John R.
Kwong, Peter D.
TI Structural Basis of Immune Evasion at the Site of CD4 Attachment on
HIV-1 gp120
SO SCIENCE
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; HUMAN MONOCLONAL-ANTIBODY; NEUTRALIZING
ANTIBODIES; BINDING-SITE; EFFICIENT NEUTRALIZATION; ENVELOPE
GLYCOPROTEINS; INFECTED INDIVIDUALS; PROTEIN; PANEL; CRYSTALLIZATION
AB The site on HIV-1 gp120 that binds to the CD4 receptor is vulnerable to antibodies. However, most antibodies that interact with this site cannot neutralize HIV-1. To understand the basis of this resistance, we determined co-crystal structures for two poorly neutralizing, CD4-binding site (CD4BS) antibodies, F105 and b13, in complexes with gp120. Both antibodies exhibited approach angles to gp120 similar to those of CD4 and a rare, broadly neutralizing CD4BS antibody, b12. Slight differences in recognition, however, resulted in substantial differences in F105- and b13-bound conformations relative to b12-bound gp120. Modeling and binding experiments revealed these conformations to be poorly compatible with the viral spike. This incompatibility, the consequence of slight differences in CD4BS recognition, renders HIV-1 resistant to all but the most accurately targeted antibodies.
C1 [Chen, Lei; Kwon, Young Do; Zhou, Tongqing; Wu, Xueling; O'Dell, Sijy; Pancera, Marie; Tang, Min; Xu, Ling; Yang, Zhi-Yong; Nabel, Gary J.; Wyatt, Richard; Mascola, John R.; Kwong, Peter D.] NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
[Cavacini, Lisa; Posner, Marshall R.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Head & Neck Oncol Program, Boston, MA 02115 USA.
[Hessell, Ann J.; Burton, Dennis R.] Scripps Res Inst, Dept Immunol, La Jolla, CA 92037 USA.
[Hessell, Ann J.; Burton, Dennis R.] Scripps Res Inst, Dept Microbial Sci, La Jolla, CA 92037 USA.
[Hessell, Ann J.; Burton, Dennis R.] Scripps Res Inst, Int AIDS Vaccine Initiat Neutralizing Antibody Ct, La Jolla, CA 92037 USA.
[Zhang, Mei-Yun; Dimitrov, Dimiter S.] NCI, Ctr Canc Res, Frederick, MD 21702 USA.
[Arthos, James] NIAID, Immunoregulat Lab, NIH, Bethesda, MD 20892 USA.
[Burton, Dennis R.] Massachusetts Gen Hosp, MIT, Ragon Inst, Boston, MA 02114 USA.
[Burton, Dennis R.] Harvard Univ, Boston, MA 02114 USA.
[Sodroski, Joseph] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Immunol & AIDS, Boston, MA 02115 USA.
RP Kwong, PD (reprint author), NIAID, Vaccine Res Ctr, NIH, Bethesda, MD 20892 USA.
EM pdkwong@nih.gov; pdkwong@nih.gov
RI Zhang, Mei-Yun/E-9908-2010; Kwon, Young Do/A-6957-2010; Zhou,
Tongqing/A-6880-2010
OI Zhou, Tongqing/0000-0002-3935-4637
FU NIH; International AIDS Vaccine Initiative; Bill and Melinda Gates
Foundation Grand Challenges in Global Heath Initiative
FX L. Chen produced and assessed for crystallization CD4BS antibodies with
unconstrained gp120, crystallized the F105-gp120 complex, assisted with
F105-gp120 data collection and structure solution, and carried out
mutagenesis and SPR binding experiments. Y. D. K. assisted with
F105-gp120 crystallization, data collection, and structure solution and
refined and analyzed the F105-gp120 structure. T. Z. purified,
crystallized, solved, and analyzed the b13-gp120 complex. X. W., S. O.'
D. and J. R. M. assessed neutralization potency and breadth of CD4,
patient sera, and CD4BS antibodies. L. Chen and M. P. carried out
cell-surface JR-FL binding experiments. M. T. and R. W. provided YU2
core gp120; L. X. and G. J. N. provided stabilized-core gp120; Z.-Y. Y.
and G. J. N. converted b13 from Fab to IgG format and provided b13 IgG;
L. Cavacini and M. R. P. provided F105; M.-Y. Z. and D. S. D. provided
m6, m14, and m18; A. J. H. and D. R. B. provided b3, b6, b11, b12; and
J. A. provided dodecameric CD4. J. A., D. R. B., D. S. D., G. J. N., M.
R. P., J. S., R. W., and J. R. M. assisted with analysis and writing,
and P. D. K. assisted with crystallography and experimental planning and
wrote the first draft. Figures, tables, and supporting online material
were produced by L. Chen, Y. D. K., M. P., T. Z. and X. W. We thank L.
Shapiro and members of the Structural Biology Section, Vaccine Research
Center (VRC), for discussions and comments on the manuscript, M. Connors
for patient serum, M. Fung for antibodies G3-42 and G3-299, J. Robinson
for antibodies 1.5e and F91, J. Stuckey for assistance with figures and
tables, S. Subramaniam for EM tomograms, C. Winter and C. Huang for S2
production of core YU2 gp120, X. Yang for preparation of JR-FL gp120,
and the Flow Cytometry Core, VRC, for assistance with antibody binding
to cell-surface-expressed HIV-1 spikes. Support for this work was
provided by the Intramural Research Program of NIH, the International
AIDS Vaccine Initiative, a grant from the Bill and Melinda Gates
Foundation Grand Challenges in Global Heath Initiative, and grants from
NIH. The use of insertion device 22 (Southeast Region Collaborative
Access Team) at the Advanced Photon Source was supported by the U. S.
Department of Energy, Basic Energy Sciences, Office of Science, under
contract number W-31-109-Eng-38. Coordinates and structure factors for
the F105-gp120 complex (accession code 3HI1) and the b13-gp120 complexes
(accession codes 3IDX and 3IDY for C222 and C2221 forms, respectively)
have been deposited with the Protein Data Bank.
NR 33
TC 187
Z9 192
U1 0
U2 21
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD NOV 20
PY 2009
VL 326
IS 5956
BP 1123
EP 1127
DI 10.1126/science.1175868
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 521UW
UT WOS:000271951000048
PM 19965434
ER
PT J
AU Flem, ET
Kasymbekova, KT
Vainio, K
Gentsch, J
Abdikarimov, ST
Glass, RI
Bresee, JS
AF Flem, Elmira T.
Kasymbekova, Kaliya T.
Vainio, Kirsti
Gentsch, Jon
Abdikarimov, Sabirjan T.
Glass, Roger I.
Bresee, Joseph S.
TI Rotavirus infection in hospitalized children and estimates of disease
burden in Kyrgyzstan, 2005-2007
SO VACCINE
LA English
DT Article
DE Rotavirus; Gastroenteritis; Epidemiology
ID POLYMERASE CHAIN-REACTION; VACCINE; POPULATION; EFFICACY; DEATHS; SAFETY
AB To estimate the rotavirus-associated burden in Kyrgyzstan, we conducted hospital surveillance among children <5 years old with diarrhoea during 2005-2007. Of 3756 children hospitalized with diarrhoea, 26% had rotavirus detected in stool samples by an enzyme immunoassay. The virus genotype G1P[8] was identified in 60% of 190 characterized samples from 2005 to 2006. The estimated risk for rotavirus hospitalization by age 5 years was 1 in 28 children. One quarter of all gastroenteritis hospitalizations in children <5 years old in Kyrgyzstan may be attributable to rotavirus. Rotavirus vaccination could be an important health intervention to reduce the burden of rotavirus gastroenteritis. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Flem, Elmira T.; Vainio, Kirsti] Norwegian Inst Publ Hlth, Div Infect Dis Control, N-0403 Oslo, Norway.
[Kasymbekova, Kaliya T.; Abdikarimov, Sabirjan T.] Minist Hlth, Dept State Sanit Epidemiol Surveillance, Bishkek, Kyrgyzstan.
[Gentsch, Jon; Bresee, Joseph S.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Glass, Roger I.] NIH, Fogarty Int, Bethesda, MD 20892 USA.
RP Flem, ET (reprint author), Norwegian Inst Publ Hlth, Div Infect Dis Control, POB 4404, N-0403 Oslo, Norway.
EM elmira.flem@fhi.no
FU Program for Appropriate Technology in Health (PATH); GAVI Alliance;
Research Council of Norway; Norwegian Institute of Public Health; U.S.
Centers for Disease Control and Prevention
FX This work was performed under a collaborative agreement with the Program
for Appropriate Technology in Health (PATH) and was funded in full or in
part by the GAVI Alliance, the Research Council of Norway, the Norwegian
Institute of Public Health and the U.S. Centers for Disease Control and
Prevention.
NR 28
TC 9
Z9 9
U1 0
U2 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 20
PY 2009
VL 27
BP F35
EP F39
DI 10.1016/j.vaccine.2009.08.087
PG 5
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 541KQ
UT WOS:000273415000008
PM 19931716
ER
PT J
AU Le, LT
Nguyen, TV
Nguyen, PM
Huong, NT
Huong, NT
Huong, NTM
Hanh, TB
Ha, DN
Anh, DD
Gentsch, JR
Wang, YH
Esona, MD
Glass, RI
Steele, AD
Kilgore, PE
Man, NV
Jiang, BM
Hien, ND
AF Le, Luan T.
Nguyen, Trang V.
Nguyen, Phuong M.
Huong, Nguyen T.
Huong, Ngo T.
Huong, Nguyen T. M.
Hanh, Tran B.
Ha, Dang N.
Anh, Dang D.
Gentsch, Jon R.
Wang, Yuhuan
Esona, Mathew D.
Glass, Roger I.
Steele, A. Duncan
Kilgore, Paul E.
Man, Nguyen V.
Jiang, Baoming
Hien, Nguyen D.
TI Development and characterization of candidate rotavirus vaccine strains
derived from children with diarrhoea in Vietnam
SO VACCINE
LA English
DT Article
DE Rotavirus vaccine; Diarrhoea; Vietnam
ID POLYMERASE-CHAIN-REACTION; SEQUENCE-ANALYSIS; IDENTIFICATION; VIRUSES;
BURDEN
AB In Vietnam, rotavirus infection accounts for more than one-half of all hospitalizations for diarrhoea among children less than 5 years of age. While new vaccines to prevent rotavirus diarrhoea have been developed and introduced into some countries by multinational manufacturers, the ability for developing countries such as Vietnam to introduce several new and important vaccines into the routine infant immunization schedule may be challenging. In order to be partially self-sufficient in vaccine production, Vietnam has pursued the development of several rotavirus strains as candidate vaccines using isolates obtained from Vietnamese children with diarrhoea. This paper describes the origin, isolation and characterization of 3 human rotavirus strains being considered for further vaccine development in Vietnam. The goal is to prepare a monovalent G1P [8] rotavirus vaccine using one of these strains obtained in Vietnam and naturally attenuated by multiple passages in cell culture. While this is an ambitious project that will require several years' work, we are using the lessons learned to improve the overall quality of vaccine production including the use of Vero cell techniques for the manufacture of other vaccines in Vietnam. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Le, Luan T.; Huong, Nguyen T.; Huong, Ngo T.; Huong, Nguyen T. M.; Hanh, Tran B.; Ha, Dang N.; Man, Nguyen V.; Hien, Nguyen D.] POLYVAC, Ctr Res & Prod Vaccines & Biol, Hanoi, Vietnam.
[Nguyen, Trang V.; Nguyen, Phuong M.; Anh, Dang D.] Natl Inst Hyg & Epidemiol, Hanoi, Vietnam.
[Gentsch, Jon R.; Wang, Yuhuan; Esona, Mathew D.; Jiang, Baoming] US Ctr Dis Control & Prevent, Div Viral Dis, Atlanta, GA 30333 USA.
[Glass, Roger I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Steele, A. Duncan] PATH, Seattle, WA USA.
[Kilgore, Paul E.] Int Vaccine Inst, Seoul, South Korea.
RP Le, LT (reprint author), POLYVAC, Ctr Res & Prod Vaccines & Biol, 135 Loduc St, Hanoi, Vietnam.
EM luanpolyvac@gmail.com; bxj4@cdc.gov
RI Kilgore, Paul/L-1462-2013
OI Kilgore, Paul/0000-0003-3214-4482
FU Ministry of Health and the Ministry of Science and Technology, Vietnam;
World Health Organisation
FX Supported by grants form the Ministry of Health and the Ministry of
Science and Technology, Vietnam, and the World Health Organisation.
NR 14
TC 1
Z9 1
U1 0
U2 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
EI 1873-2518
J9 VACCINE
JI Vaccine
PD NOV 20
PY 2009
VL 27
SU 5
BP F130
EP F138
DI 10.1016/j.vaccine.2009.08.086
PG 9
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 541KQ
UT WOS:000273415000026
ER
PT J
AU Wilopo, SA
Soenarto, Y
Bresee, JS
Tholib, A
Aminah, S
Cahyono, A
Gentsch, JR
Kilgore, P
Glass, RI
AF Wilopo, Siswanto Agus
Soenarto, Yati
Bresee, Joseph S.
Tholib, Abu
Aminah, Sri
Cahyono, Anton
Gentsch, Jon R.
Kilgore, Paul
Glass, Roger I.
TI Rotavirus surveillance to determine disease burden and epidemiology in
Java, Indonesia, August 2001 through April 2004
SO VACCINE
LA English
DT Article
DE Epidemiology; Gastroenteritis; Rotavirus; Burden of disease; Indonesia
ID ACUTE DIARRHEA; HONG-KONG; CHILDREN; GASTROENTERITIS; INFECTION;
MORTALITY; VACCINES; JAKARTA; NETWORK
AB This study estimates rotavirus disease burden in children under age 3 years presenting with acute gastroenteritis to hospitals in Purworejo district and Yogyakarta city from August 2001 to April 2004. Among a total of 8929 hospitalized children, 1397 (16%) presented with acute gastroenteritis and of the 1321 stool samples tested, 705 (53%) were positive for rotavirus. Rotavirus infections were most common among children aged 7-23 months and rotavirus was more common during the dry season (June through August). Logistic regression analysis showed no differences in socioeconomic indicators between the rotavirus positive and negative admissions. Rotavirus vaccination may prevent a large proportion of all hospitalizations of young children under 3 years of age presenting with acute gastroenteritis. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Wilopo, Siswanto Agus] Gadjah Mada Univ, CHN RL, Yogyakarta, Indonesia.
[Wilopo, Siswanto Agus] Gadjah Mada Univ, Dept Publ Hlth, Yogyakarta, Indonesia.
[Soenarto, Yati] Dr Sardjito Hosp, Dept Pediat, Yogyakarta, Indonesia.
[Bresee, Joseph S.; Gentsch, Jon R.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Tholib, Abu] Gadjah Mada Univ, Dept Microbiol, Fac Med, Bulaksumur 55281, Yogyakarta, Indonesia.
[Aminah, Sri] RSUD Wirosaban Hosp, Dept Pediat, Yogyakarta, Indonesia.
[Cahyono, Anton] RSUD Purworedjo Dist Hosp, Dept Pediat, Purworedjo, Indonesia.
[Kilgore, Paul] Int Vaccine Inst, Seoul, South Korea.
[Glass, Roger I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Wilopo, SA (reprint author), Gadjah Mada Univ, Ctr Reprod Hlth, Dept Publ Hlth, Fac Med, IKM Bldg 1st Floor,Farmako 1 St,Sekip Utara, Bulaksumur 55281, Yogyakarta, Indonesia.
EM sawilopo@yahoo.com
RI Kilgore, Paul/L-1462-2013
OI Kilgore, Paul/0000-0003-3214-4482
FU Rotavirus Vaccine Program, PATH [GAV.1142-01-07211-SPS]
FX This work was performed under a collaborative arrangement with PATH and
CDC and was funded in full or in part by the Rotavirus Vaccine Program,
PATH (GAV.1142-01-07211-SPS).
NR 28
TC 5
Z9 5
U1 1
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 20
PY 2009
VL 27
BP F61
EP F66
DI 10.1016/j.vaccine.2009.09.004
PG 6
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 541KQ
UT WOS:000273415000013
PM 19931722
ER
PT J
AU Yee, EL
Fang, ZY
Liu, N
Hadler, SC
Liang, XF
Wang, HQ
Zhu, X
Jiang, BM
Parashar, U
Widdowson, MA
Glass, RI
AF Yee, Eileen L.
Fang, Zhao-Yin
Liu, Na
Hadler, Stephen C.
Liang, Xiaofeng
Wang, Huaqing
Zhu, Xu
Jiang, Baoming
Parashar, Umesh
Widdowson, Marc-Alain
Glass, Roger I.
TI Importance and challenges of accurately counting rotavirus deaths in
China, 2002
SO VACCINE
LA English
DT Article
DE Rotavirus; Mortality; Vaccine
ID CHILDREN; DIARRHEA; DISEASE; BURDEN
AB Rotavirus mortality is an important component of the total burden of rotavirus disease for children under 5 years old, but accurate estimation is difficult for many developing countries. Here we applied a more direct method to improve estimates of rotavirus mortality in China using 2002 Chinese-specific data. Results indicate that in 2002, approximately 13,400 children under 5 years old in China died from rotavirus and 70% of these deaths occur in rural areas. Thus, a national rotavirus immunization program targeting rural areas with high mortality from diarrhoea could dramatically reduce these deaths and urban areas could reduce childhood hospitalizations attributed to rotavirus by 43%. Published by Elsevier Ltd.
C1 [Yee, Eileen L.; Jiang, Baoming; Parashar, Umesh; Widdowson, Marc-Alain; Glass, Roger I.] Ctr Dis Control & Prevent, Natl Ctr Immunizat & Resp Dis, Div Viral Dis, Epidemiol Branch, Atlanta, GA 30333 USA.
[Fang, Zhao-Yin; Liu, Na] Chinese Ctr Dis Control & Prevent, Natl Inst Viral Dis Control & Prevent, Viral Gastroenteritis Div, Beijing, Peoples R China.
[Hadler, Stephen C.] WHO, Expanded Programme Immunizat, Beijing, Peoples R China.
[Liang, Xiaofeng; Wang, Huaqing] Chinese Ctr Dis Control & Prevent, Natl Immunizat Program, Beijing, Peoples R China.
[Zhu, Xu] UNICEF China, Hlth Nutr & WES Sect, Beijing, Peoples R China.
[Glass, Roger I.] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
RP Yee, EL (reprint author), Ctr Dis Control & Prevent, Natl Ctr Immunizat & Resp Dis, Div Viral Dis, Epidemiol Branch, 1600 Clifton Rd NE,MS E02, Atlanta, GA 30333 USA.
EM bwd3@cdc.gov
OI Widdowson, Marc-Alain/0000-0002-0682-6933
FU Centers for Disease Control and Prevention
FX This Study was supported by the Centers for Disease Control and
Prevention.
NR 12
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U1 0
U2 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0264-410X
J9 VACCINE
JI Vaccine
PD NOV 20
PY 2009
VL 27
BP F46
EP F49
DI 10.1016/j.vaccine.2009.08.065
PG 4
WC Immunology; Medicine, Research & Experimental
SC Immunology; Research & Experimental Medicine
GA 541KQ
UT WOS:000273415000010
PM 19931719
ER
PT J
AU Novozhilov, AS
Koonin, EV
AF Novozhilov, Artem S.
Koonin, Eugene V.
TI Exceptional error minimization in putative primordial genetic codes
SO BIOLOGY DIRECT
LA English
DT Article
ID AMINO-ACID SYNTHESIS; COEVOLUTION THEORY; PRIMITIVE EARTH; TRIPLET-CODE;
EVOLUTION; ORIGIN; OPTIMIZATION; ASSOCIATION; ATMOSPHERES; CHEMISTRY
AB Background: The standard genetic code is redundant and has a highly non-random structure. Codons for the same amino acids typically differ only by the nucleotide in the third position, whereas similar amino acids are encoded, mostly, by codon series that differ by a single base substitution in the third or the first position. As a result, the code is highly albeit not optimally robust to errors of translation, a property that has been interpreted either as a product of selection directed at the minimization of errors or as a non-adaptive by-product of evolution of the code driven by other forces.
Results: We investigated the error-minimization properties of putative primordial codes that consisted of 16 supercodons, with the third base being completely redundant, using a previously derived cost function and the error minimization percentage as the measure of a code's robustness to mistranslation. It is shown that, when the 16-supercodon table is populated with 10 putative primordial amino acids, inferred from the results of abiotic synthesis experiments and other evidence independent of the code's evolution, and with minimal assumptions used to assign the remaining supercodons, the resulting 2-letter codes are nearly optimal in terms of the error minimization level.
Conclusion: The results of the computational experiments with putative primordial genetic codes that contained only two meaningful letters in all codons and encoded 10 to 16 amino acids indicate that such codes are likely to have been nearly optimal with respect to the minimization of translation errors. This near-optimality could be the outcome of extensive early selection during the co-evolution of the code with the primordial, error-prone translation system, or a result of a unique, accidental event. Under this hypothesis, the subsequent expansion of the code resulted in a decrease of the error minimization level that became sustainable owing to the evolution of a high-fidelity translation system.
C1 [Novozhilov, Artem S.; Koonin, Eugene V.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
EM novozhil@ncbi.nlm.nih.gov; koonin@ncbi.nlm.nih.gov
RI Novozhilov, Artem/D-7544-2012; Novozhilov, Artem/C-9248-2013
OI Novozhilov, Artem/0000-0001-5469-2557
FU DHHS (NIH, National Library of Medicine)
FX The authors' research is supported by intramural funds of the DHHS (NIH,
National Library of Medicine).
NR 69
TC 13
Z9 13
U1 0
U2 7
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD NOV 19
PY 2009
VL 4
AR 44
DI 10.1186/1745-6150-4-44
PG 15
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 526XZ
UT WOS:000272330900001
PM 19925661
ER
PT J
AU Gordeuk, VR
Campbell, A
Rana, S
Nouraie, M
Niu, XM
Minniti, CP
Sable, C
Darbari, D
Dham, N
Onyekwere, O
Ammosova, T
Nekhai, S
Kato, GJ
Gladwin, MT
Castro, OL
AF Gordeuk, Victor R.
Campbell, Andrew
Rana, Sohail
Nouraie, Mehdi
Niu, Xiaomei
Minniti, Caterina P.
Sable, Craig
Darbari, Deepika
Dham, Niti
Onyekwere, Onyinye
Ammosova, Tatiana
Nekhai, Sergei
Kato, Gregory J.
Gladwin, Mark T.
Castro, Oswaldo L.
TI Relationship of erythropoietin, fetal hemoglobin, and hydroxyurea
treatment to tricuspid regurgitation velocity in children with sickle
cell disease
SO BLOOD
LA English
DT Article
ID ENDOTHELIAL PROGENITOR CELLS; PULMONARY-HYPERTENSION; ECHOCARDIOGRAPHIC
ABNORMALITIES; JET VELOCITY; RISK-FACTORS; ANEMIA; DEATH; MORTALITY;
HEMOLYSIS; ASSOCIATION
AB Hydroxyurea and higher hemoglobin F improve the clinical course and survival in sickle cell disease, but their roles in protecting from pulmonary hypertension are not clear. We studied 399 children and adolescents with sickle cell disease at steady state; 38% were being treated with hydroxyurea. Patients on hydroxyurea had higher hemoglobin concentration and lower values for a hemolytic component derived from 4 markers of hemolysis (P <= .002) but no difference in tricuspid regurgitation velocity compared with those not receiving hydroxyurea; they also had higher hemoglobin F (P < .001) and erythropoietin (P <= .012) levels. Hemoglobin F correlated positively with erythropoietin even after adjustment for hemoglobin concentration (P < .001). Greater hemoglobin F and erythropoietin each independently predicted higher regurgitation velocity in addition to the hemolytic component (P <= .023). In conclusion, increase in hemoglobin F in sickle cell disease may be associated with relatively lower tissue oxygen delivery as reflected in higher erythropoietin concentration. Greater levels of erythropoietin or hemoglobin F were independently associated with higher tricuspid regurgitation velocity after adjustment for degree of hemolysis, suggesting an independent relationship of hypoxia with higher systolic pulmonary artery pressure. The hemolysis-lowering and hemoglobin F-augmenting effects of hydroxyurea may exert countervailing influences on pulmonary blood pressure in sickle cell disease. ( Blood. 2009; 114: 4639-4644)
C1 [Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20060 USA.
[Campbell, Andrew] Univ Michigan, Ann Arbor, MI 48109 USA.
[Minniti, Caterina P.; Kato, Gregory J.] NHLBI, Pulm & Vasc Med Branch, Bethesda, MD 20892 USA.
[Minniti, Caterina P.; Kato, Gregory J.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Sable, Craig; Darbari, Deepika; Dham, Niti] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Div Pulm Allergy & Crit Care Med, Pittsburgh, PA 15260 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Hemostasis & Vasc Biol Res Inst, Pittsburgh, PA 15260 USA.
RP Gordeuk, VR (reprint author), Howard Univ, Ctr Sickle Cell Dis, 2041 Georgia Ave NW, Washington, DC 20060 USA.
EM vgordeuk@howard.edu
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
FU National Heart, Lung, and Blood Institute (NHLBI) [2 R25 HL003679-08, 1
R01 HL079912-02]; National Center for Research Resources (NCRR),
National Institutes of Health (NIH) [2MOI RR10284-10]
FX This study was supported in part by grant nos. 2 R25 HL003679-08 and 1
R01 HL079912-02 from the National Heart, Lung, and Blood Institute (
NHLBI); by Howard University General Clinical Research Center ( GCRC)
grant no. 2MOI RR10284-10 from the National Center for Research
Resources (NCRR), National Institutes of Health (NIH); and by the
intramural research program of the NIH.
NR 40
TC 26
Z9 27
U1 0
U2 6
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2009
VL 114
IS 21
BP 4639
EP 4644
DI 10.1182/blood-2009-04-218040
PG 6
WC Hematology
SC Hematology
GA 521WQ
UT WOS:000271957400007
PM 19724057
ER
PT J
AU Arons, E
Suntum, T
Stetler-Stevenson, M
Kreitman, RJ
AF Arons, Evgeny
Suntum, Tara
Stetler-Stevenson, Maryalice
Kreitman, Robert J.
TI VH4-34(+) hairy cell leukemia, a new variant with poor prognosis despite
standard therapy
SO BLOOD
LA English
DT Article
ID ENCODED MONOCLONAL-ANTIBODIES; V-H GENE; SYSTEMIC-LUPUS-ERYTHEMATOSUS;
CHRONIC LYMPHOCYTIC-LEUKEMIA; TERM-FOLLOW-UP; B-LYMPHOCYTES; ABDOMINAL
LYMPHADENOPATHY; SOMATIC HYPERMUTATION; COLD AGGLUTININS; ANTI-I
AB Hairy cell leukemia variant (HCLv) presents with high disease burden, lack of typical antigens like CD25, and poor response to standard treatments like cladribine. Occasionally, patients with classic HCL respond poorly. Clinical and molecular features of HCL and HCLv has not been compared. Rearrangements expressing immunoglobulin VH chain were sequenced, including 22 from 20 patients with HCLv and 63 from 62 patients with classic HCL. Most patients were seeking relapsed/refractory trials, representing a poor-prognosis population. VH4-34, a gene commonly used in autoimmune disorders, was observed in 8 (40%) HCLv and 6 (10%) classic (P = .004) HCL patients. Compared with 71 VH4-34(-) rearrangements, 14 VH4-34(+) rearrangements were more frequently (P < .001) unmutated, defined as greater than 98% homologous to germline sequence. VH-434(+) patients had greater white blood cell counts at diagnosis (P = .002), lower response rate ( P < .001) and progression-free survival ( P = .007) after initial cladribine, and shorter overall survival from diagnosis (P < .001). Response and survival were more closely related to VH4-34 status than to whether or not patients had HCLv. VH4-34(-) HCL is an important disorder that only partly overlaps with the previously described HCLv. Response to initial single-agent cladribine therapy is suboptimal; these patients should be considered for alternative approaches, including antibody-related therapy. ( Blood. 2009; 114:4687-4695)
C1 [Arons, Evgeny; Suntum, Tara; Kreitman, Robert J.] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Stetler-Stevenson, Maryalice] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
RP Kreitman, RJ (reprint author), NCI, Mol Biol Lab, NIH, 37-5124B,37 Convent Dr,MSC 4255, Bethesda, MD 20892 USA.
EM kreitmar@mail.nih.gov
FU NCI; NIH
FX This work was supported by the intramural program, NCI, NIH.
NR 71
TC 60
Z9 61
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2009
VL 114
IS 21
BP 4687
EP 4695
DI 10.1182/blood-2009-01-201731
PG 9
WC Hematology
SC Hematology
GA 521WQ
UT WOS:000271957400012
PM 19745070
ER
PT J
AU Kimura, A
Rieger, MA
Simone, JM
Chen, WP
Wickre, MC
Zhu, BM
Hoppe, PS
O'Shea, JJ
Schroeder, T
Hennighausen, L
AF Kimura, Akiko
Rieger, Michael A.
Simone, James M.
Chen, Weiping
Wickre, Mark C.
Zhu, Bing-Mei
Hoppe, Philipp S.
O'Shea, John J.
Schroeder, Timm
Hennighausen, Lothar
TI The transcription factors STAT5A/B regulate GM-CSF-mediated
granulopoiesis
SO BLOOD
LA English
DT Article
ID COLONY-STIMULATING FACTOR; PHYSIOLOGICAL NEGATIVE REGULATOR;
HEMATOPOIETIC STEM-CELLS; FACTOR-RECEPTOR; EMERGENCY GRANULOPOIESIS;
LYMPHOID DEVELOPMENT; GENE-EXPRESSION; DEFICIENT MICE; GROWTH-FACTOR;
GRANULOCYTE
AB Neutrophils play a vital role in the immune defense, which is evident by the severity of neutropenia causing life-threatening infections. Granulocyte macrophage-colony stimulating factor (GM-CSF) controls homeostatic and emergency development of granulocytes. However, little is known about the contribution of the downstream mediating transcription factors signal transducer and activator of transcription 5A and 5B (STAT5A/B). To elucidate the function of this pathway, we generated mice with complete deletion of both Stat5a/b genes in hematopoietic cells. In homeostasis, peripheral neutrophils were markedly decreased in these animals. Moreover, during emergency situations, such as myelosuppression, Stat5a/b mutant mice failed to produce enhanced levels of neutrophils and were unable to respond to GM-CSF. Both the GM-CSF permitted survival of mature neutrophils and the generation of granulocytes from granulocyte-macrophage progenitors (GMPs) were markedly reduced in Stat5a/b mutants. GMPs showed impaired colony-formation ability with reduced number and size of colonies on GM-CSF stimulation. Moreover, continuous cell fate analyses by time-lapse microscopy and single cell tracking revealed that Stat5a/b-null GMPs showed both delayed cell-cycle progression and increased cell death. Finally, transcriptome analysis indicated that STAT5A/B directs GM-CSF signaling through the regulation of proliferation and survival genes. ( Blood. 2009; 114: 4721-4728)
C1 [Kimura, Akiko; Wickre, Mark C.; Zhu, Bing-Mei; Hennighausen, Lothar] NIDDK, Lab Genet & Physiol, NIH, Bethesda, MD 20892 USA.
[Rieger, Michael A.; Hoppe, Philipp S.; Schroeder, Timm] German Res Ctr Environm Hlth GmbH, Helmholtz Zentrum Muenchen, Inst Stem Cell Res, Neuherberg, Germany.
[Simone, James M.] NIAMSD, Flow Cytometry Sect, Off Sci & Technol, NIH, Bethesda, MD 20892 USA.
[Chen, Weiping] NIDDK, Microarray Core Facil, Genom Core Lab, NIH, Bethesda, MD 20892 USA.
[O'Shea, John J.] NIAMSD, Mol Immunol & Inflammat Branch, NIH, Bethesda, MD 20892 USA.
RP Hennighausen, L (reprint author), NIDDK, Lab Genet & Physiol, NIH, Bldg 8,Rm 101, Bethesda, MD 20892 USA.
EM lotharh@niddk.nih.gov
RI Schroeder, Timm/F-8448-2010
OI Schroeder, Timm/0000-0001-9320-0252
FU German Research Council (DFG); NIDDK/NIH; Deutsche
Forschungsgemeinschaft
FX This work was supported by the German Research Council (DFG) to T. S.
and the intramural program of the NIDDK/NIH and the Deutsche
Forschungsgemeinschaft Mercator Visiting Professor program to L. H.
NR 49
TC 33
Z9 35
U1 1
U2 2
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 19
PY 2009
VL 114
IS 21
BP 4721
EP 4728
DI 10.1182/blood-2009-04-216390
PG 8
WC Hematology
SC Hematology
GA 521WQ
UT WOS:000271957400016
PM 19779039
ER
PT J
AU Lisco, A
Vanpouille, C
Margolis, L
AF Lisco, Andrea
Vanpouille, Christophe
Margolis, Leonid
TI War and Peace between Microbes: HIV-1 Interactions with Coinfecting
Viruses
SO CELL HOST & MICROBE
LA English
DT Review
ID HEPATITIS-C VIRUS; ACTIVE ANTIRETROVIRAL THERAPY; IMMUNE-SYSTEM;
REVERSE-TRANSCRIPTASE; HUMAN-PAPILLOMAVIRUS; HUMAN HERPESVIRUS-6;
CHEMOKINE RECEPTOR; NATURAL-HISTORY; LYMPHOID-TISSUE; DOWN-REGULATION
C1 [Lisco, Andrea; Vanpouille, Christophe; Margolis, Leonid] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
RP Margolis, L (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
EM margolil@mail.nih.gov
NR 58
TC 16
Z9 16
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1931-3128
J9 CELL HOST MICROBE
JI Cell Host Microbe
PD NOV 19
PY 2009
VL 6
IS 5
BP 403
EP 408
DI 10.1016/j.chom.2009.10.010
PG 6
WC Microbiology; Parasitology; Virology
SC Microbiology; Parasitology; Virology
GA 529TE
UT WOS:000272539700005
PM 19917495
ER
PT J
AU Bauer, AK
Fostel, J
Degraff, LM
Rondini, EA
Walker, C
Grissom, SF
Foley, J
Kleeberger, SR
AF Bauer, Alison K.
Fostel, Jennifer
Degraff, Laura M.
Rondini, Elizabeth A.
Walker, Christopher
Grissom, Sherry F.
Foley, Julie
Kleeberger, Steven R.
TI Transcriptomic analysis of pathways regulated by toll-like receptor 4 in
a murine model of chronic pulmonary inflammation and carcinogenesis
SO MOLECULAR CANCER
LA English
DT Article
ID EPIDERMAL-GROWTH-FACTOR; CELL LUNG-CANCER; GENE-EXPRESSION;
OCCUPATIONAL-EXPOSURE; SIGNALING PATHWAY; TRANSGENIC MICE; TUMOR
PROMOTION; EGFR MUTATIONS; MOUSE; RISK
AB Background: Therapeutic strategies exist for human pulmonary neoplasia, however due to the heterogeneity of the disease, most are not very effective. The innate immunity gene, toll-like receptor 4 (TLR4), protects against chronic pulmonary inflammation and tumorigenesis in mice, but the mechanism is unclear. This study was designed to identify TLR4-mediated gene expression pathways that may be used as prognostic indicators of susceptibility to lung tumorigenesis in mice and provide insight into the mechanism.
Methods: Whole lung mRNA was isolated from C.C3H-Tlr4(Lps-d) (BALB(Lps-d); Tlr4 mutant) and BALB/c (Tlr4 normal) mice following butylated hydroxytoluene (BHT)-treatment (four weekly ip. injections; 150-200 mg/kg/each; "promotion"). mRNA from micro-dissected tumors (adenomas) and adjacent uninvolved tissue from both strains were also compared 27 wks after a single carcinogen injection (3-methylcholanthrene (MCA), 10 mu g/g; "control") or followed by BHT (6 weekly ip. injections; 125-200 mg/kg/each; "progression"). Bronchoalveolar lavage fluid was analyzed for inflammatory cell content and total protein determination, a marker of lung hyperpermeability; inflammation was also assessed using immunohistochemical staining for macrophages (F4/80) and lymphocytes (CD3) in mice bearing tumors (progression).
Results: During promotion, the majority of genes identified in the BALB(Lps-d) compared to BALB/c mice (P < 0.05) were involved in epithelial growth factor receptor (EGFR) signaling (e. g. epiregulin (Ereg)), secreted phosphoprotein 1(Spp1)), which can lead to cell growth and eventual tumor development. Inflammation was significantly higher in BALB(Lps-d) compared to BALB/c mice during progression, similar to the observed response during tumor promotion in these strains. Increases in genes involved in signaling through the EGFR pathway (e. g. Ereg, Spp1) were also observed during progression in addition to continued inflammation, chemotactic, and immune response gene expression in the BALB(Lps-d) versus BALB/c mice (P < 0.05), which appears to provide more favorable conditions for cell growth and tumor development. In support of these findings, the BALB/c mice also had significantly reduced expression of many immune response and inflammatory genes in both the tumors and uninvolved tissue.
Conclusion: This transcriptomic study determined the protective effect of TLR4 in lung carcinogenesis inhibition of multiple pathways including EGFR (e. g. Ereg), inflammatory response genes (e.g. Cxcl5), chemotaxis (e.g. Ccr1) and other cell proliferation genes (e. g. Arg1, Pthlh). Future studies will determine the utility of these pathways as indicators of immune system deficiencies and tumorigenesis.
C1 [Bauer, Alison K.; Rondini, Elizabeth A.] Michigan State Univ, Dept Pathobiol & Diagnost Invest, E Lansing, MI 48824 USA.
[Fostel, Jennifer; Degraff, Laura M.; Walker, Christopher; Kleeberger, Steven R.] Natl Inst Environm Hlth Sci, Lab Resp Biol, Res Triangle Pk, NC USA.
[Grissom, Sherry F.] Natl Inst Environm Hlth Sci, Mol Toxicol Lab, Res Triangle Pk, NC USA.
[Foley, Julie] Natl Inst Environm Hlth Sci, Lab Cellular & Mol Pathol, Res Triangle Pk, NC USA.
RP Bauer, AK (reprint author), Michigan State Univ, Dept Pathobiol & Diagnost Invest, E Lansing, MI 48824 USA.
EM akbauer@msu.edu; fostel@niehs.nih.gov; miller12@niehs.nih.gov;
rondinie@msu.edu; christopher.walker2@duke.edu;
sherryfgrissom@gmail.com; foley1@niehs.nih.gov; kleeber1@niehs.nih.gov
FU Division of Intramural Research of the NIEHS [HHSN273200700046U];
National Institute of Environmental Health Science; Michigan State
University
FX The authors would like to thank Drs. Alex Merrick and Pierre Bushel for
critically reviewing the manuscript. J Fostel was supported by the
Division of Intramural Research of the NIEHS contract HHSN273200700046U.
S. R. K., L. M. D., C. W., J. F. and S. F. G. were supported by the
Division of Intramural Research of the National Institute of
Environmental Health Science. A. K. B. and E. A. R. were supported by
Michigan State University internal funds.
NR 55
TC 15
Z9 17
U1 0
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD NOV 19
PY 2009
VL 8
AR 107
DI 10.1186/1476-4598-8-107
PG 17
WC Biochemistry & Molecular Biology; Oncology
SC Biochemistry & Molecular Biology; Oncology
GA 526IY
UT WOS:000272282800001
PM 19925653
ER
PT J
AU Glocker, EO
Kotlarz, D
Boztug, K
Gertz, EM
Schaffer, AA
Noyan, F
Perro, M
Diestelhorst, J
Allroth, A
Murugan, D
Hatscher, N
Pfeifer, D
Sykora, KW
Sauer, M
Kreipe, H
Lacher, M
Nustede, R
Woellner, C
Baumann, U
Salzer, U
Koletzko, S
Shah, N
Segal, AW
Sauerbrey, A
Buderus, S
Snapper, SB
Grimbacher, B
Klein, C
AF Glocker, Erik-Oliver
Kotlarz, Daniel
Boztug, Kaan
Gertz, E. Michael
Schaeffer, Alejandro A.
Noyan, Fatih
Perro, Mario
Diestelhorst, Jana
Allroth, Anna
Murugan, Dhaarini
Haetscher, Nadine
Pfeifer, Dietmar
Sykora, Karl-Walter
Sauer, Martin
Kreipe, Hans
Lacher, Martin
Nustede, Rainer
Woellner, Cristina
Baumann, Ulrich
Salzer, Ulrich
Koletzko, Sibylle
Shah, Neil
Segal, Anthony W.
Sauerbrey, Axel
Buderus, Stephan
Snapper, Scott B.
Grimbacher, Bodo
Klein, Christoph
TI Inflammatory Bowel Disease and Mutations Affecting the Interleukin-10
Receptor
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID AUTOSOMAL RECESSIVE ENTEROCOLITIS; GENOME-WIDE ASSOCIATION;
CROHNS-DISEASE; INTESTINAL INFLAMMATION; CYTOKINE PRODUCTION;
ULCERATIVE-COLITIS; SEQUENCE VARIANTS; CRYSTAL-STRUCTURE; LOCI
CONTRIBUTE; IL-10
AB BACKGROUND
The molecular cause of inflammatory bowel disease is largely unknown.
METHODS
We performed genetic-linkage analysis and candidate-gene sequencing on samples from two unrelated consanguineous families with children who were affected by early-onset inflammatory bowel disease. We screened six additional patients with early-onset colitis for mutations in two candidate genes and carried out functional assays in patients' peripheral-blood mononuclear cells. We performed an allogeneic hematopoietic stem-cell transplantation in one patient.
RESULTS
In four of nine patients with early-onset colitis, we identified three distinct homozygous mutations in genes IL10RA and IL10RB, encoding the IL10R1 and IL10R2 proteins, respectively, which form a heterotetramer to make up the interleukin-10 receptor. The mutations abrogate interleukin-10-induced signaling, as shown by deficient STAT3 (signal transducer and activator of transcription 3) phosphorylation on stimulation with interleukin-10. Consistent with this observation was the increased secretion of tumor necrosis factor alpha and other proinflammatory cytokines from peripheral-blood mononuclear cells from patients who were deficient in IL10R subunit proteins, suggesting that interleukin-10-dependent "negative feedback" regulation is disrupted in these cells. The allogeneic stem-cell transplantation performed in one patient was successful.
CONCLUSIONS
Mutations in genes encoding the IL10R subunit proteins were found in patients with early-onset enterocolitis, involving hyperinflammatory immune responses in the intestine. Allogeneic stem-cell transplantation resulted in disease remission in one patient.
C1 [Kotlarz, Daniel; Boztug, Kaan; Noyan, Fatih; Diestelhorst, Jana; Allroth, Anna; Murugan, Dhaarini; Haetscher, Nadine; Sykora, Karl-Walter; Sauer, Martin; Klein, Christoph] Hannover Med Sch, Dept Pediat Hematol Oncol, D-30625 Hannover, Germany.
[Kreipe, Hans] Hannover Med Sch, Dept Pathol, D-30625 Hannover, Germany.
[Nustede, Rainer] Hannover Med Sch, Dept Pediat Surg, D-30625 Hannover, Germany.
[Baumann, Ulrich] Hannover Med Sch, Dept Pediat Pulmonol, D-30625 Hannover, Germany.
[Glocker, Erik-Oliver; Perro, Mario; Woellner, Cristina; Grimbacher, Bodo] Royal Free Hosp, Dept Immunol, London NW3 2QG, England.
[Segal, Anthony W.] UCL, Dept Med, London, England.
[Shah, Neil] UCL, Great Ormond St Hosp, Dept Paediat Gastroenterol, London, England.
[Gertz, E. Michael; Schaeffer, Alejandro A.] NIH, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Pfeifer, Dietmar] Univ Freiburg, Med Ctr, Dept Hematol Oncol, Core Facil Genom 2, D-7800 Freiburg, Germany.
[Salzer, Ulrich] Univ Hosp Freiburg, Dept Rheumatol & Clin Immunol, Freiburg, Germany.
[Lacher, Martin; Koletzko, Sibylle] Univ Munich, Dr von Haunersches Kinderspital, Munich, Germany.
[Sauerbrey, Axel] HELIOS Hosp Erfurt, Dept Pediat, Erfurt, Germany.
[Buderus, Stephan] St Marien Hosp Bonn, Dept Pediat, Bonn, Germany.
[Snapper, Scott B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Snapper, Scott B.] Harvard Univ, Sch Med, Boston, MA USA.
RP Klein, C (reprint author), Hannover Med Sch, Dept Pediat Hematol Oncol, Carl Neuberg Str 1, D-30625 Hannover, Germany.
EM b.grimbacher@ucl.ac.uk; klein.christoph@mh-hannover.de
RI Schaffer, Alejandro/F-2902-2012;
OI Segal, Anthony/0000-0001-7602-9043; Gertz, E.
Michael/0000-0001-8390-4387
FU European Commission Marie Curie Excellence program
[MEXT-CT-2006-042316]; Deutsche Forschungsgemeinschaft [SFB621]; German
Federal Ministry of Education and Research (PID-NET); Intramural
Research Program of the National Institutes of Health; Deutsche Jose
Carreras Leukmie-Stiftung; Else-Krner-Fresenius-Stiftung
FX Supported by grants from the European Commission Marie Curie Excellence
program (MEXT-CT-2006-042316,to Dr. Grim- bacher), Deutsche
Forschungsgemeinschaft (SFB621, to Dr. Klein), and the German Federal
Ministry of Education and Research (PID-NET), to Drs. Klein and
Grimbacher; by the Intramural Research Program of the National
Institutes of Health; and by fellowships from Deutsche Jose Carreras
Leukmie-Stiftung (to Dr. Kotlarz) and Else-Krner-Fresenius-Stiftung ( to
Dr. Boztug).
NR 45
TC 504
Z9 523
U1 7
U2 23
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 19
PY 2009
VL 361
IS 21
BP 2033
EP 2045
DI 10.1056/NEJMoa0907206
PG 13
WC Medicine, General & Internal
SC General & Internal Medicine
GA 521DA
UT WOS:000271898600008
PM 19890111
ER
PT J
AU Zhang, Q
Davis, JC
Lamborn, IT
Freeman, AF
Jing, H
Favreau, AJ
Matthews, HF
Davis, J
Turner, ML
Uzel, G
Holland, SM
Su, HC
AF Zhang, Qian
Davis, Jeremiah C.
Lamborn, Ian T.
Freeman, Alexandra F.
Jing, Huie
Favreau, Amanda J.
Matthews, Helen F.
Davis, Joie
Turner, Maria L.
Uzel, Gulbu
Holland, Steven M.
Su, Helen C.
TI Combined Immunodeficiency Associated with DOCK8 Mutations
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID HYPER-IGE SYNDROME; T-CELL IMMUNODEFICIENCY; STAT3 MUTATIONS;
DIFFERENTIATION; DEFICIENCIES; ACTIVATOR; DELETION; DISEASES; EGRESS;
FAMILY
AB BACKGROUND
Recurrent sinopulmonary and cutaneous viral infections with elevated serum levels of IgE are features of some variants of combined immunodeficiency. The genetic causes of these variants are unknown.
METHODS
We collected longitudinal clinical data on 11 patients from eight families who had recurrent sinopulmonary and cutaneous viral infections. We performed comparative genomic hybridization arrays and targeted gene sequencing. Variants with predicted loss-of-expression mutations were confirmed by means of a quantitative reverse-transcriptase-polymerase-chain-reaction assay and immunoblotting. We evaluated the number and function of lymphocytes with the use of in vitro assays and flow cytometry.
RESULTS
Patients had recurrent otitis media, sinusitis, and pneumonias; recurrent Staphylococcus aureus skin infections with otitis externa; recurrent, severe herpes simplex virus or herpes zoster infections; extensive and persistent infections with molluscum contagiosum; and human papillomavirus infections. Most patients had severe atopy with anaphylaxis; several had squamous-cell carcinomas, and one had T-cell lymphoma-leukemia. Elevated serum IgE levels, hypereosinophilia, low numbers of T cells and B cells, low serum IgM levels, and variable IgG antibody responses were common. Expansion in vitro of activated CD8 T cells was impaired. Novel homozygous or compound heterozygous deletions and point mutations in the gene encoding the dedicator of cytokinesis 8 protein (DOCK8) led to the absence of DOCK8 protein in lymphocytes.
CONCLUSIONS
Autosomal recessive DOCK8 deficiency is associated with a novel variant of combined immunodeficiency.
C1 [Su, Helen C.] NIAID, NIH, Host Def Lab, Bethesda, MD 20892 USA.
[Freeman, Alexandra F.; Davis, Joie; Uzel, Gulbu; Holland, Steven M.] NIAID, Lab Clin Infect Dis, Bethesda, MD 20892 USA.
[Favreau, Amanda J.] NIAID, Res Technol Branch, Bethesda, MD 20892 USA.
[Matthews, Helen F.] NIAID, Immunol Lab, Bethesda, MD 20892 USA.
[Davis, Jeremiah C.] Howard Hughes Med Inst, Bethesda, MD 20817 USA.
[Turner, Maria L.] NCI, Dermatol Branch, Bethesda, MD 20892 USA.
RP Su, HC (reprint author), NIAID, NIH, Host Def Lab, CRC 5W3940,MSC 1456, Bethesda, MD 20892 USA.
EM hsu@niaid.nih.gov
RI Su, Helen/H-9541-2015;
OI Su, Helen/0000-0002-5582-9110; Zhang, Qian/0000-0002-9040-3289
FU National Institutes of Health; National Institute of Allergy and
Infectious Diseases; National Cancer Institute; Howard Hughes Medical
Institute-National Institutes of Health Research Scholar Program
FX Supported by the Intramural Research Program of the National Institutes
of Health, the National Institute of Allergy and Infectious Diseases,
and the National Cancer Institute, and by a grant from the Howard Hughes
Medical Institute-National Institutes of Health Research Scholar Program
( to Mr. Davis). Sequencing was performed by the Genomics Unit of the
Rocky Mountain Laboratories Research Technologies Section of the
National Institute of Allergy and Infectious Diseases.
NR 39
TC 252
Z9 260
U1 2
U2 8
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 19
PY 2009
VL 361
IS 21
BP 2046
EP 2055
DI 10.1056/NEJMoa0905506
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 521DA
UT WOS:000271898600009
PM 19776401
ER
PT J
AU Kelsall, B
AF Kelsall, Brian
TI Interleukin-10 in Inflammatory Bowel Disease
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
ID RECOMBINANT HUMAN INTERLEUKIN-10; ACTIVE CROHNS-DISEASE; SUSCEPTIBILITY;
EFFICACY; MULTIPLE; SAFETY; LOCI
C1 NIAID, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Kelsall, B (reprint author), NIAID, Lab Mol Immunol, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
NR 13
TC 6
Z9 6
U1 1
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 19
PY 2009
VL 361
IS 21
BP 2091
EP 2093
DI 10.1056/NEJMe0909225
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 521DA
UT WOS:000271898600016
PM 19890110
ER
PT J
AU Ahmet, I
Spangler, E
Shukitt-Hale, B
Joseph, JA
Ingram, DK
Talan, M
AF Ahmet, Ismayil
Spangler, Edward
Shukitt-Hale, Barbara
Joseph, James A.
Ingram, Donald K.
Talan, Mark
TI Survival and Cardioprotective Benefits of Long-Term Blueberry Enriched
Diet in Dilated Cardiomyopathy Following Myocardial Infarction in Rats
SO PLOS ONE
LA English
DT Article
ID MITOCHONDRIAL PERMEABILITY TRANSITION; CARDIAC MYOCYTE APOPTOSIS;
QUALITY-OF-LIFE; HEART-FAILURE; BEHAVIORAL DEFICITS; DISEASE; DEATH;
SUPPLEMENTATION; DAMAGE
AB Background: Despite remarkable progress in treatment of chronic heart failure (CHF) over the last two decades, mortality, personal suffering and cost remain staggering, and effective interventions are still a challenge. Previously we reported that a blueberry-enriched diet (BD) attenuated necroapoptosis and inflammation in periinfarct area in a rat model of myocardial infarction (MI).
Objectives: To test the hypothesis that BD will attenuate the course of CHF, including mortality and cardiac remodeling during the first year after induction of MI in rats.
Method and Results: Two weeks after coronary artery ligation, rats were divided into two groups of similar average MI size, measured by echocardiography, and then 12-mo dietary regimens were initiated as follows: ad libitum regular diet (control, CD, n = 27) and isocaloric food with 2% blueberry supplement (BD, n = 27) also available ad libitum. These dietary groups were compared to each other and to sham group (SH). Mortality over the 12 mo was reduced by 22% in BD compared with CD (p<0.01). In the course of developing CHF, BD had no effect on the body weight, heart rate or blood pressure. Bimonthly Echo revealed significant attenuation of the LV chamber remodeling, LV posterior wall thinning, and MI expansion in BD compared with CD. In fact, BD arrested the MI expansion.
Conclusion: This is the first experimental evidence that a blueberry-enriched diet has positive effects on the course of CHF and thus warrants consideration for clinical evaluation.
RP Ahmet, I (reprint author), NIA, Lab Cardiovasc Sci, NIH, Baltimore, MD 21224 USA.
EM talanm@grc.nia.nih.gov
FU Intramural NIH HHS
NR 25
TC 18
Z9 18
U1 1
U2 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 19
PY 2009
VL 4
IS 11
AR e7975
DI 10.1371/journal.pone.0007975
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 522NJ
UT WOS:000272004600024
PM 19936253
ER
PT J
AU D'Armiento, JM
Scharf, SM
Roth, MD
Connett, JE
Ghio, A
Sternberg, D
Goldin, JG
Louis, TA
Mao, JT
O'Connor, GT
Ramsdell, JW
Ries, AL
Schluger, NW
Sciurba, FC
Skeans, MA
Voelker, H
Walter, RE
Wendt, CH
Weinmann, GG
Wise, RA
Foronjy, RF
AF D'Armiento, Jeanine M.
Scharf, Steven M.
Roth, Michael D.
Connett, John E.
Ghio, Andrew
Sternberg, David
Goldin, Jonathan G.
Louis, Thomas A.
Mao, Jenny T.
O'Connor, George T.
Ramsdell, Joe W.
Ries, Andrew L.
Schluger, Neil W.
Sciurba, Frank C.
Skeans, Melissa A.
Voelker, Helen
Walter, Robert E.
Wendt, Christine H.
Weinmann, Gail G.
Wise, Robert A.
Foronjy, Robert F.
TI Eosinophil and T cell markers predict functional decline in COPD
patients
SO RESPIRATORY RESEARCH
LA English
DT Article
ID OBSTRUCTIVE PULMONARY-DISEASE; SYNCYTIAL VIRUS-INFECTION;
CIGARETTE-SMOKE; AIRWAY INFLAMMATION; RESPIRATORY VIRUSES;
CHRONIC-BRONCHITIS; EFFECTOR ACTIVITY; EXACERBATIONS; LYMPHOCYTES;
EMPHYSEMA
AB Background: The major marker utilized to monitor COPD patients is forced expiratory volume in one second (FEV1). However, asingle measurement of FEV1 cannot reliably predict subsequent decline. Recent studies indicate that T lymphocytes and eosinophils are important determinants of disease stability in COPD. We therefore measured cytokine levels in the lung lavage fluid and plasma of COPD patients in order to determine if the levels of T cell or eosinophil related cytokines were predictive of the future course of the disease.
Methods: Baseline lung lavage and plasma samples were collected from COPD subjects with moderately severe airway obstruction and emphysematous changes on chest CT. The study participants were former smokers who had not had a disease exacerbation within the past six months or used steroids within the past two months. Those subjects who demonstrated stable disease over the following six months (Delta FEV1 % predicted = 4.7 +/- 7.2; N = 34) were retrospectively compared with study participants who experienced a rapid decline in lung function (Delta FEV1 % predicted = -16.0 +/- 6.0; N = 16) during the same time period and with normal controls (N = 11). Plasma and lung lavage cytokines were measured from clinical samples using the Luminex multiplex kit which enabled the simultaneous measurement of several T cell and eosinophil related cytokines.
Results and Discussion: Stable COPD participants had significantly higher plasma IL-2 levels compared to participants with rapidly progressive COPD (p = 0.04). In contrast, plasma eotaxin-1 levels were significantly lower in stable COPD subjects compared to normal controls (p < 0.03). In addition, lung lavage eotaxin-1 levels were significantly higher in rapidly progressive COPD participants compared to both normal controls (p < 0.02) and stable COPD participants (p < 0.05).
Conclusion: These findings indicate that IL-2 and eotaxin-1 levels may be important markers of disease stability in advanced emphysema patients. Prospective studies will need to confirm whether measuring IL-2 or eotaxin-1 can identify patients at risk for rapid disease progression.
C1 [D'Armiento, Jeanine M.; Sternberg, David; Schluger, Neil W.; Foronjy, Robert F.] Columbia Univ, Dept Med, New York, NY 10027 USA.
[D'Armiento, Jeanine M.; Sternberg, David; Schluger, Neil W.; Foronjy, Robert F.] Columbia Univ, Dept Surg, New York, NY USA.
[Scharf, Steven M.] Univ Maryland, Dept Med, Baltimore, MD 21201 USA.
[Roth, Michael D.; Goldin, Jonathan G.; Mao, Jenny T.; Skeans, Melissa A.; Voelker, Helen; Wendt, Christine H.] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90024 USA.
[Roth, Michael D.; Goldin, Jonathan G.; Mao, Jenny T.; Skeans, Melissa A.; Voelker, Helen; Wendt, Christine H.] Univ Calif Los Angeles, Dept Biol, Los Angeles, CA 90024 USA.
[Connett, John E.] Univ Minnesota, Dept Med, CCBR, Twin Cities, CA USA.
[Connett, John E.] Univ Minnesota, Dept Biostat, CCBR, Twin Cities, CA USA.
[Ghio, Andrew; Wise, Robert A.] US EPA, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA.
[Louis, Thomas A.; Walter, Robert E.] Johns Hopkins Univ, Dept Med, Baltimore, MD USA.
[O'Connor, George T.] Boston Univ, Dept Med, Boston, MA 02215 USA.
[Ramsdell, Joe W.; Ries, Andrew L.] Univ Calif San Diego, Dept Med, San Diego, CA 92103 USA.
[Sciurba, Frank C.] Univ Pittsburgh, Dept Med, Pittsburgh, PA USA.
[Weinmann, Gail G.] NIH, Bethesda, MD 20892 USA.
RP Foronjy, RF (reprint author), Columbia Univ, Dept Med, New York, NY 10027 USA.
EM jmd12@columbia.edu; sscharf@medicine.umaryland.edu;
MRoth@mednet.ucla.edu; john-c@ccbr.umn.edu; Ghio.Andy@epamail.epa.gov;
das9018@nyp.org; JGoldin@mednet.ucla.edu; tlouis@jhsph.edu;
JMao@mednet.ucla.edu; goconnor@bu.edu; jramsdell@ucsd.edu;
aries@ucsd.edu; ns311@columbia.edu; sciurbafc@msx.upmc.edu;
melissas@ccbr.umn.edu; voelk002@umn.edu; walterb@bu.edu;
wendt005@tc.umn.edu; gweinmann@nih.gov; rwise@welch.jhu.edu;
rff5@columbia.edu
RI Wendt, Chris/C-6823-2012
FU NHLBI NIH HHS [L30 HL074905, N01-HR-96140, N01-HR-96141-001,
N01-HR-96142, N01-HR-96143, N01-HR-96144, N01-HR-96145, R01 HL098528,
R01HL086936-03]
NR 45
TC 20
Z9 20
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1465-9921
J9 RESP RES
JI Respir. Res.
PD NOV 19
PY 2009
VL 10
AR 113
DI 10.1186/1465-9921-10-113
PG 13
WC Respiratory System
SC Respiratory System
GA 526MH
UT WOS:000272293200001
PM 19925666
ER
PT J
AU Sul, B
Iwasa, KH
AF Sul, Bora
Iwasa, Kuni H.
TI Effectiveness of Hair Bundle Motility as the Cochlear Amplifier
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID MECHANOELECTRICAL-TRANSDUCTION CHANNELS; CHICK BASILAR PAPILLA; CELL
STEREOCILIA; MECHANICAL RESPONSES; LIMITING FREQUENCY; TECTORIAL
MEMBRANE; NEGATIVE STIFFNESS; ACTIN-FILAMENTS; FAST ADAPTATION; BIRD
COCHLEA
AB The effectiveness of hair bundle motility in mammalian and avian ears is studied by examining energy balance for a small sinusoidal displacement of the hair bundle. The condition that the energy generated by a hair bundle must be greater than energy loss due to the shear in the subtectorial gap per hair bundle leads to a limiting frequency that can be supported by hair-bundle motility. Limiting frequencies are obtained for two motile mechanisms for fast adaptation, the channel re-closure model and a model that assumes that fast adaptation is an interplay between gating of the channel and the myosin motor. The limiting frequency obtained for each of these models is an increasing function of a factor that is determined by the morphology of hair bundles and the cochlea. Primarily due to the higher density of hair cells in the avian inner ear, this factor is similar to 10-fold greater for the avian ear than the mammalian ear, which has much higher auditory frequency limit. This result is consistent with a much greater significance of hair bundle motility in the avian ear than that in the mammalian ear.
C1 [Sul, Bora; Iwasa, Kuni H.] Natl Inst Deafness & Other Commun Disorders, Biophys Sect, Lab Cellular Biol, NIH, Rockville, MD USA.
RP Iwasa, KH (reprint author), Natl Inst Deafness & Other Commun Disorders, Biophys Sect, Lab Cellular Biol, NIH, Rockville, MD USA.
EM iwasa@nih.gov
OI Iwasa, Kuni/0000-0002-9397-7704
FU National Institute on Deafness and Other Communication Disorders,
National Institutes of Health, Bethesda, MD
FX This work was supported by the intramural program of the National
Institute on Deafness and Other Communication Disorders, National
Institutes of Health, Bethesda, MD.
NR 65
TC 11
Z9 11
U1 0
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 18
PY 2009
VL 97
IS 10
BP 2653
EP 2663
DI 10.1016/j.bpj.2009.08.039
PG 11
WC Biophysics
SC Biophysics
GA 521JQ
UT WOS:000271917700002
PM 19917218
ER
PT J
AU Snyder, JS
Choe, JS
Clifford, MA
Jeurling, SI
Hurley, P
Brown, A
Kamhi, JF
Cameron, HA
AF Snyder, Jason S.
Choe, Jessica S.
Clifford, Meredith A.
Jeurling, Sara I.
Hurley, Patrick
Brown, Ashly
Kamhi, J. Frances
Cameron, Heather A.
TI Adult-Born Hippocampal Neurons Are More Numerous, Faster Maturing, and
More Involved in Behavior in Rats than in Mice
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID GENERATED GRANULE CELLS; ENHANCED SYNAPTIC PLASTICITY; MORRIS
WATER-MAZE; LONG-TERM-MEMORY; DENTATE GYRUS; SPATIAL MEMORY;
NEUROGENESIS; BRAIN; MOUSE; EXPRESSION
AB Neurons are born throughout adulthood in the hippocampus and show enhanced plasticity compared with mature neurons. However, there are conflicting reports on whether or not young neurons contribute to performance in behavioral tasks, and there is no clear relationship between the timing of maturation of young neurons and the duration of neurogenesis reduction in studies showing behavioral deficits. We asked whether these discrepancies could reflect differences in the properties of young neurons in mice and rats. We report that young neurons in adult rats show a mature neuronal marker profile and activity-induced immediate early gene expression 1-2 weeks earlier than those in mice. They are also twice as likely to escape cell death, and are 10 times more likely to be recruited into learning circuits. This comparison holds true in two different strains of mice, both of which show high rates of neurogenesis relative to other background strains. Differences in adult neurogenesis are not limited to the hippocampus, as the density of new neocortical neurons was 5 times greater in rats than in mice. Finally, in a test of function, we find that the contribution of young neurons to fear memory is much greater in rats than in mice. These results reveal substantial differences in new neuron plasticity and function between these two commonly studied rodent species.
C1 [Snyder, Jason S.; Choe, Jessica S.; Clifford, Meredith A.; Jeurling, Sara I.; Hurley, Patrick; Brown, Ashly; Kamhi, J. Frances; Cameron, Heather A.] NIMH, Unit Neuroplast, NIH, Bethesda, MD 20892 USA.
RP Snyder, JS (reprint author), NIMH, Unit Neuroplast, NIH, Bldg 35-3C911,MSC3718, Bethesda, MD 20892 USA.
EM snyderjason@mail.nih.gov
RI Snyder, Jason/F-3435-2011; Cameron, Heather/E-6221-2011;
OI Cameron, Heather/0000-0002-3245-5777; Kamhi, J.
Frances/0000-0002-3806-0506; Snyder, Jason/0000-0002-5509-0272
FU National Institutes of Health; National Institute of Mental Health
[Z01-MH002784]
FX This research was supported by the Intramural Program of the National
Institutes of Health, National Institute of Mental Health, Z01-MH002784
( H. A. C.). We thank Sarah Kellner, Andrea Moderi, and Kaitlin Sanzone
for assistance with histological analyses and Anastasia Sowers and James
Mitchell for assistance with the irradiation procedures.
NR 64
TC 184
Z9 188
U1 1
U2 6
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 18
PY 2009
VL 29
IS 46
BP 14484
EP 14495
DI 10.1523/JNEUROSCI.1768-09.2009
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 521SO
UT WOS:000271944500011
PM 19923282
ER
PT J
AU Scimemi, A
Tian, H
Diamond, JS
AF Scimemi, Annalisa
Tian, Hua
Diamond, Jeffrey S.
TI Neuronal Transporters Regulate Glutamate Clearance, NMDA Receptor
Activation, and Synaptic Plasticity in the Hippocampus
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID LONG-TERM POTENTIATION; D-ASPARTATE RECEPTORS; RELEASED GLUTAMATE;
PYRAMIDAL CELLS; RAT HIPPOCAMPUS; IN-VITRO; SYNAPSES; SUBUNIT; CURRENTS;
EAAC1
AB In the mammalian brain, the specificity of excitatory synaptic transmission depends on rapid diffusion of glutamate away from active synapses and the powerful uptake capacity of glutamate transporters in astrocytes. The extent to which neuronal glutamate transporters influence the lifetime of glutamate in the extracellular space remains unclear. Here we show that EAAC1, the predominant neuronal glutamate transporter at excitatory synapses in hippocampal area CA1, buffers glutamate released during synaptic events and prolongs the time course of its clearance by astrocytes. EAAC1 does not significantly alter activation of receptors in the synaptic cleft. Instead, it reduces recruitment of perisynaptic/extrasynaptic NR2B-containing NMDARs, thereby facilitating induction of long-term potentiation by short bursts of high-frequency stimulation. We describe novel roles of EAAC1 in regulating glutamate diffusion and propose that NMDARs at different subsynaptic locations can make distinct contributions to the regulation of synaptic strength.
C1 [Scimemi, Annalisa; Tian, Hua; Diamond, Jeffrey S.] Natl Inst Neurol Disorders & Stroke, Synapt Physiol Sect, NIH, Bethesda, MD 20892 USA.
RP Scimemi, A (reprint author), Natl Inst Neurol Disorders & Stroke, Synapt Physiol Sect, NIH, 35 Convent Dr,Bldg 35,Room 3C1006-3C1000, Bethesda, MD 20892 USA.
EM scimemia@ninds.nih.gov; diamondj@ninds.nih.gov
RI Scimemi, Annalisa/O-5396-2014; Diamond, Jeffrey/C-1835-2015
OI Scimemi, Annalisa/0000-0003-4975-093X; Diamond,
Jeffrey/0000-0002-1770-2629
FU National Institute of Neurological Disorders and Stroke (NINDS)
Intramural Research Program and Human Frontier Science Program
[RGP50/2006]
FX This work was supported by the National Institute of Neurological
Disorders and Stroke (NINDS) Intramural Research Program and Human
Frontier Science Program (RGP50/2006). We thank N. C. Danbolt for the
EAAC1 antibody, the NINDS EM facility for technical assistance, and D.
M. Kullmann and C. J. McBain for comments on this manuscript. Thanks to
M. Dittrich for help with the MCell software and M. Beato, K. Paradiso,
and A. V. Tzingounis for valuable discussions. A. S. performed
electrophysiological recordings, EM analysis, 2P-LSM imaging, diffusion
measurements, and modeling. H. T. performed molecular biology
experiments. A. S. and J. S. D. designed the research and wrote this
manuscript.
NR 51
TC 77
Z9 78
U1 1
U2 9
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 18
PY 2009
VL 29
IS 46
BP 14581
EP 14595
DI 10.1523/JNEUROSCI.4845-09.2009
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 521SO
UT WOS:000271944500020
PM 19923291
ER
PT J
AU Shahzad-Ul-Hussan, S
Cai, ML
Bewley, CA
AF Shahzad-ul-Hussan, Syed
Cai, Mengli
Bewley, Carole A.
TI Unprecedented Glycosidase Activity at a Lectin Carbohydrate-Binding Site
Exemplified by the Cyanobacterial Lectin MVL
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID ANTI-HIV PROTEIN; SPERM-EGG INTERACTION; STRUCTURAL BASIS; CYANOVIRIN-N;
SUBSTRATE-BINDING; DIPOLAR COUPLINGS; COMPLEX; NMR; SPECIFICITY; POTENT
AB Carbohydrate binding proteins, or lectins, are engendered with the ability to bind specific carbohydrate structures, thereby mediating cell-cell and cell-pathogen interactions. Lectins are distinct from carbohydrate modifying enzymes and antibodies, respectively, as they do not carry out glycosidase or glycosyl transferase reactions, and they are of nonimmune origin. Cyanobacterial and algal lectins have become prominent in recent years due to their unique biophysical traits, such as exhibiting novel protein folds and unusually high carbohydrate affinity, and ability to potently inhibit HIV-1 entry through high affinity carbohydrate-mediated interactions with the HIV envelope glycoprotein gp120. The antiviral cyanobacterial lectin Microcystis viridis lectin (MVL), which contains two high affinity oligomannose binding sites, is one such example. Here we used glycan microarray profiling, NMR spectroscopy, and mutagenesis to show that one of the two oligomannose binding sites of MVL can catalyze the cleavage of chitin fragments (such as chitotriose) to GlcNAc, to determine the mode of MVL binding to and cleavage of chitotriose, to identify Asp75 as the primary catalytic residue involved in this cleavage, and to solve the solution structure of an inactive mutant of MVL in complex with this unexpected substrate. These studies represent the first demonstration of dual catalytic activity and carbohydrate recognition for discrete oligosaccharides at the same carbohydrate-binding site in a lectin. Sequence comparisons between the N- and C-domains of MVL, together with the sequences of new MVL homologues identified through bioinformatics, provide insight into the evolving roles of carbohydrate recognition.
C1 [Shahzad-ul-Hussan, Syed; Bewley, Carole A.] NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Cai, Mengli] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Bewley, CA (reprint author), NIDDKD, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM caroleb@mail.nih.gov
FU NIDDK; NIH; NIAID; NIGMS [M62116]
FX We thank Dr. Richard Alvarez for glycan microarray profiling, Mr. Ali
Shah for assistance with protein expression and purification, and Drs.
Maria-Teresa Gutierrez-Lugo, Marius Clore, Son Lain and Y. C. Lee for
contributive discussions during the course of this work. This research
was supported in part by the Intramural Research Program, NIDDK, NIH;
the AIDS-Targeted Antiviral Program of the Office of the Director, NIH
(C.A.B.); an instrument grant from the Division of AIDS Research, NIAID
(C.A.B.); and NIGMS - The Consortium for Functional Glycomics, Core H
(GM62116).
NR 44
TC 6
Z9 7
U1 2
U2 11
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 18
PY 2009
VL 131
IS 45
BP 16500
EP 16508
DI 10.1021/ja905929c
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA 518VK
UT WOS:000271723000044
PM 19856962
ER
PT J
AU Baker, SG
AF Baker, Stuart G.
TI Putting Risk Prediction in Perspective: Relative Utility Curves
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID BREAST-CANCER RISK; MODELS; VALIDATION; TESTS
AB Risk prediction models based on medical history or results of tests are increasingly common in the cancer literature. An important use of these models is to make treatment decisions on the basis of estimated risk. The relative utility curve is a simple method for evaluating risk prediction in a medical decision-making framework. Relative utility curves have three attractive features for the evaluation of risk prediction models. First, they put risk prediction into perspective because relative utility is the fraction of the expected utility of perfect prediction obtained by the risk prediction model at the optimal cut point. Second, they do not require precise specification of harms and benefits because relative utility is plotted against a summary measure of harms and benefits (ie, the risk threshold). Third, they are easy to compute from standard tables of data found in many articles on risk prediction. An important use of relative utility curves is to evaluate the addition of a risk factor to the risk prediction model. To illustrate an application of relative utility curves, an analysis was performed on previously published data involving the addition of breast density to a risk prediction model for invasive breast cancer.
C1 NCI, Biometry Res Grp, Canc Prevent Div, Bethesda, MD 20892 USA.
RP Baker, SG (reprint author), NCI, Biometry Res Grp, Canc Prevent Div, EPN 3131,6130 Execut Blvd,MSC 7354, Bethesda, MD 20892 USA.
EM sb16i@nih.gov
NR 15
TC 44
Z9 44
U1 1
U2 4
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 18
PY 2009
VL 101
IS 22
BP 1538
EP 1542
DI 10.1093/jnci/djp353
PG 5
WC Oncology
SC Oncology
GA 523PL
UT WOS:000272086400007
PM 19843888
ER
PT J
AU Baris, D
Karagas, MR
Verrill, C
Johnson, A
Andrew, AS
Marsit, CJ
Schwenn, M
Colt, JS
Cherala, S
Samanic, C
Waddell, R
Cantor, KP
Schned, A
Rothman, N
Lubin, J
Fraumeni, JF
Hoover, RN
Kelsey, KT
Silverman, DT
AF Baris, Dalsu
Karagas, Margaret R.
Verrill, Castine
Johnson, Alison
Andrew, Angeline S.
Marsit, Carmen J.
Schwenn, Molly
Colt, Joanne S.
Cherala, Sai
Samanic, Claudine
Waddell, Richard
Cantor, Kenneth P.
Schned, Alan
Rothman, Nathaniel
Lubin, Jay
Fraumeni, Joseph F., Jr.
Hoover, Robert N.
Kelsey, Karl T.
Silverman, Debra T.
TI A Case-Control Study of Smoking and Bladder Cancer Risk: Emergent
Patterns Over Time
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID ENVIRONMENTAL TOBACCO-SMOKE; MODELING TOTAL EXPOSURE; CIGARETTE-SMOKING;
LUNG-CANCER; AROMATIC-AMINES; CHANGING CIGARETTE; HISTOLOGIC TYPE;
POOLED ANALYSIS; CELL CARCINOMA; INTENSITY
AB Cigarette smoking is a well-established risk factor for bladder cancer. The effects of smoking duration, intensity (cigarettes per day), and total exposure (pack-years); smoking cessation; exposure to environmental tobacco smoke; and changes in the composition of tobacco and cigarette design over time on risk of bladder cancer are unclear.
We examined bladder cancer risk in relation to smoking practices based on interview data from a large, population-based case-control study conducted in Maine, New Hampshire, and Vermont from 2001 to 2004 (N = 1170 urothelial carcinoma case patients and 1413 control subjects). We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression. To examine changes in smoking-induced bladder cancer risk over time, we compared odds ratios from New Hampshire residents in this study (305 case patients and 335 control subjects) with those from two case-control studies conducted in New Hampshire in 1994-1998 and in 1998-2001 (843 case patients and 1183 control subjects).
Regular and current cigarette smokers had higher risks of bladder cancer than never-smokers (for regular smokers, OR = 3.0, 95% CI = 2.4 to 3.6; for current smokers, OR = 5.2, 95% CI = 4.0 to 6.6). In New Hampshire, there was a statistically significant increasing trend in smoking-related bladder cancer risk over three consecutive periods (1994-1998, 1998-2001, and 2002-2004) among former smokers (OR = 1.4, 95% CI = 1.0 to 2.0; OR = 2.0, 95% CI = 1.4 to 2.9; and OR = 2.6, 95% CI = 1.7 to 4.0, respectively) and current smokers (OR = 2.9, 95% CI = 2.0 to 4.2; OR = 4.2, 95% CI = 2.8 to 6.3; OR = 5.5, 95% CI = 3.5 to 8.9, respectively) (P for homogeneity of trends over time periods = .04). We also observed that within categories of intensity, odds ratios increased approximately linearly with increasing pack-years smoked, but the slope of the increasing trend declined with increasing intensity.
Smoking-related risks of bladder cancer appear to have increased in New Hampshire since the mid-1990s. Based on our modeling of pack-years and intensity, smoking fewer cigarettes over a long time appears more harmful than smoking more cigarettes over a shorter time, for equal total pack-years of cigarettes smoked.
C1 [Baris, Dalsu; Colt, Joanne S.; Samanic, Claudine; Cantor, Kenneth P.; Rothman, Nathaniel; Lubin, Jay; Fraumeni, Joseph F., Jr.; Hoover, Robert N.; Silverman, Debra T.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Karagas, Margaret R.; Andrew, Angeline S.; Schned, Alan] Dartmouth Med Sch, Dept Community & Family Med, Hannover, NH, Germany.
[Marsit, Carmen J.; Kelsey, Karl T.] Brown Univ, Dept Community Hlth & Pathol & Lab Med, Providence, RI 02912 USA.
[Verrill, Castine; Schwenn, Molly] Maine Canc Registry, Augusta, ME USA.
[Cherala, Sai] New Hampshire Canc Registry, Concord, NH USA.
[Johnson, Alison] Vermont Canc Registry, Burlington, VT USA.
RP Baris, D (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,EPS Rm 8008, Bethesda, MD 20852 USA.
EM barisd@mail.nih.gov
RI Kelsey, Karl/I-1252-2014;
OI Marsit, Carmen/0000-0003-4566-150X
FU Intramural NIH HHS; NCI NIH HHS [CA121147, R01 CA057494, R01 CA121147,
R01 CA57494]; NIEHS NIH HHS [P42 ES007373]
NR 48
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U1 0
U2 7
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 18
PY 2009
VL 101
IS 22
BP 1553
EP 1561
DI 10.1093/jnci/djp361
PG 9
WC Oncology
SC Oncology
GA 523PL
UT WOS:000272086400009
PM 19917915
ER
PT J
AU Hollingshead, MG
AF Hollingshead, Melinda G.
TI Response: Re: Antitumor Efficacy Testing in Rodents
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Letter
ID ADP-RIBOSE POLYMERASE; 0 CLINICAL-TRIAL; DRUG DEVELOPMENT
C1 [Hollingshead, Melinda G.] NCI, Biol Testing Branch, Dev Therapeut Program, Div Canc Treatment & Diag, Frederick, MD 21701 USA.
RP Hollingshead, MG (reprint author), NCI, Div Canc Treatment, Fairview Ctr, Ste 205,1003 W 7th St, Frederick, MD 21701 USA.
EM hollingm@mail.nih.gov
NR 5
TC 0
Z9 0
U1 0
U2 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 18
PY 2009
VL 101
IS 22
BP 1593
EP 1594
DI 10.1093/jnci/djp360
PG 2
WC Oncology
SC Oncology
GA 523PL
UT WOS:000272086400014
ER
PT J
AU Mandelblatt, JS
Cronin, KA
Bailey, S
Berry, DA
de Koning, HJ
Draisma, G
Huang, H
Lee, SJ
Munsell, M
Plevritis, SK
Ravdin, P
Schechter, CB
Sigal, B
Stoto, MA
Stout, NK
van Ravesteyn, NT
Venier, J
Zelen, M
Feuer, EJ
AF Mandelblatt, Jeanne S.
Cronin, Kathleen A.
Bailey, Stephanie
Berry, Donald A.
de Koning, Harry J.
Draisma, Gerrit
Huang, Hui
Lee, Sandra J.
Munsell, Mark
Plevritis, Sylvia K.
Ravdin, Peter
Schechter, Clyde B.
Sigal, Bronislava
Stoto, Michael A.
Stout, Natasha K.
van Ravesteyn, Nicolien T.
Venier, John
Zelen, Marvin
Feuer, Eric J.
CA Canc Intervention Surveillance Mod
TI Effects of Mammography Screening Under Different Screening Schedules:
Model Estimates of Potential Benefits and Harms
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Article
ID CARCINOMA IN-SITU; COST-EFFECTIVENESS ANALYSIS; BREAST-CANCER MORTALITY;
UPPER AGE LIMIT; RANDOMIZED-TRIALS; FOLLOW-UP; UNITED-STATES; OLDER
WOMEN; OVERDIAGNOSIS; OVERTREATMENT
AB Background: Despite trials of mammography and widespread use, optimal screening policy is controversial.
Objective: To evaluate U. S. breast cancer screening strategies.
Design: 6 models using common data elements.
Data Sources: National data on age-specific incidence, competing mortality, mammography characteristics, and treatment effects.
Target Population: A contemporary population cohort.
Time Horizon: Lifetime.
Perspective: Societal.
Interventions: 20 screening strategies with varying initiation and cessation ages applied annually or biennially.
Outcome Measures: Number of mammograms, reduction in deaths from breast cancer or life-years gained (vs. no screening), false-positive results, unnecessary biopsies, and overdiagnosis.
Results of Base-Case Analysis: The 6 models produced consistent rankings of screening strategies. Screening biennially maintained an average of 81% (range across strategies and models, 67% to 99%) of the benefit of annual screening with almost half the number of false-positive results. Screening biennially from ages 50 to 69 years achieved a median 16.5% (range, 15% to 23%) reduction in breast cancer deaths versus no screening. Initiating biennial screening at age 40 years (vs. 50 years) reduced mortality by an additional 3% (range, 1% to 6%), consumed more resources, and yielded more false-positive results. Biennial screening after age 69 years yielded some additional mortality reduction in all models, but overdiagnosis increased most substantially at older ages.
Results of Sensitivity Analysis: Varying test sensitivity or treatment patterns did not change conclusions.
Limitation: Results do not include morbidity from false-positive results, patient knowledge of earlier diagnosis, or unnecessary treatment.
Conclusion: Biennial screening achieves most of the benefit of annual screening with less harm. Decisions about the best strategy depend on program and individual objectives and the weight placed on benefits, harms, and resource considerations.
C1 [Mandelblatt, Jeanne S.] Lombardi Comprehens Canc Ctr, Washington, DC 20007 USA.
Georgetown Univ, Med Ctr, Washington, DC 20007 USA.
NIH, Bethesda, MD 20892 USA.
Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
Erasmus Univ, Med Ctr, Rotterdam, Netherlands.
Harvard Univ, Sch Publ Hlth, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA.
Harvard Pilgrim Hlth Care, Boston, MA USA.
Stanford Univ, Palo Alto, CA 94304 USA.
Albert Einstein Coll Med, New York, NY USA.
RP Mandelblatt, JS (reprint author), Lombardi Comprehens Canc Ctr, 3300 Whitehaven St,NW,Suite 4100, Washington, DC 20007 USA.
EM mandelbj@georgetown.edu
FU NCI [2U01CA088270, 2U01CA088283, 2U01CA088248, F32 CA125984,
HHSN261200800769P, HHSN261200800002C]; NCI-funded BCSC [U01CA63740,
U01CA86076, U01CA86082, U01CA63736, U01CA70013, U01CA69976, U01CA63731,
U01CA70040]; U.S. state public health departments and cancer registries
FX By NCI cooperative agreements (2U01CA088270, 2U01CA088283, 2U01CA088248,
and F32 CA125984). Portions of this work were performed under contract
HHSN261200800769P. Data collection in the BCSC was supported by
NCI-funded BCSC cooperative agreements (U01CA63740, U01CA86076,
U01CA86082, U01CA63736, U01CA70013, U01CA69976, U01CA63731, and
U01CA70040) and several U.S. state public health departments and cancer
registries. CISNET data management and Web site support were provided by
Cornerstone Systems Northwest (NCI contract HHSN261200800002C).
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U2 25
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD NOV 17
PY 2009
VL 151
IS 10
BP 738
EP W247
PG 15
WC Medicine, General & Internal
SC General & Internal Medicine
GA 524LP
UT WOS:000272145100007
PM 19920274
ER
PT J
AU Levine, RJ
Vatten, LJ
Horowitz, GL
Qian, C
Romundstad, PR
Yu, KF
Hollenberg, AN
Hellevik, AI
Asvold, BO
Karumanchi, SA
AF Levine, Richard J.
Vatten, Lars J.
Horowitz, Gary L.
Qian, Cong
Romundstad, Pal R.
Yu, Kai F.
Hollenberg, Anthony N.
Hellevik, Alf I.
Asvold, Bjorn O.
Karumanchi, S. Ananth
TI Pre-eclampsia, soluble fms-like tyrosine kinase 1, and the risk of
reduced thyroid function: nested case-control and population based study
SO BRITISH MEDICAL JOURNAL
LA English
DT Article
ID UNITED-STATES POPULATION; HYPOTHYROIDISM; PREGNANCY; DISEASE; SUNITINIB;
WOMEN; TRIAL; DYSFUNCTION; MECHANISMS; ANTIBODIES
AB Objective To determine if pre-eclampsia is associated with reduced thyroid function during and after pregnancy.
Design Nested case-control study during pregnancy and population based follow-up study after pregnancy.
Setting Calcium for Pre-eclampsia Prevention trial of healthy pregnant nulliparous women in the United States during 1992-5, and a Norwegian population based study (Nord-Trondelag Health Study or HUNT-2) during 1995-7 with linkage to the medical birth registry of Norway.
Participants All 141 women (cases) in the Calcium for Preeclampsia Prevention trial with serum measurements before 21 weeks' gestation (baseline) and after onset of pre-eclampsia (before delivery), 141 normotensive controls with serum measurements at similar gestational ages, and 7121 women in the Nord-Trondelag Health Study whose first birth had occurred in 1967 or later and in whom serum levels of thyroid stimulating hormone had been subsequently measured.
Main outcome measures Thyroid function tests and human chorionic gonadotrophin and soluble fms-like tyrosine kinase 1 concentrations in the Calcium for Preeclampsia Prevention cohort and odds ratios for levels of thyroid stimulating hormone above the reference range, according to pre-eclampsia status in singleton pregnancies before the Nord-Trondelag Health Study.
Results In predelivery specimens of the Calcium for Preeclampsia Prevention cohort after the onset of preeclampsia, thyroid stimulating hormone levels increased 2.42 times above baseline compared with a 1.48 times increase in controls. The ratio of the predelivery to baseline ratio of cases to that of the controls was 1.64 (95% confidence interval 1.29 to 2.08). Free triiodothyronine decreased more in the women with preeclampsia than in the controls (case ratio to control ratio 0.96, 95% confidence interval 0.92 to 0.99). The predelivery specimens but not baseline samples from women with pre-eclampsia were significantly more likely than those from controls to have concentrations of thyroid stimulating hormone above the reference range (adjusted odds ratio 2.2, 95% confidence interval 1.1 to 4.4). Both in women who developed pre-eclampsia and in normotensive controls the increase in thyroid stimulating hormone concentration between baseline and predelivery specimens was strongly associated with increasing quarters of predelivery soluble fms-like tyrosine kinase 1 (P for trend 0.002 and <0.001, respectively). In the Nord-Trondelag Health Study, women with a history of pre-eclampsia in their first pregnancy were more likely than other women (adjusted odds ratio 1.7, 95% confidence interval 1.1 to 2.5) to have concentrations of thyroid stimulating hormone above the reference range (>3.5 mIU/l). In particular, they were more likely to have high concentrations of thyroid stimulating hormone without thyroid peroxidase antibodies (adjusted odds ratio 2.6, 95% confidence interval 1.3 to 5.0), suggesting hypothyroid function in the absence of an autoimmune process. This association was especially strong (5.8, 1.3 to 25.5) if pre-eclampsia had occurred in both the first and the second pregnancies.
Conclusion Increased serum concentration of soluble fms-like tyrosine kinase 1 during pre-eclampsia is associated with subclinical hypothyroidism during pregnancy. Pre-eclampsia may also predispose to reduced thyroid function in later years.
C1 [Levine, Richard J.; Yu, Kai F.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, US Dept HHS, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA.
[Vatten, Lars J.; Romundstad, Pal R.; Hellevik, Alf I.] Norwegian Univ Sci & Technol, Fac Med, Dept Publ Hlth, N-7034 Trondheim, Norway.
[Horowitz, Gary L.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA.
[Horowitz, Gary L.; Hollenberg, Anthony N.; Karumanchi, S. Ananth] Harvard Univ, Sch Med, Boston, MA USA.
[Qian, Cong] Glotech, Rockville, MD USA.
[Hollenberg, Anthony N.; Karumanchi, S. Ananth] Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02215 USA.
[Karumanchi, S. Ananth] Beth Israel Deaconess Med Ctr, Dept Obstet & Gynecol, Boston, MA 02215 USA.
[Karumanchi, S. Ananth] Howard Hughes Med Inst, Boston, MA 02115 USA.
RP Levine, RJ (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, US Dept HHS, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA.
EM LevineRJ@mail.nih.gov; sananth@bidmc.harvard.edu
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development [N01-HD-5-3398]; National Institute of Child Health and
Human Development [N01-HD-1-3121-3126, N01-HD-3154, N01-HD-5-3246];
National Heart, Lung, and Blood Institute; Norwegian University of
Science and Technology; Central Norway Regional Health Authority
FX This study was supported by the Eunice Kennedy Shriver National
Institute of Child Health and Human Development (contract N01-HD-5-3398)
and by salary support from the intramural research programme of the
National Institutes of Health. The Calcium for Preeclampsia Prevention
trial was supported by the National Institute of Child Health and Human
Development (contracts N01-HD-1-3121-3126, N01-HD-3154, and
N01-HD-5-3246), with cofunding from the National Heart, Lung, and Blood
Institute. SAK is supported by a clinical scientist award by the
Burroughs Wellcome Fund and is an investigator of the Howard Hughes
Medical Institute and an established investigator of the American Heart
Association. The Nord-Trondelag Health Study is a collaborative effort
of the Norwegian University of Science and Technology, the Norwegian
Institute of Public Health, and the Nord-Trondelag County Council. This
substudy of the Nord-Trondelag Health Study was supported by the
Norwegian University of Science and Technology and by the Central Norway
Regional Health Authority.
NR 35
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U2 1
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0959-8146
J9 BRIT MED J
JI Br. Med. J.
PD NOV 17
PY 2009
VL 339
AR b4336
DI 10.1136/bmj.b4336
PG 8
WC Medicine, General & Internal
SC General & Internal Medicine
GA 523SZ
UT WOS:000272096100002
PM 19920004
ER
PT J
AU Franco, OH
Massaro, JM
Civil, J
Cobain, MR
O'Malley, B
D'Agostino, RB
AF Franco, Oscar H.
Massaro, Joseph M.
Civil, Jacky
Cobain, Mark R.
O'Malley, Brendan
D'Agostino, Ralph B., Sr.
TI Trajectories of Entering the Metabolic Syndrome The Framingham Heart
Study
SO CIRCULATION
LA English
DT Article
DE cardiovascular diseases; Framingham study; metabolic syndrome;
prevention; syndrome X
ID C-REACTIVE PROTEIN; MIDDLE-AGED MEN; DIABETES-MELLITUS; DISEASE;
ASSOCIATION; DEFINITION; FAMILIES; WOMEN
AB Background-We evaluated the progression of the metabolic syndrome (MetS) and its components, the trajectories followed by individuals entering MetS, and the manner in which different trajectories predict cardiovascular disease and mortality.
Methods and Results-Using data from 3078 participants from the Framingham Offspring Study (a cohort study) who attended examinations 4 (1987), 5 (1991), and 6 (1995), we evaluated the progression of MetS and its components. MetS was defined according to the Adult Treatment Panel III criteria. Using logistic regression, we evaluated the predictive ability of the presence of each component of the MetS on the subsequent development of MetS. Additionally, we examined the probability of developing cardiovascular disease or mortality (until 2007) by having specific combinations of 3 that diagnose MetS. The prevalence of MetS almost doubled in 10 years of follow-up. Hyperglycemia and central obesity experienced the highest increase. High blood pressure was most frequently present when a diagnosis of MetS occurred (77.3%), and the presence of central obesity conferred the highest risk of developing MetS (odds ratio, 4.75; 95% confidence interval, 3.78 to 5.98). Participants who entered the MetS having a combination of central obesity, high blood pressure, and hyperglycemia had a 2.36-fold (hazard ratio, 2.36; 95% confidence interval, 1.54 to 3.61) increase of incident cardiovascular events and a 3-fold (hazard ratio, 3.09, 95% confidence interval, 1.93 to 4.94) increased risk of mortality.
Conclusions-Particular trajectories and combinations of factors on entering the MetS confer higher risks of incident cardiovascular disease and mortality in the general population and among those with MetS. Intense efforts are required to identify populations with these particular combinations and to provide them with adequate treatment at early stages of disease. (Circulation. 2009; 120: 1943-1950.)
C1 [Franco, Oscar H.] Univ Warwick, Dept Publ Hlth, Hlth Sci Res Inst, Warwick Med Sch, Coventry CV4 7AL, W Midlands, England.
[Franco, Oscar H.; Civil, Jacky; Cobain, Mark R.; O'Malley, Brendan] Unilever Corp Res, Sharnbrook, Beds, England.
[Massaro, Joseph M.] Boston Univ, Dept Math Stat & Biostat, Boston, MA 02215 USA.
[D'Agostino, Ralph B., Sr.] NHLBI, Framingham Heart Study, Framingham, MA USA.
RP Franco, OH (reprint author), Univ Warwick, Dept Publ Hlth, Hlth Sci Res Inst, Warwick Med Sch, B-160, Coventry CV4 7AL, W Midlands, England.
EM O.H.Franco@warwick.ac.uk
OI Massaro, Joseph/0000-0002-2682-4812; O'Malley,
Brendan/0000-0003-0822-3455
FU Unilever plc.
FX This study was funded by Unilever plc. The funding organization did not
participate in the design and conduct of the study; collection,
management, analysis, and interpretation of the data; and preparation,
review, and approval of the manuscript.
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
EI 1524-4539
J9 CIRCULATION
JI Circulation
PD NOV 17
PY 2009
VL 120
IS 20
BP 1943
EP 1950
DI 10.1161/CIRCULATIONAHA.109.855817
PG 8
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520QJ
UT WOS:000271860500003
PM 19884471
ER
PT J
AU Sauseng, P
Klimesch, W
Heise, KF
Gruber, WR
Holz, E
Karim, AA
Glennon, M
Gerloff, C
Birbaumer, N
Hummel, FC
AF Sauseng, Paul
Klimesch, Wolfgang
Heise, Kirstin F.
Gruber, Walter R.
Holz, Elisa
Karim, Ahmed A.
Glennon, Mark
Gerloff, Christian
Birbaumer, Niels
Hummel, Friedhelm C.
TI Brain Oscillatory Substrates of Visual Short-Term Memory Capacity
SO CURRENT BIOLOGY
LA English
DT Article
ID TRANSCRANIAL MAGNETIC STIMULATION; EEG ALPHA-ACTIVITY; WORKING-MEMORY;
INDIVIDUAL-DIFFERENCES; PHASE SYNCHRONIZATION; THETA-OSCILLATIONS;
NEURONAL OSCILLATIONS; SPATIAL ATTENTION; NEURAL MEASURES; CORTEX
AB The amount of information that can be stored in visual short-term memory is strictly limited to about four items [1]. Therefore, memory capacity relies not only on the successful retention of relevant information but also on efficient suppression of distracting information, visual attention, and executive functions [2-5]. However, completely separable neural signatures for these memory capacity-limiting factors remain to be identified. Because of its functional diversity [6-9], oscillatory brain activity may off er a utile solution. In the present study, we show that capacity-determining mechanisms, namely retention of relevant information and suppression of distracting information, are based on neural substrates independent of each other: the successful maintenance of relevant material in short-term memory is associated with cross-frequency phase synchronization between theta (rhythmical neural activity around 5 Hz) and gamma (>50 Hz) oscillations at posterior parietal recording sites. On the other hand, electroencephalographic alpha activity (around 10 Hz) predicts memory capacity based on efficient suppression of irrelevant information in short-term memory. Moreover, repetitive transcranial magnetic stimulation at alpha frequency can modulate short-term memory capacity by influencing the ability to suppress distracting information. Taken together, the current study provides evidence for a double dissociation of brain oscillatory correlates of visual short-term memory capacity.
C1 [Sauseng, Paul; Heise, Kirstin F.; Gerloff, Christian; Hummel, Friedhelm C.] Univ Hamburg, Univ Krankenhaus Hamburg Eppendorf, Dept Neurol, Brain Imaging & Neurostimulat Lab, D-20246 Hamburg, Germany.
[Sauseng, Paul; Klimesch, Wolfgang; Gruber, Walter R.; Holz, Elisa] Salzburg Univ, Dept Psychol, A-5020 Salzburg, Austria.
[Karim, Ahmed A.; Birbaumer, Niels] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, D-72074 Tubingen, Germany.
[Karim, Ahmed A.] Int Max Planck Res Sch Neural & Behav Sci, D-72074 Tubingen, Germany.
[Glennon, Mark] Natl Univ Ireland, Sch Psychol, Galway, Ireland.
[Birbaumer, Niels] Natl Inst Neurol Disorders & Stroke, Human Cort Physiol Sect, NIH, Bethesda, MD 20892 USA.
RP Sauseng, P (reprint author), Univ Hamburg, Univ Krankenhaus Hamburg Eppendorf, Dept Neurol, Brain Imaging & Neurostimulat Lab, Martinistr 52, D-20246 Hamburg, Germany.
EM p.sauseng@uke.uni-hamburg.de
RI Cognitive Neuroscience, Centre for/C-7888-2011; Sauseng,
Paul/A-5273-2009;
OI Heise, Kirstin-Friederike/0000-0003-3666-8531
FU Austrian Academy of Sciences; Deutsche Forschungsgemeinschaft [B1
195/51-1]
FX This research was supported by the Austrian Academy of Sciences (P.S. is
the recipient of an APART fellowship of the Austrian Academy of
Sciences) and the Deutsche Forschungsgemeinschaft (B1 195/51-1). We
thank R. Freunberger for helpful comments and T. Schwaiger for
assistance during data recording.
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U1 7
U2 36
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
J9 CURR BIOL
JI Curr. Biol.
PD NOV 17
PY 2009
VL 19
IS 21
BP 1846
EP 1852
DI 10.1016/j.cub.2009.08.062
PG 7
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 522AS
UT WOS:000271970200028
PM 19913428
ER
PT J
AU McCulloch, DR
Nelson, CM
Dixon, LJ
Silver, DL
Wylie, JD
Lindner, V
Sasaki, T
Cooley, MA
Argraves, WS
Apte, SS
AF McCulloch, Daniel R.
Nelson, Courtney M.
Dixon, Laura J.
Silver, Debra L.
Wylie, James D.
Lindner, Volkhard
Sasaki, Takako
Cooley, Marion A.
Argraves, W. Scott
Apte, Suneel S.
TI ADAMTS Metalloproteases Generate Active Versican Fragments that Regulate
Interdigital Web Regression
SO DEVELOPMENTAL CELL
LA English
DT Article
ID PROGRAMMED CELL-DEATH; MOUSE LIMB; IN-VIVO; FIBULIN-1 GENE; C-ELEGANS;
TGF-BETA; EMBRYO; MORPHOGENESIS; EXPRESSION; AGGRECAN
AB We show that combinatorial mouse alleles for the secreted metalloproteases Adamts5, Adamts20 (bt), and Adamts9 result in fully penetrant soft-tissue syndactyly. Interdigital webs in Adamts5(-/-);bt/bt mice had reduced apoptosis and decreased cleavage of the proteoglycan versican; however, the BMP-FGF axis, which regulates interdigital apoptosis was unaffected. BMP4 induced apoptosis, but without concomitant versican proteolysis. Haploinsufficiency of either Vcan or Fbln1, a cofactor for versican processing by ADAMTS5, led to highly penetrant syndactyly in bt mice, suggesting that cleaved versican was essential for web regression. The local application of an aminoterminal versican fragment corresponding to ADAMTS-processed versican, induced cell death in Adamts5(-/-);bt/bt webs. Thus, ADAMTS proteases cooperatively maintain versican proteolysis above a required threshold to create a permissive environment for apoptosis. The data highlight the developmental significance of proteolytic action on the ECM, not only as a clearance mechanism, but also as a means to generate bioactive versican fragments.
C1 [McCulloch, Daniel R.; Nelson, Courtney M.; Dixon, Laura J.; Wylie, James D.; Apte, Suneel S.] Cleveland Clin, Lerner Res Inst, Dept Biomed Engn, Cleveland, OH 44195 USA.
[Silver, Debra L.] NHGRI, Genet Dis Res Branch, Bethesda, MD 20892 USA.
[Lindner, Volkhard] Maine Med Ctr, Res Inst, Scarborough, ME 04074 USA.
[Sasaki, Takako] Oregon Hlth & Sci Univ, Dept Biochem & Mol Biol, Portland, OR 97239 USA.
[Cooley, Marion A.; Argraves, W. Scott] Med Univ S Carolina, Dept Anat & Cell Biol, Charleston, SC 29403 USA.
RP Apte, SS (reprint author), Cleveland Clin, Lerner Res Inst, Dept Biomed Engn, ND20,9500 Euclid Ave, Cleveland, OH 44195 USA.
EM aptes@ccf.org
RI McCulloch, Daniel/N-9142-2013;
OI McCulloch, Daniel/0000-0003-0269-5857; Wylie, James/0000-0003-2657-0311
FU National Institutes of Health [AR49930, AR53890, HL095067, AR050953];
Arthritis Foundation; American Heart Association [0755346U]
FX We thank Roche Pharmaceuticals, Corey Mjaatvedt and Christine B. Kern
for hdf mice, David Beier for bt mice, Vernique Lefebvre, Radhika Atit,
and Richard Harland for cDNAs, Preston Alexander and John Sandy for
ADAMTS5 antibodies, Amanda Allamong and Michael Braun for assistance
with histology, and James Lang for photography. Dieter Zimmermann
provided the versican expression plasmid. This work was supported by
National Institutes of Health grants to S.S.A (AR49930 and AR53890) and
W.S.A. (HL095067), the Arthritis Foundation (Northeast Ohio Chapter
Award to S.S.A.) and the American Heart Association (Grant-in-Aid
0755346U to W.S.A.). Histology and mCT was done at the Cleveland Clinic
Musculoskeletal Core Center (supported by NIH grant AR050953).
NR 52
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U1 2
U2 4
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1534-5807
J9 DEV CELL
JI Dev. Cell
PD NOV 17
PY 2009
VL 17
IS 5
BP 687
EP 698
DI 10.1016/j.devcel.2009.09.008
PG 12
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 523US
UT WOS:000272100700013
PM 19922873
ER
PT J
AU Byun, JS
Wong, MM
Cui, WW
Idelman, G
Li, Q
De Siervi, A
Bilke, S
Haggerty, CM
Player, A
Wang, YH
Thirman, MJ
Kaberlein, JJ
Petrovas, C
Koup, RA
Longo, D
Ozato, K
Gardner, K
AF Byun, Jung S.
Wong, Madeline M.
Cui, Wenwu
Idelman, Gila
Li, Quentin
De Siervi, Adriana
Bilke, Sven
Haggerty, Cynthia M.
Player, Audrey
Wang, Yong Hong
Thirman, Michael J.
Kaberlein, Joseph J.
Petrovas, Constantinos
Koup, Richard A.
Longo, Dan
Ozato, Keiko
Gardner, Kevin
TI Dynamic bookmarking of primary response genes by p300 and RNA polymerase
II complexes
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gene regulation; histone acetylation; transcription; ELL; epigenetics
ID BROMODOMAIN PROTEIN BRD4; IMMEDIATE-EARLY GENES; ELONGATION-FACTOR;
T-CELLS; C-FOS; COACTIVATOR COMPLEXES; CHROMATIN-STRUCTURE; ACTIVE
PROMOTERS; HUMAN GENOME; P-TEFB
AB Profiling the dynamic interaction of p300 with proximal promoters of human T cells identified a class of genes that rapidly coassemble p300 and RNA polymerase II (pol II) following mitogen stimulation. Several of these p300 targets are immediate early genes, including FOS, implicating a prominent role for p300 in the control of primary genetic responses. The recruitment of p300 and pol II rapidly transitions to the assembly of several elongation factors, including the positive transcriptional elongation factor (P-TEFb), the bromo-domain-containing protein (BRD4), and the elongin-like eleven nineteen lysine-rich leukemia protein (ELL). However, transcription at many of these rapidly induced genes is transient, wherein swift departure of P-TEFb, BRD4, and ELL coincides with termination of transcriptional elongation. Unexpectedly, both p300 and pol II remain accumulated or "bookmarked'' at the proximal promoter long after transcription has terminated, demarking a clear mechanistic separation between the recruitment and elongation phases of transcription in vivo. The bookmarked pol II is depleted of both serine-2 and serine-5 phosphorylation of its C-terminal domain and remains proximally positioned at the promoter for hours. Surprisingly, these p300/pol II bookmarked genes can be readily reactivated, and elongation factors can be reassembled by subsequent addition of nonmitogenic agents that, alone, have minimal effects on transcription in the absence of prior preconditioning by mitogen stimulation. These findings suggest that p300 is likely to play an important role in biological processes in which transcriptional bookmarking or preconditioning influences cellular growth and development through the dynamic priming of genes for response to rechallenge by secondary stimuli.
C1 [Byun, Jung S.; Wong, Madeline M.; Cui, Wenwu; Idelman, Gila; Li, Quentin; Haggerty, Cynthia M.; Gardner, Kevin] NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
[De Siervi, Adriana] Univ Buenos Aires, Dept Biochem, Buenos Aires, DF, Argentina.
[Bilke, Sven; Player, Audrey; Wang, Yong Hong] NCI, Genet Branch, Bethesda, MD 20892 USA.
[Thirman, Michael J.; Kaberlein, Joseph J.] Univ Chicago, Med Ctr, Chicago, IL 60637 USA.
[Petrovas, Constantinos; Koup, Richard A.] NIH, Vaccine Res Ctr, Bethesda, MD 20892 USA.
[Longo, Dan] NIA, Immunol Lab, Baltimore, MD 21224 USA.
[Ozato, Keiko] NICHHD, Lab Mol Growth Regulat, Bethesda, MD 20892 USA.
RP Gardner, K (reprint author), NCI, Lab Receptor Biol & Gene Express, Bethesda, MD 20892 USA.
EM gardnerk@mail.nih.gov
FU NIH; National Cancer Institute; National Institute on Aging
FX We thank R. Owens, E. Kawasaki, B. Lewis, C. Smith, and K. Adelman for
helpful discussions and acknowledge Q. Wang and I. Collins for technical
contributions. This research was supported by the Intramural Research
Program of the NIH, the National Cancer Institute and the National
Institute on Aging.
NR 42
TC 40
Z9 41
U1 0
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 17
PY 2009
VL 106
IS 46
BP 19292
EP 19297
DI 10.1073/pnas.0905469106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 521GC
UT WOS:000271907400015
PM 19880750
ER
PT J
AU Weiss, JM
Back, TC
Scarzello, AJ
Subleski, JJ
Hall, VL
Stauffer, JK
Chen, X
Micic, D
Alderson, K
Murphy, WJ
Wiltrout, RH
AF Weiss, Jonathan M.
Back, Timothy C.
Scarzello, Anthony J.
Subleski, Jeff J.
Hall, Veronica L.
Stauffer, Jimmy K.
Chen, Xin
Micic, Dejan
Alderson, Kory
Murphy, William J.
Wiltrout, Robert H.
TI Successful immunotherapy with IL-2/anti-CD40 induces the
chemokine-mediated mitigation of an immunosuppressive tumor
microenvironment
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE chemokines; tumor immunotherapy; CD40
ID RENAL-CELL CARCINOMA; REGULATORY T-CELLS; MACROPHAGE INFILTRATION;
ANTITUMOR RESPONSES; MALIGNANT-MELANOMA; SUPPRESSOR-CELLS;
INTERFERON-GAMMA; IFN-GAMMA; TNF-ALPHA; EXPRESSION
AB Treatment of mice bearing orthotopic, metastatic tumors with anti-CD40 antibody resulted in only partial, transient anti-tumor effects whereas combined treatment with IL-2/anti-CD40, induced tumor regression. The mechanisms for these divergent anti-tumor responses were examined by profiling tumor-infiltrating leukocyte subsets and chemokine expression within the tumor microenvironment after immunotherapy. IL-2/anti-CD40, but not anti-CD40 alone, induced significant infiltration of established tumors by NK and CD8(+) T cells. To further define the role of chemokines in leukocyte recruitment into tumors, we evaluated anti-tumor responses in mice lacking the chemokine receptor, CCR2. The antitumor effects and leukocyte recruitment mediated by anti-CD40 alone, were completely abolished in CCR2(-/-) mice. In contrast, IL-2/anti-CD40-mediated leukocyte recruitment and reductions in primary tumors and metastases were maintained in CCR2(-/-) mice. Treatment of mice with IL-2/anti-CD40, but not anti-CD40 alone, also caused an IFN-gamma-dependent increase in the expression of multiple Th1 chemokines within the tumor microenvironment. Interestingly, although IL-2/anti-CD40 treatment increased Tregs in the spleen, it also caused a coincident IFN-gamma-dependent reduction in CD4(+)/FoxP3(+) Tregs, myeloid-derived suppressor cells and Th2 chemokine expression specifically within the tumor microenvironment that was not observed after treatment with anti-CD40 alone. Similar effects were observed using IL-15 in combination with anti-CD40. Taken together, our data demonstrate that IL-2/antiCD40, but not anti-CD40 alone, can preferentially reduce the overall immunosuppressive milieu within the tumor microenvironment. These results suggest that the use of anti-CD40 in combination with IL-2 or IL-15 may hold substantially more promise for clinical cancer treatment than anti-CD40 alone.
C1 [Weiss, Jonathan M.; Back, Timothy C.; Scarzello, Anthony J.; Subleski, Jeff J.; Hall, Veronica L.; Stauffer, Jimmy K.; Chen, Xin; Micic, Dejan; Wiltrout, Robert H.] NCI, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
[Alderson, Kory; Murphy, William J.] Univ Calif Davis, Dept Dermatol, Davis, CA 95616 USA.
RP Wiltrout, RH (reprint author), NCI, Expt Immunol Lab, Canc & Inflammat Program, Frederick, MD 21702 USA.
EM wiltrour@mail.nih.gov
RI Chen, Xin/I-6601-2015
OI Chen, Xin/0000-0002-2628-4027
FU National Institutes of Health National Cancer Institute; National Cancer
Institute [N01-CO-12400, R01-CA-95572]
FX We thank Drs. Giorgio Trinchieri and John Ortaldo for critically
reviewing the manuscript. This work was supported by the Intramural
Research Program of the National Institutes of Health National Cancer
Institute and with federal funds from the National Cancer Institute
under Contracts N01-CO-12400 and R01-CA-95572 (to W.J.M.).
NR 35
TC 37
Z9 39
U1 1
U2 2
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 17
PY 2009
VL 106
IS 46
BP 19455
EP 19460
DI 10.1073/pnas.0909474106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 521GC
UT WOS:000271907400043
PM 19892741
ER
PT J
AU Lee, SJ
Trostel, A
Le, P
Harinarayanan, R
FitzGerald, PC
Adhya, S
AF Lee, Sang Jun
Trostel, Andrei
Le, Phuoc
Harinarayanan, Rajendran
FitzGerald, Peter C.
Adhya, Sankar
TI Cellular stress created by intermediary metabolite imbalances
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE galactose metabolism; gene signals; intracellular stress; tiling arrays
ID ESCHERICHIA-COLI; GALACTOSE METABOLISM; HEREDITARY DEFECTS;
GENE-EXPRESSION; MUTANTS; REPRESSION; PROMOTERS; INDUCTION; PROTEIN
AB Small molecules generally activate or inhibit gene transcription as externally added substrates or as internally accumulated end-products, respectively. Rarely has a connection been made that links an intracellular intermediary metabolite as a signal of gene expression. We report that a perturbation in the critical step of a metabolic pathway-the D-galactose amphibolic pathway changes the dynamics of the pathways leading to accumulation of the intermediary metabolite UDP-galactose. This accumulation causes cell stress and transduces signals that alter gene expression so as to cope with the stress by restoring balance in the metabolite pool. This underscores the importance of studying the global effects of alterations in the level of intermediary metabolites in causing stress and coping with it by transducing signals to genes to reach a stable state of equilibrium (homeostasis). Such studies are an essential component in the integration of metabolomics, proteomics, and transcriptomics.
C1 [Lee, Sang Jun; Trostel, Andrei; Le, Phuoc; Adhya, Sankar] NCI, Mol Biol Lab, NIH, Bethesda, MD 20892 USA.
[Harinarayanan, Rajendran] NICHHD, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
[FitzGerald, Peter C.] NICHHD, Genome Anal Unit, Bethesda, MD 20892 USA.
RP Adhya, S (reprint author), NCI, Mol Biol Lab, NIH, Bldg 37, Bethesda, MD 20892 USA.
EM sadhya@helix.nih.gov
FU National Institutes of Health; National Cancer Institute; Center for
Cancer Research
FX We thank R. Edgar, D. E. A. Lewis, M. Cashel for helpful discussions,
and R. Edgar and R. A. Weisberg for critical reading of the manuscript
and suggestions. We thank D.J. Jin and C.L. Turnbough, Jr. for the gift
of bacterial strains. This work was supported by the Intramural Research
Program of the National Institutes of Health, National Cancer Institute,
Center for Cancer Research.
NR 30
TC 32
Z9 32
U1 1
U2 15
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 17
PY 2009
VL 106
IS 46
BP 19515
EP 19520
DI 10.1073/pnas.0910586106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 521GC
UT WOS:000271907400053
PM 19887636
ER
PT J
AU Iwatani, Y
Chan, DSB
Liu, L
Yoshii, H
Shibata, J
Yamamoto, N
Levin, JG
Gronenborn, AM
Sugiura, W
AF Iwatani, Yasumasa
Chan, Denise S. B.
Liu, Lin
Yoshii, Hiroaki
Shibata, Junko
Yamamoto, Naoki
Levin, Judith G.
Gronenborn, Angela M.
Sugiura, Wataru
TI HIV-1 Vif-mediated ubiquitination/degradation of APOBEC3G involves four
critical lysine residues in its C-terminal domain
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE structure model; deaminase; antiviral
ID IMMUNODEFICIENCY-VIRUS TYPE-1; VIRION INFECTIVITY FACTOR;
UBIQUITIN-LIGASE COMPLEX; FUNCTIONAL IMPLICATIONS; ANTIVIRAL ACTIVITY;
CRYSTAL-STRUCTURE; CATALYTIC DOMAIN; ENZYME APOBEC3G; SOCS-BOX;
DEGRADATION
AB During coevolution with the host, HIV-1 developed the ability to hijack the cellular ubiquitin/proteasome degradation pathway to counteract the antiviral activity of APOBEC3G (A3G), a host cytidine deaminase that can block HIV-1 replication. Abrogation of A3G function involves the HIV-1 Vif protein, which binds A3G and serves as an adapter molecule to recruit A3G to a Cullin5-based E3 ubiquitin ligase complex. Structure-guided mutagenesis of A3G focused on the 14 most surface-exposed Lys residues allowed us to identify four Lys residues (Lys-297, 301, 303, and 334) that are required for Vif-mediated A3G ubiquitination and degradation. Substitution of Arg for these residues confers Vif resistance and restores A3G's antiviral activity in the presence of Vif. In our model, the critical four Lys residues cluster at the C terminus, opposite to the known N-terminal Vif-interaction region in the protein. Thus, spatial constraints imposed by the E3 ligase complex may be an important determinant in Vif-dependent A3G ubiquitination.
C1 [Iwatani, Yasumasa; Yoshii, Hiroaki; Shibata, Junko; Sugiura, Wataru] Natl Hosp Org Nagoya Med Ctr, Clin Res Ctr, Naka Ku, Aichi 4600001, Japan.
[Iwatani, Yasumasa; Sugiura, Wataru] Nagoya Univ, Grad Sch Med, Aichi 4668550, Japan.
[Iwatani, Yasumasa; Yamamoto, Naoki; Sugiura, Wataru] Natl Inst Infect Dis, AIDS Res Ctr, Tokyo 1628640, Japan.
[Chan, Denise S. B.; Liu, Lin; Gronenborn, Angela M.] Univ Pittsburgh, Sch Med, Dept Biol Struct, Pittsburgh, PA 15260 USA.
[Chan, Denise S. B.] Univ Hong Kong, Dept Chem, Hong Kong, Hong Kong, Peoples R China.
[Levin, Judith G.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Mol Genet Lab, NIH, Bethesda, MD 20892 USA.
RP Iwatani, Y (reprint author), Natl Hosp Org Nagoya Med Ctr, Clin Res Ctr, Naka Ku, 4-1-1 San No Maru, Aichi 4600001, Japan.
EM iwataniy@nnh.hosp.go.jp
OI Gronenborn, Angela M/0000-0001-9072-3525
FU Ministry of Education, Culture, Sports, Science and Technology, Japan;
National Institutes of Health [GM082251]; National Institutes of Health,
Eunice Kennedy Shriver National Institute of Child Health and Human
Development; Ministry of Health, Labor, and Welfare, Japan
FX This work was supported in part by a grant-in-aid for Scientific
Research from the Ministry of Education, Culture, Sports, Science and
Technology, Japan (to Y.I.); National Institutes of Health Grant
GM082251 (to A.M.G); the Intramural Research Program of the National
Institutes of Health, Eunice Kennedy Shriver National Institute of Child
Health and Human Development (to J.G.L.); and a grant-in-aid for AIDS
Research from the Ministry of Health, Labor, and Welfare, Japan (to
W.S.).
NR 48
TC 32
Z9 34
U1 1
U2 4
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 17
PY 2009
VL 106
IS 46
BP 19539
EP 19544
DI 10.1073/pnas.0906652106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 521GC
UT WOS:000271907400057
PM 19887642
ER
PT J
AU Ji, YY
Yang, F
Papaleo, F
Wang, HX
Gao, WJ
Weinberger, DR
Lu, B
AF Ji, Yuanyuan
Yang, Feng
Papaleo, Francesco
Wang, Huai-Xing
Gao, Wen-Jun
Weinberger, Daniel R.
Lu, Bai
TI Role of dysbindin in dopamine receptor trafficking and cortical GABA
function
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE dopamine D2 receptor; schizophrenia; prefrontal cortex
ID LYSOSOME-RELATED ORGANELLES; PREFRONTAL CORTEX; MEMBRANE TRAFFICKING;
SUSCEPTIBILITY GENE; D2 RECEPTORS; SCHIZOPHRENIA; INTERNEURONS;
MECHANISMS; PROTEIN; BLOC-1
AB Dysbindin has been implicated in the pathogenesis of schizophrenia, but little is known about how dysbindin affects neuronal function in the circuitry underlying psychosis and related behaviors. Using a dysbindin knockout line (dys(-/-)) derived from the natural dysbindin mutant Sandy mice, we have explored the role of dysbindin in dopamine signaling and neuronal function in the prefrontal cortex (PFC). Combined cell imaging and biochemical experiments revealed a robust increase in the dopamine receptor D2, but not D1, on cell surface of neurons from dys(-/-) cortex. This was due to an enhanced recycling and insertion, rather than reduced endocytosis, of D2. Disruption of dysbindin gene resulted in a marked decrease in the excitability of fast-spiking (FS) GABA-ergic interneurons in both PFC and striatum. Dys(-/-) mice also exhibited a decreased inhibitory input to pyramidal neurons in layer V of PFC. The increased D2 signaling in dys(-/-) FS interneurons was associated with a more pronounced increase in neuronal firing in response to D2 agonist, compared to that in wild-type interneurons. Taken together, these results suggest that dysbindin regulates PFC function by facilitating D2-mediated modulation of GABAergic function.
C1 [Ji, Yuanyuan; Yang, Feng; Lu, Bai] NICHHD, Sect Neural Dev & Plast, Bethesda, MD 20892 USA.
[Papaleo, Francesco; Weinberger, Daniel R.; Lu, Bai] Natl Inst Mental Hlth, Genes Cognit & Psychosis Program, Bethesda, MD 20892 USA.
[Wang, Huai-Xing; Gao, Wen-Jun] Drexel Univ, Coll Med, Dept Neurobiol & Anat, Philadelphia, PA 19129 USA.
RP Lu, B (reprint author), NICHHD, Sect Neural Dev & Plast, Bethesda, MD 20892 USA.
EM bailu@mail.nih.gov
RI Yang, Feng/C-9530-2011; Lu, Bai/A-4018-2012;
OI Papaleo, Francesco/0000-0002-6326-0657
FU National Institute of Child Health and Human Development; National
Institute of Mental Health
FX We thank Dr. David R. Sibley (National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda) for
N-terminal FLAG-D2 human cDNA and Dr. Richard T. Swank (Roswell Park
Cancer Institute, Buffalo, NY) for genotyping information of
dys-/- mice. This work is supported by the Intramural
Research Programs of the National Institute of Child Health and Human
Development and the National Institute of Mental Health.
NR 44
TC 77
Z9 81
U1 0
U2 5
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 17
PY 2009
VL 106
IS 46
BP 19593
EP 19598
DI 10.1073/pnas.0904289106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 521GC
UT WOS:000271907400066
PM 19887632
ER
PT J
AU Bristow, GC
Lane, TA
Walker, M
Chen, L
Sei, Y
Hyde, TM
Kleinman, JE
Harrison, PJ
Eastwood, SL
AF Bristow, Greg C.
Lane, Tracy A.
Walker, Mary
Chen, Li
Sei, Yoshi
Hyde, Thomas M.
Kleinman, Joel E.
Harrison, Paul J.
Eastwood, Sharon L.
TI Expression of Kinase Interacting with Stathmin (KIS, UHMK1) in human
brain and lymphoblasts: effects of schizophrenia and genotype
SO BRAIN RESEARCH
LA English
DT Article
DE Bipolar disorder; Gene expression; Psychosis; Schizophrenia; UHMK1
ID CYTOSOLIC ROUTING DETERMINANTS; PEPTIDE-PROCESSING ENZYME;
MESSENGER-RNA; PROTEIN-KINASE; GENETIC ASSOCIATION; CHROMOSOME 1Q23.3;
P27(KIP1); MIGRATION; CORTEX; DOMAINS
AB Single nucleotide polymorphisms (SNPs) within the gene encoding the serine/threonine kinase KIS (Kinase interacting with Stathmin, also known as UHMK1) have recently been associated with schizophrenia. As none of the disease associated SNPs are coding, they may confer susceptibility by altering some facet of KIS expression. Here we have characterised the cellular distribution of KIS in human brain using in situ hybridisation and immunohistochemistry, and quantified KIS protein and mRNA in two large brain series to determine if KIS expression is altered in schizophrenia or bipolar disorder or in relation to a schizophrenia-associated SNP (rs7513662). Post-mortem tissue from the superior temporal gyrus of schizophrenia and control subjects, and also dorsolateral prefrontal cortex, anterior cingulate cortex, and cerebellum from schizophrenia, bipolar disorder, and control subjects were used. KIS expression was measured by quantitative PCR (mRNA) and immunoautoradiography (protein), and was also quantified by immunoblot in lymphoblast cell lines derived from schizophrenia and control subjects. Our results demonstrate that KIS is expressed in neurons, and its encoded protein is localised to the nucleus and cytoplasm. No difference in KIS expression was found between diagnostic groups, or in the lymphoblast cell lines, and no effect of rs7S13662 genotype on KIS expression was found. Hence, these data do not provide support for the hypothesis that altered expression is the mechanism by which genetic variation of KIS may increase susceptibility to schizophrenia, nor evidence that KIS expression is altered in the disease itself, at least in terms of the parameters studied here. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Bristow, Greg C.; Lane, Tracy A.; Walker, Mary; Chen, Li; Harrison, Paul J.; Eastwood, Sharon L.] Warneford Hosp, Univ Dept Psychiat, Oxford OX3 7JX, England.
[Sei, Yoshi] NIMH, Blood Genom Lab, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
[Hyde, Thomas M.; Kleinman, Joel E.] NIMH, Sect Neuropathol, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program,IRP,NIH, Bethesda, MD 20892 USA.
RP Eastwood, SL (reprint author), Warneford Hosp, Univ Dept Psychiat, Neurosci Bldg, Oxford OX3 7JX, England.
EM sharon.eastwood@psych.ox.ac.uk
OI Bristow, Greg/0000-0002-6395-6806
FU Intramural NIH HHS [Z01 MH002903-01]; Medical Research Council [,
G0500180]
NR 30
TC 4
Z9 4
U1 0
U2 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 16
PY 2009
VL 1301
BP 197
EP 206
DI 10.1016/j.brainres.2009.08.090
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 523UN
UT WOS:000272100200022
PM 19747464
ER
PT J
AU Schuck, S
Prinz, WA
Thorn, KS
Voss, C
Walter, P
AF Schuck, Sebastian
Prinz, William A.
Thorn, Kurt S.
Voss, Christiane
Walter, Peter
TI Membrane expansion alleviates endoplasmic reticulum stress independently
of the unfolded protein response
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID TRANSCRIPTIONAL REGULATORY NETWORKS; PHOSPHOLIPID BIOSYNTHETIC GENES;
PLASMA-CELL DIFFERENTIATION; SACCHAROMYCES-CEREVISIAE; TRANSMEMBRANE
PROTEIN; INDUCIBLE MEMBRANES; LIPID BIOSYNTHESIS; PHOSPHATIDIC-ACID;
FACTOR XBP-1; YEAST
AB Cells constantly adjust the sizes and shapes of their organelles according to need. In this study, we examine endoplasmic reticulum (ER) membrane expansion during the unfolded protein response (UPR) in the yeast Saccharomyces cerevisiae. We find that membrane expansion occurs through the generation of ER sheets, requires UPR signaling, and is driven by lipid biosynthesis. Uncoupling ER size control and the UPR reveals that membrane expansion alleviates ER stress independently of an increase in ER chaperone levels. Converting the sheets of the expanded ER into tubules by reticulon overexpression does not affect the ability of cells to cope with ER stress, showing that ER size rather than shape is the key factor. Thus, increasing ER size through membrane synthesis is an integral yet distinct part of the cellular program to overcome ER stress.
C1 [Schuck, Sebastian; Walter, Peter] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94158 USA.
[Schuck, Sebastian; Thorn, Kurt S.; Walter, Peter] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94158 USA.
[Prinz, William A.; Voss, Christiane] NIDDK, Lab Cell Biochem & Biol, NIH, Bethesda, MD 20892 USA.
RP Schuck, S (reprint author), Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94158 USA.
EM sebastian.schuck@ucsf.edu
RI di Ronza, Alberto/H-7674-2016;
OI di Ronza, Alberto/0000-0002-9813-5143; Thorn, Kurt/0000-0001-9310-288X
FU Intramural NIH HHS
NR 61
TC 127
Z9 129
U1 1
U2 14
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD NOV 16
PY 2009
VL 187
IS 4
BP 525
EP 536
DI 10.1083/jcb.200907074
PG 12
WC Cell Biology
SC Cell Biology
GA 520HI
UT WOS:000271833400010
PM 19948500
ER
PT J
AU Zhang, YW
Hughes, KJ
Zahm, SH
Zhang, YQ
Holford, TR
Dai, L
Bai, YN
Han, XS
Qin, Q
Lan, Q
Rothman, N
Zhu, Y
Leaderer, B
Zheng, TZ
AF Zhang, Yawei
Hughes, Kathryn J.
Zahm, Shelia Hoar
Zhang, Yaqun
Holford, Theodore R.
Dai, Li
Bai, Yana
Han, Xuesong
Qin, Qin
Lan, Qing
Rothman, Nathaniel
Zhu, Yong
Leaderer, Brian
Zheng, Tongzhang
TI Genetic Variations in Xenobiotic Metabolic Pathway Genes, Personal Hair
Dye Use, and Risk of Non-Hodgkin Lymphoma
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE genetics; hair dyes; lymphoma; non-Hodgkin; xenobiotics
ID GLUTATHIONE-S-TRANSFERASE; LUNG-CANCER; N-ACETYLTRANSFERASE-1 NAT1;
BIOTRANSFORMATION ENZYMES; MOLECULAR-GENETICS; GSTT1 GENOTYPES;
POLYMORPHISMS; ASSOCIATION; SMOKING; GSTM3
AB From 1996 to 2000, the authors conducted a population-based case-control study among Connecticut women to test the hypothesis that genetic variation in xenobiotic metabolic pathway genes modifies the relation between hair dye use and risk of non-Hodgkin lymphoma. No effect modifications were found for women who started using hair dyes in 1980 or afterward. For women who started using hair dye before 1980 as compared with never users, a statistically significantly increased risk of non-Hodgkin lymphoma was found for carriers of CYP2C9 Ex3-52C > T TT/CT genotypes (odds ratio (OR) = 2.9, 95% confidence interval (CI): 1.4, 6.1), CYP2E1 -332T > A AT/AA genotypes (OR = 2.0, 95% CI: 1.2, 3.4), a homozygous or heterozygous 3-base-pair deletion in intron 6 of GSTM3 (OR = 2.3, 95% CI: 1.3, 4.1), GSTP1 Ex5-24A > G AA genotypes (OR = 1.8, 95% CI: 1.1, 2.9), or NAT2 genotypes conferring intermediate/rapid acetylator status (OR = 1.6, 95% CI: 1.0, 2.7). The observed associations were mainly seen for follicular lymphoma. In contrast, no significantly increased risk was observed for starting hair dye use before 1980 (relative to never use) among women who were homozygous wild-type for the CYP2C9, CYP2E1, or GSTM3 polymorphisms, women carrying 1 or 2 copies of the variant GSTP1 allele, or women who were slow NAT2 acetylators. A possible role of genetic variation in xenobiotic metabolism in the carcinogenicity of hair dye use needs to be confirmed in larger studies.
C1 [Zhang, Yawei; Hughes, Kathryn J.; Holford, Theodore R.; Dai, Li; Bai, Yana; Han, Xuesong; Zhu, Yong; Leaderer, Brian; Zheng, Tongzhang] Yale Univ, Sch Publ Hlth, New Haven, CT 06520 USA.
[Zahm, Shelia Hoar; Lan, Qing; Rothman, Nathaniel] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Zhang, Yaqun] Gansu Prov Design & Res Inst Environm Sci, Lanzhou, Peoples R China.
[Dai, Li] Sichuan Univ, W China Univ Hosp 2, Natl Ctr Birth Defect Monitoring, Chengdu 610064, Peoples R China.
[Bai, Yana] Lanzhou Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Lanzhou 730000, Peoples R China.
[Qin, Qin] Univ So Maine, Ctr Toxicol & Environm Hlth, Portland, ME 04103 USA.
RP Zhang, YW (reprint author), Yale Univ, Sch Publ Hlth, 60 Coll St,LEPH 440,POB 208034, New Haven, CT 06520 USA.
EM yawei.zhang@yale.edu
RI Zahm, Shelia/B-5025-2015
FU National Cancer Institute [CA62006]; National Institutes of Health (NIH)
[1D43TW007864-01]; National Center for Research Resources, NIH [UL1
RR024139]
FX This study was supported by grant CA62006 from the National Cancer
Institute; the Intramural Research Program of the National Cancer
Institute, National Institutes of Health (NIH); and Fogarty training
grant 1D43TW007864-01 from the NIH. Publication of this article was made
possible by Clinical and Translational Science Award UL1 RR024139 from
the National Center for Research Resources, NIH, and by the NIH Roadmap
for Medical Research.
NR 35
TC 6
Z9 6
U1 0
U2 5
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2009
VL 170
IS 10
BP 1222
EP 1230
DI 10.1093/aje/kwp263
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 514FN
UT WOS:000271379800004
PM 19822571
ER
PT J
AU Villanueva, CM
Silverman, DT
Kogevinas, M
AF Villanueva, Cristina M.
Silverman, Debra T.
Kogevinas, Manolis
TI Re: "Determinants of Quality of Interview and Impact on Risk Estimates
in a Case-Control Study of Bladder Cancer" - Three Authors Reply
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Letter
C1 [Villanueva, Cristina M.; Kogevinas, Manolis] Ctr Res Environm Epidemiol CREAL, Barcelona 08003, Spain.
[Villanueva, Cristina M.; Kogevinas, Manolis] IMIM Hosp Mar, Municipal Inst Med Res, Barcelona 08003, Spain.
[Villanueva, Cristina M.; Kogevinas, Manolis] CIBERESP, Barcelona 08003, Spain.
[Silverman, Debra T.] NCI, Occupat & Environm Epidemiol Branch, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Kogevinas, Manolis] Natl Sch Publ Hlth, Athens 11521, Greece.
RP Villanueva, CM (reprint author), Ctr Res Environm Epidemiol CREAL, Barcelona 08003, Spain.
EM cvillanueva@creal.cat
RI Benavides, Fernando/A-5137-2008; Villanueva, Cristina/N-1942-2014;
Kogevinas, Manolis/C-3918-2017
OI Benavides, Fernando/0000-0003-0747-2660; Villanueva,
Cristina/0000-0002-0783-1259;
NR 2
TC 0
Z9 0
U1 0
U2 2
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 15
PY 2009
VL 170
IS 10
BP 1319
EP 1320
DI 10.1093/aje/kwp286
PG 2
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 514FN
UT WOS:000271379800015
ER
PT J
AU Gunay-Aygun, M
AF Gunay-Aygun, Meral
TI Liver and Kidney Disease in Ciliopathies
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Review
DE ductal plate malformation; congenital hepatic fibrosis; Caroli syndrome;
polycystic liver disease; portal hypertension; polycystic kidney
disease; nephronophthisis; cystic dysplastic kidneys; medullary sponge
kidney; multicystic dysplastic kidneys; primary cilia; ciliopathy
ID CONGENITAL HEPATIC-FIBROSIS; MOON-BIEDL SYNDROME; INTRAHEPATIC
BILE-DUCTS; DIGITAL SYNDROME TYPE-1; AUTOSOMAL-DOMINANT; POLYCYSTIC
LIVER; JOUBERT-SYNDROME; RENAL-DISEASE; PANCREATIC DYSPLASIA;
JEUNE-SYNDROME
AB Hepatorenal fibrocystic diseases (HRFCDs) are among the most common inherited human disorders. The discovery that proteins defective in the autosomal dominant and recessive polycystic kidney diseases (ADPKD and ARPKD) localize to the primary cilia and the recognition of the role these organelles play in the pathogenesis of HRFCDs led to the term "ciliopathies." While ADPKD and ARPKD are the most common ciliopathies associated with both liver and kidney disease, variable degrees of renal and/or hepatic involvement occur in many other ciliopathies, including Joubert, Bardet-Biedl, Meckel-Gruber, and oral-facial-digital syndromes. The ductal plate malformation (DPM), a developmental abnormality of the portobiliary system, is the basis of the liver disease in ciliopathies that manifest congenital hepatic fibrosis (CHF), Caroli syndrome (CS), and polycystic liver disease (PLD). Hepatocellular function remains relatively preserved in ciliopathy-associated liver diseases. The major morbidity associated with CHF is portal hypertension (PH), often leading to esophageal varices and hypersplenism. In addition, CD predisposes to recurrent cholangitis. PLD is not typically associated with PH, but may result in complications due to mass effects. The kidney pathology in ciliopathies ranges from non-functional cystic dysplastic kidneys to an isolated urinary concentration defect; the disorders contributing to this pathology, in addition to ADPKD and ARPKD, include nephronophithisis (NPHP), glomerulocystic kidney disease and medullary sponge kidneys. Decreased urinary concentration ability, resulting in polyuria and polydypsia, is the first and most common renal symptom in ciliopathies. While the majority of ADPKD, ARPKD, and NPHP patients require renal transplantation, the frequency and rate of progression to renal failure varies considerably in other ciliopathies. This review focuses on the kidney and liver disease found in the different ciliopathies. Published 2009 Wiley-Liss, Inc.(dagger)
C1 [Gunay-Aygun, Meral] NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Gunay-Aygun, Meral] Johns Hopkins Univ, Sch Medicine, Baltimore, MD 21218 USA.
RP Gunay-Aygun, M (reprint author), NHGRI, Sect Human Biochem Genet, Med Genet Branch, NIH, 10 Ctr Dr,Bldg 10,Rm 10C103, Bethesda, MD 20892 USA.
EM mgaygun@mail.nih.gov
FU Intramural NIH HHS [Z99 HG999999]
NR 109
TC 72
Z9 75
U1 4
U2 8
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4868
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD NOV 15
PY 2009
VL 151C
IS 4
BP 296
EP 306
DI 10.1002/ajmg.c.30225
PG 11
WC Genetics & Heredity
SC Genetics & Heredity
GA 516MT
UT WOS:000271547300004
PM 19876928
ER
PT J
AU Parisi, MA
AF Parisi, Melissa A.
TI Clinical and Molecular Features of Joubert syndrome and Related
Disorders
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Review
DE Joubert syndrome; COACH syndrome; molar tooth sign; ciliary disorder;
ciliopathy; cerebellar vermis hypoplasia
ID MECKEL-GRUBER-SYNDROME; MOLAR TOOTH SIGN; BARDET-BIEDL-SYNDROME;
OCULO-RENAL SYNDROMES; SENIOR-LOKEN-SYNDROME; AHI1 GENE-MUTATIONS;
SYNDROME TYPE-B; CEREBELLAR VERMIS; JUVENILE NEPHRONOPHTHISIS;
CENTROSOMAL PROTEIN
AB Joubert syndrome (JBTS; OMIM 213300) is a rare, autosomal recessive disorder characterized by a specific congenital malformation of the hindbrain and a broad spectrum of other phenotypic findings that is now known to be caused by defects in the structure and/or function of the primary cilium. The complex hindbrain malformation that is characteristic of JBTS can be identified on axial magnetic resonance imaging and is known as the molar tooth sign (MTS); other diagnostic criteria include intellectual disability, hypotonia, and often, abnormal respiratory pattern and/or abnormal eye movements. In addition, a broad spectrum of other anomalies characterize Joubert syndrome and related disorders (JSRD), and may include retinal dystrophy, ocular coloboma, oral frenulae and tongue tumors, polydactyly, cystic renal disease (including cystic dysplasia or juvenile nephronophthisis), and congenital hepatic fibrosis. The clinical course can be variable, but most children with this condition survive infancy to reach adulthood. At least eight genes cause JSRD, with some genotype-phenotype correlations emerging, including the association between mutations in the MKS3 gene and hepatic fibrosis characteristic of the JSRD subtype known as COACH syndrome. Several of the causative genes for JSRD are implicated in other ciliary disorders, such as juvenile nephronophthisis and Meckel syndrome, illustrating the close association between these conditions and their overlapping clinical features that reflect a shared etiology involving the primary cilium. (C) 2009 Wiley-Liss, Inc.
C1 [Parisi, Melissa A.] Seattle Childrens Hosp, Seattle, WA USA.
[Parisi, Melissa A.] Univ Washington, Seattle, WA 98195 USA.
RP Parisi, MA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Intellectual & Dev Disabil Branch, NIH, Bethesda, MD 20892 USA.
EM parisima@mail.nih.gov
FU National Institutes of Health [K23NS45832, P30HD002274]; March of Dimes
Endowment for Healthier Babies
FX Grant sponsor: National Institutes of Health; Grant numbers: K23NS45832,
P30HD002274; Grant sponsor: March of Dimes Endowment for Healthier
Babies.
NR 108
TC 68
Z9 73
U1 2
U2 8
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4868
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD NOV 15
PY 2009
VL 151C
IS 4
BP 326
EP 340
DI 10.1002/ajmg.c.30229
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 516MT
UT WOS:000271547300007
PM 19876931
ER
PT J
AU Fessler, MB
AF Fessler, Michael B.
TI Simvastatin as a Potential Therapeutic for Acute Respiratory Distress
Syndrome
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Letter
ID PULMONARY INFLAMMATION; OXIDATIVE STRESS; REDUCTASE
C1 NIEHS, Res Triangle Pk, NC 27709 USA.
RP Fessler, MB (reprint author), NIEHS, POB 12233, Res Triangle Pk, NC 27709 USA.
NR 6
TC 1
Z9 1
U1 0
U2 1
PU AMER THORACIC SOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD NOV 15
PY 2009
VL 180
IS 10
BP 1031
EP 1031
PG 1
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 519VR
UT WOS:000271797600022
PM 19897776
ER
PT J
AU Bezrukov, L
Blank, PS
Polozov, IV
Zimmerberg, J
AF Bezrukov, Ludmila
Blank, Paul S.
Polozov, Ivan V.
Zimmerberg, Joshua
TI An adhesion-based method for plasma membrane isolation: Evaluating
cholesterol extraction from cells and their membranes
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE Fibroblast cells; Cholesterol/phospholipid ratio; Differential
extraction; Methyl-beta-cyclodextrin; Polylysine
ID COATED POLYACRYLAMIDE BEADS; HELA-CELLS; PHOSPHOLIPID-COMPOSITION; GLASS
BEADS; POLYLYSINE; HEMAGGLUTININ; PURIFICATION; FIBROBLASTS; ASYMMETRY;
SURFACE
AB A method to isolate large quantities of directly accessible plasma membrane from attached cells is presented. The method is based on the adhesion of cells to an adsorbed layer of polylysine on glass plates, followed by hypotonic lysis with ice-cold distilled water and subsequent washing steps. Optimal conditions for coating glass plates and time for cell attachment were established. No additional chemical or mechanical treatments were used. Contamination of the isolated plasma membrane by cell organelles was less than 5%. The method uses inexpensive, commercially available polylysine and reusable glass plates. Plasma membrane preparations can be made in 15 min. Using this method, we determined that methyl-beta-cyclodextrin differentially extracts cholesterol from fibroblast cells and their plasma membranes and that these differences are temperature dependent. Determination of the cholesterol/phospholipid ratio from intact cells does not reflect methyl-beta-cyclodextrin plasma membrane extraction properties. Published by Elsevier Inc.
C1 [Bezrukov, Ludmila; Blank, Paul S.; Polozov, Ivan V.; Zimmerberg, Joshua] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Zimmerberg, J (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Phys Biol, Natl Inst Hlth, Bethesda, MD 20892 USA.
EM zimmerbj@mail.nih.gov
FU National Institutes of Health; Eunice Kennedy Shriver National Institute
of Health and Human Development
FX The authors thank K. Melikov, E. Zaitseva, and J. Mazar for fruitful
discussions and suggestions. This study was supported by the Intramural
Research Program of the National Institutes of Health, Eunice Kennedy
Shriver National Institute of Health and Human Development.
NR 27
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Z9 13
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 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD NOV 15
PY 2009
VL 394
IS 2
BP 171
EP 176
DI 10.1016/j.ab.2009.07.027
PG 6
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 534GI
UT WOS:000272884000004
PM 19631189
ER
PT J
AU Cope, K
Seifried, H
Seifried, R
Milner, J
Kris-Etherton, P
Harrison, EH
AF Cope, Keary
Seifried, Harold
Seifried, Rebecca
Milner, John
Kris-Etherton, Penny
Harrison, Earl H.
TI A gas chromatography-mass spectrometry method for the quantitation of
N-nitrosoproline and N-acetyl-S-allylcysteine in human urine:
Application to a study of the effects of garlic consumption on
nitrosation
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE Biomarkers; Allyl sulfur compounds; Nitrosation; Nutrition; Cancer
ID ALLYL-L-CYSTEINE; DRINKING-WATER; ASCORBIC-ACID; ENDOGENOUS NITROSATION;
EXCRETION; NITRATE; MECHANISMS; NITRITE; CANCER; NITROSODIMETHYLAMINE
AB Biomarkers in urine can provide useful information about the bioactivation of chemical carcinogens and can be used to investigate the chemoprotective properties of dietary nutrients. N-Nitrosoproline (NPRO) excretion has been used as an index for endogenous nitrosation. In vitro and animal studies have reported that compounds in garlic may suppress nitrosation and inhibit carcinogenesis. We present a new method for extraction and sensitive detection of both NPRO and N-acetyl-S-allylcysteine from urine. The latter is a metabolite of S-allylcysteine, which is found in garlic. Urine was acidified and the organic acids were extracted by reversed-phase extraction (RP-SPE) and use of a polymeric weak anion exchange (WAX-SPE) resin. NPRO was quantified by isotope dilution gas chromatography-mass spectrometry (GC-MS) using [(13)C(5)]NPRO and N-nitrosopipecolinic acid (NPIC) as internal standards. This method was used to analyze urine samples from a study that was designed to test whether garlic supplementation inhibits NPRO synthesis. Using this method, 2.4 to 46.0 ng NPRO/ml urine was detected. The method is straightforward and reliable, and it can be performed with readily available GC-MS instruments. N-Acetyl-S-allylcysteine was quantified in the same fraction and detectable at levels of 4.1 to 176.4 ng/ml urine. The results suggest that 3 to 5 g of garlic supplements inhibited NPRO synthesis to an extent similar to a 0.5-g dose of ascorbic acid or a commercial supplement of aged garlic extract. Urinary NPRO concentration was inversely associated with the N-acetyl-S-allylcysteine concentration. It is possible that allyl sulfur compounds found in garlic may inhibit nitrosation in humans. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Harrison, Earl H.] Ohio State Univ, Dept Human Nutr, Columbus, OH 43210 USA.
[Cope, Keary; Seifried, Rebecca; Harrison, Earl H.] USDA Human Nutr Res Ctr, Phytonutrients Lab, Beltsville, MD 20705 USA.
[Seifried, Harold; Milner, John] NCI, Nutr Sci Res Grp, Canc Prevent Div, Rockville, MD 20892 USA.
[Seifried, Rebecca; Milner, John; Kris-Etherton, Penny] Penn State Univ, Dept Nutr Sci, University Pk, PA 16802 USA.
RP Harrison, EH (reprint author), Ohio State Univ, Dept Human Nutr, Columbus, OH 43210 USA.
EM harrison.304@osu.edu
FU NHLBI NIH HHS [R01 HL049879, R01 HL049879-08]; NIDDK NIH HHS [R01
DK044498, R01 DK044498-09]
NR 28
TC 2
Z9 2
U1 0
U2 11
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD NOV 15
PY 2009
VL 394
IS 2
BP 243
EP 248
DI 10.1016/j.ab.2009.07.035
PG 6
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 534GI
UT WOS:000272884000014
PM 19643074
ER
PT J
AU Pan, BX
Ito, W
Morozov, A
AF Pan, Bing-Xing
Ito, Wataru
Morozov, Alexei
TI Divergence Between Thalamic and Cortical Inputs to Lateral Amygdala
During Juvenile-Adult Transition in Mice
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Amygdala; development; fear; juvenile; LTP; synaptic transmission
ID LONG-TERM POTENTIATION; SYNAPTIC PLASTICITY; SILENT SYNAPSES;
TRANSMITTER RELEASE; GLUTAMATE UPTAKE; FEAR; PATHWAY; BRAIN; LTP;
ADOLESCENCE
AB Background: Adolescence is considered a critical time of life for emotional development in humans. During this period the amygdala, which regulates emotions, undergoes structural reorganization. Auditory fear conditioning, a form of amygdala-dependent emotional learning, occurs differently in juvenile and adult rodents. Because this learning is mediated by plastic changes in the thalamic and cortical inputs to lateral amygdala (LA), we investigated changes in synaptic properties of these inputs during juvenile-to-adult transition.
Methods: Whole-cell patch clamp recording in amygdala slices from juvenile and young adult mice was conducted to investigate long-term potentiation and basal synaptic transmission in the thalamic and cortical inputs to LA.
Results: We show that physiological differences develop between thalamic and cortical afferents to LA during the juvenile-to-adult transition. Although in juvenile mice the two pathways have similar properties, in young adult mice the thalamic pathway has reduced plasticity, increased number of quanta released by a single action potential, and decreased proportion of silent synapses.
Conclusions: Changes in thalamic but not cortical inputs to amygdala take place during late development and might contribute to differences in auditory fear conditioning between juveniles and adults.
C1 [Pan, Bing-Xing; Ito, Wataru; Morozov, Alexei] NIMH, Unit Behav Genet, Mol Pathophysiol Lab, NIH, Bethesda, MD 20892 USA.
RP Morozov, A (reprint author), NIMH, Unit Behav Genet, Mol Pathophysiol Lab, NIH, 35 Convent Dr, Bethesda, MD 20892 USA.
EM morozova@mail.nih.gov
RI PAN, BINGXING/C-7870-2011
FU National Institute of Mental Health
FX This research was supported by the National Institute of Mental Health
Intramural Research Program. We thank, Chao Yang for editorial work.
NR 48
TC 11
Z9 12
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD NOV 15
PY 2009
VL 66
IS 10
BP 964
EP 971
DI 10.1016/j.biopsych.2009.07.006
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 515UC
UT WOS:000271497400010
PM 19699473
ER
PT J
AU Youssef, D
Potter, E
Jha, M
De Clercq, E
Balzarini, J
Stables, JP
Jha, A
AF Youssef, Dani
Potter, Elizabeth
Jha, Mamta
De Clercq, Erik
Balzarini, Jan
Stables, James P.
Jha, Amitabh
TI Design, synthesis and bioevaluation of novel maleamic amino acid ester
conjugates of 3,5-bisarylmethylene-4-piperidones as cytostatic agents
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE 3,5-Bisarylmethylene-4-piperidones; Cytostatic activity; Anticancer;
Topoisomerase inhibitions; QSAR
ID DNA TOPOISOMERASE-II; CYTOTOXIC PROPERTIES; ANTICANCER AGENTS; ANALOGS;
3,5-BIS(ARYLIDENE)-4-PIPERIDONES; INHIBITION; MECHANISM; TOXICITY;
KINASE; CELLS
AB A novel series of maleamic amino acid ester conjugates of 3,5-bisarylmethylene-4-piperidones were prepared to investigate the efficacy of micronutrient conjugation in enhancing cytotoxic potency by improving selectivity and delivery. These compounds, prepared as anticancer agents, were expected to demonstrate enhanced selectivity towards malignant cells through the inhibition of topoisomerase II alpha via protein thiolation. The cytostatic effects of these compounds were evaluated against three cell lines, namely murine L1210 leukemia cells, human Molt 4/C8 and CEM T-lymphocyte cells. All compounds were found to have greater potency than the reference drug melphalan. Several compounds were found to potently inhibit topoisomerase IIa and displayed cytostatic activity in the nanomolar range. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Youssef, Dani; Potter, Elizabeth; Jha, Mamta; Jha, Amitabh] Acadia Univ, Dept Chem, Wolfvile, NS B4P 2R6, Canada.
[Youssef, Dani] Univ St Anna, Dept Sci, Pointe De Leglise, NS B0W 1M0, Canada.
[De Clercq, Erik; Balzarini, Jan] Katholieke Univ Leuven, Rega Inst Med Res, B-3000 Louvain, Belgium.
[Stables, James P.] NINDS, Rockville, MD 20852 USA.
RP Jha, A (reprint author), Acadia Univ, Dept Chem, Wolfvile, NS B4P 2R6, Canada.
EM ajha@acadiau.ca
RI Jha, Amitabh/B-5452-2010; Youssef, Diaa/H-9813-2012
OI Jha, Amitabh/0000-0002-6305-0721;
FU Nova Scotia Health Research Foundation; Concerted Research Actions [GOA
05/19]
FX The authors thank the following agencies for financial support, the Nova
Scotia Health Research Foundation (A. J., E. P.) and the Concerted
Research Actions (GOA 05/19) (J. B.). Appreciation is extended to Mrs.
Lisette van Berckelaer for conducting the Molt 4/C8, CEM, and L1210
assays, and the National Institute of Neurological Disorders and Stroke,
USA, for undertaking the short term toxicity studies in mice. Dr. Sherri
McFarland (Acadia University) is thanked for demonstrating the
topoisomerase assay protocol.
NR 31
TC 9
Z9 9
U1 0
U2 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD NOV 15
PY 2009
VL 19
IS 22
BP 6364
EP 6367
DI 10.1016/j.bmcl.2009.09.069
PG 4
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 509PH
UT WOS:000271029600023
PM 19819135
ER
PT J
AU Fuller, CD
Wang, SJ
Choi, M
Czito, BG
Cornell, J
Welzel, TM
McGlynn, KA
Luh, JY
Thomas, CR
AF Fuller, Clifton D.
Wang, Samuel J.
Choi, Mehee
Czito, Brian G.
Cornell, John
Welzel, Tania M.
McGlynn, Katherine A.
Luh, Join Y.
Thomas, Charles R., Jr.
TI Multimodality Therapy for Locoregional Extrahepatic Cholangiocarcinoma A
Population-Based Analysis
SO CANCER
LA English
DT Article
DE cholangiocarcinoma; bile duct cancer; radiotherapy; surgery; lognormal
survival
ID BILE-DUCT CARCINOMA; EXTERNAL-BEAM RADIOTHERAPY; RESECTED BILIARY
MALIGNANCIES; SEER DATABASE ANALYSIS; ADJUVANT RADIOTHERAPY; HILAR
CHOLANGIOCARCINOMA; RADICAL RESECTION; RADIATION-THERAPY; IMPROVED
SURVIVAL; BREAST-CANCER
AB BACKGROUND: Although surgical resection is the mainstay of treatment for extrahepatic cholangiocarcinoma, the majority of patients present with advanced disease. Due in part to numeric rarity, the optimum role of radiotherapy (RT) for extrahepatic cholangiocarcinoma, as well as its relative benefit, is an area of debate. The specific aim of this series was to estimate survival for extrahepatic cholangiocarcinoma patients receiving surgery and adjuvant RT using a robust population-based data set. METHODS: Data were extracted from the Surveillance, Epidemiology, and End Results (SEER) limited-use data set for selected extrahepatic cholangiocarcinoma cases. Lognormal multivariate survival analysis was implemented to estimate survival for patients for treatment cohorts based on extent of surgical intervention and RT. RESULTS: Parametric estimated median survival for patients receiving total/radical resection+RT was 26 months; it was 25 months for total/radical resection alone, 25 months for subtotal/debulking resection+RT, 21 months for subtotal/debulking resection, 12 months for RT alone, and 9 months for those not receiving surgery or RT. Parametric multivariate analysis revealed age, American Joint Committee on Cancer Stage, grade, and surgical/radiation regimen as statistically significant covariates with survival. Surgery alone and adjuvant RT cohorts demonstrated evidence of improved survival compared with no treatment; comparatively, RT alone was associated with survival decrement. Early improvement in survival in adjuvant cohorts was not observed at later time points. CONCLUSIONS: Survival estimates using SEER data suggest an early survival advantage for adjuvant RT for patients with locoregional extrahepatic cholangiocarcinoma. Although future prospective series are needed to confirm these observations, SEER data represent the largest domestic population-based extrahepatic cholangiocarcinoma cohort, and may provide useful baseline survival estimates for future studies. Cancer 2009;115:5175-83. Published 2009 by the American Cancer Society*.
C1 [Fuller, Clifton D.; Luh, Join Y.] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiat Oncol, San Antonio, TX 78229 USA.
[Fuller, Clifton D.] Univ Texas Hlth Sci Ctr San Antonio, Dept Radiol, Grad Div Radiol Sci, San Antonio, TX 78229 USA.
[Fuller, Clifton D.; Wang, Samuel J.; Choi, Mehee; Thomas, Charles R., Jr.] Oregon Hlth & Sci Univ, Inst Canc, Dept Radiat Med, Portland, OR 97201 USA.
[Czito, Brian G.] Duke Univ, Dept Radiat Oncol, Durham, NC USA.
[Cornell, John] Univ Texas Hlth Sci Ctr San Antonio, Dept Epidemiol & Biostat, San Antonio, TX 78229 USA.
[Welzel, Tania M.; McGlynn, Katherine A.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Luh, Join Y.] St Joseph Hosp, Eureka, CA USA.
RP Fuller, CD (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Radiat Oncol, 7703 Floyd Curl Dr,MSC 7889, San Antonio, TX 78229 USA.
EM fullercd@uthscsa.edu
OI Fuller, Clifton/0000-0002-5264-3994
FU National Institutes of Health/National Institute of Biomedical Imaging
and BioEngineering/UTHSCSA [5T32EB000817-04]
FX Dr. Fuller received funding support from the National Institutes of
Health/National Institute of Biomedical Imaging and
BioEngineering/UTHSCSA Graduate Division of Radiological Sciences
Multidisciplinary Training Grant in Human Imaging (5T32EB000817-04).
NR 63
TC 26
Z9 26
U1 0
U2 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2009
VL 115
IS 22
BP 5175
EP 5183
DI 10.1002/cncr.24572
PG 9
WC Oncology
SC Oncology
GA 516SW
UT WOS:000271564100010
PM 19637356
ER
PT J
AU Abdeen, A
Chou, AJ
Healey, JH
Khanna, C
Osborne, TS
Hewitt, SM
Kim, M
Wang, D
Moody, K
Gorlick, R
AF Abdeen, Ayesha
Chou, Alexander J.
Healey, John H.
Khanna, Chand
Osborne, Tanasa S.
Hewitt, Stephen M.
Kim, Mimi
Wang, Dan
Moody, Karen
Gorlick, Richard
TI Correlation Between Clinical Outcome and Growth Factor Pathway
Expression in Osteogenic Sarcoma
SO CANCER
LA English
DT Article
DE osteosarcoma; immunohistochemistry; survival; signal transduction
ID POOR-PROGNOSIS; OSTEOSARCOMA; CHEMOTHERAPY; METASTASIS; EXPERIENCE; VEGF
AB BACKGROUND: Multiple cell-signaling ligands and receptors-including vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), endothelial growth factor (EGF), v-akt murine thymoma viral oncogene homolog (AKT), platelet-derived growth factor (PDGF), mitogen-activated protein kinase (MAPK), and 70-kilodalton (kD) protein S6 kinase (p70S6 kinase)-reportedly are variably expressed in osteogenic sarcoma. Expression of these proteins may have future implications for prognostication and targeted therapy. The objective of the current study was to determine the relation between clinical outcome and the expression of these proteins. METHODS: A paraffin-embedded microarray of 48 human osteogenic sarcoma tissue specimens was stained with the antibodies against VEGF, IGF, EGF, AKT, PDGF, MAPK, and p70S6 kinase. Staining for each protein included the total protein and, when applicable, the phosphorylated version of the protein. Immunohistochemical staining was then correlated with patient survival (overall survival [OS] and event-free survival [EFS]), histologic response to chemotherapy, and serum markers. RESULTS: There was a negative correlation between VEGF receptor 3 (VEGF-R3) and both OS and EFS. VEGF-B was correlated with a poor histologic response to chemotherapy. Serum markers were not correlated with any specific proteins. When using a P value of .05, multiple correlations were observed between proteins of various pathways. CONCLUSIONS: The current results suggested that the VEGF pathway is a critical signaling pathway in osteogenic sarcoma. These data have identified specific proteins within these pathways toward which future investigations should be directed to further clarify their prognostic potential. Cancer 2009;115:5243-50. Published 2009 by the American Cancer Society.*
C1 [Abdeen, Ayesha; Healey, John H.] Cornell Univ, Weill Med Coll, Mem Sloan Kettering Canc Ctr, Dept Orthopaed Surg, New York, NY 10021 USA.
[Chou, Alexander J.] Cornell Univ, Weill Med Coll, Mem Sloan Kettering Canc Ctr, Dept Pediat, New York, NY 10021 USA.
[Khanna, Chand; Osborne, Tanasa S.] NCI, Tumor & Metastasis Biol Sect, Pediat Oncol Branch, LLR, Bethesda, MD 20892 USA.
[Hewitt, Stephen M.] NCI, TARP, Pathol Lab, LLR, Bethesda, MD 20892 USA.
[Kim, Mimi; Wang, Dan] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA.
[Moody, Karen; Gorlick, Richard] Yeshiva Univ, Albert Einstein Coll Med, Montefiore Med Ctr, Dept Pediat, Bronx, NY USA.
RP Gorlick, R (reprint author), Childrens Hosp Montefiore, Div Pediat Hematol Oncol, 3415 Bainbridge Ave,Rosenthal Bldg,Room 300, Bronx, NY 10467 USA.
EM rgorlick@montefiore.org
OI Hewitt, Stephen/0000-0001-8283-1788; Chou, Alexander/0000-0002-7926-3326
NR 11
TC 41
Z9 44
U1 0
U2 4
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 15
PY 2009
VL 115
IS 22
BP 5243
EP 5250
DI 10.1002/cncr.24562
PG 8
WC Oncology
SC Oncology
GA 516SW
UT WOS:000271564100018
PM 19670450
ER
PT J
AU Dignam, JJ
Huang, L
Ries, L
Reichman, M
Mariotto, A
Feuer, E
AF Dignam, James J.
Huang, Lan
Ries, Lynn
Reichman, Marsha
Mariotto, Angela
Feuer, Eric
TI Estimating Breast Cancer-Specific and Other-Cause Mortality in Clinical
Trial and Population-Based Cancer Registry Cohorts
SO CANCER
LA English
DT Article
DE relative survival; cause-specific survival; breast cancer; life tables
ID SURGICAL ADJUVANT BREAST; RELATIVE SURVIVAL RATES; INDIVIDUAL PATIENT
DATA; RESULTS SEER PROGRAM; 18 RANDOMIZED-TRIALS; LOCOREGIONAL
RECURRENCES; TUMOR RECURRENCE; COLON-CANCER; END-POINTS; EPIDEMIOLOGY
AB BACKGROUND: To compute net cancer-specific survival rates using population data sources (eg, the National Cancer Institute's Surveillance, Epidemiology, and End Results [SEER] Program), 2 approaches primarily are used: relative survival (observed survival adjusted for life expectancy) and cause-specific survival based on death certificates. The authors of this report evaluated the performance of these estimates relative to a third approach based on detailed clinical follow-up history. METHODS: By using data from Cancer Cooperative Group clinical trials in breast cancer, the authors estimated 1) relative survival, 2) breast cancer-specific survival (BCSS) determined from death certificates, and 3) BCSS obtained by attributing cause according to clinical events after diagnosis, which, for this analysis was considered the benchmark "true" estimate. Noncancer life expectancy also was compared between trial participants, SEER registry patients, and the general population. RESULTS: Among trial patients, relative survival overestimated true BCSS in patients with lymph node-negative breast cancer; whereas, in patients with lymph node-positive breast cancer, the 2 estimates were similar. For higher risk patients (younger age, larger tumors), relative survival accurately estimated true BCSS. In lower risk patients, death certificate BCSS was more accurate than relative survival. Noncancer life expectancy was more favorable among trial participants than in the general population and among SEER patients. Tumor size at diagnosis, which is a potential surrogate for screening use, partially accounted for this difference. CONCLUSIONS: In the clinical trials, relative survival accurately estimated BCSS in patients who had higher risk disease despite more favorable other-cause mortality than the population at large. In patients with lower risk disease, the estimate using death certificate information was more accurate. For SEER data and other data sources where detailed postdiagnosis clinical history was unavailable, death certificate-based estimates of cause-specific survival may be a superior choice. Cancer 2009;115:5272-83. (C) 2009 American Cancer Society.
C1 [Dignam, James J.] Univ Chicago, Dept Hlth Studies, Chicago, IL 60637 USA.
[Dignam, James J.] Univ Chicago, Canc Res Ctr, Chicago, IL 60637 USA.
[Huang, Lan; Ries, Lynn; Reichman, Marsha; Mariotto, Angela; Feuer, Eric] NCI, Div Canc Control & Populat Sci, Bethesda, MD 20892 USA.
RP Dignam, JJ (reprint author), Univ Chicago, Dept Hlth Studies, 5841 S Maryland Ave,MC 2007, Chicago, IL 60637 USA.
EM jdignam@health.bsd.uchicago.edu
FU US. National Cancer Institute [263-MQ-611334, NCI-U10-CA-69,
NCI-U10-CA-651, NCI-U10-CA-12, NCI-U10-CA-027]; Susan G. Komen for the
Cure Foundation
FX Supported by, contract 263-MQ-611334 to J.J.D. from the Division of
Cancer Control and Population Sciences/Surveillance Research
Program/Statistical Research and Applications Branch of the US. National
Cancer Institute and by a research grant from the Susan G. Komen for the
Cure Foundation. The clinical trials were Supported by Public Health
Service grants NCI-U10-CA-69,651 and NCI-U10-CA-12,027 from the US.
National Cancer Institute.
NR 24
TC 20
Z9 20
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 15
PY 2009
VL 115
IS 22
BP 5272
EP 5283
DI 10.1002/cncr.24617
PG 12
WC Oncology
SC Oncology
GA 516SW
UT WOS:000271564100021
PM 19670456
ER
PT J
AU Fujisawa, T
Joshi, B
Nakajima, A
Puri, RK
AF Fujisawa, Toshio
Joshi, Bharat
Nakajima, Atsushi
Puri, Raj K.
TI A Novel Role of Interleukin-13 Receptor alpha 2 in Pancreatic Cancer
Invasion and Metastasis
SO CANCER RESEARCH
LA English
DT Article
ID PROTEIN-KINASE PATHWAYS; PSEUDOMONAS EXOTOXIN; MATRIX
METALLOPROTEINASES; SIGNAL-TRANSDUCTION; IN-VIVO; CELLS; CHAIN;
EXPRESSION; FIBROSIS; TARGET
AB Whereas interleukin-13 receptor alpha 2 chain (IL-13R alpha 2) is over-expressed in a variety of human solid cancers including pancreatic cancer, we investigated its significance in cancer invasion and metastasis. We used two pancreatic cancer cell lines, IL-13R alpha 2-negative HPAF-H and IL-13R alpha 2-positive HS766T, and generated IL-13Ra2 stably transfected HPAF-II as well as IL-13Ra2 RNA interference knocked-down HS766T cells. Ability of invasion and signal transduction was compared between IL-13R alpha 2-negative and IL-13R alpha 2-positive cells and tumor metastasis was assessed in murine model for human pancreatic cancer with orthotopic implantation of tumors. IL-13 treatment enhanced cell invasion in IL13R alpha 2-positive cancer cell lines but not in IL-13R alpha 2-negative cell lines. Furthermore, gene transfer of IL-13R alpha 2 in negative cell lines enhanced invasion, whereas its silencing downmodulated invasion of pancreatic cell lines in a Matrigel invasion assay. In vivo study revealed that II-13R alpha 2-positive cancer metastasized to lymph nodes, liver, and peritoneum at. a significantly higher rate compared with IL-13R alpha 2-negative tumors. The expression of IL-13R alpha 2 in metastatic lesions was found to be increased compared with primary tumors, and mice with IL-13R alpha 2-positive cancer displayed cachexia and poor prognosis. Invasion and metastasis also correlated with increased matrix metalloproteinase protease activity in these cells. Mechanistically, IL-13 activated extracellular signal-regulated kinase 1/2 and activator protein-1 nuclear factors in IL-13R alpha 2-positive pancreatic cancer cell lines but not in IL-13R alpha 2-negative cell lines. Taken together, our results show for the first time that IL-13 can signal through IL-13R alpha 2 in pancreatic cancer cells and IL-13Ra2 may serve as a prognostic biomarker of invasion and metastasis in pancreatic cancer. [Cancer Res 2009;69(22):8678-85]
C1 [Fujisawa, Toshio; Joshi, Bharat; Puri, Raj K.] US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA.
[Nakajima, Atsushi] Yokohama City Univ, Sch Med, Div Gastroenterol, Yokohama, Kanagawa 232, Japan.
RP Puri, RK (reprint author), US FDA, Tumor Vaccines & Biotechnol Branch, Div Cellular & Gene Therapies, Ctr Biol Evaluat & Res, NIH Bldg 29B,Room 2NN20 HFM 735,29 Lincoln Dr, Bethesda, MD 20892 USA.
EM raj.puri@fda.hhs.gov
NR 35
TC 47
Z9 53
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2009
VL 69
IS 22
BP 8678
EP 8685
DI 10.1158/0008-5472.CAN-09-2100
PG 8
WC Oncology
SC Oncology
GA 520JC
UT WOS:000271839200020
PM 19887609
ER
PT J
AU Vo, DD
Prins, RM
Begley, JL
Donahue, TR
Morris, LF
Bruhn, KW
de la Rocha, P
Yang, MY
Mok, S
Garban, HJ
Craft, N
Economou, JS
Marincola, FM
Wang, E
Ribas, A
AF Vo, Dan D.
Prins, Robert M.
Begley, Jonathan L.
Donahue, Timothy R.
Morris, Lilah F.
Bruhn, Kevin W.
de la Rocha, Pilar
Yang, Meng-Yin
Mok, Stephen
Garban, Hermes J.
Craft, Noah
Economou, James S.
Marincola, Francesco M.
Wang, Ena
Ribas, Antoni
TI Enhanced Antitumor Activity Induced by Adoptive T-Cell Transfer and
Adjunctive Use of the Histone Deacetylase Inhibitor LAQ824
SO CANCER RESEARCH
LA English
DT Article
ID MYELOID-LEUKEMIA CELLS; MHC CLASS-I; LISTERIA-MONOCYTOGENES VACCINE;
SUBERIC BISHYDROXAMATE; DENDRITIC CELLS; MELANOMA-CELLS; EXPRESSION;
MODULATION; NVP-LAQ824; APOPTOSIS
AB Tumors grow in the presence of antigen-specific T cells, suggesting the existence of intrinsic cancer cell escape mechanisms. We hypothesized that a histone deacetylase (HDAC) inhibitor could sensitize tumor cells to immunotherapy because this class of agents has been reported to increase tumor antigen expression and shift gene expression to a proapoptotic milieu in cancer cells. To test this question, we treated 1116 murine melanoma with the combination of the HDAC inhibitor LAQ824 and the adoptive transfer of gp100 melanoma antigen-specific pmel-1 T cells. The combined therapy significantly improved antitumor activity through several mechanisms: (a) increase in MHC and tumor-associated antigen expression by tumor cells; (b) decrease in competing endogenous lymphocytes in recipient mice, resulting in a proliferative advantage for the adoptively transferred cells; and (c) improvement in the functional activity of the adoptively transferred lymphocytes. We confirmed the beneficial effects of this HDAC inhibitor as a sensitizer to immunotherapy in a different model of prophylactic prime-boost vaccination with the melanoma antigen tyrosinase-related protein 2, which also showed a significant improvement in antitumor activity against B16 melanoma. In conclusion, the HDAC inhibitor LAQ824 significantly enhances tumor immunotherapy through effects on target tumor cells as well as improving the antitumor activity of tumor antigen-specific lymphocytes. [Cancer Res 2009;69(22):8693-9]
C1 [Ribas, Antoni] Univ Calif Los Angeles, Dept Med, Div Hematol Oncol, Med Ctr, Los Angeles, CA 90095 USA.
[Vo, Dan D.; Donahue, Timothy R.; Morris, Lilah F.; de la Rocha, Pilar; Mok, Stephen; Garban, Hermes J.; Economou, James S.; Ribas, Antoni] Univ Calif Los Angeles, Dept Surg, Div Surg Oncol, Los Angeles, CA 90095 USA.
[Prins, Robert M.; Yang, Meng-Yin] Univ Calif Los Angeles, Dept Neurosurg, Los Angeles, CA 90095 USA.
[Prins, Robert M.; Economou, James S.; Ribas, Antoni] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
[Bruhn, Kevin W.; Craft, Noah] Harbor UCLA Med Ctr, Dept Med, Div Dermatol, Los Angeles Biomed Res Inst, Torrance, CA 90509 USA.
[Marincola, Francesco M.; Wang, Ena] NIH, Infect Dis & Immunogenet Sect, Dept Transfus Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Ribas, A (reprint author), Univ Calif Los Angeles, Dept Med, Div Hematol Oncol, Med Ctr, 11-934 Factor Bldg,10833 Le Conte Ave, Los Angeles, CA 90095 USA.
EM aribas@mednet.ucla.edu
RI Bruhn, Kevin/F-9772-2013;
OI Garban, Hermes/0000-0001-7754-5357; Prins, Robert/0000-0002-6282-6583
FU Harry J. Hoyd Charitable Trust; Waxman Foundation; W.M. Keck Foundation;
Monkarsh land; NIH [CAI6042]; [P50 CA086306]
FX Harry J. Hoyd Charitable Trust, P50 CA086306, Waxman Foundation. W.M.
Keck Foundation, and Monkarsh land. Flow cytometry was done at the
University of California-Los Angeles Jonsson Comprehensive Cancer Center
Core Facility, which is supported by the NIH award CAI6042.
NR 38
TC 56
Z9 57
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2009
VL 69
IS 22
BP 8693
EP 8699
DI 10.1158/0008-5472.CAN-09-1456
PG 7
WC Oncology
SC Oncology
GA 520JC
UT WOS:000271839200022
PM 19861533
ER
PT J
AU Espey, MG
Chen, Q
Levine, M
AF Espey, Michael Graham
Chen, Qi
Levine, Mark
TI Comment re: Vitamin C Antagonizes the Cytotoxic Effects of Chemotherapy
SO CANCER RESEARCH
LA English
DT Letter
ID DEHYDROASCORBIC ACID
C1 [Espey, Michael Graham; Chen, Qi; Levine, Mark] NIDDK, Mol & Clin Nutr Sect, NIH, Bethesda, MD 20892 USA.
RP Espey, MG (reprint author), NIDDK, Mol & Clin Nutr Sect, NIH, Bethesda, MD 20892 USA.
RI Chen, Qi/D-8278-2015
OI Chen, Qi/0000-0002-7173-8411
NR 8
TC 5
Z9 5
U1 0
U2 4
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
J9 CANCER RES
JI Cancer Res.
PD NOV 15
PY 2009
VL 69
IS 22
BP 8830
EP 8830
DI 10.1158/0008-5472.CAN-08-3798
PG 1
WC Oncology
SC Oncology
GA 520JC
UT WOS:000271839200039
PM 19843868
ER
PT J
AU Figueroa, A
Fujita, Y
Gorospe, M
AF Figueroa, Angelica
Fujita, Yasuyuki
Gorospe, Myriam
TI Hacking RNA Hakai promotes tumorigenesis by enhancing the RNA-binding
function of PSF
SO CELL CYCLE
LA English
DT Article
DE E-cadherin; PSF; PTB-associated splicing factor; proliferation; tumor
progression; RNA binding protein; oncogene
ID RENAL-CELL CARCINOMA; E-CADHERIN; SPLICING FACTOR; MESSENGER-RNA;
PROTEIN; IDENTIFICATION; P54(NRB)/NONO; TRANSCRIPTION; LOCALIZATION;
ONCOPROTEIN
AB Hakai, an E3 ubiquitin ligase for the E-cadherin complex, plays a crucial role in lowering cell-cell contacts in epithelial cells, a hallmark feature of tumor progression. Recently, Hakai was also found to interact with PSF (PTB-associated splicing factor). While PSF can function as a DNA-binding protein with a tumor suppressive function, its association with Hakai promotes PSF's RNA-binding ability and post-transcriptional influence on target mRNAs. Hakai overexpression enhanced the binding of PSF to mRNAs encoding cancer-related proteins, while knockdown of Hakai reduced the RNA-binding ability of PSF. Furthermore, the knockdown of PSF suppressed Hakai-induced cell proliferation. Thus, Hakai can affect the oncogenic phenotype both by altering E-cadherin-based intercellular adhesions and by increasing PSF's ability to bind RNAs that promote cancer-related gene expression.
C1 [Figueroa, Angelica] Univ A Coruna, Inst Invest Biomed A Coruna, Complejo Hosp, La Coruna, Spain.
[Fujita, Yasuyuki] UCL, MRC Lab Mol Cell Biol, London, England.
[Fujita, Yasuyuki] UCL, Cell Biol Unit, London, England.
[Fujita, Yasuyuki] UCL, Dept Cell & Dev Biol, London, England.
[Gorospe, Myriam] NIA, LCMB, NIH, Baltimore, MD 21224 USA.
RP Figueroa, A (reprint author), Univ A Coruna, Inst Invest Biomed A Coruna, Complejo Hosp, La Coruna, Spain.
EM angelica.figueroa.conde-valvis@sergas.es
RI Fujita, Yasuyuki/A-4324-2012
FU Secretaria Xeral I+D+I, Xunta de Galicia, Spain; NIA-IRP, NIH
FX A. F. is supported by Parga Pondal Program, Secretaria Xeral I+D+I,
Xunta de Galicia, Spain. Y. F. is supported by MRC funding to the Cell
Biology Unit. M. G. is supported by the NIA-IRP, NIH.
NR 31
TC 12
Z9 12
U1 0
U2 2
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 15
PY 2009
VL 8
IS 22
BP 3648
EP 3651
PG 4
WC Cell Biology
SC Cell Biology
GA 525MB
UT WOS:000272219000017
PM 19855157
ER
PT J
AU Lopez-Otin, C
Palavalli, LH
Samuels, Y
AF Lopez-Otin, Carlos
Palavalli, Lavanya H.
Samuels, Yardena
TI Protective roles of matrix metalloproteinases From mouse models to human
cancer
SO CELL CYCLE
LA English
DT Article
DE matrix metalloproteinases; MMP-8; tumor suppressor gene; mouse model;
somatic mutation
ID HUMAN BREAST; TUMOR; GENE; PROGRESSION; SUPPRESSOR; THERAPY;
IDENTIFICATION; CHROMOSOME; ESOPHAGEAL; REVEALS
AB Matrix metalloproteinases (MMPs) have long been linked to cancer progression owing to their ability to breakdown tissue barriers for metastatic spread. Accordingly, multiple studies have examined the potential value of these enzymes as targets for cancer therapy. Unfortunately, most clinical trials with MMP inhibitors have yielded negative results which has made necessary to re-evaluate the role of these proteases in cancer. Recent works mainly based on the use of mouse models deficient in specific MMPs have revealed that these enzymes play many roles in cancer distinct from matrix destruction, influencing early steps of tumor evolution, and expanding their pro-tumorigenic properties. However, these in vivo studies have also shown that, unexpectedly, some MMP family members like MMP8 may have paradoxical anti-tumor functions. Nevertheless, the final validation of these MMPs as bona fide tumor suppressors requested the identification of the putative genetic or epigenetic changes underlying their inactivation during cancer development. To this purpose, very recent large-scale genomic studies have explored the possibility that MMPs could be genetically altered in a panel of human malignant tumors from different sources. These studies have demonstrated that MMP8 is a frequently mutated gene in human melanoma. Functional analysis of the identified mutations has confirmed that all of them lead to the loss-of-function of MMP8 and enhance the progression of melanoma, thus providing definitive evidence that MMP8 is a tumor-suppressor gene. Parallel studies have extended these findings to other MMP-related metalloproteinases such as ADAMTS15, which has been found to be genetically inactivated in human colorectal cancer. This review describes the identification and validation of some MMPs and related enzymes as anti-tumor proteases and speculates about the molecular mechanisms underlying their protective roles in tumor development. Finally, the review explores the clinical applications derived from the identification of MMPs that favour the host instead of the tumor.
C1 [Palavalli, Lavanya H.; Samuels, Yardena] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
[Lopez-Otin, Carlos] Univ Oviedo, Inst Univ Oncol, Dept Bioquim & Biol Mol, Fac Med, Oviedo, Spain.
RP Samuels, Y (reprint author), NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA.
EM samuelsy@mail.nih.gov
RI Lopez-Otin, Carlos/C-6657-2013
OI Lopez-Otin, Carlos/0000-0001-6964-1904
FU Ministerio de Ciencia e Innovacion-Spain, Fundacion; European Union
FP7-MicroEnviMet; National Human Genome Research Institute; National
Institutes of Health
FX This work was supported by grants from Ministerio de Ciencia e
Innovacion-Spain, Fundacion "M. Botin", the European Union
FP7-MicroEnviMet (to C.L.-O.) and the Intramural Research Programs of
the National Human Genome Research Institute, National Institutes of
Health, USA (to Y. S.).
NR 38
TC 51
Z9 51
U1 0
U2 2
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 15
PY 2009
VL 8
IS 22
BP 3657
EP 3662
PG 6
WC Cell Biology
SC Cell Biology
GA 525MB
UT WOS:000272219000019
PM 19844170
ER
PT J
AU Jian, BX
Nagineni, CN
Meleth, S
Grizzle, W
Bland, K
Chaudry, I
Raju, R
AF Jian, Bixi
Nagineni, Chandrasekharam N.
Meleth, Sreelatha
Grizzle, William
Bland, Kirby
Chaudry, Irshad
Raju, Raghavan
TI Anosmin-1 involved in neuronal cell migration is hypoxia inducible and
cancer regulated
SO CELL CYCLE
LA English
DT Article
DE HIF-1 alpha; anosmin; hypogonadism; colon cancer; apoptosis; tumor;
metastasis; anosmia
ID GROWTH-FACTOR-BETA; KALLMANN-SYNDROME; ENDOPLASMIC-RETICULUM;
GENE-EXPRESSION; HYDROXYLATION; ACTIVATION; FIBROSIS; ADHESION; PATHWAY;
TWIST
AB Functional expression of KAL1 gene is critical in the migration of GnRH neurons from the olfactory placode to the hypothalamus in embryogenesis. This gene thus far has not been shown to play a functional role in any other physiological or pathological process either in the developed brain or in peripheral tissues. We show here that KAL1 gene expression is decreased in early stage and increased in later stages of cancers. Screening of colon, lung and ovarian cancer cDNA panels indicated significant decrease in KAL1 expression in comparison to corresponding uninvolved tissues. However, KAL1 expression increased with the progression of cancer from early (I and II) stages to later (III and IV) stages of the cancer. There was a direct correlation between the TGF beta and KAL1 expression in colon cancer cDNA. Using colon cancer cell lines, we showed that TGF beta induces KAL1 gene expression and secretion of anosmin-1 protein (KAL1 coded protein). We further report that hypoxia induces anosmin-1 expression; anosmin-1 protects cancer cells from apoptosis activated by hypoxia and increases cancer cell mobility. Using siRNA technique we found that KAL1 expression following hypoxia is hypoxia-inducible factor (HIF-1)alpha dependent. Our results suggest that KAL1 gene expression plays an important role in cancer metastasis and protection from apoptosis.
C1 [Jian, Bixi; Bland, Kirby; Chaudry, Irshad; Raju, Raghavan] Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
[Meleth, Sreelatha] Univ Alabama, Comprehens Canc Ctr Biostat, Birmingham, AL 35294 USA.
[Grizzle, William] Univ Alabama, Dept Pathol, Birmingham, AL 35294 USA.
[Chaudry, Irshad; Raju, Raghavan] Univ Alabama, Dept Microbiol, Birmingham, AL 35294 USA.
[Nagineni, Chandrasekharam N.] NEI, NIH, Bethesda, MD 20892 USA.
RP Raju, R (reprint author), Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
EM RRaju@uab.edu
RI Raju, Raghavan/E-9219-2011
FU HSF-GEF Scholar Award
FX This work was supported by the HSF-GEF Scholar Award.
NR 30
TC 15
Z9 15
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 15
PY 2009
VL 8
IS 22
BP 3770
EP 3776
PG 7
WC Cell Biology
SC Cell Biology
GA 525MB
UT WOS:000272219000034
PM 19844165
ER
PT J
AU Mai, W
Kawakami, K
Shakoori, A
Kyo, S
Miyashita, K
Yokoi, K
Jin, MJ
Shimasaki, T
Motoo, Y
Minamoto, T
AF Mai, Wei
Kawakami, Kazuyuki
Shakoori, Abbas
Kyo, Satoru
Miyashita, Katsuyoshi
Yokoi, Kenji
Jin, Mingji
Shimasaki, Takeo
Motoo, Yoshiharu
Minamoto, Toshinari
TI Deregulated GSK3 beta Sustains Gastrointestinal Cancer Cells Survival by
Modulating Human Telomerase Reverse Transcriptase and Telomerase
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID GLYCOGEN-SYNTHASE KINASE-3-BETA; HUMAN COLON-CANCER; COLORECTAL-CANCER;
CELLULAR SENESCENCE; GENE-TRANSCRIPTION; ONCOGENE ADDICTION;
PANCREATIC-CANCER; GASTRIC-CANCER; BETA-CATENIN; KAPPA-B
AB Purpose: Glycogen synthase kinase-3 beta (GSK3 beta) regulates multiple cell signaling pathways and has been implicated in glucose intolerance, neurodegenerative disorders, and inflammation. We investigated the expression, activity, and putative pathologic role of GSK3 beta in gastrointestinal, pancreatic, and liver cancers.
Experimental Design: Colon, stomach, pancreatic, and liver cancer cell lines; nonneoplastic HEK293 cells; and matched pairs of normal and tumor tissues of stomach and colon cancer patients were examined for GSK3 beta expression and its phosphorylation at serine 9 (inactive form) and tyrosine 216 (active form) by Western immunoblotting and for GSK3 beta activity by in vitro kinase assay. The effects of small-molecule GSK3 beta inhibitors and of RNA interference on cell survival, proliferation, and apoptosis were examined in vitro and on human colon cancer cell xenografts in athymic mice. The effects of GSK3 beta inhibition on human telomerase reverse transcriptase (hTERT) expression and telomerase activity were compared between colon cancer and HEK293 cells.
Results: Cancer cell lines and most cancer tissues showed increased GSK3 beta expression and increased tyrosine 216 phosphorylation and activity but decreased serine 9 phosphorylation compared with HEK293 cells and nonneoplastic tissues. Inhibition of GSK3 beta resulted in attenuated cell survival and proliferation and increased apoptosis in most cancer cell lines and in HT-29 xenografts in rodents but not in HEK293 cells. GSK3 beta inhibition in colon cancer cells was associated with decreased hTERT expression and telomerase activity.
Conclusion: The results indicate that deregulated GSK3 beta sustains gastrointestinal cancer cells survival through modulation of hTERT and telomerase. (Clin Cancer Res 2009;15(22):6810-19)
C1 [Minamoto, Toshinari] Kanazawa Univ, Canc Res Inst, Div Translat & Clin Oncol, Kanazawa, Ishikawa 9200934, Japan.
[Kyo, Satoru] Kanazawa Univ, Dept Obstet & Gynecol, Grad Sch Med Sci, Kanazawa, Ishikawa 9200934, Japan.
[Miyashita, Katsuyoshi] Kanazawa Univ, Dept Neurosurg, Grad Sch Med Sci, Kanazawa, Ishikawa 9200934, Japan.
[Yokoi, Kenji] Kanazawa Univ, Dept Cardiothorac & Gen Surg, Grad Sch Med Sci, Kanazawa, Ishikawa 9200934, Japan.
[Shakoori, Abbas] NCI, Sect Canc Genom, NIH, Bethesda, MD 20892 USA.
[Shimasaki, Takeo; Motoo, Yoshiharu] Kanazawa Med Univ, Dept Med Oncol, Uchinada, Ishikawa 92002, Japan.
[Yokoi, Kenji] Univ Texas MD Anderson Canc Ctr, Dept Canc Biol, Houston, TX 77030 USA.
RP Minamoto, T (reprint author), Kanazawa Univ, Canc Res Inst, Div Translat & Clin Oncol, 13-1 Takara Machi, Kanazawa, Ishikawa 9200934, Japan.
EM minamoto@staff.kanazawa-u.ac.jp
RI Yokoi, Kenji/J-1216-2014
FU Japanese Ministry of Education, Science, Sports, Technology and Culture;
Ministry of Health, Labour and Welfare; Japan Society for the Promotion
of Science
FX Supported in part by Grants-in-Aid for Scientific Research from the
Japanese Ministry of Education, Science, Sports, Technology and Culture;
from the Ministry of Health, Labour and Welfare; and from the Japan
Society for the Promotion of Science.
NR 51
TC 45
Z9 46
U1 0
U2 1
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2009
VL 15
IS 22
BP 6810
EP 6819
DI 10.1158/1078-0432.CCR-09-0973
PG 10
WC Oncology
SC Oncology
GA 520EJ
UT WOS:000271822600010
PM 19903789
ER
PT J
AU Hong, DS
Sebti, SM
Newman, RA
Blaskovich, MA
Ye, L
Gagel, RF
Moulder, S
Wheler, JJ
Naing, A
Tannir, NM
Ng, CS
Sherman, SI
El Naggar, AK
Khan, R
Trent, J
Wright, JJ
Kurzrock, R
AF Hong, David S.
Sebti, Said M.
Newman, Robert A.
Blaskovich, Michelle A.
Ye, Lei
Gagel, Robert F.
Moulder, Stacy
Wheler, Jennifer J.
Naing, Aung
Tannir, Nizar M.
Ng, Chaan S.
Sherman, Steven I.
El Naggar, Adel K.
Khan, Rabia
Trent, Jon
Wright, John J.
Kurzrock, Razelle
TI Phase I Trial of a Combination of the Multikinase Inhibitor Sorafenib
and the Farnesyltransferase Inhibitor Tipifarnib in Advanced
Malignancies
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID RENAL-CELL CARCINOMA; FARNESYL TRANSFERASE INHIBITORS; THYROID-CANCER;
MYELODYSPLASTIC SYNDROME; KINASE INHIBITOR; SOLID TUMORS; R115777;
THERAPY; TARGET
AB Purpose: We evaluated the safety, maximum tolerated dose, pharmacokinetics, and biological effects of the combination of the Raf-1, RET, KIT, platelet-derived growth factor receptor, and vascular endothelial growth factor receptor 2 kinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib.
Experimental Design: A standard 3 + 3 phase I dose-escalation design was used with a 28-day cycle (sorafenib daily and tipifarnib for 21 days, by mouth).
Results: Fifty patients were treated; 43 reached restaging evaluation after cycle 2. The most common side effects were grade 1 to 2 rash, hyperglycemia, and diarrhea. Dose-limiting toxicity was rash, and the recommended phase 11 dose is sorafenib 400 mg p.o. qam/200 mg p.o. qpm and tipifarnib p.o. 100 mg bd. Despite the low doses of tipifarnib, one quarter of patients had >= 50% reduction in farnesyltransferase levels. Interestingly, six of eight patients with medullary thyroid cancer had durable stable disease (n = 3) or partial remissions (n = 3), lasting 12 to 26+ months. Five of the six responders had available tissue, and RET gene mutations were identified in them. Prolonged (>= 6 months) stable disease was also seen in nine patients as follows: papillary thyroid cancer (n = 4; 18+ to 27+ months), adrenocortical cancer (n = 2; 7 and 11 months), and one each of melanoma (platelet-derived growth factor receptor mutation positive; 14 months), renal (6 months), and pancreatic cancer (6 months).
Conclusions: Our study shows that the combination of tipifarnib and sorafenib is well tolerated. Activity was seen, especially in patients with medullary thyroid cancer, a tumor characterized by RET mutations. (Clin Cancer Res 2009;15(22):7061-8)
C1 [Hong, David S.; Wheler, Jennifer J.; Naing, Aung; Khan, Rabia; Kurzrock, Razelle] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Invest Canc Therapeut, Phase Clin Trials Program 1, Houston, TX 77030 USA.
[Newman, Robert A.] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Expt Canc Therapeut, Houston, TX 77030 USA.
[Ye, Lei; Gagel, Robert F.; Sherman, Steven I.] Univ Texas MD Anderson Canc Ctr, Div Internal Med, Dept Endocrine Neoplasia & Hormonal Disorders, Houston, TX 77030 USA.
[Moulder, Stacy] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Breast Med Oncol, Houston, TX 77030 USA.
[Tannir, Nizar M.] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept GU Med Oncol, Houston, TX 77030 USA.
[Ng, Chaan S.] Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Radiol, Houston, TX 77030 USA.
[El Naggar, Adel K.] Univ Texas MD Anderson Canc Ctr, Dept Pathol, Houston, TX 77030 USA.
[Trent, Jon] Univ Texas MD Anderson Canc Ctr, Dept Sarcoma, Houston, TX 77030 USA.
[Sebti, Said M.; Blaskovich, Michelle A.] Univ S Florida, H Lee Moffitt Canc Ctr & Res Inst, Dept Drug Discovery Program, Tampa, FL USA.
[Sebti, Said M.; Blaskovich, Michelle A.] Univ S Florida, Dept Oncol Sci, Tampa, FL USA.
[Wright, John J.] NCI, Canc Therapy Evaluat Program, Bethesda, MD 20892 USA.
RP Hong, DS (reprint author), Univ Texas MD Anderson Canc Ctr, Div Canc Med, Dept Invest Therapeut, Phase Program 1, 1515 Holcombe Blvd, Houston, TX 77030 USA.
EM dshong@mdanderson.org
OI Sherman, Steven/0000-0002-3079-5153
FU NIH [5 U01 CA062461]; Translational Initiative [25XS0688]
FX Grant support: NIH grant 5 U01 CA062461 (R. Kurzrock) and Translational
Initiative Grant 25XS0688 (D.S. Hong).
NR 30
TC 53
Z9 54
U1 0
U2 6
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1078-0432
J9 CLIN CANCER RES
JI Clin. Cancer Res.
PD NOV 15
PY 2009
VL 15
IS 22
BP 7061
EP 7068
DI 10.1158/1078-0432.CCR-09-1241
PG 8
WC Oncology
SC Oncology
GA 520EJ
UT WOS:000271822600038
PM 19903778
ER
PT J
AU Deeks, SG
Gange, SJ
Kitahata, MM
Saag, MS
Justice, AC
Hogg, RS
Eron, JJ
Brooks, JT
Rourke, SB
Gill, MJ
Bosch, RJ
Benson, CA
Collier, AC
Martin, JN
Klein, MB
Jacobson, LP
Rodriguez, B
Sterling, TR
Kirk, GD
Napravnik, S
Rachlis, AR
Calzavara, LM
Horberg, MA
Silverberg, MJ
Gebo, KA
Kushel, MB
Goedert, JJ
McKaig, RG
Moore, RD
AF Deeks, Steven G.
Gange, Stephen J.
Kitahata, Mari M.
Saag, Michael S.
Justice, Amy C.
Hogg, Robert S.
Eron, Joseph J.
Brooks, John T.
Rourke, Sean B.
Gill, M. John
Bosch, Ronald J.
Benson, Constance A.
Collier, Ann C.
Martin, Jeffrey N.
Klein, Marina B.
Jacobson, Lisa P.
Rodriguez, Benigno
Sterling, Timothy R.
Kirk, Gregory D.
Napravnik, Sonia
Rachlis, Anita R.
Calzavara, Liviana M.
Horberg, Michael A.
Silverberg, Michael J.
Gebo, Kelly A.
Kushel, Margot B.
Goedert, James J.
McKaig, Rosemary G.
Moore, Richard D.
CA N Amer AIDS Cohort Collaboration R
TI Trends in Multidrug Treatment Failure and Subsequent Mortality among
Antiretroviral Therapy-Experienced Patients with HIV Infection in North
America
SO CLINICAL INFECTIOUS DISEASES
LA English
DT Article
ID HUMAN-IMMUNODEFICIENCY-VIRUS; VIROLOGICAL FAILURE; DRUG-RESISTANCE;
HIV-1-INFECTED PATIENTS; RISK; COHORT; PROGRESSION; PREVALENCE;
PREDICTORS; INHIBITORS
AB Background. Although combination antiretroviral therapy continues to evolve, with potentially more effective options emerging each year, the ability of therapy to prevent multiple regimen failure and mortality in clinical practice remains poorly defined.
Methods. Sixteen cohorts representing over 60 sites contributed data on all individuals who initiated combination antiretroviral therapy. We identified those individuals who experienced virologic failure (defined as a human immunodeficiency virus [HIV] RNA level 11000 copies/mL),received modified therapy, and subsequently had a second episode of virologic failure. Multivariate Cox regression was used to assess factors associated with time to second regimen failure and the time to death after the onset of second regimen failure.
Results. Of the 42,790 individuals who received therapy, 7159 experienced a second virologic failure. The risk of second virologic failure decreased from 1996 (56 cases per 100 person-years) through 2005 (16 cases per 100 person-years; P < .001). The cumulative mortality after onset of second virologic failure was 26% at 5 years and decreased over time. A history of AIDS, a lower CD4(+) T cell count, and a higher plasma HIV RNA level were each independently associated with mortality. Similar trends were observed when analysis was limited to the subset of previously treatment-naive patients
Conclusions. Although the rates of multiple regimen failure have decreased dramatically over the past decade, mortality rates for those who have experienced failure of at least 2 regimens have remained high. Plasma HIV RNA levels, CD4(+) T cell counts at time of treatment failure, and a history of AIDS remain independent risk factors for death, which emphasizes that these factors remain important targets for those in need of more-aggressive therapeutic interventions.
C1 [Deeks, Steven G.; Martin, Jeffrey N.; Kushel, Margot B.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Benson, Constance A.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Horberg, Michael A.; Silverberg, Michael J.] Kaiser Permanente No Calif, Oakland, CA USA.
[Gange, Stephen J.; Jacobson, Lisa P.; Kirk, Gregory D.; Gebo, Kelly A.; Moore, Richard D.] Johns Hopkins Univ, Baltimore, MD USA.
[Goedert, James J.; McKaig, Rosemary G.] NIH, Bethesda, MD 20892 USA.
[Kitahata, Mari M.; Collier, Ann C.] Univ Washington, Seattle, WA 98195 USA.
[Saag, Michael S.] Univ Alabama, Birmingham, AL USA.
[Justice, Amy C.] Yale Univ, New Haven, CT USA.
[Eron, Joseph J.; Napravnik, Sonia] Univ N Carolina, Chapel Hill, NC USA.
[Brooks, John T.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Bosch, Ronald J.] Harvard Univ, Boston, MA 02115 USA.
[Rodriguez, Benigno] Case Western Reserve Univ, Cleveland, OH USA.
[Sterling, Timothy R.] Vanderbilt Univ, Nashville, TN USA.
[Hogg, Robert S.] Simon Fraser Univ, Vancouver, BC, Canada.
[Rourke, Sean B.; Rachlis, Anita R.; Calzavara, Liviana M.] Univ Toronto, Toronto, ON, Canada.
[Gill, M. John] Univ Calgary, Calgary, AB, Canada.
[Klein, Marina B.] McGill Univ, Montreal, PQ, Canada.
RP Deeks, SG (reprint author), San Francisco Gen Hosp, Ward 84,Bldg 80,995 Potrero Ave, San Francisco, CA 94110 USA.
EM sdeeks@php.ucsf.edu
RI Hogg, Robert/B-2783-2012; Rodriguez, Benigno/C-3365-2009; Gill,
John/G-7083-2016;
OI Rodriguez, Benigno/0000-0001-9736-7957; Gill, John/0000-0002-8546-8790;
Gange, Stephen/0000-0001-7842-512X; Hogg, Robert/0000-0003-3463-5488
FU NCI NIH HHS [N02CP55504, Z01 CP010176]; NCRR NIH HHS [M01 RR000071, M01
RR000079, M01 RR000083, M01 RR000722, M01-RR00071, M01-RR00079,
M01-RR00083]; NIAAA NIH HHS [R01 AA016893, R01-AA16893, U01 AA013566,
U01-AA013566]; NIAID NIH HHS [AI-69432, K01 AI071754, K01-AI071754,
K23-AI-61-0320, P30 AI027757, P30 AI027767, P30 AI050410, P30 AI054999,
P30-AI27757, P30-AI27767, P30-AI50410, P30-AI54999, R24 AI067039,
R24-AI067039, U01 AI031834, U01 AI034989, U01 AI034993, U01 AI034994,
U01 AI035004, U01 AI035039, U01 AI035040, U01 AI035041, U01 AI035042,
U01 AI035043, U01 AI037613, U01 AI037984, U01 AI038855, U01 AI038858,
U01 AI042590, U01 AI068634, U01 AI068636, U01 AI069432, U01 AI069918,
U01 AI069918-01, U01-AI069918, U01-AI31834, U01-AI34989, U01-AI34993,
U01-AI34994, U01-AI35004, U01-AI35039, U01-AI35040, U01-AI35041,
U01-AI35042, U01-AI35043, U01-AI37613, U01-AI37984, U01-AI38855,
U01-AI38858, U01-AI42590, U01-AI68634, U01-AI68636, UM1 AI069432]; NICHD
NIH HHS [U01 HD032632, U01-HD32632]; NIDA NIH HHS [R01-DA11602, R01
DA004334, R01 DA011602, R01 DA012568, R01-DA04334, R01-DA12568, R56
DA004334]; NIMH NIH HHS [R01 MH054907, R01-MH54907]; PHS HHS
[AHQ290-01-0012, K24-00432]
NR 28
TC 28
Z9 28
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 1058-4838
J9 CLIN INFECT DIS
JI Clin. Infect. Dis.
PD NOV 15
PY 2009
VL 49
IS 10
BP 1582
EP 1590
DI 10.1086/644768
PG 9
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EH
UT WOS:000271146200021
PM 19845473
ER
PT J
AU Rajagopal, R
Huang, J
Dattilo, LK
Kaartinen, V
Mishina, Y
Deng, CX
Umans, L
Zwijsen, A
Roberts, AB
Beebe, DC
AF Rajagopal, Ramya
Huang, Jie
Dattilo, Lisa K.
Kaartinen, Vesa
Mishina, Yuji
Deng, Chu-Xia
Umans, Lieve
Zwijsen, An
Roberts, Anita B.
Beebe, David C.
TI The type I BMP receptors, Bmpr1a and Acvr1, activate multiple signaling
pathways to regulate lens formation
SO DEVELOPMENTAL BIOLOGY
LA English
DT Article
DE Lens formation; Bone morphogenetic proteins; Smads
ID EARLY MOUSE EMBRYO; CONDITIONAL KNOCKOUT; PRESUMPTIVE LENS;
CHICK-EMBRYO; DEFECTS; PROLIFERATION; INDUCTION; CELLS; MICE; EYE
AB BMPs play multiple roles in development and BMP signaling is essential for lens formation. However, the mechanisms by which BMP receptors function in vertebrate development are incompletely understood. To determine the downstream effectors of BMP signaling and their functions in the ectoderm that will form the lens, we deleted the genes encoding the type 1 BMP receptors. Bmpr1a and Acvr1, and the canonical transducers of BMP signaling, Smad4, Smad1 and Smad5. Bmpr1a and Acvr1 regulated cell survival and proliferation, respectively. Absence of both receptors interfered with the expression of proteins involved in normal lens development and prevented lens formation, demonstrating that BMPs induce lens formation by acting directly on the prospective lens ectoderm. Remarkably, the canonical Smad signaling pathway was not needed for most of these processes. Lens formation, placode cell proliferation, the expression of FoxE3, a lens-specific transcription factor, and the lens protein, alpha A-crystallin were regulated by BMP receptors in a Smad-independent manner. Placode cell survival was promoted by R-Smad signaling, but in a manner that did not involve Smad4. Of the responses tested, only maintaining a high level of Sox2 protein, a transcription factor expressed early in placode formation, required the canonical Smad pathway. A key function of Smad-independent BMP receptor signaling may be reorganization of actin cytoskeleton to drive lens invagination. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Kaartinen, Vesa] Univ So Calif, Childrens Hosp Los Angeles, Keck Sch Med, Dev Biol Program,Dept Pathol & Surg, Los Angeles, CA 90027 USA.
[Mishina, Yuji] Natl Inst Environm Hlth Sci, Lab Reprod & Dev Toxicol, Mol Dev Biol Grp, Res Triangle Pk, NC USA.
[Deng, Chu-Xia] NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD USA.
[Umans, Lieve; Zwijsen, An] VIB, Dept Mol & Dev Genet, Lab Mol Biol Celgen, Louvain, Belgium.
[Umans, Lieve; Zwijsen, An] Katholieke Univ Leuven, Ctr Human Genet, Lab Mol Biol Celgen, Louvain, Belgium.
[Roberts, Anita B.] NCI, Lab Cell Regulat & Carcinogenesis, NIH, Bethesda, MD 20892 USA.
[Rajagopal, Ramya; Huang, Jie; Dattilo, Lisa K.; Beebe, David C.] Washington Univ, Dept Ophthalmol, St Louis, MO 63110 USA.
[Rajagopal, Ramya; Huang, Jie; Dattilo, Lisa K.; Beebe, David C.] Washington Univ, Dept Visual Sci, St Louis, MO 63110 USA.
RP Beebe, DC (reprint author), Washington Univ, Dept Ophthalmol & Visual Sci, 660 S Euclid Ave,Campus Box 8096,Rm 101 McMillan, St Louis, MO 63110 USA.
EM beebe@wustl.edu
RI Huang, Jie/D-7728-2014; deng, chuxia/N-6713-2016;
OI Kaartinen, Vesa/0000-0002-9432-510X
FU Research to Prevent Blindness; NIH [EY02687, EY04853, 5R01HL074862,
5R01DE013085]
FX We thank Drs. Ruth Ashery-Padan and Judy West-Mays for providing the
Le-Cre mice and are grateful for the expert technical assistance of
Chenghua Wu and Mary Feldmeier with genotyping and Belinda McMahan and
Jean Jones with histology and immunohistochemistry. We are indebted to
Drs. Jeffrey Miner and Peter Carlsson for the laminin and FoxE3
antibodies, respectively. This work was supported by an unrestricted
grant from Research to Prevent Blindness and NIH Core Grant EY02687 to
the Department of Ophthalmology and Visual Sciences, NIH grant EY04853
to DCB and 5R01HL074862 and 5R01DE013085 to VK. Drs. Lieve Umans and An
Zwijsen are indebted to Dr. Danny Huylebroeck for his support of their
work.
NR 44
TC 49
Z9 51
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 0012-1606
J9 DEV BIOL
JI Dev. Biol.
PD NOV 15
PY 2009
VL 335
IS 2
BP 305
EP 316
DI 10.1016/j.ydbio.2009.08.027
PG 12
WC Developmental Biology
SC Developmental Biology
GA 517GJ
UT WOS:000271601000002
PM 19733164
ER
PT J
AU Xie, JC
Sun, BG
Wang, SB
Ito, Y
AF Xie, Jianchun
Sun, Baoguo
Wang, Shuaibin
Ito, Yoichiro
TI Isolation and purification of nootkatone from the essential oil of
fruits of Alpinia oxyphylla Miquel by high-speed counter-current
chromatography
SO FOOD CHEMISTRY
LA English
DT Article
DE Counter-current chromatography; Alpinia oxyphylla Miquel;
Sesquiterpenoid; Nootkatone; Flavor; Bioactive component
ID PREPARATIVE ISOLATION; SEPARATION
AB HSCCC technique in a semi-preparative scale was successfully applied in isolation and purification of nootkatone from the essential oil of fruits of Alpinia oxyphylla Miquel. Twelve kinds of two-phase solvent systems. consisting of seven non-aqueous and five organic-aqueous solvent systems, were selected with not only suitable partition coefficients of nootkatone but also suitable separation factors between nootkatone and valencene, the dominant impurity in the essential oil. Further on HSCCC, n-hexane-chloroform-acetonitrile (10:1:10, v/v) amongst the non-aqueous solvent systems and n-hexane-methanol-water (5:4:1, v/v) amongst the organic-aqueous solvent systems were separately screened out. However, n-hexane-methanol-water (5:4:1, v/v) was thought optimal due to quite shorter elution time and better HSCCC peak form. By eluting the lower phase of this solvent system in head-tail mode, 3.1 mg of nootkatone was obtained at a purity of 92.30% by GC-MS from 80 mg of crude essential oil in one step operation in less than 4 h. The chemical structure of nootkatone fraction was confirmed by EI-MS and (1)H NMR. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Xie, Jianchun; Sun, Baoguo; Wang, Shuaibin] Beijing Technol & Business Univ, Sch Chem & Environm Engn, Beijing 100048, Peoples R China.
[Ito, Yoichiro] NHLBI, Bioseparat Technol Biochem & Biophys Ctr, NIH, Bethesda, MD 20892 USA.
RP Xie, JC (reprint author), Beijing Technol & Business Univ, Sch Chem & Environm Engn, Beijing 100048, Peoples R China.
EM xjchun@th.btbu.edu.cn
FU Beijing Municipal Talent Development Organization [20051D0500310];
National Natural Science Foundation of China [NSFC20676003]
FX The present work was supported by Beijing Municipal Talent Development
Organization (No. 20051D0500310) and National Natural Science Foundation
of China (NSFC20676003).
NR 16
TC 20
Z9 22
U1 2
U2 23
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0308-8146
J9 FOOD CHEM
JI Food Chem.
PD NOV 15
PY 2009
VL 117
IS 2
BP 375
EP 380
DI 10.1016/j.foodchem.2009.04.011
PG 6
WC Chemistry, Applied; Food Science & Technology; Nutrition & Dietetics
SC Chemistry; Food Science & Technology; Nutrition & Dietetics
GA 465RP
UT WOS:000267604800031
PM 20209043
ER
PT J
AU Qian, L
Hu, XM
Zhang, D
Snyder, A
Wu, HM
Li, YC
Wilson, B
Lu, RB
Hong, JS
Flood, PM
AF Qian, Li
Hu, Xiaoming
Zhang, Dan
Snyder, Amanda
Wu, Hung-Ming
Li, Yachen
Wilson, Belinda
Lu, Ru-Band
Hong, Jau-Shyong
Flood, Patrick M.
TI beta 2 Adrenergic Receptor Activation Induces Microglial NADPH Oxidase
Activation and Dopaminergic Neurotoxicity Through an
ERK-Dependent/Protein Kinase A-Independent Pathway
SO GLIA
LA English
DT Article
DE beta 2AR; oxidative stress; neuroinflammation
ID LIPOPOLYSACCHARIDE-INDUCED NEUROTOXICITY; BETA-ADRENERGIC AGONISTS;
TUMOR-NECROSIS-FACTOR; BETA(2)-ADRENERGIC RECEPTOR; PARKINSONS-DISEASE;
PROTEIN-KINASE; RESPIRATORY BURST; TETRAZOLIUM SALT; RAT-BRAIN; CELLS
AB Activation of the beta 2 adrenergic receptor (beta 2AR) on immune cells has been reported to possess anti-inflammatory properties, however, the pro-inflammatory properties of beta 2AR activation remain unclear. In this study, using rat primary mesencephalic neuron-glia cultures, we report that salmeterol, a long-acting beta 2AR agonist, selectively induces dopaminergic (DA) neurotoxicity through its ability to activate microglia. Salmeterol selectively increased the production of reactive oxygen species (ROS) by NADPH oxidase (PHOX), the major superoxide-producing enzyme in microglia. A key role of PHOX in mediating salmeterol-induced neurotoxicity was demonstrated by the inhibition of DA neurotoxicity in cultures pretreated with diphenylene-iodonium (DPI), an inhibitor of PHOX activity. Mechanistic studies revealed the activation of microglia by salmeterol results in the selective phosphorylation of ERK, a signaling pathway required for the translocation of the PHOX cytosolic subunit p47(phox) to the cell membrane. Furthermore, we found ERK inhibition, but not protein kinase A (PKA) inhibition, significantly abolished salmeterol-induced superoxide production, p47(phox) translocation, and its ability to mediate neurotoxicity. Together, these findings indicate that beta 2AR activation induces microglial PHOX activation and DA neurotoxicity through an ERK-dependent/PKA-independent pathway. (C) 2009 Wiley-Liss, Inc.
C1 [Qian, Li; Snyder, Amanda; Flood, Patrick M.] Univ N Carolina, Comprehens Ctr Inflammatory Disorders, Chapel Hill, NC 27599 USA.
[Qian, Li; Hu, Xiaoming; Zhang, Dan; Wu, Hung-Ming; Li, Yachen; Wilson, Belinda; Hong, Jau-Shyong] NIEHS, Neuropharmacol Sect, Pharmacol Lab, NIH, Res Triangle Pk, NC 27709 USA.
[Wu, Hung-Ming; Lu, Ru-Band] Natl Cheng Kung Univ, Coll Med, Inst Behav Med, Tainan 70101, Taiwan.
[Wu, Hung-Ming; Lu, Ru-Band] Natl Cheng Kung Univ, Coll Med, Dept Psychiat, Tainan 70101, Taiwan.
RP Flood, PM (reprint author), Univ N Carolina, Comprehens Ctr Inflammatory Disorders, Chapel Hill, NC 27599 USA.
EM pat_flood@dentistry.unc.edu
FU National Institute for Dental and Craniofacial Research [DE-13079];
NIH/NIEHS
FX Grant sponsor: National Institute for Dental and Craniofacial Research;
Grant number: DE-13079; Grant sponsor: NIH/NIEHS (Intramural Research
Program).
NR 46
TC 16
Z9 16
U1 0
U2 6
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0894-1491
J9 GLIA
JI Glia
PD NOV 15
PY 2009
VL 57
IS 15
BP 1600
EP 1609
DI 10.1002/glia.20873
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 508MG
UT WOS:000270934900003
PM 19330844
ER
PT J
AU Antoniou, AC
Sinilnikova, OM
McGuffog, L
Healey, S
Nevanlinna, H
Heikkinen, T
Simard, J
Spurdle, AB
Beesley, J
Chen, XQ
Neuhausen, SL
Ding, YC
Couch, FJ
Wang, XS
Fredericksen, Z
Peterlongo, P
Peissel, B
Bonanni, B
Viel, A
Bernard, L
Radice, P
Szabo, CI
Foretova, L
Zikan, M
Claes, K
Greene, MH
Mai, PL
Rennert, G
Lejbkowicz, F
Andrulis, IL
Ozcelik, H
Glendon, G
Gerdes, AM
Thomassen, M
Sunde, L
Caligo, MA
Laitman, Y
Kontorovich, T
Cohen, S
Kaufman, B
Dagan, E
Baruch, RG
Friedman, E
Harbst, K
Barbany-Bustinza, G
Rantala, J
Ehrencrona, H
Karlsson, P
Domchek, SM
Nathanson, KL
Osorio, A
Blanco, I
Lasa, A
Benitez, J
Hamann, U
Hogervorst, FBL
Rookus, MA
Collee, JM
Devilee, P
Ligtenberg, MJ
van der Luijt, RB
Aalfs, CM
Waisfisz, Q
Wijnen, J
van Roozendaal, CEP
Peock, S
Cook, M
Frost, D
Oliver, C
Platte, R
Evans, DG
Lalloo, F
Eeles, R
Izatt, L
Davidson, R
Chu, C
Eccles, D
Cole, T
Hodgson, S
Godwin, AK
Stoppa-Lyonnet, D
Buecher, B
Leone, M
Bressac-de Paillerets, B
Remenieras, A
Caron, O
Lenoir, GM
Sevenet, N
Longy, M
Ferrer, SF
Prieur, F
Goldgar, D
Miron, A
John, EM
Buys, SS
Daly, MB
Hopper, JL
Terry, MB
Yassin, Y
Singer, C
Gschwantler-Kaulich, D
Staudigl, C
Hansen, TVO
Barkardottir, RB
Kirchhoff, T
Pal, P
Kosarin, K
Offit, K
Piedmonte, M
Rodriguez, GC
Wakeley, K
Boggess, JF
Basil, J
Schwartz, PE
Blank, SV
Toland, AE
Montagna, M
Casella, C
Imyanitov, EN
Allavena, A
Schmutzler, RK
Versmold, B
Engel, C
Meindl, A
Ditsch, N
Arnold, N
Niederacher, D
Deissler, H
Fiebig, B
Suttner, C
Schonbuchner, I
Gadzicki, D
Caldes, T
de la Hoya, M
Pooley, KA
Easton, DF
Chenevix-Trench, G
AF Antoniou, Antonis C.
Sinilnikova, Olga M.
McGuffog, Lesley
Healey, Sue
Nevanlinna, Heli
Heikkinen, Tuomas
Simard, Jacques
Spurdle, Amanda B.
Beesley, Jonathan
Chen, Xiaoqing
Neuhausen, Susan L.
Ding, Yuan C.
Couch, Fergus J.
Wang, Xianshu
Fredericksen, Zachary
Peterlongo, Paolo
Peissel, Bernard
Bonanni, Bernardo
Viel, Alessandra
Bernard, Loris
Radice, Paolo
Szabo, Csilla I.
Foretova, Lenka
Zikan, Michal
Claes, Kathleen
Greene, Mark H.
Mai, Phuong L.
Rennert, Gad
Lejbkowicz, Flavio
Andrulis, Irene L.
Ozcelik, Hilmi
Glendon, Gord
Gerdes, Anne-Marie
Thomassen, Mads
Sunde, Lone
Caligo, Maria A.
Laitman, Yael
Kontorovich, Tair
Cohen, Shimrit
Kaufman, Bella
Dagan, Efrat
Baruch, Ruth Gershoni
Friedman, Eitan
Harbst, Katja
Barbany-Bustinza, Gisela
Rantala, Johanna
Ehrencrona, Hans
Karlsson, Per
Domchek, Susan M.
Nathanson, Katherine L.
Osorio, Ana
Blanco, Ignacio
Lasa, Adriana
Benitez, Javier
Hamann, Ute
Hogervorst, Frans B. L.
Rookus, Matti A.
Collee, J. Margriet
Devilee, Peter
Ligtenberg, Marjolijn J.
van der Luijt, Rob B.
Aalfs, Cora M.
Waisfisz, Quinten
Wijnen, Juul
van Roozendaal, Cornelis E. P.
Peock, Susan
Cook, Margaret
Frost, Debra
Oliver, Clare
Platte, Radka
Evans, D. Gareth
Lalloo, Fiona
Eeles, Rosalind
Izatt, Louise
Davidson, Rosemarie
Chu, Carol
Eccles, Diana
Cole, Trevor
Hodgson, Shirley
Godwin, Andrew K.
Stoppa-Lyonnet, Dominique
Buecher, Bruno
Leone, Melanie
Bressac-de Paillerets, Brigitte
Remenieras, Audrey
Caron, Olivier
Lenoir, Gilbert M.
Sevenet, Nicolas
Longy, Michel
Ferrer, Sandra Fert
Prieur, Fabienne
Goldgar, David
Miron, Alexander
John, Esther M.
Buys, Saundra S.
Daly, Mary B.
Hopper, John L.
Terry, Mary Beth
Yassin, Yosuf
Singer, Christian
Gschwantler-Kaulich, Daphne
Staudigl, Christine
Hansen, Thomas V. O.
Barkardottir, Rosa Bjork
Kirchhoff, Tomas
Pal, Prodipto
Kosarin, Kristi
Offit, Kenneth
Piedmonte, Marion
Rodriguez, Gustavo C.
Wakeley, Katie
Boggess, John F.
Basil, Jack
Schwartz, Peter E.
Blank, Stephanie V.
Toland, Amanda E.
Montagna, Marco
Casella, Cinzia
Imyanitov, Evgeny N.
Allavena, Anna
Schmutzler, Rita K.
Versmold, Beatrix
Engel, Christoph
Meindl, Alfons
Ditsch, Nina
Arnold, Norbert
Niederacher, Dieter
Deissler, Helmut
Fiebig, Britta
Suttner, Christian
Schoenbuchner, Ines
Gadzicki, Dorothea
Caldes, Trinidad
de la Hoya, Miguel
Pooley, Karen A.
Easton, Douglas F.
Chenevix-Trench, Georgia
CA Kathleen Cuningham Fdn Consortium
OCGN
HEBON
EMBRACE
GEMO
Breast Canc Family Registry
CIMBA
TI Common variants in LSP1, 2q35 and 8q24 and breast cancer risk for BRCA1
and BRCA2 mutation carriers
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ESTROGEN-RECEPTOR; OVARIAN-CANCER;
SUSCEPTIBILITY; GENE; POPULATION; EXPRESSION; ALLELES
AB Genome-wide association studies of breast cancer have identified multiple single nucleotide polymorphisms (SNPs) that are associated with increased breast cancer risks in the general population. In a previous study, we demonstrated that the minor alleles at three of these SNPs, in FGFR2, TNRC9 and MAP3K1, also confer increased risks of breast cancer for BRCA1 or BRCA2 mutation carriers. Three additional SNPs rs3817198 at LSP1, rs13387042 at 2q35 and rs13281615 at 8q24 have since been reported to be associated with breast cancer in the general population, and in this study we evaluated their association with breast cancer risk in 9442 BRCA1 and 5665 BRCA2 mutation carriers from 33 study centres. The minor allele of rs3817198 was associated with increased breast cancer risk only for BRCA2 mutation carriers [hazard ratio (HR) = 1.16, 95% CI: 1.07-1.25, P-trend = 2.8 x 10(-4)]. The best fit for the association of SNP rs13387042 at 2q35 with breast cancer risk was a dominant model for both BRCA1 and BRCA2 mutation carriers (BRCA1: HR = 1.14, 95% CI: 1.04-1.25, P = 0.0047; BRCA2: HR = 1.18 95% CI: 1.04-1.33, P = 0.0079). SNP rs13281615 at 8q24 was not associated with breast cancer for either BRCA1 or BRCA2 mutation carriers, but the estimated association for BRCA2 mutation carriers (per-allele HR = 1.06, 95% CI: 0.98-1.14) was consistent with odds ratio estimates derived from population-based case-control studies. The LSP1 and 2q35 SNPs appear to interact multiplicatively on breast cancer risk for BRCA2 mutation carriers. There was no evidence that the associations vary by mutation type depending on whether the mutated protein is predicted to be stable or not.
C1 [Antoniou, Antonis C.; McGuffog, Lesley; Peock, Susan; Cook, Margaret; Frost, Debra; Oliver, Clare; Platte, Radka; Pooley, Karen A.; Easton, Douglas F.; EMBRACE] Univ Cambridge, Dept Publ Hlth & Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
[Sinilnikova, Olga M.; Leone, Melanie] Univ Lyon, CNRS, Hosp Civils Lyon,Ctr Leon Berard,UMR5201, Unite Mixte Genet Constitut Canc Frequents, Lyon, France.
[Healey, Sue; Spurdle, Amanda B.; Beesley, Jonathan; Chen, Xiaoqing; Chenevix-Trench, Georgia] Queensland Inst Med Res, Brisbane, Qld 4029, Australia.
[Nevanlinna, Heli; Heikkinen, Tuomas] Univ Helsinki, Cent Hosp, Dept Obstet & Gynecol, FIN-00290 Helsinki, Finland.
[Simard, Jacques] Univ Laval, Quebec City, PQ, Canada.
[Simard, Jacques] Univ Quebec, Ctr Hosp, Canada Res Chair Oncogenet, Canc Genom Lab, Quebec City, PQ, Canada.
[Kathleen Cuningham Fdn Consortium] Peter MacCallum Canc Inst, Melbourne, Vic 3002, Australia.
[Neuhausen, Susan L.; Ding, Yuan C.] Univ Calif Irvine, Dept Epidemiol, Irvine, CA USA.
[Couch, Fergus J.; Wang, Xianshu; Fredericksen, Zachary] Mayo Clin, Rochester, MN USA.
[Peterlongo, Paolo; Peissel, Bernard; Radice, Paolo] Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
[Peterlongo, Paolo; Radice, Paolo] Fdn Ist FIRC Oncol Molecolare, Milan, Italy.
[Bonanni, Bernardo; Bernard, Loris] Ist Europeo Oncol, Milan, Italy.
[Viel, Alessandra] IRCCS, Ctr Riferimento Oncol, Aviano, Italy.
[Bernard, Loris] Cogentech, Consortium Genom Technol, Milan, Italy.
[Szabo, Csilla I.] Mayo Clin, Coll Med, Dept Lab Med & Pathol, Rochester, MN USA.
[Foretova, Lenka] Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
[Zikan, Michal] Charles Univ Prague, Dept Biochem & Expt Oncol, Fac Med 1, Prague, Czech Republic.
[Claes, Kathleen] Ghent Univ Hosp, Ctr Med Genet, B-9000 Ghent, Belgium.
[Greene, Mark H.; Mai, Phuong L.] US Natl Canc Inst, Clin Genet Branch, Rockville, MD USA.
[Rennert, Gad; Lejbkowicz, Flavio] CHS Natl Canc Control Ctr, Haifa, Israel.
[Rennert, Gad; Lejbkowicz, Flavio] Carmel Hosp, Dept Community Med & Epidemiol, Haifa, Israel.
[Rennert, Gad; Lejbkowicz, Flavio] B Rappaport Fac Med, Haifa, Israel.
[Andrulis, Irene L.; Glendon, Gord; OCGN] Canc Care Ontario, Ontario Canc Genet Network, Toronto, ON M5G 2L7, Canada.
[Andrulis, Irene L.] Mt Sinai Hosp, Fred A Litwin Ctr Canc Genet, Samuel Lunenfeld Res Inst, Toronto, ON, Canada.
[Andrulis, Irene L.] Univ Toronto, Dept Mol Genet, Toronto, ON, Canada.
[Gerdes, Anne-Marie; Thomassen, Mads] Odense Univ Hosp, Dept Biochem Pharmacol & Genet, DK-5000 Odense, Denmark.
[Sunde, Lone] Aarhus Univ Hosp, Dept Clin Genet, DK-8000 Aarhus, Denmark.
[Caligo, Maria A.] Univ Pisa, Div Surg Mol & Ultrastructural Pathol, Dept Oncol, Pisa, Italy.
[Caligo, Maria A.] Pisa Univ Hosp, Pisa, Italy.
[Laitman, Yael; Kontorovich, Tair; Cohen, Shimrit; Friedman, Eitan] Chaim Sheba Med Ctr, Susanne Levy Gertner Oncogenet Unit, IL-52621 Tel Hashomer, Israel.
[Kaufman, Bella] Chaim Sheba Med Ctr, Inst Oncol, IL-52621 Tel Hashomer, Israel.
[Kaufman, Bella; Friedman, Eitan] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel.
[Dagan, Efrat; Baruch, Ruth Gershoni] Rambam Med Ctr, Genet Inst, Haifa, Israel.
[Harbst, Katja] Lund Univ, Dept Oncol, S-22100 Lund, Sweden.
[Barbany-Bustinza, Gisela; Rantala, Johanna] Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden.
[Ehrencrona, Hans] Uppsala Univ, Dept Genet & Pathol, Uppsala, Sweden.
[Karlsson, Per] Sahlgrenska Univ, Dept Oncol, Gothenburg, Sweden.
[Domchek, Susan M.; Nathanson, Katherine L.] Univ Penn, Philadelphia, PA 19104 USA.
[Osorio, Ana; Benitez, Javier] Ctr Invest Biomed Red Enfermedades Raras CIBERERE, Inst Salud Carlos III, Madrid, Spain.
[Osorio, Ana; Benitez, Javier] Spanish Natl Canc Ctr CNIO, Human Canc Genet Programme, Human Genet Grp, Madrid, Spain.
[Blanco, Ignacio] Catalan Inst Oncol ICO, Canc Genet Counseling Program, Barcelona, Spain.
[Lasa, Adriana] Hosp Santa Creu & Sant Pau, Genet Serv, Barcelona, Spain.
[Hamann, Ute] Deutsch Krebsforschungszentrum, Neuenheimer Feld 580 69120, D-6900 Heidelberg, Germany.
[Hogervorst, Frans B. L.] Netherlands Canc Inst, Dept Pathol, Family Canc Clin, NL-1066 CX Amsterdam, Netherlands.
[Rookus, Matti A.] Netherlands Canc Inst, Dept Epidemiol, Amsterdam, Netherlands.
[Collee, J. Margriet] Erasmus Univ, Dept Clin Genet, Rotterdam Family Canc Clin, Med Ctr, NL-3000 DR Rotterdam, Netherlands.
[Devilee, Peter] Dept Genet Epidemiol, Leiden, Netherlands.
[Wijnen, Juul] Leiden Univ, Med Ctr, Ctr Human & Clin Genet, Leiden, Netherlands.
[Ligtenberg, Marjolijn J.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6525 ED Nijmegen, Netherlands.
[van der Luijt, Rob B.] Univ Utrecht, Med Ctr, Dept Clin Mol Genet, NL-3508 TC Utrecht, Netherlands.
[Aalfs, Cora M.] Univ Amsterdam, Acad Med Ctr, Dept Clin Genet, NL-1105 AZ Amsterdam, Netherlands.
[Waisfisz, Quinten] Vrije Univ Amsterdam, Med Ctr, Dept Clin Genet, Amsterdam, Netherlands.
[van Roozendaal, Cornelis E. P.] Univ Med Ctr, Dept Clin Genet, Maastricht, Netherlands.
[Evans, D. Gareth; Lalloo, Fiona] Cent Manchester Univ Hosp, NHS Fdn Trust, Manchester Acad Hlth Sci Ctr, Manchester, Lancs, England.
[Eeles, Rosalind] Inst Canc Res, Translat Canc Genet Team, London SW3 6JB, England.
[Eeles, Rosalind] Royal Marsden NHS Fdn Trust, London, England.
[Izatt, Louise] Guys Hosp, Clin Genet, London SE1 9RT, England.
[Davidson, Rosemarie] Ferguson Smith Ctr Clin Genet, Glasgow, Lanark, Scotland.
[Chu, Carol] Yorkshire Reg Genet Serv, Leeds, W Yorkshire, England.
[Eccles, Diana] Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England.
[Cole, Trevor] Birmingham Womens Hosp Healthcare, NHS Trust, W Midlands Reg Genet Serv, Birmingham, W Midlands, England.
[Hodgson, Shirley] Univ London, Dept Canc Genet, St Georges Hosp, London, England.
[Godwin, Andrew K.; Daly, Mary B.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Stoppa-Lyonnet, Dominique] Univ Paris 05, Paris, France.
[Stoppa-Lyonnet, Dominique; GEMO] Inst Curie, INSERM U509, Serv Genet Oncol, Paris, France.
[Buecher, Bruno] Inst Curie, Dept Genet, Paris, France.
[Bressac-de Paillerets, Brigitte; Remenieras, Audrey; Lenoir, Gilbert M.] Inst Cancrol Gustave Roussy, Dept Genet, Villejuif, France.
[Bressac-de Paillerets, Brigitte] Inst Cancerol Gustave Roussy, INSERM U946, Villejuif, France.
[Caron, Olivier] Inst Cancerol Gustave Roussy, Dept Med, Villejuif, France.
[Lenoir, Gilbert M.] Inst Cancerol Gustave Roussy, CNRS FRE2939, Villejuif, France.
[Sevenet, Nicolas; Longy, Michel] Inst Bergonie, Lab Genet Constitutionnelle, Bordeaux, France.
[Longy, Michel] Inst Bergonie, INSERM U916, Bordeaux, France.
[Ferrer, Sandra Fert] Hop Hotel Dieu, Ctr Hosp, Lab Genet Chromosom, Chambery, France.
[Prieur, Fabienne] CHU St Etienne, Serv Genet Clin Chromosom, St Etienne, France.
[Goldgar, David] Univ Utah, Dept Dermatol, Salt Lake City, UT 84112 USA.
[Miron, Alexander; Yassin, Yosuf] Dana Farber Canc Inst, Boston, MA 02115 USA.
[John, Esther M.] No Calif Canc Ctr, Fremont, CA USA.
[John, Esther M.] Stanford Univ, Sch Med, Stanford, CA 94305 USA.
[Buys, Saundra S.] Univ Utah, Hlth Sci Ctr, Huntsman Canc Inst, Salt Lake City, UT USA.
[Hopper, John L.] Univ Melbourne, Melbourne, Australia.
[Terry, Mary Beth] Columbia Univ, New York, NY USA.
[Singer, Christian; Gschwantler-Kaulich, Daphne; Staudigl, Christine] Med Univ Vienna, Div Special Gynecol, Dept OB GYN, Vienna, Austria.
[Hansen, Thomas V. O.] Univ Copenhagen, Rigshosp, Dept Clin Biochem, DK-2100 Copenhagen, Denmark.
[Barkardottir, Rosa Bjork] Landspitali Univ Hosp, Dept Pathol, Reykjavik, Iceland.
[Kirchhoff, Tomas; Pal, Prodipto; Kosarin, Kristi; Offit, Kenneth] Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA.
[Piedmonte, Marion] Roswell Pk Canc Inst, GOG Stat & Data Ctr, Buffalo, NY 14263 USA.
[Rodriguez, Gustavo C.] Evanston NW Healthcare, NorthShore Univ Hlth Syst, Evanston, IL 60201 USA.
[Wakeley, Katie] Tufts Univ, New England Med Ctr, Boston, MA 02111 USA.
[Boggess, John F.] Univ N Carolina, Chapel Hill, NC 27599 USA.
[Basil, Jack] St Elizabeth Hosp, Edgewood, KY 41017 USA.
[Schwartz, Peter E.] Yale Univ, Sch Med, New Haven, CT 06510 USA.
[Blank, Stephanie V.] NYU, Sch Med, New York, NY 10016 USA.
[Toland, Amanda E.] Ohio State Univ, Dept Internal Med, Columbus, OH 43210 USA.
[Toland, Amanda E.] Ohio State Univ, Div Human Canc Genet, Ctr Comprehens Canc, Columbus, OH 43210 USA.
[Montagna, Marco; Casella, Cinzia] IRCCS, Ist Oncologico Veneto, Immunol & Mol Oncol Unit, Padua, Italy.
[Imyanitov, Evgeny N.] NN Petrov Inst Res Inst, St Petersburg, Russia.
[Allavena, Anna] Univ Turin, Dept Genet Biol & Biochem, Turin, Italy.
[Schmutzler, Rita K.; Versmold, Beatrix; Arnold, Norbert] Univ Cologne, Dept Obstet & Gynaecol, Div Mol Gynaeco Oncol, Cologne, Germany.
[Engel, Christoph] Univ Leipzig, Inst Med Informat Stat & Epidemiol, Leipzig, Germany.
[Meindl, Alfons] Tech Univ Munich, Dept Obstet & Gynaecol, Munich, Germany.
[Ditsch, Nina] Univ Munich, Dept Obstet & Gynecol, Munich, Germany.
Univ Schleswig Holstein, Dept Obstet & Gynaecol, Campus Kiel, Germany.
[Niederacher, Dieter] Univ Duesseldorf, Dept Obstet & Gynaecol, Mol Genet Lab, Dusseldorf, Germany.
[Deissler, Helmut] Univ Ulm, Dept Obstet & Gynaecol, Ulm, Germany.
[Fiebig, Britta] Univ Regensburg, Inst Human Genet, Regensburg, Germany.
[Suttner, Christian] Univ Heidelberg, Inst Human Genet, Heidelberg, Germany.
[Schoenbuchner, Ines] Univ Wurzburg, Inst Human Genet, D-8700 Wurzburg, Germany.
[Gadzicki, Dorothea] Med Univ, Inst Cellular & Mol Pathol, Hannover, Germany.
[Caldes, Trinidad; de la Hoya, Miguel] Hosp Clinico San Carlos 28040, Madrid, Spain.
RP Antoniou, AC (reprint author), Strangeways Res Lab, CR UK Genet Epidemiol, Cambridge CB1 8RN, England.
EM antonis@srl.cam.ac.uk
RI Spurdle, Amanda/A-4978-2011; Ehrencrona, Hans/M-5619-2014; Arnold,
Norbert/E-3012-2010; Toland, Amanda/E-4202-2011; montagna,
marco/E-2225-2012; Andrulis, Irene/E-7267-2013; Sunde, Lone/H-7402-2013;
Hoogerbrugge, Nicoline/O-1016-2013; Radice, Paolo/O-3119-2013; Blanco,
Ignacio/D-2565-2013; Ditsch, Nina/F-6267-2014; Osorio, Ana/I-4324-2014;
Bernard, Loris/K-5953-2014; GLADIEFF, Laurence/O-5129-2014; Ligtenberg,
Marjolijn/N-9666-2013; Peissel, Bernard/E-8187-2017;
OI Spurdle, Amanda/0000-0003-1337-7897; Ehrencrona,
Hans/0000-0002-5589-3622; Arnold, Norbert/0000-0003-4523-8808; montagna,
marco/0000-0002-4929-2150; Blanco, Ignacio/0000-0002-7414-7481; Osorio,
Ana/0000-0001-8124-3984; GLADIEFF, Laurence/0000-0002-6980-9719;
Ligtenberg, Marjolijn/0000-0003-1290-1474; Peissel,
Bernard/0000-0001-9233-3571; Nordling, Margareta/0000-0002-4047-4994;
Nathanson, Katherine/0000-0002-6740-0901; Eeles,
Rosalind/0000-0002-3698-6241; Sunde, Lone/0000-0002-8479-165X;
Nevanlinna, Heli/0000-0002-0916-2976; Kirchhoff,
Tomas/0000-0002-9055-2364; Evans, Gareth/0000-0002-8482-5784
FU Cancer Research UK; Associazione Italiana per la Ricerca sul Cancro
FX The CIMBA genotyping, data management and statistical analysis are
supported by Cancer Research UK. A.C.A. is a Cancer Research UK Senior
Cancer Research Fellow. We thank Ellen Goode for organizing the
distribution of the standard DNA plates.
NR 26
TC 72
Z9 74
U1 4
U2 22
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2009
VL 18
IS 22
BP 4442
EP 4456
DI 10.1093/hmg/ddp372
PG 15
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 510RB
UT WOS:000271107300019
PM 19656774
ER
PT J
AU Periasamy, S
Kolenbrander, PE
AF Periasamy, Saravanan
Kolenbrander, Paul E.
TI Mutualistic Biofilm Communities Develop with Porphyromonas gingivalis
and Initial, Early, and Late Colonizers of Enamel
SO JOURNAL OF BACTERIOLOGY
LA English
DT Article
ID FUSOBACTERIUM-NUCLEATUM; DENTAL PLAQUE; STREPTOCOCCUS-GORDONII; ORAL
BACTERIA; COAGGREGATION; SALIVA; COMMUNICATION; COLONIZATION; LACTOSE;
FLOW
AB Porphyromonas gingivalis is present in dental plaque as early as 4 h after tooth cleaning, but it is also associated with periodontal disease, a late-developing event in the microbial successions that characterize daily plaque development. We report here that P. gingivalis ATCC 33277 is remarkable in its ability to interact with a variety of initial, early, middle, and late colonizers growing solely on saliva. Integration of P. gingivalis into multispecies communities was investigated by using two in vitro biofilm models. In flow cells, bacterial growth was quantified using fluorescently conjugated antibodies against each species, and static biofilm growth on saliva-submerged polystyrene pegs was analyzed by quantitative real-time PCR using species-specific primers. P. gingivalis could not grow as a single species or together with initial colonizer Streptococcus oralis but showed mutualistic growth when paired with two other initial colonizers, Streptococcus gordonii and Actinomyces oris, as well as with Veillonella sp. (early colonizer), Fusobacterium nucleatum (middle colonizer), and Aggregatibacter actinomycetemcomitans (late colonizer). In three-species flow cells, P. gingivalis grew with Veillonella sp. and A. actinomycetemcomitans but not with S. oralis and A. actinomycetemcomitans. Also, it grew with Veillonella sp. and F. nucleatum but not with S. oralis and F. nucleatum, indicating that P. gingivalis and S. oralis are not compatible. However, P. gingivalis grew in combination with S. gordonii and S. oralis, demonstrating its ability to overcome the incompatibility when cultured with a second initially colonizing species. Collectively, these data help explain the observed presence of P. gingivalis at all stages of dental plaque development.
C1 [Periasamy, Saravanan; Kolenbrander, Paul E.] NIDCR, Oral Infect & Immun Branch, NIH, Bethesda, MD 20892 USA.
RP Kolenbrander, PE (reprint author), NIDCR, Oral Infect & Immun Branch, NIH, Bldg 30,Room 310,30 Convent Dr,MSC 4350, Bethesda, MD 20892 USA.
EM pkolenbrander@dir.nidcr.nih.gov
FU National Institute of Dental and Craniofacial Research; National
Institutes of Health
FX This research was supported in part by the Intramural Research Program
of the National Institute of Dental and Craniofacial Research, National
Institutes of Health and in part by the Colgate-Palmolive Co. CRADA.
NR 23
TC 94
Z9 100
U1 4
U2 23
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0021-9193
J9 J BACTERIOL
JI J. Bacteriol.
PD NOV 15
PY 2009
VL 191
IS 22
BP 6804
EP 6811
DI 10.1128/JB.01006-09
PG 8
WC Microbiology
SC Microbiology
GA 511UO
UT WOS:000271195300006
PM 19749049
ER
PT J
AU Kang, YS
Zhao, XH
Lovaas, J
Eisenberg, E
Greene, LE
AF Kang, Young-Shin
Zhao, Xiaohong
Lovaas, Jenna
Eisenberg, Evan
Greene, Lois E.
TI Clathrin-independent internalization of normal cellular prion protein in
neuroblastoma cells is associated with the Arf6 pathway
SO JOURNAL OF CELL SCIENCE
LA English
DT Article
DE Prion; Clathrin; Raft; Arf6
ID ENDOCYTIC PATHWAY; TRAFFICKING; DISEASE; INHIBITION; DOMAINS; TOXIN;
CARGO
AB To understand the role of clathrin-mediated endocytosis in the internalization of normal cellular prion protein (PrP(c)) in neuronal cells, N2a cells were depleted of clathrin by RNA interference. PrP(c) internalization via the constitutive endocytic pathway in the absence of Cu(2+) and the stimulated pathway in the presence of Cu(2+) were measured in both control and clathrin-depleted cells. Depletion of clathrin had almost no effect on the internalization of PrP(c) either in the presence or absence of Cu(2+), in contrast to the marked reduction observed in transferrin uptake. By contrast, the internalization of PrP(c) was inhibited by the raft-disrupting drugs filipin and nystatin, and by the dominant-negative dynamin-1 mutant dynamin-1 K44A, both in the presence and absence of Cu(2+). The internalized PrP(c) was found to colocalize with cargo that traffic in the Arf6 pathway and in large vacuoles in cells expressing the Arf6 dominant-active mutant. These results show that PrP(c) is internalized in a clathrin-independent pathway that is associated with Arf6.
C1 [Kang, Young-Shin; Zhao, Xiaohong; Lovaas, Jenna; Eisenberg, Evan; Greene, Lois E.] NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
RP Greene, LE (reprint author), NHLBI, Cell Biol Lab, NIH, Bethesda, MD 20892 USA.
EM greenel@helix.nih.gov
NR 36
TC 15
Z9 16
U1 0
U2 0
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
CAMBS, ENGLAND
SN 0021-9533
J9 J CELL SCI
JI J. Cell Sci.
PD NOV 15
PY 2009
VL 122
IS 22
BP 4062
EP 4069
DI 10.1242/jcs.046292
PG 8
WC Cell Biology
SC Cell Biology
GA 518HJ
UT WOS:000271681300007
PM 19843586
ER
PT J
AU Zhou, ZG
Wang, YL
Bryant, SH
AF Zhou, Zhigang
Wang, Yanli
Bryant, Stephen H.
TI Computational Analysis of the Cathepsin B Inhibitors Activities Through
LR-MMPBSA Binding Affinity Calculation Based on Docked Complex
SO JOURNAL OF COMPUTATIONAL CHEMISTRY
LA English
DT Article
DE cathepsin B protein; free energy of binding; virtual screening;
modeling; drug design; regression; PubChem
ID ATOM FORCE-FIELD; CYSTEINE PROTEASES; ENZYMATIC-REACTIONS;
ALZHEIMERS-DISEASE; ACCURATE DOCKING; LIGAND-BINDING; DRUG DESIGN; HIV-1
RT; MM-PBSA; CANCER
AB Cathepsin B. a ubiquitous lysosomal cysteine protease, is involved in many biological processes related to several human diseases. Inhibitors targeting the enzyme have been investigated as possible diseases treatments. A set of 37 compounds were recently found active in a high throughput screening assay to inhibit the catalytic activity of Cathepsin B, with chemical structures and biological test results available to the public in the PubChem BioAssay Database (AID 820). In this study, we compare these experimental activities to the results of theoretical predictions from binding affinity calculation with it LR-MM-PNSA approach based oil clocked complexes. Strong correlations (r(2) = 0.919 and q(2) = 0.887 for the best) are observed between the theoretical predictions and experimental biological activity. The models are cross-validated by four independent predictive experiments with randomly split compounds into training and test sets. Our results also show that the results based oil protein dimer show better correlations with experimental activity when compared to results based on monomer in the in silico calculations. (C) 2009 Wiley Periodicals, Inc.* J Comput Chem 30: 2165-2175, 2009
C1 [Zhou, Zhigang; Wang, Yanli; Bryant, Stephen H.] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
RP Bryant, SH (reprint author), NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20894 USA.
EM bryant@ncbi.nlm.nih.gov
FU Intramural NIH HHS [Z01 LM100604-04, Z99 LM999999]
NR 41
TC 7
Z9 7
U1 1
U2 17
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0192-8651
J9 J COMPUT CHEM
JI J. Comput. Chem.
PD NOV 15
PY 2009
VL 30
IS 14
BP 2165
EP 2175
DI 10.1002/jcc.21214
PG 11
WC Chemistry, Multidisciplinary
SC Chemistry
GA 496AL
UT WOS:000269939600001
PM 19242965
ER
PT J
AU Choi, CW
Chung, YJ
Slape, C
Aplan, PD
AF Choi, Chul Won
Chung, Yang Jo
Slape, Christopher
Aplan, Peter D.
TI A NUP98-HOXD13 Fusion Gene Impairs Differentiation of B and T
Lymphocytes and Leads to Expansion of Thymocytes with Partial TCRB Gene
Rearrangement
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; IN-SITU
HYBRIDIZATION; MYELODYSPLASTIC SYNDROMES; BONE-MARROW; TRANSGENIC MICE;
CELL; PROGENITOR; LINEAGE; TRANSPLANTATION
AB Expression of a NUP98-HOXD13 (NHD13) fusion gene leads to myelodysplastic syndrome in mice. In addition to ineffective hematopoiesis, we observed that NHD13 mice were lymphopenic; the lymphopenia was due to a decrease in both T and B lymphocytes. Although the pro-B cell (B220(+)/CD43(+)) populations from the NHD13 and wild-type mice were similar, the NHD13 mice showed decreased pre-B cells (B220(+)/CD43(-)), indicating impaired differentiation at the pro-B to pre-B stage. Thymi from NHD13 mice were smaller and overexpressed Hoxa cluster genes, including Hoxa7, Hoxa9, and Hoxa10. In addition, the NHD13 thymi contained fewer thymocytes, with an increased percentage of CD4(-)/CD8(-) (double-negative (DN)) cells and a decreased percentage of CD4(+)/CD8(+) (double-positive) cells; the DN1/DN2 population was increased and the DN3/DN4 population was decreased, suggesting a partial block at the DN2 to DN3 transition. To determine clonality of the thymocytes, we used degenerate RT-PCR to identify clonal Tcrb gene rearrangements. Five of six NHD13 thymi showed an unusual Tcrb gene rearrangement pattern with common, clonal DJ rearrangements, but distinct V-D junctions, suggesting a marked clonal expansion of thymocytes that had undergone a DJ rearrangement, but not completed a VDJ rearrangement. Taken together, these findings demonstrate that expression of the NHD13 transgene inhibits lymphoid as well as myeloid and erythroid differentiation, results in overexpression of Hoxa cluster genes, and leads to a precursor T cell lymphoblastic leukemia/lymphoma. The Journal of Immunology, 2009,183: 6227-6235.
C1 [Choi, Chul Won; Chung, Yang Jo; Slape, Christopher; Aplan, Peter D.] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20889 USA.
RP Aplan, PD (reprint author), Navy 8,Room 5101,8901 Wisconsin Ave, Bethesda, MD 20889 USA.
EM aplanp@mail.nih.gov
RI Slape, Christopher/H-8586-2016; Aplan, Peter/K-9064-2016
OI Slape, Christopher/0000-0002-8407-3092;
FU National Institutes of Health, National Cancer Institute
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute.
NR 30
TC 12
Z9 13
U1 0
U2 1
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2009
VL 183
IS 10
BP 6227
EP 6235
DI 10.4049/jimmunol.0901121
PG 9
WC Immunology
SC Immunology
GA 519KQ
UT WOS:000271765700024
PM 19841179
ER
PT J
AU Cohen, R
Torres, A
Ma, HT
Holowka, D
Baird, B
AF Cohen, Roy
Torres, Alexis
Ma, Hong-Tao
Holowka, David
Baird, Barbara
TI Ca2+ Waves Initiate Antigen-Stimulated Ca2+ Responses in Mast Cells
SO JOURNAL OF IMMUNOLOGY
LA English
DT Article
ID CAPACITATIVE CALCIUM-ENTRY; BASOPHILIC LEUKEMIA-CELL; ACCOMPANY
NEUTROPHIL POLARIZATION; OPERATED CRAC CHANNELS; HIGH-SPEED MICROSCOPY;
CURRENT I-CRAC; BONE-MARROW; FORMYLMETHIONYLLEUCYLPHENYLALANINE
STIMULATION; 2-AMINOETHOXYDIPHENYL BORATE; INOSITOL TRISPHOSPHATE
AB Ca2+ mobilization is central to many cellular processes, including stimulated exocytosis and cytokine production in mast cells. Using single cell stimulation by IgE-specific Ag and high-speed imaging of conventional or genetically encoded Ca2+ sensors in rat basophilic leukemia and bone marrow-derived rat mast cells, we observe Ca2+ waves that originate most frequently from the tips of extended cell protrusions, as well as Ca2+ oscillations throughout the cell that usually follow the initiating Ca2+ wave. In contrast, Ag conjugated to the tip of a micropipette stimulates local, repetitive Ca2+ puffs at the region of cell contact. Initiating Ca2+ waves are observed in most rat basophilic leukemia cells stimulated with soluble Ag and are sensitive to inhibitors of Ca2+ release from endoplasmic reticulum stores and to extracellular Ca2+, but they do not depend on store-operated Ca2+ entry. Knockdown of transient receptor potential channel (TRPC)1 and TRPC3 channel proteins by short hairpin RNA reduces the sensitivity of these cells to Ag and shifts the wave initiation site from protrusions to the cell body. Our results reveal spatially encoded Ca2+ signaling in response to immunoreceptor activation that utilizes TRPC channels to specify the initiation site of the Ca2+ response. The Journal of Immunology, 2009, 183: 6478-6488.
C1 [Cohen, Roy; Torres, Alexis; Holowka, David; Baird, Barbara] Cornell Univ, Dept Chem & Chem Biol, Ithaca, NY 14850 USA.
[Ma, Hong-Tao] NHLBI, Lab Mol Immunol, NIH, Bethesda, MD 20892 USA.
RP Holowka, D (reprint author), Cornell Univ, Dept Chem & Chem Biol, Ithaca, NY 14850 USA.
EM dah24@cornell.edu
FU National Institutes of Health [AI022449]; Nanobiotechnology Center at
Cornell [NSF:ECS-9876771]; National Heart, Lung, and Blood Institute,
National Institutes of Health
FX This work was supported by National Institutes of Health Grant AI022449
and by the Nanobiotechnology Center at Cornell (NSF:ECS-9876771).
H.-T.M. is supported by the International Program of the National Heart,
Lung, and Blood Institute, National Institutes of Health.
NR 77
TC 23
Z9 23
U1 1
U2 7
PU AMER ASSOC IMMUNOLOGISTS
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0022-1767
J9 J IMMUNOL
JI J. Immunol.
PD NOV 15
PY 2009
VL 183
IS 10
BP 6478
EP 6488
DI 10.4049/jimmunol.0901615
PG 11
WC Immunology
SC Immunology
GA 519KQ
UT WOS:000271765700051
PM 19864608
ER
PT J
AU Taha, TE
Kumwenda, J
Cole, SR
Hoover, DR
Kafulafula, G
Fowler, MG
Thigpen, MC
Li, Q
Kumwenda, NI
Mofenson, L
AF Taha, Taha E.
Kumwenda, Johnstone
Cole, Stephen R.
Hoover, Donald R.
Kafulafula, George
Fowler, Mary Glenn
Thigpen, Michael C.
Li, Qing
Kumwenda, Newton I.
Mofenson, Lynne
TI Postnatal HIV-1 Transmission after Cessation of Infant Extended
Antiretroviral Prophylaxis and Effect of Maternal Highly Active
Antiretroviral Therapy
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID BREAST-MILK; INTERRUPTION; OUTCOMES; MOTHER; WOMEN; CHILD
AB Background. The association between postnatal human immunodeficiency virus type 1 (HIV-1) transmission and maternal highly active antiretroviral therapy (HAART) after infant extended antiretroviral prophylaxis was assessed.
Methods. A follow-up study was conducted for the Post-Exposure Prophylaxis of Infants trial in Blantyre, Malawi (PEPI-Malawi). In PEPI-Malawi, breast-feeding infants of HIV-infected women were randomized at birth to receive a either control regimen (single-dose nevirapine plus 1 week of zidovudine); the control regimen plus nevirapine to age 14 weeks; or the control regimen plus nevirapine and zidovudine to age 14 weeks. Infant HIV infection, maternal CD4 cell count, and HAART use were determined. Maternal HAART use was categorized as HAART eligible but untreated (CD4 cell count of <250 cells/mu L, no HAART received), HAART eligible and treated (CD4 cell count of <250 cells/mu L, HAART received), and HAART ineligible (CD4 cell count of >= 250 cells/mu L). The incidence of HIV infection and the association between postnatal HIV transmission and maternal HAART were calculated among infants who were HIV negative at 14 weeks.
Results. Of 2318 infants, 130 (5.6%) acquired HIV infection, and 310 mothers (13.4%) received HAART. The rates of HIV transmission (in cases per 100 person-years) were as follows: for the HAART-eligible/untreated category, 10.56 (95% confidence interval [CI], 7.91-13.82); for the HAART-eligible/treated category, 1.79 (95% CI, 0.58-4.18); and for the HAART-ineligible category, 3.66 (95% CI, 2.86-4.61). The HIV transmission rate ratio for the HAART-eligible/treated category versus the HAART-eligible/untreated category, adjusted for infant prophylaxis, was 0.18 (95% CI, 0.07-0.44).
Conclusions. Postnatal HIV transmission continues after cessation of infant prophylaxis. HAART-eligible women should start treatment early for their own health and to reduce postnatal HIV transmission to their infants.
C1 [Taha, Taha E.; Li, Qing; Kumwenda, Newton I.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Fowler, Mary Glenn] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Mofenson, Lynne] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Cole, Stephen R.] Univ N Carolina, Sch Publ Hlth, Chapel Hill, NC USA.
[Hoover, Donald R.] Rutgers State Univ, Piscataway, NJ USA.
[Thigpen, Michael C.] Ctr Dis Control & Prevent, Div HIV AIDS Prevent, Natl Ctr HIV AIDS Viral Hepatitis STD & TB Preven, Atlanta, GA USA.
[Kumwenda, Johnstone; Kafulafula, George] Univ Malawi, Coll Med, Blantyre, Malawi.
RP Taha, TE (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Rm E7138,615 N Wolfe St, Baltimore, MD 21205 USA.
EM ttaha@jhsph.edu
OI Mofenson, Lynne/0000-0002-2818-9808
NR 28
TC 45
Z9 47
U1 0
U2 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2009
VL 200
IS 10
BP 1490
EP 1497
DI 10.1086/644598
PG 8
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EQ
UT WOS:000271147100002
PM 19832114
ER
PT J
AU Ripamonti, C
Orenstein, A
Kutty, G
Huang, L
Schuhegger, R
Sing, A
Fantoni, G
Atzori, C
Vinton, C
Huber, C
Conville, PS
Kovacs, JA
AF Ripamonti, Chiara
Orenstein, Abigail
Kutty, Geetha
Huang, Laurence
Schuhegger, Regina
Sing, Andreas
Fantoni, Giovanna
Atzori, Chiara
Vinton, Carol
Huber, Charles
Conville, Patricia S.
Kovacs, Joseph A.
TI Restriction Fragment Length Polymorphism Typing Demonstrates Substantial
Diversity among Pneumocystis jirovecii Isolates
SO JOURNAL OF INFECTIOUS DISEASES
LA English
DT Article
ID MAJOR SURFACE GLYCOPROTEIN; INTERNAL TRANSCRIBED SPACER; HIV-INFECTED
PATIENTS; F SP. HOMINIS; EXPRESSION SITE; CARINII; GENES; PNEUMONIA;
TRANSMISSION; REGIONS
AB Better understanding of the epidemiology and transmission patterns of human Pneumocystis should lead to improved strategies for preventing Pneumocystis pneumonia (PCP). We have developed a typing method for Pneumocystis jirovecii that is based on restriction fragment length polymorphism (RFLP) analysis after polymerase chain reaction amplification of an similar to 1300 base-pair region of the msg gene family, which comprises an estimated 50-100 genes/genome. The RFLP pattern was reproducible in samples containing >1000 msg copies/reaction and was stable over time, based on analysis of serial samples from the same patient. In our initial analysis of 48 samples, we found that samples obtained from different individuals showed distinct banding patterns; only samples obtained from the same patient showed an identical RFLP pattern. Despite this substantial diversity, samples tended to cluster on the basis of country of origin. In an evaluation of samples obtained from an outbreak of PCP in kidney transplant recipients in Germany, RFLP analysis demonstrated identical patterns in samples that were from 12 patients previously linked to this outbreak, as well as from 2 additional patients. Our results highlight the presence of a remarkable diversity in human Pneumocystis strains. RFLP may be very useful for studying clusters of PCP in immunosuppressed patients, to determine whether there is a common source of infection.
C1 [Ripamonti, Chiara; Orenstein, Abigail; Kutty, Geetha; Fantoni, Giovanna; Vinton, Carol; Kovacs, Joseph A.] NIH, Dept Crit Care Med, Ctr Clin, Bethesda, MD 20892 USA.
[Huber, Charles; Conville, Patricia S.] NIH, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
[Huang, Laurence] Univ Calif San Francisco, San Francisco Gen Hosp, Dept Med, San Francisco, CA USA.
[Schuhegger, Regina; Sing, Andreas] Bavarian Hlth & Food Safety Author Bavarian LGL, Oberschleissheim, Germany.
[Atzori, Chiara] Luigi Sacco Hosp, Dept Infect Dis, Milan, Italy.
RP Kovacs, JA (reprint author), NIH, Dept Crit Care Med, Cin Ctr, 10 Rm 2C145,MSC 1662, Bethesda, MD 20892 USA.
EM jkovacs@nih.gov
FU National Institutes of Health (NIH) Clinical Center; NIH [K24 HL087713,
R01 HL090335]
FX Financial support: Intramural Research Program of the National
Institutes of Health (NIH) Clinical Center and NIH (K24 HL087713 and R01
HL090335 to L. H.).
NR 25
TC 10
Z9 12
U1 0
U2 1
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0022-1899
J9 J INFECT DIS
JI J. Infect. Dis.
PD NOV 15
PY 2009
VL 200
IS 10
BP 1616
EP 1622
DI 10.1086/644643
PG 7
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 511EQ
UT WOS:000271147100019
PM 19795979
ER
PT J
AU Ishibashi, T
Lee, PR
Baba, H
Fields, RD
AF Ishibashi, Tomoko
Lee, Philip R.
Baba, Hiroko
Fields, R. Douglas
TI Leukemia Inhibitory Factor Regulates the Timing of Oligodendrocyte
Development and Myelination in the Postnatal Optic Nerve
SO JOURNAL OF NEUROSCIENCE RESEARCH
LA English
DT Article
DE myelin; LIF; oligodendrocyte; astrocyte; optic nerve; transcription;
OPC; differentiation
ID ACTION-POTENTIALS; PRECURSOR CELLS; SPINAL-CORD; TRANSCRIPTIONAL
CONTROL; PROTEOLIPID PROTEIN; GROWTH-FACTOR; EXPRESSION;
DIFFERENTIATION; DEMYELINATION; SURVIVAL
AB Leukemia inhibitory factor (LIF) promotes the survival of oligodendrocytes both in vitro and in an animal model of multiple sclerosis, but the possible role of LIF signaling in myelination during normal development has not been investigated. We find that LIF(-/-) mice have a pronounced myelination defect in optic nerve at postnatal day 10. Myelin basic protein (MBP)- and proteolipid protein (PLP)-positive myelin was evident throughout the optic nerve in the wild-type mice, but staining was present only at the chiasmal region in LIF(-/-) mice of the same age. Further experiments suggest that the myelination defect was a consequence of a delay in maturation of oligodendrocyte precursor cell (OPC) population. The number of Olig2-positive cells was dramatically decreased in optic nerve of LIF(-/-) mice, and the distribution of Olig2-positive cells was restricted to the chiasmal region of the nerve in a steep gradient toward the retina. Gene expression profiling and cell culture experiments revealed that OPCs from P10 optic nerve of LIF(-/-) mice remained in a highly proliferative immature stage compared with littermate controls. Interestingly by postnatal day 14, MBP immunostaining in the LIF(-/-) optic nerve was comparable to that of LIF(+/+) mice. These results suggest that, during normal development of mouse optic nerve, there is a defined developmental time window when LIF is required for correct myelination. Myelination seems to recover by postnatal day 14, so LIF is not necessary for the completion of myelination during postnatal development. (C) 2009 Wiley-Liss, Inc.
C1 [Ishibashi, Tomoko; Lee, Philip R.; Fields, R. Douglas] NIH, Nervous Syst Dev & Plast Sect, Bethesda, MD 20892 USA.
[Ishibashi, Tomoko; Baba, Hiroko] Tokyo Univ Pharm & Life Sci, Tokyo, Japan.
RP Fields, RD (reprint author), NIH, Nervous Syst Dev & Plast Sect, NICHD Bldg 35,Room 2A211,MSC 371335 Lincoln Dr, Bethesda, MD 20892 USA.
EM fieldsd@mail.nih.gov
FU NICHD; Japan Society for the Promotion of Science [19800043]
FX Contract grant sponsor: NICHD; Contract grant sponsor: Japan Society for
the Promotion of Science; Contract grant number: 19800043 (to T. I.).
NR 46
TC 29
Z9 31
U1 0
U2 2
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0360-4012
J9 J NEUROSCI RES
JI J. Neurosci. Res.
PD NOV 15
PY 2009
VL 87
IS 15
BP 3343
EP 3355
DI 10.1002/jnr.22173
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 507HR
UT WOS:000270843400012
PM 19598242
ER
PT J
AU Hoshino, Y
Katano, H
Zou, P
Hohman, P
Marques, A
Tyring, SK
Follmann, D
Cohen, JI
AF Hoshino, Yo
Katano, Harutaka
Zou, Ping
Hohman, Patricia
Marques, Adriana
Tyring, Stephen K.
Follmann, Dean
Cohen, Jeffrey I.
TI Long-Term Administration of Valacyclovir Reduces the Number of
Epstein-Barr Virus (EBV)-Infected B Cells but Not the Number of EBV DNA
Copies per B Cell in Healthy Volunteers
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID INFECTIOUS-MONONUCLEOSIS; CEREBROSPINAL-FLUID; IN-VIVO; ACYCLOVIR;
REPLICATION; RECIPIENTS; LYMPHOMA; THERAPY
AB Epstein-Barr virus (EBV) establishes a latent infection in B cells in the blood, and the latent EBV load in healthy individuals is generally stable over time, maintaining a "set point." It is unknown if the EBV load changes after long-term antiviral therapy in healthy individuals. We treated volunteers with either valacyclovir (valaciclovir) or no antiviral therapy for 1 year and measured the amount of EBV DNA in B cells every 3 months with a novel, highly sensitive assay. The number of EBV-infected B cells decreased in subjects receiving valacyclovir (half-life of 11 months; P = 0.02) but not in controls (half-life of 31 years; P = 0.86). The difference in the slopes of the lines for the number of EBV-infected B cells over time for the valacyclovir group versus the control group approached significance (P = 0.054). In contrast, the number of EBV DNA copies per B cell remained unchanged in both groups (P = 0.62 and P = 0.92 for the control and valacyclovir groups, respectively). Valacyclovir reduces the frequency of EBV-infected B cells when administered over a long period and, in theory, might allow eradication of EBV from the body if reinfection does not occur.
C1 [Hoshino, Yo; Katano, Harutaka; Zou, Ping; Cohen, Jeffrey I.] NIAID, Med Virol Sect, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Hohman, Patricia; Marques, Adriana] NIAID, Clin Studies Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Tyring, Stephen K.] Univ Texas Hlth Sci Ctr, Dept Dermatol, Houston, TX USA.
[Follmann, Dean] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
RP Cohen, JI (reprint author), NIAID, Med Virol Sect, Lab Clin Infect Dis, NIH, Bldg 10,Room 11N234,10 Ctr Dr,MSC 1888, Bethesda, MD 20892 USA.
EM jcohen@niaid.nih.gov
FU National Institute of Allergy and Infectious Diseases
FX This study was supported by the intramural research program of the
National Institute of Allergy and Infectious Diseases.
NR 24
TC 21
Z9 22
U1 1
U2 3
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2009
VL 83
IS 22
BP 11857
EP 11861
DI 10.1128/JVI.01005-09
PG 5
WC Virology
SC Virology
GA 510JJ
UT WOS:000271084100044
PM 19740997
ER
PT J
AU Migueles, SA
Weeks, KA
Nou, E
Berkley, AM
Rood, JE
Osborne, CM
Hallahan, CW
Cogliano-Shutta, NA
Metcalf, JA
McLaughlin, M
Kwan, R
Mican, JM
Davey, RT
Connors, M
AF Migueles, Stephen A.
Weeks, Kristin A.
Nou, Eric
Berkley, Amy M.
Rood, Julia E.
Osborne, Christine M.
Hallahan, Claire W.
Cogliano-Shutta, Nancy A.
Metcalf, Julia A.
McLaughlin, Mary
Kwan, Richard
Mican, Joann M.
Davey, Richard T., Jr.
Connors, Mark
TI Defective Human Immunodeficiency Virus-Specific CD8(+) T-Cell
Polyfunctionality, Proliferation, and Cytotoxicity Are Not Restored by
Antiretroviral Therapy
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID LONG-TERM NONPROGRESSORS; VIRAL REPLICATION CAPACITY; ACUTE HIV-1
INFECTION; HIV-1-INFECTED SUBJECTS; ELITE SUPPRESSORS; TYPE-1 INFECTION;
IMMUNE CONTROL; ANTIGEN LOAD; INTERLEUKIN-2; EXPRESSION
AB Identifying the functions of human immunodeficiency virus (HIV)-specific CD8(+) T cells that are not merely modulated by the level of virus but clearly distinguish patients with immune control from those without such control is of paramount importance. Features of the HIV-specific CD8(+) T-cell response in antiretroviral-treated patients ( designated Rx < 50) and untreated patients (long-term nonprogressors [LTNP]) matched for very low HIV RNA levels were comprehensively examined. The proliferative capacity of HIV-specific CD8(+) T cells was not restored in Rx < 50 to the level observed in LTNP, even though HIV-specific CD4(+) T-cell proliferation in the two patient groups was comparable. This diminished HIV-specific CD8(+) T-cell proliferation in Rx < 50 was primarily due to a smaller fraction of antigen-specific cells recruited to divide and not to the numbers of divisions that proliferating cells had undergone. Exogenous interleukin-2 (IL-2) induced proliferating cells to divide further but did not rescue the majority of antigen-specific cells with defective proliferation. In addition, differences in HIV-specific CD8(+) T-cell proliferation could not be attributed to differences in cellular subsets bearing a memory phenotype, IL-2 production, or PD-1 expression. Although polyfunctionality of HIV-specific CD8(+) T cells in Rx < 50 was not restored to the levels observed in LTNP despite prolonged suppression of HIV RNA levels, per-cell cytotoxic capacity was the functional feature that most clearly distinguished the cells of LTNP from those of Rx < 50. Taken together, these data suggest that there are selective qualitative abnormalities within the HIV-specific CD8(+) T-cell compartment that persist under conditions of low levels of antigen.
C1 [Migueles, Stephen A.; Weeks, Kristin A.; Nou, Eric; Berkley, Amy M.; Rood, Julia E.; Osborne, Christine M.; Cogliano-Shutta, Nancy A.; Metcalf, Julia A.; McLaughlin, Mary; Kwan, Richard; Mican, Joann M.; Davey, Richard T., Jr.; Connors, Mark] NIAID, LIR, NIH, Bethesda, MD 20892 USA.
[Hallahan, Claire W.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
RP Connors, M (reprint author), NIAID, LIR, NIH, 10 Rm 11B-09,10 Ctr Dr,MSC 1876, Bethesda, MD 20892 USA.
EM mconnors@niaid.nih.gov
FU Intramural Research Program of the NIH; National Institute of Allergy
and Infectious Diseases
FX This research was supported in part by the Intramural Research Program
of the NIH, National Institute of Allergy and Infectious Diseases.
NR 51
TC 88
Z9 89
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2009
VL 83
IS 22
BP 11876
EP 11889
DI 10.1128/JVI.01153-09
PG 14
WC Virology
SC Virology
GA 510JJ
UT WOS:000271084100046
PM 19726501
ER
PT J
AU Bok, K
Abente, EJ
Realpe-Quintero, M
Mitra, T
Sosnovtsev, SV
Kapikian, AZ
Green, KY
AF Bok, Karin
Abente, Eugenio J.
Realpe-Quintero, Mauricio
Mitra, Tanaji
Sosnovtsev, Stanislav V.
Kapikian, Albert Z.
Green, Kim Y.
TI Evolutionary Dynamics of GII.4 Noroviruses over a 34-Year Period
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID NORWALK-LIKE VIRUSES; POSITIVE SELECTION PRESSURE; QUASI-SPECIES
DYNAMICS; BLOOD GROUP ANTIGENS; VIRAL GASTROENTERITIS;
HUMAN-POPULATIONS; GII-4 NOROVIRUS; CAPSID PROTEIN; P2 DOMAIN; EPIDEMIC
AB Noroviruses are a major cause of epidemic gastroenteritis in children and adults, and GII.4 has been the predominant genotype since its first documented occurrence in 1987. This study examined the evolutionary dynamics of GII.4 noroviruses over more than three decades to investigate possible mechanisms by which these viruses have emerged to become predominant. Stool samples (n = 5,424) from children hospitalized at the Children's Hospital in Washington, DC, between 1974 and 1991 were screened for the presence of noroviruses by a custom multiplex real-time reverse transcription-PCR. The complete genome sequences of five GII.4 noroviruses ( three of which predate 1987 by more than a decade) in this archival collection were determined and compared to the sequences of contemporary strains. Evolutionary analysis determined that the GII.4 VP1 capsid gene evolved at a rate of 4.3 x 10(-3) nucleotide substitutions/site/year. Only six sites in the VP1 capsid protein were found to evolve under positive selection, most of them located in the shell domain. No unique mutations were observed in or around the two histoblood group antigen (HBGA) binding sites in the P region, indicating that this site has been conserved since the 1970s. The VP1 proteins from the 1974 to 1977 noroviruses contained a unique sequence of four consecutive amino acids in the P2 region, which formed an exposed protrusion on the modeled capsid structure. This protrusion and other observed sequence variations did not affect the HBGA binding profiles of recombinant virus-like particles derived from representative 1974 and 1977 noroviruses compared with more recent noroviruses. Our analysis of archival GII.4 norovirus strains suggests that this genotype has been circulating for more than three decades and provides new ancestral strain sequences for the analysis of GII.4 evolution.
C1 [Bok, Karin] NIAID, Norovirus Gastroenteritis Unit, Infect Dis Lab, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Bok, K (reprint author), NIAID, Norovirus Gastroenteritis Unit, Infect Dis Lab, NIH,Dept Hlth & Human Serv, 50 South Dr,Bldg 50,Room 6316, Bethesda, MD 20892 USA.
EM bokk@niaid.nih.gov
OI Abente, Eugenio/0000-0002-3390-2786
FU NIH; NIAID
FX This research was supported by the Intramural Research Program of the
NIH, NIAID.
NR 49
TC 135
Z9 141
U1 1
U2 9
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2009
VL 83
IS 22
BP 11890
EP 11901
DI 10.1128/JVI.00864-09
PG 12
WC Virology
SC Virology
GA 510JJ
UT WOS:000271084100047
PM 19759138
ER
PT J
AU Beliakova-Bethell, N
Terry, LJ
Bilanchone, V
DaSilva, R
Nagashima, K
Wente, SR
Sandmeyer, S
AF Beliakova-Bethell, Nadejda
Terry, Laura J.
Bilanchone, Virginia
DaSilva, Rhonda
Nagashima, Kunio
Wente, Susan R.
Sandmeyer, Suzanne
TI Ty3 Nuclear Entry Is Initiated by Viruslike Particle Docking on GLFG
Nucleoporins
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID AVIAN-SARCOMA VIRUS; TRANSFER-RNA GENES; PORE COMPLEX; NUCLEOCYTOPLASMIC
TRANSPORT; SACCHAROMYCES-CEREVISIAE; LOCALIZATION SIGNAL;
RETROTRANSPOSON TF1; NONDIVIDING CELLS; EXPORT RECEPTOR; POLY(A)(+) RNA
AB Yeast retrotransposons form intracellular particles within which replication occurs. Because fungal nuclear membranes do not break down during mitosis, similar to retroviruses infecting nondividing cells, the cDNA produced must be translocated through nuclear pore complexes. The Saccharomyces cerevisiae long terminal repeat retrotransposon Ty3 assembles its Gag3 and Gag3-Pol3 precursor polyproteins into viruslike particles in association with perinuclear P-body foci. These perinuclear clusters of Ty3 viruslike particles localized to sites of clustered nuclear pore complexes (NPCs) in a nup120 Delta mutant, indicating that Ty3 particles and NPCs interact physically. The NPC channels are lined with nucleoporins (Nups) with extended FG (Phe-Gly) motif repeat domains, further classified as FG, FxFG, or GLFG repeat types. These domains mediate partitioning of proteins between the cytoplasm and the nucleus. Here we have systematically examined the requirements for FG repeat domains in Ty3 nuclear transport. The GLFG domains interacted in vitro with virus-like particle Gag3, and this interaction was disrupted by mutations in the amino-terminal domain of Gag3, which is predicted to lie on the external surface of the particles. Accordingly, Ty3 transposition was decreased in strains with the GLFG repeats deleted. The spacer-nucleocapsid domain of Gag3, which is predicted to be internal to the particle, interacted with GLFG repeats and nucleocapsid localized to the nucleus. We conclude that Ty3 particle docking on nuclear pores is facilitated by interactions between Gag3 and GLFG Nups and that nuclear entry of the preintegration complex is further promoted by nuclear localization signals within the nucleocapsid and integrase.
C1 [Beliakova-Bethell, Nadejda; Bilanchone, Virginia; Sandmeyer, Suzanne] Univ Calif Irvine, Dept Biol Chem, Irvine, CA 92697 USA.
[Terry, Laura J.; Wente, Susan R.] Vanderbilt Univ, Dept Cell & Dev Biol, Med Ctr, Nashville, TN 37232 USA.
[DaSilva, Rhonda; Nagashima, Kunio] SAIC Frederick Inc, Elect Microscope Lab, NCI Frederick, Frederick, MD 21702 USA.
RP Sandmeyer, S (reprint author), Univ Calif Irvine, Dept Biol Chem, Irvine, CA 92697 USA.
EM sbsandme@uci.edu
FU National Institutes of Health [R01 GM33281, R01 GM051219, 5 T32 AI
07319, 5 T32 CA 009385]; National Cancer Institute [NO1-CO-12400]
FX This research was supported in part by funds from National Institutes of
Health grants R01 GM33281 to S. B. S. and R01 GM051219 to S. R. W. The
research was also funded in part by National Cancer Institute contract
NO1-CO-12400 to K. N. N. B.-B. and L. J. T. were supported by National
Institutes of Health Training Grants 5 T32 AI 07319 and 5 T32 CA 009385,
respectively.
NR 64
TC 10
Z9 10
U1 0
U2 1
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
EI 1098-5514
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2009
VL 83
IS 22
BP 11914
EP 11925
DI 10.1128/JVI.01192-09
PG 12
WC Virology
SC Virology
GA 510JJ
UT WOS:000271084100049
PM 19759143
ER
PT J
AU Lanke, KHW
van der Schaar, HM
Belov, GA
Feng, Q
Duijsings, D
Jackson, CL
Ehrenfeld, E
van Kuppeveld, FJM
AF Lanke, Kjerstin H. W.
van der Schaar, Hilde M.
Belov, George A.
Feng, Qian
Duijsings, Daniel
Jackson, Catherine L.
Ehrenfeld, Ellie
van Kuppeveld, Frank J. M.
TI GBF1, a Guanine Nucleotide Exchange Factor for Arf, Is Crucial for
Coxsackievirus B3 RNA Replication
SO JOURNAL OF VIROLOGY
LA English
DT Article
ID CELLULAR-PROTEIN SECRETION; ADP-RIBOSYLATION FACTOR;
ENDOPLASMIC-RETICULUM; BREFELDIN-A; MEMBRANE ASSOCIATION;
VIRAL-PROTEINS; POLIOVIRUS RNA; 3A PROTEINS; GOLGI; INHIBITION
AB The replication of enteroviruses is sensitive to brefeldin A (BFA), an inhibitor of endoplasmic reticulum-to-Golgi network transport that blocks activation of guanine exchange factors (GEFs) of the Arf GTPases. Mammalian cells contain three BFA-sensitive Arf GEFs: GBF1, BIG1, and BIG2. Here, we show that coxsackievirus B3 (CVB3) RNA replication is insensitive to BFA in MDCK cells, which contain a BFA-resistant GBF1 due to mutation M832L. Further evidence for a critical role of GBF1 stems from the observations that viral RNA replication is inhibited upon knockdown of GBF1 by RNA interference and that replication in the presence of BFA is rescued upon overexpression of active, but not inactive, GBF1. Overexpression of Arf proteins or Rab1B, a GTPase that induces GBF1 recruitment to membranes, failed to rescue RNA replication in the presence of BFA. Additionally, the importance of the interaction between enterovirus protein 3A and GBF1 for viral RNA replication was investigated. For this, the rescue from BFA inhibition of wild-type (wt) replicons and that of mutant replicons of both CVB3 and poliovirus (PV) carrying a 3A protein that is impaired in binding GBF1 were compared. The BFA-resistant GBF1-M832L protein efficiently rescued RNA replication of both wt and mutant CVB3 and PV replicons in the presence of BFA. However, another BFA-resistant GBF1 protein, GBF1-A795E, also efficiently rescued RNA replication of the wt replicons, but not that of mutant replicons, in the presence of BFA. In conclusion, this study identifies a critical role for GBF1 in CVB3 RNA replication, but the importance of the 3A-GBF1 interaction requires further study.
C1 [Lanke, Kjerstin H. W.; van der Schaar, Hilde M.; Duijsings, Daniel; van Kuppeveld, Frank J. M.] Radboud Univ Nijmegen, Med Ctr, Nijmegen Ctr Mol Life Sci, Dept Med Microbiol, NL-6500 HB Nijmegen, Netherlands.
[Lanke, Kjerstin H. W.; van der Schaar, Hilde M.; Duijsings, Daniel; van Kuppeveld, Frank J. M.] Radboud Univ Nijmegen, Med Ctr, Nijmegen Inst Infect Inflammat & Immun, NL-6500 HB Nijmegen, Netherlands.
[Belov, George A.; Feng, Qian; Ehrenfeld, Ellie] NIAID, NIH, Bethesda, MD 20892 USA.
[Jackson, Catherine L.] CNRS, Lab Enzymol & Biochem Struct, Gif Sur Yvette, France.
RP van Kuppeveld, FJM (reprint author), Radboud Univ Nijmegen, Med Ctr, Nijmegen Ctr Mol Life Sci, Dept Med Microbiol, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM f.vankuppeveld@ncmls.ru.nl
RI Belov, George/B-4625-2008; Jackson, Catherine/A-3421-2013
OI Belov, George/0000-0002-0892-1731; Jackson,
Catherine/0000-0002-0843-145X
FU Netherlands Organization for Scientific Research [NWO-VIDI-917.46.306,
NWO-ECHO-700.57.001]; NIAID, NIH
FX This work was partly supported by grants from The Netherlands
Organization for Scientific Research (NWO-VIDI-917.46.306 and
NWO-ECHO-700.57.001 to F. V. K.) and by the intramural research program
of the NIAID, NIH.
NR 35
TC 71
Z9 72
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0022-538X
J9 J VIROL
JI J. Virol.
PD NOV 15
PY 2009
VL 83
IS 22
BP 11940
EP 11949
DI 10.1128/JVI.01244-09
PG 10
WC Virology
SC Virology
GA 510JJ
UT WOS:000271084100051
PM 19740986
ER
PT J
AU Wang, PF
Lin, CQ
Smith, ER
Guo, H
Sanderson, BW
Wu, M
Gogol, M
Alexander, T
Seidel, C
Wiedemann, LM
Ge, K
Krumlauf, R
Shilatifard, A
AF Wang, Pengfei
Lin, Chengqi
Smith, Edwin R.
Guo, Hong
Sanderson, Brian W.
Wu, Min
Gogol, Madelaine
Alexander, Tara
Seidel, Christopher
Wiedemann, Leanne M.
Ge, Kai
Krumlauf, Robb
Shilatifard, Ali
TI Global Analysis of H3K4 Methylation Defines MLL Family Member Targets
and Points to a Role for MLL1-Mediated H3K4 Methylation in the
Regulation of Transcriptional Initiation by RNA Polymerase II
SO MOLECULAR AND CELLULAR BIOLOGY
LA English
DT Article
ID LYSINE-4 METHYLTRANSFERASE COMPLEX; MIXED-LINEAGE LEUKEMIA; HISTONE-H3
LYSINE-4; GENE-EXPRESSION; H2B MONOUBIQUITINATION; HUMAN GENOME;
CHROMATIN; COMPASS; TRITHORAX; PROTEIN
AB A common landmark of activated genes is the presence of trimethylation on lysine 4 of histone H3 (H3K4) at promoter regions. Set1/COMPASS was the founding member and is the only H3K4 methylase in Saccharomyces cerevisiae; however, in mammals, at least six H3K4 methylases, Set1A and Set1B and MLL1 to MLL4, are found in COMPASS-like complexes capable of methylating H3K4. To gain further insight into the different roles and functional targets for the H3K4 methylases, we have undertaken a genome-wide analysis of H3K4 methylation patterns in wild-type Mll1(+/+) and Mll1(-/-) mouse embryonic fibroblasts (MEFs). We found that Mll1 is required for the H3K4 trimethylation of less than 5% of promoters carrying this modification. Many of these genes, which include developmental regulators such as Hox genes, show decreased levels of RNA polymerase II recruitment and expression concomitant with the loss of H3K4 methylation. Although Mll1 is only required for the methylation of a subset of Hox genes, menin, a component of the Mll1 and Mll2 complexes, is required for the overwhelming majority of H3K4 methylation at Hox loci. However, the loss of MLL3/MLL4 and/or the Set1 complexes has little to no effect on the H3K4 methylation of Hox loci or their expression levels in these MEFs. Together these data provide insight into the redundancy and specialization of COMPASS-like complexes in mammals and provide evidence for a possible role for Mll1-mediated H3K4 methylation in the regulation of transcriptional initiation.
C1 [Wang, Pengfei; Lin, Chengqi; Smith, Edwin R.; Sanderson, Brian W.; Wu, Min; Gogol, Madelaine; Alexander, Tara; Seidel, Christopher; Wiedemann, Leanne M.; Krumlauf, Robb; Shilatifard, Ali] Stowers Inst Med Res, Kansas City, MO 64110 USA.
[Guo, Hong; Ge, Kai] NIDDK, Nucl Receptor Biol Sect, Clin Endocrinol Branch, NIH, Bethesda, MD 20892 USA.
[Wiedemann, Leanne M.] Univ Kansas, Sch Med, Dept Pathol & Lab Med, Kansas City, KS USA.
[Krumlauf, Robb] Univ Kansas, Sch Med, Dept Anat & Cell Biol, Kansas City, KS USA.
RP Shilatifard, A (reprint author), Stowers Inst Med Res, 1000 East 50th St, Kansas City, MO 64110 USA.
EM ASH@Stowers.org
OI Ge, Kai/0000-0002-7442-5138
FU NCI [5R01CA089455]; Stowers Institute for Medical Research
FX This work was supported by grants from the NCI to A. S. (5R01CA089455)
and by support of A. S. and R. K. by the Stowers Institute for Medical
Research.
NR 60
TC 163
Z9 167
U1 3
U2 13
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 0270-7306
J9 MOL CELL BIOL
JI Mol. Cell. Biol.
PD NOV 15
PY 2009
VL 29
IS 22
BP 6074
EP 6085
DI 10.1128/MCB.00924-09
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 511ZB
UT WOS:000271209600009
PM 19703992
ER
PT J
AU Zou, QH
Wu, CW
Stein, EA
Zang, YF
Yang, YH
AF Zou, Qihong
Wu, Changwei W.
Stein, Elliot A.
Zang, Yufeng
Yang, Yihong
TI Static and dynamic characteristics of cerebral blood flow during the
resting state
SO NEUROIMAGE
LA English
DT Article
DE CBF; Static; Dynamic; Functional connectivity; ALFF; ReHo; Resting state
ID INDEPENDENT COMPONENT ANALYSIS; BOLD SIGNAL FLUCTUATIONS; DEFAULT-MODE
NETWORK; FUNCTIONAL CONNECTIVITY; HUMAN BRAIN; LOW-FREQUENCY; REGIONAL
HOMOGENEITY; ALZHEIMERS-DISEASE; GLOBAL SIGNAL; SMALL-WORLD
AB In this study, the static and dynamic characteristics of cerebral blood flow (CBF) in the resting state were investigated using an arterial spin labeling (ASL) perfusion imaging technique. Consistent with previous PET results, static CBF measured by ASL was significantly higher in the posterior cingulate cortex (PCC), thalamus, insula/superior temporal gyrus (STG) and medial prefrontal cortex (MPFC) than the average CBF of the brain. The dynamic measurement of CBF fluctuations showed high correlation ( functional connectivity) between components in the default mode network. These brain regions also had high local temporal synchrony and high fluctuation amplitude, as measured by regional homogeneity (ReHo) and amplitude of low-frequency fluctuation (ALFF) analyses. The spatial pattern of the static CBF correlated well with that of the dynamic indices. The high static and dynamic activities in the PCC, MPFC, insula/STG and thalamus suggest that these regions play a vital role in maintaining and facilitating fundamental brain functions. Published by Elsevier Inc.
C1 [Zou, Qihong; Zang, Yufeng] Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, Beijing 100875, Peoples R China.
[Zou, Qihong; Wu, Changwei W.; Stein, Elliot A.; Yang, Yihong] NIDA, Neuroimaging Res Branch, NIH, Baltimore, MD 21224 USA.
[Wu, Changwei W.] Natl Taiwan Univ, Dept Elect Engn, Taipei 10764, Taiwan.
RP Zang, YF (reprint author), Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, 19 Xinjiekouwai St, Beijing 100875, Peoples R China.
EM zangyf@bnu.edu.cn; yihongyang@intra.nida.nih.gov
RI ZANG, Yu-Feng/J-1558-2012
OI ZANG, Yu-Feng/0000-0003-1833-8010
FU Intramural Research Program of the National Institute on Drug Abuse
(NIDA); National Institute of Health (NIH)
FX This work was supported by the Intramural Research Program of the
National Institute on Drug Abuse (NIDA), National Institute of Health
(NIH). The authors thank Dr. Christian F. Beckmann for providing dual
regression method for ICA denoising, Dr. Xinian Zuo for preparing the
vessel mask and suggestions for removing noise using ICA, and Dr. Thomas
J. Ross and Dr. Yong He for helpful discussions.
NR 59
TC 94
Z9 96
U1 1
U2 19
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2009
VL 48
IS 3
BP 515
EP 524
DI 10.1016/j.neuroimage.2009.07.006
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 558EQ
UT WOS:000274724000004
PM 19607928
ER
PT J
AU Hakk, H
Diliberto, JJ
Birnbaum, LS
AF Hakk, Heldur
Diliberto, Janet J.
Birnbaum, Linda S.
TI The effect of dose on 2,3,7,8-TCDD tissue distribution, metabolism and
elimination in CYP1A2 (-/-) knockout and C57BL/6N parental strains of
mice
SO TOXICOLOGY AND APPLIED PHARMACOLOGY
LA English
DT Article
DE 2,3,7,8-Tetrachlorodibenzo-p-dioxin TCDD; CYP1A2; Knockout mice;
Metabolism; Mouse major urinary protein
ID DIBENZO-P-DIOXINS; RESPONSE RELATIONSHIPS;
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; METHYLSULFONYL METABOLITE;
POLYCHLORINATED BIPHENYL; HEPATIC SEQUESTRATION; RAT; BINDING;
EXCRETION; PROTEINS
AB Numerous metabolism studies have demonstrated that the toxic contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is poorly metabolized. A hallmark feature of TCDD exposure is induction of hepatic CYP1A2 and subsequent sequestration leading to high liver-to-fat concentration ratios. This study was initiated to determine whether TCDD was inherently poorly metabolized or unavailable for metabolism because of sequestration to CYP1A2. [H-3]TCDD was administered as a single, oral dose (0.1 and 10 mu g/kg) to 12 male C57BL/6N mice or 12 CYP1A2 (-/-) mice. At 96 h, less than 5% of the dose was eliminated in the urine of all groups, and TCDD detected in urine was bound to mouse major urinary protein (mMUP). Feces were the major elimination pathway (24-31% of dose), and fecal extracts and non-extractables were quantitated by HPLC for metabolites. No great differences in urinary or fecal elimination (% dose) were observed between the high and low dose treatments. TCDD concentrations were the highest in adipose tissue for CYP1A2 knockout mice but in liver for C57BL/6N mice supporting the role of hepatic CYP1A2 in the sequestration of TCDD. Overall metabolism between parental and knockout strains showed no statistical differences at either the high or low doses. The data suggested that metabolism of TCDD is inherently slow, due principally to CYP1A7, and that hepatic CYP1A2 is not an active participant in the metabolism of TCDD in male mice. Rather, CYP1A2 governs the pharmacokinetics of TCDD by making it unavailable for hepatic CYP1A1 through sequestration and attenuating extrahepatic tissue disposition. Published by Elsevier Inc.
C1 [Hakk, Heldur] ARS, USDA, Biosci Res Lab, Fargo, ND USA.
[Diliberto, Janet J.] US EPA ORD, Natl Hlth Effects & Environm Res Lab, Expt Toxicol Div, Res Triangle Pk, NC USA.
[Birnbaum, Linda S.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
RP Hakk, H (reprint author), ARS, USDA, Biosci Res Lab, POB 5674, Fargo, ND USA.
EM heldur.hakk@ars.usda.gov
NR 42
TC 20
Z9 21
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 0041-008X
EI 1096-0333
J9 TOXICOL APPL PHARM
JI Toxicol. Appl. Pharmacol.
PD NOV 15
PY 2009
VL 241
IS 1
BP 119
EP 126
DI 10.1016/j.taap.2009.08.009
PG 8
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 514QH
UT WOS:000271409400011
PM 19695277
ER
PT J
AU Horkay, F
Basser, PJ
Londono, DJ
Hecht, AM
Geissler, E
AF Horkay, Ferenc
Basser, Peter J.
Londono, David J.
Hecht, Anne-Marie
Geissler, Erik
TI Ions in hyaluronic acid solutions
SO JOURNAL OF CHEMICAL PHYSICS
LA English
DT Article
ID POLYELECTROLYTE SOLUTIONS; CARTILAGE AGGRECAN; LIGHT-SCATTERING;
POLYSACCHARIDES; ORGANIZATION; VISCOSITY; SALT; DNA
AB Hyaluronic acid (HA) is an anionic biopolymer that is almost ubiquitous in biological tissues. An attempt is made to determine the dominant features that account for both its abundance and its multifunctional role, and which set it apart from other types of biopolymers. A combination of osmotic and scattering techniques is employed to quantify its dynamic and static properties in near-physiological solution conditions, where it is exposed both to mono- and divalent counterions. An equation of state is derived for the osmotic pressure Pi in the semidilute concentration region, in terms of two variables, the polymer concentration c and the ionic strength J of the added salt, according to which Pi=1.4x10(3)c(9/4)/J(3/4) kPa, where c and J are expressed in mole. Over the physiological ion concentration range, the effect of the sodium chloride and calcium chloride on the osmotic properties of HA solutions is fully accounted for by their contributions to the ionic strength. The absence of precipitation, even at high CaCl(2) concentrations, distinguishes this molecule from other biopolymers such as DNA. Dynamic light scattering measurements reveal that the collective diffusion coefficient in HA solutions exceeds that in aqueous solutions of typical neutral polymers by a factor of approximately 5. This property ensures rapid adjustment to, and recovery from, stress applied to HA-containing tissue. Small angle x-ray scattering measurements confirm the absence of appreciable structural reorganization over the observed length scale range 10-1000 angstrom, as a result of calcium-sodium ion exchange. The scattered intensity in the transfer momentum range q>0.03 angstrom(-1) varies as 1/q, indicating that the HA chain segments in semidilute solutions are linear over an extended concentration range. The osmotic compression modulus c partial derivative Pi/partial derivative c, a high value of which is a prerequisite in structural biopolymers, is several times greater than in typical neutral polymer solutions. (C) 2009 American Institute of Physics. [doi: 10.1063/1.3262308]
C1 [Horkay, Ferenc; Basser, Peter J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Tissue Biophys & Biomimet, Program Phys Biol, NIH, Bethesda, MD 20892 USA.
[Londono, David J.] Dupont Nemours & Co, Dupont Cent Res, Expt Stn, Wilmington, DE 19880 USA.
[Hecht, Anne-Marie; Geissler, Erik] Univ Grenoble 1, CNRS, Spectrometrie Phys Lab, UMR 5588, F-38402 St Martin Dheres, France.
RP Horkay, F (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Sect Tissue Biophys & Biomimet, Program Phys Biol, NIH, 13 South Dr, Bethesda, MD 20892 USA.
EM horkay@helix.nih.gov
RI Basser, Peter/H-5477-2011
FU NICHD, NIH; National Science Foundation [DMR-9423101]
FX This research was supported by the Intramural Research Program of the
NICHD, NIH. We express our gratitude to the Advanced Photon Source,
Argonne National Laboratory, for access to the DND-CAT small angle
instrument. This work is partially based upon activities supported by
the National Science Foundation under Grant No. DMR-9423101.
NR 35
TC 16
Z9 16
U1 1
U2 25
PU AMER INST PHYSICS
PI MELVILLE
PA CIRCULATION & FULFILLMENT DIV, 2 HUNTINGTON QUADRANGLE, STE 1 N O 1,
MELVILLE, NY 11747-4501 USA
SN 0021-9606
J9 J CHEM PHYS
JI J. Chem. Phys.
PD NOV 14
PY 2009
VL 131
IS 18
AR 184902
DI 10.1063/1.3262308
PG 8
WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical
SC Chemistry; Physics
GA 528NY
UT WOS:000272454500041
PM 19916626
ER
PT J
AU Bray, GA
Chatellier, A
Duncan, C
Greenway, FL
Levy, E
Ryan, DH
Polonsky, KS
Tobian, J
Ehrmann, D
Matulik, MJ
Clark, B
Czech, K
DeSandre, C
Hilbrich, R
McNabb, W
Semenske, AR
Goldstein, BJ
Smith, KA
Wildman, W
Pepe, C
Goldberg, RB
Calles, J
Ojito, J
Castillo-Florez, S
Florez, HJ
Giannella, A
Lara, O
Veciana, B
Haffner, SM
Montez, MG
Lorenzo, C
Martinez, A
Hamman, RF
Testaverde, L
Bouffard, A
Dabelea, D
Jenkins, T
Lenz, D
Perreault, L
Price, DW
Steinke, SC
Horton, ES
Poirier, CS
Swift, K
Caballero, E
Jackson, SD
Lambert, L
Lawton, KE
Ledbury, S
Kahn, SE
Montgomery, BK
Fujimoto, W
Knopp, RH
Lipkin, EW
Marr, M
Murillo, A
Trence, D
Kitabchi, AE
Murphy, ME
Applegate, WB
Bryer-Ash, M
Dagogo-Jack, S
Frieson, SL
Lambeth, H
Lichtermann, LC
Otkaei, H
Rutledge, LMK
Sherman, AR
Smith, CM
Soberman, JE
Williams-Cleaves, B
Metzger, BE
Molitch, ME
Johnson, MK
Giles, MM
Larsen, D
Niznik, C
Pen, SC
Schinleber, PA
Nathan, DM
McKitrick, C
Turgeon, H
Abbott, K
Altshuler, D
Anderson, E
Bissett, L
Cagliero, E
D'Anna, K
Delahanty, L
Florez, JC
Goldman, V
Poulos, A
Tseng, B
Barrett-Connor, E
Carrion-Petersen, ML
Horne, J
Leos, D
Mudaliar, S
Smith, J
Vejvoda, K
Pi-Sunyer, FX
Lee, JE
Foo, ST
Hagamen, S
Marrero, DG
Kelly, SM
Ackermann, RT
Fineberg, ES
Hadden, A
Jackson, MA
Kirkman, MS
Mather, KJ
Roach, PJ
Wheeler, ML
Ratner, RE
Aroda, V
Shapiro, S
Bavido-Arrage, C
Gibbs, P
Uwaifo, G
Wiggins, R
Saad, MF
Watson, K
Botrous, M
Jinagouda, S
Budget, M
Conzues, C
Magpuri, P
Ngo, K
Xapthalamous, K
White, NH
Das, S
Santiago, A
Brown, AL
Wernimont, C
Saudek, CD
Whittington, T
Clark, JM
Greene, A
Jiggetts, D
Mosley, H
Reusing, J
Rubin, RR
Stephen, S
Utsey, E
Schade, DS
Adams, KS
Hemphill, C
Hyde, P
Butler, L
Canady, JL
Colleran, K
Gonzales, Y
Hernandez-McGinnis, DA
Katz, P
King, C
Crandall, J
Brown-Friday, JO
Adorno, E
Duffy, H
Martinez, H
Pompi, D
Shamoon, H
Walker, EA
Wylie-Rosett, J
Orchard, T
Jeffries, S
Kramer, MK
Smith, M
Kriska, A
Pettigrew, J
Semler, L
Venditti, E
Weinzierl, V
Arakaki, RF
Baker-Ladao, NK
Isonaga, MK
Bermudez, NE
Mau, MK
Knowler, WC
Cooeyate, N
Hoskin, MA
Natewa, C
Percy, CA
Acton, KJ
Andre, VL
Begay, S
Bucca, BC
Cook, S
Doughty, MS
Glass, J
Glass, M
Hanson, RL
Hassenpflug, D
Ingraham, LE
Kobus, KM
Krakoff, J
Manus, C
McCabe, C
Michaels, S
Morgan, T
Nelson, JA
Roy, RJ
Smart, M
Tonemah, DP
Wilson, C
Fowler, S
Brenneman, T
Abebe, S
Bamdad, J
Callaghan, J
Christophi, CA
Edelstein, SL
Gao, Y
Gooding, R
Gottlieb, A
Grover, N
Hoffman, H
Jablonski, K
Katz, R
Kolinjivadi, P
Lachin, JM
Ma, Y
Reamer, S
Sapozhnikova, A
Sherif, H
Temprosa, M
Venditti, EM
Kriska, AM
Semler, L
Weinzierl, V
Marcovina, S
Strylewicz, G
Albers, J
Prineas, RJ
Alexander, T
Campbell, C
Hall, S
Hensley, S
Li, Y
Mills, M
Soliman, E
Zhang, Z
Fradkin, J
Garfield, S
Mayer-Davis, E
Moran, RR
Ganiats, T
Sarkin, AJ
AF Bray, G. A.
Chatellier, A.
Duncan, C.
Greenway, F. L.
Levy, E.
Ryan, D. H.
Polonsky, K. S.
Tobian, J.
Ehrmann, D.
Matulik, M. J.
Clark, B.
Czech, K.
DeSandre, C.
Hilbrich, R.
McNabb, W.
Semenske, A. R.
Goldstein, B. J.
Smith, K. A.
Wildman, W.
Pepe, C.
Goldberg, R. B.
Calles, J.
Ojito, J.
Castillo-Florez, S.
Florez, H. J.
Giannella, A.
Lara, O.
Veciana, B.
Haffner, S. M.
Montez, M. G.
Lorenzo, C.
Martinez, A.
Hamman, R. F.
Testaverde, L.
Bouffard, A.
Dabelea, D.
Jenkins, T.
Lenz, D.
Perreault, L.
Price, D. W.
Steinke, S. C.
Horton, E. S.
Poirier, C. S.
Swift, K.
Caballero, E.
Jackson, S. D.
Lambert, L.
Lawton, K. E.
Ledbury, S.
Kahn, S. E.
Montgomery, B. K.
Fujimoto, W.
Knopp, R. H.
Lipkin, E. W.
Marr, M.
Murillo, A.
Trence, D.
Kitabchi, A. E.
Murphy, M. E.
Applegate, W. B.
Bryer-Ash, M.
Dagogo-Jack, S.
Frieson, S. L.
Lambeth, H.
Lichtermann, L. C.
Otkaei, H.
Rutledge, L. M. K.
Sherman, A. R.
Smith, C. M.
Soberman, J. E.
Williams-Cleaves, B.
Metzger, B. E.
Molitch, M. E.
Johnson, M. K.
Giles, M. M.
Larsen, D.
Niznik, C.
Pen, S. C.
Schinleber, P. A.
Nathan, D. M.
McKitrick, C.
Turgeon, H.
Abbott, K.
Altshuler, D.
Anderson, E.
Bissett, L.
Cagliero, E.
D'Anna, K.
Delahanty, L.
Florez, J. C.
Goldman, V.
Poulos, A.
Tseng, B.
Barrett-Connor, E.
Carrion-Petersen, M. L.
Horne, J.
Leos, D.
Mudaliar, S.
Smith, J.
Vejvoda, K.
Pi-Sunyer, F. X.
Lee, J. E.
Foo, S. T.
Hagamen, S.
Marrero, D. G.
Kelly, S. M.
Ackermann, R. T.
Fineberg, E. S.
Hadden, A.
Jackson, M. A.
Kirkman, M. S.
Mather, K. J.
Roach, P. J.
Wheeler, M. L.
Ratner, R. E.
Aroda, V.
Shapiro, S.
Bavido-Arrage, C.
Gibbs, P.
Uwaifo, Gl
Wiggins, R.
Saad, M. F.
Watson, K.
Botrous, M.
Jinagouda, S.
Budget, M.
Conzues, C.
Magpuri, P.
Ngo, K.
Xapthalamous, K.
White, N. H.
Das, S.
Santiago, A.
Brown, A. L.
Wernimont, C.
Saudek, C. D.
Whittington, T.
Clark, J. M.
Greene, A.
Jiggetts, D.
Mosley, H.
Reusing, J.
Rubin, R. R.
Stephen, S.
Utsey, E.
Schade, D. S.
Adams, K. S.
Hemphill, C.
Hyde, P.
Butler, L.
Canady, J. L.
Colleran, K.
Gonzales, Y.
Hernandez-McGinnis, D. A.
Katz, P.
King, C.
Crandall, J.
Brown-Friday, J. O.
Adorno, E.
Duffy, H.
Martinez, H.
Pompi, D.
Shamoon, H.
Walker, E. A.
Wylie-Rosett, J.
Orchard, T.
Jeffries, S.
Kramer, M. K.
Smith, M.
Kriska, A.
Pettigrew, J.
Semler, L.
Venditti, E.
Weinzierl, V.
Arakaki, R. F.
Baker-Ladao, N. K.
Isonaga, M. K.
Bermudez, N. E.
Mau, M. K.
Knowler, W. C.
Cooeyate, N.
Hoskin, M. A.
Natewa, C.
Percy, C. A.
Acton, K. J.
Andre, V. L.
Begay, S.
Bucca, B. C.
Cook, S.
Doughty, M. S.
Glass, J.
Glass, M.
Hanson, R. L.
Hassenpflug, D.
Ingraham, L. E.
Kobus, K. M.
Krakoff, J.
Manus, C.
McCabe, C.
Michaels, S.
Morgan, T.
Nelson, J. A.
Roy, R. J.
Smart, M.
Tonemah, D. P.
Wilson, C.
Fowler, S.
Brenneman, T.
Abebe, S.
Bamdad, J.
Callaghan, J.
Christophi, C. A.
Edelstein, S. L.
Gao, Y.
Gooding, R.
Gottlieb, A.
Grover, N.
Hoffman, H.
Jablonski, K.
Katz, R.
Kolinjivadi, P.
Lachin, J. M.
Ma, Y.
Reamer, S.
Sapozhnikova, A.
Sherif, H.
Temprosa, M.
Venditti, E. M.
Kriska, A. M.
Semler, L.
Weinzierl, V.
Marcovina, S.
Strylewicz, G.
Albers, J.
Prineas, R. J.
Alexander, T.
Campbell, C.
Hall, S.
Hensley, S.
Li, Y.
Mills, M.
Soliman, E.
Zhang, Z.
Fradkin, J.
Garfield, S.
Mayer-Davis, E.
Moran, R. R.
Ganiats, T.
Sarkin, A. J.
CA Diabet Prevention Program Res Grp
TI 10-year follow-up of diabetes incidence and weight loss in the Diabetes
Prevention Program Outcomes Study
SO LANCET
LA English
DT Article
ID IMPAIRED GLUCOSE-TOLERANCE; LIFE-STYLE INTERVENTION; COST-EFFECTIVENESS;
RISK-FACTORS; METFORMIN; MELLITUS; PEOPLE; TRIAL; REDUCTION; DIAGNOSIS
AB Background In the 2.8 years of the Diabetes Prevention Program (DPP) randomised clinical trial, diabetes incidence in high-risk adults was reduced by 58% with intensive lifestyle intervention and by 31% with metformin, compared with placebo. We investigated the persistence of these effects in the long term.
Methods All active DPP participants were eligible for continued follow-up. 2766 of 3150 (88%) enrolled for a median additional follow-up of 5.7 years (IQR 5.5-5.8). 910 participants were from the lifestyle, 924 from the metformin, and 932 were from the original placebo groups. On the basis of the benefits from the intensive lifestyle intervention in the DPP, all three groups were offered group-implemented lifestyle intervention. Metformin treatment was continued in the original metformin group (850 mg twice daily as tolerated), with participants unmasked to assignment, and the original lifestyle intervention group was offered additional lifestyle support. The primary outcome was development of diabetes according to American Diabetes Association criteria. Analysis was by intention-to-treat. This study is registered with ClinicalTrials.gov, number NCT00038727.
Findings During the 10.0-year (IQR 9.0-10.5) follow-up since randomisation to DPP, the original lifestyle group lost, then partly regained weight. The modest weight loss with metformin was maintained. Diabetes incidence rates during the DPP were 4.8 cases per 100 person-years (95% CI 4.1-5.7) in the intensive lifestyle intervention group, 7.8 (6.8-8.8) in the metformin group, and 11.0 (9.8-12.3) in the placebo group. Diabetes incidence rates in this follow-up study were similar between treatment groups: 5.9 per 100 person-years (5.1-6.8) for lifestyle, 4.9 (4.2-5.7) for metformin, and 5.6 (4.8-6.5) for placebo. Diabetes incidence in the 10 years since DPP randomisation was reduced by 34% (24-42) in the lifestyle group and 18% (7-28) in the metformin group compared with placebo.
Interpretation During follow-up after DPP, incidences in the former placebo and metformin groups fell to equal those in the former lifestyle group, but the cumulative incidence of diabetes remained lowest in the lifestyle group. Prevention or delay of diabetes with lifestyle intervention or metformin can persist for at least 10 years.
C1 [Bray, G. A.; Fowler, S.; Brenneman, T.; Abebe, S.; Bamdad, J.; Callaghan, J.; Christophi, C. A.; Edelstein, S. L.; Gao, Y.; Gooding, R.; Gottlieb, A.; Grover, N.; Hoffman, H.; Jablonski, K.; Katz, R.; Kolinjivadi, P.; Lachin, J. M.; Ma, Y.; Reamer, S.; Sapozhnikova, A.; Sherif, H.; Temprosa, M.] George Washington Univ, Diabet Prevent Program Coordinating Ctr, Ctr Biostat, Rockville, MD 20852 USA.
[Bray, G. A.; Chatellier, A.; Duncan, C.; Greenway, F. L.; Levy, E.; Ryan, D. H.] Pennington Biomed Res Ctr, Baton Rouge, LA USA.
[Polonsky, K. S.; Tobian, J.; Ehrmann, D.; Matulik, M. J.; Clark, B.; Czech, K.; DeSandre, C.; Hilbrich, R.; McNabb, W.; Semenske, A. R.] Univ Chicago, Chicago, IL 60637 USA.
[Goldstein, B. J.; Smith, K. A.; Wildman, W.; Pepe, C.] Thomas Jefferson Univ, Jefferson Med Coll, Philadelphia, PA 19107 USA.
[Goldberg, R. B.; Calles, J.; Ojito, J.; Castillo-Florez, S.; Florez, H. J.; Giannella, A.; Lara, O.; Veciana, B.] Univ Miami, Miami, FL USA.
[Haffner, S. M.; Montez, M. G.; Lorenzo, C.; Martinez, A.] Univ Texas Hlth Sci Ctr San Antonio, San Antonio, TX 78229 USA.
[Hamman, R. F.; Testaverde, L.; Bouffard, A.; Dabelea, D.; Jenkins, T.; Lenz, D.; Perreault, L.; Price, D. W.; Steinke, S. C.] Univ Colorado, Denver, CO 80202 USA.
[Horton, E. S.; Poirier, C. S.; Swift, K.; Caballero, E.; Jackson, S. D.; Lambert, L.; Lawton, K. E.; Ledbury, S.] Joslin Diabet Ctr, Boston, MA 02215 USA.
[Kahn, S. E.; Montgomery, B. K.; Fujimoto, W.; Knopp, R. H.; Lipkin, E. W.; Marr, M.; Murillo, A.; Trence, D.] Univ Washington, Seattle, WA 98195 USA.
[Kitabchi, A. E.; Murphy, M. E.; Applegate, W. B.; Bryer-Ash, M.; Dagogo-Jack, S.; Frieson, S. L.; Lambeth, H.; Lichtermann, L. C.; Otkaei, H.; Rutledge, L. M. K.; Sherman, A. R.; Smith, C. M.; Soberman, J. E.; Williams-Cleaves, B.] Univ Tennessee, Memphis, TN USA.
[Metzger, B. E.; Molitch, M. E.; Johnson, M. K.; Giles, M. M.; Larsen, D.; Niznik, C.; Pen, S. C.; Schinleber, P. A.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Nathan, D. M.; McKitrick, C.; Turgeon, H.; Abbott, K.; Altshuler, D.; Anderson, E.; Bissett, L.; Cagliero, E.; D'Anna, K.; Delahanty, L.; Florez, J. C.; Goldman, V.; Poulos, A.; Tseng, B.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Barrett-Connor, E.; Carrion-Petersen, M. L.; Horne, J.; Leos, D.; Mudaliar, S.; Smith, J.; Vejvoda, K.] Univ Calif San Diego, San Diego, CA 92103 USA.
[Pi-Sunyer, F. X.; Lee, J. E.; Foo, S. T.; Hagamen, S.] St Lukes Roosevelt Hosp, New York, NY 10025 USA.
[Marrero, D. G.; Kelly, S. M.; Ackermann, R. T.; Fineberg, E. S.; Hadden, A.; Jackson, M. A.; Kirkman, M. S.; Mather, K. J.; Roach, P. J.; Wheeler, M. L.] Indiana Univ, Indianapolis, IN 46204 USA.
[Ratner, R. E.; Aroda, V.; Shapiro, S.; Bavido-Arrage, C.; Gibbs, P.; Uwaifo, Gl; Wiggins, R.] Medstar Res Inst, Washington, DC USA.
[Saad, M. F.; Watson, K.; Botrous, M.; Jinagouda, S.; Budget, M.; Conzues, C.; Magpuri, P.; Ngo, K.; Xapthalamous, K.] Univ Calif Los Angeles, Univ So Calif, Res Ctr, Alhambra, CA USA.
[White, N. H.; Das, S.; Santiago, A.; Brown, A. L.; Wernimont, C.] Washington Univ, St Louis, MO USA.
[Saudek, C. D.; Whittington, T.; Clark, J. M.; Greene, A.; Jiggetts, D.; Mosley, H.; Reusing, J.; Rubin, R. R.; Stephen, S.; Utsey, E.] Johns Hopkins Sch Med, Baltimore, MD USA.
[Schade, D. S.; Adams, K. S.; Hemphill, C.; Hyde, P.; Butler, L.; Canady, J. L.; Colleran, K.; Gonzales, Y.; Hernandez-McGinnis, D. A.; Katz, P.; King, C.] Univ New Mexico, Albuquerque, NM 87131 USA.
[Crandall, J.; Brown-Friday, J. O.; Adorno, E.; Duffy, H.; Martinez, H.; Pompi, D.; Shamoon, H.; Walker, E. A.; Wylie-Rosett, J.] Albert Einstein Coll Med, Bronx, NY 10467 USA.
[Orchard, T.; Jeffries, S.; Kramer, M. K.; Smith, M.; Kriska, A.; Pettigrew, J.; Semler, L.; Venditti, E.; Weinzierl, V.] Univ Pittsburgh, Pittsburgh, PA USA.
[Arakaki, R. F.; Baker-Ladao, N. K.; Isonaga, M. K.; Bermudez, N. E.; Mau, M. K.] Univ Hawaii, Honolulu, HI 96822 USA.
[Knowler, W. C.; Cooeyate, N.; Hoskin, M. A.; Natewa, C.; Percy, C. A.; Acton, K. J.; Andre, V. L.; Begay, S.; Bucca, B. C.; Cook, S.; Doughty, M. S.; Glass, J.; Glass, M.; Hanson, R. L.; Hassenpflug, D.; Ingraham, L. E.; Kobus, K. M.; Krakoff, J.; Manus, C.; McCabe, C.; Michaels, S.; Morgan, T.; Nelson, J. A.; Roy, R. J.; Smart, M.; Tonemah, D. P.; Wilson, C.] SW Amer Indian Ctr, Phoenix, AZ USA.
[Knowler, W. C.; Cooeyate, N.; Hoskin, M. A.; Natewa, C.; Percy, C. A.; Acton, K. J.; Andre, V. L.; Begay, S.; Bucca, B. C.; Cook, S.; Doughty, M. S.; Glass, J.; Glass, M.; Hanson, R. L.; Hassenpflug, D.; Ingraham, L. E.; Kobus, K. M.; Krakoff, J.; Manus, C.; McCabe, C.; Michaels, S.; Morgan, T.; Nelson, J. A.; Roy, R. J.; Smart, M.; Tonemah, D. P.; Wilson, C.] SW Amer Indian Ctr, Shiprock, NM USA.
[Knowler, W. C.; Cooeyate, N.; Hoskin, M. A.; Natewa, C.; Percy, C. A.; Acton, K. J.; Andre, V. L.; Begay, S.; Bucca, B. C.; Cook, S.; Doughty, M. S.; Glass, J.; Glass, M.; Hanson, R. L.; Hassenpflug, D.; Ingraham, L. E.; Kobus, K. M.; Krakoff, J.; Manus, C.; McCabe, C.; Michaels, S.; Morgan, T.; Nelson, J. A.; Roy, R. J.; Smart, M.; Tonemah, D. P.; Wilson, C.] SW Amer Indian Ctr, Zuni, NM USA.
[Marcovina, S.; Strylewicz, G.; Albers, J.] Cent Biochem Lab, Seattle, WA USA.
[Prineas, R. J.; Alexander, T.; Campbell, C.; Hall, S.; Hensley, S.; Li, Y.; Mills, M.; Soliman, E.; Zhang, Z.] Epidemiol Cardiol Res Ctr Epicare, Winston Salem, NC USA.
[Fradkin, J.; Garfield, S.] NIDDK, NIH, Bethesda, MD USA.
[Mayer-Davis, E.; Moran, R. R.] Nutr Coding Ctr, Columbia, SC USA.
[Ganiats, T.; Sarkin, A. J.] Qual Well Being Ctr, La Jolla, CA USA.
RP Bray, GA (reprint author), George Washington Univ, Diabet Prevent Program Coordinating Ctr, Ctr Biostat, 6110 Execut Blvd,Suite 750, Rockville, MD 20852 USA.
EM dppmail@biostat.bsc.gwu.edu
RI Altshuler, David/A-4476-2009; Uwaifo, Gabriel/M-2361-2016
OI Altshuler, David/0000-0002-7250-4107; Uwaifo,
Gabriel/0000-0002-6962-9304
FU National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK), National Institutes of Health
FX This study was funded by the National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK) as a cooperative agreement. We
thank the participants of the Diabetes Prevention Program and Diabetes
Prevention Program Outcomes Study for their commitment and dedication;
the National Institute of Diabetes and Digestive and Kidney Diseases
(NIDDK) of the National Institutes of Health for funding to the clinical
and coordinating centres that designed and undertook the study, and
collected, managed, analysed and interpreted the data; and the General
Clinical Research Center Program and the National Center for Research
Resources for support of data collection at many of the clinical
centres. The Southwestern American Indian Centers were supported
directly by the NIDDK, including its Intramural Research Program, and by
the Indian Health Service. Funding was also provided by the National
Institute of Child Health and Human Development, the National Institute
on Aging, the National Eye Institute, the National Heart Lung and Blood
Institute, the Office of Women's Health, the National Center for
Minority Health and Human Disease, the Centers for Disease Control and
Prevention, and the American Diabetes Association. Lipha (Merck-Sante)
provided medicines, and LifeScan donated materials. The opinions
expressed are those of the investigators and do not necessarily reflect
the views of the funding agencies.
NR 28
TC 800
Z9 806
U1 12
U2 82
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD NOV 14
PY 2009
VL 374
IS 9702
BP 1677
EP 1686
DI 10.1016/S0140-6736(09)61457-4
PG 10
WC Medicine, General & Internal
SC General & Internal Medicine
GA 522LP
UT WOS:000271999700023
ER
PT J
AU Landi, MT
Chatterjee, N
Yu, K
Goldin, LR
Goldstein, AM
Rotunno, M
Mirabello, L
Jacobs, K
Wheeler, W
Yeager, M
Bergen, AW
Li, QZ
Consonni, D
Pesatori, AC
Wacholder, S
Thun, M
Diver, R
Oken, M
Virtamo, J
Albanes, D
Wang, ZM
Burdette, L
Doheny, KF
Pugh, EW
Laurie, C
Brennan, P
Hung, R
Gaborieau, V
McKay, JD
Lathrop, M
McLaughlin, J
Wang, Y
Tsao, MS
Spitz, MR
Wang, YF
Krokan, H
Vatten, L
Skorpen, F
Arnesen, E
Benhamou, S
Bouchard, C
Metsapalu, A
Vooder, T
Nelis, M
Valk, K
Field, JK
Chen, C
Goodman, G
Sulem, P
Thorleifsson, G
Rafnar, T
Eisen, T
Sauter, W
Rosenberger, A
Bickeboller, H
Risch, A
Chang-Claude, J
Wichmann, HE
Stefansson, K
Houlston, R
Amos, CI
Fraumeni, JF
Savage, SA
Bertazzi, PA
Tucker, MA
Chanock, S
Caporaso, NE
AF Landi, Maria Teresa
Chatterjee, Nilanjan
Yu, Kai
Goldin, Lynn R.
Goldstein, Alisa M.
Rotunno, Melissa
Mirabello, Lisa
Jacobs, Kevin
Wheeler, William
Yeager, Meredith
Bergen, Andrew W.
Li, Qizhai
Consonni, Dario
Pesatori, Angela C.
Wacholder, Sholom
Thun, Michael
Diver, Ryan
Oken, Martin
Virtamo, Jarmo
Albanes, Demetrius
Wang, Zhaoming
Burdette, Laurie
Doheny, Kimberly F.
Pugh, Elizabeth W.
Laurie, Cathy
Brennan, Paul
Hung, Rayjean
Gaborieau, Valerie
McKay, James D.
Lathrop, Mark
McLaughlin, John
Wang, Ying
Tsao, Ming-Sound
Spitz, Margaret R.
Wang, Yufei
Krokan, Hans
Vatten, Lars
Skorpen, Frank
Arnesen, Egil
Benhamou, Simone
Bouchard, Christine
Metsapalu, Andres
Vooder, Tonu
Nelis, Mari
Vaelk, Kristian
Field, John K.
Chen, Chu
Goodman, Gary
Sulem, Patrick
Thorleifsson, Gudmar
Rafnar, Thorunn
Eisen, Timothy
Sauter, Wiebke
Rosenberger, Albert
Bickeboeller, Heike
Risch, Angela
Chang-Claude, Jenny
Wichmann, H. Erich
Stefansson, Kari
Houlston, Richard
Amos, Christopher I.
Fraumeni, Joseph F., Jr.
Savage, Sharon A.
Bertazzi, Pier Alberto
Tucker, Margaret A.
Chanock, Stephen
Caporaso, Neil E.
TI A Genome-wide Association Study of Lung Cancer Identifies a Region of
Chromosome 5p15 Associated with Risk for Adenocarcinoma
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID TELOMERASE REVERSE-TRANSCRIPTASE; IDIOPATHIC PULMONARY-FIBROSIS;
SUSCEPTIBILITY LOCUS; FAMILY-HISTORY; MUTATIONS; VARIANTS; POPULATION;
EXPRESSION; TERT; METAANALYSIS
AB Three genetic loci for lung cancer risk have been identified by genome-wide association studies (GWAS), but inherited susceptibility to specific histologic types of king cancer is not well established. We conducted a GWAS of lung cancer and its major histologic types, genotyping 515,922 single-nucleotide polymorphisms (SNPs) in 5739 lung cancer cases and 5848 controls from one population-based case-control study and three cohort studies. Results were combined with summary data from ten additional studies, for a total of 13,300 cases and 19,666 controls of European descent. Four Studies also provided histology data for replication, resulting in 3333 adenocarcinomas (AD), 2589 squamous cell carcinomas (SQ), and 1418 small cell carcinomas (SQ. In analyses by histology, rs2736100 (TERT), on chromosome 5p15.33, was associated with risk of adenocarcinoma (odds ratio [OR] = 1.23, 95% confidence interval [CI] = 1.13-1.33, p = 3.02 x 10(-7)), but not with other histologic types (OR = 1.01, p = 0.84 and OR = 1.00, p = 0.93 for SQ and SC, respectively). This finding was confirmed in each replication study and overall meta-analysis (OR = 1.24, 95% CI = 1.17-1.31, p = 3.74 x 10(-14) for AD; OR = 0.99, p = 0.69 and OR = 0.97, p = 0.48 for SQ and SC, respectively). Other previously reported association signals on 15q25 and 6p21 were also refined, but no additional loci reached genome-wide significance. In conclusion, a lung cancer GWAS identified a distinct hereditary contribution to adenocarcinoma.
C1 [Landi, Maria Teresa; Chatterjee, Nilanjan; Yu, Kai; Goldin, Lynn R.; Goldstein, Alisa M.; Rotunno, Melissa; Mirabello, Lisa; Jacobs, Kevin; Yeager, Meredith; Li, Qizhai; Wacholder, Sholom; Albanes, Demetrius; Wang, Zhaoming; Burdette, Laurie; Fraumeni, Joseph F., Jr.; Savage, Sharon A.; Tucker, Margaret A.; Chanock, Stephen; Caporaso, Neil E.] NCI, Div Canc Epidemiol, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Wheeler, William] Informat Management Serv Inc, Rockville, MD 20852 USA.
[Bergen, Andrew W.] SRI Int, Ctr Hlth Sci, Mol Genet program, Menlo Pk, CA 94025 USA.
[Li, Qizhai] Chinese Acad Sci, Acad Math & Syst Sci, Key Lab Syst & Control, Beijing 100190, Peoples R China.
[Consonni, Dario; Pesatori, Angela C.; Bertazzi, Pier Alberto] Osped Maggiore Policlin Mangiagalli & Regina Elen, Fdn Ist Ricevero & Cura Carattere Sci, Epidemiol Unit, I-20122 Milan, Italy.
[Consonni, Dario; Pesatori, Angela C.; Bertazzi, Pier Alberto] Univ Milan, Dept Occupat & Environm Hlth, I-20122 Milan, Italy.
[Thun, Michael; Diver, Ryan] Amer Canc Soc Epidemiol & Surveillance Res, Atlanta, GA 30301 USA.
[Oken, Martin] Univ Minnesota, Hubert H Humphrey Canc Ctr, Minneapolis, MN 55455 USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki 00280, Finland.
[Doheny, Kimberly F.; Pugh, Elizabeth W.] Johns Hopkins Univ, Sch Med, Inst Med Genet, Ctr Inherited Dis Res, Baltimore, MD 21224 USA.
[Laurie, Cathy] Univ Washington, Dept Biostat, Seattle, WA 98195 USA.
[Brennan, Paul; Gaborieau, Valerie; McKay, James D.] Int Agcy Res Canc, F-69372 Lyon, France.
[Hung, Rayjean; McLaughlin, John; Wang, Ying] Univ Toronto, Dalla Lana Sch Publ Hlth, Div Epidemiol, Samuel Lunenfeld Res Inst, Toronto, ON M5T 3L9, Canada.
[Lathrop, Mark; Benhamou, Simone] Fdn Jean Dausset, Ctr Etud Polymorphisme Humain, F-75010 Paris, France.
[Tsao, Ming-Sound] Princess Margaret Hosp, Univ Hlth Network, Dept Pathol, Toronto, ON M5T 3L9, Canada.
[Spitz, Margaret R.; Amos, Christopher I.] Univ Texas Houston, MD Anderson Canc Ctr, Dept Epidemiol, Houston, TX 77030 USA.
[Wang, Yufei; Houlston, Richard] Inst Canc Res, Sect Canc Genet, Sutton SM2 5NG, Surrey, England.
[Krokan, Hans; Vatten, Lars; Skorpen, Frank] Norwegian Univ Sci & Technol, Fac Med, N-7489 Trondheim, Norway.
[Arnesen, Egil] Univ Tromso, Dept Community Med, N-9037 Tromso, Norway.
[Benhamou, Simone] INSERM, F-75010 Paris, France.
[Bouchard, Christine] Geneva Canc Registry, CH-1205 Geneva, Switzerland.
[Metsapalu, Andres; Vooder, Tonu; Nelis, Mari; Vaelk, Kristian] Univ Tartu, Inst Mol & Cell Biol, Estonian Bioctr, EE-51010 Tartu, Estonia.
[Metsapalu, Andres; Vooder, Tonu; Nelis, Mari; Vaelk, Kristian] Univ Tartu, Estonian Genome Project, Estonian Bioctr, EE-51010 Tartu, Estonia.
[Field, John K.] Univ Liverpool, Canc Res Ctr, Roy Castle Lung Canc Res Program, Liverpool L3 97A, Merseyside, England.
[Chen, Chu; Goodman, Gary] Fred Hutchinson Canc Res Ctr, Publ Hlth Sci Div, Seattle, WA 98109 USA.
[Sulem, Patrick; Thorleifsson, Gudmar; Rafnar, Thorunn; Stefansson, Kari] DeCODE Genet, IS-101 Reykjavik, Iceland.
[Eisen, Timothy] Univ Cambridge, Dept Oncol, Cambridge CB2 2RE, England.
[Sauter, Wiebke; Wichmann, H. Erich] German Res Ctr Environm Hlth, Helmholtz Ctr Munich, Inst Epidemiol, D-85764 Neuherberg, Germany.
[Wichmann, H. Erich] Univ Munich, Inst Med Informat Biometry & Epidemiol, Chair Epidemiol, D-81377 Munich, Germany.
[Wichmann, H. Erich] Univ Munich, Klinikum Grosshadern, D-81377 Munich, Germany.
[Rosenberger, Albert; Bickeboeller, Heike] Univ Gottingen, Dept Genet Epidemiol, Sch Med, D-37073 Gottingen, Germany.
[Risch, Angela; Chang-Claude, Jenny] German Canc Res Ctr, Div Epigenom & Canc Risk Factors, D-69120 Heidelberg, Germany.
RP Landi, MT (reprint author), NCI, Div Canc Epidemiol, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
EM landim@mail.nih.gov
RI Hung, Rayjean/A-7439-2013; McLaughlin, John/E-4577-2013; Tucker,
Margaret/B-4297-2015; Albanes, Demetrius/B-9749-2015; Savage,
Sharon/B-9747-2015; Benhamou, Simone/K-6554-2015; Risch,
Angela/H-2669-2013; bertazzi, pietro alberto/D-5039-2017;
OI Houlston, Richard/0000-0002-5268-0242; Savage,
Sharon/0000-0001-6006-0740; Risch, Angela/0000-0002-8026-5505; bertazzi,
pietro alberto/0000-0003-3475-2449; pesatori,
angela/0000-0002-0261-3252; Field, John/0000-0003-3951-6365
FU Medical Research Council [G9900432]; NCI NIH HHS [R01 CA127219, R01
CA127219-02, R01 CA127219-04]
NR 54
TC 295
Z9 299
U1 2
U2 22
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD NOV 13
PY 2009
VL 85
IS 5
BP 679
EP 691
DI 10.1016/j.ajhg.2009.09.012
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 521JH
UT WOS:000271916500014
PM 19836008
ER
PT J
AU Bhatti, P
Kampa, D
Alexander, BH
McClure, C
Ringer, D
Doody, MM
Sigurdson, AJ
AF Bhatti, Parveen
Kampa, Diane
Alexander, Bruce H.
McClure, Christopher
Ringer, Danny
Doody, Michele M.
Sigurdson, Alice J.
TI Blood spots as an alternative to whole blood collection and the effect
of a small monetary incentive to increase participation in genetic
association studies
SO BMC MEDICAL RESEARCH METHODOLOGY
LA English
DT Article
ID US RADIOLOGIC TECHNOLOGISTS; DNA BANKING; CANCER
AB Background: Collection of buccal cells from saliva for DNA extraction offers a less invasive and convenient alternative to venipuncture blood collection that may increase participation in genetic epidemiologic studies. However, dried blood spot collection, which is also a convenient method, offers a means of collecting peripheral blood samples from which analytes in addition to DNA can be obtained.
Methods: To determine if offering blood spot collection would increase participation in genetic epidemiologic studies, we conducted a study of collecting dried blood spot cards by mail from a sample of female cancer cases (n = 134) and controls (n = 256) who were previously selected for a breast cancer genetics study and declined to provide a venipuncture blood sample. Participants were also randomized to receive either a $2.00 bill or no incentive with the blood spot collection kits.
Results: The average time between the venipuncture sample refusal and recruitment for the blood spot collection was 4.4 years. Thirty-seven percent of cases and 28% of controls provided a dried blood spot card. While the incentive was not associated with participation among controls (29% for $2.00 incentive vs. 26% for no incentive, p = 0.6), it was significantly associated with participation among the breast cancer cases (48% vs. 27%, respectively, p = 0.01). There did not appear to be any bias in response since no differences between cases and controls and incentive groups were observed when examining several demographic, work history and radiation exposure variables.
Conclusion: This study demonstrates that collection of dried blood spot cards in addition to venipuncture blood samples may be a feasible method to increase participation in genetic case-control studies.
C1 [Bhatti, Parveen] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, Seattle, WA 98104 USA.
[Bhatti, Parveen; Doody, Michele M.; Sigurdson, Alice J.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Kampa, Diane; Alexander, Bruce H.] Univ Minnesota, Sch Publ Hlth, Div Environm Hlth Sci, Minneapolis, MN USA.
[McClure, Christopher; Ringer, Danny] Res Triangle Inst, Rockville, MD USA.
RP Bhatti, P (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Program Epidemiol, 1124 Columbia St, Seattle, WA 98104 USA.
EM pbhatti@fhcrc.org; dkampa@umn.edu; balex@umn.edu; cmcclure@rti.org;
dringer@rti.org; doodym@mail.nih.gov; sigurdsa@mail.nih.giv
FU Intramural Research Program of the Division of Cancer Epidemiology and
Genetics [NO1-CP-31018, NO2-CP-31013, NO2-CP-31003]; National Cancer
Institute; National Institutes of Health; Department of Health and Human
Services
FX We are grateful to the radiologic technologists who participated in the
USRT Study; Jerry Reid of the American Registry of Radiologic
Technologists for continued support of this study; Allison Iwan of the
University of Minnesota for coordinating the blood spot collection and
Kim Doeden of Research Triangle International for preparing the blood
spot collection pictogram. This study was supported in part by contracts
NO1-CP-31018, NO2-CP-31013, and NO2-CP-31003 from the Intramural
Research Program of the Division of Cancer Epidemiology and Genetics,
National Cancer Institute, National Institutes of Health, Department of
Health and Human Services.
NR 13
TC 11
Z9 12
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2288
J9 BMC MED RES METHODOL
JI BMC Med. Res. Methodol.
PD NOV 13
PY 2009
VL 9
AR 76
DI 10.1186/1471-2288-9-76
PG 6
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 527ZH
UT WOS:000272409300001
PM 19912630
ER
PT J
AU Beard, WA
Shock, DD
Batra, VK
Pedersen, LC
Wilson, SH
AF Beard, William A.
Shock, David D.
Batra, Vinod K.
Pedersen, Lars C.
Wilson, Samuel H.
TI DNA Polymerase beta Substrate Specificity SIDE CHAIN MODULATION OF THE
"A-RULE"
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID INDUCED-FIT MECHANISM; ABASIC SITE; STRUCTURAL BASIS; NUCLEOTIDE
INCORPORATION; CRYSTAL-STRUCTURES; BASE SUBSTITUTION; TERNARY COMPLEXES;
TEMPLATE-PRIMER; MINOR-GROOVE; T-OPPOSITE
AB Apurinic/apyrimidinic (AP) sites are continuously generated in genomic DNA. Left unrepaired, AP sites represent noninstructional premutagenic lesions that are impediments to DNA synthesis. When DNA polymerases encounter an AP site, they generally insert dAMP. This preferential insertion is referred to as the A-rule. Crystallographic structures of DNA polymerase (pol) beta, a family X polymerase, with active site mismatched nascent base pairs indicate that the templating (i.e. coding) base is repositioned outside of the template binding pocket thereby diminishing interactions with the incorrect incoming nucleotide. This effectively produces an abasic site because the template pocket is devoid of an instructional base. However, the template pocket is not empty; an arginine residue (Arg-283) occupies the space vacated by the templating nucleotide. In this study, we analyze the kinetics of pol beta insertion opposite an AP site and show that the preferential incorporation of dAMP is lost with the R283A mutant. The crystallographic structures of pol beta bound to gapped DNA with an AP site analog (tertrahydrofuran) in the gap (binary complex) and with an incoming nonhydrolyzable dATP analog (ternary complex) were solved. These structures reveal that binding of the dATP analog induces a closed polymerase conformation, an unstable primer terminus, and an upstream shift of the templating residue even in the absence of a template base. Thus, dATP insertion opposite an abasic site and dATP misinsertions have common features.
C1 [Beard, William A.; Shock, David D.; Batra, Vinod K.; Pedersen, Lars C.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, NIH, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, NIH, 111 TW Alexander Dr,POB 12233,MD F3-01, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU National Institutes of Health, NIEHS [Z01-ES0500158, Z01-ES050161];
National Institutes of Health [1U19CA105010]
FX This work was supported, in whole or in part, by Research Projects
Z01-ES0500158 and Z01-ES050161 (to S. H. W.) in the Intramural Research
Program, National Institutes of Health, NIEHS, and was in association
with National Institutes of Health Grant 1U19CA105010.
NR 62
TC 32
Z9 32
U1 0
U2 0
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 13
PY 2009
VL 284
IS 46
BP 31680
EP 31689
DI 10.1074/jbc.M109.029843
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 516VZ
UT WOS:000271572700023
PM 19759017
ER
PT J
AU Pletnev, S
Gurskaya, NG
Pletneva, NV
Lukyanov, KA
Chudakov, DM
Martynov, VI
Popov, VO
Kovalchuk, MV
Wlodawer, A
Dauter, Z
Pletnev, V
AF Pletnev, Sergei
Gurskaya, Nadya G.
Pletneva, Nadya V.
Lukyanov, Konstantin A.
Chudakov, Dmitri M.
Martynov, Vladimir I.
Popov, Vladimir O.
Kovalchuk, Mikhail V.
Wlodawer, Alexander
Dauter, Zbigniew
Pletnev, Vladimir
TI Structural Basis for Phototoxicity of the Genetically Encoded
Photosensitizer KillerRed
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID RED FLUORESCENT PROTEIN; INTERNAL WATER CHAIN; IN-VIVO;
CRYSTAL-STRUCTURE; ELECTRON-TRANSFER; CHROMOPHORE FORMATION; MONOMERIC
RED; CYTOCHROME F; CANCER-CELLS; WHOLE-BODY
AB KillerRed is the only known fluorescent protein that demonstrates notable phototoxicity, exceeding that of the other green and red fluorescent proteins by at least 1,000-fold. KillerRed could serve as an instrument to inactivate target proteins or to kill cell populations in photodynamic therapy. However, the nature of KillerRed phototoxicity has remained unclear, impeding the development of more phototoxic variants. Here we present the results of a high resolution crystallographic study of KillerRed in the active fluorescent and in the photobleached non-fluorescent states. A unique and striking feature of the structure is a water-filled channel reaching the chromophore area from the end cap of the beta-barrel that is probably one of the key structural features responsible for phototoxicity. A study of the structure-function relationship of KillerRed, supported by structure-based, site-directed mutagenesis, has also revealed the key residues most likely responsible for the phototoxic effect. In particular, Glu(68) and Ser(119), located adjacent to the chromophore, have been assigned as the primary trigger of the reaction chain.
C1 [Dauter, Zbigniew] NCI, Synchrotron Radiat Res Sect, Macromol Crystallog Lab, SAIC Frederick Inc, Argonne, IL 60439 USA.
[Gurskaya, Nadya G.; Pletneva, Nadya V.; Lukyanov, Konstantin A.; Chudakov, Dmitri M.; Martynov, Vladimir I.; Pletnev, Vladimir] Russian Acad Sci, Shemyakin Ovchinnikov Inst Bioorgan Chem, Moscow 117997, Russia.
[Popov, Vladimir O.] Russian Acad Sci, AN Bach Inst Biochem, Moscow 117234, Russia.
[Kovalchuk, Mikhail V.] Russian Acad Sci, Inst Crystallog, Moscow 119333, Russia.
[Wlodawer, Alexander] NCI, Prot Struct Sect, Macromol Crystallog Lab, NIH, Frederick, MD 21702 USA.
RP Pletnev, S (reprint author), SAIC Frederick Inc, Basic Res Program, Argonne, IL 60439 USA.
EM svp@ncifcrf.gov
RI Chudakov, Dmitriy/G-7741-2014; Pletneva, Nadya/F-7839-2014; Pletnev,
Vladimir/Q-6151-2016; Martynov, Vladimir/S-3483-2016
OI Chudakov, Dmitriy/0000-0003-0430-790X; Martynov,
Vladimir/0000-0003-4923-6842
FU National Institutes of Health Intramural Research Program, NCI, Center
for Cancer Research; National Institutes of Health, NCI
[HHSN2612008000001E]; Russian Foundation for Basic Research
[07-04-00054, 08-04-01702-a]; Russian Federal Agency for Science and
Innovations [02.513.12.3013]; Molecular and Cell Biology Program RAS;
President of the Russian Federation [MD-2780.2009.4]; United States
Department of Energy, Office of Science, Office of Basic Energy Sciences
[W-31-109-Eng-38]
FX This work was supported, in whole or in part, by the National Institutes
of Health Intramural Research Program, NCI, Center for Cancer Research
and by National Institutes of Health, NCI, Contract HHSN2612008000001E.
This project was also supported in part by Russian Foundation for Basic
Research Grants 07-04-00054 and 08-04-01702-a; by Russian Federal Agency
for Science and Innovations Grant 02.513.12.3013; by the Molecular and
Cell Biology Program RAS; and by grants from the President of the
Russian Federation (MD-2780.2009.4). Use of the Advanced Photon Source
was supported by the United States Department of Energy, Office of
Science, Office of Basic Energy Sciences, under Contract
W-31-109-Eng-38.
NR 58
TC 61
Z9 63
U1 0
U2 14
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 13
PY 2009
VL 284
IS 46
BP 32028
EP 32039
DI 10.1074/jbc.M109.054973
PG 12
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 516VZ
UT WOS:000271572700058
PM 19737938
ER
PT J
AU Wang, H
Hu, LP
Dalen, K
Dorward, H
Marcinkiewicz, A
Russell, D
Gong, DW
Londos, C
Yamaguchi, T
Holm, C
Rizzo, MA
Brasaemle, D
Sztalryd, C
AF Wang, Hong
Hu, Liping
Dalen, Knut
Dorward, Heidi
Marcinkiewicz, Amy
Russell, Deanna
Gong, Dawei
Londos, Constantine
Yamaguchi, Tomohiro
Holm, Cecilia
Rizzo, Mark A.
Brasaemle, Dawn
Sztalryd, Carole
TI Activation of Hormone-sensitive Lipase Requires Two Steps, Protein
Phosphorylation and Binding to the PAT-1 Domain of Lipid Droplet Coat
Proteins
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID ADIPOSE TRIGLYCERIDE LIPASE; FLUORESCENCE POLARIZATION MICROSCOPY;
A-MEDIATED LIPOLYSIS; PERILIPIN-A; ENDOPLASMIC-RETICULUM; STIMULATED
LIPOLYSIS; ADIPOCYTE LIPOLYSIS; 3T3-L1 ADIPOCYTES; STORAGE DROPLET;
ALPHA-SYNUCLEIN
AB Lipolysis is an important metabolic pathway controlling energy homeostasis through degradation of triglycerides stored in lipid droplets and release of fatty acids. Lipid droplets of mammalian cells are coated with one or more members of the PAT protein family, which serve important functions in regulating lipolysis. In this study, we investigate the mechanisms by which PAT family members, perilipin A, adipose differentiation-related protein (ADFP), and LSDP5, control lipolysis catalyzed by hormone-sensitive lipase (HSL), a major lipase in adipocytes and several non-adipose cells. We applied fluorescence microscopic tools to analyze proteins in situ in cultured Chinese hamster ovary cells using fluorescence recovery after photo-bleaching and anisotropy Forster resonance energy transfer. Fluorescence recovery after photobleaching data show that ADFP and LSDP5 exchange between lipid droplet and cytoplasmic pools, whereas perilipin A does not. Differences in protein mobility do not correlate with PAT protein-mediated control of lipolysis catalyzed by HSL or endogenous lipases. Forster resonance energy transfer and co-immunoprecipitation experiments reveal that each of the three PAT proteins bind HSL through interaction of the lipase with amino acids within the highly conserved amino-terminal PAT-1 domain. ADFP and LSDP5 bind HSL under basal conditions, whereas phosphorylation of serine residues within three amino-terminal protein kinase A consensus sequences of perilipin A is required for HSL binding and maximal lipolysis. Finally, protein kinase A-mediated phosphorylation of HSL increases lipolysis in cells expressing ADFP or LSDP5; in contrast, phosphorylation of perilipin A exerts the major control over HSL-mediated lipolysis when perilipin is the main lipid droplet protein.
C1 [Wang, Hong; Hu, Liping; Gong, Dawei; Sztalryd, Carole] Univ Maryland, Sch Med, Dept Med, Div Endocrinol, Baltimore, MD 21201 USA.
[Wang, Hong; Hu, Liping; Sztalryd, Carole] Univ Maryland, Sch Med, Baltimore Vet Affairs Hlth Care Ctr, Geriatr Res Educ & Clin Ctr, Baltimore, MD 21201 USA.
[Dalen, Knut; Dorward, Heidi; Londos, Constantine; Rizzo, Mark A.] NIDDK, Cellular & Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
[Marcinkiewicz, Amy; Russell, Deanna; Brasaemle, Dawn] Rutgers State Univ, Dept Nutr Sci, New Brunswick, NJ 08901 USA.
[Holm, Cecilia] Lund Univ, Dept Expt Med Sci, SE-22184 Lund, Sweden.
[Rizzo, Mark A.] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
[Yamaguchi, Tomohiro] Hyogo Med Univ, Grad Sch Life Sci, Kamigori, Hyogo 6781297, Japan.
RP Sztalryd, C (reprint author), Univ Maryland, Sch Med, Dept Med, Div Endocrinol, Rm 445,Howard Hall,660 W Redwood St, Baltimore, MD 21201 USA.
EM csztalry@grecc.umaryland.edu
RI Dalen, Knut Tomas/C-4719-2016;
OI Dalen, Knut Tomas/0000-0002-0270-5982; Brasaemle,
Dawn/0000-0002-8553-8285
FU National Institutes of Health [RO1 DK075017, RO1 DK054797]; NIDDK
Intramural Research Programs; American Diabetes Association
[1-05-CD-17]; Geriatric Research, Education, and Clinical Center,
Baltimore Veterans Affairs Health Care Center; Clinical Nutrition
Research Unit of Maryland [DK072488]
FX This work was supported, in whole or in part, by National Institutes of
Health Grants RO1 DK075017 (to C. S.) and RO1 DK054797 (to D. L. B.) and
NIDDK Intramural Research Programs. This work was also supported by
Career Development Award 1-05-CD-17 from the American Diabetes
Association (to C. S.), the Geriatric Research, Education, and Clinical
Center, Baltimore Veterans Affairs Health Care Center, and the Clinical
Nutrition Research Unit of Maryland Grant DK072488.
NR 44
TC 77
Z9 80
U1 0
U2 9
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 13
PY 2009
VL 284
IS 46
BP 32116
EP 32125
DI 10.1074/jbc.M109.006726
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 516VZ
UT WOS:000271572700066
PM 19717842
ER
PT J
AU McElwee, MK
Song, MO
Freedman, JH
AF McElwee, Matthew K.
Song, Min Ok
Freedman, Jonathan H.
TI Copper Activation of NF-kB Signaling in HepG2 Cells
SO JOURNAL OF MOLECULAR BIOLOGY
LA English
DT Article
DE copper; NF-kappa B; HepG2 cells; gene expression; microarray
ID KAPPA-B ACTIVATION; HEPATITIS-C VIRUS; TOXIC MILK MOUSE;
GENE-EXPRESSION; HEPATOCELLULAR-CARCINOMA; WILSONS-DISEASE; METAL-IONS;
IN-VIVO; LIVER; PHOSPHORYLATION
AB Copper is a persistent environmental contaminant, and exposure to elevated levels of this transition metal can result in a variety of pathologies. Copper affects the transcription of multiple defense and repair genes to protect against metal-induced pathologies. HepG2 cells were treated with copper under multiple conditions and microarray analyses were previously performed to better understand the mechanisms by which copper affects the transcription of stress-responsive genes. Analysis of the microarray data indicated that copper modulates multiple signal transduction pathways, including those mediated by NF-kappa B. Luciferase assays, quantitative reverse transcription real-time PCR, and chemical inhibition in HepG2 cells validated the microarray results and confirmed that NF-kappa B was activated by stress-inducible concentrations of copper. In addition, two novel NF-kappa B-regulated genes, SRXN1 (sulfiredoxin 1 homolog) and ZFAND2A (zinc-finger, AN1-type domain 2A), were identified. Our results indicate that the activation of NF-kappa B may be important for survival under elevated concentrations of copper. Published by Elsevier Ltd.
C1 [McElwee, Matthew K.; Song, Min Ok; Freedman, Jonathan H.] NIEHS, Mol Toxicol Lab, NIH, DHHS, Res Triangle Pk, NC 27709 USA.
[McElwee, Matthew K.] Duke Univ, Nicholas Sch Environm, Durham, NC 27708 USA.
RP Freedman, JH (reprint author), NIEHS, Mol Toxicol Lab, NIH, DHHS, Box 12233,MD E1-05,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM freedma1@niehs.nih.gov
FU National Institutes of Health [U19ES011375, P42 ES10356]; National
Institutes of Health; National Institute of Environmental Health
Sciences [Z01ES102045]
FX This work was supported (in part) by National Institutes of Health
Grants U19ES011375 and P42 ES10356 and by the Intramural Research
Program of the National Institutes of Health and National Institute of
Environmental Health Sciences (Z01ES102045).
NR 47
TC 24
Z9 24
U1 1
U2 6
PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
PI LONDON
PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND
SN 0022-2836
J9 J MOL BIOL
JI J. Mol. Biol.
PD NOV 13
PY 2009
VL 393
IS 5
BP 1013
EP 1021
DI 10.1016/j.jmb.2009.08.077
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 517ER
UT WOS:000271596500002
PM 19747488
ER
PT J
AU Wolf, RC
Vasic, N
Sambataro, F
Hose, A
Frasch, K
Schmid, M
Walter, H
AF Wolf, Robert Christian
Vasic, Nenad
Sambataro, Fabio
Hoese, Annett
Frasch, Karel
Schmid, Markus
Walter, Henrik
TI Temporally anticorrelated brain networks during working memory
performance reveal aberrant prefrontal and hippocampal connectivity in
patients with schizophrenia
SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY
LA English
DT Review
DE Functional connectivity; Functional magnetic resonance imaging;
Hippocampus; Independent component analysis; Prefrontal cortex;
Schizophrenia
ID ALTERED EFFECTIVE CONNECTIVITY; POSITRON-EMISSION-TOMOGRAPHY;
TASK-INDUCED DEACTIVATION; BOLD SIGNAL FLUCTUATIONS; DEFAULT MODE
NETWORK; FUNCTIONAL CONNECTIVITY; CORTICAL DYSFUNCTION; CORTEX
DYSFUNCTION; FMRI ACTIVATION; DEPRESSION
AB Functional neuroimaging studies on cognitive dysfunction in schizophrenia have suggested regional brain activation changes in the dorsolateral prefrontal cortex and the medial temporal lobe. However, less is known about the functional coupling of these areas during cognitive performance. In this study, we used functional magnetic resonance imaging, a verbal working memory (WM) task and multivariate statistical techniques to investigate the functional coupling of temporally anticorrelated neural networks during cognitive processing in patients with schizophrenia (n=16) compared to healthy controls (n=16). Independent component analysis identified 18 independent components (ICs) among which two ICs were selected for further analyses. These ICs included temporally anticorrelated networks which were most highly associated with the delay period of the task in both healthy controls and patients with schizophrenia. Functional network abnormalities in patients with schizophrenia were detected within a "task-positive" lateral frontoparietal network, where increased functional connectivity was found in bilateral dorsolateral prefrontal regions. In addition, aberrant functional coupling of the hippocampal cortex in patients with schizophrenia was detected within a "task-negative" medial frontotemporal network. In patients with schizophrenia, functional connectivity indices in the left dorsolateral prefrontal cortex and the right hippocampal cortex were positively correlated with accuracy during the WM task, while the connectivity strength in the right dorsolateral prefrontal cortex was negatively correlated with measures of symptom severity. These data suggest that within two temporally anticorrelated network states, patients with schizophrenia exhibit increased and persistent dorsolateral prefrontal and hippocampal connectivity during WM performance. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Wolf, Robert Christian; Vasic, Nenad; Schmid, Markus] Univ Ulm, Dept Psychiat & Psychotherapy 3, D-89075 Ulm, Germany.
[Sambataro, Fabio] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, NIH, Bethesda, MD 20892 USA.
[Hoese, Annett; Frasch, Karel] Univ Ulm, Dept Psychiat & Psychotherapy 2, Gunzburg, Germany.
[Walter, Henrik] Univ Bonn, Div Med Psychol, Dept Psychiat, Bonn, Germany.
RP Wolf, RC (reprint author), Univ Ulm, Dept Psychiat & Psychotherapy 3, Leimgrubenweg 12-14, D-89075 Ulm, Germany.
EM christian.wolf@uni-ulm.de
RI Sambataro, Fabio/E-3426-2010; Walter, Henrik/O-2612-2013;
OI Sambataro, Fabio/0000-0003-2102-416X; Frasch, Karel/0000-0003-3308-4258
NR 82
TC 47
Z9 47
U1 3
U2 16
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0278-5846
J9 PROG NEURO-PSYCHOPH
JI Prog. Neuro-Psychopharmacol. Biol. Psychiatry
PD NOV 13
PY 2009
VL 33
IS 8
BP 1464
EP 1473
DI 10.1016/j.pnpbp.2009.07.032
PG 10
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 532RL
UT WOS:000272767100023
PM 19666074
ER
PT J
AU Baskar, S
Suschak, JM
Samija, I
Srinivasan, R
Childs, RW
Pavletic, SZ
Bishop, MR
Rader, C
AF Baskar, Sivasubramanian
Suschak, Jessica M.
Samija, Ivan
Srinivasan, Ramaprasad
Childs, Richard W.
Pavletic, Steven Z.
Bishop, Michael R.
Rader, Christoph
TI A human monoclonal antibody drug and target discovery platform for
B-cell chronic lymphocytic leukemia based on allogeneic hematopoietic
stem cell transplantation and phage display
SO BLOOD
LA English
DT Article
ID GRAFT-VERSUS-LEUKEMIA; CHRONIC MYELOGENOUS LEUKEMIA; MINOR
HISTOCOMPATIBILITY ANTIGEN; BONE-MARROW-TRANSPLANTATION; AFFINITY
MATURATION; COMPLETE RESPONSE; MULTIPLE-MYELOMA; IMMUNE-RESPONSES;
POTENTIAL TARGET; EXPRESSION
AB Allogeneic hematopoietic stem cell transplantation (alloHSCT) is the only potentially curative treatment available for patients with B-cell chronic lymphocytic leukemia (B-CLL). Here, we show that post-alloHSCT antibody repertoires can be mined for the discovery of fully human monoclonal antibodies to B-CLL cellsurface antigens. Sera collected from B-CLL patients at defined times after alloHSCT showed selective binding to primary B-CLL cells. Pre-alloHSCT sera, donor sera, and control sera were negative. To identify post-alloHSCT serum antibodies and subsequently B-CLL cell-surface antigens they recognize, we generated a human antibody-binding fragment (Fab) library from post-alloHSCT peripheral blood mononuclear cells and selected it on primary B-CLL cells by phage display. A panel of Fab with B-CLL cell-surface reactivity was strongly enriched. Selection was dominated by highly homologous Fab predicted to bind the same antigen. One Fab was converted to immunoglobulin G1 and analyzed for reactivity with peripheral blood mononuclear cells from B-CLL patients and healthy volunteers. Cell-surface antigen expression was restricted to primary B cells and up-regulated in primary B-CLL cells. Mining post-alloHSCT antibody repertoires offers a novel route to discover fully human monoclonal antibodies and identify antigens of potential therapeutic relevance to B-CLL and possibly other cancers. Trials described herein were registered at www.clinicaltrials.gov as nos. NCT00055744 and NCT00003838. (Blood. 2009;114:4494-4502)
C1 [Rader, Christoph] NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Srinivasan, Ramaprasad; Childs, Richard W.] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA.
RP Rader, C (reprint author), NCI, Expt Transplantat & Immunol Branch, Ctr Canc Res, NIH, 9000 Rockville Pike,Bldg 10 CRC,Rm 3-3150, Bethesda, MD 20892 USA.
EM raderc@mail.nih.gov
OI Samija, Ivan/0000-0002-5633-5745
FU Intramural Research Program of the Center for Cancer Research; National
Cancer Institute, NIH; National Foundation for Science, Higher Education
and Technological Development of the Republic of Croatia
FX This work was supported by the Intramural Research Program of the Center
for Cancer Research, National Cancer Institute, NIH (C.R.) and through a
stipend from the National Foundation for Science, Higher Education and
Technological Development of the Republic of Croatia (I.S.).
NR 50
TC 8
Z9 8
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 12
PY 2009
VL 114
IS 20
BP 4494
EP 4502
DI 10.1182/blood-2009-05-222786
PG 9
WC Hematology
SC Hematology
GA 518WW
UT WOS:000271727500022
PM 19667400
ER
PT J
AU Chang, CC
Zhou, XB
Taylor, JJ
Huang, WT
Ren, XW
Monzon, F
Feng, YD
Rao, PH
Lu, XY
Fabio, F
Hilsenbeck, S
Creighton, CJ
Jaffe, ES
Lau, CC
AF Chang, Chung-Che
Zhou, Xiaobo
Taylor, Jesalyn J.
Huang, Wan-Ting
Ren, Xianwen
Monzon, Federico
Feng, Yongdong
Rao, Pulivarthi H.
Lu, Xin-Yan
Fabio, Facchetti
Hilsenbeck, Susan
Creighton, Chad J.
Jaffe, Elaine S.
Lau, Ching-Ching
TI Genomic profiling of plasmablastic lymphoma using array comparative
genomic hybridization (aCGH): revealing significant overlapping genomic
lesions with diffuse large B-cell lymphoma
SO JOURNAL OF HEMATOLOGY & ONCOLOGY
LA English
DT Article
ID ACTIVE ANTIRETROVIRAL THERAPY; ORAL-CAVITY; MICROARRAY; GENES;
IDENTIFICATION; EXPRESSION; ERA
AB Background: Plasmablastic lymphoma (PL) is a subtype of diffuse large B-cell lymphoma (DLBCL). Studies have suggested that tumors with PL morphology represent a group of neoplasms with clinopathologic characteristics corresponding to different entities including extramedullary plasmablastic tumors associated with plasma cell myeloma (PCM). The goal of the current study was to evaluate the genetic similarities and differences among PL, DLBCL (AIDS-related and non AIDS-related) and PCM using array-based comparative genomic hybridization.
Results: Examination of genomic data in PL revealed that the most frequent segmental gain (>40%) include: 1p36.11-1p36.33, 1p34.1-1p36.13, 1q21.1-1q23.1, 7q11.2-7q11.23, 11q12-11q13.2 and 22q12.2-22q13.3. This correlated with segmental gains occurring in high frequency in DLBCL (AIDS-related and non AIDS-related) cases. There were some segmental gains and some segmental loss that occurred in PL but not in the other types of lymphoma suggesting that these foci may contain genes responsible for the differentiation of this lymphoma. Additionally, some segmental gains and some segmental loss occurred only in PL and AIDS associated DLBCL suggesting that these foci may be associated with HIV infection. Furthermore, some segmental gains and some segmental loss occurred only in PL and PCM suggesting that these lesions may be related to plasmacytic differentiation.
Conclusion: To the best of our knowledge, the current study represents the first genomic exploration of PL. The genomic aberration pattern of PL appears to be more similar to that of DLBCL (AIDS-related or non AIDS-related) than to PCM. Our findings suggest that PL may remain best classified as a subtype of DLBCL at least at the genome level.
C1 [Chang, Chung-Che; Taylor, Jesalyn J.; Monzon, Federico; Feng, Yongdong] Methodist Hosp, Dept Pathol, Houston, TX 77030 USA.
[Chang, Chung-Che; Taylor, Jesalyn J.; Monzon, Federico; Feng, Yongdong] Methodist Hosp, Res Inst, Houston, TX 77030 USA.
[Chang, Chung-Che; Monzon, Federico] Weill Cornell Med Coll, Dept Pathol, New York, NY USA.
[Zhou, Xiaobo; Ren, Xianwen] Methodist Hosp, Dept Bioinformat Core, Houston, TX 77030 USA.
[Rao, Pulivarthi H.; Lu, Xin-Yan; Lau, Ching-Ching] Baylor Coll Med, Texas Childrens Canc Ctr, Dept Pediat, Houston, TX 77030 USA.
[Fabio, Facchetti] Univ Brescia, Dept Pathol 1, Spedali Civili, Brescia, Italy.
[Hilsenbeck, Susan] Dept Med, Houston, TX USA.
[Hilsenbeck, Susan; Creighton, Chad J.] Dan L Duncan Canc Ctr, Houston, TX USA.
[Creighton, Chad J.] Div Biostat, Houston, TX USA.
[Jaffe, Elaine S.] NCI, Dept Hematol, NIH, Bethesda, MD 20892 USA.
RP Chang, CC (reprint author), Methodist Hosp, Dept Pathol, Houston, TX 77030 USA.
EM jeffchang@tmhs.org; XZhou@tmhs.org; jesalynt@hotmail.com;
huang_minnie@hotmail.com; renxwise@gmail.com; FAMonzon@tmhs.org;
YFeng@tmhs.org; prao@bcm.edu; xxlu@txccc.org; facchett@med.unibs.it;
sgh@bcm.edu; creighto@bcm.edu; ejaffe@mail.nih.gov; clau@txccc.org
FU National Institute of Dental and Craniofacial Research, National
Institute of Health [DE017086]
FX The authors would like to express appreciation to AIDS and Cancer
Specimen Resource, National Cancer Institute for providing some
specimens for this study. This study was supported by a grant from
National Institute of Dental and Craniofacial Research, National
Institute of Health (DE017086) (C-C. C.).
NR 20
TC 24
Z9 27
U1 0
U2 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-8722
J9 J HEMATOL ONCOL
JI J. Hematol. Oncol.
PD NOV 12
PY 2009
VL 2
AR 47
DI 10.1186/1756-8722-2-47
PG 6
WC Oncology; Hematology
SC Oncology; Hematology
GA 528ZE
UT WOS:000272484700002
PM 19909553
ER
PT J
AU Park, KD
Morieux, P
Salome, C
Cotten, SW
Reamtong, O
Eyers, C
Gaskell, SJ
Stables, JP
Liu, RH
Kohn, H
AF Park, Ki Duk
Morieux, Pierre
Salome, Christophe
Cotten, Steven W.
Reamtong, Onrapak
Eyers, Claire
Gaskell, Simon J.
Stables, James P.
Liu, Rihe
Kohn, Harold
TI Lacosamide Isothiocyanate-Based Agents: Novel Agents To Target and
Identify Lacosamide Receptors
SO JOURNAL OF MEDICINAL CHEMISTRY
LA English
DT Article
ID N-BENZYLACETAMIDE DERIVATIVES; GATED SODIUM-CHANNELS; ANTIEPILEPTIC
DRUGS; ANTICONVULSANT ACTIVITIES; MEDIATED PHENOMENA; OPIOID RECEPTORS;
IRREVERSIBLE LIGANDS; AFFINITY LIGANDS; AMINO-ACIDS;
BENZODIAZEPINE-RECEPTORS
AB (R)-Lacosamide ((R)-2, (R)-N-benzyl 2-acetamido-3-methoxypropionamide) has recently gained regulatory approval for the treatment of partial-onset seizures in adults. Whole animal pharmacological studies have documented that (R)-2 function is unique: A robust strategy is advanced for the discovery of interacting proteins associated with function and toxicity of (R)-2 through the use of (R)-2 analogues, 3, which contain "affinity bait (AB)" and "chemical reporter (CR)" functional groups. In 3, covalent modification of the interacting proteins proceeds at the AB moiety, and detection or isolation of the selectively captured protein occurs through the bioorthogonal CR group upon reaction with all appropriate probe. We report the synthesis, pharmacological evaluation, and interrogation of the mouse soluble brain proteome using 3 where the AB group is an isothiocyanate moiety. One compound, (R)-N-(4-isothiocyanato)benzyl 2-acetamido-3-(prop-2-ynyloxy)propionamide ((R)-9), exhibited excellent Seizure protection in mice, and like (R)-2, anticonvulsant activity principally resided in the (R)-stereoisomer. Several proteins were preferentially labeled by (R)-9 compared with (S)-9, including collapsin response mediator protein 2.
C1 [Park, Ki Duk; Morieux, Pierre; Salome, Christophe; Cotten, Steven W.; Liu, Rihe; Kohn, Harold] Univ N Carolina, Div Med Chem & Nat Prod, Eshelman Sch Pharm, Chapel Hill, NC 27599 USA.
[Reamtong, Onrapak; Eyers, Claire; Gaskell, Simon J.] Univ Manchester, Manchester Interdisciplinary Bioctr, Michael Barber Ctr Mass Spectrometry, Manchester M1 7DN, Lancs, England.
[Stables, James P.] NINDS, Anticonvulsant Screening Program, NIH, Rockville, MD 20892 USA.
[Liu, Rihe] Univ N Carolina, Carolina Ctr Genome Sci, Chapel Hill, NC 27599 USA.
[Kohn, Harold] Univ N Carolina, Dept Chem, Chapel Hill, NC 27599 USA.
RP Liu, RH (reprint author), Univ N Carolina, Div Med Chem & Nat Prod, Eshelman Sch Pharm, Chapel Hill, NC 27599 USA.
EM rliu@email.unc.edu; hkohn@email.unc.edu
RI Eyers, Claire/C-6291-2013
OI Eyers, Claire/0000-0002-3223-5926
FU NINDS and the Anticonvulsant Screening Program (ASP) at the National
Institutes of Health; National Institute of Netll-ological Disorders and
Stroke [R01NS054112, F31NS060358]; Korean Government (MOEHRD)
[KRF-2006-352-C00042]
FX The authors thank the NINDS and the Anticonvulsant Screening Program
(ASP) at the National Institutes of Health for kindly performing the
pharmacological studies via the ASP's contract site at the University of
Utah with Drs. H. Wolfe, H. S. White, and K. Wilcox. Funds for this
study was generously provided by Grants R01NS054112 (H.K., R.L.) and
F31NS060358 (P.M.) from the National Institute of Netll-ological
Disorders and Stroke and by the Korean Research Foundation Grant funded
by the Korean Government (MOEHRD) Grant KRF-2006-352-C00042 (K.D.P.).
The content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institute of
Neurological Disorders and Stroke of- the National Institutes of Health.
Harold Kohn has a royalty-stake position in (R)-2.
NR 85
TC 29
Z9 30
U1 1
U2 5
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0022-2623
J9 J MED CHEM
JI J. Med. Chem.
PD NOV 12
PY 2009
VL 52
IS 21
BP 6897
EP 6911
DI 10.1021/jm9012054
PG 15
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 514WW
UT WOS:000271427900041
PM 19795888
ER
PT J
AU Scott, I
AF Scott, Iain
TI No special cases in efforts to stop immigration fraud
SO NATURE
LA English
DT Letter
C1 NHLBI, Bethesda, MD 20892 USA.
RP Scott, I (reprint author), NHLBI, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM scotti@nhlbi.nih.gov
NR 0
TC 0
Z9 0
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 12
PY 2009
VL 462
IS 7270
BP 159
EP 159
DI 10.1038/462159a
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517YM
UT WOS:000271655100019
PM 19907474
ER
PT J
AU Keiser, MJ
Setola, V
Irwin, JJ
Laggner, C
Abbas, AI
Hufeisen, SJ
Jensen, NH
Kuijer, MB
Matos, RC
Tran, TB
Whaley, R
Glennon, RA
Hert, J
Thomas, KLH
Edwards, DD
Shoichet, BK
Roth, BL
AF Keiser, Michael J.
Setola, Vincent
Irwin, John J.
Laggner, Christian
Abbas, Atheir I.
Hufeisen, Sandra J.
Jensen, Niels H.
Kuijer, Michael B.
Matos, Roberto C.
Tran, Thuy B.
Whaley, Ryan
Glennon, Richard A.
Hert, Jerome
Thomas, Kelan L. H.
Edwards, Douglas D.
Shoichet, Brian K.
Roth, Bryan L.
TI Predicting new molecular targets for known drugs
SO NATURE
LA English
DT Article
ID SEROTONIN RECEPTORS; REUPTAKE INHIBITOR; CHEMICAL BIOLOGY; DOUBLE-BLIND;
AGONIST; N,N-DIMETHYLTRYPTAMINE; HALLUCINOGEN; PHARMACOLOGY;
PROMISCUITY; MECHANISM
AB Although drugs are intended to be selective, at least some bind to several physiological targets, explaining side effects and efficacy. Because many drug-target combinations exist, it would be useful to explore possible interactions computationally. Here we compared 3,665 US Food and Drug Administration (FDA)-approved and investigational drugs against hundreds of targets, defining each target by its ligands. Chemical similarities between drugs and ligand sets predicted thousands of unanticipated associations. Thirty were tested experimentally, including the antagonism of the beta(1) receptor by the transporter inhibitor Prozac, the inhibition of the 5-hydroxytryptamine (5-HT) transporter by the ion channel drug Vadilex, and antagonism of the histamine H(4) receptor by the enzyme inhibitor Rescriptor. Overall, 23 new drug-target associations were confirmed, five of which were potent (<100 nM). The physiological relevance of one, the drug N,N-dimethyltryptamine (DMT) on serotonergic receptors, was confirmed in a knockout mouse. The chemical similarity approach is systematic and comprehensive, and may suggest side-effects and new indications for many drugs.
C1 [Keiser, Michael J.; Irwin, John J.; Laggner, Christian; Hert, Jerome; Thomas, Kelan L. H.; Edwards, Douglas D.; Shoichet, Brian K.] Univ Calif San Francisco, Dept Pharmaceut Chem, San Francisco, CA 94143 USA.
[Keiser, Michael J.] Univ Calif San Francisco, Grad Grp Bioinformat, San Francisco, CA 94143 USA.
[Setola, Vincent; Kuijer, Michael B.; Matos, Roberto C.; Tran, Thuy B.; Whaley, Ryan; Roth, Bryan L.] Case Western Reserve Univ, Sch Med, Dept Pharmacol, NIMH Psychoact Drug Screening Program, Cleveland, OH 44106 USA.
[Abbas, Atheir I.] Case Western Reserve Univ, Sch Med, Dept Biochem, Cleveland, OH 44106 USA.
[Hufeisen, Sandra J.; Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, Chapel Hill Sch Med, Div Med Chem & Nat Prod, Chapel Hill, NC 27759 USA.
[Hufeisen, Sandra J.; Jensen, Niels H.; Roth, Bryan L.] Univ N Carolina, Chapel Hill Sch Med, Dept Pharmacol, Chapel Hill, NC 27759 USA.
[Glennon, Richard A.] Virginia Commonwealth Univ, Dept Med Chem, Sch Pharm, Med Coll Virginia Campus, Richmond, VA 23298 USA.
[Thomas, Kelan L. H.] Univ Michigan Hlth Syst, Ann Arbor, MI 48109 USA.
RP Shoichet, BK (reprint author), Univ Calif San Francisco, Dept Pharmaceut Chem, 1700 4th St, San Francisco, CA 94143 USA.
EM shoichet@cgl.ucsf.edu; bryan_roth@med.unc.edu
RI Hert, Jerome/A-8158-2008; Roth, Bryan/F-3928-2010; Keiser,
Michael/F-2825-2016;
OI Keiser, Michael/0000-0002-1240-2192; Irwin, John/0000-0002-1195-6417;
Thomas, Kelan/0000-0003-2818-270X; Hert/0000-0003-3062-8029
FU National Institutes of Health (NIH); National Science Foundation;
European Commission; Max Kade Foundation; NARSAD; Michael Hooker Chair
FX Supported by grants from the National Institutes of Health (NIH)
supporting chemoinformatics (to B. K. S. and J. J. I.) and NIH grants
and contracts supporting drug discovery and receptor pharmacology (to B.
L. R). M. J. K., J. H. and C. L. were supported by fellowships from the
National Science Foundation, the 6th FP of the European Commission, and
the Max Kade Foundation, respectively. B. L. R. was also supported by a
Distinguished Investigator Award from the NARSAD and the Michael Hooker
Chair. We thank T. Oprea of Sunset Molecular for WOMBAT, Elsevier MDL
for the MDDR, Scitegic for PipelinePilot, J. Overington of the European
Bioinformatics Institute (EMBL-EBI) for StARlite, Daylight Chemical
Information Systems Inc. for the Daylight toolkit, and J. Gingrich for
5-HT2A knockout mice.
NR 53
TC 685
Z9 703
U1 14
U2 116
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 12
PY 2009
VL 462
IS 7270
BP 175
EP U48
DI 10.1038/nature08506
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517YM
UT WOS:000271655100034
PM 19881490
ER
PT J
AU Soeda, A
Park, M
Lee, D
Mintz, A
Androutsellis-Theotokis, A
McKay, RD
Engh, J
Iwama, T
Kunisada, T
Kassam, AB
Pollack, IF
Park, DM
AF Soeda, A.
Park, M.
Lee, D.
Mintz, A.
Androutsellis-Theotokis, A.
McKay, R. D.
Engh, J.
Iwama, T.
Kunisada, T.
Kassam, A. B.
Pollack, I. F.
Park, D. M.
TI Hypoxia promotes expansion of the CD133-positive glioma stem cells
through activation of HIF-1 alpha
SO ONCOGENE
LA English
DT Article
DE glioma; cancer stem cell; HIF-1 alpha; hypoxia; CD133
ID INDUCIBLE FACTOR 1-ALPHA; CENTRAL-NERVOUS-SYSTEM; ENDOTHELIAL
GROWTH-FACTOR; TUMOR ANGIOGENESIS; TRANSCRIPTIONAL ACTIVITY; HUMAN
GLIOBLASTOMA; CANCER CELLS; FACTOR-I; EXPRESSION; PROLIFERATION
AB Hypoxia contributes to the progression of a variety of cancers by activating adaptive transcriptional programs that promote cell survival, motility and tumor angiogenesis. Although the importance of hypoxia and subsequent hypoxia-inducible factor-1 alpha (HIF-1 alpha) activation in tumor angiogenesis is well known, their role in the regulation of glioma-derived stem cells is unclear. In this study, we show that hypoxia (1% oxygen) promotes the self-renewal capacity of CD133-positive human glioma-derived cancer stem cells (CSCs). Propagation of the glioma-derived CSCs in a hypoxic environment also led to the expansion of cells bearing CXCR4 (CD184), CD44(low) and A2B5 surface markers. The enhanced self-renewal activity of the CD133-positive CSCs in hypoxia was preceded by upregulation of HIF-1 alpha. Knockdown of HIF-1 alpha abrogated the hypoxia-mediated CD133-positive CSC expansion. Inhibition of the phosphatidylinositol 3-kinase (PI3K)-Akt or ERK1/2 pathway reduced the hypoxia-driven CD133 expansion, suggesting that these signaling cascades may modulate the hypoxic response. Finally, CSCs propagated at hypoxia robustly retained the undifferentiated phenotype, whereas CSCs cultured at normoxia did not. These results suggest that response to hypoxia by CSCs involves the activation of HIF-1a to enhance the self-renewal activity of CD133-positive cells and to inhibit the induction of CSC differentiation. This study illustrates the importance of the tumor microenvironment in determining cellular behavior. Oncogene (2009) 28, 3949-3959; doi:10.1038/onc.2009.252; published online 31 August 2009
C1 [Park, D. M.] Univ Pittsburgh, Inst Canc, UPMC Canc Pavil, Brain Tumor Program, Pittsburgh, PA 15232 USA.
[Mintz, A.; Engh, J.; Kassam, A. B.; Pollack, I. F.; Park, D. M.] Univ Pittsburgh, Dept Neurol Surg, Pittsburgh, PA 15232 USA.
[Androutsellis-Theotokis, A.; McKay, R. D.] NIH, Mol Biol Lab, Bethesda, MD 20892 USA.
[Iwama, T.] Gifu Univ, Sch Med, Dept Neurosurg, Gifu 500, Japan.
[Kunisada, T.] Gifu Univ, Sch Med, Dept Tissue & Organ Dev Regenerat & Adv Med Sci, Gifu 500, Japan.
[Park, D. M.] Univ Pittsburgh, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15232 USA.
RP Park, DM (reprint author), Univ Pittsburgh, Inst Canc, UPMC Canc Pavil, Brain Tumor Program, 5th Floor,5150 Ctr Ave, Pittsburgh, PA 15232 USA.
EM parkdm@upmc.edu
RI Park, Deric/C-5675-2013;
OI Kunisada, Takahiro/0000-0003-1651-2716
FU Uehara Memorial Foundation
FX Akio Soeda is in part supported by the Uehara Memorial Foundation.
NR 51
TC 287
Z9 303
U1 4
U2 35
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0950-9232
J9 ONCOGENE
JI Oncogene
PD NOV 12
PY 2009
VL 28
IS 45
BP 3949
EP 3959
DI 10.1038/onc.2009.252
PG 11
WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics &
Heredity
GA 530AC
UT WOS:000272560300001
PM 19718046
ER
PT J
AU Cadet, JL
Mccoy, MT
Cai, NS
Krasnova, IN
Ladenheim, B
Beauvais, G
Wilson, N
Wood, W
Becker, KG
Hodges, AB
AF Cadet, Jean Lud
Mccoy, Michael T.
Cai, Ning Sheng
Krasnova, Irina N.
Ladenheim, Bruce
Beauvais, Genevieve
Wilson, Natascha
Wood, William, III
Becker, Kevin G.
Hodges, Amber B.
TI Methamphetamine Preconditioning Alters Midbrain Transcriptional
Responses to Methamphetamine-Induced Injury in the Rat Striatum
SO PLOS ONE
LA English
DT Article
ID THYROTROPIN-RELEASING-HORMONE; PROTEIN-TYROSINE PHOSPHATASES; DISMUTASE
TRANSGENIC MICE; MESSENGER-RNA EXPRESSION; NEUROTROPHIC FACTOR;
DOPAMINERGIC-NEURONS; GENE-EXPRESSION; CEREBRAL-ISCHEMIA; HEME
OXYGENASE-1; FREE-RADICALS
AB Methamphetamine (METH) is an illicit drug which is neurotoxic to the mammalian brain. Numerous studies have revealed significant decreases in dopamine and serotonin levels in the brains of animals exposed to moderate-to-large METH doses given within short intervals of time. In contrast, repeated injections of small nontoxic doses of the drug followed by a challenge with toxic METH doses afford significant protection against monoamine depletion. The present study was undertaken to test the possibility that repeated injections of the drug might be accompanied by transcriptional changes involved in rendering the nigrostriatal dopaminergic system refractory to METH toxicity. Our results confirm that METH preconditioning can provide significant protection against METH-induced striatal dopamine depletion. In addition, the presence and absence of METH preconditioning were associated with substantial differences in the identity of the genes whose expression was affected by a toxic METH challenge. Quantitative PCR confirmed METH-induced changes in genes of interest and identified additional genes that were differentially impacted by the toxic METH challenge in the presence of METH preconditioning. These genes include small heat shock 27 kD 27 protein 2 (HspB2), thyrotropin-releasing hormone (TRH), brain derived neurotrophic factor (BDNF), c-fos, and some encoding antioxidant proteins including CuZn superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx)-1, and heme oxygenase-1 (Hmox-1). These observations are consistent, in part, with the transcriptional alterations reported in models of lethal ischemic injuries which are preceded by ischemic or pharmacological preconditioning. Our findings suggest that multiple molecular pathways might work in tandem to protect the nigrostriatal dopaminergic pathway against the deleterious effects of the toxic psychostimulant. Further analysis of the molecular and cellular pathways regulated by these genes should help to provide some insight into the neuroadaptive potentials of the brain when repeatedly exposed to drugs of abuse.
RP Cadet, JL (reprint author), NIDA, Mol Neuropsychiat Res Branch, DHHS, NIH,Intramural Res Program, Baltimore, MD USA.
EM jcadet@intra.nida.nih.gov
OI Becker, Kevin/0000-0002-6794-6656
NR 128
TC 28
Z9 28
U1 4
U2 11
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 12
PY 2009
VL 4
IS 11
AR e7812
DI 10.1371/journal.pone.0007812
PG 16
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 518UW
UT WOS:000271721400011
PM 19915665
ER
PT J
AU Koonin, EV
Wolf, YI
AF Koonin, Eugene V.
Wolf, Yuri I.
TI Is evolution Darwinian or/and Lamarckian?
SO BIOLOGY DIRECT
LA English
DT Review
ID HORIZONTAL GENE-TRANSFER; PROVIDES ACQUIRED-RESISTANCE; STRESS-INDUCED
MUTAGENESIS; GENOME-WIDE HYPERMUTATION; STATIONARY-PHASE; TUMOR
MICROENVIRONMENT; ANTIBIOTIC-RESISTANCE; METABOLIC NETWORKS; TRANSFERRED
GENES; DIRECTED MUTATION
AB Background: The year 2009 is the 200th anniversary of the publication of Jean-Bapteste Lamarck's Philosophie Zoologique and the 150th anniversary of Charles Darwin's On the Origin of Species. Lamarck believed that evolution is driven primarily by non-randomly acquired, beneficial phenotypic changes, in particular, those directly affected by the use of organs, which Lamarck believed to be inheritable. In contrast, Darwin assigned a greater importance to random, undirected change that provided material for natural selection.
The concept: The classic Lamarckian scheme appears untenable owing to the non-existence of mechanisms for direct reverse engineering of adaptive phenotypic characters acquired by an individual during its life span into the genome. However, various evolutionary phenomena that came to fore in the last few years, seem to fit a more broadly interpreted (quasi) Lamarckian paradigm. The prokaryotic CRISPR-Cas system of defense against mobile elements seems to function via a bona fide Lamarckian mechanism, namely, by integrating small segments of viral or plasmid DNA into specific loci in the host prokaryote genome and then utilizing the respective transcripts to destroy the cognate mobile element DNA (or RNA). A similar principle seems to be employed in the piRNA branch of RNA interference which is involved in defense against transposable elements in the animal germ line. Horizontal gene transfer (HGT), a dominant evolutionary process, at least, in prokaryotes, appears to be a form of (quasi) Lamarckian inheritance. The rate of HGT and the nature of acquired genes depend on the environment of the recipient organism and, in some cases, the transferred genes confer a selective advantage for growth in that environment, meeting the Lamarckian criteria. Various forms of stress-induced mutagenesis are tightly regulated and comprise a universal adaptive response to environmental stress in cellular life forms. Stress-induced mutagenesis can be construed as a quasi-Lamarckian phenomenon because the induced genomic changes, although random, are triggered by environmental factors and are beneficial to the organism.
Conclusion: Both Darwinian and Lamarckian modalities of evolution appear to be important, and reflect different aspects of the interaction between populations and the environment.
C1 [Koonin, Eugene V.; Wolf, Yuri I.] Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
RP Koonin, EV (reprint author), Natl Lib Med, Natl Ctr Biotechnol Informat, NIH, Bethesda, MD 20894 USA.
EM koonin@ncbi.nlm.nih.gov; wolf@ncbi.nlm.nih.gov
FU Intramural NIH HHS
NR 104
TC 101
Z9 106
U1 8
U2 93
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6150
J9 BIOL DIRECT
JI Biol. Direct
PD NOV 11
PY 2009
VL 4
AR 42
DI 10.1186/1745-6150-4-42
PG 14
WC Biology
SC Life Sciences & Biomedicine - Other Topics
GA 526XV
UT WOS:000272330400001
PM 19906303
ER
PT J
AU Hansen, DF
Feng, HQ
Zhou, Z
Bai, YW
Kay, LE
AF Hansen, D. Flemming
Feng, Haniqiao
Zhou, Zheng
Bai, Yawen
Kay, Lewis E.
TI Selective Characterization of Microsecond Motions in Proteins by NMR
Relaxation
SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY
LA English
DT Article
ID CHEMICAL-SHIFT ANISOTROPY; MAGNETIC-RESONANCE RELAXATION;
LIQUID-CRYSTALLINE PHASE; MODEL-FREE APPROACH; CONFORMATIONAL DYNAMICS;
BACKBONE DYNAMICS; CHAPERONE CHZ1; SPECTROSCOPY; EXCHANGE; DOMAIN
AB The three-dimensional structures of macromolecules fluctuate over a wide range of time-scales. Separating the individual dynamic processes according to frequency is of importance in relating protein motions to biological function and stability. We present here a general NMR method for the specific characterization of microsecond motions at backbone positions in proteins even in the presence of other dynamics such as large-amplitude nanosecond motions and millisecond chemical exchange processes. The method is based on measurement of relaxation rates of four bilinear coherences and relies on the ability of strong continuous radio frequency fields to quench millisecond chemical exchange. The utility of the methodology is demonstrated and validated through two specific examples focusing on the thermostable proteins, ubiquitin and protein L, where it is found that small-amplitude microsecond dynamics are more pervasive than previously thought. Specifically, these motions are localized to a helices, loop regions, and regions along the rim of beta sheets in both of the proteins examined. A third example focuses on a 28 kDa ternary complex of the chaperone Chz1 and the histones H2A.Z/H2B, where it is established that pervasive microsecond motions are localized to a region of the chaperone that is important for stabilizing the complex. It is further shown that these motions can be well separated from extensive millisecond dynamics that are also present and that derive from exchange of Chz1 between bound and free states. The methodology is straightforward to implement, and data recorded at only a single static magnetic field are required.
C1 [Hansen, D. Flemming; Kay, Lewis E.] Univ Toronto, Dept Mol Genet, Toronto, ON M5S 1A8, Canada.
[Hansen, D. Flemming; Kay, Lewis E.] Univ Toronto, Dept Biochem, Toronto, ON M5S 1A8, Canada.
[Hansen, D. Flemming; Kay, Lewis E.] Univ Toronto, Dept Chem, Toronto, ON M5S 1A8, Canada.
[Feng, Haniqiao; Zhou, Zheng; Bai, Yawen] NCI, Biochem & Mol Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Hansen, DF (reprint author), Univ Toronto, Dept Mol Genet, 100 Coll St, Toronto, ON M5S 1A8, Canada.
EM flemming@pound.med.utoronto.ca; kay@pound.med.utoronto.ca
FU Canadian Institutes of Health Research (CIHR); Canada Research Chair in
Biochemistry
FX We would like to thank Professors Silke Wiesner (Max Planck Institute
for Developmental Biology, Tubingen, Germany) and Voula Kanelis
(University of Toronto, Canada) for preparing the human ubiquitin and
protein L samples, respectively. This work was supported by a grant from
the Canadian Institutes of Health Research (CIHR). D.F.H. acknowledges a
postdoctoral fellowship from CIHR. L.E.K. is the recipient of a Canada
Research Chair in Biochemistry.
NR 62
TC 29
Z9 29
U1 1
U2 20
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0002-7863
J9 J AM CHEM SOC
JI J. Am. Chem. Soc.
PD NOV 11
PY 2009
VL 131
IS 44
BP 16257
EP 16265
DI 10.1021/ja906842s
PG 9
WC Chemistry, Multidisciplinary
SC Chemistry
GA 516AJ
UT WOS:000271513700061
PM 19842628
ER
PT J
AU Ju, JH
Maeng, JS
Lee, DY
Piszczek, G
Gelmann, EP
Gruschus, JM
AF Ju, Jeong Ho
Maeng, Jin-Soo
Lee, Duck-Yeon
Piszczek, Grzegory
Gelmann, Edward P.
Gruschus, James M.
TI Interactions of The Acidic Domain and SRF Interacting Motifs with the
NKX3.1 Homeodomain
SO BIOCHEMISTRY
LA English
DT Article
ID PROSTATE-CANCER; DNA-BINDING; VND/NK-2 HOMEODOMAIN; PROTEIN; GENE;
HOMEOPROTEIN; EXPRESSION; MUTATIONS; DELETION; RESIDUE
AB NKX3.1 is a prostate tumor Suppressor belonging to the NK-2 family of homeodomain (HD) transcription factors NK-2family members often possess as( retch of 10-15 residues enriched in acidic amino acids, the acidic domain (AD), in the flexible, disordered region N-terminal to the HD. Interactions between the N-terminal region of NKX3 1 and its homeodomain affect protein stability and DNA binding. CD spectroscopy measuring the thermal unfolding of NKX3 I Constructs showed a 2 degrees C intramolecular stabilization of the H 1) by the N-terminal region containing the acidic domain (residues 85-96) CD of mixtures of various N-terminal peptides With it construct containing just the HD showed that the acidic domain and the following legion, the SRF interacting (SI) motif (residues 99-105), was necessary For this stabilization. Phosphorylation of the acidic domain is known to slow proteasomal degradation of NKX3.1 in prostate cells, and MAR spectroscopy Was Used 10 measure and map the Interaction of the HD with phosphorylated and nonphosphorylated forms of the AD peptide The interaction with the phosphorylated AD peptide was considerably stronger (K-d = 0 5 +/- 0 2 mM). resulting in large chemical shift perturbations For residues Ser 150 and Arg 175 in the HD, as well as a 2 degrees C increase ill the HD thermal stability compared to that of the nonphosphorylated form. NKX3 1 constructs with AD phosphorylation site threonine residues (89 and 93) mutated to glutamate were 4 degrees C more stable than HD alone Using polymer theory, effective concentrations for interactions between domains connected by flexible linkers are predicted to be ill the millimolar range, and thus. the weak intramolecular interactions observed here could conceivably modulate or compete With stronger, intermolecular interactions with the NKX3.1 HD
C1 [Lee, Duck-Yeon; Piszczek, Grzegory; Gruschus, James M.] NHLBI, NIH, Bethesda, MD 20892 USA.
[Ju, Jeong Ho; Gelmann, Edward P.] Columbia Univ, Herbert Irving Comprehens Canc Ctr, Div Hematol Oncol, New York, NY 10032 USA.
[Maeng, Jin-Soo] Sch Biol Sci & Technol, Kwangju 500757, South Korea.
RP Gruschus, JM (reprint author), NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA.
FU National Heart. Lung and Blood Institute; Natinal Institute of
Environmental Health Sciences [ES09888]
FX This work was supported to part by the Intramural Research Program of
the National Heart. Lung and Blood Institute and by Natinal Institute of
Environmental Health Sciences Grant ES09888 to EPG
NR 29
TC 4
Z9 5
U1 0
U2 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 10
PY 2009
VL 48
IS 44
BP 10601
EP 10607
DI 10.1021/bi9013374
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 512IU
UT WOS:000271242200015
PM 19780584
ER
PT J
AU Lubet, RA
Yao, RS
Grubbs, CJ
You, M
Wang, Y
AF Lubet, Ronald A.
Yao, Ruisheng
Grubbs, Clinton J.
You, Ming
Wang, Yian
TI Induced expression of drug metabolizing enzymes by preventive agents:
Role of the antioxidant response element
SO CHEMICO-BIOLOGICAL INTERACTIONS
LA English
DT Article
DE Chemopreventive agents; Phase I/II inducers; Antioxidant response
element
ID MAMMARY CARCINOGENESIS; PHENOLIC ANTIOXIDANTS; BETA-NAPHTHOFLAVONE;
CIGARETTE-SMOKE; DNA-ADDUCTS; CANCER; INHIBITION; RATS; CHEMOPREVENTION;
INDOLE-3-CARBINOL
AB Identifying agents that block tumor initiation is a goal of cancer prevention. The ability of a chemically varied group of agents to induce various drug metabolizing genes in livers of rats was examined. Sprague-Dawley rats were treated for 7 days with various agents in the diet or by gavage. The agents examined, which might be expected to respond via specific nuclear receptors (CAR. AhR) as well as antioxidant response elements (AREs), included Phase I/II inducers [5,6-benzoflavone (BF, 5000 mg/kg diet), diallyl sulfide (DAS, 500 mg/kg BW/clay). ethoxyqum (EXC, 300 mg/kg BW/day) and phenobarbital (PB, 500 mg/kg diet)] or pure Phase II inducers [1,2-dithiol-3-thione (DTT, 500 mg/kg diet), and cyclopentadithiolthione (CPDTT, 175 mg/kg BW/day)]. Liver RNA expression was analyzed employing oligonucleotide microarrays. The agents yielded unique expression profiles. In genes with known AREs, the induction ratios (Levels Treated/Levels Controls) were: quinone oxidoreductase (BF, 8.1; DTT. 3.2:1; CPDTT, 3:1; DAS, 1.81; Exo, 1.7;1), glutatione transferase Pi (DTT, 36:1; CPDTT, 34:1: EXO, 8:1; DAS, 5:1; BF, 2.5:1;), and alclehyde keto reductase 7A3 (AFAR) (DTT and CPDTT 14:1: DAS, 6:1; EXC, 4:1; PB, 1.5:1).When the search included a wider variety of Phase II drug metabolizing enzymes, no clear pattern was observed. Agent induced gene expression and preventive activity in published carcinogen induced tumor models showed limited correlation: questioning whether measuring the induction of one or two genes (e.g., quinone reductase) is a surrogate for overall Phase 11 inducing (antioxidant) and potential anti-tumor activity. Published by Elsevier Ireland Ltd.
C1 [Lubet, Ronald A.] NCI, Canc Prevent Div, Rockville, MD 20852 USA.
[Yao, Ruisheng; You, Ming; Wang, Yian] Washington Univ, Sch Med, Dept Surg, St Louis, MO 63110 USA.
[Yao, Ruisheng; You, Ming; Wang, Yian] Washington Univ, Sch Med, Alvin J Siteman Canc Ctr, St Louis, MO 63110 USA.
[Grubbs, Clinton J.] Univ Alabama, Dept Surg, Birmingham, AL 35294 USA.
RP Lubet, RA (reprint author), NCI, Canc Prevent Div, Execut Plaza N,Suite 2110,6130 Execut Blvd, Rockville, MD 20852 USA.
EM lubetr@mail.nih.gov
FU NCI [HHSN261200433001C]
FX The authors would like to thank Ms. Mary Jo Cagle and Jeanne Hale for
their editorial assistance in the preparation of this manuscript. The
funding for the studies was provided in part by NCI Contract Number
HHSN261200433001C.
NR 36
TC 11
Z9 11
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0009-2797
J9 CHEM-BIOL INTERACT
JI Chem.-Biol. Interact.
PD NOV 10
PY 2009
VL 182
IS 1
BP 22
EP 28
DI 10.1016/j.cbi.2009.08.011
PG 7
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology
GA 510XK
UT WOS:000271127100004
PM 19695238
ER
PT J
AU Anderson, WF
Jatoi, I
Sherman, ME
AF Anderson, William F.
Jatoi, Ismail
Sherman, Mark E.
TI Qualitative Age Interactions in Breast Cancer Studies: Mind the Gap
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Editorial Material
ID RISK-FACTORS; GENE-EXPRESSION; UNITED-STATES; SEER PROGRAM; YOUNG AGE;
WOMEN; EPIDEMIOLOGY; PROGNOSIS; PATTERNS; RECEPTOR
C1 [Anderson, William F.; Sherman, Mark E.] NCI, Dept Hlth & Human Serv, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Jatoi, Ismail] Natl Naval Med Ctr, Breast Care Ctr, Bethesda, MD USA.
RP Anderson, WF (reprint author), NCI, Dept Hlth & Human Serv, NIH, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
FU Intramural NIH HHS [Z01 CP010183-06]
NR 44
TC 20
Z9 21
U1 0
U2 0
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5308
EP 5311
DI 10.1200/JCO.2009.22.9450
PG 4
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900004
PM 19826117
ER
PT J
AU Piekarz, RL
Frye, R
Turner, M
Wright, JJ
Allen, SL
Kirschbaum, MH
Zain, J
Prince, HM
Leonard, JP
Geskin, LJ
Reeder, C
Joske, D
Figg, WD
Gardner, ER
Steinberg, SM
Jaffe, ES
Stetler-Stevenson, M
Lade, S
Fojo, AT
Bates, SE
AF Piekarz, Richard L.
Frye, Robin
Turner, Maria
Wright, John J.
Allen, Steven L.
Kirschbaum, Mark H.
Zain, Jasmine
Prince, H. Miles
Leonard, John P.
Geskin, Larisa J.
Reeder, Craig
Joske, David
Figg, William D.
Gardner, Erin R.
Steinberg, Seth M.
Jaffe, Elaine S.
Stetler-Stevenson, Maryalice
Lade, Stephen
Fojo, A. Tito
Bates, Susan E.
TI Phase II Multi-Institutional Trial of the Histone Deacetylase Inhibitor
Romidepsin As Monotherapy for Patients With Cutaneous T-Cell Lymphoma
SO JOURNAL OF CLINICAL ONCOLOGY
LA English
DT Article
ID SEZARY-SYNDROME; MYCOSIS-FUNGOIDES; DEPSIPEPTIDE FR901228;
CLINICAL-TRIALS; CANCER-THERAPY; FK228; DIFFERENTIATION; IDENTIFICATION;
POPULATION; INDUCERS
AB Purpose
Romidepsin (depsipeptide or FK228) is a member of a new class of antineoplastic agents active in T-cell lymphoma, the histone deacetylase inhibitors. On the basis of observed responses in a phase I trial, a phase II trial of romidepsin in patients with T-cell lymphoma was initiated.
Patients and Methods
The initial cohort was limited to patients with cutaneous T-cell lymphoma (CTCL), or subtypes mycosis fungoides or Sezary syndrome, who had received no more than two prior cytotoxic regimens. There were no limits on other types of therapy. Subsequently, the protocol was expanded to enroll patients who had received more than two prior cytotoxic regimens.
Results
Twenty-seven patients were enrolled onto the first cohort, and a total of 71 patients are included in this analysis. These patients had undergone a median of four prior treatments, and 62 patients (87%) had advanced-stage disease ( stage IIB, n = 15; stage III, n = 6; or stage IV, n = 41). Toxicities included nausea, vomiting, fatigue, and transient thrombocytopenia and granulocytopenia. Pharmacokinetics were evaluated with the first administration of romidepsin. Complete responses were observed in four patients, and partial responses were observed in 20 patients for an overall response rate of 34% (95% CI, 23% to 46%). The median duration of response was 13.7 months.
Conclusion
The histone deacetylase inhibitor romidepsin has single-agent clinical activity with significant and durable responses in patients with CTCL.
C1 NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
NCI, Canc Therapy Evaluat Program, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
SAIC Frederick, Clin Pharmacol Program, Frederick, MD USA.
N Shore Univ Hosp, Manhasset, NY USA.
New York Presbyterian Hosp, New York, NY USA.
City Hope Natl Canc Ctr, Duarte, CA USA.
Univ Pittsburgh, Pittsburgh, PA USA.
Mayo Clin Scottsdale, Scottsdale, AZ USA.
Peter MacCallum Canc Ctr, Melbourne, Vic, Australia.
Univ Melbourne, Melbourne, Vic, Australia.
Sir Charles Gairdner Hosp, Nedlands, WA 6009, Australia.
RP Piekarz, RL (reprint author), 10 Ctr Dr,MSC 1903,Bldg 10,Rm 12N226, Bethesda, MD 20892 USA.
EM rpiekarz@nih.gov
RI Figg Sr, William/M-2411-2016;
OI Allen, Steven/0000-0002-3482-3182
FU National Institutes of Health (NIH) [N01-CO-12400]; National Cancer
Institute; Center for Cancer Research; Gloucester Pharmaceuticals,
Cambridge, MA
FX Supported in part by the Intramural Research Program of the National
Institutes of Health (NIH), National Cancer Institute, Center for Cancer
Research and by a Cooperative Research and Development Agreement with
Gloucester Pharmaceuticals, Cambridge, MA; also supported in part by
federal funds from the National Cancer Institute, NIH, under Grant No.
N01-CO-12400 (E.R.G.).
NR 36
TC 335
Z9 348
U1 2
U2 14
PU AMER SOC CLINICAL ONCOLOGY
PI ALEXANDRIA
PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA
SN 0732-183X
J9 J CLIN ONCOL
JI J. Clin. Oncol.
PD NOV 10
PY 2009
VL 27
IS 32
BP 5410
EP 5417
DI 10.1200/JCO.2008.21.6150
PG 8
WC Oncology
SC Oncology
GA 516GT
UT WOS:000271530900020
PM 19826128
ER
PT J
AU Sa, JM
Twu, O
Hayton, K
Reyes, S
Fay, MP
Ringwald, P
Wellems, TE
AF Sa, Juliana Martha
Twu, Olivia
Hayton, Karen
Reyes, Sahily
Fay, Michael P.
Ringwald, Pascal
Wellems, Thomas E.
TI Geographic patterns of Plasmodium falciparum drug resistance
distinguished by differential responses to amodiaquine and chloroquine
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE malaria; pfcrt; pfmdr1
ID PAPUA-NEW-GUINEA; GENE HAPLOTYPE SVMNT; TRANSPORTER PFCRT;
SULFADOXINE-PYRIMETHAMINE; QUININE RESISTANCE; PFMDR1 MUTATIONS;
EAST-AFRICA; WILD-TYPE; MALARIA; SENSITIVITY
AB Chloroquine (CQ) resistance (CQR) in Plasmodium falciparum originated from at least six foci in South America, Asia, and Oceania. Malaria parasites from these locations exhibit contrasting resistance phenotypes that are distinguished by point mutations and microsatellite polymorphisms in and near the CQR transporter gene, pfcrt, and the multidrug resistance transporter gene, pfmdr1. Amodiaquine (AQ), a 4-aminoquinoline related to CQ, is recommended and often used successfully against CQ-resistant P. falciparum in Africa, but it is largely ineffective across large regions of South America. The relationship of different pfcrt and pfmdr1 combinations to these drug-resistant phenotypes has been unclear. In two P. falciparum genetic crosses, particular pfcrt and pfmdr1 alleles from South America interact to yield greater levels of resistance to monodesethylamodiaquine (MDAQ; the active metabolite of AQ) than to CQ, whereas a pfcrt allele from Southeast Asia and Africa is linked to greater CQ than MDAQ resistance with all partner pfmdr1 alleles. These results, together with (i) available haplotype data from other parasites; (ii) evidence for an emerging focus of AQ resistance in Tanzania; and (iii) the persistence of 4-aminoquinoline-resistant parasites in South America, where CQ and AQ use is largely discontinued, suggest that different histories of drug use on the two continents have driven the selection of distinct suites of pfcrt and pfmdr1 mutations. Increasing use of AQ in Africa poses the threat of a selective sweep of highly AQ-resistant, CQ-resistant parasites with pfcrt and pfmdr1 mutations that are as advantaged and persistent as in South America.
C1 [Sa, Juliana Martha; Twu, Olivia; Hayton, Karen; Reyes, Sahily; Wellems, Thomas E.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Fay, Michael P.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Ringwald, Pascal] WHO, Global Malaria Program, CH-1211 Geneva 27, Switzerland.
RP Wellems, TE (reprint author), NIAID, Lab Malaria & Vector Res, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM twellems@niaid.nih.gov
OI Twu, Olivia/0000-0002-5175-3016; Fay, Michael P./0000-0002-8643-9625
FU The Intramural Research Program of the National Institutes of Health,
National Institute of Allergy and Infectious Diseases
FX We thank Jianbing Mu for assistance in genotyping the P. falciparum
clones; Hongying Jiang, Xinzhuan Su, Jeff Skinner, Vivek Gopalan, Jason
Barnett, Yentram Huyen, and William Knight for assistance with in vitro
drug assays and automated analysis of IC50s and IC90s; and Erika Phelps,
Sarnia Laurent, Michael Krause, and Rick Fairhurst for assistance with
QTL mapping, DNA sequencing, and discussions. The Intramural Research
Program of the National Institutes of Health, National Institute of
Allergy and Infectious Diseases, supported this research.
NR 71
TC 111
Z9 113
U1 1
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 10
PY 2009
VL 106
IS 45
BP 18883
EP 18889
DI 10.1073/pnas.0911317106
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517SJ
UT WOS:000271637500005
PM 19884511
ER
PT J
AU Das, R
Andre, I
Shen, Y
Wu, YB
Lemak, A
Bansal, S
Arrowsmith, CH
Szyperski, T
Baker, D
AF Das, Rhiju
Andre, Ingemar
Shen, Yang
Wu, Yibing
Lemak, Alexander
Bansal, Sonal
Arrowsmith, Cheryl H.
Szyperski, Thomas
Baker, David
TI Simultaneous prediction of protein folding and docking at high
resolution
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE homo-oligomers; molecular replacement; NMR structure inference; protein
structure prediction; symmetry
ID RESIDUAL DIPOLAR COUPLINGS; NMR CHEMICAL-SHIFTS; X-RAY-STRUCTURE;
COILED-COIL; ROSETTA; COMPLEXES; ASSEMBLIES; SEQUENCES; SYMMETRY;
TARGETS
AB Interleaved dimers and higher order symmetric oligomers are ubiquitous in biology but present a challenge to de novo structure prediction methodology: The structure adopted by a monomer can be stabilized largely by interactions with other monomers and hence not the lowest energy state of a single chain. Building on the Rosetta framework, we present a general method to simultaneously model the folding and docking of multiple-chain interleaved homo-oligomers. For more than a third of the cases in a benchmark set of interleaved homo-oligomers, the method generates near-native models of large alpha-helical bundles, interlocking beta sandwiches, and interleaved alpha/beta motifs with an accuracy high enough for molecular replacement based phasing. With the incorporation of NMR chemical shift information, accurate models can be obtained consistently for symmetric complexes with as many as 192 total amino acids; a blind prediction was within 1 angstrom rmsd of the traditionally determined NMR structure, and fit independently collected RDC data equally well. Together, these results show that the Rosetta "fold-and-dock'' protocol can produce models of homo-oligomeric complexes with nearatomic-level accuracy and should be useful for crystallographic phasing and the rapid determination of the structures of multimers with limited NMR information.
C1 [Das, Rhiju; Andre, Ingemar; Baker, David] Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
[Shen, Yang] NIDDKD, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
[Wu, Yibing; Szyperski, Thomas] SUNY Buffalo, Dept Chem, Buffalo, NY 14260 USA.
[Wu, Yibing; Szyperski, Thomas] SUNY Buffalo, Dept Biol Struct, Buffalo, NY 14260 USA.
[Wu, Yibing; Szyperski, Thomas] SUNY Buffalo, NE Struct Genom Consortium, Buffalo, NY 14260 USA.
[Lemak, Alexander; Arrowsmith, Cheryl H.] Univ Toronto, Dept Med Biophys, Ontario Canc Inst, Toronto, ON M5G IL5, Canada.
[Lemak, Alexander; Arrowsmith, Cheryl H.] Univ Toronto, NE Struct Genom Consortium, Toronto, ON M5G IL5, Canada.
[Bansal, Sonal] Washington Univ, Sch Med, Dept Biochem & Mol Biophys, St Louis, MO 63108 USA.
RP Baker, D (reprint author), Univ Washington, Dept Biochem, Seattle, WA 98195 USA.
EM dabaker@u.washington.edu
RI Shen, Yang/C-3064-2008; Andre, Ingemar/O-4777-2014; Baker,
David/K-8941-2012
OI Shen, Yang/0000-0003-1408-8034; Andre, Ingemar/0000-0002-4753-8233;
Baker, David/0000-0001-7896-6217
FU Howard Hughes Medical Institute; Knut and Alice Wallenberg Foundation;
Jane Coffin Childs Foundation and a Burroughs-Wellcome Career Award;
Intramural Research Program of the National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases;
National Institutes of Health Protein Structure Initiative
[U54-GM074958]; Canada Research Chair in Structural Proteomics
FX We thank Keith Laidig and Darwin Alonso for flawless administration of
computational resources; the users of Rosetta@ home for donating their
computer time; developers in the Rosetta community for contributions to
our shared codebase; and Suzanne Pfeffer for informing us about the
GCC185 coiled-coil sequence before the release of its crystal structure.
This work was supported by the Howard Hughes Medical Institute ( to D.
B.), the Knut and Alice Wallenberg Foundation ( to I. A.), the Jane
Coffin Childs Foundation and a Burroughs-Wellcome Career Award at the
Scientific Interface ( to R. D.), the Intramural Research Program of the
National Institutes of Health National Institute of Diabetes and
Digestive and Kidney Diseases ( to Y. S.), and the National Institutes
of Health Protein Structure Initiative Grant U54-GM074958 ( to T. S. and
C. H. A.). C. H. A. holds a Canada Research Chair in Structural
Proteomics.
NR 39
TC 88
Z9 88
U1 2
U2 21
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 10
PY 2009
VL 106
IS 45
BP 18978
EP 18983
DI 10.1073/pnas.0904407106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517SJ
UT WOS:000271637500021
PM 19864631
ER
PT J
AU Ieva, R
Bernstein, HD
AF Ieva, Raffaele
Bernstein, Harris D.
TI Interaction of an autotransporter passenger domain with BamA during its
translocation across the bacterial outer membrane
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE autotransporter; Bam complex; outer membrane; protein secretion;
virulence factors
ID ESCHERICHIA-COLI; PROTEIN; SECRETION; BIOGENESIS; MECHANISM; COMPONENT;
CLEAVAGE; COMPLEX; YAET; GENE
AB Autotransporters are a superfamily of virulence factors produced by Gram-negative bacteria consisting of a large N-terminal extracellular domain ("passenger domain'') and a C-terminal beta barrel domain ("beta domain''). The mechanism by which the passenger domain is translocated across the outer membrane (OM) is unknown. Here we show that the insertion of a small linker into the passenger domain of the Escherichia coli O157:H7 autotransporter EspP effectively creates a translocation intermediate by transiently stalling translocation near the site of the insertion. Using a site-specific photocrosslinking approach, we found that residues adjacent to the stall point interact with BamA, a component of a heterooligomeric complex (Bam complex) that catalyzes OM protein assembly, and that residues closer to the EspP N terminus interact with the periplasmic chaperones SurA and Skp. The EspP-BamA interaction was short-lived and could be detected only when passenger domain translocation was stalled. These results support a model in which molecular chaperones prevent misfolding of the passenger domain before its secretion and the Bam complex catalyzes both the integration of the beta domain into the OM and the translocation of the passenger domain across the OM in a C-to N-terminal direction.
C1 [Ieva, Raffaele; Bernstein, Harris D.] NIDDKD, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
RP Bernstein, HD (reprint author), NIDDKD, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA.
EM harris_bernstein@nih.gov
RI Ieva, Raffaele/J-9207-2014
OI Ieva, Raffaele/0000-0002-3405-0650
FU National Institute of Diabetes and Digestive and Kidney Diseases
FX We thank Natacha Ruiz and Tom Silhavy for providing the BamA antisera
used in preliminary experiments and Janine Peterson for providing
technical assistance. We also thank Nathalie Dautin and Susan Buchanan
for their critical reading of the manuscript. This work was supported by
the National Institute of Diabetes and Digestive and Kidney Diseases
Intramural Research Program.
NR 28
TC 103
Z9 104
U1 0
U2 11
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 10
PY 2009
VL 106
IS 45
BP 19120
EP 19125
DI 10.1073/pnas.0907912106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517SJ
UT WOS:000271637500045
PM 19850876
ER
PT J
AU Joksimovic, M
Anderegg, A
Roy, A
Campochiaro, L
Yun, B
Kittappa, R
McKay, R
Awatramani, R
AF Joksimovic, Milan
Anderegg, Angela
Roy, Anil
Campochiaro, Laura
Yun, Beth
Kittappa, Raja
McKay, Ronald
Awatramani, Rajeshwar
TI Spatiotemporally separable Shh domains in the midbrain define distinct
dopaminergic progenitor pools
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE dopamine; Sonic hedgehog; lineage; substantia nigra
ID EMBRYONIC STEM-CELLS; FLOOR PLATE CELLS; PARKINSONS-DISEASE;
SUBSTANTIA-NIGRA; GENETIC LINEAGES; SONIC-HEDGEHOG; MUTANT MICE;
NEURONS; FATE; IDENTIFICATION
AB Midbrain dopamine neurons (mDA) are important regulators of diverse physiological functions, including movement, attention, and reward behaviors. Accordingly, aberrant function of dopamine neurons underlies a wide spectrum of disorders, such as Parkinson's disease (PD), dystonia, and schizophrenia. The distinct functions of the dopamine system are carried out by neuroanatomically discrete subgroups of dopamine neurons, which differ in gene expression, axonal projections, and susceptibility in PD. The developmental underpinnings of this heterogeneity are undefined. We have recently shown that in the embryonic CNS, mDA originate from the midbrain floor plate, a ventral midline structure that is operationally defined by the expression of the molecule Shh. Here, we develop these findings to reveal that in the embryonic midbrain, the spatiotemporally dynamic Shh domain defines multiple progenitor pools. We deduce 3 distinct progenitor pools, medial, intermediate, and lateral, which contribute to different mDA clusters. The earliest progenitors to express Shh, here referred to as the medial pool, contributes neurons to the rostral linear nucleus and mDA of the ventral tegmental area/interfascicular regions, but remarkably, little to the substantia nigra pars compacta. The intermediate Shh+ progenitors give rise to neurons of all dopaminergic nuclei, including the SNpc. The last and lateral pool of Shh+ progenitors generates a cohort that populates the red nucleus, Edinger Westphal nucleus, and supraoculomotor nucleus and cap. Subsequently, these lateral Shh+ progenitors produce mDA. This refined ontogenetic definition will expand understanding of dopamine neuron biology and selective susceptibility, and will impact stem cell-derived therapies and models for PD.
C1 [Joksimovic, Milan; Anderegg, Angela; Roy, Anil; Campochiaro, Laura; Yun, Beth; Awatramani, Rajeshwar] Northwestern Univ, Feinberg Sch Med, Dept Neurol, Chicago, IL 60611 USA.
[Joksimovic, Milan; Anderegg, Angela; Roy, Anil; Campochiaro, Laura; Yun, Beth; Awatramani, Rajeshwar] Ctr Genet Med, Chicago, IL 60611 USA.
[Kittappa, Raja; McKay, Ronald] NINDS, Mol Biol Lab, Bethesda, MD 20892 USA.
RP Awatramani, R (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Neurol, 7-113 Lurie Bldg,303 E Super St, Chicago, IL 60611 USA.
EM r-awatramani@northwestern.edu
RI Joksimovic, Milan/A-4952-2016
OI Joksimovic, Milan/0000-0002-3936-4632
FU Whitehall Foundation; Brain Research Foundation; American Parkinson's
Disease Association; Parkinson's Disease Foundation
FX We thank Dr. Cliff Tabin for Shh: CreGFP and Shh: CreERT2 mice and Shh
cDNA; Dr. Michael German for anti-Lmx1a; Drs. Thomas Muller and Carmen
Birchmeier for anti-Lmx1b; and Dr. Eric Turner for antiBrn3a antibodies.
We thank Dr. Doug Kim for useful comments and Dr. Abdelhak Belmadani and
Bor-Shuen Wang for imaging and technical assistance. R. A. was supported
by the Whitehall Foundation, Brain Research Foundation, and the American
Parkinson's Disease Association. M. J. was supported by the Parkinson's
Disease Foundation.
NR 40
TC 62
Z9 63
U1 0
U2 3
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 10
PY 2009
VL 106
IS 45
BP 19185
EP 19190
DI 10.1073/pnas.0904285106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517SJ
UT WOS:000271637500056
PM 19850875
ER
PT J
AU Guettier, JM
Gautam, D
Scarselli, M
de Azua, IR
Li, JH
Rosemond, E
Ma, XC
Gonzalez, FJ
Armbruster, BN
Lu, HY
Roth, BL
Wess, J
AF Guettier, Jean-Marc
Gautam, Dinesh
Scarselli, Marco
de Azua, Inigo Ruiz
Li, Jian Hua
Rosemond, Erica
Ma, Xiaochao
Gonzalez, Frank J.
Armbruster, Blaine N.
Lu, Huiyan
Roth, Bryan L.
Wess, Juergen
TI A chemical-genetic approach to study G protein regulation of beta cell
function in vivo
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE beta cells; G protein-coupled receptors; transgenic mice; type 2
diabetes
ID MUSCARINIC ACETYLCHOLINE-RECEPTOR; PHASIC INSULIN RELEASE; COUPLED
RECEPTORS; GLUCOSE; MECHANISMS; EXPRESSION; SECRETION
AB Impaired functioning of pancreatic beta cells is a key hallmark of type 2 diabetes. beta cell function is modulated by the actions of different classes of heterotrimeric G proteins. The functional consequences of activating specific beta cell G protein signaling pathways in vivo are not well understood at present, primarily due to the fact that beta cell G protein-coupled receptors (GPCRs) are also expressed by many other tissues. To circumvent these difficulties, we developed a chemical-genetic approach that allows for the conditional and selective activation of specific beta cell G proteins in intact animals. Specifically, we created two lines of transgenic mice each of which expressed a specific designer GPCR in beta cells only. Importantly, the two designer receptors differed in their G protein-coupling properties (G(q/11) versus G(s)). They were unable to bind endogenous ligand(s), but could be efficiently activated by an otherwise pharmacologically inert compound (clozapine-N-oxide), leading to the conditional activation of either beta cell G(q/11) or G(s) G proteins. Here we report the findings that conditional and selective activation of beta cell G(q/11) signaling in vivo leads to striking increases in both first-and second-phase insulin release, greatly improved glucose tolerance in obese, insulin-resistant mice, and elevated beta cell mass, associated with pathway-specific alterations in islet gene expression levels. Selective stimulation of beta cell G(s) triggered qualitatively similar in vivo metabolic effects. Thus, this developed chemical-genetic strategy represents a powerful approach to study G protein regulation of beta cell function in vivo.
C1 [Guettier, Jean-Marc; Gautam, Dinesh; Scarselli, Marco; de Azua, Inigo Ruiz; Li, Jian Hua; Rosemond, Erica; Wess, Juergen] NIDDKD, Mol Signaling Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
[Ma, Xiaochao; Gonzalez, Frank J.] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
[Lu, Huiyan] NIDDKD, Mouse Transgen Core Facil, NIH, Bethesda, MD 20892 USA.
[Armbruster, Blaine N.; Roth, Bryan L.] Univ N Carolina, Dept Pharmacol, Chapel Hill Med Sch, Chapel Hill, NC 27514 USA.
[Armbruster, Blaine N.; Roth, Bryan L.] Univ N Carolina, Div Med Chem & Nat Prod, Chapel Hill Med Sch, Chapel Hill, NC 27514 USA.
RP Guettier, JM (reprint author), NIDDKD, Mol Signaling Sect, Bioorgan Chem Lab, NIH, Bethesda, MD 20892 USA.
EM guettierj@mail.nih.gov; jwess@helix.nih.gov
RI Roth, Bryan/F-3928-2010; Li, Jianhua/B-7671-2011;
OI Li, Jianhua/0000-0002-5744-3182; Scarselli, Marco/0000-0001-5087-3182
FU Intramural Research Program; National Institute of Diabetes and
Digestive and Kidney Diseases; National Institutes of Health; U. S.
Department of Health and Human Services; National Institutes of Health
[U19MH82441, NO1MH80004, RO1MH61887]
FX We thank Ms. Xiaohong Zhang and Ms. Yinghong Cui for excellent technical
assistance; Dr. Elliot Ross (UT Southwestern Medical Center, Dallas, TX)
for providing the turkey beta1-adrenergic receptor expression
vector; The National Institutes of Health Inter-institute Endocrine
Training Program, particularly Drs. M. C. Skarulis, L. K. Nieman, D.
LeRoith, and P. Gorden for support of this work. This work was supported
by the Intramural Research Program, the National Institute of Diabetes
and Digestive and Kidney Diseases, National Institutes of Health; U. S.
Department of Health and Human Services; and National Institutes of
Health Grants U19MH82441, NO1MH80004, and RO1MH61887.
NR 24
TC 96
Z9 96
U1 0
U2 7
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 10
PY 2009
VL 106
IS 45
BP 19197
EP 19202
DI 10.1073/pnas.0906593106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 517SJ
UT WOS:000271637500058
PM 19858481
ER
PT J
AU Ramot, Y
Nyska, A
Lieuallen, W
Maly, A
Flake, G
Kissling, GE
Brix, A
Malarkey, DE
Hooth, MJ
AF Ramot, Yuval
Nyska, Abraham
Lieuallen, Warren
Maly, Alex
Flake, Gordon
Kissling, Grace E.
Brix, Amy
Malarkey, David E.
Hooth, Michelle J.
TI Inflammatory and chloracne-like skin lesions in B6C3F1 mice exposed to
3,3 ',4,4 '-tetrachloroazobenzene for 2 years
SO TOXICOLOGY
LA English
DT Article
DE TCAB; Dioxin; Chloracne; Mice; Inflammation
ID SPRAGUE-DAWLEY-RATS; DIOXIN-LIKE COMPOUNDS; POLYCYCLIC
AROMATIC-HYDROCARBONS; POLYCHLORINATED-BIPHENYLS;
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN TCDD; CHRONIC TOXICITY; HUMAN
KERATINOCYTES; HAIRLESS MOUSE; ORAL TREATMENT; CARCINOGENICITY
AB Exposure to dioxin and dioxin-like compounds (DLCs) has been connected to the induction of chloracne in humans and animals. 3,3',4,4'-Tetrachloroazobenzene (TCAB) is an environmental contaminant that induces chloracne in humans. TCAB has been studied only to a limited extent in laboratory animals. While performing a 2-year gavage study in B6C3F1 mice to evaluate the toxic and carcinogenic effects of TCAB, we also explored potential chloracnegenic properties. Groups of 50 male and 50 female B6C3F1 mice were exposed by gavage to TCAB at dose levels of 0, 3, 10 and 30 mg/kg for 5 days a week for 2 years. The animals developed treatment-related gross inflammatory skin lesions, which were characterized histologically by inflammation, fibrosis, hyperplasia, and ulcers. Additionally, many of the animals developed follicular dilatation and sebaceous gland atrophy, consistent with chloracne-like lesions. This current 2-year study supports recently published papers showing susceptibility to chloracne in mouse strains other than hairless mice. The chloracne-like lesions were not clinically evident; therefore, our study highlights the need for careful examination of the skin in order to identify subtle lesions consistent with chloracne-like changes in rodents exposed to dioxin and DLCs. Since previous short-term studies did not demonstrate any skin lesions, we suggest that reliable assessment of all safety issues involving dioxin and DLCs requires evaluation following chronic exposure. Such studies in animal models will help to elucidate the mechanisms of dioxin-related health hazards. Published by Elsevier Ireland Ltd.
C1 [Flake, Gordon; Kissling, Grace E.; Malarkey, David E.; Hooth, Michelle J.] NIEHS, Natl Toxicol Program, Res Triangle Pk, NC 27709 USA.
[Ramot, Yuval] Hadassah Hebrew Univ, Med Ctr, IL-91200 Jerusalem, Israel.
[Nyska, Abraham] Tel Aviv Univ, IL-36576 Tel Aviv, Israel.
[Lieuallen, Warren] Charles River Labs Pathol Associates, Durham, NC 27703 USA.
[Brix, Amy] Expt Pathol Labs, Res Triangle Pk, NC 27709 USA.
RP Hooth, MJ (reprint author), NIEHS, Natl Toxicol Program, POB 12233,Mail Drop K2-13,111 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM hooth@niehs.nih.gov
FU NIH, National Institute of Environmental Health Sciences [1 Z01
ES045004-11 BB]
FX The authors gratefully acknowledge Ms. JoAnne Johnson, Dr. Robert Sills,
and Dr. Nigel Walker from the NTP/NIEHS for their critical review of the
manuscript. This research was supported [in part] by the Intramural
Research Program of the NIH, National Institute of Environmental Health
Sciences under Research Project Number 1 Z01 ES045004-11 BB.
NR 87
TC 6
Z9 6
U1 0
U2 2
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD NOV 9
PY 2009
VL 265
IS 1-2
BP 1
EP 9
DI 10.1016/j.tox.2009.08.017
PG 9
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 518SM
UT WOS:000271713500001
PM 19737593
ER
PT J
AU Nakamura, T
Ito, Y
Yanagiba, Y
Ramdhan, DH
Kono, Y
Naito, H
Hayashi, Y
Li, YF
Aoyama, T
Gonzalez, FJ
Nakajima, T
AF Nakamura, Toshiki
Ito, Yuki
Yanagiba, Yukie
Ramdhan, Doni Hikmat
Kono, Yasuhide
Naito, Hisao
Hayashi, Yumi
Li, Yufei
Aoyama, Toshifumi
Gonzalez, Frank J.
Nakajima, Tamie
TI Microgram-order ammonium perfluorooctanoate may activate mouse
peroxisome proliferator-activated receptor alpha, but not human PPAR
alpha
SO TOXICOLOGY
LA English
DT Article
DE Ammonium perflurooctanate; Peroxisome proliferator-activated receptor
(PPAR) alpha; Humanized PPAR alpha mouse; Ppar alpha-null mouse; Lipid
metabolism
ID FLUOROCHEMICAL PRODUCTION WORKERS; RAT-LIVER; PFOA CONCENTRATIONS; NULL
MICE; WILD-TYPE; ACID; EXPRESSION; INDUCTION; TRICHLOROETHYLENE;
PURIFICATION
AB Perfluorooctanoic acid (PFOA) is a ligand for peroxisome proliferator-activated receptor (PPAR)alpha, which exhibits marked species differences in expression and function, especially between rodents and humans. We investigated the functional difference in PFOA response between mice and humans, using a humanized PPAR alpha transgenic mouse line. Three genotyped mice, 129/5v wild-type (mPPAR alpha), Ppar alpha-null mice and humanized PPAR alpha (hPPAR alpha) mice (8-week-old males) were divided into three groups: the first was treated with water daily for 2 weeks by gavage (control group), and the remaining two groups were treated with 0.1 and 0.3 mg/kg ammonium perflurooctanate (APFO), respectively, for 2 weeks by gavage. The APFO dosages used did not influence the plasma triglyceride or total cholesterol levels in any mouse line, but the high dose increased both hepatic lipid levels only in mPPAR alpha mice. APFO increased mRNA and/or protein levels of PPAR alpha target genes cytochrome P450 Cyp4a10, peroxisomal thiolase and bifunctional protein only in the liver of mPPAR alpha mice, but not in Ppar alpha-null or hPPAR alpha mice. This chemical also increased expression of mitochondrial very long chain acyl-CoA dehydrogenase only in the liver of mPPAR alpha mice. Taken together, human PPAR alpha may be less responsive to PFOA than that of mice when a relatively low dose is applied. This information may be very valuable in considering whether PFOA influences the lipid metabolism in humans. (c) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [Nakamura, Toshiki; Ito, Yuki; Yanagiba, Yukie; Ramdhan, Doni Hikmat; Kono, Yasuhide; Naito, Hisao; Hayashi, Yumi; Li, Yufei; Nakajima, Tamie] Nagoya Univ, Dept Occupat & Environm Hlth, Grad Sch Med, Showa Ku, Aichi 4668550, Japan.
[Aoyama, Toshifumi] Shinshu Univ, Dept Metab Regulat, Grad Sch Med, Nagano 3908621, Japan.
[Gonzalez, Frank J.] NCI, Lab Metab, NIH, Bethesda, MD 20892 USA.
RP Nakajima, T (reprint author), Nagoya Univ, Dept Occupat & Environm Hlth, Grad Sch Med, Showa Ku, 65 Tsurumai Cho, Aichi 4668550, Japan.
EM tnasu23@med.nagoya-u.ac.jp
RI Ito, Yuki/C-3698-2008
FU Japan Society for the Promotion of Science [B. 14370121, B. 17390169]
FX We wish to thank Mr. Nakagawa, Department of Occupational and
Environmental Health, Nagoya University Graduate School of Medicine for
his valuable assistance. This study was supported in part by
Grants-in-Aid for Scientific Research from the Japan Society for the
Promotion of Science (B. 14370121 and B. 17390169).
NR 43
TC 20
Z9 23
U1 1
U2 5
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD NOV 9
PY 2009
VL 265
IS 1-2
BP 27
EP 33
DI 10.1016/j.tox.2009.09.004
PG 7
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 518SM
UT WOS:000271713500004
PM 19751795
ER
PT J
AU Maguire, AM
High, KA
Auricchio, A
Wright, JF
Pierce, EA
Testa, F
Mingozzi, F
Bennicelli, JL
Ying, GS
Rossi, S
Fulton, A
Marshall, KA
Banfi, S
Chung, DC
Morgan, JIW
Hauck, B
Zelenaia, O
Zhu, XS
Raffini, L
Coppieters, F
De Baere, E
Shindler, KS
Volpe, NJ
Surace, EM
Acerra, C
Lyubarsky, A
Redmond, TM
Stone, E
Sun, JW
McDonnell, JW
Leroy, BP
Simonelli, F
Bennett, J
AF Maguire, Albert M.
High, Katherine A.
Auricchio, Alberta
Wright, J. Fraser
Pierce, Eric A.
Testa, Francesco
Mingozzi, Federico
Bennicelli, Jeannette L.
Ying, Gui-shuang
Rossi, Settimio
Fulton, Ann
Marshall, Kathleen A.
Banfi, Sandra
Chung, Daniel C.
Morgan, Jessica I. W.
Hauck, Bernd
Zelenaia, Olga
Zhu, Xiaosong
Raffini, Leslie
Coppieters, Frauke
De Baere, Elfride
Shindler, Kenneth S.
Volpe, Nicholas J.
Surace, Enrico M.
Acerra, Carmela
Lyubarsky, Arkady
Redmond, T. Michael
Stone, Edwin
Sun, Junwei
McDonnell, Jennifer Wellman
Leroy, Bart P.
Simonelli, Francesca
Bennett, Jean
TI Age-dependent effects of RPE65 gene therapy for Leber's congenital
amaurosis: a phase 1 dose-escalation trial
SO LANCET
LA English
DT Article
ID VISUAL CYCLE; RETINITIS-PIGMENTOSA; VISION; MUTATIONS; BLINDNESS; ROD;
ISOMEROHYDROLASE; ISOMERASE; KINETICS; SAFETY
AB Background Gene therapy has the potential to reverse disease or prevent further deterioration of vision in patients with incurable inherited retinal degeneration. We therefore did a phase 1 trial to assess the effect of gene therapy on retinal and visual function in children and adults with Leber's congenital amaurosis.
Methods We assessed the retinal and visual function in 12 patients (aged 8-44 years) with RPE65-associated Leber's congenital amaurosis given one subretinal injection of adeno-associated virus (AAV) containing a gene encoding a protein needed for the isomerohydrolase activity of the retinal pigment epithelium (AAV2-hRPE65v2) in the worst eye at low (1.5x10(10) vector genomes), medium (4.8x10(10) vector genomes), or high dose (1.5x10(11) vector genomes) for up to 2 years.
Findings AAV2-hRPE65v2 was well tolerated and all patients showed sustained improvement in subjective and objective measurements of vision (ie, dark adaptometry, pupillometry, electroretinography, nystagmus, and ambulatory behaviour). Patients had at least a 2 log unit increase in pupillary light responses, and an 8-year-old child had nearly the same level of light sensitivity as that in age-matched normal-sighted individuals. The greatest improvement was noted in children, all of whom gained ambulatory vision. The study is registered with ClinicalTrials.gov, number NCT00516477.
Interpretation The safety, extent, and stability of improvement in vision in all patients support the use of AAV mediated gene therapy for treatment of inherited retinal diseases, with early intervention resulting in the best potential gain.
C1 [Bennett, Jean] Univ Penn, Stellar Chance Labs 309C, Scheie Eye Inst, FM Kirby Ctr Mol Ophthalmol, Philadelphia, PA 19104 USA.
[Maguire, Albert M.; High, Katherine A.; Wright, J. Fraser; Mingozzi, Federico; Marshall, Kathleen A.; Hauck, Bernd; Zelenaia, Olga; Sun, Junwei; McDonnell, Jennifer Wellman; Bennett, Jean] Childrens Hosp Philadelphia, Ctr Cellular & Mol Therapeut, Abramson Pediat Res Ctr, Philadelphia, PA 19104 USA.
[Maguire, Albert M.; Pierce, Eric A.; Zhu, Xiaosong] Childrens Hosp Philadelphia, Dept Ophthalmol, Philadelphia, PA 19104 USA.
[High, Katherine A.; Raffini, Leslie] Univ Penn, Childrens Hosp Philadelphia, Dept Hematol, Dept Pediat, Philadelphia, PA 19104 USA.
[High, Katherine A.; Stone, Edwin] Univ Penn, Howard Hughes Med Inst, Philadelphia, PA 19104 USA.
[High, Katherine A.; Stone, Edwin] Univ Iowa, Howard Hughes Med Inst, Iowa City, IA 52242 USA.
[Auricchio, Alberta; Banfi, Sandra; Surace, Enrico M.] TIGEM, Naples, Italy.
[Auricchio, Alberta] Univ Naples Federico 2, Dept Pediat, Naples, Italy.
[Testa, Francesco; Rossi, Settimio; Acerra, Carmela; Simonelli, Francesca] Univ Naples 2, Dept Ophthalmol, Naples, Italy.
[Ying, Gui-shuang; Volpe, Nicholas J.] Univ Penn, Scheie Eye Inst, Dept Ophthalmol, Ctr Prevent Ophthalmol & Biostat, Philadelphia, PA 19104 USA.
[Fulton, Ann] Childrens Hosp Boston, Dept Ophthalmol, Boston, MA USA.
[Coppieters, Frauke; De Baere, Elfride; Leroy, Bart P.] Univ Ghent, Ctr Med Genet, B-9000 Ghent, Belgium.
Univ Penn, Scheie Eye Inst, Neuroophthalmol Serv, Dept Ophthalmol, Philadelphia, PA 19104 USA.
[Redmond, T. Michael] NEI, Lab Retinal Cell & Mol Biol, NIH, Bethesda, MD 20892 USA.
[Stone, Edwin] Univ Iowa, Coll Med, Dept Ophthalmol, Carver Ctr, Iowa City, IA 52242 USA.
[Wright, J. Fraser] Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
[Leroy, Bart P.] Univ Ghent, Dept Ophthalmol, B-9000 Ghent, Belgium.
[Leroy, Bart P.] Ghent Univ Hosp, B-9000 Ghent, Belgium.
RP Bennett, J (reprint author), Univ Penn, Stellar Chance Labs 309C, Scheie Eye Inst, FM Kirby Ctr Mol Ophthalmol, 422 Curie Blvd, Philadelphia, PA 19104 USA.
EM jebennet@mail.med.upenn.edu
RI Shindler, Kenneth/D-2095-2009; Testa, Francesco/J-3185-2012; Rossi,
Settimio/J-4922-2012;
OI Testa, Francesco/0000-0002-1482-1577; Simonelli,
Francesca/0000-0001-8520-6769; AURICCHIO, Alberto/0000-0002-0832-2472;
Redmond, T. Michael/0000-0002-1813-5291; Surace, Enrico
Maria/0000-0002-2975-942X; BANFI, Sandro/0000-0002-6541-8833; Pierce,
Eric/0000-0002-2354-4102
FU Funding Center for Cellular and Molecular Therapeutics at the Children's
Hospital of Philadelphia; Foundation Fighting Blindness; Telethon;
Research to Prevent Blindness; F M Kirby Foundation; Mackall Foundation
Trust; Regione Campania Convenzione; European Union; Associazione
Italiana Amaurosi Congenita di Leber; Fund for Scientific Research; Fund
for Research in Ophthalmology; National Center for Research Resources
FX Funding Center for Cellular and Molecular Therapeutics at the Children's
Hospital of Philadelphia, Foundation Fighting Blindness, Telethon,
Research to Prevent Blindness, F M Kirby Foundation, Mackall Foundation
Trust, Regione Campania Convenzione, European Union, Associazione
Italiana Amaurosi Congenita di Leber, Fund for Scientific Research, Fund
for Research in Ophthalmology, and National Center for Research
Resources.
NR 26
TC 373
Z9 386
U1 3
U2 35
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD NOV 7
PY 2009
VL 374
IS 9701
BP 1597
EP 1605
DI 10.1016/S0140-6736(09)61836-5
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 518EZ
UT WOS:000271674600033
PM 19854499
ER
PT J
AU Chen, E
Finkel, T
AF Chen, Edmund
Finkel, Toren
TI The Tortoise, the Hare, and the FoxO
SO CELL STEM CELL
LA English
DT Editorial Material
ID OXIDATIVE STRESS; CELLS; MAINTENANCE; HOMEOSTASIS
AB Maintaining stem cell quiescence is intimately connected to preserving long-term self-renewal potential. In this issue of Cell Stem Cell, Paik et al. (2009) and Renault et al. (2009) demonstrate a role for FoxO transcription factors in regulating neural stem cell proliferation and in maintaining stem and progenitor cell homeostasis.
C1 [Chen, Edmund; Finkel, Toren] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
RP Finkel, T (reprint author), NHLBI, Translat Med Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM finkelt@nih.gov
NR 11
TC 6
Z9 6
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1934-5909
J9 CELL STEM CELL
JI Cell Stem Cell
PD NOV 6
PY 2009
VL 5
IS 5
BP 451
EP 452
DI 10.1016/j.stem.2009.10.011
PG 2
WC Cell & Tissue Engineering; Cell Biology
SC Cell Biology
GA 522SR
UT WOS:000272019500001
PM 19896431
ER
PT J
AU Seth, M
Zhang, ZS
Mao, L
Graham, V
Burch, J
Stiber, J
Tsiokas, L
Winn, M
Abramowitz, J
Rockman, HA
Birnbaumer, L
Rosenberg, P
AF Seth, Malini
Zhang, Zhu-Shan
Mao, Lan
Graham, Victoria
Burch, Jarrett
Stiber, Jonathan
Tsiokas, Leonidas
Winn, Michelle
Abramowitz, Joel
Rockman, Howard A.
Birnbaumer, Lutz
Rosenberg, Paul
TI TRPC1 Channels Are Critical for Hypertrophic Signaling in the Heart
SO CIRCULATION RESEARCH
LA English
DT Article
DE transient receptor potential channels; G protein receptor signaling;
cardiac hypertrophy
ID METABOTROPIC GLUTAMATE RECEPTORS; SMOOTH-MUSCLE-CELLS;
CARDIAC-HYPERTROPHY; CATION CHANNEL; GROWTH CONES; ACTIVATION; GENE;
MYOCYTES; HOMER; MICE
AB Rationale: Cardiac muscle adapts to increase workload by altering cardiomyocyte size and function resulting in cardiac hypertrophy. G protein-coupled receptor signaling is known to govern the hypertrophic response through the regulation of ion channel activity and downstream signaling in failing cardiomyocytes.
Objective: Transient receptor potential canonical (TRPC) channels are G protein-coupled receptor operated channels previously implicated in cardiac hypertrophy. Our objective of this study is to better understand how TRPC channels influence cardiomyocyte calcium signaling.
Methods and Results: Here, we used whole cell patch clamp of adult cardiomyocytes to show upregulation of a nonselective cation current reminiscent of TRPC channels subjected to pressure overload. This TRPC current corresponds to the increased TRPC channel expression noted in hearts of mice subjected to pressure overload. Importantly, we show that mice lacking TRPC1 channels are missing this putative TRPC current. Moreover, Trpc1(-/-) mice fail to manifest evidence of maladaptive cardiac hypertrophy and maintain preserved cardiac function when subjected to hemodynamic stress and neurohormonal excess. In addition, we provide a mechanistic basis for the protection conferred to Trpc1(-/-) mice as mechanosensitive signaling through calcineurin/NFAT, mTOR and Akt is altered in Trpc1(-/-) mice.
Conclusions: From these studies, we suggest that TRPC1 channels are critical for the adaptation to biomechanical stress and TRPC dysregulation leads to maladaptive cardiac hypertrophy and failure. (Circ Res. 2009;105:1023-1030.)
C1 [Seth, Malini; Zhang, Zhu-Shan; Mao, Lan; Graham, Victoria; Burch, Jarrett; Stiber, Jonathan; Winn, Michelle; Rockman, Howard A.; Rosenberg, Paul] Duke Univ, Sch Med, Dept Med, Durham, NC 27706 USA.
[Tsiokas, Leonidas] Univ Oklahoma, Hlth Sci Ctr, Dept Cell Biol, Oklahoma City, OK USA.
[Abramowitz, Joel; Birnbaumer, Lutz] NIEHS, Neurobiol Lab, Res Triangle Pk, NC 27709 USA.
RP Rosenberg, P (reprint author), Suite 200,4321 Med Pk Dr, Durham, NC 27704 USA.
EM rosen029@mc.duke.edu
RI Abramowitz, Joel/A-2620-2015;
OI Rosenberg, Paul/0000-0002-5659-160X
FU NIH [R01-HL093470]; Muscular Dystrophy Association; NIH; National
Institute of Environmental Health Sciences
FX This work was supported by NIH grant R01-HL093470 (to P. R.), the Mandel
Center at Duke (P.R.), and a Muscular Dystrophy Association research
award (P.R.) and, in part, by the Intramural Program of the NIH,
National Institute of Environmental Health Sciences ( to J.A. and L.B.).
NR 45
TC 99
Z9 108
U1 0
U2 5
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7330
J9 CIRC RES
JI Circ.Res.
PD NOV 6
PY 2009
VL 105
IS 10
BP 1023
EP U190
DI 10.1161/CIRCRESAHA.109.206581
PG 17
WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Hematology
GA 515XE
UT WOS:000271505400011
PM 19797170
ER
PT J
AU Kim, KK
Adelstein, RS
Kawamoto, S
AF Kim, Kee K.
Adelstein, Robert S.
Kawamoto, Sachiyo
TI Identification of Neuronal Nuclei (NeuN) as Fox-3, a New Member of the
Fox-1 Gene Family of Splicing Factors
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID NEURAL STEM-CELLS; HEAVY CHAIN-B; DIAGNOSTIC HISTOPATHOLOGY; HUMAN
TISSUES; MARKER NEUN; SPINAL-CORD; ADULT MICE; IN-VIVO; PROTEIN;
EXPRESSION
AB NeuN (neuronal nuclei) is a neuron-specific nuclear protein which is identified by immunoreactivity with a monoclonal antibody, anti-NeuN. Anti-NeuN has been used widely as a reliable tool to detect most postmitotic neuronal cell types in neuroscience, developmental biology, and stem cell research fields as well as diagnostic histopathology. To date, however, the identity of its antigen, NeuN itself, has been unknown. Here, we identify NeuN as the Fox-3 gene product by providing the following evidence: 1) Mass spectrometry analysis of anti-NeuN immunoreactive protein yields the Fox-3 amino acid sequence. 2) Recombinant Fox-3 is recognized by anti-NeuN. 3) Short hairpin RNAs targeting Fox-3 mRNA down-regulate NeuN expression. 4) Fox-3 expression is restricted to neural tissues. 5) Anti-Fox-3 immunostaining and anti-NeuN immunostaining overlap completely in neuronal nuclei. We also show that a protein cross-reactive with anti-NeuN is the synaptic vesicle protein, synapsin I. Anti-NeuN recognizes synapsin I in immunoblots with one order of magnitude lower affinity than Fox-3, and does not recognize synapsin I using immunohistology. Fox-3 (also called hexaribonucleotide-binding protein 3 and D11Bwg0517e) contains an RNA recognition motif and is classified as a member of the Fox-1 gene family that binds specifically to an RNA element, UGCAUG. We demonstrate that Fox-3 functions as a splicing regulator using neural cell-specific alternative splicing of the non-muscle myosin heavy chain II-B pre-mRNA as a model. Identification of NeuN as Fox-3 clarifies an important element of neurobiology research.
C1 [Kim, Kee K.; Adelstein, Robert S.; Kawamoto, Sachiyo] NHLBI, Mol Cardiol Lab, NIH, Bethesda, MD 20892 USA.
RP Kawamoto, S (reprint author), NHLBI, Mol Cardiol Lab, NIH, Bldg 10,Rm 6C209,10 Ctr Dr MSC 1762, Bethesda, MD 20892 USA.
EM kawamots@mail.nih.gov
RI Kim, Kee/F-8784-2011;
OI Adelstein, Robert/0000-0002-8683-2144
FU Division of Intramural Research; NHLBI; National Institutes of Health
FX This work was supported, in whole or in part, by the Division of
Intramural Research, NHLBI, National Institutes of Health.
NR 40
TC 156
Z9 161
U1 0
U2 10
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 6
PY 2009
VL 284
IS 45
BP 31052
EP 31061
DI 10.1074/jbc.M109.052969
PG 10
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 514EZ
UT WOS:000271378400034
PM 19713214
ER
PT J
AU Ghosh, A
Rossi, ML
Aulds, J
Croteau, D
Bohr, VA
AF Ghosh, Avik
Rossi, Marie L.
Aulds, Jason
Croteau, Deborah
Bohr, Vilhelm A.
TI Telomeric D-loops Containing 8-Oxo-2 '-deoxyguanosine Are Preferred
Substrates for Werner and Bloom Syndrome Helicases and Are Bound by POT1
SO JOURNAL OF BIOLOGICAL CHEMISTRY
LA English
DT Article
ID SINGLE-STRANDED-DNA; RECQ HELICASES; MAMMALIAN TELOMERES; OXIDATIVE
STRESS; SYNDROME PROTEIN; SYNDROME GENE; WRN PROTEIN; IN-VITRO; BINDING;
SITE
AB 8-Oxo-2'-deoxyguanosine (8-oxodG) is one of the most important oxidative DNA lesions, and G-rich telomeric DNA is especially susceptible to oxidative DNA damage. RecQ helicases WRN and BLM and telomere- binding protein POT1 are thought to play roles in telomere maintenance. This study examines the ability of WRN, BLM, and RecQ5 to unwind and POT1 to bind telomeric D-loops containing 8-oxodG. The results demonstrate that WRN and BLM preferentially unwind telomeric D-loops containing 8-oxodG and that POT1 binds with higher affinity to telomeric D-loops with 8-oxodG but shows no preference for telomeric single-stranded DNA with 8-oxodG. We speculate that telomeric D-loops with 8-oxodG may have a greater tendency to form G-quadruplex DNA structures than telomeric DNA lacking 8-oxodG.
C1 [Bohr, Vilhelm A.] NIA, Lab Mol Gerontol, NIH, Biomed Res Ctr, Baltimore, MD 21224 USA.
RP Bohr, VA (reprint author), NIA, Lab Mol Gerontol, NIH, Biomed Res Ctr, 251 Bayview Blvd, Baltimore, MD 21224 USA.
EM BohrV@.nih.gov
FU National Institute on Aging
FX This work was supported, in whole or in part, by the National Institutes
of Health Intramural Program of the National Institute on Aging.
NR 51
TC 35
Z9 35
U1 0
U2 7
PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
SN 0021-9258
J9 J BIOL CHEM
JI J. Biol. Chem.
PD NOV 6
PY 2009
VL 284
IS 45
BP 31074
EP 31084
DI 10.1074/jbc.M109.027532
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 514EZ
UT WOS:000271378400036
PM 19734539
ER
PT J
AU Prokunina-Olsson, L
Hall, JL
AF Prokunina-Olsson, Ludmila
Hall, Jennifer L.
TI No effect of cancer-associated SNP rs6983267 in the 8q24 region on
co-expression of MYC and TCF7L2 in normal colon tissue
SO MOLECULAR CANCER
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; COLORECTAL-CANCER; PROSTATE-CANCER; CHROMOSOME
8Q24; C-MYC; SMALL-INTESTINE; RISK; GENE; EXPRESSION; TARGET
AB A single nucleotide polymorphism (SNP) rs6983267, located within the 8q24 region, is strongly associated with risk of colorectal and prostate cancer. It has been suggested that the mechanism of this association is related to differential interaction of TCF7L2 protein (previously known as TCF-4) with alleles of rs6983267, influencing the expression of a well-known oncogene, MYC, located 335 Kb telomeric. Here, we tested the correlation between mRNA expression of MYC and several alternatively spliced forms of TCF7L2 in 117 non-cancer colon samples. We observed a strong correlation (r = 0.60, p < 10(-6)) between expression of MYC and a unique splicing form of TCF7L2. The level of MYC expression in these samples was associated with expression of some TCF7L2 splicing forms but not with genotypes of rs6983267, or interaction of rs6983267 with TCF7L2 expression. These findings suggest that some splicing forms of TCF7L2 may be functionally important for regulation of MYC expression in colon tissue but this regulation is not directly dependent on rs6983267.
C1 [Prokunina-Olsson, Ludmila] NCI, Lab Translat Gen, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Hall, Jennifer L.] Univ Minnesota, Dept Med, Lillehei Heart Inst, Minneapolis, MN 55455 USA.
RP Prokunina-Olsson, L (reprint author), NCI, Lab Translat Gen, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
EM prokuninal@mail.nih.gov; jlhall@umn.edu
OI Prokunina-Olsson, Ludmila/0000-0002-9622-2091
FU NCI/NIH (LPO); R21 award [1R21DK078029-01]
FX We thank Yi-Ping Fu for help with statistical analysis. The study was
supported by the intramural research program of NCI/NIH (LPO) and by an
R21 award to JLH (1R21DK078029-01). We would like to thank Cullan Welch,
Nikki Usher, and Marj Carlson for their technical assistance with the
tissue processing.
NR 33
TC 15
Z9 16
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-4598
J9 MOL CANCER
JI Mol. Cancer
PD NOV 6
PY 2009
VL 8
AR 96
DI 10.1186/1476-4598-8-96
PG 5
WC Biochemistry & Molecular Biology; Oncology
SC Biochemistry & Molecular Biology; Oncology
GA 526IL
UT WOS:000272281400001
PM 19895682
ER
PT J
AU Ren, D
Labandeira, CC
Santiago-Blay, JA
Rasnitsyn, A
Shih, C
Bashkuev, A
Logan, MAV
Hotton, CL
Dilcher, D
AF Ren, Dong
Labandeira, Conrad C.
Santiago-Blay, Jorge A.
Rasnitsyn, Alexandr
Shih, ChungKun
Bashkuev, Alexei
Logan, M. Amelia V.
Hotton, Carol L.
Dilcher, David
TI A Probable Pollination Mode Before Angiosperms: Eurasian, Long-Proboscid
Scorpionflies
SO SCIENCE
LA English
DT Article
ID REPRODUCTIVE STRUCTURES; INSECT POLLINATION; POLLEN MORPHOLOGY; FOSSIL
EVIDENCE; DIVERSITY; DIPTERA; DIVERSIFICATION; COEVOLUTION; BRACHYCERA;
MOUTHPARTS
AB The head and mouthpart structures of 11 species of Eurasian scorpionflies represent three extinct and closely related families during a 62-million-year interval from the late Middle Jurassic to the late Early Cretaceous. These taxa had elongate, siphonate ( tubular) proboscides and fed on ovular secretions of extinct gymnosperms. Five potential ovulate host-plant taxa co-occur with these insects: a seed fern, conifer, ginkgoopsid, pentoxylalean, and gnetalean. The presence of scorpionfly taxa suggests that siphonate proboscides fed on gymnosperm pollination drops and likely engaged in pollination mutualisms with gymnosperms during the mid-Mesozoic, long before the similar and independent coevolution of nectar-feeding flies, moths, and beetles on angiosperms. All three scorpionfly families became extinct during the later Early Cretaceous, coincident with global gymnosperm-to-angiosperm turnover.
C1 [Ren, Dong; Shih, ChungKun] Capital Normal Univ, Coll Life Sci, Beijing 100048, Peoples R China.
[Labandeira, Conrad C.; Santiago-Blay, Jorge A.; Hotton, Carol L.; Dilcher, David] Smithsonian Inst, Natl Museum Nat Hist, Dept Paleobiol, Washington, DC 20013 USA.
[Labandeira, Conrad C.] Univ Maryland, Dept Entomol, College Pk, MD 20742 USA.
[Santiago-Blay, Jorge A.] Gallaudet Univ, Dept Biol, Washington, DC 20003 USA.
[Rasnitsyn, Alexandr] Russian Acad Sci, Inst Paleontol, Moscow 117997, Russia.
[Rasnitsyn, Alexandr] Nat Hist Museum, Dept Palaeontol, London SW7 5BD, England.
[Logan, M. Amelia V.] Smithsonian Inst, Natl Museum Nat Hist, Dept Mineral Sci, Washington, DC 20013 USA.
[Hotton, Carol L.] Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20892 USA.
[Dilcher, David] Univ Florida, Florida Museum Nat Hist, Gainesville, FL 32611 USA.
RP Labandeira, CC (reprint author), Capital Normal Univ, Coll Life Sci, Beijing 100048, Peoples R China.
EM labandec@si.edu
FU National Science Foundation of China [30430100, 40872022]; Natural
Science Foundation of Beijing [5082002]; Key and PHR Program of the
Beijing Municipal Commission of Education; Origin and Evolution of the
Biosphere program of the Presidium of the Russian Academy of Sciences;
Intramural Research Program of the National Library of Medicine
FX This is contribution 152 of the Evolution of Terrestrial Ecosystems
consortium at the National Museum of Natural History and contribution
614 of the Florida Museum of Natural History. Supported by the National
Science Foundation of China ( grants 30430100 and 40872022), the Natural
Science Foundation of Beijing ( grant 5082002), and the Key and PHR
Program of the Beijing Municipal Commission of Education ( D. R.); the
Origin and Evolution of the Biosphere program of the Presidium of the
Russian Academy of Sciences ( A. B.); and the Intramural Research
Program of the National Library of Medicine. We thank F. Marsh for
drafting the figures, T. Lott for a presubmission review, P. Crane for
comments, T. Rose for assistance on the geochemical analyses, J. Corman
for collection of data, B. Wagner and R. Johnson for translations, P.
Peltier for proofreading, and W. Wu for general assistance. X. Wang
provided data and images for Problematospermum ovale, and D. Grimaldi of
the American Museum of Natural History ( New York) made an important
specimen available for study.
NR 54
TC 113
Z9 128
U1 2
U2 49
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD NOV 6
PY 2009
VL 326
IS 5954
BP 840
EP 847
DI 10.1126/science.1178338
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 515KG
UT WOS:000271468000041
PM 19892981
ER
PT J
AU Coutellier, L
Wurbel, H
AF Coutellier, Laurence
Wuerbel, Hanno
TI Early environmental cues affect object recognition memory in adult
female but not male C57BL/6 mice
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Maternal environment; Object recognition memory; Predator cues;
Offspring
ID POSTNATAL MATERNAL ENVIRONMENT; COGNITIVE FUNCTION; STRESS REACTIVITY;
CARE; RESPONSES; RATS; BEHAVIOR; EXPRESSION; ENRICHMENT; FEAR
AB We studied the effects of variations in maternal environment on maternal behaviour and offspring memory in mice by exposing lactating C57BL/6J dams to predator cues and/or environmental enrichment. At 10 weeks of age, object recognition memory in the offspring was assessed. The presence of enrichment in the maternal environment had no effect on offspring memory. In contrast, female offspring of dams that were not exposed to predator cues displayed a significant preference for the novel object (p = 0.05) and a significantly higher preference score (PS) than female offspring of dams that were exposed to predator cues (F= 4.23, p = 0.05) indicating an impairment in object recognition memory in the latter. Conversely, there was no evidence of object recognition memory in male offspring, except for males of dams exposed to predator cues without shelter (p = 0.03). These effects can be explained by an interaction between variations in maternal care and the stressfulness of the rearing conditions since a regression analysis revealed an inverse relationship between the level of licking-grooming and the PS, but only in female offspring reared by dams exposed to the predator cues (beta = -0.96, p = 0.001). The present findings thus provide some evidence that early rearing conditions may affect cognitive abilities of mice. The data also suggest that these effects may be sex-specific, and that females may be more sensitive to early environmental variations than males. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Coutellier, Laurence] NIMH, Sect Fundamental Neurosci, NIH, Bethesda, MD 20892 USA.
[Wuerbel, Hanno] Univ Giessen, Div Anim Welf & Ethol, D-35392 Giessen, Germany.
RP Coutellier, L (reprint author), NIMH, Sect Fundamental Neurosci, NIH, 35 Convent Dr, Bethesda, MD 20892 USA.
EM coutellierl@mail.nih.gov
RI Wurbel, Hanno/D-6281-2012
OI Wurbel, Hanno/0000-0002-2934-3010
NR 24
TC 13
Z9 13
U1 2
U2 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 5
PY 2009
VL 203
IS 2
BP 312
EP 315
DI 10.1016/j.bbr.2009.05.001
PG 4
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 475MP
UT WOS:000268364100021
PM 19427334
ER
PT J
AU Flegel, WA
AF Flegel, Willy Albert
TI Immunogenicity reloaded
SO BLOOD
LA English
DT Editorial Material
C1 Natl Inst Hlth, Bethesda, MD 20892 USA.
RP Flegel, WA (reprint author), Natl Inst Hlth, Bethesda, MD 20892 USA.
NR 5
TC 3
Z9 3
U1 0
U2 0
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 5
PY 2009
VL 114
IS 19
BP 3979
EP 3980
DI 10.1182/blood-2009-09-241448
PG 4
WC Hematology
SC Hematology
GA 515TJ
UT WOS:000271495500005
PM 19892725
ER
PT J
AU Li, ZY
Wang, HS
Xue, LQ
Shin, DM
Roopenian, D
Xu, W
Qi, CF
Sangster, MY
Orihuela, CJ
Tuomanen, E
Rehg, JE
Cui, XL
Zhang, QG
Morse, HC
Morris, SW
AF Li, Zhaoyang
Wang, Hongsheng
Xue, Liquan
Shin, Dong-Mi
Roopenian, Derry
Xu, Wu
Qi, Chen-Feng
Sangster, Mark Y.
Orihuela, Carlos J.
Tuomanen, Elaine
Rehg, Jerold E.
Cui, Xiaoli
Zhang, Quangeng
Morse, Herbert C., III
Morris, Stephan W.
TI E mu-BCL10 mice exhibit constitutive activation of both canonical and
noncanonical NF-kappa B pathways generating marginal zone (MZ) B-cell
expansion as a precursor to splenic MZ lymphoma
SO BLOOD
LA English
DT Article
ID POSITIVE SELECTION; MALT LYMPHOMA; NUCLEAR EXPRESSION; PLASMA-CELL; B1B
CELLS; T-CELL; BCL10; LYMPHOCYTES; BAFF; APRIL
AB BCL10, required for nuclear factor kappa B (NF-kappa B) activation during antigen-driven lymphocyte responses, is aberrantly expressed in mucosa-associated lymphoid tissue-type marginal zone (MZ) lymphomas because of chromosomal translocations. E mu-driven human BCL10 transgenic (Tg) mice, which we created and characterize here, had expanded populations of MZ B cells and reduced follicular and B1a cells. Splenic B cells from Tg mice exhibited constitutive activation of both canonical and noncanonical NF-kappa B signaling pathways is associated with increased expression of NF-kappa B target genes. These genes included Tnfsf13b, which encodes the B-cell activating factor (BAFF). In addition, levels of BAFF were significantly increased in sera from Tg mice. MZ B cells of Tg mice exhibited reduced turnover in vivo and enhanced survival in vitro, indicative of lymphoaccumulation rather than lymphoproliferation as the cause of MZ expansion. In vivo antibody responses to both T-independent, and especially T-dependent, antigens were significantly reduced in Tg mice. Mortality was accelerated in Tg animals, and some mice older than 8 months had histologic and molecular findings indicative of clonal splenic MZ lymphoma. These results suggest that, in addition to constitutive activation of BCL10 in MZ B cells, other genetic factors or environmental influences are required for short latency oncogenic transformation. (Blood. 2009; 114:4158-4168)
C1 [Zhang, Quangeng] Capital Med Univ, Dept Immunol, Beijing 100069, Peoples R China.
[Li, Zhaoyang; Wang, Hongsheng; Shin, Dong-Mi; Qi, Chen-Feng; Morse, Herbert C., III] NIAID, Immunopathol Lab, NIH, Rockville, MD 20852 USA.
[Xue, Liquan; Rehg, Jerold E.; Cui, Xiaoli; Morris, Stephan W.] St Jude Childrens Hosp, Dept Pathol, Memphis, TN 38105 USA.
[Xue, Liquan; Rehg, Jerold E.; Cui, Xiaoli; Morris, Stephan W.] St Jude Childrens Hosp, Dept Oncol, Memphis, TN 38105 USA.
[Roopenian, Derry] Jackson Lab, Bar Harbor, ME 04609 USA.
[Xu, Wu] Univ Louisiana, Dept Chem, Lafayette, LA USA.
[Sangster, Mark Y.] Univ Tennessee, Dept Microbiol, Knoxville, TN 37996 USA.
[Orihuela, Carlos J.] Univ Texas Hlth Sci Ctr San Antonio, Dept Microbiol & Immunol, San Antonio, TX 78229 USA.
[Tuomanen, Elaine] St Jude Childrens Hosp, Dept Infect Dis, Memphis, TN 38105 USA.
RP Zhang, QG (reprint author), Capital Med Univ, Dept Immunol, Rm 1121,2nd Teaching Bldg,10 Xi Tou Tiao, Beijing 100069, Peoples R China.
EM zhangqg@ccmu.edu.cn; hmorse@niaid.nih.gov; steve.morris@stjude.org
RI Li, Chaoyang/A-7980-2012;
OI Morse, Herbert/0000-0002-9331-3705
FU Intramural Research Program of the National Institutes of Health;
National Institute of Allergy and Infectious Diseases; National Cancer
Institute [R01 CA87064]; Cancer Center [CA21765]; American Lebanese
Syrian Associated Charities (ALSAC); St Jude Children's Research
Hospital
FX This work was supported in part by the Intramural Research Program of
the National Institutes of Health, National Institute of Allergy and
Infectious Diseases and by National Cancer Institute (NCI; grant R01
CA87064, S.W.M.), Cancer Center (CORE; grant CA21765), and the American
Lebanese Syrian Associated Charities (ALSAC), St Jude Children's
Research Hospital.
NR 50
TC 31
Z9 33
U1 0
U2 1
PU AMER SOC HEMATOLOGY
PI WASHINGTON
PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA
SN 0006-4971
J9 BLOOD
JI Blood
PD NOV 5
PY 2009
VL 114
IS 19
BP 4158
EP 4168
DI 10.1182/blood-2008-12-192583
PG 11
WC Hematology
SC Hematology
GA 515TJ
UT WOS:000271495500029
PM 19696203
ER
PT J
AU Drazen, JM
Van Der Weyden, MB
Sahni, P
Rosenberg, J
Marusic, A
Laine, C
Kotzin, S
Horton, R
Hebert, PC
Haug, C
Godlee, F
Frizelle, FA
de Leeuw, PW
DeAngelis, CD
AF Drazen, Jeffrey M.
Van Der Weyden, Martin B.
Sahni, Peush
Rosenberg, Jacob
Marusic, Ana
Laine, Christine
Kotzin, Sheldon
Horton, Richard
Hebert, Paul C.
Haug, Charlotte
Godlee, Fiona
Frizelle, Frank A.
de Leeuw, Peter W.
DeAngelis, Catherine D.
TI Uniform Format for Disclosure of Competing Interests in ICMJE Journals.
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Editorial Material
C1 [Kotzin, Sheldon] Natl Lib Med, Bethesda, MD 20894 USA.
RI Marusic, Ana/E-7683-2013;
OI Marusic, Ana/0000-0001-6272-0917; Sahni, Peush/0000-0002-6910-062X
NR 0
TC 48
Z9 53
U1 0
U2 1
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 5
PY 2009
VL 361
IS 19
BP 1896
EP 1897
DI 10.1056/NEJMe0909052
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 514OZ
UT WOS:000271405800017
PM 19825973
ER
PT J
AU Tsaneva-Atanasova, K
Sherman, A
AF Tsaneva-Atanasova, Krasimira
Sherman, Arthur
TI Accounting for Near-Normal Glucose Sensitivity in K(ir)6.2[AAA]
Transgenic Mice
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID PANCREATIC-BETA-CELLS; K-ATP CHANNELS; SINGLE POTASSIUM CHANNELS;
INSULIN-SECRETION; B-CELLS; ELECTRICAL-ACTIVITY; CA2+ CONCENTRATION;
INTRACELLULAR ATP; MINIMAL MODEL; MEMBRANE
AB K(ir)6.2[AAA] transgenic mouse islets exhibit mosaicism such that similar to 70% of the beta-cells have nonfunctional ATP-sensitive potassium (K-ATP) channels, whereas the remainder have normal KATP function. Despite this drastic reduction, the glucose dose-response curve is only shifted by similar to 2 mM. We use a previously published mathematical model, in which K-ATP conductance is increased by rises in cytosolic calcium through indirect effects on metabolism, to investigate how cells could compensate for the loss of K-ATP conductance. Compensation is favored by the assumption that only a small fraction of K-ATP channels are open during oscillations, which renders it easy to upregulate the open fraction via a modest elevation of calcium. We show further that strong gap-junctional coupling of both membrane potential and calcium is needed to overcome the stark heterogeneity of cell properties in these mosaic islets.
C1 [Tsaneva-Atanasova, Krasimira; Sherman, Arthur] NIDDK, Lab Biol Modeling, NIH, Bethesda, MD USA.
RP Sherman, A (reprint author), NIDDK, Lab Biol Modeling, NIH, Bethesda, MD USA.
EM asherman@nih.gov
RI Tsaneva-Atanasova, Krasimira/A-7153-2011;
OI Tsaneva-Atanasova, Krasimira/0000-0002-6294-7051
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health, Bethesda, MD
FX A.S. Was Supported by the intramural research program of the National
Institute of Diabetes and Digestive and Kidney Diseases, National
Institutes of Health, Bethesda, MD.
NR 57
TC 7
Z9 7
U1 0
U2 0
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 4
PY 2009
VL 97
IS 9
BP 2409
EP 2418
DI 10.1016/j.bpj.2009.07.060
PG 10
WC Biophysics
SC Biophysics
GA 515FU
UT WOS:000271454000006
PM 19883583
ER
PT J
AU Zhu, FQ
Hummer, G
AF Zhu, Fangqiang
Hummer, Gerhard
TI Gating Transition of Pentameric Ligand-Gated Ion Channels
SO BIOPHYSICAL JOURNAL
LA English
DT Article
ID NICOTINIC ACETYLCHOLINE-RECEPTOR; KCSA POTASSIUM CHANNEL; NORMAL-MODE
ANALYSIS; MOLECULAR-DYNAMICS SIMULATIONS; ELASTIC NETWORK MODEL;
X-RAY-STRUCTURE; MECHANOSENSITIVE CHANNEL; CONFORMATIONAL-CHANGE; ENERGY
LANDSCAPES; OPEN-STATE
AB Pentameric ligand-gated ion channels are an important family of membrane proteins and play key roles in physiological processes, including signal transduction at chemical synapses. Here, we study the conformational changes associated with the opening and closing of the channel pore. Based on recent crystal structures of two prokaryotic members of the family in open and closed states, respectively, mixed elastic network models are constructed for the transmembrane domain. To explore the conformational changes in the gating transition, a coarse-grained transition path is computed that smoothly connects the closed and open conformations of the channel. We find that the conformational transition involves no major rotations of the transmembrane helices, and is instead characterized by a concerted tilting of helices M2 and M3. In addition, helix M2 changes its bending state, which results in an early closure of the pore during the open-to-closed transition.
C1 [Zhu, Fangqiang; Hummer, Gerhard] NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
RP Hummer, G (reprint author), NIDDK, Chem Phys Lab, NIH, Bethesda, MD 20892 USA.
EM hummer@helix.nih.gov
RI Hummer, Gerhard/A-2546-2013
OI Hummer, Gerhard/0000-0001-7768-746X
FU National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health
FX This research was supported by the Intramural Research Program of the
National Institute of Diabetes and Digestive and Kidney Diseases,
National Institutes of Health.
NR 49
TC 30
Z9 30
U1 0
U2 6
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0006-3495
J9 BIOPHYS J
JI Biophys. J.
PD NOV 4
PY 2009
VL 97
IS 9
BP 2456
EP 2463
DI 10.1016/j.bpj.2009.08.020
PG 8
WC Biophysics
SC Biophysics
GA 515FU
UT WOS:000271454000011
PM 19883588
ER
PT J
AU Costanzo-Garvey, DL
Pfluger, PT
Dougherty, MK
Stock, JL
Boehm, M
Chaika, O
Fernandez, MR
Fisher, K
Kortum, RL
Hong, EG
Jun, JY
Ko, HJ
Schreiner, A
Volle, DJ
Treece, T
Swift, AL
Winer, M
Chen, D
Wu, M
Leon, LR
Shaw, AS
McNeish, J
Kim, JK
Morrison, DK
Tschop, MH
Lewis, RE
AF Costanzo-Garvey, Diane L.
Pfluger, Paul T.
Dougherty, Michele K.
Stock, Jeffery L.
Boehm, Matthew
Chaika, Oleg
Fernandez, Mario R.
Fisher, Kurt
Kortum, Robert L.
Hong, Eun-Gyoung
Jun, John Y.
Ko, Hwi Jin
Schreiner, Aimee
Volle, Deanna J.
Treece, Tina
Swift, Amy L.
Winer, Mike
Chen, Denise
Wu, Min
Leon, Lisa R.
Shaw, Andrey S.
McNeish, John
Kim, Jason K.
Morrison, Deborah K.
Tschoep, Matthias H.
Lewis, Robert E.
TI KSR2 Is an Essential Regulator of AMP Kinase, Energy Expenditure, and
Insulin Sensitivity
SO CELL METABOLISM
LA English
DT Article
ID ACTIVATED PROTEIN-KINASE; GLUCOSE-TRANSPORT; CELLULAR-ENERGY;
SKELETAL-MUSCLE; IN-VIVO; SCAFFOLD; PHOSPHORYLATION; OBESITY;
IDENTIFICATION; SUPPRESSOR
AB Kinase suppressors of Ras 1 and 2 (KSR1 and KSR2) function as molecular scaffolds to potently regulate the MAP kinases ERK1/2 and affect multiple cell fates. Here we show that KSR2 interacts with and modulates the activity of AMPK. KSR2 regulates AMPK-dependent glucose uptake and fatty acid oxidation in mouse embryonic fibroblasts and glycolysis in a neuronal cell line. Disruption of KSR2 in vivo impairs AMPK-regulated processes affecting fatty acid oxidation and thermogenesis to cause obesity. Despite their increased adiposity, ksr2(-/-) mice are hypophagic and hyperactive but expend less energy than wild-type mice. In addition, hyperinsulinemic-euglycemic clamp studies reveal that ksr2(-/-) mice are profoundly insulin resistant. The expression of genes mediating oxidative phosphorylation is also downregulated in the adipose tissue of ksr2(-/-) mice. These data demonstrate that ksr2(-/-) mice are highly efficient in conserving energy, revealing a novel role for KSR2 in AMPK-mediated regulation of energy metabolism.
C1 [Costanzo-Garvey, Diane L.; Boehm, Matthew; Chaika, Oleg; Fernandez, Mario R.; Fisher, Kurt; Kortum, Robert L.; Schreiner, Aimee; Volle, Deanna J.; Treece, Tina; Lewis, Robert E.] Univ Nebraska Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA.
[Pfluger, Paul T.; Tschoep, Matthias H.] Univ Cincinnati, Dept Med, Obes Res Ctr, Cincinnati, OH 45237 USA.
[Dougherty, Michele K.; Morrison, Deborah K.] NCI, Lab Cell & Dev Signaling, Ctr Canc Res, NIH, Frederick, MD 21702 USA.
[Stock, Jeffery L.; McNeish, John] Pfizer Global Res & Dev, Genet Technol, Groton, CT 06340 USA.
[Hong, Eun-Gyoung; Jun, John Y.; Ko, Hwi Jin; Kim, Jason K.] Penn State Coll Med, Penn State Mouse Metab Phenotyping Ctr, Dept Cellular & Mol Physiol, Hershey, PA 17033 USA.
[Swift, Amy L.; Winer, Mike; Chen, Denise; Wu, Min] Seahorse Biosci, N Billerica, MA 01862 USA.
[Leon, Lisa R.] USA, Thermal Mt Med Div, Environm Med Res Inst, Natick, MA 01760 USA.
[Shaw, Andrey S.] Washington Univ, Sch Med, Howard Hughes Med Inst, St Louis, MO 63110 USA.
[Shaw, Andrey S.] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA.
RP Lewis, RE (reprint author), Univ Nebraska Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA.
EM rlewis@unmc.edu
RI Pfluger, Paul/B-4889-2010; Tschoep, Matthias/I-5443-2014;
OI Tschoep, Matthias/0000-0002-4744-371X
FU National Institutes of Health (NIH) [DK52809, DK69987, DK59630, DK56863,
P20 RR016469]; Nebraska Research Initiative; Skala Fellowship;
University of Nebraska Medical Center (UNMC); American Diabetes
Association
FX We thank the members of the Lewis laboratory for comments and criticism.
M. Birnbaum (University of Pennsylvania) is thanked for his gift of the
constitutively active AMPK construct. This work was supported by
National Institutes of Health (NIH) grants to R.E.L. (DK52809) and
M.H.T. (DK69987, DK59630, and DK56863) and by support from the Nebraska
Research Initiative (to R.E.L.). M.R.F was supported by the Skala
Fellowship, and M.B. was supported by the Bukey Fellowship from the
University of Nebraska Medical Center (UNMC). K.F. was supported by a
Physician/Scientist Training Award from the American Diabetes
Association. The UNMC Microarray Core Facility receives partial support
from NIH grant P20 RR016469. For those studies conducted at United
States Army Research Institute Environmental Medicine (USARIEM), the
opinions or assertions contained herein are the private views of the
author(s) and are not to be construed as official or reflecting the
views of the Army or the Department of Defense. Any citations of
commercial organizations and trade names in this report do not
constitute an official Department of the Army endorsement of approval of
the products or services of these organizations.
NR 43
TC 60
Z9 60
U1 0
U2 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD NOV 4
PY 2009
VL 10
IS 5
BP 366
EP 378
DI 10.1016/j.cmet.2009.09.010
PG 13
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 515UP
UT WOS:000271498700006
PM 19883615
ER
PT J
AU Kemper, JK
Xiao, Z
Ponugoti, B
Miao, J
Fang, S
Kanamaluru, D
Tsang, S
Wu, SY
Chiang, CM
Veenstra, TD
AF Kemper, Jongsook Kim
Xiao, Zhen
Ponugoti, Bhaskar
Miao, Ji
Fang, Sungsoon
Kanamaluru, Deepthi
Tsang, Stephanie
Wu, Shwu-Yuan
Chiang, Cheng-Ming
Veenstra, Timothy D.
TI FXR Acetylation Is Normally Dynamically Regulated by p300 and SIRT1 but
Constitutively Elevated in Metabolic Disease States
SO CELL METABOLISM
LA English
DT Article
ID BILE-ACID BIOSYNTHESIS; FARNESOID-X-RECEPTOR; NUCLEAR RECEPTOR;
GLUCOSE-HOMEOSTASIS; PGC-1-ALPHA; SHP; ACTIVATION; COMPLEX;
TRANSCRIPTION; CHOLESTEROL
AB The nuclear bile acid receptor FXR is critical for regulation of lipid and glucose metabolism. Here, we report that FXR is a target of SIRT1, a deacetylase that mediates nutritional and hormonal modulation of hepatic metabolism. Lysine 217 of FXR is the major acetylation site targeted by p300 and SIRT1. Acetylation of FXR increases its stability but inhibits heterodimerization with RXR alpha, DNA binding, and transactivation activity. Downregulation of hepatic SIRT1 increased FXR acetylation with deleterious metabolic outcomes. Surprisingly, in mouse models of metabolic disease, FXR interaction with SIRT1 and p300 was dramatically altered, FXR acetylation levels were elevated, and overexpression of SIRT1 or resveratrol treatment reduced acetylated FXR levels. Our data demonstrate that FXR acetylation is normally dynamically regulated by p300 and SIRT1 but is constitutively elevated in metabolic disease states. Small molecules that inhibit FXR acetylation by targeting SIRT1 or p300 may be promising therapeutic agents for metabolic disorders.
C1 [Kemper, Jongsook Kim; Ponugoti, Bhaskar; Miao, Ji; Fang, Sungsoon; Kanamaluru, Deepthi; Tsang, Stephanie] Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA.
[Xiao, Zhen; Veenstra, Timothy D.] NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Wu, Shwu-Yuan; Chiang, Cheng-Ming] Univ Texas SW Med Ctr Dallas, Dept Biochem, Simmons Comprehens Canc Ctr, Dallas, TX 75390 USA.
[Wu, Shwu-Yuan; Chiang, Cheng-Ming] Univ Texas SW Med Ctr Dallas, Dept Pharmacol, Dallas, TX 75390 USA.
RP Kemper, JK (reprint author), Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA.
EM jongsook@uiuc.edu
RI PONUGOTI, BHASKAR/H-2230-2011
FU NIH [CA103867, CA124760, DK062777, DK80032]; National Cancer Institute,
National Institutes of Health [N01-CO-12400]
FX We are grateful to P. Puigserver for Ad-siSIRT1 and Ad-flag-SIRT1, P.
Edwards for FXR deletion constructs, M. Leid for GST-SIRT1 constructs,
R. Sato for plasmids CMV-3 flag-FXR and G4DBD-FXR, W. Gu and T. Finkel
for plasmids for SIRT1 WT and mutant, M. Ananthanarayanan for
(FXRE)3-tkluc, Yoon K. Lee for the Shp-luc reporter plasmid, and T.
Imamura for the HA-Ub plasmid. Special thanks to Dr. T.M. Willson for
providing GW4064. We also thank B. Kemper for helpful discussions. This
study was supported by NIH grants CA103867 and CA124760 to C.-M.C. and
NIH DK062777, NIH DK80032, and ADA basic research award to J.K.K. This
project has been funded in whole or in part with federal funds from the
National Cancer Institute, National Institutes of Health under Contract
N01-CO-12400 to T.D.V.
NR 39
TC 137
Z9 143
U1 2
U2 11
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 1550-4131
J9 CELL METAB
JI Cell Metab.
PD NOV 4
PY 2009
VL 10
IS 5
BP 392
EP 404
DI 10.1016/j.cmet.2009.09.009
PG 13
WC Cell Biology; Endocrinology & Metabolism
SC Cell Biology; Endocrinology & Metabolism
GA 515UP
UT WOS:000271498700008
PM 19883617
ER
PT J
AU Merikangas, KR
Lehner, T
Risch, NJ
AF Merikangas, Kathleen Ries
Lehner, Thomas
Risch, Neil J.
TI Gene-Environment Interactions and Depression Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
ID POLYMORPHISM
C1 [Merikangas, Kathleen Ries; Lehner, Thomas] NIMH, Genet Epidemiol Res Branch, Bethesda, MD 20892 USA.
[Risch, Neil J.] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA.
RP Merikangas, KR (reprint author), NIMH, Genet Epidemiol Res Branch, Bethesda, MD 20892 USA.
EM kathleen.merikangas@nih.gov
NR 2
TC 3
Z9 3
U1 1
U2 2
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0098-7484
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 4
PY 2009
VL 302
IS 17
BP 1861
EP 1862
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 514DU
UT WOS:000271375300011
ER
PT J
AU Dorgan, JF
Stanczyk, FZ
Egleston, BL
Kahle, LL
Shaw, CM
Spittle, CS
Godwin, AK
Brinton, LA
AF Dorgan, Joanne F.
Stanczyk, Frank Z.
Egleston, Brian L.
Kahle, Lisa L.
Shaw, Christiana M.
Spittle, Cynthia S.
Godwin, Andrew K.
Brinton, Louise A.
TI Prospective Case-Control Study of Serum Mullerian Inhibiting Substance
and Breast Cancer Risk
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID POLYCYSTIC-OVARY-SYNDROME; POSTMENOPAUSAL WOMEN; MENSTRUAL-CYCLE;
HORMONE-LEVELS; FREE TESTOSTERONE; GROWTH; AGE; SECRETION; AROMATASE;
DECLINE
AB Mullerian inhibiting substance (MIS) is a member of the transforming growth factor beta family of growth and differentiation factors that inhibits elongation and branching of mammary ducts and has been shown to inhibit mammary tumor growth in vitro and in animal models. The objective of this study was to determine whether serum MIS levels are associated with breast cancer risk.
We conducted a prospective case-control study of 309 participants who were registered in the Columbia, Missouri Serum Bank. Each of 105 in situ or invasive breast cancer case patients with prediagnostic serum collected before menopause was matched to two control subjects by age, date, menstrual cycle day, and time of day of blood collection. MIS was measured in serum by using an enzyme-linked immunosorbent assay, and estradiol and testosterone concentrations were quantified by using specific radioimmunoassays. Data were analyzed using conditional logistic regression. All tests of statistical significance were two-sided.
The relative odds ratio of breast cancer for women in increasing MIS quartiles were 1, 2.8 (95% confidence interval [CI] = 1.0 to 7.4), 5.9 (95% CI = 2.4 to 14.6), and 9.8 (95% CI = 3.3 to 28.9, P-trend < .001). The association of MIS with breast cancer was weaker in women who were not taking oral contraceptives at the time of blood collection, but adjustment for estradiol and testosterone levels did not materially alter results for these women. The association of MIS with breast cancer did not vary by age at blood collection but was stronger among women who were diagnosed with breast cancer at an older age than among those who were diagnosed at a younger age.
MIS may be a novel biomarker of increased breast cancer risk. Additional research including confirmatory epidemiological studies and mechanistic studies is needed.
C1 [Dorgan, Joanne F.; Egleston, Brian L.; Shaw, Christiana M.; Spittle, Cynthia S.; Godwin, Andrew K.] Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
[Stanczyk, Frank Z.] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
[Stanczyk, Frank Z.] Univ So Calif, Keck Sch Med, Dept Obstet & Gynecol, Los Angeles, CA 90033 USA.
[Kahle, Lisa L.] Informat Management Serv Inc, Rockville, MD USA.
[Brinton, Louise A.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
RP Dorgan, JF (reprint author), Fox Chase Canc Ctr, 333 Cottman Ave, Philadelphia, PA 19111 USA.
EM joanne.dorgan@fccc.edu
RI Brinton, Louise/G-7486-2015
OI Brinton, Louise/0000-0003-3853-8562
FU Department of Defense [BC062367]; National Institutes of Health
[P30CA006927]; National Institutes of Health intramural research program
FX Department of Defense (BC062367 to J.F.D.), National Institutes of
Health (P30CA006927), and National Institutes of Health intramural
research program.
NR 31
TC 8
Z9 9
U1 0
U2 2
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-. Natl. Cancer Inst.
PD NOV 4
PY 2009
VL 101
IS 21
BP 1501
EP 1509
DI 10.1093/jnci/djp331
PG 9
WC Oncology
SC Oncology
GA 516WX
UT WOS:000271575100010
PM 19820206
ER
PT J
AU Parisiadou, L
Xie, CS
Cho, HJ
Lin, X
Gu, XL
Long, CX
Lobbestael, E
Baekelandt, V
Taymans, JM
Sun, LX
Cai, HB
AF Parisiadou, Loukia
Xie, Chengsong
Cho, Hyun Jin
Lin, Xian
Gu, Xing-Long
Long, Cai-Xia
Lobbestael, Evy
Baekelandt, Veerle
Taymans, Jean-Marc
Sun, Lixin
Cai, Huaibin
TI Phosphorylation of Ezrin/Radixin/Moesin Proteins by LRRK2 Promotes the
Rearrangement of Actin Cytoskeleton in Neuronal Morphogenesis
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID PARKINSONS-DISEASE; KINASE-ACTIVITY; ERM PROTEINS; HIPPOCAMPAL-NEURONS;
AXON FORMATION; GROWTH CONES; IN-VIVO; MUTATIONS; MORPHOLOGY; MOTILITY
AB Leucine-rich repeat kinase 2 (LRRK2) functions as a putative protein kinase of ezrin, radixin, and moesin (ERM) family proteins. A Parkinson's disease-related G2019S substitution in the kinase domain of LRRK2 further enhances the phosphorylation of ERM proteins. The phosphorylated ERM (pERM) proteins are restricted to the filopodia of growing neurites in which they tether filamentous actin (F-actin) to the cytoplasmic membrane and regulate the dynamics of filopodia protrusion. Here, we show that, in cultured neurons derived from LRRK2 G2019S transgenic mice, the number of pERM-positive and F-actin-enriched filopodia was significantly increased, and this correlates with the retardation of neurite outgrowth. Conversely, deletion of LRRK2, which lowered the pERM and F-actin contents in filopodia, promoted neurite outgrowth. Furthermore, inhibition of ERM phosphorylation or actin polymerization rescued the G2019S-dependent neuronal growth defects. These data support a model in which the G2019S mutation of LRRK2 causes a gain-of-function effect that perturbs the homeostasis of pERM and F-actin in sprouting neurites critical for neuronal morphogenesis.
C1 [Parisiadou, Loukia; Xie, Chengsong; Cho, Hyun Jin; Lin, Xian; Gu, Xing-Long; Long, Cai-Xia; Sun, Lixin; Cai, Huaibin] NIA, Unit Transgenesis, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Lobbestael, Evy; Baekelandt, Veerle; Taymans, Jean-Marc] Katholieke Univ Leuven, Lab Neurobiol & Gene Therapy, Div Mol Med, Dept Mol & Cellular Med,Fac Med, B-3000 Leuven, Belgium.
RP Cai, HB (reprint author), NIA, Unit Transgenesis, Neurogenet Lab, NIH, Bldg 35,Room 1A116,MSC 3707,35 Convent Dr, Bethesda, MD 20892 USA.
EM caih@mail.nih.gov
RI gu, xinglong/A-3054-2011; Cai, Huaibin/H-3359-2013;
OI gu, xinglong/0000-0002-0437-5606; Cai, Huaibin/0000-0002-8596-6108;
Taymans, Jean-Marc/0000-0001-5503-5524
FU National Institutes of Health (NIH) [AG000944-01]; Fonds
Wetenschappelijk Onderzoek (FWO) [G.0666.09]; Science and Technology in
Flanders [IWT SBO/80020]; Katholieke Universiteit Leuven [IOF-KP/07/001,
OT/08/052A]
FX This work was supported in part by National Institutes of Health
(NIH)-National Institute on Aging Intramural Research Program Grant
AG000944-01 and by Fonds Wetenschappelijk Onderzoek (FWO) Vlaanderen
Grant G.0666.09, Institute for the Promotion of Innovation by Science
and Technology in Flanders Grant IWT SBO/80020, and Katholieke
Universiteit Leuven Grants IOF-KP/07/001 and OT/08/052A. E. L. is a
research assistant and J.-M. T. is a postdoctoral researcher of the
Flemish Fund for Scientific Research (FWO Vlaanderen). We thank Dr. Zu-
Hang Sheng for his helpful suggestions, Chris Van Den Haute and Anke
Vander Perren for technical support, and the NIH Fellows Editorial Board
for editing this manuscript.
NR 39
TC 170
Z9 171
U1 2
U2 9
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 4
PY 2009
VL 29
IS 44
BP 13971
EP 13980
DI 10.1523/JNEUROSCI.3799-09.2009
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 515LG
UT WOS:000271471400023
PM 19890007
ER
PT J
AU Simon, RM
Paik, S
Hayes, DF
AF Simon, Richard M.
Paik, Soonmyung
Hayes, Daniel F.
TI Use of Archived Specimens in Evaluation of Prognostic and Predictive
Biomarkers
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Editorial Material
ID CLINICAL-TRIAL DESIGN; BREAST-CANCER; TUMOR-MARKERS; COLORECTAL-CANCER;
AMERICAN SOCIETY; RECOMMENDATIONS; ONCOLOGY; VALIDATION; PACLITAXEL;
MUTATIONS
AB The development of tumor biomarkers ready for clinical use is complex. We propose a refined system for biomarker study design, conduct, analysis, and evaluation that incorporates a hierarchal level of evidence scale for tumor marker studies, including those using archived specimens. Although fully prospective randomized clinical trials to evaluate the medical utility of a prognostic or predictive biomarker are the gold standard, such trials are costly, so we discuss more efficient indirect "prospective-retrospective" designs using archived specimens. In particular, we propose new guidelines that stipulate that 1) adequate amounts of archived tissue must be available from enough patients from a prospective trial (which for predictive factors should generally be a randomized design) for analyses to have adequate statistical power and for the patients included in the evaluation to be clearly representative of the patients in the trial; 2) the test should be analytically and preanalytically validated for use with archived tissue; 3) the plan for biomarker evaluation should be completely specified in writing before the performance of biomarker assays on archived tissue and should be focused on evaluation of a single completely defined classifier; and 4) the results from archived specimens should be validated using specimens from one or more similar, but separate, studies.
C1 [Simon, Richard M.] NCI, Biometr Res Branch, Bethesda, MD 20892 USA.
[Paik, Soonmyung] Univ Pittsburgh, Div Pathol, Natl Surg Adjuvant Breast & Bowel Project, Pittsburgh, PA USA.
[Hayes, Daniel F.] Univ Michigan, Ctr Comprehens Canc, Breast Oncol Program, Ann Arbor, MI 48109 USA.
RP Simon, RM (reprint author), NCI, Biometr Res Branch, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM rsimon@nih.gov
NR 28
TC 447
Z9 451
U1 0
U2 15
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 4
PY 2009
VL 101
IS 21
BP 1446
EP 1452
DI 10.1093/jnci/djp335
PG 7
WC Oncology
SC Oncology
GA 516WX
UT WOS:000271575100006
PM 19815849
ER
PT J
AU Taube, SE
Clark, GM
Dancey, JE
McShane, LM
Sigman, CC
Gutman, SI
AF Taube, Sheila E.
Clark, Gary M.
Dancey, Janet E.
McShane, Lisa M.
Sigman, Caroline C.
Gutman, Steven I.
TI A Perspective on Challenges and Issues in Biomarker Development and Drug
and Biomarker Codevelopment
SO JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID GROWTH-FACTOR RECEPTOR; CELL LUNG-CANCER; HER2-POSITIVE BREAST-CANCER;
METASTATIC COLORECTAL-CANCER; CLINICAL-TRIAL DESIGN; ADJUVANT
CHEMOTHERAPY; PREDICTIVE MARKER; KRAS MUTATIONS; GENE-MUTATIONS;
OVARIAN-CANCER
AB A workshop sponsored by the National Cancer Institute and the US Food and Drug Administration addressed past lessons learned and ongoing challenges faced in biomarker development and drug and biomarker codevelopment. Participants agreed that critical decision points in the product life cycle depend on the level of understanding of the biology of the target and its interaction with the drug, the preanalytical and analytical factors affecting biomarker assay performance, and the clinical disease process. The more known about the biology and the greater the strength of association between an analytical signal and clinical result, the more efficient and less risky the development process will be. Rapid entry into clinical practice will only be achieved by using a rigorous scientific approach, including careful specimen collection and standardized and quality-controlled data collection. Early interaction with appropriate regulatory bodies will ensure studies are appropriately designed and biomarker test performance is well characterized.
C1 [Taube, Sheila E.] ST Consulting, Glen Echo, MD 20812 USA.
[Clark, Gary M.] ArrayBiopharma Inc, Biostat & Data Management, Boulder, CO USA.
[Dancey, Janet E.] Ontario Inst Canc Res, Toronto, ON, Canada.
[McShane, Lisa M.] NCI, Biometr Res Branch, Bethesda, MD 20892 USA.
[Sigman, Caroline C.] CCS Associates, Mountain View, CA USA.
[Gutman, Steven I.] Univ Cent Florida, Coll Med, Tampa, FL USA.
RP Taube, SE (reprint author), ST Consulting, POB 260, Glen Echo, MD 20812 USA.
EM taubese63@alumni.brandeis.edu
FU National Cancer Institute
FX National Cancer Institute. C. S. also received National Cancer Institute
support for scientific and editorial assistance.
NR 60
TC 61
Z9 62
U1 0
U2 8
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
J9 J NATL CANCER I
JI J. Natl. Cancer Inst.
PD NOV 4
PY 2009
VL 101
IS 21
BP 1453
EP 1463
DI 10.1093/jnci/djp334
PG 11
WC Oncology
SC Oncology
GA 516WX
UT WOS:000271575100007
PM 19855077
ER
PT J
AU Shao, W
Kearney, M
Maldarelli, F
Mellors, JW
Stephens, RM
Lifson, JD
KewalRamani, VN
Ambrose, Z
Coffin, JM
Palmer, SE
AF Shao, Wei
Kearney, Mary
Maldarelli, Frank
Mellors, John W.
Stephens, Robert M.
Lifson, Jeffrey D.
KewalRamani, Vineet N.
Ambrose, Zandrea
Coffin, John M.
Palmer, Sarah E.
TI RT-SHIV subpopulation dynamics in infected macaques during anti-HIV
therapy
SO RETROVIROLOGY
LA English
DT Article
ID IMMUNODEFICIENCY-VIRUS TYPE-1; TO-CHILD TRANSMISSION; DRUG-RESISTANCE
MUTATIONS; REVERSE-TRANSCRIPTASE; WITHIN-HOST; ANTIRETROVIRAL THERAPY;
MINORITY POPULATIONS; PROTEASE INHIBITORS; RANDOMIZED-TRIAL; RHESUS
MACAQUES
AB Background: To study the dynamics of wild-type and drug-resistant HIV-1 RT variants, we developed a methodology that follows the fates of individual genomes over time within the viral quasispecies. Single genome sequences were obtained from 3 pigtail macaques infected with a recombinant simian immunodeficiency virus containing the RT coding region from HIV-1 (RT-SHIV) and treated with short-course efavirenz monotherapy 13 weeks post-infection followed by daily combination antiretroviral therapy (ART) beginning at week 17. Bioinformatics tools were constructed to trace individual genomes from the beginning of infection to the end of the treatment.
Results: A well characterized challenge RT-SHIV inoculum was used to infect three monkeys. The RT-SHIV inoculum had 9 variant subpopulations and the dominant subpopulation accounted for 80% of the total genomes. In two of the three monkeys, the inoculated wild-type virus was rapidly replaced by new wild type variants. By week 13, the original dominant subpopulation in the inoculum was replaced by new dominant subpopulations, followed by emergence of variants carrying known NNRTI resistance mutations. However, during ART, virus subpopulations containing resistance mutations did not outgrow the wide-type subpopulations until a minor subpopulation carrying linked drug resistance mutations (K103N/M184I) emerged. We observed that persistent viremia during ART is primarily made up of wild type subpopulations. We also found that subpopulations carrying the V75L mutation, not known to be associated with NNRTI resistance, emerged initially in week 13 in two macaques. Eventually, all subpopulations from these two macaques carried the V75L mutation.
Conclusion: This study quantitatively describes virus evolution and population dynamics patterns in an animal model. The fact that wild type subpopulations remained as dominant subpopulations during ART treatment suggests that the presence or absence of at least some known drug resistant mutations may not greatly affect virus replication capacity in vivo. Additionally, the emergence and prevalence of V75L indicates that this mutation may provide the virus a selective advantage, perhaps escaping the host immure system surveillance. Our new method to quantitatively analyze viral population dynamics enabled us to observe the relative competitiveness and adaption of different viral variants and provided a valuable tool for studying HIV subpopulation emergence, persistence, and decline during ART.
C1 [Shao, Wei; Stephens, Robert M.] NCI, Adv Biomed Comp Ctr, SAIC Frederick Inc, Frederick, MD USA.
[Kearney, Mary; Maldarelli, Frank; KewalRamani, Vineet N.; Palmer, Sarah E.] NCI, HIV Drug Resistance Program, Frederick, MD USA.
[Mellors, John W.; Ambrose, Zandrea] Univ Pittsburgh, Sch Med, Div Infect Dis, Pittsburgh, PA USA.
[Lifson, Jeffrey D.] NCI, AIDS & Canc Virus Program, SAIC Frederick Inc, Frederick, MD USA.
[Coffin, John M.] Tufts Univ, Boston, MA 02111 USA.
[Palmer, Sarah E.] Swedish Inst Infect Dis Control, Dept Virol, Stockholm, Sweden.
[Palmer, Sarah E.] Karolinska Inst, Stockholm, Sweden.
RP Shao, W (reprint author), NCI, Adv Biomed Comp Ctr, SAIC Frederick Inc, Frederick, MD USA.
EM shaow@mail.nih.gov; kearneym@mail.nih.gov; fmalli@mail.nih.gov;
Mellors@dom.pitt.edu; stephensr@mail.nih.gov; Jeffrey.Lifson@nih.gov;
vineet@ncifcrf.gov; zaa4@pitt.edu; coffinj@mail.nih.gov;
sarah.palmer@smi.se
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; George Kirby Foundation; American Foundation for
AIDS Research (amfAR) [106404-33-RFMC, 107149-44-RGRL]; Swedish Research
Council
FX The authors thank Dr. Shiu-Lok Hu for directing the animal study and Dr.
Michael Piatak, Jr. and Kelli Oswald for assistance with plasma viral
load determinations. Funding for this research was provided by the
National Cancer Institute's intramural Center for Cancer Research and in
part with federal funds from the National Cancer Institute, National
Institutes of Health, under Contract No. HHSN261200800001E. JMC was a
research professor of the American Cancer Society, with support from the
George Kirby Foundation. ZA was funded, in part, by grants
106404-33-RFMC and 107149-44-RGRL from the American Foundation for AIDS
Research (amfAR). Sarah Palmer was funded, in part, by the Swedish
Research Council.
NR 34
TC 12
Z9 12
U1 0
U2 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD NOV 4
PY 2009
VL 6
AR 101
DI 10.1186/1742-4690-6-101
PG 13
WC Virology
SC Virology
GA 518FI
UT WOS:000271675600001
PM 19889213
ER
PT J
AU Alkhalil, A
Strand, S
Mucker, E
Huggins, JW
Jahrling, PB
Ibrahim, SM
AF Alkhalil, Abdulnaser
Strand, Sarah
Mucker, Eric
Huggins, John W.
Jahrling, Peter B.
Ibrahim, Sofi M.
TI Inhibition of Monkeypox virus replication by RNA interference
SO VIROLOGY JOURNAL
LA English
DT Article
ID DOUBLE-STRANDED-RNA; POXVIRUS INFECTIONS; CIDOFOVIR; GENE; DELIVERY;
CELLS; SIRNAS; TRANSCRIPTION; POLYMERASE; DISEASE
AB The Orthopoxvirus genus of Poxviridae family is comprised of several human pathogens, including cowpox (CPXV), Vaccinia (VACV), monkeypox (MPV) and Variola (VARV) viruses. Species of this virus genus cause human diseases with various severities and outcome ranging from mild conditions to death in fulminating cases. Currently, vaccination is the only protective measure against infection with these viruses and no licensed antiviral drug therapy is available. In this study, we investigated the potential of RNA interference pathway (RNAi) as a therapeutic approach for orthopox virus infections using MPV as a model. Based on genome-wide expression studies and bioinformatic analysis, we selected 12 viral genes and targeted them by small interference RNA (siRNA). Forty-eight siRNA constructs were developed and evaluated in vitro for their ability to inhibit viral replication. Two genes, each targeted with four different siRNA constructs in one pool, were limiting to viral replication. Seven siRNA constructs from these two pools, targeting either an essential gene for viral replication (A6R) or an important gene in viral entry (E8L), inhibited viral replication in cell culture by 65-95% with no apparent cytotoxicity. Further analysis with wild-type and recombinant MPV expressing green fluorescence protein demonstrated that one of these constructs, siA6-a, was the most potent and inhibited viral replication for up to 7 days at a concentration of 10 nM. These results emphasis the essential role of A6R gene in viral replication, and demonstrate the potential of RNAi as a therapeutic approach for developing oligonucleotide-based drug therapy for MPV and other orthopox viruses.
C1 [Alkhalil, Abdulnaser; Strand, Sarah; Mucker, Eric; Huggins, John W.; Ibrahim, Sofi M.] USA, Med Res Inst Infect Dis, Ft Detrick, MD 21702 USA.
[Jahrling, Peter B.] NIAID, Emerging Viral Pathogens Sect, NIH, Bethesda, MD 20892 USA.
RP Alkhalil, A (reprint author), USA, Med Res Inst Infect Dis, Ft Detrick, MD 21702 USA.
EM naser.alkhalil@amedd.army.mil; sarah.strand@amedd.army.mil;
muckerEM@amedd.army.mil; hugginsJW@amedd.army.mil;
peter.jahrling@amedd.army.mil; sofi.ibrahim@amedd.army.mil
FU Defense Threat Reduction Agency [4.10022_07_RD_B]
FX We thank Mohamed Ait Ichou, Jason Farlow, Lorraine Farinick, and
Catherine Kenyon for thoughtful discussions, critical review, and
assistance during manuscript preparation. The research described herein
was supported by a grant from the Defense Threat Reduction Agency,
Project number 4.10022_07_RD_B.
NR 46
TC 13
Z9 13
U1 1
U2 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1743-422X
J9 VIROL J
JI Virol. J.
PD NOV 4
PY 2009
VL 6
AR 188
DI 10.1186/1743-422X-6-188
PG 10
WC Virology
SC Virology
GA 526OB
UT WOS:000272299300003
PM 19889227
ER
PT J
AU Yabroff, KR
Saraiya, M
Meissner, HI
Haggstrom, DA
Wideroff, L
Yuan, G
Berkowitz, Z
Davis, WW
Benard, VB
Coughlin, SS
AF Yabroff, K. Robin
Saraiya, Mona
Meissner, Helen I.
Haggstrom, David A.
Wideroff, Louise
Yuan, Gigi
Berkowitz, Zahava
Davis, William W.
Benard, Vicki B.
Coughlin, Steven S.
TI Specialty Differences in Primary Care Physician Reports of Papanicolaou
Test Screening Practices: A National Survey, 2006 to 2007
SO ANNALS OF INTERNAL MEDICINE
LA English
DT Article
ID CERVICAL-CANCER PREVENTION; UNITED-STATES; OLDER WOMEN;
HUMAN-PAPILLOMAVIRUS; ABNORMAL MAMMOGRAMS; COST-EFFECTIVENESS; HEALTH;
BREAST; NEOPLASIA; SERVICES
AB Background: Cervical cancer screening guidelines were substantially revised in 2002 and 2003. Little information is available about primary care physicians' current Papanicolaou (Pap) test screening practices, including initiation, frequency, and stopping.
Objective: To assess current Pap test screening practices in the United States.
Design: Cross-sectional survey.
Setting: Nationally representative sample of physicians during 2006 to 2007.
Participants: 1212 primary care physicians.
Measurements: The survey included questions about physician and practice characteristics and recommendations for Pap screening presented as clinical vignettes describing women by age and by sexual and screening histories. A composite measure-guideline-consistent recommendations-was created by using responses to vignettes in which major guidelines were uniform.
Results: Most physicians reported providing Pap tests to their eligible patients (91.0% [95% CI, 89.0% to 92.6%]). Among Pap test providers (n = 1114), screening practices, including number of tests ordered or performed, use of patient reminder systems, and cytology method used, varied by physician specialty (P < 0.001). Although most Pap test providers reported that screening guidelines were very influential in their clinical practice, few had guideline-consistent recommendations for starting and stopping Pap screening across multiple vignettes (22.3% [CI, 19.9% to 25.0%]). Guideline-consistent recommendations varied by specialty (obstetrics/gynecology, 16.4%; internal medicine, 27.5%; and family or general practice, 21.1%). Compared with obstetricians/gynecologists, internal medicine specialists and family or general practice specialists were more likely to have guideline-consistent screening recommendations (odds ratio, 1.98 [CI, 1.22 to 3.23] and 1.45 [CI, 0.99 to 2.13], respectively) in multivariate analysis.
Limitation: Physician self-report may reflect idealized rather than actual practice.
Conclusion: Primary care physicians' recommendations for Pap test screening are not consistent with screening guidelines, reflecting overuse of screening. Implementation of effective interventions that focus on potentially modifiable physician and practice factors is needed to improve screening practice. Primary Funding Source: National Cancer Institute, Centers for Disease Control and Prevention, and Agency for Healthcare Research and Quality.
C1 [Yabroff, K. Robin] NCI, Hlth Serv, Bethesda, MD 20892 USA.
NIH, Bethesda, MD 20892 USA.
Informat Management Serv Inc, Silver Spring, MD USA.
Ctr Dis Control & Prevent, Atlanta, GA USA.
Regenstrief Inst Hlth Care, Vet Affairs Med Ctr, Indianapolis, IN USA.
Indiana Univ, Sch Med, Indianapolis, IN USA.
Dept Vet Affairs, Washington, DC USA.
RP Yabroff, KR (reprint author), NCI, Hlth Serv, Execut Plaza N,Room 4005,6130 Execut Blvd, Bethesda, MD 20892 USA.
EM yabroffr@mail.nih.gov
RI Hernandez, Jessica/G-6527-2011;
OI Yabroff, K. Robin/0000-0003-0644-5572
FU National Cancer Institute [N02-PC51308]; Centers for Disease Control and
Prevention [Y3-PC-6017-01]; Agency for Healthcare Research and Quality
[Y3-PC-5019-01, Y3-PC-5019-02]
FX By the National Cancer Institute (contract N02-PC51308), Centers for
Disease Control and Prevention (interagency agreement Y3-PC-6017-01),
and Agency for Healthcare Research and Quality ( interagency agreements
Y3-PC-5019-01 and Y3-PC-5019-02).
NR 49
TC 65
Z9 67
U1 0
U2 1
PU AMER COLL PHYSICIANS
PI PHILADELPHIA
PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA
SN 0003-4819
EI 1539-3704
J9 ANN INTERN MED
JI Ann. Intern. Med.
PD NOV 3
PY 2009
VL 151
IS 9
BP 602
EP W197
PG 12
WC Medicine, General & Internal
SC General & Internal Medicine
GA 514IM
UT WOS:000271387700002
PM 19884621
ER
PT J
AU Arora, G
Gona, P
Salton, CJ
Chuang, ML
Jhaveri, RR
Velagaleti, RS
Yeon, SB
O'Donnell, CJ
Manning, WJ
AF Arora, Garima
Gona, Philmon
Salton, Carol J.
Chuang, Michael L.
Jhaveri, Rahul R.
Velagaleti, Raghava S.
Yeon, Susan B.
O'Donnell, Christopher J.
Manning, Warren J.
TI Normal Right Ventricle Anatomy and Function in a Longitudinally Followed
Cohort Free of Hypertension and Cardiovascular Disease: A Cardiovascular
Magnetic Resonance Study of the Framingham Heart Study Offspring Cohort
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Arora, Garima; Salton, Carol J.; Chuang, Michael L.; Jhaveri, Rahul R.; Yeon, Susan B.; O'Donnell, Christopher J.; Manning, Warren J.] Beth Israel Deaconess Med Cntr, Boston, MA USA.
[Gona, Philmon] Boston Univ, Framingham, MA USA.
[Gona, Philmon; Velagaleti, Raghava S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
RI Arora, Garima/F-3481-2011
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S546
EP S546
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501197
ER
PT J
AU Arora, G
Gona, P
Salton, CJ
Chuang, ML
Jhaveri, RR
O'Donnell, CJ
Manning, WJ
AF Arora, Garima
Gona, Philmon
Salton, Carol J.
Chuang, Michael L.
Jhaveri, Rahul R.
O'Donnell, Christopher J.
Manning, Warren J.
TI Impact of Aging on the Normal Right Ventricle: A Cardiovascular Magnetic
Resonance Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Arora, Garima; Salton, Carol J.; Chuang, Michael L.; Jhaveri, Rahul R.; Manning, Warren J.] Beth Israel Deaconess Med Cntr, Boston, MA USA.
[Gona, Philmon] Boston Univ, Framingham, MA USA.
[Gona, Philmon; O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
RI Arora, Garima/F-3481-2011
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S338
EP S338
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500159
ER
PT J
AU Becker, LC
Herrera, JE
Yanek, LR
Yang, XP
Johnson, AD
Chen, MH
O'Donnell, CJ
Becker, DM
Faraday, N
AF Becker, Lewis C.
Herrera, J. E.
Yanek, Lisa R.
Yang, Xiao P.
Johnson, Andrew D.
Chen, Ming-Huei
O'Donnell, Christopher J.
Becker, Diane M.
Faraday, Nauder
TI A Variant in Intron 1 of the Platelet Endothelial Aggregation Receptor-1
(PEAR1) Gene is Strongly Associated With Increased Platelet
Aggregability
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Becker, Lewis C.; Herrera, J. E.; Yanek, Lisa R.; Yang, Xiao P.; Becker, Diane M.; Faraday, Nauder] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Johnson, Andrew D.; O'Donnell, Christopher J.] NIH, Framingham, MA USA.
[Chen, Ming-Huei] Boston Univ, Boston, MA 02215 USA.
RI Johnson, Andrew/G-6520-2013
NR 0
TC 4
Z9 4
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S599
EP S599
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501414
ER
PT J
AU Berkowitz, SJ
Yan, R
Fernandez, VR
Wu, C
Rosen, B
Redheuil, A
Bluemke, DA
Lima, JA
AF Berkowitz, Seth J.
Yan, Raymond
Fernandez, Veronica R.
Wu, Colin
Rosen, Boza
Redheuil, Alban
Bluemke, David A.
Lima, Joao A.
TI The Relationship Between Left Ventricular Hypertrophy and Temporal
Decline in Myocardial Function: Longitudinal Analysis of Myocardial
Tagging in the Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Berkowitz, Seth J.; Yan, Raymond; Fernandez, Veronica R.; Redheuil, Alban; Lima, Joao A.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Wu, Colin; Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
[Rosen, Boza] Univ Utah, Hlth Sci Cntr, Salt Lake City, UT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S304
EP S304
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500025
ER
PT J
AU Cao, JJ
Gudnason, V
Sigurdson, S
Eiriksdottir, G
Launer, L
Harris, T
Arai, AE
AF Cao, Jie J.
Gudnason, Vilmundur
Sigurdson, Sigurdur
Eiriksdottir, Gudny
Launer, Lenore
Harris, Tamara
Arai, Andrew E.
TI Association of Left Ventricular Concentric Hypertrophy and Thoracic
Aortic Calcification With Cardiac Morbidity and Mortality in Elderly
Subjects in the ICELAND-MI Substudy of AGES-Reykjavik
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Cao, Jie J.] St Francis Hosp, Roslyn, NY USA.
[Gudnason, Vilmundur; Sigurdson, Sigurdur; Eiriksdottir, Gudny] Iceland Heart Assoc, Reykjavik, Iceland.
[Launer, Lenore; Harris, Tamara; Arai, Andrew E.] NIH, Bethesda, MD 20892 USA.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S304
EP S304
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500024
ER
PT J
AU Chavakis, E
Hain, A
Orlandi, A
Carmona, G
Quertermous, T
Chavakis, T
Dimmeler, S
AF Chavakis, Emmanouil
Hain, Andreas
Orlandi, Alessia
Carmona, Guillaume
Quertermous, Thomas
Chavakis, Triantafyllos
Dimmeler, Stefanie
TI Del-1, a New Beta2-integrin Ligand, Which Inhibits Mobilization,
Adhesion and Homing of Progenitor Cells
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Chavakis, Emmanouil; Hain, Andreas; Orlandi, Alessia; Carmona, Guillaume; Dimmeler, Stefanie] Goethe Univ Frankfurt, Frankfurt, Germany.
[Quertermous, Thomas] Stanford Univ, Stanford, CA 94305 USA.
[Chavakis, Triantafyllos] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1029
EP S1029
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503526
ER
PT J
AU Eijgelsheim, M
Newton-Cheh, C
Sotoodehnia, N
de Bakker, PI
Muller, M
Morrison, AC
Smith, AV
Isaacs, A
Sanna, S
Dorr, M
Navarro, P
Fuchsberger, C
Wilson, JF
Pramstaller, PP
van Duijn, CM
Lakatta, EG
Felix, SB
Gudnason, V
Pfeufer, A
Heckbert, SR
Stricker, BH
Boerwinkle, E
O'Donnell, CJ
AF Eijgelsheim, Mark
Newton-Cheh, Christpher
Sotoodehnia, Nona
de Bakker, Paul I.
Mueller, Martina
Morrison, Alanna C.
Smith, Albert V.
Isaacs, Aaron
Sanna, Serena
Doerr, Marcus
Navarro, Pau
Fuchsberger, Christian
Wilson, James F.
Pramstaller, Peter P.
van Duijn, Cornelia M.
Lakatta, Edward G.
Felix, Stephan B.
Gudnason, Vilmundur
Pfeufer, Arne
Heckbert, Susan R.
Stricker, Bruno H.
Boerwinkle, Eric
O'Donnell, Christopher J.
TI Genome-wide Association Analysis of 25,330 Individuals Identifies
Multiple Loci Associated With Resting Heart Rate
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Eijgelsheim, Mark; Isaacs, Aaron; van Duijn, Cornelia M.; Stricker, Bruno H.] Erasmus MC, Rotterdam, Netherlands.
[Newton-Cheh, Christpher] Massachusetts Gen Hosp, Ctr Human Genet Res, Cardiovasc Res Ctr, Boston, MA 02114 USA.
[Sotoodehnia, Nona; Heckbert, Susan R.] Univ Washington, Seattle, WA 98195 USA.
[de Bakker, Paul I.] Broad Inst Harvard & MIT, Program Med Populat Genet, Boston, MA USA.
[Mueller, Martina] Helmholtz Ctr Munich, Munich, Germany.
[Morrison, Alanna C.; Boerwinkle, Eric] Univ Texas Houston, Houston, TX USA.
[Smith, Albert V.; Gudnason, Vilmundur] Iceland Heart Assoc Res Inst, Kopavagur, Iceland.
[Sanna, Serena] Ist Neurogenet & Neurofarmacol, Monserrato, Italy.
[Doerr, Marcus] Ernst Moritz Arndt Univ Greifswald, Greifswald, Germany.
[Navarro, Pau] Western Gen Hosp, Edinburgh EH4 2XU, Midlothian, Scotland.
[Fuchsberger, Christian; Pramstaller, Peter P.] European Acad Bozen, Bolzano, Italy.
[Wilson, James F.] Univ Edinburgh, Edinburgh, Midlothian, Scotland.
[Lakatta, Edward G.] NIA, Baltimore, MD 21224 USA.
[O'Donnell, Christopher J.] NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
RI Fuchsberger, Christian/C-9646-2010; Pfeufer, Arne/B-6634-2013;
Pramstaller, Peter/C-2357-2008; de Bakker, Paul/B-8730-2009; Gudnason,
Vilmundur/K-6885-2015
OI de Bakker, Paul/0000-0001-7735-7858; Gudnason,
Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S579
EP S579
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501330
ER
PT J
AU Einstein, AJ
Elliston, CD
Arai, AE
Chen, MY
Mather, R
Pearson, GD
DeLapaz, RL
Nickoloff, EL
Dutta, A
Brenner, DJ
AF Einstein, Andrew J.
Elliston, Carl D.
Arai, Andrew E.
Chen, Marcus Y.
Mather, Richard
Pearson, Gregory D.
DeLapaz, Robert L.
Nickoloff, Edward L.
Dutta, Ajoy
Brenner, David J.
TI Radiation Dose From Single Heartbeat Coronary CT Angiography Performed
Using a 320 Detector-Row Volume Scanner
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Einstein, Andrew J.; Elliston, Carl D.; Pearson, Gregory D.; DeLapaz, Robert L.; Nickoloff, Edward L.; Dutta, Ajoy; Brenner, David J.] Columbia Univ, Med Cntr, New York, NY USA.
[Arai, Andrew E.; Chen, Marcus Y.] NHLBI, Bethesda, MD 20892 USA.
[Mather, Richard] Toshiba Amer Med Syst, Tustin, CA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S311
EP S311
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500053
ER
PT J
AU Fleg, JL
Leifer, E
Kitzman, DW
Whellan, DJ
Kokkinos, P
Wolfel, G
Gardin, JM
AF Fleg, Jerome L.
Leifer, Eric
Kitzman, Dalane W.
Whellan, David J.
Kokkinos, Peter
Wolfel, Gene
Gardin, Julius M.
TI Clinical and Doppler Echocardiographic Correlates of VE/VCO2 Slope in
Systolic Heart Failure: The HF-ACTION Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Fleg, Jerome L.; Leifer, Eric] NHLBI, NIH, Bethesda, MD 20892 USA.
[Kitzman, Dalane W.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Whellan, David J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Kokkinos, Peter] Washington VA Med Ctr, Washington, DC USA.
[Wolfel, Gene] Univ Colorado, Hlth Sci Ctr, Denver, CO USA.
[Gardin, Julius M.] Hackensack Univ, Med Ctr, Hackensack, NJ USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S365
EP S365
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500263
ER
PT J
AU Forman, DE
Clare, R
Kitzman, DW
Ellis, SJ
Chiara, T
Fletcher, G
Fleg, JL
Kraus, WE
AF Forman, Daniel E.
Clare, Robert
Kitzman, Dalane W.
Ellis, Stephen J.
Chiara, Toni
Fletcher, Gerald
Fleg, Jerome L.
Kraus, William E.
TI Impact of Age on Aerobic Capacity in Patients With Systolic Heart
Failure: The HF-ACTION Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Forman, Daniel E.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Clare, Robert; Ellis, Stephen J.] Duke Clin Res Inst, Durham, NC USA.
[Kitzman, Dalane W.] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Chiara, Toni] Univ Florida, Gainesville, FL USA.
[Fletcher, Gerald] Mayo Clin, Jacksonville, FL 32224 USA.
[Fleg, Jerome L.] NHLBI, Bethesda, MD 20892 USA.
[Kraus, William E.] Duke Univ, Med Ctr, Durham, NC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S550
EP S550
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501211
ER
PT J
AU Gaskins, RB
Lagasse, L
Hai, L
Shankaran, S
Lester, BM
Bada, H
Bauer, CR
Das, A
Higgins, R
AF Gaskins, Ronnesia B.
Lagasse, Linda
Hai, Lin
Shankaran, Seetha
Lester, Barry M.
Bada, Henrietta
Bauer, Charles R.
Das, Abik
Higgins, Rosemary
TI Externalizing Behavioral Problems, Stress Reactivity and Obesity
Adolescents Within Utero Cocaine Exposure
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Gaskins, Ronnesia B.; Lagasse, Linda; Hai, Lin; Lester, Barry M.] Brown Univ, Warren Alpert Med Sch, Women & Infants Hosp Rhode Isl, Providence, RI 02912 USA.
[Shankaran, Seetha] Wayne State Univ, Detroit, MI USA.
[Bada, Henrietta] Univ Kentucky, Lexington, KY USA.
[Bauer, Charles R.] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Das, Abik] Res Triangle Inst, Res Triangle Pk, NC 27709 USA.
[Higgins, Rosemary] 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 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S492
EP S492
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500769
ER
PT J
AU Georgiopoulou, VV
Kalogeropoulos, AP
Psaty, BM
Rodondi, N
Bauer, DC
Butler, AB
Koster, A
Smith, AL
Harris, TB
Newman, AB
Kritchevsky, SB
Butler, J
AF Georgiopoulou, Vasiliki V.
Kalogeropoulos, Andreas P.
Psaty, Bruce M.
Rodondi, Nicolas
Bauer, Douglas C.
Butler, Abida B.
Koster, Annemarie
Smith, Andrew L.
Harris, Tamara B.
Newman, Anne B.
Kritchevsky, Stephen B.
Butler, Javed
TI Abnormal Lung Function and Risk for Heart Failure in the Elderly: The
Health, Aging, and Body Composition Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Georgiopoulou, Vasiliki V.; Kalogeropoulos, Andreas P.; Smith, Andrew L.; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
[Psaty, Bruce M.] Univ Washington, Seattle, WA 98195 USA.
[Rodondi, Nicolas] Univ Lausanne, Lausanne, Switzerland.
[Bauer, Douglas C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Butler, Abida B.] Louisiana State Univ, Bogalusa Med Cntr, Bogalusa, LA USA.
[Koster, Annemarie; Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Winston Salem, NC 27109 USA.
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S505
EP S505
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501035
ER
PT J
AU Goto, K
Iso, T
Suga, T
Matsui, H
Arai, M
Gonzalez, FJ
Kurabayashi, M
AF Goto, Kosaku
Iso, Tatsuya
Suga, Toshihiro
Matsui, Hiroki
Arai, Masashi
Gonzalez, Frank J.
Kurabayashi, Masahiko
TI Notch-peroxisome Proliferator Activated Receptor Gamma 2 Pathway
Regulates Transendothelial Fatty Acid Transport via Induction of Fatty
Acid Binding Protein 4 and Fatty Acid Translocase in Capillary
Endothelial Cells in Heart
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Goto, Kosaku; Iso, Tatsuya; Suga, Toshihiro; Matsui, Hiroki; Arai, Masashi; Kurabayashi, Masahiko] Gunma Univ, Grad Sch Med, Gunma, Japan.
[Gonzalez, Frank J.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1115
EP S1115
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504090
ER
PT J
AU He, M
Cornelis, MC
Franks, PW
Zhang, CL
Hu, FB
Qi, L
AF He, Meian
Cornelis, Marilyn C.
Franks, Paul W.
Zhang, Cuilin
Hu, Frank B.
Qi, Lu
TI Obesity Genotype Score and Cardiovascular Risk in Women With Type 2
Diabetes
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [He, Meian; Cornelis, Marilyn C.; Hu, Frank B.; Qi, Lu] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Franks, Paul W.] Umea Univ Hosp, S-90185 Umea, Sweden.
[Zhang, Cuilin] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Rockville, 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 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S467
EP S467
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500669
ER
PT J
AU Horwich, T
Leifer, ES
Brawner, CA
Fitz-Gerald, MB
Fonarow, GC
AF Horwich, Tamara
Leifer, Eric S.
Brawner, Clinton A.
Fitz-Gerald, Meredith B.
Fonarow, Gregg C.
TI The Relationship Between Body Mass Index and Cardiopulmonary Exercise
Testing in Chronic Systolic Heart Failure
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Horwich, Tamara; Fonarow, Gregg C.] Univ Calif Los Angeles, Med Ctr, Los Angeles, CA 90024 USA.
[Leifer, Eric S.] Natl Heart Lung Blood Inst, Bethesda, MD USA.
[Brawner, Clinton A.] Henry Ford Hosp, Detroit, MI 48202 USA.
[Fitz-Gerald, Meredith B.] Univ Alabama, Birmingham, AL USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S757
EP S757
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502239
ER
PT J
AU Hsu, DT
Zak, V
Mahony, L
Sleeper, LA
Atz, AM
Levine, JC
Barker, PC
Ravishankar, C
McCrindle, BW
Williams, RV
Altmann, K
Ghanayem, NS
Margossian, R
Chung, WK
Border, WL
Pearson, GD
Stylianou, MP
Mital, S
AF Hsu, Daphne T.
Zak, Victor
Mahony, Lynn
Sleeper, Lynn A.
Atz, Andrew M.
Levine, Jami C.
Barker, Piers C.
Ravishankar, Chitra
McCrindle, Brian W.
Williams, Richard V.
Altmann, Karen
Ghanayem, Nancy S.
Margossian, Renee
Chung, Wendy K.
Border, William L.
Pearson, Gail D.
Stylianou, Mario P.
Mital, Seema
TI Enalapril Does Not Improve Growth or Ventricular Function in Infants
With Single Ventricle: A Multicenter Clinical Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Hsu, Daphne T.] Childrens Hosp Montefiore, Bronx, NY USA.
[Zak, Victor; Sleeper, Lynn A.] New England Res Inst, Watertown, MA 02172 USA.
[Mahony, Lynn] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Atz, Andrew M.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Levine, Jami C.; Margossian, Renee] Childrens Hosp, Boston, MA 02115 USA.
[Barker, Piers C.] Duke Univ, Med Ctr, Durham, NC USA.
[Ravishankar, Chitra] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[McCrindle, Brian W.; Mital, Seema] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Williams, Richard V.] Primary Childrens Med Ctr, Salt Lake City, UT 84103 USA.
[Altmann, Karen; Chung, Wendy K.] Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
[Ghanayem, Nancy S.] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Border, William L.] Cincinnati Childrens Hosp, Cincinnati, OH USA.
[Pearson, Gail D.; Stylianou, Mario P.] NHLBI, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S560
EP S561
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501254
ER
PT J
AU Hsu, LY
Groves, DW
Kellman, P
Aletras, AH
Aral, AE
AF Hsu, Li-Yueh
Groves, Daniel W.
Kellman, Peter
Aletras, Anthony H.
Aral, Andrew E.
TI Quantification of Absolute Myocardial Blood Flow With Contrast Enhanced
MRI Approaching a Pixel Resolution: Validation vs. Microspheres
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Hsu, Li-Yueh; Groves, Daniel W.; Kellman, Peter; Aletras, Anthony H.; Aral, Andrew E.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S299
EP S299
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500004
ER
PT J
AU Huang, CM
Wang, KL
Cheng, HM
Vhuang, SY
Ting, CT
Lakatta, EG
Yin, F
Chou, P
Chen, CH
AF Huang, Chi-Ming
Wang, Kang-Ling
Cheng, Hao-Min
Vhuang, Shao-Yuan
Ting, Chih-Tai
Lakatta, Edward G.
Yin, Frank
Chou, Pesus
Chen, Chen-Huan
TI Central or Ambulatory Peripheral Blood Pressure: Which Best Relates to
Target-organs and Future Mortality?
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Huang, Chi-Ming; Wang, Kang-Ling; Cheng, Hao-Min; Chen, Chen-Huan] Taipei Vet Gen Hosp, Taipei, Taiwan.
[Vhuang, Shao-Yuan] Acad Sinica, Taipei 115, Taiwan.
[Ting, Chih-Tai] Taichung Vet Gen Hosp, Taichung, Taiwan.
[Lakatta, Edward G.] NIA, Baltimore, MD 21224 USA.
[Yin, Frank] Washington Univ, St Louis, MO USA.
[Chou, Pesus] Natl Yang Ming Univ, Taipei 112, Taiwan.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1060
EP S1060
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503655
ER
PT J
AU Isenberg, JS
Bauer, E
Qin, Y
Miller, T
Bandle, R
Csanyi, G
Pagano, PJ
Bauer, PM
Schnermann, JB
Roberts, DD
AF Isenberg, Jeffrey S.
Bauer, Eileen
Qin, Yan
Miller, Thomas
Bandle, Russell
Csanyi, Gabor
Pagano, Patrick J.
Bauer, Phillip M.
Schnermann, Jurgen B.
Roberts, David D.
TI Thrombospondin-1, via CD47, Blocks Endothelial-Dependent Arterial
Relaxation by Limiting Endothelial Nitric Oxide Synthase Activation
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Isenberg, Jeffrey S.; Bauer, Eileen; Csanyi, Gabor; Pagano, Patrick J.; Bauer, Phillip M.] Univ Pittsburgh, Sch Med, Pittsburgh, PA USA.
[Qin, Yan; Miller, Thomas; Bandle, Russell; Schnermann, Jurgen B.; Roberts, David D.] NIH, Bethesda, MD 20892 USA.
RI Roberts, David/A-9699-2008
OI Roberts, David/0000-0002-2481-2981
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1132
EP S1132
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504168
ER
PT J
AU Jain, A
McClelland, RL
Polak, JF
Shea, SJ
Burke, GL
Bild, DE
Watson, KE
Budoff, MJ
Liu, K
Post, W
Folsom, AR
Lima, JA
Bluemke, DA
AF Jain, Aditya
McClelland, Robyn L.
Polak, Joseph F.
Shea, Steven J.
Burke, Gregory L.
Bild, Diane E.
Watson, Karol E.
Budoff, Matthew J.
Liu, Kiang
Post, Wendy
Folsom, Aaron R.
Lima, Joao A.
Bluemke, David A.
TI Imaging Measures for Prediction of Cardiovascular Events in Men and
Women: The Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Jain, Aditya; Post, Wendy; Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[McClelland, Robyn L.] Univ Washington, Seattle, WA 98195 USA.
[Polak, Joseph F.] Tufts Univ, Boston, MA 02111 USA.
[Shea, Steven J.] Columbia Univ, New York, NY USA.
[Burke, Gregory L.] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Bild, Diane E.] NHLBI, Bethesda, MD 20892 USA.
[Watson, Karol E.] Univ Calif Los Angeles, Los Angeles, CA USA.
[Budoff, Matthew J.] Harbor UCLA Med Ctr, Los Angeles Biomed Res Inst, Torrance, CA 90509 USA.
[Liu, Kiang] Northwestern Univ, Chicago, IL 60611 USA.
[Folsom, Aaron R.] Univ Minnesota, Minneapolis, MN USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S463
EP S463
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500650
ER
PT J
AU Johnson, AD
Ehret, GB
Rice, K
Verwoert, GC
Launer, LJ
Gudnason, V
Larson, MG
Chakravarti, A
Psaty, BM
van Duijn, CM
Levy, D
AF Johnson, Andrew D.
Ehret, Georg B.
Rice, Kenneth
Verwoert, Germaine C.
Launer, Lenore J.
Gudnason, Vilmundur
Larson, Martin G.
Chakravarti, Aravinda
Psaty, Bruce M.
van Duijn, Cornelia M.
Levy, Daniel
CA CHARGE Consortium
TI Association of Hypertension Drug Target Genes With Blood Pressure and
Hypertension: Results From a Genome-wide Association Study in 29,136
Individuals
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Johnson, Andrew D.; Levy, Daniel] NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Ehret, Georg B.; Chakravarti, Aravinda] Johns Hopkins Univ, Baltimore, MD USA.
[Rice, Kenneth; Psaty, Bruce M.] Univ Washington, Seattle, WA 98195 USA.
[Verwoert, Germaine C.; van Duijn, Cornelia M.] Erasmus Univ, Med Ctr, Rotterdam, Netherlands.
[Launer, Lenore J.] NIA, Bethesda, MD 20892 USA.
[Gudnason, Vilmundur] Iceland Heart Assoc, Reykjavik, Iceland.
[Larson, Martin G.] Boston Univ, Framingham, MA USA.
RI Rice, Kenneth/A-4150-2013; Johnson, Andrew/G-6520-2013; Gudnason,
Vilmundur/K-6885-2015
OI Rice, Kenneth/0000-0001-5779-4495; Gudnason,
Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S588
EP S588
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501368
ER
PT J
AU Johnson, AD
Yanek, LR
Chen, MH
Kraja, AT
Larson, MG
Lin, R
Tofler, GH
Becker, DM
Yang, Q
Province, MA
O'Donnell, CJ
Becker, LC
AF Johnson, Andrew D.
Yanek, Lisa R.
Chen, Ming-Huei
Kraja, Aldi T.
Larson, Martin G.
Lin, Rosa
Tofler, Geoffrey H.
Becker, Diane M.
Yang, Qiong
Province, Michael A.
O'Donnell, Christopher J.
Becker, Lewis C.
TI Multiple Platelet Aggregation Genes Are Identified by Genome-wide
Association Meta-analyses
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Johnson, Andrew D.; Tofler, Geoffrey H.; O'Donnell, Christopher J.] NHLBI, Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Yanek, Lisa R.; Becker, Diane M.; Becker, Lewis C.] Johns Hopkins Univ, Baltimore, MD USA.
[Chen, Ming-Huei; Yang, Qiong] Boston Univ, Boston, MA 02215 USA.
[Kraja, Aldi T.; Lin, Rosa; Province, Michael A.] Washington Univ, St Louis, MO USA.
[Larson, Martin G.] Boston Univ, Framingham, MA USA.
RI Johnson, Andrew/G-6520-2013; Yang, Qiong/G-5438-2014
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S588
EP S588
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501366
ER
PT J
AU Johnson, AD
Bhimavarapu, A
Benjamin, EJ
Fox, C
Levy, D
Jarvik, GP
O'Donnell, CJ
AF Johnson, Andrew D.
Bhimavarapu, Anupama
Benjamin, Emelia J.
Fox, Caroline
Levy, Daniel
Jarvik, Gail P.
O'Donnell, Christopher J.
TI Notifiable Genetic Variants on Commercially Available SNP Arrays:
Implications for Research Participants in Genome-wide Association
Studies for Cardiovascular Disease
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Johnson, Andrew D.; Fox, Caroline; Levy, Daniel; O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Bhimavarapu, Anupama] Harvard Univ, Sch Med, Cambridge, MA USA.
[Benjamin, Emelia J.] Boston Univ, Boston, MA 02215 USA.
[Jarvik, Gail P.] Univ Washington, Seattle, WA 98195 USA.
RI Johnson, Andrew/G-6520-2013; Jarvik, Gail/N-6476-2014
OI Jarvik, Gail/0000-0002-6710-8708
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S559
EP S559
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501247
ER
PT J
AU Johnson, BD
Eteiba, W
Sharaf, B
Pepine, CJ
Reis, SA
Rogers, W
Kelsey, SF
Vido, D
Bittner, V
Sopko, G
Shaw, LJ
Merz, NB
AF Johnson, B. Delia
Eteiba, Wafia
Sharaf, Barry
Pepine, Carl J.
Reis, Steven A.
Rogers, William
Kelsey, Sheryl F.
Vido, Diane
Bittner, Vera
Sopko, George
Shaw, Leslee J.
Merz, Noel Bairey
TI Sudden Cardiac Death and Severity of Obstructive Coronary Artery
Disease: A Report From the NHLBI-Sponsored Women's Ischemia Syndrome
Evaluation (WISE) Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Johnson, B. Delia; Eteiba, Wafia; Kelsey, Sheryl F.] Univ Pittsburgh GSPH, Pittsburgh, PA USA.
[Sharaf, Barry] Rhode Isl Hosp, Providence, RI USA.
[Pepine, Carl J.] Univ Florida, Gainesville, FL USA.
[Reis, Steven A.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
[Rogers, William; Bittner, Vera] Univ Alabama, Birmingham, AL USA.
[Vido, Diane] Allegheny Gen Hosp, Pittsburgh, PA 15212 USA.
[Sopko, George] NIH, Bethesda, MD 20892 USA.
[Shaw, Leslee J.] Emory Univ, Atlanta, GA 30322 USA.
[Merz, Noel Bairey] Cedars Sinai Med Ctr, Los Angeles, CA USA.
NR 0
TC 1
Z9 1
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S394
EP S394
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500374
ER
PT J
AU Kadakia, MB
Fox, CS
Scirica, BM
Murphy, SA
Bonaca, MP
Morrow, DA
AF Kadakia, Mitul B.
Fox, Caroline S.
Scirica, Benjamin M.
Murphy, Sabina A.
Bonaca, Marc P.
Morrow, David A.
TI Central Obesity and Cardiovascular Outcomes in Patients With Acute
Coronary Syndromes: Observations From the MERLIN-TIMI 36 Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kadakia, Mitul B.; Scirica, Benjamin M.; Murphy, Sabina A.; Bonaca, Marc P.; Morrow, David A.] Brigham & Womens Hosp, TIMI Study Grp, Boston, MA 02115 USA.
[Kadakia, Mitul B.; Scirica, Benjamin M.; Murphy, Sabina A.; Bonaca, Marc P.; Morrow, David A.] Harvard Univ, Sch Med, Boston, MA 02115 USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S510
EP S510
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501052
ER
PT J
AU Kalogeropoulos, AP
Georgiopoulou, VV
Psaty, BM
Rodondi, N
Smith, AL
Harrison, DG
Liu, YM
Hoffmann, U
Bauer, DC
Newman, AB
Kritchevsky, SB
Harris, TB
Butler, J
AF Kalogeropoulos, Andreas P.
Georgiopoulou, Vasiliki V.
Psaty, Bruce M.
Rodondi, Nicolas
Smith, Andreas L.
Harrison, David G.
Liu, Yongmei
Hoffmann, Udo
Bauer, Douglas C.
Newman, Anne B.
Kritchevsky, Stephen B.
Harris, Tamara B.
Butler, Javed
TI Inflammatory Markers and Incident Heart Failure Risk in Older Adults:
The Health, Aging, and Body Composition Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kalogeropoulos, Andreas P.; Georgiopoulou, Vasiliki V.; Smith, Andreas L.; Harrison, David G.; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
[Psaty, Bruce M.] Univ Washington, Seattle, WA 98195 USA.
[Rodondi, Nicolas] Univ Lausanne, Lausanne, Switzerland.
[Liu, Yongmei; Kritchevsky, Stephen B.] Wake Forest Univ, Winston Salem, SC USA.
[Hoffmann, Udo] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
[Bauer, Douglas C.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Newman, Anne B.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, Tamara B.] NIA, Intramural Rsch Program, Bethesda, MD 20892 USA.
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S505
EP S505
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501036
ER
PT J
AU Kalogeropoulos, AP
Georgiopoulou, VV
Agha, SA
Giamouzis, G
Smith, AL
Kritchevsky, SB
Najjar, S
Bibbins-Domingo, K
Sutton-Tyrrell, K
Harris, TB
Butler, J
AF Kalogeropoulos, Andreas P.
Georgiopoulou, Vasiliki V.
Agha, Syed A.
Giamouzis, Grigorios
Smith, Andrew L.
Kritchevsky, Stephen B.
Najjar, Samir
Bibbins-Domingo, Kristen
Sutton-Tyrrell, Kim
Harris, Tamara B.
Butler, Javed
TI Systolic Blood Pressure and Heart Failure Risk in the Elderly: The
Health, Aging, and Body Composition Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kalogeropoulos, Andreas P.; Georgiopoulou, Vasiliki V.; Agha, Syed A.; Giamouzis, Grigorios; Smith, Andrew L.; Butler, Javed] Emory Univ, Atlanta, GA 30322 USA.
[Kritchevsky, Stephen B.] Wake Forest Univ, Winston Salem, SC USA.
[Najjar, Samir; Harris, Tamara B.] NIA, Intramural Rsch Program, Bethesda, MD 20892 USA.
[Bibbins-Domingo, Kristen] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Sutton-Tyrrell, Kim] Univ Pittsburgh, Pittsburgh, PA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S505
EP S506
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501037
ER
PT J
AU Kaludercic, N
Takimoto, E
Nagayama, T
Lai, E
Bedja, D
Chen, K
Gabrielson, K
Shih, JC
Pacak, K
Kass, DA
Di Lisa, F
Paolocci, N
AF Kaludercic, Nina
Takimoto, Eiki
Nagayama, Takahiro
Lai, Edwin
Bedja, Djahida
Chen, Kevin
Gabrielson, Kathleen
Shih, Jean C.
Pacak, Karel
Kass, David A.
Di Lisa, Fabio
Paolocci, Nazareno
TI Pharmacological and Genetic Inhibition of Monoamine Oxidase A Prevents
Enhanced Norepinephrine Catabolism and Heart Failure After Pressure
Overload
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kaludercic, Nina; Takimoto, Eiki; Nagayama, Takahiro; Bedja, Djahida; Gabrielson, Kathleen; Kass, David A.; Paolocci, Nazareno] Johns Hopkins Univ, Baltimore, MD USA.
[Lai, Edwin; Pacak, Karel] NICHD, NIH, Bethesda, MD USA.
[Chen, Kevin; Shih, Jean C.] Univ So Calif, Los Angeles, CA USA.
[Di Lisa, Fabio] Univ Padua, Padua, Italy.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S720
EP S720
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502085
ER
PT J
AU Kim, HC
Greenland, P
Rossouw, J
Manson, J
Cochrane, B
Lasser, N
Limacher, M
Lloyd-Jones, D
Margolis, K
Robinson, J
AF Kim, Hyeon Chang
Greenland, Philip
Rossouw, Jacques
Manson, JoAnn
Cochrane, Barbara
Lasser, Norman
Limacher, Marian
Lloyd-Jones, Donald
Margolis, Karen
Robinson, Jennifer
TI Multi-marker Prediction of Coronary Heart Disease Risk: The Women's
Health Initiative
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kim, Hyeon Chang; Greenland, Philip; Lloyd-Jones, Donald] Northwestern Univ, Chicago, IL 60611 USA.
[Rossouw, Jacques] NHLBI, Bethesda, MD 20892 USA.
[Manson, JoAnn] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Cochrane, Barbara] Univ Washington, Seattle, WA 98195 USA.
[Lasser, Norman] Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA.
[Limacher, Marian] Univ Florida, Gainesville, FL USA.
[Margolis, Karen] HealthPartners Rsch Fdn & Med Grp, Minneapolis, MN USA.
[Robinson, Jennifer] Univ Iowa, Iowa City, IA USA.
RI Lloyd-Jones, Donald/C-5899-2009
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S424
EP S424
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500497
ER
PT J
AU Kovacic, JC
Gupta, R
Lee, AC
Ma, MC
Fang, F
Tolbert, CN
Walls, AD
Beltran, LE
San, H
Chen, GB
Boehm, M
AF Kovacic, Jason C.
Gupta, Rohit
Lee, Angela C.
Ma, Mingchao
Fang, Fang
Tolbert, Claire N.
Walls, Avram D.
Beltran, Leilani E.
San, Hong
Chen, Guibin
Boehm, Manfred
TI STAT3-dependent Acute RANTES Production in Vascular Smooth Muscle Cells
Modulates Inflammation Following Arterial Injury
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Kovacic, Jason C.; Gupta, Rohit; Lee, Angela C.; Ma, Mingchao; Fang, Fang; Tolbert, Claire N.; Walls, Avram D.; Beltran, Leilani E.; Chen, Guibin; Boehm, Manfred] NHLBI, NIH, Bethesda, MD 20892 USA.
[San, Hong] NHGRI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1078
EP S1078
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503735
ER
PT J
AU Lipshultz, SE
Williams, P
Shearer, WT
Rich, K
Leister, E
Hazra, R
Kaltman, J
Jacobson, D
Dooley, L
Wilkinson, JD
Scott, G
Colan, SD
AF Lipshultz, Steven E.
Williams, Paige
Shearer, William T.
Rich, Kenneth
Leister, Erin
Hazra, Rohan
Kaltman, Jonathan
Jacobson, Denise
Dooley, Laurie
Wilkinson, James D.
Scott, Gwendolyn
Colan, Steven D.
CA PHACS Study Team
TI Increased Left Ventricular and Aortic Dimensions in Long-Term Muttiagent
Antiretroviral Therapy (ART)-Treated HIV-Infected Children: The NIH
Multicenter Pediatric HIV/AIDS Cohort Study (PHACS)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Lipshultz, Steven E.; Wilkinson, James D.; Scott, Gwendolyn] Univ Miami, Miller Sch Med, Miami, FL 33136 USA.
[Williams, Paige; Leister, Erin; Jacobson, Denise] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Shearer, William T.] Baylor Coll Med, Houston, TX 77030 USA.
[Shearer, William T.] Texas Childrens Hosp, Houston, TX 77030 USA.
[Rich, Kenneth] Univ Illinois, Chicago, IL USA.
[Hazra, Rohan] NICHHD, Bethesda, MD 20892 USA.
[Kaltman, Jonathan] NHLBI, Bethesda, MD 20892 USA.
[Dooley, Laurie] Frontier Sci Technol & Rsch Fdn, Amherst, NY USA.
[Colan, Steven D.] Childrens Hosp, Boston, MA 02115 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S909
EP S909
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503053
ER
PT J
AU Liu, JK
Taylor, HA
Fox, CS
Sung, JH
Hickson, D
Sarpong, D
Ekunwe, L
May, WD
AF Liu, Jiankang
Taylor, Herman A.
Fox, Caroline S.
Sung, Jung Hye
Hickson, DeMarc
Sarpong, Daniel
Ekunwe, Lynette
May, Warren D.
TI Pericardial Fat and Cardiovascular Disease Risk Factors: The Jackson
Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Liu, Jiankang; Taylor, Herman A.; May, Warren D.] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Dis Epidemiol Study, Boston, MA USA.
[Sung, Jung Hye; Hickson, DeMarc; Sarpong, Daniel; Ekunwe, Lynette] Jackson State Univ, Jackson, MS USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S402
EP S403
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500412
ER
PT J
AU Liu, LJ
Eisen, HJ
Sullivan, DH
Kanaya, A
Rodondi, N
Satterfield, S
Sutton-Tyrrell, K
Harris, TB
AF Liu, Longjian
Eisen, Howard J.
Sullivan, Dennis H.
Kanaya, Alka
Rodondi, Nicolas
Satterfield, Suzanne
Sutton-Tyrrell, Kim
Harris, Tamara B.
CA Hlth ABC Study
TI Serum Leptin Concentration, Body Mass Index and Incident Heart Failure:
The Health, Aging, and Body Composition Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Liu, Longjian] Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19104 USA.
[Eisen, Howard J.] Drexel Univ, Coll Med, Philadelphia, PA 19104 USA.
[Sullivan, Dennis H.] Cent Arkansas Vet Healthcare Syst, Little Rock, AR USA.
[Sullivan, Dennis H.] Univ Arkansas Med Sci, Little Rock, AR 72205 USA.
[Kanaya, Alka] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Rodondi, Nicolas] Univ Lausanne, Lausanne, Switzerland.
[Satterfield, Suzanne] Univ Tennessee, Memphis, TN USA.
[Sutton-Tyrrell, Kim] Univ Pittsburgh, Pittsburgh, PA USA.
[Harris, Tamara B.] NIA, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S399
EP S399
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500397
ER
PT J
AU Marine, JE
Shetty, V
Chow, GV
Wright, J
Gerstenblith, G
Najjar, SS
Fleg, JL
AF Marine, Joseph E.
Shetty, Veena
Chow, Grant V.
Wright, Jeanette
Gerstenblith, Gary
Najjar, Samer S.
Fleg, Jerome L.
TI Prognostic Significance of Exercise-induced Non-sustained Ventricular
Tachycardia in Asymptomatic Volunteers: The Baltimore Longitudinal Study
of Aging
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Marine, Joseph E.; Chow, Grant V.; Gerstenblith, Gary] Johns Hopkins Univ, Sch Med, Baltimore, MD 20892 USA.
[Shetty, Veena] MedStar Res Inst, Hyattsville, MD USA.
[Wright, Jeanette; Najjar, Samer S.] NIA, Baltimore, MD USA.
[Fleg, Jerome L.] NHLBI, 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 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S661
EP S661
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501672
ER
PT J
AU Massing, MW
Chambless, LE
Jiang, NT
Ni, HY
AF Massing, Mark W.
Chambless, Lloyd E.
Jiang, Niantao
Ni, Hanyu
TI Heart Failure Diagnostic Codes: Concordance of Medical Records and
Medicare Administrative Claims. The ARIC Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Massing, Mark W.; Chambless, Lloyd E.; Jiang, Niantao] Univ N Carolina, Chapel Hill, NC USA.
[Ni, Hanyu] NHLBI, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S399
EP S399
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500396
ER
PT J
AU McDermott, MM
Liu, K
Ferrucci, L
Tian, L
Green, D
Guralnik, J
Tao, HM
Ridker, P
Criqui, M
AF McDermott, Mary M.
Liu, Kiang
Ferrucci, Luigi
Tian, Lu
Green, David
Guralnik, Jack
Tao, Huimin
Ridker, Paul
Criqui, Michael
TI High Levels of Homocysteine and D-dimer Are Associated With Faster
Functional Decline Among Men and Women With Lower Extremity Peripheral
Arterial Disease
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [McDermott, Mary M.; Liu, Kiang; Tian, Lu; Green, David; Tao, Huimin] Northwestern Univ, Chicago, IL 60611 USA.
[Ferrucci, Luigi; Guralnik, Jack] NIH, Bethesda, MD 20892 USA.
[Ridker, Paul] Harvard Univ, Boston, MA 02115 USA.
[Criqui, Michael] Univ Calif San Diego, San Diego, CA 92103 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1148
EP S1149
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504237
ER
PT J
AU Mewton, N
Viallon, M
Kellman, P
Stemmer, A
Rappachi, S
Bi, XM
Zuehlsdorff, S
Revel, D
Croisille, P
AF Mewton, Nathan
Viallon, Magalie
Kellman, Peter
Stemmer, Alto
Rappachi, Stanislas
Bi, Xiaoming
Zuehlsdorff, Sven
Revel, Didier
Croisille, Pierre
TI Observer Performance With State-of-the-Art T2 Weighted
Sequences-T2p-singleshot SSFP, TSESSFP( ACUTE), IR-TSE (TIRM) and BLADE-
for the Detection of Acute Myocardial Injury
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Rappachi, Stanislas; Revel, Didier; Croisille, Pierre] Hop Cardiovasc L Pradel, CREATIS, Bron, France.
[Viallon, Magalie] Hop Cantonal Univ Geneva, Geneva, Switzerland.
[Kellman, Peter] NHLBI, NIH, Bethesda, MD 20892 USA.
[Stemmer, Alto] Siemens Med Solut, Healthcare Sector, Erlangen, Germany.
[Bi, Xiaoming; Zuehlsdorff, Sven] Siemens Med Solut, Healthcare Sector, Chicago, IL USA.
RI Croisille, Pierre/H-4928-2014; Magalie, Viallon/H-4471-2014; Revel,
Didier/M-4553-2014; Clarysse, Patrick/G-6371-2014
OI Croisille, Pierre/0000-0003-4019-3460; Magalie,
Viallon/0000-0001-9118-0438; Clarysse, Patrick/0000-0002-5495-7655
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S322
EP S322
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500094
ER
PT J
AU Miao, CL
Chen, SG
Macedo, R
Carr, JJ
Brown, E
Lai, SH
Liu, K
Li, DB
Vogel-Clausen, J
Lima, JA
Ding, JZ
Bluemke, D
AF Miao, Cuilian
Chen, Shaoguang
Macedo, Robson
Carr, J. Jeffrey
Brown, Elizabeth
Lai, Shenghan
Liu, Kiang
Li, Debiao
Vogel-Clausen, Jens
Lima, Joao A.
Ding, Jingzhong
Bluemke, David
TI The Association of Pericardial Fat With Coronary Artery Plaque by MRI:
The Multi-ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Miao, Cuilian; Chen, Shaoguang; Macedo, Robson; Lai, Shenghan; Vogel-Clausen, Jens; Lima, Joao A.] Johns Hopkins Med Inst, Baltimore, MD 21205 USA.
[Carr, J. Jeffrey; Ding, Jingzhong] Wake Forest Univ Hlth Sci, Winston Salem, NC USA.
[Brown, Elizabeth] Univ Washington, Seattle, WA 98195 USA.
[Liu, Kiang] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Li, Debiao] Northwestern Univ, Sch Med, Chicago, IL 60611 USA.
[Bluemke, David] NIH, Bethesda, MD 20892 USA.
RI Li, Debiao/B-7622-2009; Carr, John/A-1938-2012
OI Carr, John/0000-0002-4398-8237
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S464
EP S464
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500655
ER
PT J
AU Morawietz, H
Catar, RA
Goettsch, C
Taye, A
Muller, G
Lehmann, S
Ziegler, CG
Bornstein, SR
Krug, AW
Walther, T
AF Morawietz, Henning
Catar, Rusan A.
Goettsch, Claudia
Taye, Ashraf
Muller, Gregor
Lehmann, Susann
Ziegler, Christian G.
Bornstein, Stefan R.
Krug, Alexander W.
Walther, Thomas
TI Novel Cross-Talk Between Oxidized LDL, Angiotensin II and Oxidative
Stress After AT1 Blockade and AT1a/AT1b Double Knockout
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Morawietz, Henning; Goettsch, Claudia; Taye, Ashraf; Muller, Gregor; Lehmann, Susann; Ziegler, Christian G.; Bornstein, Stefan R.] Tech Univ Dresden, D-8027 Dresden, Germany.
[Catar, Rusan A.] Charite, Berlin, Germany.
[Krug, Alexander W.] NIH Baltimore, Baltimore, MD USA.
[Walther, Thomas] Univ Hull, Kingston Upon Hull HU6 7RX, N Humberside, England.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1133
EP S1133
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504171
ER
PT J
AU Murray, CI
Gao, WD
Zhong, X
Stanley, BA
Foster, DB
King, SB
Wink, DA
Van Eyk, JE
Paolocci, N
AF Murray, Christopher I.
Gao, Wei Dong
Zhong, Xin
Stanley, Brian A.
Foster, D. Brain
King, S. Bruce
Wink, David A.
Van Eyk, Jennifer E.
Paolocci, Nazareno
TI HNO Induces a Disulfide Bond Between Cysteine Residues on Actin (Cys
257) and Tropomyosin (Cys 190) Increasing Cardiac Force Development A
Novel, Redox-based Mechanism for Contractile Regulation
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Murray, Christopher I.; Gao, Wei Dong; Zhong, Xin; Stanley, Brian A.; Foster, D. Brain; Van Eyk, Jennifer E.; Paolocci, Nazareno] Johns Hopkins Univ, Baltimore, MD USA.
[King, S. Bruce] Wake Forest, Winston Salem, NC USA.
[Wink, David A.] NCI, Bethesda, MD 20892 USA.
RI Foster, D. Brian/C-6350-2009
OI Foster, D. Brian/0000-0002-9290-9590
NR 0
TC 1
Z9 1
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S871
EP S871
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502710
ER
PT J
AU Ohye, RG
Tabbutt, S
Sleeper, LA
Pearson, GD
Mahony, L
Newburger, JW
Lu, MM
Laussen, PC
Goldberg, CS
Ghanayem, NS
Frommelt, PC
Atz, AM
Colan, S
Jacobs, JP
Jaggers, J
Kanter, KR
Krawczeski, CD
Lewis, AB
McCrindle, BW
Minick, LL
Mital, S
Pizarro, C
Ravishankar, C
Williams, IA
Gaynor, JW
AF Ohye, Richard G.
Tabbutt, Sarah
Sleeper, Lynn A.
Pearson, Gail D.
Mahony, Lynn
Newburger, Jane W.
Lu, Minmin
Laussen, Peter C.
Goldberg, Caren S.
Ghanayem, Nancy S.
Frommelt, Peter C.
Atz, Andrew M.
Colan, Steven
Jacobs, Jeffrey P.
Jaggers, James
Kanter, Kirk R.
Krawczeski, Catherine D.
Lewis, Alan B.
McCrindle, Brian W.
Minick, L. L.
Mital, Seema
Pizarro, Christian
Ravishankar, Chitra
Williams, Ismee A.
Gaynor, J. W.
TI Outcomes of the Norwood Operation in Infants Randomized to a Modified
Blalock-Taussig versus Right Ventricle-to-Pulmonary Artery Shunt: The
Pediatric Heart Network Single Ventricle Reconstruction Trial
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Ohye, Richard G.; Goldberg, Caren S.] Univ Michigan, Congenital Heart Cntr, Ann Arbor, MI 48109 USA.
[Tabbutt, Sarah] Childrens Hosp Philadelphia, Watertown, MA USA.
[Sleeper, Lynn A.; Lu, Minmin] New England Res Inst, Boston, MA USA.
[Pearson, Gail D.] NHLBI, Bethesda, MD 20892 USA.
[Mahony, Lynn] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Newburger, Jane W.; Laussen, Peter C.; Colan, Steven] Childrens Hosp, Boston, MA 02115 USA.
[Ghanayem, Nancy S.; Frommelt, Peter C.] Childrens Hosp Wisconsin, Milwaukee, WI 53201 USA.
[Atz, Andrew M.] Med Univ S Carolina, Ann Arbor, MI USA.
[Jacobs, Jeffrey P.] Childrens Heart Inst Florida, St Petersburg, FL USA.
[Jaggers, James] Duke Univ, Med Ctr, Durham, NC USA.
[Kanter, Kirk R.] Emory Univ, Atlanta, GA 30322 USA.
[Krawczeski, Catherine D.] Cincinnati Childrens Hosp, Med Ctr, Cincinnati, OH USA.
[Lewis, Alan B.] Childrens Hosp Los Angeles, Los Angeles, CA 90027 USA.
[McCrindle, Brian W.; Mital, Seema] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Minick, L. L.] Univ Utah, Salt Lake City, UT USA.
[Pizarro, Christian] Alfred I DuPont Hosp Children, Wilmington, DE USA.
[Ravishankar, Chitra; Gaynor, J. W.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
[Williams, Ismee A.] Columbia Univ Coll Phys & Surg, New York, NY 10032 USA.
NR 0
TC 1
Z9 1
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S560
EP S560
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501252
ER
PT J
AU Owens, DS
Plehn, JF
Sigurdsson, S
Probstfield, JL
Launer, LJ
Eiriksdottir, G
Gudnason, V
Harris, TB
O'Brien, KD
AF Owens, David S.
Plehn, Jonathan F.
Sigurdsson, Sigurdur
Probstfield, Jeffrey L.
Launer, Lenore J.
Eiriksdottir, Guony
Gudnason, Vilmundur
Harris, Tamara B.
O'Brien, Kevin D.
TI Aortic Valve Calcium Scores Are Strong Predictors of Aortic Stenosis in
a Population-Based Setting: The AGES-Reykjavik Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Owens, David S.; Probstfield, Jeffrey L.; O'Brien, Kevin D.] Univ Washington, Seattle, WA 98195 USA.
[Plehn, Jonathan F.] Covance Inc, Princeton, NJ USA.
[Sigurdsson, Sigurdur; Eiriksdottir, Guony; Gudnason, Vilmundur] Iceland Heart Assoc, Reykjavik, Iceland.
[Launer, Lenore J.; Harris, Tamara B.] NIA, NIH, Bethesda, MD 20892 USA.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S313
EP S314
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500061
ER
PT J
AU Payne, AR
Berry, C
Kellman, P
Anderson, R
Chen, MY
Watkins, S
McPhaden, AR
Schenke, W
Wright, V
Lederman, RJ
Aletras, AH
Arai, AE
AF Payne, Alexander R.
Berry, Colin
Kellman, Peter
Anderson, Rachel
Chen, Marcus Y.
Watkins, Stuart
McPhaden, Alan R.
Schenke, William
Wright, Victor
Lederman, Robert J.
Aletras, Anthony H.
Arai, Andrew E.
TI T2-weighted MRI Has High Diagnostic Accuracy for Myocardial Hemorrhage
in Myocardial Infarction: A Preclinical Validation Study in Swine
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Payne, Alexander R.; Berry, Colin; Kellman, Peter; Anderson, Rachel; Chen, Marcus Y.; Schenke, William; Wright, Victor; Lederman, Robert J.; Aletras, Anthony H.; Arai, Andrew E.] NIH, Bethesda, MD 20892 USA.
[Watkins, Stuart] Golden Jubilee Natl Hosp, Glasgow, Lanark, Scotland.
[McPhaden, Alan R.] Glasgow Royal Infirm, Glasgow G4 0SF, Lanark, Scotland.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S321
EP S321
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500089
ER
PT J
AU Pencina, M
D'Agostino, RB
Fox, CS
Vasan, RS
Kannel, WB
AF Pencina, Michael
D'Agostino, Ralph B.
Fox, Caroline S.
Vasan, Ramachandran S.
Kannel, William B.
TI Obesity is Independently Associated With Long-term Risk of
Cardiovascular Mortality and Underweight With Risk of Non-cardiovascular
Mortality in Framingham Offspring Cohort
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Pencina, Michael; D'Agostino, Ralph B.] Boston Univ, Boston, MA 02215 USA.
[Fox, Caroline S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Vasan, Ramachandran S.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
NR 0
TC 2
Z9 2
U1 0
U2 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S508
EP S508
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501045
ER
PT J
AU Polak, JF
Pencina, MJ
O'Donnell, CJ
Wolf, PA
D'Agostino, R
AF Polak, Joseph F.
Pencina, Michael J.
O'Donnell, Christopher J.
Wolf, Philip A.
D'Agostino, Ralph, Sr.
TI Added Value of the Common and Internal Carotid Intima-media Thickness
(IMT) for the Prediction of Cardiovascular Events: The Framingham
Offspring Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Polak, Joseph F.] Tufts Univ, Sch Med, Tufts Med Cntr, Boston, MA 02111 USA.
[Wolf, Philip A.] Boston Univ, Sch Med, Boston, MA 02215 USA.
[O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Polak, Joseph F.] Tufts Univ, Sch Med, Tufts Med Ctr, Boston, MA 02111 USA.
[Pencina, Michael J.; Wolf, Philip A.; D'Agostino, Ralph, Sr.] Boston Univ, Sch Med, Boston, MA 02215 USA.
[O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S425
EP S425
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500501
ER
PT J
AU Polak, JF
Wong, Q
Johnson, WC
Bluemke, DA
Harrington, A
O'Leary, DH
Yanez, ND
AF Polak, Joseph F.
Wong, Quenna
Johnson, W. C.
Bluemke, David A.
Harrington, Anita
O'Leary, Daniel H.
Yanez, N. D.
TI Associations Between Inter-adventitial Diameters of the Common Carotid
Artery, Cardiovascular Risk Factors, Carotid Intima-media Thickness and
Left Ventricular Mass: The Multi-Ethnic Study of Atherosclerosis (MESA)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Polak, Joseph F.] Tufts Univ, Sch Med, Tufts Med Cntr, Boston, MA 02111 USA.
[Wong, Quenna; Johnson, W. C.; Yanez, N. D.] Univ Washington, Seattle, WA 98195 USA.
[Bluemke, David A.] Natl Inst Hlth, Bethesda, MD USA.
[O'Leary, Daniel H.] Tufts Univ, Sch Med, Carney Hosp, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S400
EP S400
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500401
ER
PT J
AU Pop-Busui, R
Waberski, BH
Cleary, PA
Herman, WH
Low, PA
Martin, CL
Lima, JA
Bluemke, D
AF Pop-Busui, Rodica
Waberski, Barbara H.
Cleary, Patricia A.
Herman, William H.
Low, Phillip A.
Martin, Catherine L.
Lima, Joao A.
Bluemke, David
TI Cardiac Autonomic Neuropathy and Left Ventricular Function in the
Diabetes Control and Complications Trial/Epidemiology of Diabetes
Intervention and Complications Study (DCCT/EDIC)
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Pop-Busui, Rodica; Herman, William H.; Martin, Catherine L.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Waberski, Barbara H.; Cleary, Patricia A.] George Washington Univ, Rockville, MD USA.
[Low, Phillip A.] Mayo Clin, Rochester, MN USA.
[Lima, Joao A.] Johns Hopkins Univ, Baltimore, MD USA.
[Bluemke, David] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S546
EP S547
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501198
ER
PT J
AU Rajesh, M
Mukhopadhyay, P
Patel, V
Batkai, S
Ungvari, Z
Hasko, G
Pacher, P
AF Rajesh, Mohanraj
Mukhopadhyay, Partha
Patel, Vivek
Batkai, Sandor
Ungvari, Zoltan
Hasko, Gyorgy
Pacher, Pal
TI Cannabidiol Attenuates Myocardial Dysfunction, Fibrosis, Inflammation,
Cell Death and Interrelated Signaling Pathways Associated With Diabetic
Cardiomyopathy
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Rajesh, Mohanraj; Mukhopadhyay, Partha; Patel, Vivek; Batkai, Sandor; Pacher, Pal] NIH, Rockville, MD USA.
[Ungvari, Zoltan] New York Med Coll, Valhalla, NY 10595 USA.
[Hasko, Gyorgy] Univ Med & Dent New Jersey, Newark, NJ 07103 USA.
RI Batkai, Sandor/G-3889-2010; Batkai, Sandor/H-7983-2014
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S868
EP S868
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831502696
ER
PT J
AU Schnabel, RB
Baumert, J
Barbalic, M
Dupuis, J
Ellinor, PT
Durda, P
Dehghan, A
Bis, JC
Witteman, JC
Hoogeveen, RC
Benjamin, EJ
Koenig, W
Tracy, RP
AF Schnabel, Renate B.
Baumert, Jens
Barbalic, Maja
Dupuis, Josee
Ellinor, Patrick T.
Durda, Peter
Dehghan, Abbas
Bis, Joshua C.
Witteman, Jacqueline C.
Hoogeveen, Ron C.
Benjamin, Emelia J.
Koenig, Wolfgang
Tracy, Russell P.
CA CHARGE Consortium
TI Duffy Antigen Receptor for Chemokines (Darc) Polymorphism Regulates
Circulating Concentrations of Monocyte Chemoattractant Protein-1 and
Other Circulating Inflammatory Mediators
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Schnabel, Renate B.] Johannes Gutenberg Univ Mainz, Mainz, 02114, Germany.
[Baumert, Jens] German Rsch Cntr Environm Hlth, Helmholtz Zentrum Munchen, Neuherberg, 05405, Germany.
[Barbalic, Maja; Hoogeveen, Ron C.] Univ Texas Hlth Sci Ctr, Human Genet Cntr, Houston, TX USA.
[Barbalic, Maja; Hoogeveen, Ron C.] Univ Texas Hlth Sci Ctr, Inst Mol Med, Houston, TX 98195 USA.
[Dupuis, Josee] Boston Univ, Sch Publ Hlth, Dept Biostat, Boston, MA USA.
[Ellinor, Patrick T.] Massachusetts Gen Hosp, Cardiovasc Rsch Cntr, Boston, MA USA.
[Durda, Peter] Univ Vermont, Coll Med, Dept Pathol, Burlington, VT USA.
[Dehghan, Abbas] Erasmus Med Cntr, Dept Epidemiol, D-7900 Rotterdam, Netherlands.
[Bis, Joshua C.] Univ Washington, Seattle, WA 05405 USA.
[Witteman, Jacqueline C.] Erasmus Med Cntr, Rotterdam, Netherlands.
[Benjamin, Emelia J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Benjamin, Emelia J.] Boston Univ, Framingham Heart Study, Framingham, MA USA.
[Koenig, Wolfgang] Univ Ulm, Dept Internal Med 2, Med Cntr, Ulm, Germany.
[Tracy, Russell P.] Univ Vermont, Coll Med, Dept Biochem, Burlington, VT USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S559
EP S559
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501249
ER
PT J
AU Schoenhoff, FS
Griswold, BF
Matt, P
Sloper, LJ
Yamazaki, M
Carlson, OD
Dietz, HC
Van Eyk, JE
McDonnell, NB
AF Schoenhoff, Florian S.
Griswold, Benjamin F.
Matt, Peter
Sloper, Leslie J.
Yamazaki, Michiyo
Carlson, Olga D.
Dietz, Harry C.
Van Eyk, Jennifer E.
McDonnell, Nazli B.
TI The Role of Circulating Transforming Growth Factor-beta in Vascular
Ehlers-Danlos Syndrome: Implications for Drug Therapy
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Schoenhoff, Florian S.; Matt, Peter; Yamazaki, Michiyo; Dietz, Harry C.; Van Eyk, Jennifer E.] Johns Hopkins Univ, Baltimore, MD USA.
[Griswold, Benjamin F.; Sloper, Leslie J.; Carlson, Olga D.; McDonnell, Nazli B.] NIA, Baltimore, MD 21224 USA.
NR 0
TC 3
Z9 3
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1048
EP S1048
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503606
ER
PT J
AU Sibley, CT
Gottlieb, I
Cox, C
Godoy, G
Spooner, AE
Bluemke, DA
Lima, JA
AF Sibley, Christopher T.
Gottlieb, Ilan
Cox, Christopher
Godoy, Gustavo
Spooner, Amy E.
Bluemke, David A.
Lima, Joao A.
TI Comparative Effect of Statins vs Niacin on MRI Measured Regression of
Carotid Atherosclerosis in a Randomized Clinical Trial: The NIA Plaque
Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Sibley, Christopher T.; Godoy, Gustavo; Lima, Joao A.] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Gottlieb, Ilan] Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
[Cox, Christopher] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Spooner, Amy E.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
RI Sibley, Christopher/C-9900-2013
NR 0
TC 9
Z9 9
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S376
EP S376
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500305
ER
PT J
AU Thanassoulis, G
Massaro, JM
Hoffman, U
Mahabadi, AA
Vasan, RS
O'Donnell, CJ
Fox, CS
AF Thanassoulis, George
Massaro, Joseph M.
Hoffman, Udo
Mahabadi, Amir A.
Vasan, Ramachandran S.
O'Donnell, Christopher J.
Fox, Caroline S.
TI Prevalence and Distribution of High Pericardial and Intra-thoracic Fat
Depots in the Framingham Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Thanassoulis, George; Mahabadi, Amir A.; Vasan, Ramachandran S.; O'Donnell, Christopher J.; Fox, Caroline S.] NHLBI, NIH, Framingham Heart Dis Epidemiol Study, Framingham, MA USA.
[Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S539
EP S540
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501172
ER
PT J
AU Thanassoulis, G
Massaro, JM
O'Donnell, CJ
Levy, D
Hoffman, U
Ellinor, PT
Wang, TJ
Vasan, RS
Fox, CS
Benjamin, EJ
AF Thanassoulis, George
Massaro, Joseph M.
O'Donnell, Christopher J.
Levy, Daniel
Hoffman, Udo
Ellinor, Patrick T.
Wang, Thomas J.
Vasan, Ramachandran S.
Fox, Caroline S.
Benjamin, Emelia J.
TI Pericardial Fat is Associated With Prevalent AF - The Framingham Heart
Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Thanassoulis, George; O'Donnell, Christopher J.; Vasan, Ramachandran S.; Fox, Caroline S.; Benjamin, Emelia J.] NHLBI, NIH, Framingham Heart Study, Framingham, MA USA.
[Massaro, Joseph M.] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Hoffman, Udo; Ellinor, Patrick T.; Wang, Thomas J.] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S519
EP S519
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501091
ER
PT J
AU Tofler, GH
Massaro, J
O'Donnell, CJ
Wilson, PW
Vasan, RS
Sutherland, PA
Lipinska, I
Meigs, JB
Levy, D
D'Agostino, RB
AF Tofler, Geoffrey H.
Massaro, Joseph
O'Donnell, Christopher J.
Wilson, Peter W.
Vasan, Ramachandran S.
Sutherland, Patrice A.
Lipinska, Izabela
Meigs, James B.
Levy, Daniel
D'Agostino, Ralph B.
TI Plasminogen Activator Inhibitor (PAI-1) and Risk of Cardiovascular
Disease: The Framingham Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Tofler, Geoffrey H.] Royal N Shore Hosp, Sydney, NSW 02215, Australia.
[Massaro, Joseph; Vasan, Ramachandran S.; Lipinska, Izabela; D'Agostino, Ralph B.] Boston Univ, Boston, MA USA.
[O'Donnell, Christopher J.; Levy, Daniel] NHLBI, Framingham, MA USA.
[O'Donnell, Christopher J.; Sutherland, Patrice A.; Levy, Daniel] Framingham Heart Dis Epidemiol Study, Framingham, MA 30322 USA.
[Wilson, Peter W.] Emory Univ, Atlanta, GA 02114 USA.
[Meigs, James B.] Massachusetts Gen Hosp, Boston, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S454
EP S454
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500614
ER
PT J
AU Vazquez, E
Sethi, AA
Sampson, M
Remaley, AT
Chaudhry, H
Cannon, RO
AF Vazquez, Edward
Sethi, Amar A.
Sampson, Maureen
Remaley, Alan T.
Chaudhry, Hira
Cannon, Richard O., III
TI "Dysfunctional" High-density Lipoprotein Despite Normal Cholesterol
Content in Sedentary Obese Women
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Vazquez, Edward; Sethi, Amar A.; Sampson, Maureen; Remaley, Alan T.; Chaudhry, Hira; Cannon, Richard O., III] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S470
EP S470
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500681
ER
PT J
AU Velagaleti, RS
Pencina, MJ
Aragam, J
Wang, TJ
Levy, D
D'Agostino, RB
Kannel, WB
Benjamin, EJ
Vasan, RS
AF Velagaleti, Raghava S.
Pencina, Michael J.
Aragam, Jayashri
Wang, Thomas J.
Levy, Daniel
D'Agostino, Ralph B.
Kannel, William B.
Benjamin, Emelia J.
Vasan, Ramachandran S.
TI Left Ventricular Hypertrophy Patterns and the Incidence of Heart
Failure: The Framingham Heart Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Velagaleti, Raghava S.; Pencina, Michael J.; Wang, Thomas J.; Levy, Daniel; D'Agostino, Ralph B.; Kannel, William B.; Benjamin, Emelia J.; Vasan, Ramachandran S.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Aragam, Jayashri] Vet Adm Hosp, W Roxbury, MA USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S415
EP S415
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500462
ER
PT J
AU Velagaleti, RS
Gona, P
Chuang, ML
Yeon, SB
Salton, CJ
Fox, CS
Massaro, J
Hoffmann, U
Manning, WJ
O'Donnell, CJ
AF Velagaleti, Raghava S.
Gona, Philimon
Chuang, Michael L.
Yeon, Susan B.
Salton, Carol J.
Fox, Caroline S.
Massaro, Joseph
Hoffmann, Udo
Manning, Warren J.
O'Donnell, Christopher J.
TI Aortic Atherosclerosis and Left Ventricular Structure in the Community
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Velagaleti, Raghava S.; Gona, Philimon; Fox, Caroline S.; Massaro, Joseph; O'Donnell, Christopher J.] NHLBI, Framingham, MA USA.
[Chuang, Michael L.; Yeon, Susan B.; Salton, Carol J.; Manning, Warren J.] Beth Israel Deaconess Med Cntr, Boston, MA USA.
[Hoffmann, Udo] Massachusetts Gen Hosp, Boston, MA 02114 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S380
EP S380
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500321
ER
PT J
AU Vickers, KC
Aponte, AM
Remaley, AT
AF Vickers, Kasey C.
Aponte, Angel M.
Remaley, Alan T.
TI A Novel Pathway for the Regulation of Hepatic Cholesterol Synthesis by
microRNA's
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Vickers, Kasey C.; Aponte, Angel M.; Remaley, Alan T.] NHLBI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S476
EP S476
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500705
ER
PT J
AU Vogel-Claussen, J
Tomas, MS
Newatia, A
Boyce, D
Pinheiro, A
Abraham, R
Abraham, T
Bluemke, DA
AF Vogel-Claussen, Jens
Tomas, Miguel Santaularia
Newatia, Amit
Boyce, Danielle
Pinheiro, Aurelio
Abraham, Roselle
Abraham, Theodore
Bluemke, David A.
TI Left Ventricular Outflow Tract (LVOT) Diameter/Aortic Valve Diameter
Ratio is an Accurate Non-invasive Cardiac MRI Marker for Estimation of
LVOT Obstruction in Patients With Hypertrophic Cardiomyopathy
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Vogel-Claussen, Jens; Tomas, Miguel Santaularia; Newatia, Amit; Boyce, Danielle; Pinheiro, Aurelio; Abraham, Roselle; Abraham, Theodore] Johns Hopkins Univ Hosp, Baltimore, MD 21287 USA.
[Bluemke, David A.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S379
EP S379
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500318
ER
PT J
AU Wang, KL
Cheng, HM
Chuang, SY
Spurgeon, H
Ting, CT
Najjar, S
Lakatta, E
Yin, F
Chou, P
Chen, CH
AF Wang, Kang-Ling
Cheng, Hao-Min
Chuang, Shao-Yuan
Spurgeon, Harold
Ting, Chih-Tai
Najjar, Samer
Lakatta, Edward
Yin, Frank
Chou, Pesus
Chen, Chen-Huan
TI Waveform Reflections and Arterial Stiffness in the Prediction of
15.1-Year All-Cause and Cardiovascular Mortalities: A Community-Based
Study
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Wang, Kang-Ling; Cheng, Hao-Min; Chen, Chen-Huan] Taipei Vet Gen Hosp, Taipei, Taiwan.
[Chuang, Shao-Yuan] Acad Sinica, Taipei 115, Taiwan.
[Spurgeon, Harold; Najjar, Samer; Lakatta, Edward] NIA, Baltimore, MD 21224 USA.
[Ting, Chih-Tai] Taichung Vet Gen Hosp, Taichung, Taiwan.
[Yin, Frank] Washington Univ, St Louis, MO USA.
[Chou, Pesus] Yang Ming Univ, Taipei, Taiwan.
RI Chuang, Shao-Yuan/B-3478-2011
NR 0
TC 0
Z9 0
U1 0
U2 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1061
EP S1062
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831503661
ER
PT J
AU Williams, RV
Travison, T
Kaltman, JR
Cecchin, F
Colan, S
Idriss, SF
Lu, M
Margossian, R
Reed, JH
Silver, EE
Stephenson, EA
Vetter, VL
AF Williams, Richard V.
Travison, Thomas
Kaltman, Jonathan R.
Cecchin, Frank
Colan, Steven
Idriss, Salim F.
Lu, Minmin
Margossian, Renee
Reed, John H.
Silver, Eric E.
Stephenson, Elizabeth A.
Vetter, Victoria L.
CA Pediat Heart Network Investigators
TI Decreased Functional Status and Ventricular Function in Fontan Patients
With Pacemakers
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Williams, Richard V.] Univ Utah, Salt Lake City, UT USA.
[Travison, Thomas; Lu, Minmin] New England Res Inst, Watertown, MA 02172 USA.
[Kaltman, Jonathan R.] NHLBI, Bethesda, MD 20892 USA.
[Cecchin, Frank; Colan, Steven; Margossian, Renee] Childrens Hosp, Boston, MA 02115 USA.
[Idriss, Salim F.] Duke Univ, Durham, NC USA.
[Reed, John H.] Med Univ S Carolina, Charleston, SC 29425 USA.
[Silver, Eric E.] Columbia Univ, New York, NY USA.
[Stephenson, Elizabeth A.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Vetter, Victoria L.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S600
EP S601
PG 2
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501419
ER
PT J
AU Wu, Q
Chambliss, KL
Oltmann, SC
Umetani, M
Yuhanna, IS
Korach, KS
Thomas, GD
Mineo, C
Kim, SH
Madak-Erdogan, Z
Maggi, A
Dineen, SP
Roland, CL
Brekken, RA
Katzenellenbogen, JA
Katzenellenbogen, BS
Shaul, PW
AF Wu, Qian
Chambliss, Ken L.
Oltmann, Sarah C.
Umetani, Michihisa
Yuhanna, Ivan S.
Korach, Kenneth S.
Thomas, Gail D.
Mineo, Chieko
Kim, Sung Hoon
Madak-Erdogan, Zeynep
Maggi, Adriana
Dineen, Sean P.
Roland, Christina L.
Brekken, Rolf A.
Katzenellenbogen, John A.
Katzenellenbogen, Benita S.
Shaul, Philip W.
TI Extranuclear Estrogen Receptor a Signaling Promotes Endothelial
Monolayer Integrity but Not Breast Cancer or Uterine Growth in Mice
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Wu, Qian; Chambliss, Ken L.; Oltmann, Sarah C.; Umetani, Michihisa; Yuhanna, Ivan S.; Thomas, Gail D.; Mineo, Chieko; Dineen, Sean P.; Roland, Christina L.; Brekken, Rolf A.; Shaul, Philip W.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Korach, Kenneth S.] NIEHS, Res Triangle Pk, NC 27709 USA.
[Kim, Sung Hoon; Madak-Erdogan, Zeynep; Katzenellenbogen, John A.; Katzenellenbogen, Benita S.] Univ Illinois, Urbana, IL 61801 USA.
[Maggi, Adriana] Univ Milan, Milan, Italy.
RI Dineen, Sean/B-6222-2013; Oltmann, Sarah/L-3245-2014; Dineen,
Sean/M-3741-2013; Dineen, Sean/K-1471-2015
OI Oltmann, Sarah/0000-0002-7180-4167; Dineen, Sean/0000-0002-2012-2238
NR 0
TC 0
Z9 0
U1 0
U2 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S1161
EP S1161
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831504293
ER
PT J
AU Yeon, SB
Salton, CJ
Gona, P
Chuang, ML
Tsao, CW
Danias, PG
Levy, D
O'Donnell, CJ
Manning, WJ
AF Yeon, Susan B.
Salton, Carol J.
Gona, Philimon
Chuang, Michael L.
Tsao, Connie W.
Danias, Peter G.
Levy, Daniel
O'Donnell, Christopher J.
Manning, Warren J.
TI Gender Differences in Left Ventricular Parameters in a Normotensive
Population: Impact of Indexation for Fat Free Mass
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Yeon, Susan B.; Salton, Carol J.; Tsao, Connie W.; Manning, Warren J.] Beth Israel Deaconess Med Cntr, Boston, MA USA.
[Gona, Philimon; Levy, Daniel; O'Donnell, Christopher J.] NHLBI, Framingham Heart Study, Framingham, MA USA.
[Gona, Philimon] NHLBI, Framingham Heart Study, Boston, MA USA.
[Gona, Philimon] Boston Univ, Framingham, MA USA.
[Gona, Philimon] Boston Univ, Boston, MA 02215 USA.
[Danias, Peter G.] Tufts Univ, Sch Med, Boston, MA 02111 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S545
EP S545
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831501193
ER
PT J
AU Zhao, Q
Gu, DF
Chen, J
Bazzano, LA
Rao, DC
Hixson, J
Jaquish, CE
Cao, J
Chen, JC
Li, JX
Rice, T
He, J
AF Zhao, Qi
Gu, Dongfeng
Chen, Jing
Bazzano, Lydia A.
Rao, D. C.
Hixson, James
Jaquish, Cashell E.
Cao, Jie
Chen, Jichun
Li, Jianxin
Rice, Treva
He, Jiang
TI Correlation Between Blood Pressure Responses to Dietary Sodium and
Potassium Intervention in a Chinese Population
SO CIRCULATION
LA English
DT Meeting Abstract
CT 82nd Scientific Session of the American-Heart-Association
CY NOV 14-18, 2009
CL Orlando, FL
SP Amer Heart Assoc
C1 [Zhao, Qi; Bazzano, Lydia A.; He, Jiang] Tulane Univ, Sch Publ Hlth & Trop Med, New Orleans, LA 70118 USA.
[Gu, Dongfeng; Cao, Jie; Chen, Jichun; Li, Jianxin] Chinese Acad Med Sci, Fuwai Hosp & Cardiovasc Inst, Beijing 100037, Peoples R China.
[Gu, Dongfeng; Cao, Jie; Chen, Jichun; Li, Jianxin] Peking Univ, Coll Med, Beijing 100871, Peoples R China.
[Gu, Dongfeng; Cao, Jie; Chen, Jichun; Li, Jianxin] Chinese Natl Ctr Cardiovasc Dis Control & Res, Beijing, Peoples R China.
[Rao, D. C.; Rice, Treva] Washington Univ, Sch Med, St Louis, MO USA.
[Hixson, James] Univ Texas Houston, Sch Publ Hlth, Houston, TX USA.
[Jaquish, Cashell E.] NIH, Bethesda, MD 20892 USA.
[He, Jiang] Tulane Univ, Sch Med, New Orleans, LA 70118 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0009-7322
J9 CIRCULATION
JI Circulation
PD NOV 3
PY 2009
VL 120
IS 18
SU 2
BP S447
EP S447
PG 1
WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 520GV
UT WOS:000271831500587
ER
PT J
AU Bird, GS
Hwang, SY
Smyth, JT
Fukushima, M
Boyles, RR
Putney, JW
AF Bird, Gary S.
Hwang, Sung-Yong
Smyth, Jeremy T.
Fukushima, Miwako
Boyles, Rebecca R.
Putney, James W., Jr.
TI STIM1 Is a Calcium Sensor Specialized for Digital Signaling
SO CURRENT BIOLOGY
LA English
DT Article
ID EMBRYONIC KIDNEY-CELLS; LOCAL CA2+ INFLUX; MAST-CELLS; CRAC CHANNEL;
ENTRY; ACTIVATION; OSCILLATIONS; RELEASE; ORAI1
AB When cells are activated by calcium-mobilizing agonists at low, physiological concentrations, the resulting calcium signals generally take the form of repetitive regenerative discharges of stored calcium, termed calcium oscillations [1]. These intracellular calcium oscillations have long fascinated biologists as a mode of digitized intracellular signaling. Recent work has highlighted the role of calcium influx as an essential component of calcium oscillations [2]. This influx occurs through a process known as store-operated calcium entry, which is initiated by calcium sensor proteins, STIM1 and STIM2, in the endoplasmic reticulum [3]. STIM2 is activated by changes in endoplasmic reticulum calcium near the resting level, whereas a threshold of calcium depletion is required for STIM1 activation [4]. Here we show that, surprisingly, it is STIM1 and not STIM2 that is exclusively involved in calcium entry during calcium oscillations. The implication is that each oscillation produces a transient drop in endoplasmic reticulum calcium and that this drop is sufficient to transiently activate STIM1. This transient activation of STIM1 can be observed in some cells by total internal reflection fluorescence microscopy. This arrangement nicely provides a clearly defined and unambiguous signaling system, translating a digital calcium release signal into calcium influx that can signal to downstream effectors.
C1 [Bird, Gary S.; Hwang, Sung-Yong; Smyth, Jeremy T.; Fukushima, Miwako; Boyles, Rebecca R.; Putney, James W., Jr.] Natl Inst Environm Hlth Sci, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA.
RP Putney, JW (reprint author), Natl Inst Environm Hlth Sci, Lab Signal Transduct, NIH, Dept Hlth & Human Serv, POB 12233, Res Triangle Pk, NC 27709 USA.
EM putney@niehs.nih.gov
OI Boyles, Rebecca/0000-0003-0073-6854
FU National Institute of Environmental Health Sciences; National Institutes
of Health
FX We thank Drs. Jerrel Yakel, Steve Shears, and Wayne DeHaven, who read
the manuscript and provided helpful comments. This work was supported by
funds from the Intramural Program of the National Institute of
Environmental Health Sciences and the National Institutes of Health.
NR 23
TC 64
Z9 65
U1 0
U2 3
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
J9 CURR BIOL
JI Curr. Biol.
PD NOV 3
PY 2009
VL 19
IS 20
BP 1724
EP 1729
DI 10.1016/j.cub.2009.08.022
PG 6
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 515UM
UT WOS:000271498400028
PM 19765994
ER
PT J
AU Ferrari, PF
Paukner, A
Ionica, C
Suomi, SJ
AF Ferrari, Pier Francesco
Paukner, Annika
Ionica, Consuel
Suomi, Stephen J.
TI Reciprocal Face-to-Face Communication between Rhesus Macaque Mothers and
Their Newborn Infants
SO CURRENT BIOLOGY
LA English
DT Article
ID CHIMPANZEES PAN-TROGLODYTES; IMITATION
AB Human mothers interact emotionally with their newborns through exaggerated facial expressions, speech, mutual gaze, and body contact, a capacity that has long been considered uniquely human [1-4]. Current developmental psychological theories propose that this pattern of mother-infant exchange promotes the regulation of infant emotions [4-6] and serves as a precursor of more complex forms of social exchange including perspective taking and empathy. Here we report that in rhesus macaques, mother-infant pairs also communicate intersubjectively via complex forms of emotional exchanges including exaggerated lipsmacking, sustained mutual gaze, mouth-mouth contacts, and neonatal imitation. Infant macaques solicit their mother's affiliative responses and actively communicate to her. However, this form of communication disappears within the infant's first month of life. Our data challenge the view that the mother-infant communicative system functions in order to sustain proximity and that infants are simply passive recipients in such interaction. Thus, emotional communication between mother and infant is not uniquely human. Instead, we can trace back to macaques the evolutionary foundation of those behaviors that are crucial for the establishment of a functional capacity to socially exchange with others.
C1 [Ferrari, Pier Francesco] Univ Parma, Dipartimento Biol Evolut & Funz, I-43100 Parma, Italy.
[Ferrari, Pier Francesco] Univ Parma, Dipartimento Neurosci, I-43100 Parma, Italy.
[Ferrari, Pier Francesco; Paukner, Annika; Ionica, Consuel; Suomi, Stephen J.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Comparat Ethol Lab, NIH, Bethesda, MD 20892 USA.
RP Ferrari, PF (reprint author), Univ Parma, Dipartimento Biol Evolut & Funz, Via Usberti 11A, I-43100 Parma, Italy.
EM pierfrancesco.ferrari@unipr.it
RI Ionica, Consuel/A-5186-2009
FU NICHD; National Institutes of Health; MIUR-COFIN; NeuroCom
FX This study was supported by the Division of Intramural Research of the
NICHD, the National Institutes of Health, MIUR-COFIN 2007, and NeuroCom.
We thank D. Stern and E. Palagi for valuable comments on an early draft
of the manuscript.
NR 23
TC 60
Z9 61
U1 3
U2 17
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0960-9822
J9 CURR BIOL
JI Curr. Biol.
PD NOV 3
PY 2009
VL 19
IS 20
BP 1768
EP 1772
DI 10.1016/j.cub.2009.08.055
PG 5
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 515UM
UT WOS:000271498400036
PM 19818617
ER
PT J
AU Rohrer, JD
Guerreiro, R
Vandrovcova, J
Uphill, J
Reiman, D
Beck, J
Isaacs, AM
Authier, A
Ferrari, R
Fox, NC
Mackenzie, IRA
Warren, JD
de Silva, R
Holton, J
Revesz, T
Hardy, J
Hardy, J
Mead, S
Rossor, MN
AF Rohrer, J. D.
Guerreiro, R.
Vandrovcova, J.
Uphill, J.
Reiman, D.
Beck, J.
Isaacs, A. M.
Authier, A.
Ferrari, R.
Fox, N. C.
Mackenzie, I. R. A.
Warren, J. D.
de Silva, R.
Holton, J.
Revesz, T.
Hardy, J.
Hardy, J.
Mead, S.
Rossor, M. N.
TI The heritability and genetics of frontotemporal lobar degeneration
SO NEUROLOGY
LA English
DT Article
ID PRIMARY-PROGRESSIVE-APHASIA; AMYOTROPHIC-LATERAL-SCLEROSIS; CORTICOBASAL
DEGENERATION; SUPRANUCLEAR PALSY; TAU-MUTATIONS; DEMENTIA; PROGRANULIN;
FREQUENCY; CONSENSUS; CRITERIA
AB Background: Frontotemporal lobar degeneration (FTLD) is a genetically and pathologically heterogeneous neurodegenerative disorder.
Methods: We collected blood samples from a cohort of 225 patients with a diagnosis within the FTLD spectrum and examined the heritability of FTLD by giving each patient a family history score, from 1 (a clear autosomal dominant history of FTLD) through to 4 (no family history of dementia). We also looked for mutations in each of the 5 disease-causing genes (MAPT, GRN, VCP, CHMP2B, and TARDP) and the FUS gene, known to cause motor neuron disease.
Results: A total of 41.8% of patients had some family history (score of 1, 2, 3, or 3.5), although only 10.2% had a clear autosomal dominant history (score of 1). Heritability varied across the different clinical subtypes of FTLD with the behavioral variant being the most heritable and frontotemporal dementia-motor neuron disease and the language syndromes (particularly semantic dementia) the least heritable. Mutations were found in MAPT (8.9% of the cohort) and GRN (8.4%) but not in any of the other genes. Of the remaining patients without mutations but with a strong family history, 7 had pathologic confirmation, falling into 2 groups: type 3 FTLD-TDP without GRN mutations (6) and FTLD-UPS (1).
Conclusion: These findings show that frontotemporal lobar degeneration (FTLD) is a highly heritable disorder but heritability varies between the different syndromes. Furthermore, while MAPT and GRN mutations account for a substantial proportion of familial cases, there are other genes yet to be discovered, particularly in patients with type 3 FTLD-TDP without a GRN mutation. Neurology (R) 2009; 73:1451-1456
C1 [Rohrer, J. D.; Fox, N. C.; Warren, J. D.; Rossor, M. N.] UCL, Inst Neurol, Dept Mol Neurosci, Dementia Res Ctr, London WC1N 3BG, England.
[Uphill, J.; Reiman, D.; Beck, J.; Isaacs, A. M.; Authier, A.; Mead, S.] UCL, Inst Neurol, Dept Mol Neurosci, MRC Prion Unit, London WC1N 3BG, England.
[Ferrari, R.; Holton, J.] UCL, Inst Neurol, Dept Neurodegenerat Dis, Reta Lila Weston Inst,Dept Mol Neurosci, London WC1N 3BG, England.
[Vandrovcova, J.; de Silva, R.; Holton, J.; Revesz, T.] UCL, Inst Neurol, Dept Mol Neurosci, Queen Sq Brain Bank, London WC1N 3BG, England.
[Ferrari, R.] Texas Tech Univ, Hlth Sci Ctr, Dept Internal Med, Lubbock, TX 79430 USA.
[Guerreiro, R.] NIA, Neurogenet Lab, NIH, Bethesda, MD 20892 USA.
[Guerreiro, R.] Univ Coimbra, Ctr Neurosci & Cell Biol, Coimbra, Portugal.
[Mackenzie, I. R. A.] Univ British Columbia, Dept Pathol & Lab Med, Vancouver Gen Hosp, Vancouver, BC V5Z 1M9, Canada.
RP Rossor, MN (reprint author), UCL, Inst Neurol, Dept Mol Neurosci, Dementia Res Ctr, Queen Sq, London WC1N 3BG, England.
EM mrossor@dementia.ion.ucl.ac.uk
RI Revesz, Tamas/A-8732-2010; Mead, Simon/E-9414-2011; Holton,
Janice/F-6831-2011; Hardy, John/C-2451-2009; Guerreiro,
Rita/A-1327-2011; de Silva, Rohan/C-1734-2008; Fox, Nick/B-1319-2009
OI Revesz, Tamas/0000-0003-2501-0259; Mead, Simon/0000-0002-4326-1468;
Holton, Janice/0000-0002-3882-5249; de Silva, Rohan/0000-0002-5052-5775;
Fox, Nick/0000-0002-6660-657X
FU Department of Health's NIHR Biomedical Research Centres; Wellcome Trust;
Medical Research Council Prion Unit; Alzheimer's Research Trust; UCL
Hospitals Clinical Research and Development Committee; Elan Corporation;
Wyeth; Lundbeck Inc.; Sanofi-Aventis; IXICO Ltd.; Pfizer Inc.; Neurochem
Inc.; MRC [G0801306, G0601846]; NIH [U01 AG024904 (Co-I)]; Alzheimer
Research Trust [ART/RF/2007/1]; Canadian Institutes of Health Research;
Pacific Alzheimer Research Foundation; Michael Smith Foundation for
Health Research; The Sarah Matheson Trust; Action Medical Research;
BrainNet Europe; Myositis Support Group; Orion Pharma; European
Commission; BrainNet Europe II; Network of Excellence; Sarah Matheson
Trust; Parkinson's Disease Society, UK; Department of Health
FX Dr. Rohrer has received research support from the Wellcome Trust
(Clinical Research Fellowship) and Brain (Exit Scholarship). R.
Guerreiro, Dr. Vandrovcova, J. Uphill, D. Reiman, and J. Beck report no
disclosures. Dr. Isaacs receives research support from the Medical
Research Council Prion Unit, Alzheimer's Research Trust, and UCL
Hospitals Clinical Research and Development Committee. A. Authier and R.
Ferrari report no disclosures. Dr. Fox has served on scientific advisory
boards for the Alzheimer's Research Forum and GE Healthcare; may accrue
revenue on Patent PCT/GB2008/001537 (issued: 04/05/2007): QA Box; has
received honoraria from GE Healthcare and Lancet Neurology (reviewer
fee); has served as a consultant to Eli Lilly and Company, Abbott, and
Lundbeck Inc.; has received research support (to the Dementia Research
Centre) from Elan Corporation, Wyeth, Lundbeck Inc., Sanofi-Aventis,
IXICO Ltd., Pfizer Inc., and Neurochem Inc.; and receives research
support from the MRC [G0801306 (PI) and G0601846 (PI)], the NIH [U01
AG024904 (Co-I)], and the Alzheimer Research Trust [ART/RF/2007/1 (PI)].
Dr. Mackenzie serves on the advisory board of the 2009 International
Conference on Alzheimer's Disease; has received funding for travel and
speaker honoraria for non-industry-sponsored activities; serves on
editorial boards for the Journal of Neuropathology & Experimental
Neurology, the Journal of Neuroinflammation, and Clinical
Neuropathology; and receives research support from Canadian Institutes
of Health Research, Pacific Alzheimer Research Foundation, and Michael
Smith Foundation for Health Research. Dr. Warren and Dr. De Silva report
no disclosures. Dr. Holton serves on the editorial board of
Neuropathology & Applied Neurobiology and has received research support
from the Alzheimer's Research Trust, The Sarah Matheson Trust, Action
Medical Research, BrainNet Europe, and the Myositis Support Group. Dr.
Revesz serves on editorial boards for Acta Neuropathological, Clinical
Neuropathology, and Neuropathology & Applied Neurobiology; has received
speaker honoraria from Boehringer Ingelheim; and receives research
support from Orion Pharma, the Alzheimer's Research Trust, the European
Commission, BrainNet Europe II, Network of Excellence, the Sarah
Matheson Trust, and the Parkinson's Disease Society, UK. Dr. Hardy
serves as a consultant to Eisai Inc. Dr. Mead receives research support
from the Medical Research Council Prion Unit and Wellcome Trust. Dr.
Rossor serves on a scientific advisory board for Elan Corporation and
Wyeth; serves as Editor-in-Chief of the Journal of Neurology,
Neurosurgery and Psychiatry, and on the editorial boards of Practical
Neurology, Dementia and Geriatric Cognitive Disorders, Neurodegenerative
Diseases, and the British Medical Journal; receives royalties from
publishing Brain's Diseases of the Nervous System (11th edition), Oxford
University Press, 2001, and Brain's Diseases of the Nervous System (12th
edition), Oxford University Press, 2009; and receives research support
from the Department of Health and the Alzheimer's Research Trust.
NR 39
TC 110
Z9 113
U1 0
U2 18
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
J9 NEUROLOGY
JI Neurology
PD NOV 3
PY 2009
VL 73
IS 18
BP 1451
EP 1456
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 514XN
UT WOS:000271429900005
PM 19884572
ER
PT J
AU Han, T
Manoharan, AP
Harkins, TT
Bouffard, P
Fitzpatrick, C
Chu, DS
Thierry-Mieg, D
Thierry-Mieg, J
Kim, JK
AF Han, Ting
Manoharan, Arun Prasad
Harkins, Tim T.
Bouffard, Pascal
Fitzpatrick, Colin
Chu, Diana S.
Thierry-Mieg, Danielle
Thierry-Mieg, Jean
Kim, John K.
TI 26G endo-siRNAs regulate spermatogenic and zygotic gene expression in
Caenorhabditis elegans
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE endogenous siRNA; germline; RNA interference
ID DIRECTED RNA-POLYMERASE; GERM-LINE DEVELOPMENT; C-ELEGANS; ENDOGENOUS
SIRNAS; INTERFERING RNAS; MESSENGER-RNAS; SOMATIC-CELLS; MOUSE OOCYTES;
PIRNA COMPLEX; DROSOPHILA
AB Endogenous small interfering RNAs (endo-siRNAs) regulate diverse gene expression programs in eukaryotes by either binding and cleaving mRNA targets or mediating heterochromatin formation; however, the mechanisms of endo-siRNA biogenesis, sorting, and target regulation remain poorly understood. Here we report the identification and function of a specific class of germline-generated endo-siRNAs in Caenorhabditis elegans that are 26 nt in length and contain a guanine at the first nucleotide position (i.e., 26G RNAs). 26G RNAs regulate gene expression during spermatogenesis and zygotic development, and their biogenesis requires the ERI-1 exonuclease and the RRF-3 RNA-dependent RNA polymerase (RdRP). Remarkably, we identified two nonoverlapping subclasses of 26G RNAs that sort into specific RNA-induced silencing complexes (RISCs) and differentially regulate distinct mRNA targets. Class I 26G RNAs target genes are expressed during spermatogenesis, whereas class II 26G RNAs are maternally inherited and silence gene expression during zygotic development. These findings implicate a class of endo-siRNAs in the global regulation of transcriptional programs required for fertility and development.
C1 [Han, Ting; Manoharan, Arun Prasad; Kim, John K.] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
[Harkins, Tim T.] Roche Appl Sci, Indianapolis, IN 46250 USA.
[Bouffard, Pascal] Roche Co, Life Sci 454, Branford, CT 06405 USA.
[Fitzpatrick, Colin; Chu, Diana S.] San Francisco State Univ, Dept Biol, San Francisco, CA 94132 USA.
[Thierry-Mieg, Danielle; Thierry-Mieg, Jean] NIH, Natl Ctr Biotechnol Informat, Natl Lib Med, Bethesda, MD 20895 USA.
[Kim, John K.] Univ Michigan, Dept Human Genet, Ann Arbor, MI 48109 USA.
RP Kim, JK (reprint author), Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
EM jnkim@umich.edu
RI THIERRY-MIEG, Jean/F-1975-2017
OI THIERRY-MIEG, Jean/0000-0002-0396-6789
FU National Science Foundation; National Institutes of Health [S06 GM52588,
HG004276-01]; National Library of Medicine
FX We thank John Moran, Harrison Gabel, Chi Zhang, Tammy Wu, Kris Gunsalus,
Scott Kennedy, Patrick Hu, and Allison Billi for helpful comments;
Sylvia Fischer (Massachusetts General Hospital) for dcr-1( ok247) total
RNA, the Caenorhabditis Genetics Center and Shohei Mitani (Tokyo Women's
Medical University) for strains, Marco Marra and Martin Hirst of the
British Columbia Cancer Centre for Solexa deep sequencing, and David
Miller of Applied Biosystems for Taqman probes. This work was supported
by a National Science Foundation CAREER Award, National Institutes of
Health Grant S06 GM52588 (to D.S.C.), the Intramural Research Program of
the National Institutes of Health and the National Library of Medicine
(to D.T.-M. and J.T.-M.), and National Institutes of Health Grant
HG004276-01 grant (to J.K.K.).
NR 45
TC 69
Z9 84
U1 0
U2 6
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 3
PY 2009
VL 106
IS 44
BP 18674
EP 18679
DI 10.1073/pnas.0906378106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 514XM
UT WOS:000271429800048
PM 19846761
ER
PT J
AU Hasumi, Y
Baba, M
Ajima, R
Hasumi, H
Valera, VA
Klein, ME
Haines, DC
Merino, MJ
Hong, SB
Yamaguchi, TP
Schmidt, LS
Linehan, WM
AF Hasumi, Yukiko
Baba, Masaya
Ajima, Rieko
Hasumi, Hisashi
Valera, Vladimir A.
Klein, Mara E.
Haines, Diana C.
Merino, Maria J.
Hong, Seung-Beom
Yamaguchi, Terry P.
Schmidt, Laura S.
Linehan, W. Marston
TI Homozygous loss of BHD causes early embryonic lethality and kidney tumor
development with activation of mTORC1 and mTORC2
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE Birt-Hogg-Dube syndrome; kidney cancer; mouse model; mTOR; tumor
suppressor
ID HOGG-DUBE-SYNDROME; POLYCYSTIC KIDNEYS; RENAL TUMORS; COMPLEX 2; GENE;
PROTEIN; CANCER; INACTIVATION; MUTATIONS; NEOPLASIA
AB Germline mutations in the BHD/FLCN tumor suppressor gene predispose patients to develop renal tumors in the hamartoma syndrome, Birt-Hogg-Dube (BHD). BHD encodes folliculin, a protein with unknown function that may interact with the energy-and nutrient-sensing AMPK-mTOR signaling pathways. To clarify BHD function in the mouse, we generated a BHD knockout mouse model. BHD homozygous null (BHD(d/d)) mice displayed early embryonic lethality at E5.5-E6.5, showing defects in the visceral endoderm. BHD heterozygous knockout (BHD(d/+)) mice appeared normal at birth but developed kidney cysts and solid tumors as they aged (median kidney-lesion-free survival = 23 months, median tumor-free survival = 25 months). As observed in human BHD kidney tumors, three different histologic types of kidney tumors developed in BHD(d/+) mice including oncocytic hybrid, oncocytoma, and clear cell with concomitant loss of heterozygosity (LOH), supporting a tumor suppressor function for BHD in the mouse. The PI3K-AKT pathway was activated in both human BHD renal tumors and kidney tumors in BHD(d/+) mice. Interestingly, total AKT protein was elevated in kidney tumors compared to normal kidney tissue, but without increased levels of AKT mRNA, suggesting that AKT may be regulated by folliculin through post translational or post-transcriptional modification. Finally, BHD inactivation led to both mTORC1 and mTORC2 activation in kidney tumors from BHD(d/+) mice and human BHD patients. These data support a role for PI3K-AKT pathway activation in kidney tumor formation caused by loss of BHD and suggest that inhibitors of both mTORC1 and mTORC2 may be effective as potential therapeutic agents for BHD-associated kidney cancer.
C1 [Hasumi, Yukiko; Baba, Masaya; Hasumi, Hisashi; Valera, Vladimir A.; Klein, Mara E.; Hong, Seung-Beom; Schmidt, Laura S.; Linehan, W. Marston] NCI, Urol Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Merino, Maria J.] NCI, Pathol Lab, NIH, Bethesda, MD 20892 USA.
[Ajima, Rieko; Yamaguchi, Terry P.] NCI, Cell Signaling Vertebrate Dev Sect, Canc & Dev Biol Lab, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Schmidt, Laura S.] NCI, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Haines, Diana C.] NCI, Pathol Histotechnol Lab, SAIC Frederick Inc, Frederick, MD 21702 USA.
RP Linehan, WM (reprint author), NCI, Urol Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM wml@nih.gov
RI Baba, Masaya/L-7490-2013
OI Baba, Masaya/0000-0002-5308-6683
FU National Institutes of Health (NIH); National Cancer Institute (NCI);
Center for Cancer Research; NCI, NIH [HHSN261200800001E]
FX We thank Louise Cromwell for excellent technical support with the mouse
studies, Serguei Kozlov for helpful discussions, Yelena Golubeva for her
technical support regarding laser microdissection (LCM), Jaime
Rodriguez-Canales and Jeffrey Hanson for their technical expertise
regarding LCM procedures, and Kristin K. Biris for her technical support
regarding in situ hybridization. This research was supported by the
Intramural Research Program of the National Institutes of Health (NIH),
National Cancer Institute (NCI), Center for Cancer Research; federal
funds from the NCI, NIH, under Contract HHSN261200800001E.
NR 26
TC 107
Z9 107
U1 0
U2 3
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 3
PY 2009
VL 106
IS 44
BP 18722
EP 18727
DI 10.1073/pnas.0908853106
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 514XM
UT WOS:000271429800056
PM 19850877
ER
PT J
AU Khan, MA
Goila-Gaur, R
Kao, S
Miyagi, E
Walker, RC
Strebel, K
AF Khan, Mohammad A.
Goila-Gaur, Ritu
Kao, Sandra
Miyagi, Eri
Walker, Robert C., Jr.
Strebel, Klaus
TI Encapsidation of APOBEC3G into HIV-1 virions involves lipid raft
association and does not correlate with APOBEC3G oligomerization
SO RETROVIROLOGY
LA English
DT Article
ID VIRUS TYPE-1 VIF; ANTIVIRAL ACTIVITY; 7SL RNA; INFECTIVITY FACTOR;
PLASMA-MEMBRANE; VIRAL-RNA; PROTEIN; PARTICLES; GAG; DETERMINANTS
AB Background: The cellular cytidine deaminase APOBEC3G (A3G), when incorporated into the human immunodeficiency virus type 1 (HIV-1), renders viral particles non-infectious. We previously observed that mutation of a single cysteine residue of A3G (C100S) inhibited A3G packaging. In addition, several recent studies showed that mutation of tryptophan 127 (W127) and tyrosine 124 (Y124) inhibited A3G encapsidation suggesting that the N-terminal CDA constitutes a viral packaging signal in A3G. It was also reported that W127 and Y124 affect A3G oligomerization.
Results: Here we studied the mechanistic basis of the packaging defect of A3G W127A and Y124A mutants. Interestingly, cell fractionation studies revealed a strong correlation between encapsidation, lipid raft association, and genomic RNA binding of A3G. Surprisingly, the presence of a C-terminal epitope tag affected lipid raft association and encapsidation of the A3G W127A mutant but had no effect on wt A3G encapsidation, lipid raft association, and interaction with viral genomic RNA. Mutation of Y124 abolished A3G encapsidation irrespective of the presence or absence of an epitope tag. Contrasting a recent report, our co-immunoprecipitation studies failed to reveal a correlation between A3G oligomerization and A3G encapsidation. In fact, our W127A and Y124A mutants both retained the ability to oligomerize.
Conclusion: Our results confirm that W127 and Y124 residues in A3G are important for encapsidation into HIV-1 virions and our data establish a novel correlation between genomic RNA binding, lipid raft association, and viral packaging of A3G. In contrast, we were unable to confirm a role of W127 and Y124 in A3G oligomerization and we thus failed to confirm a correlation between A3G oligomerization and virus encapsidation.
C1 [Khan, Mohammad A.; Goila-Gaur, Ritu; Kao, Sandra; Miyagi, Eri; Walker, Robert C., Jr.; Strebel, Klaus] NIAID, Mol Microbiol Lab, Viral Biochem Sect, NIH, Bethesda, MD 20892 USA.
RP Strebel, K (reprint author), NIAID, Mol Microbiol Lab, Viral Biochem Sect, NIH, Bldg 4,Room 310,4 Ctr Dr,MSC 0460, Bethesda, MD 20892 USA.
EM mkhan@niaid.nih.gov; rgaur@niaid.nih.gov; skao@niaid.nih.gov;
emiyagi@niaid.nih.gov; walkerrobert@niaid.nih.gov;
kstrebel@niaid.nih.gov
FU NIH Intramural AIDS Targeted Antiviral Program; Intramural Research
Program of the NIH, NIAID
FX We thank Amy Andrew for critical comments on the manuscript and Melissa
Gilden and Sandrine Opi for plasmid construction and help with reagents.
We are grateful to Michael Malim for providing pA3G, pA3G W127A,
pA3G-HA, and pA3G-HA W127A vectors. This work was supported by a Grant
from the NIH Intramural AIDS Targeted Antiviral Program to K. S. and by
the Intramural Research Program of the NIH, NIAID.
NR 43
TC 14
Z9 15
U1 0
U2 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1742-4690
J9 RETROVIROLOGY
JI Retrovirology
PD NOV 3
PY 2009
VL 6
AR 99
DI 10.1186/1742-4690-6-99
PG 12
WC Virology
SC Virology
GA 518FH
UT WOS:000271675500001
PM 19886996
ER
PT J
AU Lerbret, A
Mason, PE
Venable, RM
Cesaro, A
Saboungi, ML
Pastor, RW
Brady, JW
AF Lerbret, A.
Mason, P. E.
Venable, R. M.
Cesaro, A.
Saboungi, M. -L
Pastor, R. W.
Brady, J. W.
TI Molecular dynamics studies of the conformation of sorbitol
SO CARBOHYDRATE RESEARCH
LA English
DT Article
DE Molecular dynamics simulation; Sorbitol; Conformation; Hydrogen bonding;
Glucose
ID X-RAY-DIFFRACTION; D-GLUCITOL; ANOMERIC EQUILIBRIUM; LIQUID WATER;
FORCE-FIELD; FREE-ENERGY; C-13 NMR; SIMULATIONS; DEPENDENCE; MALTITOL
AB Molecular dynamics simulations of a 3 molal aqueous solution Of D-Sorbitol (also called D-glucitol) have been performed at 300 K, as well as at two elevated temperatures to promote conformational transitions. In principle, sorbitol is more flexible than glucose since it does not contain a constraining ring. However, a conformational analysis revealed that the sorbitol chain remains extended in solution, in contrast to the bent conformation found experimentally in the crystalline form. While there are 243 staggered conformations of the backbone possible for this open-chain polyol, only a very limited number were found to be stable in the simulations. Although many conformers were briefly sampled, only eight were significantly populated in the simulation. The carbon backbones of all but two of these eight conformers were completely extended, unlike the bent crystal conformation. These extended conformers were stabilized by a quite persistent intramolecular hydrogen bond between the hydroxyl groups of carbon C-2 and C-4. The conformational populations were found to be in good agreement with the limited available NMR data except for the C-2-C-3 torsion (spanned by the O2-O-4 hydrogen bond), where the NMR data support a more bent structure. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Lerbret, A.; Mason, P. E.; Brady, J. W.] Cornell Univ, Dept Food Sci, Ithaca, NY 14853 USA.
[Venable, R. M.; Pastor, R. W.] NHLBI, Lab Computat Biol, NIH, Bethesda, MD 20892 USA.
[Saboungi, M. -L] Ctr Rech Mat Divisee, F-45071 Orleans, France.
[Cesaro, A.] Univ Trieste, Dip Sci Vita, Trieste, Italy.
RP Brady, JW (reprint author), Cornell Univ, Dept Food Sci, Stocking Hall, Ithaca, NY 14853 USA.
EM jwb7@cornell.edu
RI Saboungi, Marie-Louise/C-5920-2013
OI Saboungi, Marie-Louise/0000-0002-0607-4815
FU National Institutes of Health [GM63018, GM70855]
FX This project was supported by grants GM63018 and GM70855 from the
National Institutes of Health. The authors thank Alexander D. MacKerell
and Gerald Lelong for helpful discussions.
NR 34
TC 18
Z9 18
U1 2
U2 16
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0008-6215
J9 CARBOHYD RES
JI Carbohydr. Res.
PD NOV 2
PY 2009
VL 344
IS 16
BP 2229
EP 2235
DI 10.1016/j.carres.2009.08.003
PG 7
WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 512MY
UT WOS:000271254800016
PM 19744646
ER
PT J
AU Carrozza, MJ
Stefanick, DF
Horton, JK
Kedar, PS
Wilson, SH
AF Carrozza, Michael J.
Stefanick, Donna F.
Horton, Julie K.
Kedar, Padmini S.
Wilson, Samuel H.
TI PARP inhibition during alkylation-induced genotoxic stress signals a
cell cycle checkpoint response mediated by ATM
SO DNA REPAIR
LA English
DT Article
DE PARP-1; PARP inhibitor; Methyl methanesulfonate; ATM; Chk2; Cell cycle
ID DNA-POLYMERASE-BETA; DOUBLE-STRAND BREAKS; BASE-EXCISION-REPAIR;
POLY(ADP-RIBOSE) POLYMERASE; IONIZING-RADIATION; KINASE INHIBITORS;
DAMAGING AGENTS; NUCLEAR ANTIGEN; CANCER-THERAPY; ACTIVATES ATM
AB By limiting cell cycle progression following detection of DNA damage, checkpoints are critical for cell survival and genome stability. Methylated DNA damage, when combined with inhibition of PARP activity, results in an ATR-dependent S phase delay of the cell cycle. Here, we demonstrate that another checkpoint kinase, ATM, also is involved in the DNA damage response following treatment with a sub-lethal concentration of MMS combined with the PARP inhibitor 4-AN. Both ATM and PARP activities are important for moderating cellular sensitivity to MMS. Loss of ATM activity, or that of its downstream effector Chk2, limited the duration of the S phase delay. The combination of MMS and 4-AN resulted in ATM and Chk2 phosphorylation and the time course of phosphorylation for both kinases correlated with the S phase delay. Chk2 phosphorylation was reduced in the absence of ATM activity. The Chk2 phosphorylation that remained in the absence of ATM appeared to be dependent on ATR and DNA-PK. The results demonstrate that, following initiation of base excision repair and inhibition of PARP activity, ATM activation is critical for preventing the cell from progressing through S phase, and for protection against MMS-induced cytotoxicity. Published by Elsevier B.V.
C1 [Carrozza, Michael J.; Stefanick, Donna F.; Horton, Julie K.; Kedar, Padmini S.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, Natl Inst Hlth, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, Natl Inst Hlth, 111 TW Alexander Dr,POB 12233, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU NIH [ES050159]; National Institute of Environmental Health Sciences;
NIH/NIEHS; Constella/SRA, LLC [HHSN273200700046U]
FX We thank Rebecca Childress and Jennifer Zeng for technical assistance.
This research was Supported by Research Project Number ES050159 in the
Intramural Research Program of the NIH, National Institute of
Environmental Health Sciences. Dr. Kedar's contribution was funded in
whole with federal funds from NIH/NIEHS, under delivery order
HHSN273200700046U to Constella/SRA, LLC.
NR 51
TC 12
Z9 12
U1 1
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD NOV 2
PY 2009
VL 8
IS 11
BP 1264
EP 1272
DI 10.1016/j.dnarep.2009.07.010
PG 9
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 518HY
UT WOS:000271683000002
PM 19717351
ER
PT J
AU Masaoka, A
Horton, JK
Beard, WA
Wilson, SH
AF Masaoka, Aya
Horton, Julie K.
Beard, William A.
Wilson, Samuel H.
TI DNA polymerase beta and PARP activities in base excision repair in
living cells
SO DNA REPAIR
LA English
DT Article
DE Base excision repair; DNA polymerase beta; Poly(ADP-ribose) polymerase;
Luciferase; Plasmid-based assay
ID STRAND BREAK REPAIR; POLY(ADP-RIBOSE) POLYMERASE-1; COCKAYNE-SYNDROME;
MAMMALIAN-CELLS; RNA-POLYMERASE; TRANSCRIPTION ELONGATION; DIFFERENT
EFFICIENCIES; INDUCED CYTOTOXICITY; MOUSE FIBROBLASTS; OXIDATIVE STRESS
AB To examine base excision repair (BER) capacity in the context of living cells, we developed and applied a plasmid-based reporter assay. Non-replicating plasmids containing unique DNA base lesions were designed to express luciferase only after lesion repair had occurred, and luciferase expression in transfected cells was measured continuously during a repair period of 14 h. Two types of DNA lesions were examined: uracil opposite T reflecting repair primarily by the single-nucleotide BER sub-pathway, and the abasic site analogue tetrahydrofuran (THF) opposite C reflecting repair by long-patch BER. We found that the repair capacity for uracil-DNA in wild type mouse fibroblasts was very strong, whereas the repair capacity for THF-DNA, although strong, was slightly weaker. Repair capacity in DNA polymerase beta (Pol beta) null cells for uracil-DNA and THF-DNA was reduced by approximately 15% and 20%, respectively, compared to that in wild type cells. In both cases, the repair deficiency was fully complemented in Pol beta null cells expressing recombinant Pol beta. The effect of inhibition of poly(ADP-ribose) polymerase (PARP) activity on repair capacity was examined by treatment of cells with the inhibitor 4-amino-1,8-naphthalimide (4-AN). PARP inhibition decreased the repair capacity for both lesions in wild type cells, and this reduction was to the same level as that seen in Pol beta null cells. In contrast, 4-AN had no effect on repair in Pol 0 null cells. The results highlight that Pol beta and PARP function in the same repair pathway, but also suggest that there is repair independent of both Pol beta and PARP activities. Thus, before the BER capacity of a cell can be predicted or modulated, a better understanding of Pol beta and PARP activity-independent BER pathways is required. Published by Elsevier B.V.
C1 [Masaoka, Aya; Horton, Julie K.; Beard, William A.; Wilson, Samuel H.] NIEHS, Struct Biol Lab, Natl Inst Hlth, Res Triangle Pk, NC 27709 USA.
RP Wilson, SH (reprint author), NIEHS, Struct Biol Lab, Natl Inst Hlth, Res Triangle Pk, NC 27709 USA.
EM wilson5@niehs.nih.gov
FU National Institutes of Health [Z01-ES050158, Z01-ES050159]; National
Institute of Environmental Health Sciences
FX We thank Kenjiro Asagoshi, Michael Carrozza, Graciela Spivak and Philip
Hanawalt for discussions and critical reading of the manuscript and Ms.
Bonnie Mesmer for editorial assistance. This research was supported by
Research Project Numbers Z01-ES050158 and Z01-ES050159 in the Intramural
Research Program of the National Institutes of Health, National
Institute of Environmental Health Sciences.
NR 68
TC 25
Z9 26
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1568-7864
J9 DNA REPAIR
JI DNA Repair
PD NOV 2
PY 2009
VL 8
IS 11
BP 1290
EP 1299
DI 10.1016/j.dnarep.2009.08.004
PG 10
WC Genetics & Heredity; Toxicology
SC Genetics & Heredity; Toxicology
GA 518HY
UT WOS:000271683000005
PM 19748837
ER
PT J
AU Watanabe, K
Nagaoka, T
Lee, JM
Bianco, C
Gonzales, M
Castro, NP
Rangel, MC
Sakamoto, K
Sun, YP
Callahan, R
Salomon, DS
AF Watanabe, Kazuhide
Nagaoka, Tadahiro
Lee, Joseph M.
Bianco, Caterina
Gonzales, Monica
Castro, Nadia P.
Rangel, Maria Cristina
Sakamoto, Kei
Sun, Youping
Callahan, Robert
Salomon, David S.
TI Enhancement of Notch receptor maturation and signaling sensitivity by
Cripto-1
SO JOURNAL OF CELL BIOLOGY
LA English
DT Article
ID GLYCOSYLPHOSPHATIDYLINOSITOL-ANCHOR; STEM-CELLS; ROLES; FURIN; PATHWAY;
CANCER; GENE
AB Nodal and Notch signaling pathways play essential roles in vertebrate development. Through a yeast two-hybrid screening, we identified Notch3 as a candidate binding partner of the Nodal coreceptor Cripto-1. Coimmunoprecipitation analysis confirmed the binding of Cripto-1 with all four mammalian Notch receptors. Deletion analyses revealed that the binding of Cripto-1 and Notch1 is mediated by the Cripto-1/FRL-1/Cryptic domain of Cripto-1 and the C-terminal region of epidermal growth factor-like repeats of Notch1. Binding of Cripto-1 to Notch1 occurred mainly in the endoplasmic reticulum-Golgi network. Cripto-1 expression resulted in the recruitment of Notch1 protein into lipid raft microdomains and enhancement of the furin-like protein convertase-mediated proteolytic maturation of Notch1 (S1 cleavage). Enhanced S1 cleavage resulted in the sensitization to ligand-induced activation of Notch signaling. In addition, knockdown of Cripto-1 expression in human and mouse embryonal carcinoma cells desensitized the ligand-induced Notch signaling activation. These results suggest a novel role of Cripto-1 in facilitating the post-translational maturation of Notch receptors.
C1 [Watanabe, Kazuhide; Nagaoka, Tadahiro; Lee, Joseph M.; Bianco, Caterina; Gonzales, Monica; Castro, Nadia P.; Rangel, Maria Cristina; Callahan, Robert; Salomon, David S.] NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Sakamoto, Kei] Tokyo Med & Dent Univ, Grad Sch, Bunkyo Ku, Tokyo 1138549, Japan.
[Sun, Youping] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
RP Watanabe, K (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM kazuhidew@yahoo.com; salomond@mail.nih.gov
RI Rangel, Maria Cristina/P-7216-2014;
OI Rangel, Maria Cristina/0000-0002-8002-9617; Nagaoka,
Tadahiro/0000-0002-9391-0243
FU National Institutes of Health
FX This work was supported by National Institutes of Health intramural
funding.
NR 21
TC 25
Z9 25
U1 1
U2 1
PU ROCKEFELLER UNIV PRESS
PI NEW YORK
PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 USA
SN 0021-9525
J9 J CELL BIOL
JI J. Cell Biol.
PD NOV 2
PY 2009
VL 187
IS 3
BP 343
EP 353
DI 10.1083/jcb.200905105
PG 11
WC Cell Biology
SC Cell Biology
GA 514DJ
UT WOS:000271374200006
PM 19948478
ER
PT J
AU Ye, XY
Johann, DJ
Hakami, RM
Xiao, Z
Meng, ZJ
Ulrich, RG
Issaq, HJ
Veenstra, TD
Blonder, J
AF Ye, Xiaoying
Johann, Donald J.
Hakami, Ramin M.
Xiao, Zhen
Meng, Zhaojing
Ulrich, Robert G.
Issaq, Haleem J.
Veenstra, Timothy D.
Blonder, Josip
TI Optimization of protein solubilization for the analysis of the CD14
human monocyte membrane proteome using LC-MS/MS
SO JOURNAL OF PROTEOMICS
LA English
DT Article
DE CD14 monocyte; Membrane proteins; Solubilization; Methanol; Detergents;
LC-MS/MS
ID SPECTROMETRY-COMPATIBLE SURFACTANTS; TANDEM MASS-SPECTROMETRY; ENZYMATIC
DIGESTION; CLEAVABLE DETERGENTS; RAT-LIVER; BACTERIORHODOPSIN;
IDENTIFICATION; CELLS; EXPRESSION; METHANOL
AB Proteomic profiling of membrane proteins is of vital importance in the search for disease biomarkers and drug development. However, the slow pace in this field has resulted mainly from the difficulty to analyze membrane proteins by mass spectrometry (MS). The objective of this investigation was to explore and optimize solubilization. of membrane proteins for shotgun membrane proteomics of the CD14 human monocytes by examining different systems that rely on: i) an organic solvent (methanol) ii) an acid-labile detergent 3-[3-(1,1-bisalkyloxyethyl)pyridin-1-yl) propane-1-sulfonate (PPS), iii) a combination of both agents (methanol+PPS). Solubilization efficiency of different buffers was first compared using bacteriorhodopsin as a model membrane protein. Selected approaches were then applied on a membrane subproteome isolated from a highly enriched human monocyte population that was similar to 98% positive for CD14 expression as determined by FACS analysis. A methanol-based buffer yielded 194 proteins of which 93 (48%) were mapped as integral membrane proteins. The combination of methanol and acid-cleavable detergent gave similar results; 203 identified proteins of which 93 (46%) were mapped integral membrane proteins. However, employing PPS 216 proteins were identified of which 75 (35%) were mapped as integral membrane proteins. These results indicate that methanol alone or in combination with PPS yielded significantly higher membrane protein identification/enrichment than the PPS alone. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Ye, Xiaoying; Xiao, Zhen; Meng, Zhaojing; Issaq, Haleem J.; Veenstra, Timothy D.; Blonder, Josip] NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
[Johann, Donald J.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
[Hakami, Ramin M.] Oak Ridge Associated Univ, Fac Res Program, Belcamp, MD 21017 USA.
[Ulrich, Robert G.] USA, Med Res Inst Infect Dis, Frederick, MD 21702 USA.
RP Blonder, J (reprint author), NCI, Lab Prote & Analyt Technol, Adv Technol Program, SAIC Frederick Inc, Frederick, MD 21702 USA.
EM blonder@ncifcrf.gov
FU National Cancer Institute; National Institutes of Health [N01-CO-12400]
FX This project has been funded in whole or in part with Federal funds from
the National Cancer Institute, National Institutes of Health, under
Contract N01-CO-12400. 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 organization imply endorsement by the United States
Government.
NR 62
TC 16
Z9 18
U1 0
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1874-3919
J9 J PROTEOMICS
JI J. Proteomics
PD NOV 2
PY 2009
VL 73
IS 1
BP 112
EP 122
DI 10.1016/j.jprot.2009.08.008
PG 11
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 522GL
UT WOS:000271985800010
PM 19709643
ER
PT J
AU Simonelli, V
D'Errico, M
Palli, D
Prasad, R
Wilson, SH
Dogliotti, E
AF Simonelli, Valeria
D'Errico, Mariarosaria
Palli, Domenico
Prasad, Rajendra
Wilson, Samuel H.
Dogliotti, Eugenia
TI Characterization of DNA polymerase beta splicing variants in gastric
cancer: The most frequent exon 2-deleted isoform is a non-coding RNA
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Article
DE DNA polymerase beta; Splicing variants; Gastric cancer; DNA repair;
ncRNA
ID BASE-EXCISION-REPAIR; MESSENGER-RNA; MICROSATELLITE INSTABILITY;
CELLULAR-TRANSFORMATION; COLORECTAL-CANCER; OXIDATIVE STRESS;
BLADDER-CANCER; OVEREXPRESSION; MUTATIONS; CELLS
AB DNA repair polymerase beta (Pol beta) gene variants are frequently associated with tumor tissues. In this study a search for Pol beta mutants and splice variants was conducted in matched normal and tumor gastric tissues and blood samples from healthy donors. No tumor associated mutations were found while a variety of alternative Pol beta splicing variants were detected with high frequency in all the specimens analysed. Quantitative PCR of the Pol beta variant lacking exon 2 (Ex2 Delta) and the isoforms with exon 11 skipping allowed to clarify that these variants are not tumor-neither tissue-specific and their levels vary greatly among different individuals. The most frequent Ex2 Delta variant was further characterized. We clearly demonstrated that this variant does not encode protein, as detected by both western blotting and immunofluorescence analysis of human AGS cells expressing HA-tagged Ex2 Delta. The lack of translation was confirmed by comparing the DNA gap-filling capacity and alkylation sensitivity of wild type and Pol beta null murine fibroblasts expressing the human Ex2 Delta variant.
We showed that the Ex2 Delta transcript is polyadenylated and its half-life is significantly longer than that of the wild type mRNA as inferred by treating AGS cells with actinomycin D. Moreover, we found that it localizes to polyribosomes suggesting a role as post-transcriptional regulator.
This study identifies a new type of DNA repair variants that do not give rise to functional proteins but to non-coding RNAs that could either modulate target mRNAs or represent unproductive splicing events. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Simonelli, Valeria; D'Errico, Mariarosaria; Dogliotti, Eugenia] Ist Super Sanita, Dept Environm & Primary Prevent, I-00161 Rome, Italy.
[Palli, Domenico] Canc Res & Prevent Inst ISPO, Mol & Nutr Epidemiol Unit, Florence, Italy.
[Prasad, Rajendra; Wilson, Samuel H.] Natl Inst Hlth Environm Sci, NIH, Chapel Hill, NC USA.
RP Dogliotti, E (reprint author), Ist Super Sanita, Dept Environm & Primary Prevent, Viale Regina Elena 299, I-00161 Rome, Italy.
EM eugenia.dogliotti@iss.it
OI Simonelli, Valeria/0000-0002-3726-518X
FU Progetto Integrato Oncologia; Regione Toscana-Ministero della Salute;
Associazione Italiana per la Ricerca Sul Cancro (AIRC); MIUR/FIRB
[RBNE01RNN]; ISS/NIH; National Institutes of Health, NIEHS
FX We would like to thank Ettore Meccia for helpful suggestions. Grant
support: Progetto Integrato Oncologia, Regione Toscana-Ministero della
Salute, Associazione Italiana per la Ricerca Sul Cancro (AIRC),
MIUR/FIRB (RBNE01RNN7), Collaborative Project ISS/NIH. This research was
supported in part by the Intramural Research Program of the National
Institutes of Health, NIEHS.
NR 46
TC 4
Z9 5
U1 0
U2 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0027-5107
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD NOV 2
PY 2009
VL 670
IS 1-2
BP 79
EP 87
DI 10.1016/j.mrfmmm.2009.07.007
PG 9
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 522RE
UT WOS:000272015200011
PM 19635489
ER
PT J
AU Lea, IA
Jackson, MA
Dunnick, JK
AF Lea, Isabel A.
Jackson, Marcus A.
Dunnick, June K.
TI Genetic pathways to colorectal cancer
SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
LA English
DT Article
DE Colorectal cancer; Gene mutation; Loss of heterozygosity
ID HUMAN BREAST; TUMORIGENESIS; METHYLATION; HYPOMETHYLATION; MUTATIONS
AB The colorectal cancer paradigm explains how genetic and histological changes lead normal epithelial cell to transform into pre-malignant adenomas then progress to malignant carcinomas. Using the Genetic Alterations in Cancer Knowledge System intragenic allele loss and gene mutation data from approximately 9000 colorectal tumors were compared to the model of colorectal tumor development. The distribution of mutations along the TP53 codons as a function of tumorigenesis also was analyzed. Alterations of APC, KRAS and TP53 were observed in a higher percentage of adenocarcinomas compared to adenomas (P < 0.05) indicating that the alterations accumulated with malignancy. Alterations in BRAF, CTNNB, HRAS and NRAS were infrequent regardless of morphology. Differences were observed in the distribution of TP53 mutations with tumorigenesis. Mutations (single base substitutions) occurred most frequently at codons 175 and 273 in both tumor types; however, in adenocarcinomas the mutation incidence at codon 248 was approximately three times that reported in adenomas. It is proposed that the higher incidence of mutation at codon 248 is a later event in colorectal tumorigenesis that occurs as the tumors become malignant. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Lea, Isabel A.; Jackson, Marcus A.] Integrated Lab Syst Inc, Res Triangle Pk, NC 27709 USA.
[Dunnick, June K.] NIEHS, Res Triangle Pk, NC 27709 USA.
RP Lea, IA (reprint author), Integrated Lab Syst Inc, POB 13501, Res Triangle Pk, NC 27709 USA.
EM ilea@ils-inc.com
FU National Institutes of Health, National Institute of Environmental
Health Sciences [N43-ES-15477]
FX This work was supported by the Intramural Research Program of the
National Institutes of Health, National Institute of Environmental
Health Sciences [contract number N43-ES-15477].
NR 18
TC 11
Z9 12
U1 0
U2 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0027-5107
J9 MUTAT RES-FUND MOL M
JI Mutat. Res.-Fundam. Mol. Mech. Mutagen.
PD NOV 2
PY 2009
VL 670
IS 1-2
BP 96
EP 98
DI 10.1016/j.mrfmmm.2009.06.011
PG 3
WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology
GA 522RE
UT WOS:000272015200013
PM 19576232
ER
PT J
AU D'Onofrio, G
Goldstein, AB
Denisco, RA
Hingson, R
Heffelfinger, JD
Post, LA
AF D'Onofrio, Gail
Goldstein, Amy B.
Denisco, Richard A.
Hingson, Ralph
Heffelfinger, James D.
Post, Lori A.
TI Emergency Medicine Public Health Research Funded by Federal Agencies:
Progress and Priorities
SO ACADEMIC EMERGENCY MEDICINE
LA English
DT Article
DE federal funding; public health; emergency medicine; emergency
departments
ID ALCOHOL INTERVENTIONS; CARE; ACCESS; RISK; DEPARTMENTS; RESISTANT; LIFE
AB The emergency department (ED) visit provides an opportunity to impact the health of the public throughout the entire spectrum of care, from prevention to treatment. As the federal government has a vested interest in funding research and providing programmatic opportunities that promote the health of the public, emergency medicine (EM) is prime to develop a research agenda to advance the field. EM researchers need to be aware of federal funding opportunities, which entails an understanding of the organizational structure of the federal agencies that fund medical research, and the rules and regulations governing applications for grants. Additionally, there are numerous funding streams outside of the National Institutes of Health (NIH; the primary federal health research agency). EM researchers should seek funding from agencies according to each agency's mission and aims. Finally, while funds from the Department of Health and Human Services (HHS) are an important source of support for EM research, we need to look beyond traditional sources and appeal to other agencies with a vested interest in promoting public health in EDs. EM requires a broad skill set from a multitude of medical disciplines, and conducting research in the field will require looking for funding opportunities in a variety of traditional and not so traditional places within and without the federal government. The following is the discussion of a moderated session at the 2009 Academic Emergency Medicine consensus conference that included panel discussants from the National Institutes of Mental Health, Drug Abuse, and Alcoholism and Alcohol Abuse and the Centers for Disease Control and Prevention (CDC). Further information is also provided to discuss those agencies and centers not represented.
C1 [D'Onofrio, Gail; Post, Lori A.] Yale Univ, Sch Med, Dept Emergency Med, New Haven, CT 06520 USA.
[Goldstein, Amy B.] NIMH, Bethesda, MD 20892 USA.
[Denisco, Richard A.] NIDA, Bethesda, MD 20892 USA.
[Hingson, Ralph] NIAAA, Bethesda, MD USA.
[Heffelfinger, James D.] Ctr Dis Control & Prevent, Atlanta, GA USA.
RP D'Onofrio, G (reprint author), Yale Univ, Sch Med, Dept Emergency Med, New Haven, CT 06520 USA.
EM gail.donofrio@yale.edu
OI D'Onofrio, Gail/0000-0002-3833-1871
FU Agency for Healthcare Research and Quality; National Institute of Mental
Health; National Institute of Drug Abuse; National Institute of
Alcoholism and Alcohol Abuse; Substance Abuse and Mental Health
Administration Services
FX The authors thank the Society for Academic Emergency Medicine for
providing the forum for this presentation. In addition, we thank the
many agencies, institutes, and centers for funding this conference,
specifically the Agency for Healthcare Research and Quality, the
National Institute of Mental Health, the National Institute of Drug
Abuse, the National Institute of Alcoholism and Alcohol Abuse, and the
Substance Abuse and Mental Health Administration Services. Finally, the
authors thank Brian Biroscak for his help in the preparation of the
manuscript. The views expressed in this article are the opinions of the
authors and do not necessarily represent the views of the Department of
Health and Human Services or the United States government.
NR 43
TC 4
Z9 4
U1 1
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1069-6563
J9 ACAD EMERG MED
JI Acad. Emerg. Med.
PD NOV
PY 2009
VL 16
IS 11
BP 1065
EP 1071
DI 10.1111/j.1553-2712.2009.00555.x
PG 7
WC Emergency Medicine
SC Emergency Medicine
GA 515JC
UT WOS:000271465000007
PM 20053224
ER
PT J
AU Tang, WK
Li, DY
Esser, L
Xia, D
AF Tang, Wai-Kwan
Li, Dongyang
Esser, Lothar
Xia, Di
TI Purification, crystallization and preliminary X-ray diffraction analysis
of disease-related mutants of p97
SO ACTA CRYSTALLOGRAPHICA SECTION F-STRUCTURAL BIOLOGY AND CRYSTALLIZATION
COMMUNICATIONS
LA English
DT Article
ID BLUE NATIVE PAGE; FRONTOTEMPORAL DEMENTIA; AAA ATPASE; PROTEIN; P97/VCP;
BONE; MYOPATHY; FAMILY
AB The human type II Lambda Lambda Lambda+ protein p97 participates in various cellular activities, presumably through its involvement in the ubiquitin-proteasome degradation pathway. Mutations in p97 have been implicated in patients with inclusion-body myopathy associated with Paget's disease of the bone and frontotemporal dementia (IBMPFD). In this work, three mutant p97 N-D1 fragments, R86A, R95G and R155H, were crystallized in the presence of ATP gamma S with PEG 3350 as a main precipitant, yielding two different crystal forms. The R155H mutant crystal belonged to space group R3, with unit-cell parameters in the hexagonal setting of a = b = 134.2, c = 182.9 angstrom, and was merohedrally twinned, with an estimated twin fraction of 0.34. The crystals of the R86A and R95G mutants belonged to space group P1, with similar unit-cell parameters of a = 90.89, b = 102.6, c = 107.2 angstrom, alpha = 97.5, beta = 90.6, gamma = 91.5 degrees and a = 92.76, b = 103.7, c = 107.7 angstrom, alpha = 97.7, beta = 91.9, gamma = 89.7 degrees, respectively.
C1 [Tang, Wai-Kwan; Li, Dongyang; Esser, Lothar; Xia, Di] NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
RP Xia, D (reprint author), NCI, Cell Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM dixia@helix.nih.gov
RI Tang, Wai Kwan/A-6158-2012
FU NIH; National Cancer Institute; Center for Cancer Research
FX The authors wish to thank the staff members of the SER-CAT beamline
(ID-22) at Advanced Photon Source, Argonne National Laboratory for their
assistance in data collection. We also thank George Leiman for editorial
assistance. This research was supported by the Intramural Research
Program of the NIH, National Cancer Institute, Center for Cancer
Research.
NR 26
TC 1
Z9 1
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1744-3091
J9 ACTA CRYSTALLOGR F
JI Acta Crystallogr. F-Struct. Biol. Cryst. Commun.
PD NOV
PY 2009
VL 65
BP 1166
EP 1170
DI 10.1107/S174430910904055X
PG 5
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Biophysics; Crystallography
SC Biochemistry & Molecular Biology; Biophysics; Crystallography
GA 514US
UT WOS:000271421800022
PM 19923742
ER
PT J
AU Jegalian, AG
Facchetti, F
Jaffe, ES
AF Jegalian, Armin G.
Facchetti, Fabio
Jaffe, Elaine S.
TI Plasmacytoid Dendritic Cells Physiologic Roles and Pathologic States
SO ADVANCES IN ANATOMIC PATHOLOGY
LA English
DT Review
DE plasmacytoid dendritic cell; interferon-alpha; blastic plasmacytoid
dendritic cell neoplasm; CD4(+)/CD56(+) hematodermic neoplasm
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; INTERFERON-PRODUCING CELLS; CD4(+)/CD56(+)
HEMATODERMIC NEOPLASM; CHRONIC MYELOMONOCYTIC LEUKEMIA; LINEAGE-NEGATIVE
MALIGNANCIES; DRAINING LYMPH-NODES; TOLL-LIKE RECEPTORS; MURINE
BONE-MARROW; T-CELLS; I INTERFERON
AB Plasmacytoid dendritic cells (PDCs) have perplexed pathologists for decades, undergoing multiple adjustments in nomenclature as their lineage and functions have been characterized. Although PDCs account for less than 0.1% of peripheral blood mononuclear cells, they serve as a principal source of interferon-a and are also known as interferon-I producing cells (IPCs). Upon activation in vitro, they can differentiate into dendritic cells, and recent studies have substantiated a potential role in antigen presentation. Thus, PDCs may act as a link between innate and adaptive immunity. Normally found in small quantities in primary and secondary lymphoid organs, PDCs accumulate in a variety of inflammatory conditions, including Kikuchi-Fujimoto lymphadenopathy, hyaline-vascular Castleman disease, and autoimmune diseases, and in certain malignancies such as classical Hodgkin lymphoma and carcinomas. Demonstrating potential for neoplastic transformation reflective of varying stages of maturation, clonal proliferations range from PDC nodules most commonly associated with chronic myelomonocytic leukemia to the rare but highly aggressive malignancy now known as blastic plasmacytoid dendritic cell neoplasm (BPDCN). Formerly called blastic natural killer cell lymphoma or CD4(+)/CD56(+) hematodermic neoplasm, BPDCN, unlike natural killer cell lymphomas, is not associated with Epstein-Barr virus infection and is generally not curable with treatment regimens for non-Hodgkin lymphomas. In fact, this entity is no longer considered to be a lymphoma and instead represents a unique precursor hematopoietic neoplasm. Acute leukemia therapy regimens may lead to sustained clinical remission of BPDCN, with bone marrow transplantation in first complete remission potentially curative in adult patients.
C1 [Jegalian, Armin G.; Jaffe, Elaine S.] NCI, Pathol Lab, Hematopathol Sect, Bethesda, MD 20892 USA.
[Facchetti, Fabio] Univ Brescia, Dept Pathol, Brescia, Italy.
RP Jaffe, ES (reprint author), 10 Ctr Dr,MSC 1500,Bldg 10,Room 2B42, Bethesda, MD 20892 USA.
EM elainejaffe@nih.gov
RI Facchetti, Fabio/E-7190-2010
OI Facchetti, Fabio/0000-0003-4975-2388
NR 151
TC 52
Z9 66
U1 0
U2 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1072-4109
J9 ADV ANAT PATHOL
JI Adv. Anat. Pathol.
PD NOV
PY 2009
VL 16
IS 6
BP 392
EP 404
PG 13
WC Pathology
SC Pathology
GA 515OU
UT WOS:000271482500003
PM 19851130
ER
PT J
AU Liu, CL
Yang, Y
Gange, SJ
Weber, K
Sharp, GB
Wilson, TE
Levine, A
Robison, E
Goparaju, L
Ganhdi, M
Merenstein, D
AF Liu, Chenglong
Yang, Yang
Gange, Stephen J.
Weber, Kathleen
Sharp, Gerald B.
Wilson, Tracey E.
Levine, Alexandra
Robison, Esther
Goparaju, Lakshmi
Ganhdi, Monica
Merenstein, Dan
TI Disclosure of Complementary and Alternative Medicine Use to Health Care
Providers among HIV-Infected Women
SO AIDS PATIENT CARE AND STDS
LA English
DT Article
ID ST JOHNS WORT; ANTIRETROVIRAL THERAPY; ADHERENCE; SATISFACTION; ADULTS;
AIDS; MEN
AB To determine prevalence and predictors of complementary and alternative medicine (CAM) use disclosure to health care providers and whether CAM use disclosure is associated with highly active antiretroviral therapy (HAART) adherence among HIV-infected women, we analyzed longitudinal data collected between October 1994 and March 2002 from HIV-infected CAM-using women enrolled in the Women's Interagency HIV Study. Repeated measures Poisson regression models were constructed to evaluate associations of selected predictors with CAM use disclosure and association between CAM use disclosure and HAART adherence. A total of 1377 HIV-infected women reported CAM use during study follow-up and contributed a total of 4689 CAM-using person visits. The overall prevalence of CAM use disclosure to health care providers was 36% across study visits. Women over 45 years old, with a college education, or with health insurance coverage were more likely to disclose their CAM use to health care providers, whereas women identified as non-Hispanic Black or other ethnicities were less likely to communicate their CAM usage. More health care provider visits, more CAM domains used, and higher health care satisfaction scores had significant relationships with increased levels of CAM use disclosure. Restricting analysis to use of herbal or nonherbal medications only, similar results were obtained. Compared to other CAM domains, mind-body practice had the lowest prevalence of CAM use disclosure. Additionally, CAM use disclosure was significantly associated with higher HAART adherence. From this study, we showed that a high percentage of HIV-infected women did not discuss their CAM use with health care providers. Interventions targeted towards both physicians and patients may enhance communication of CAM use, avoid potential adverse events and drug interactions, and enhance HAART adherence.
C1 [Liu, Chenglong; Goparaju, Lakshmi] Georgetown Univ, Dept Med, Washington, DC 20007 USA.
[Yang, Yang] Georgetown Univ, Dept Biostat Bioinformat & Biomath, Washington, DC 20007 USA.
[Gange, Stephen J.] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
[Weber, Kathleen] John H Stroger Hosp Cook Cty, Chicago, IL USA.
[Sharp, Gerald B.] NIAID, Epidemiol Branch, Basic Sci Program, NIH, Bethesda, MD 20892 USA.
[Wilson, Tracey E.] SUNY Hlth Sci Ctr, Dept Prevent Med & Community Hlth, Brooklyn, NY 11203 USA.
[Levine, Alexandra] City Hope Natl Med Ctr, Duarte, CA 91010 USA.
[Robison, Esther] Montefiore Med Ctr, Bronx, NY 10467 USA.
[Ganhdi, Monica] Univ Calif San Francisco, Dept Med, San Francisco, CA USA.
[Merenstein, Dan] Georgetown Univ, Dept Family Med, Med Ctr, Washington, DC 20007 USA.
RP Liu, CL (reprint author), Georgetown Univ, Dept Med, 2233 Wisconsin Ave NW,Suite 214, Washington, DC 20007 USA.
EM cl278@georgetown.edu
OI Gange, Stephen/0000-0001-7842-512X
FU National Cancer Institute; National Institute on Drug Abuse
[UO1-AI-35004, UO1-AI-31834, UO1-AI-34994, UO1-AI-34989, UO1-AI-34993,
UO1-AI-42590]; National Institute of Child Health and Human Development
[UO1-HD-32632]; National Center for Research Resources [MO1-RR-00071,
MO1-RR-00079, MO1-RR-00083]
FX Data in this manuscript were collected by the Women's Interagency HIV
Study (WIHS) Collaborative Study Group with centers (Principal
Investigators) at New York City/Bronx Consortium (Kathryn Anastos);
Brooklyn, New York (Howard Minkoff); Washington, D.C. Metropolitan
Consortium (Mary Young); The Connie Wofsy Study Consortium of Northern
California (Ruth Greenblatt); Los Angeles County/Southern California
Consortium (Alexandra Levine); Chicago Consortium (Mardge Cohen); Data
Coordinating Center (Stephen Gange). WIHS is funded by the National
Institute of Allergy and Infectious Diseases with supplemental funding
from the National Cancer Institute and the National Institute on Drug
Abuse (UO1-AI-35004, UO1-AI-31834, UO1-AI-34994, UO1-AI-34989,
UO1-AI-34993, and UO1-AI-42590). Funding is also provided by the
National Institute of Child Health and Human Development (UO1-HD-32632)
and the National Center for Research Resources (MO1-RR-00071,
MO1-RR-00079, MO1-RR-00083).
NR 33
TC 19
Z9 21
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1087-2914
J9 AIDS PATIENT CARE ST
JI Aids Patient Care STDS
PD NOV
PY 2009
VL 23
IS 11
BP 965
EP 971
DI 10.1089/apc.2009.0134
PG 7
WC Public, Environmental & Occupational Health; Infectious Diseases
SC Public, Environmental & Occupational Health; Infectious Diseases
GA 522KD
UT WOS:000271995700008
PM 19821723
ER
PT J
AU Ruscetti, EF
Petrow-Sadowski, C
Janik, J
Huang, Y
Bertolette, D
Morris, J
Waldmann, T
Jones, K
AF Ruscetti, E. F.
Petrow-Sadowski, C.
Janik, J.
Huang, Y.
Bertolette, D.
Morris, J.
Waldmann, T.
Jones, K.
TI In Vivo and in Vitro HTLV-1-Infection of Plasmacytoid Dendritic Cells:
Pathogenic Considerations
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Ruscetti, E. F.; Huang, Y.; Bertolette, D.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
[Petrow-Sadowski, C.; Jones, K.] SAIC Frederick, Basic Sci Program, Frederick, MD USA.
[Janik, J.; Morris, J.; Waldmann, T.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1202
EP 1202
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200028
ER
PT J
AU Akahata, Y
Matsuura, E
Jacobson, S
Oh, U
AF Akahata, Y.
Matsuura, E.
Jacobson, S.
Oh, U.
TI High Expression of CD244 and SAP Regulated CD8+T Cell Responses of
Patients with HTLV-I Associated Neurologic Disease
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Akahata, Y.; Matsuura, E.; Jacobson, S.; Oh, U.] NINDS, NIH, Bethesda, MD 20892 USA.
RI MATSUURA, EIJI/E-1231-2013
OI MATSUURA, EIJI/0000-0001-8215-8853
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1203
EP 1204
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200032
ER
PT J
AU Gordon, S
Weissman, A
Cecchinato, V
Zaffiri, L
Andresen, V
Jones, K
Ferrari, MG
Chung, HK
Ruscetti, F
Franchini, G
AF Gordon, S.
Weissman, A.
Cecchinato, V
Zaffiri, L.
Andresen, V
Jones, K.
Ferrari, M. G.
Chung, H. K.
Ruscetti, F.
Franchini, G.
TI HTLV-II Establishes a Persistent Infection in Rhesus Macaques and Does
Not Exacerbate SIV Infection
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 NCI, Anim Models & Retroviral Vaccines Sect, NIH, Bethesda, MD 20892 USA.
NCI, Basic Res Program, Saic Frederick Inc, NIH, Frederick, MD 21701 USA.
Adv Biosci Labs Inc, Kensington, MD 20895 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1212
EP 1212
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200054
ER
PT J
AU Akahata, Y
Matsuura, E
Jacobson, S
Oh, U
AF Akahata, Y.
Matsuura, E.
Jacobson, S.
Oh, U.
TI Minocycline Modulates Antigen-Specific CTL Activity through Inactivation
of Mononuclear Phagocytes in Patients with HAM/TSP
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Akahata, Y.; Matsuura, E.; Jacobson, S.; Oh, U.] Natl Inst Neurol Disorders & Stroke, NIH, Bethesda, MD USA.
RI MATSUURA, EIJI/E-1231-2013
OI MATSUURA, EIJI/0000-0001-8215-8853
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1214
EP 1215
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200060
ER
PT J
AU Oh, U
Akahata, Y
Turner, R
Graham, J
Waldmann, T
Jacobson, S
AF Oh, U.
Akahata, Y.
Turner, R.
Graham, J.
Waldmann, T.
Jacobson, S.
TI The Use of Humanized-MiK-????1, a Monoclonal Antibody Against CD122, In
HTLV-I-Associated Myelopathy Tropical Spastic Paraparesis (HAM/TSP)
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Oh, U.; Akahata, Y.; Turner, R.; Graham, J.; Jacobson, S.] NINDS, Viral Immunol Sect, NIH, Bethesda, MD 20892 USA.
[Waldmann, T.] NCI, Metab Branch, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1216
EP 1216
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200063
ER
PT J
AU Matsuura, E
Yao, K
Jacobson, S
Oh, U
Akahata, Y
Tanaka, Y
AF Matsuura, E.
Yao, K.
Jacobson, S.
Oh, U.
Akahata, Y.
Tanaka, Y.
TI Interaction of Cytotoxic T Lymphocytes and Monocytes: Role in HTLV-I
Associated Neurologic Disease
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Matsuura, E.; Yao, K.; Jacobson, S.; Oh, U.; Akahata, Y.; Tanaka, Y.] NINDS, NIH, Bethesda, MD USA.
RI MATSUURA, EIJI/E-1231-2013
OI MATSUURA, EIJI/0000-0001-8215-8853
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1218
EP 1218
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200068
ER
PT J
AU Lambert, S
Bouttier, M
Vassy, R
Seigneuret, M
Petrow-Sadowski, C
Janvier, S
Heveker, N
Ruscetti, FW
Perret, G
Jones, KS
Pique, C
AF Lambert, S.
Bouttier, M.
Vassy, R.
Seigneuret, M.
Petrow-Sadowski, C.
Janvier, S.
Heveker, N.
Ruscetti, F. W.
Perret, G.
Jones, K. S.
Pique, C.
TI Molecular Mimicry between the HTLV-1 SU and VEGF(165) Governs HTLV-1
Entry through Heparan Sulfate Proteoglycans and Neuropilin 1
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Lambert, S.; Bouttier, M.; Seigneuret, M.; Pique, C.] Univ Paris 05, CNRS, INSERM, UMR 8104,U567, F-75014 Paris, France.
[Vassy, R.; Perret, G.] Univ Paris 13, UMR 7033, Bobigny, France.
[Petrow-Sadowski, C.; Jones, K. S.] NCI, Basic Sci Program, SAIC Frederick Inc, Frederick, MD 21701 USA.
[Janvier, S.; Heveker, N.] Univ Montreal, Dept Biochim, Quebec City, PQ, Canada.
[Janvier, S.; Heveker, N.] Hop St Justine, Ctr Rech 6737, Quebec City, PQ, Canada.
[Ruscetti, F. W.] NCI, Lab Expt Immunol, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21701 USA.
RI PERRET, gerard/A-7379-2008; Heveker, Nikolaus/G-5306-2012
OI PERRET, gerard/0000-0003-0645-3337;
NR 0
TC 0
Z9 0
U1 0
U2 2
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1224
EP 1225
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200084
ER
PT J
AU Fukumoto, R
Andresen, V
Bialuk, I
Cecchinato, V
Walser, JC
Valeri, VW
Nauroth, JM
Gessain, A
Nicot, C
Franchini, G
AF Fukumoto, R.
Andresen, V
Bialuk, I
Cecchinato, V
Walser, J. -C
Valeri, V. W.
Nauroth, J. M.
Gessain, A.
Nicot, C.
Franchini, G.
TI In Vivo Genetic Mutations Define Predominant Functions of the Human
T-Cell Leukemia/Lymphoma Virus P12I Protein
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Fukumoto, R.; Andresen, V; Bialuk, I; Cecchinato, V; Valeri, V. W.; Nauroth, J. M.; Franchini, G.] Natl Canc Inst, Anim Models & Retroviral Vaccines Sect, Bethesda, MD USA.
[Walser, J. -C] NIDDK, Lab Mol & Cellular Biol, Bethesda, MD USA.
[Gessain, A.] Inst Pasteur, Unite DepideMol & Physiopathol Virus OncogeNes, Dept Virol, Paris, France.
[Nicot, C.] Univ Kansas, Med Ctr, Dept Microbiol Mol Genet & Immunol, Kansas City, KS 66103 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1226
EP 1226
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200088
ER
PT J
AU Andresen, V
Nicot, C
Franchini, G
Fukumoto, R
Parks, RW
Datta, US
Cecchinato, V
AF Andresen, V
Nicot, C.
Franchini, G.
Fukumoto, R.
Parks, R. W.
Datta, U. S.
Cecchinato, V
TI The HTLV-1 P13 II Protein Interacts with Tax, Inhibits Tax Dependent
Transcription and Decreases Viral Replication
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Andresen, V; Nicot, C.; Franchini, G.; Fukumoto, R.; Parks, R. W.; Datta, U. S.; Cecchinato, V] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1227
EP 1227
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200090
ER
PT J
AU Tosi, G
Badarou, L
Andresen, V
Franchini, G
Accolla, RS
AF Tosi, G.
Badarou, L.
Andresen, V
Franchini, G.
Accolla, R. S.
TI CIITA, the Master Regulator of MHC Class II Gene Transcription, Targets
the Viral Transactivator Tax-1 to Inhibit HTLV-I Viral Replication and
NFKB Activation
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Tosi, G.; Badarou, L.; Accolla, R. S.] Univ Insubria, Dept Clin & Biol Sci, Varese, Italy.
[Andresen, V; Franchini, G.] NCI, Anim Models & Retroviral Vaccines Sect, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1245
EP 1245
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200131
ER
PT J
AU Prooyen, NV
Franchini, G
Gold, H
Bialuk, I
Fukumoto, R
Andresen, V
AF Prooyen, N., V
Franchini, G.
Gold, H.
Bialuk, I
Fukumoto, R.
Andresen, V
TI Effect of HTLV-1 ORF I Protein Products on the Immunological Synapse and
Actin Remodeling
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Prooyen, N., V; Franchini, G.; Gold, H.; Bialuk, I; Fukumoto, R.; Andresen, V] NCI, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1246
EP 1247
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200135
ER
PT J
AU Janik, JE
O'mahony, D
Wharfe, G
Morris, JC
Urquhart, N
Seam, P
Fioravanti, S
Waldmann, TA
AF Janik, J. E.
O'mahony, D.
Wharfe, G.
Morris, J. C.
Urquhart, N.
Seam, P.
Fioravanti, S.
Waldmann, T. A.
TI Phase II Trial of Denileukin Diftitox in Adult T-Cell Leukemia/Lymphoma
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Janik, J. E.; O'mahony, D.; Wharfe, G.; Morris, J. C.; Urquhart, N.; Seam, P.; Fioravanti, S.; Waldmann, T. A.] NCI, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1252
EP 1253
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200150
ER
PT J
AU Evangelou, I
McFarland, H
Jacobson, S
Oh, U
AF Evangelou, I
McFarland, H.
Jacobson, S.
Oh, U.
TI Detection and Quantification of Cervical and Thoracic Spinal Cord
Atrophy of HAM/TSP Patients Using a 3D Semi-Automatic Technique
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Evangelou, I; McFarland, H.; Jacobson, S.; Oh, U.] NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1270
EP 1270
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200191
ER
PT J
AU Jones, KS
Andresen, V
Valeri, VW
Petrow-Sadowski, C
Bertolette, D
Franchini, G
Ruscetti, F
AF Jones, K. S.
Andresen, V.
Valeri, V. W.
Petrow-Sadowski, C.
Bertolette, D.
Franchini, G.
Ruscetti, F.
TI P30II is Required for the Persistent Infection of Dendritic Cells by
HTLV-1
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Jones, K. S.; Petrow-Sadowski, C.] SAIC Frederick, Basic Sci Program, Frederick, MD USA.
[Andresen, V.; Valeri, V. W.; Franchini, G.] NCI, Anim Models & Retroviral Vacc Sect, NIH, Bethesda, MD 20892 USA.
[Bertolette, D.; Ruscetti, F.] NCI, Canc & Inflammat Program, Frederick, MD 21701 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1286
EP 1286
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200229
ER
PT J
AU Bialuk, I
Gessain, A
Castro, BG
Franchini, G
Walser, JC
Graham, J
Alcantara, LC
Fukumoto, R
Jacobson, S
Andresen, V
AF Bialuk, I.
Gessain, A.
Castro, B. G.
Franchini, G.
Walser, J. C.
Graham, J.
Alcantara, L. C.
Fukumoto, R.
Jacobson, S.
Andresen, V.
TI The 8 kDa Form Encoded by the HTLV-I ORF-I is Associated with Low
Provirus Levels in a Subset of HTLV-I Infected Individuals
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 NCI, NIH, Bethesda, MD 20892 USA.
Med Univ Bialystok, Bialystok, Poland.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1297
EP 1297
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200258
ER
PT J
AU Graham, J
Jacobson, S
Oh, U
Akahata, Y
AF Graham, J.
Jacobson, S.
Oh, U.
Akahata, Y.
TI The Effect of the Histone Deacetylase Inhibitor Valproic Acid on Tax
Expression, Spontaneous Degranulation and Cell Survival in HTLV-I
Infected Peripheral Blood Mononuclear Cells
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Graham, J.; Jacobson, S.; Oh, U.; Akahata, Y.] NIH, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1297
EP 1298
PG 2
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200259
ER
PT J
AU Rende, F
Cavallari, I
Silic-Benussi, M
Corradin, A
Toulza, F
Valeri, VW
Chieco-Bianchi, L
D'Agostino, DM
Jacobson, S
Franchini, G
Bangham, CRM
Ciminale, V
AF Rende, F.
Cavallari, I.
Silic-Benussi, M.
Corradin, A.
Toulza, F.
Valeri, V. W.
Chieco-Bianchi, L.
D'Agostino, D. M.
Jacobson, S.
Franchini, G.
Bangham, C. R. M.
Ciminale, V.
TI Temporal Regulation of HTLV-1 Gene Expression
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 [Rende, F.; Cavallari, I.; Silic-Benussi, M.; Chieco-Bianchi, L.; D'Agostino, D. M.; Ciminale, V.] Univ Padua, Dept Oncol & Surg Sci, I-35100 Padua, Italy.
[Corradin, A.] Univ Padua, Dept Informat Engn, I-35100 Padua, Italy.
[Toulza, F.; Bangham, C. R. M.] Univ London Imperial Coll Sci Technol & Med, Dept Immunol, London, England.
[Jacobson, S.] NINDS, Viral Immunol Sect, Neuroimmunol Branch, NIH, Bethesda, MD 20892 USA.
[Franchini, G.] NCI, Anim Models & Retroviral Vaccines Sect, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1297
EP 1297
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200257
ER
PT J
AU Mahieux, R
Gessain, A
Sadowski, CP
Bertolette, D
Ruscetti, F
Jones, K
Afonso, P
Chevalier, S
Huang, Y
AF Mahieux, R.
Gessain, A.
Sadowski, C. P.
Bertolette, D.
Ruscetti, F.
Jones, K.
Afonso, P.
Chevalier, S.
Huang, Y.
TI The Receptor Complex Associated with HTLV-3 ENV-Mediated Binding and
Entry is Distinct from, but Overlaps with, the Receptor Complexes of
HTLV-1 and HTLV-2
SO AIDS RESEARCH AND HUMAN RETROVIRUSES
LA English
DT Meeting Abstract
CT 14th International Conference on Human Retrovirology HTLV and Related
Retroviruses
CY JUL 01-04, 2009
CL Salvador, BRAZIL
C1 Saic Frederick Inc, Natick, MA USA.
NCI Frederick, Frederick, MD USA.
Inst Pasteur, Paris, France.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 0889-2229
J9 AIDS RES HUM RETROV
JI Aids Res. Hum. Retrovir.
PD NOV
PY 2009
VL 25
IS 11
BP 1298
EP 1298
PG 1
WC Immunology; Infectious Diseases; Virology
SC Immunology; Infectious Diseases; Virology
GA 524ZF
UT WOS:000272182200260
ER
PT J
AU Ciccocioppo, R
Gehlert, DR
Ryabinin, A
Kaur, S
Cippitelli, A
Thorsell, A
Le, AD
Hipskind, PA
Hamdouchi, C
Lu, JL
Hembre, EJ
Cramer, J
Song, M
McKinzie, D
Morin, M
Economidou, D
Stopponi, S
Cannella, N
Braconi, S
Kallupi, M
de Guglielmo, G
Massi, M
George, DT
Gilman, J
Hersh, J
Tauscher, JT
Hunt, SP
Hommer, D
Heilig, M
AF Ciccocioppo, Roberto
Gehlert, Donald R.
Ryabinin, Andrey
Kaur, Simranjit
Cippitelli, Andrea
Thorsell, Annika
Le, Anh D.
Hipskind, Philip A.
Hamdouchi, Chafiq
Lu, Jianliang
Hembre, Erik J.
Cramer, Jeffrey
Song, Min
McKinzie, David
Morin, Michelle
Economidou, Daina
Stopponi, Serena
Cannella, Nazzareno
Braconi, Simone
Kallupi, Marsida
de Guglielmo, Giordano
Massi, Maurizio
George, David T.
Gilman, Jody
Hersh, Jacqueline
Tauscher, Johannes T.
Hunt, Stephen P.
Hommer, Daniel
Heilig, Markus
TI Stress-related neuropeptides and alcoholism: CRH, NPY, and beyond
SO ALCOHOL
LA English
DT Article; Proceedings Paper
CT Conference on Alcoholism and Stress - A Framework for Future Treatment
Strategies
CY MAY 06-08, 2008
CL Volterra, ITALY
DE CRH; Nociceptin/orphanin FQ; Neurokinins; Substance P; Neuropeptide Y;
Urocortin
ID CORTICOTROPIN-RELEASING-FACTOR; EDINGER-WESTPHAL NUCLEUS;
PITUITARY-ADRENAL AXIS; NOCICEPTIN/ORPHANIN FQ; SEEKING BEHAVIOR;
LATERAL SEPTUM; UROCORTIN EXPRESSION; ETHANOL-CONSUMPTION; INDUCED
HYPOTHERMIA; RECEPTORS MEDIATE
AB This article summarizes the proceedings of a symposium held at the conference on "Alcoholism and Stress: A Framework for Future Treatment Strategies" in Volterra, Italy, May 6-9, 2008. Chaired by Markus Heilig and Roberto Ciccocioppo, this symposium offered a forum for the presentation of recent data linking neuropetidergic neurotransmission to the regulation of different alcohol-related behaviors in animals and in humans. Dr. Donald Gehlert described the development of a new corticotrophin-releasing factor receptor I antagonist and showed its efficacy in reducing alcohol consumption and stress-induced relapse in different animal models of alcohol abuse. Dr. Andrey Ryabinin reviewed recent findings in his laboratory, indicating a role of the urocortin I receptor system in the regulation of alcohol intake. Dr. Annika Thorsell showed data supporting the significance of the neuropeptide Y receptor system in the modulation of behaviors associated with a history of ethanol intoxication. Dr. Roberto Ciccocioppo focused his presentation on the nociceptin/orphanin FQ (N/OFQ) receptors as treatment targets for alcoholism. Finally, Dr. Markus Heilig showed recent preclinical and clinical evidence suggesting that neurokinin I antagonism may represent a promising new treatment for alcoholism. Collectively, these investigators highlighted the significance of neuropeptidergic neurotransmission in the regulation of neurobiological mechanisms of alcohol addiction. Data also revealed the importance of these systems as treatment targets for the development of new medication for alcoholism. (C) 2009 Elsevier Inc. All rights reserved.
C1 [Ciccocioppo, Roberto; Cippitelli, Andrea; Economidou, Daina; Stopponi, Serena; Cannella, Nazzareno; Braconi, Simone; Kallupi, Marsida; de Guglielmo, Giordano; Massi, Maurizio] Univ Camerino, Dept Expt Med & Publ Hlth, I-62032 Camerino, Macerata, Italy.
[Gehlert, Donald R.; Hipskind, Philip A.; Hamdouchi, Chafiq; Lu, Jianliang; Hembre, Erik J.; Cramer, Jeffrey; Song, Min; McKinzie, David; Morin, Michelle; Tauscher, Johannes T.] Lilly Res Labs, Indianapolis, IN 46285 USA.
[Ryabinin, Andrey; Kaur, Simranjit] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97239 USA.
[Cippitelli, Andrea; Thorsell, Annika; George, David T.; Gilman, Jody; Hersh, Jacqueline; Hommer, Daniel; Heilig, Markus] NIAAA, Lab Clin & Translat Studies, NIH, Bethesda, MD 20892 USA.
[Le, Anh D.] Univ Toronto, Ctr Addict & Mental Hlth, Toronto, ON M5S 2S1, Canada.
[Hunt, Stephen P.] UCL, Dept Anat & Dev Biol, London WC1E 6BT, England.
RP Ciccocioppo, R (reprint author), Univ Camerino, Dept Expt Med & Publ Hlth, Via Madonna Carceri, I-62032 Camerino, Macerata, Italy.
EM roberto.ciccocioppo@unicam.it
RI Tauscher, Johannes/M-5976-2016;
OI Heilig, Markus/0000-0003-2706-2482; Kallupi,
Marsida/0000-0002-8688-709X; Cannella, Nazzareno/0000-0002-2891-8679;
Thorsell, Annika/0000-0003-3535-3845
FU NIAAA NIH HHS [AA016647, AA013738, AA01435, R01 AA013108, R01 AA013738,
R01 AA013738-05, R01 AA014351, R01 AA014351-05, U01 AA016647, U01
AA016647-04]
NR 73
TC 32
Z9 32
U1 1
U2 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-8329
J9 ALCOHOL
JI Alcohol
PD NOV
PY 2009
VL 43
IS 7
BP 491
EP 498
DI 10.1016/j.alcohol.2009.08.003
PG 8
WC Substance Abuse; Pharmacology & Pharmacy; Toxicology
SC Substance Abuse; Pharmacology & Pharmacy; Toxicology
GA 526SU
UT WOS:000272314700002
PM 19913192
ER
PT J
AU Witkiewitz, K
Holmes, A
Ray, LA
Murphy, JG
Richardson, HN
Chen, YC
McDevitt-Murphy, ME
Cruz, MT
Roberto, M
AF Witkiewitz, Katie
Holmes, Andrew
Ray, Lara A.
Murphy, James G.
Richardson, Heather N.
Chen, Yi-Chyan
McDevitt-Murphy, Meghan E.
Cruz, Maureen T.
Roberto, Marisa
TI Young Investigator Award Symposium
SO ALCOHOL
LA English
DT Article; Proceedings Paper
CT Conference on Alcoholism and Stress - A Framework for Future Treatment
Strategies
CY MAY 06-08, 2008
CL Volterra, ITALY
DE Alcohol; Stress; Human; Mouse; Rat; Glutamate; Naltrexone; HPA axis
ID CORTICOTROPIN-RELEASING-FACTOR; PITUITARY-ADRENAL AXIS;
ETHANOL-DEPENDENT RATS; POSTTRAUMATIC-STRESS-DISORDER; ANXIETY-LIKE
BEHAVIOR; CHRONIC SWIM STRESS; NMDA RECEPTOR NR2A; ALCOHOL DEPENDENCE;
ADRENOCORTICAL AXIS; NORMAL VOLUNTEERS
AB This article highlights the research presented at the inaugural meeting of Alcoholism and Stress: A Framework for future Treatment Strategies. This meeting was held on May 6-8, 2008 in Volterra, Italy. It is an international meeting dedicated to developing preventive strategies and pharmacotherapeutic remedies for stress- and alcohol-related disorders. For the first time, the National Institute on Alcohol Abuse and Alcoholism (NIAAA) conferred a Young Investigator Award to promote the work of young researchers and highlight their outstanding achievements in the fields of addiction medicine and stress disorders. The awardees were Dr. Katie Witkiewitz (University of Washington), Dr. Andrew Holmes (NIAAA), Dr. Lara A. Ray (Brown University), Dr. James Murphy (University of Memphis), and Dr. Heather Richardson (The Scripps Research Institute). The symposium was chaired by Drs. Fulton Crews and Antonio Noronha. (C) 2009 Published by Elsevier Inc.
C1 [Richardson, Heather N.; Cruz, Maureen T.; Roberto, Marisa] Scripps Res Inst, Comm Neurobiol Addict Disorders, La Jolla, CA 92037 USA.
[Witkiewitz, Katie] Univ Washington, Inst Alcohol & Drug Abuse, Seattle, WA 98105 USA.
[Holmes, Andrew] NIAAA, Sect Behav Sci & Genet, Lab Integrat Neurosci, NIH, Rockville, MD 20852 USA.
[Ray, Lara A.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA.
[Murphy, James G.; McDevitt-Murphy, Meghan E.] Univ Memphis, Dept Psychol, Memphis, TN 38152 USA.
[Richardson, Heather N.] Univ Massachusetts, Dept Psychol Neurosci, Amherst, MA 01003 USA.
[Chen, Yi-Chyan] Triserv Gen Hosp, Natl Def Med Ctr, Dept Psychiat, Taipei, Taiwan.
RP Roberto, M (reprint author), Scripps Res Inst, Comm Neurobiol Addict Disorders, La Jolla, CA 92037 USA.
OI Richardson, Heather/0000-0001-7659-1212
FU NIAAA NIH HHS [P60 AA006420]
NR 99
TC 0
Z9 0
U1 2
U2 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0741-8329
J9 ALCOHOL
JI Alcohol
PD NOV
PY 2009
VL 43
IS 7
BP 499
EP 508
DI 10.1016/j.alcohol.2009.06.004
PG 10
WC Substance Abuse; Pharmacology & Pharmacy; Toxicology
SC Substance Abuse; Pharmacology & Pharmacy; Toxicology
GA 526SU
UT WOS:000272314700003
PM 19913193
ER
PT J
AU Mason, BJ
Shaham, Y
Weiss, F
Le, AD
AF Mason, Barbara J.
Shaham, Yavin
Weiss, Friedbert
Le, A. D.
TI Stress, alcohol craving, and relapse risk: mechanisms and viable
treatment targets
SO ALCOHOL
LA English
DT Article; Proceedings Paper
CT Conference on Alcoholism and Stress - A Framework for Future Treatment
Strategies
CY MAY 06-08, 2008
CL Volterra, ITALY
ID CORTICOTROPIN-RELEASING-FACTOR; YOHIMBINE-INDUCED INCREASES; SEEKING;
RATS; RECEPTORS; AGONIST; REINSTATEMENT; ABSTINENCE; GLUTAMATE; LY379268
C1 [Mason, Barbara J.; Weiss, Friedbert] Scripps Res Inst, La Jolla, CA 92037 USA.
[Shaham, Yavin] NIDA, Baltimore, MD USA.
[Le, A. D.] Univ Toronto, Toronto, ON, Canada.
RP Mason, BJ (reprint author), Scripps Res Inst, 10550 N Torrey Pines Rd, La Jolla, CA 92037 USA.
EM mason@scripps.edu
RI shaham, yavin/G-1306-2014; Mason, Barbara/P-6604-2016
FU NIAAA NIH HHS [R01 AA010531-13, R01 AA010531, R01 AA012602, R01
AA012602-09, R01 AA013108, R01AA012602, R37 AA014028, R37 AA014028-06,
R37AA014028]; NIDA NIH HHS [R37 DA007348, R37 DA007348-14]
NR 17
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 0741-8329
J9 ALCOHOL
JI Alcohol
PD NOV
PY 2009
VL 43
IS 7
SI SI
BP 541
EP 543
DI 10.1016/j.alcohol.2009.09.024
PG 3
WC Substance Abuse; Pharmacology & Pharmacy; Toxicology
SC Substance Abuse; Pharmacology & Pharmacy; Toxicology
GA 526SU
UT WOS:000272314700007
PM 19913197
ER
PT J
AU Levine, M
Eck, P
AF Levine, Mark
Eck, Peter
TI Vitamin C: working on the x-axis
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Editorial Material
ID ASCORBIC-ACID
C1 [Levine, Mark] NIDDK, Mol & Clin Nutr Sect, Digest Dis Branch, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
[Eck, Peter] Univ Manitoba, Dept Human Nutr Sci, Richardson Ctr Funct Foods & Nutraceut, Winnipeg, MB, Canada.
RP Levine, M (reprint author), NIDDK, Mol & Clin Nutr Sect, Digest Dis Branch, Intramural Res Program,NIH, Bldg 10,Room 4D52,MSC 1372,10 Ctr Dr, Bethesda, MD 20892 USA.
EM mark.levine@nih.gov
OI Eck, Peter/0000-0003-2371-9774
NR 10
TC 10
Z9 10
U1 0
U2 0
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV 1
PY 2009
VL 90
IS 5
BP 1121
EP 1123
DI 10.3945/ajcn.2009.28687
PG 3
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 508TO
UT WOS:000270959500002
PM 19812178
ER
PT J
AU Savastano, DM
Gorbach, AM
Eden, HS
Brady, SM
Reynolds, JC
Yanovski, JA
AF Savastano, David M.
Gorbach, Alexander M.
Eden, Henry S.
Brady, Sheila M.
Reynolds, James C.
Yanovski, Jack A.
TI Adiposity and human regional body temperature
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID RESTING ENERGY-EXPENDITURE; ARTERIOVENOUS ANASTOMOSES; SUBCUTANEOUS FAT;
METABOLIC-RATE; BLOOD-FLOW; SKIN; TISSUE; OBESE; VESSELS; SYSTEM
AB Background: Human obesity is associated with increased heat production; however, subcutaneous adipose tissue provides an insulating layer that impedes heat loss. To maintain normothermia, therefore, obese individuals must increase their heat dissipation.
Objective: The objective was to test the hypothesis that temperature in a heat-dissipating region of the hand is elevated in obese adults.
Design: Obese [body mass index (in kg/m(2)) >= 30] and normal-weight (NW; body mass index = 18-25) adults were studied under thermoneutral conditions at rest. Core body temperature was measured by using ingested telemetric capsules. The temperatures of the third fingernail bed of the right hand and of abdominal skin from an area 1.5 cm inferior to the umbilicus were determined by using infrared thermography. Abdominal skin temperatures were also measured via adhesive thermistors that were placed over a prominent skin-surface blood vessel and over an adjacent nonvessel location. The groups were compared by analysis of covariance with age, sex, race, and room temperature as covariates.
Results: Core temperature did not differ significantly between the 23 obese and 13 NW participants (P = 0.74). However, infrared thermography-measured fingernail-bed temperature was significantly higher in obese subjects than in NW subjects (33.9 6 +/- 0.7 degrees C compared with 28.6 +/- 0.9 degrees C; P < 0.001). Conversely, infrared thermography-measured abdominal skin temperature was significantly lower in obese subjects than in NW subjects (31.8 +/- 0.2 degrees C compared with 32.8 +/- 0.3 degrees C; P = 0.02). Nonvessel abdominal skin temperatures measured by thermistors were also lower in obese subjects (P = 0.04).
Conclusions: Greater subcutaneous abdominal adipose tissue in obese adults may provide a significant insulating layer that blunts abdominal heat transfer. Augmented heat release from the hands may offset heat retention in areas of the body with greater adiposity, thereby helping to maintain normothermia in obesity. This trial was registered at clinicaltrials.gov as NCT00266500. Am J Clin Nutr 2009; 90: 1124-31.
C1 [Savastano, David M.; Brady, Sheila M.; Yanovski, Jack A.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Growth & Obes, Program Dev Endocrinol & Genet, Bethesda, MD 20892 USA.
[Gorbach, Alexander M.; Eden, Henry S.] Natl Inst Biomed Imaging & Bioengn, Lab Bioengn & Phys Sci, Bethesda, MD USA.
[Reynolds, James C.] NIH, Dept Diagnost Radiol, Hatfield Clin Res Ctr, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Yanovski, JA (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth, Unit Growth & Obes, Program Dev Endocrinol & Genet, NIH,Hatfield Clin Res Ctr, 10 Ctr Dr,Room 1-3330,MSC 1103, Bethesda, MD 20892 USA.
EM jy15i@nih.gov
OI Yanovski, Jack/0000-0001-8542-1637
FU Intramural NIH HHS [Z01 EB000032-01]
NR 41
TC 54
Z9 58
U1 0
U2 20
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV 1
PY 2009
VL 90
IS 5
BP 1124
EP 1131
DI 10.3945/ajcn.2009.27567
PG 8
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 508TO
UT WOS:000270959500003
PM 19740972
ER
PT J
AU Manini, TM
Everhart, JE
Anton, SD
Schoeller, DA
Cummings, SR
Mackey, DC
Delmonico, MJ
Bauer, DC
Simonsick, EM
Colbert, LH
Visser, M
Tylavsky, F
Newman, AB
Harris, TB
AF Manini, Todd M.
Everhart, James E.
Anton, Stephen D.
Schoeller, Dale A.
Cummings, Steve R.
Mackey, Dawn C.
Delmonico, Matthew J.
Bauer, Douglas C.
Simonsick, Eleanor M.
Colbert, Lisa H.
Visser, Marjolein
Tylavsky, Frances
Newman, Anne B.
Harris, Tamara B.
CA Hlth Aging & Body Composition Stud
TI Activity energy expenditure and change in body composition in late life
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID DOUBLY-LABELED WATER; PHYSICAL-ACTIVITY; RESPIRATORY CHAMBER;
RESISTANCE-EXERCISE; SKELETAL-MUSCLE; WEIGHT CHANGE; OLDER MEN; HUMANS;
PEOPLE; WOMEN
AB Background: Change in body composition, specifically loss of fat-free mass and gain in fat mass, in older adults is a major pathway leading to the onset of functional decline and physical disability.
Objective: The objective was to determine the association of activity-related energy expenditure with change in body mass and composition among older men and women.
Design: Total energy expenditure ( TEE) was assessed over 2 wk by using the doubly labeled water method in 302 community-dwelling older adults aged 70-82 y. Resting metabolic rate (RMR) was measured by using indirect calorimetry, and the thermic effect of meals was estimated at 10% of TEE. Activity energy expenditure (AEE) was calculated as [TEE(0.9) - RMR]. Total body mass, fat-free mass (FFM), and fat mass ( FM) were assessed by dual-energy X-ray absorptiometry annually over a mean (+/- SD) of 4.9 +/- 1.3 y.
Results: In multivariate models adjusted for baseline age, smoking status, and race, men and women had a decline ( in kg/y) in body mass ( men: -0.34, 95% CI: -0.71, 0.02; women: -0.45, 95% CI: -0.71, -0.19) and FFM ( men: -0.48, 95% CI: -0.67, -0.29; women: -0.14, 95% CI: -0.026, -0.03). No changes (in kg/y) were observed in FM ( men: 0.14, 95% CI: -0.10, 0.38; women: -0.28, 95% CI: -0.49, -0.07). In men and women, higher AEE at baseline was associated with greater FFM. The average change in these outcomes (ie, slope), however, was similar across tertiles of AEE.
Conclusions: These data suggest that accumulated energy expenditure from all physical activities is associated with greater FFM, but the effect does not alter the trajectory of FFM change in late life. Am J Clin Nutr 2009; 90: 1336-42.
C1 [Manini, Todd M.; Anton, Stephen D.] Univ Florida, Dept Aging & Geriatr Res, Gainesville, FL 32611 USA.
[Harris, Tamara B.] NIA, Lab Epidemiol Demog & Biometry, Bethesda, MD 20892 USA.
[Everhart, James E.] NIDDKD, Bethesda, MD 20892 USA.
[Schoeller, Dale A.] Univ Wisconsin, Dept Nutr Sci, Madison, WI 53706 USA.
[Colbert, Lisa H.] Univ Wisconsin, Dept Kinesiol, Madison, WI 53706 USA.
[Delmonico, Matthew J.] Univ Rhode Isl, Dept Kinesiol, Kingston, RI 02881 USA.
[Visser, Marjolein] Vrije Univ Amsterdam, Fac Earth & Life Sci, Inst Hlth Sci, Amsterdam, Netherlands.
[Visser, Marjolein] Vrije Univ Amsterdam, Med Ctr, EMGO, Amsterdam, Netherlands.
[Tylavsky, Frances] Univ Tennessee, Dept Biostat & Epidemiol, Memphis, TN USA.
[Cummings, Steve R.; Mackey, Dawn C.] Calif Pacific Med Ctr, San Francisco Coordinating Ctr, San Francisco, CA USA.
[Newman, Anne B.] Univ Pittsburgh, Dept Epidemiol, Pittsburgh, PA 15261 USA.
[Simonsick, Eleanor M.] NIA, Clin Res Branch, Baltimore, MD 21224 USA.
[Bauer, Douglas C.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Bauer, Douglas C.] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA.
RP Manini, TM (reprint author), Univ Florida, Dept Aging & Geriatr Res, POB 112610, Gainesville, FL 32611 USA.
EM tmanini@aging.ufl.edu
RI Newman, Anne/C-6408-2013
OI Newman, Anne/0000-0002-0106-1150
FU NIA Claude D. Pepper Center [P30AG028740]; Institute on Aging at the
University of Florida; NIH, National Institute on Aging [N01AG-6-2106,
N01-AG-6-2101, N01-AG-6-2103]; National Institute of Diabetes and
Digestive and Kidney Diseases
FX Supported by the NIA Claude D. Pepper Center (P30AG028740) and a grant
from the Institute on Aging at the University of Florida. The Health,
Aging and Body Composition Study was supported by the Intramural
Research Program of the NIH, National Institute on Aging (contracts
N01AG-6-2106, N01-AG-6-2101, and N01-AG-6-2103) with additional support
from the National Institute of Diabetes and Digestive and Kidney
Diseases.
NR 31
TC 18
Z9 19
U1 1
U2 4
PU AMER SOC CLINICAL NUTRITION
PI BETHESDA
PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-3300, BETHESDA, MD 20814-3998
USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV 1
PY 2009
VL 90
IS 5
BP 1336
EP 1342
DI 10.3945/ajcn.2009.27659
PG 7
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 508TO
UT WOS:000270959500030
PM 19740971
ER
PT J
AU Yong, LC
Petersen, MR
Sigurdson, AJ
Sampson, LA
Ward, EM
AF Yong, Lee C.
Petersen, Martin R.
Sigurdson, Alice J.
Sampson, Laura A.
Ward, Elizabeth M.
TI High dietary antioxidant intakes are associated with decreased
chromosome translocation frequency in airline pilots
SO AMERICAN JOURNAL OF CLINICAL NUTRITION
LA English
DT Article
ID IONIZING-RADIATION; FREE-RADICALS; VITAMINS C; CANCER; VEGETABLES;
DAMAGE; REPRODUCIBILITY; QUESTIONNAIRE; CAROTENOIDS; VALIDITY
AB Background: Dietary antioxidants may protect against DNA damage induced by endogenous and exogenous sources, including ionizing radiation (IR), but data from IR-exposed human populations are limited.
Objective: The objective was to examine the association between the frequency of chromosome translocations, as a biomarker of cumulative DNA damage, and intakes of vitamins C and E and carotenoids in 82 male airline pilots.
Design: Dietary intakes were estimated by using a self-administered semiquantitative food-frequency questionnaire. Translocations were scored by using fluorescence in situ hybridization with whole chromosome paints. Negative binomial regression was used to estimate rate ratios and 95% CIs, adjusted for potential confounders.
Results: Significant and inverse associations were observed between translocation frequency and intakes of vitamin C, beta-carotene, beta-cryptoxanthin, and lutein-zeaxanthin from food (P < 0.05). Translocation frequency was not associated with the intake of vitamin E, alpha-carotene, or lycopene from food; total vitamin C or E from food and supplements; or vitamin C or E or multivitamin supplements. The adjusted rate ratios ( 95% CI) for >= median compared with, = median compared with, median combined intakes of vitamins C and E, beta- carotene, beta-cryptoxanthin, and lutein-zeaxanthin from food: 0.27 (0.14, 0.55).
Conclusion: High combined intakes of vitamins C and E, beta- carotene, beta-cryptoxanthin, and lutein-zeaxanthin from food, or a diet high in their food sources, may protect against cumulative DNA damage in IR-exposed persons. Am J Clin Nutr 2009;90:1402-10.
C1 [Yong, Lee C.] NIOSH, Ctr Dis Control & Prevent, Industrywide Studies Branch, Div Surveillance Hazard Evaluat & Field Studies, Cincinnati, OH 45226 USA.
[Sigurdson, Alice J.] NCI, NIH, Bethesda, MD 20892 USA.
[Sampson, Laura A.] Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA.
[Ward, Elizabeth M.] Amer Canc Soc, Atlanta, GA 30329 USA.
RP Yong, LC (reprint author), NIOSH, Ctr Dis Control & Prevent, Industrywide Studies Branch, Div Surveillance Hazard Evaluat & Field Studies, 4676 Columbia Pkwy,R-15, Cincinnati, OH 45226 USA.
EM lay7@cdc.gov
FU National Institute for Occupational Safety and Health and the National
Cancer Institute [Y1CP802904]; Intramural Research Program of the
Division of Cancer Epidemiology and Genetics, National Cancer Institute
FX Supported in part by an interagency agreement between the National
Institute for Occupational Safety and Health and the National Cancer
Institute ( contract Y1CP802904) and by the Intramural Research Program
of the Division of Cancer Epidemiology and Genetics, National Cancer
Institute.
NR 40
TC 11
Z9 11
U1 0
U2 2
PU AMER SOC NUTRITION-ASN
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0002-9165
J9 AM J CLIN NUTR
JI Am. J. Clin. Nutr.
PD NOV 1
PY 2009
VL 90
IS 5
BP 1402
EP 1410
DI 10.3945/ajcn.2009.28207
PG 9
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 508TO
UT WOS:000270959500038
PM 19793852
ER
PT J
AU Sinha, R
Park, Y
Graubard, BI
Leitzmann, MF
Hollenbeck, A
Schatzkin, A
Cross, AJ
AF Sinha, Rashmi
Park, Yikyung
Graubard, Barry I.
Leitzmann, Michael F.
Hollenbeck, Albert
Schatzkin, Arthur
Cross, Amanda J.
TI Meat and Meat-related Compounds and Risk of Prostate Cancer in a Large
Prospective Cohort Study in the United States
SO AMERICAN JOURNAL OF EPIDEMIOLOGY
LA English
DT Article
DE amines; benzo(a)pyrene; heme; meat; nitrates; nitrites; polycyclic
hydrocarbons, aromatic; prostatic neoplasms
ID HETEROCYCLIC AMINE CONTENT; FOOD-FREQUENCY QUESTIONNAIRE;
HEALTH-AMERICAN-ASSOCIATION; RETIRED-PERSONS DIET; COLORECTAL-CANCER;
ANIMAL PRODUCTS; N-NITROSATION; RED MEAT; NATIONAL-INSTITUTES;
NETHERLANDS COHORT
AB The authors examined associations between meat consumption (type, cooking method, and related mutagens), heme iron, nitrite/nitrate, and prostate cancer in a cohort of 175,343 US men aged 50-71 years. During 9 years of follow-up (1995-2003), they ascertained 10,313 prostate cancer cases (1,102 advanced) and 419 fatal cases. Hazard ratios comparing the fifth intake quintile with the first revealed elevated risks associated with red and processed meat for total (red meat: hazard ratio (HR) = 1.12, 95% confidence interval (CI): 1.04, 1.21; processed meat: HR = 1.07, 95% CI: 1.00, 1.14) and advanced (red meat: HR = 1.31, 95% CI: 1.05, 1.65; processed meat: HR = 1.32, 95% CI: 1.08, 1.61) prostate cancer. Heme iron, barbecued/grilled meat, and benzo[a]pyrene were all positively associated with total (HR = 1.09 (95% CI: 1.02, 1.17), HR = 1.11 (95% CI: 1.03, 1.19), and HR = 1.09 (95% CI: 1.00, 1.18), respectively) and advanced (HR = 1.28 (95% CI: 11.03, 1.58), HR = 1.36 (95% CI: 1.10, 1.69), and HR = 1.28 (95% CI: 1.00, 1.65), respectively) disease. Nitrite (HR = 1.24, 95% CI: 1.02, 1.51) and nitrate (HR = 1.31, 95% CI: 1.07, 1.61) intakes were associated with advanced prostate cancer. There were no clear associations for fatal prostate cancer. Red and processed meat may be positively associated with prostate cancer via mechanisms involving heme iron, nitrite/nitrate, grilling/barbecuing, and benzo[a]pyrene.
C1 [Sinha, Rashmi; Park, Yikyung; Graubard, Barry I.; Schatzkin, Arthur; Cross, Amanda J.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Leitzmann, Michael F.] Univ Regensburg, Inst Epidemiol & Prevent Med, Regensburg, Germany.
[Hollenbeck, Albert] AARP, Washington, DC USA.
RP Sinha, R (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Rockville, MD 20892 USA.
EM sinhar@nih.gov
RI Sinha, Rashmi/G-7446-2015;
OI Sinha, Rashmi/0000-0002-2466-7462; Park, Yikyung/0000-0002-6281-489X
NR 62
TC 63
Z9 63
U1 3
U2 19
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0002-9262
J9 AM J EPIDEMIOL
JI Am. J. Epidemiol.
PD NOV 1
PY 2009
VL 170
IS 9
BP 1165
EP 1177
DI 10.1093/aje/kwp280
PG 13
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 511KR
UT WOS:000271163700013
PM 19808637
ER
PT J
AU Singer, ST
Kim, HY
Olivieri, NF
Kwiatkowski, JL
Coates, TD
Carson, S
Neufeld, E
Cunningham, MJ
Giardina, PJ
Mueller, BU
Quinn, CT
Fung, E
Vichinsky, E
AF Singer, Sylvia Titi
Kim, Hae-Young
Olivieri, Nancy F.
Kwiatkowski, Janet L.
Coates, Thomas D.
Carson, Susan
Neufeld, Ellis
Cunningham, Melody J.
Giardina, Patricia J.
Mueller, Brigitta U.
Quinn, Charles T.
Fung, Ellen
Vichinsky, Elliott
CA Thalassemia Clinical Res Network
TI Hemoglobin H-constant spring in North America: An alpha Thalassemia with
frequent complications
SO AMERICAN JOURNAL OF HEMATOLOGY
LA English
DT Letter
ID INTERMEDIA PATIENTS; CHINESE PATIENTS; MARROW ACTIVITY; IRON OVERLOAD;
DISEASE; CALIFORNIA; GENOTYPES; FEATURES; ANEMIA
AB Hemoglobin H-constant spring (Hb H-CS), the most common nondeletional alpha thalassemia in Asia is increasingly recognized in North America due to shifts in immigration patterns. In California, alpha (alpha)-thalassemia syndromes are the second most frequent finding among newborns screened for hemoglobinopathies with a two-fold increase compared to a decade earlier [1,2]. Though known to have a more severe anemia than Hb H disease, the other clinical findings of Hb H-CS are not well described. Moreover, beneficial therapies that have become available in the last decade are often not applied to their care. This analysis of 46 patients enrolled in the Thalassemia Clinical Research Network (TCRN) age 13+/- 10 years old, with Hb H-CS revealed moderate anemia (mean 8.7 +/- 1.5 g/dl), regular transfusion therapy in 24% of patients, and spienomegaly or prior splenectomy in one-third of them. Serum transferin receptor (sTfr), was elevated; (44.4 +/- 18 mcg/ml normal range 2.9-8.3 mcg/ml), reflecting ineffective erythropoiesis, which in turn leads to high iron absorption and increased ferritin levels in younger (median = 187 ng/ml) and older (median = 465 ng/ml) nontransfused patients. These findings along with moderate growth delay and low bone mass were more prevalent in Hlb H-CS patients compared to deletional Hlb H disease. Our results highlight the required monitoring of the extent of anemia, growth, splenomegaly, iron overload, gallstones, bone density and assessment of need for transfusions and specific treatments for disease complications.
C1 [Singer, Sylvia Titi] Childrens Hosp, NHLBI, Oakland, CA 94609 USA.
[Singer, Sylvia Titi; Fung, Ellen; Vichinsky, Elliott; Thalassemia Clinical Res Network] Res Ctr Oakland, Oakland, CA 94609 USA.
[Kim, Hae-Young] New England Res Inst, Watertown, MA 02172 USA.
[Olivieri, Nancy F.] Toronto Gen Hosp, Univ Hlth Network, Toronto, ON, Canada.
[Kwiatkowski, Janet L.] Childrens Hosp Philadelphia, Div Hematol, Philadelphia, PA 19104 USA.
[Coates, Thomas D.; Carson, Susan] Childrens Hosp Los Angeles, Childrens Ctr Canc & Blood Dis, Los Angeles, CA 90027 USA.
[Neufeld, Ellis; Cunningham, Melody J.] Childrens Hosp, Boston, MA 02115 USA.
[Giardina, Patricia J.] Weill Cornell Med Coll, New York, NY USA.
[Mueller, Brigitta U.] Texas Childrens Hosp, Baylor Coll Med, Houston, TX 77030 USA.
[Quinn, Charles T.] Univ Texas SW Med Ctr Dallas, Div Pediat Hematol Oncol, Dallas, TX 75390 USA.
RP Singer, ST (reprint author), Childrens Hosp, NHLBI, 747 52nd St, Oakland, CA 94609 USA.
EM tsinger@mail.cho.org
RI Vichinsky, Elliott/F-8541-2011; Quinn, Charles/J-6842-2012;
OI Vichinsky, Elliott/0000-0002-0500-9579; Quinn,
Charles/0000-0002-2372-2175; Coates, Thomas/0000-0001-9878-6029
FU NCRR NIH HHS [M01 RR001271]; NHLBI NIH HHS [U01 HL065232, U01 HL065233,
U01 HL065238, U01 HL065239, U01 HL065244, U01 HL065260]
NR 21
TC 10
Z9 10
U1 0
U2 1
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0361-8609
J9 AM J HEMATOL
JI Am. J. Hematol.
PD NOV
PY 2009
VL 84
IS 11
BP 759
EP 761
DI 10.1002/ajh.21523
PG 3
WC Hematology
SC Hematology
GA 516KC
UT WOS:000271539900013
PM 19787795
ER
PT J
AU Lampl, M
Kusanovic, JP
Erez, O
Gotsch, F
Espinoza, J
Goncalves, L
Lee, W
Gomez, R
Nien, JK
Frongillo, EA
Romero, R
AF Lampl, Michelle
Kusanovic, Juan Pedro
Erez, Offer
Gotsch, Francesca
Espinoza, Jimmy
Goncalves, Luis
Lee, Wesley
Gomez, Ricardo
Kae Nien, Jyh
Frongillo, Edward A.
Romero, Roberto
TI Growth Perturbations in a Phenotype with Rapid Fetal Growth Preceding
Preterm Labor and Term Birth
SO AMERICAN JOURNAL OF HUMAN BIOLOGY
LA English
DT Article
ID FOR-GESTATIONAL-AGE; INTRAUTERINE GROWTH; IMPRINTED GENES; IN-UTERO;
RESTRICTED FETUSES; AMNIOTIC-FLUID; FATTY LIVER; WEIGHT; PREGNANCY;
HORMONE
AB The variability in fetal growth rates and gestation duration in humans is not well understood. Of interest are women presenting with an episode of preterm labor and subsequently delivering a term neonate, who is small relative to peers of similar gestational age. To further understand these relationships, fetal growth patterns predating an episode of preterm labor were investigated. Retrospective analysis of fetal biometry assessed by serial ultrasound in a prospectively studied sample of pregnancies in Santiago, Chile, tested the hypothesis that fetal growth patterns among uncomplicated pregnancies (n = 3,706) and those with an episode of preterm labor followed by term delivery (n = 184) were identical across the time intervals 16-22 weeks, 22-28 weeks, and 28-34 weeks in a multilevel mixed-effects regression. The hypothesis was not supported. Fetal weight growth rate was faster from 16 weeks among pregnancies with an episode of preterm labor (P < 0.05), declined across midgestation (22-28 weeks, P < 0.05), and rebounded between 28 and 34 weeks (P = 0.06). This was associated with perturbations in abdominal circumference growth and proportionately larger biparietal diameter from 22 gestational weeks (P = 0.03), greater femur (P = 0.01), biparietal diameter (P = 0.001) and head circumference (P = 0.02) dimensions relative to abdominal circumference across midgestation (22-28 weeks), followed by proportionately smaller femur diaphyseal length (P = 0.02) and biparietal diameter (P = 0.03) subsequently. A distinctive rapid growth phenotype characterized fetal growth preceding an episode of preterm labor among this sample of term-delivered neonates. Perturbations in abdominal circumference growth and patterns of proportionality suggest an altered growth strategy pre-dating the preterm labor episode. Am. J. Hum. Biol. 21:782-792, 2009. (C) 2009 Wiley-Liss, Inc.
C1 [Lampl, Michelle] Emory Univ, Dept Anthropol, Atlanta, GA 30322 USA.
[Lampl, Michelle; Kusanovic, Juan Pedro; Erez, Offer; Gotsch, Francesca; Espinoza, Jimmy; Goncalves, Luis; Lee, Wesley; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Dev, Perinatol Res Branch, NIH, DHHS, Bethesda, MD USA.
[Lampl, Michelle] Emory Univ, Predict Hlth Ctr Hlth Discovery, Atlanta, GA 30322 USA.
[Kusanovic, Juan Pedro; Erez, Offer] Wayne State Univ, Dept Obstet & Gynecol, Hutzel Womens Hosp, Detroit, MI USA.
[Gomez, Ricardo; Kae Nien, Jyh] Pontificia Univ Catolica Chile, Sotero Rio Hosp, Ctr Perinatal Diag & Res CEDIP, Puente Alto, Chile.
[Frongillo, Edward A.] Univ S Carolina, Dept Hlth Promot Educ & Behav, Columbia, SC 29208 USA.
[Romero, Roberto] Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI USA.
RP Lampl, M (reprint author), Emory Univ, Dept Anthropol, Atlanta, GA 30322 USA.
EM mlampl@emory.edu
RI Lampl, Michelle/B-1619-2013
FU Intramural Program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development, NIH, DHHS
FX Contract grant sponsor: Intramural Program of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, NIH, DHHS
NR 74
TC 7
Z9 7
U1 0
U2 3
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1042-0533
J9 AM J HUM BIOL
JI Am. J. Hum. Biol.
PD NOV-DEC
PY 2009
VL 21
IS 6
BP 782
EP 792
DI 10.1002/ajhb.20880
PG 11
WC Anthropology; Biology
SC Anthropology; Life Sciences & Biomedicine - Other Topics
GA 517BZ
UT WOS:000271589100010
PM 19298010
ER
PT J
AU Masi, CM
Hawkley, LC
Xu, X
Veenstra, TD
Cacioppo, JT
AF Masi, Christopher M.
Hawkley, Louise C.
Xu, Xia
Veenstra, Timothy D.
Cacioppo, John T.
TI Serum Estrogen Metabolites and Systolic Blood Pressure Among Middle-Aged
and Older Women and Men
SO AMERICAN JOURNAL OF HYPERTENSION
LA English
DT Article
ID ESTRADIOL METABOLITES; HYPERTENSION; PREVALENCE; AWARENESS; RECEPTOR;
TRENDS; CELLS
AB BACKGROUND
Hypertension is more common among men at younger ages and among women after age 60, suggesting a possible link between endogenous estrogens and systolic blood pressure (SBP) We tested whether serum 17 beta-estradiol (E(2)) or any of its metabolites were associated with SBP among middle-aged and older adults.
METHODS
Using a cross-sectional study design, we examined data from a population-based sample of 98 adults living in Cook County, Illinois. Age ranged between 55 and 69 years and body mass index (BMI) ranged between 19.8 and 50.6 kg/m(2). Serum was analyzed for 17 beta-E(2) and 14 estrogen metabolites (EMS) using mass spectrometry. SBP was measured using a tonometric device that records a pulse wave at the radial artery. Demographic and health history information were obtained via questionnaires.
RESULTS
Univariate analysis revealed an inverse relationship between SBP and both natural log (in) 16 alpha-hydroxyestrone (OHE(1)) (r = -0.360, P < 0.05) and In 16-ketoestradiol (ketoE(2)) (r = -0.360, P < 0.05) among women but not men. No significant correlations were found between SBP and 17 beta-E(2) in either sex. In multivariate analysis which adjusted for age, race, ethnicity, BMI, and use of cardiovascular medications, In 16 alpha-hydroxyestrone (16 alpha-OHE(1)) (B = -5.3, s.e. = 2.1, P < 0.05) and In 16-ketoE(2) (B = -4.7, s.e. = 1.9, P < 0.05) continued to be negatively associated with SBP among postmenopausal women.
CONCLUSIONS
These data suggest that serum 16 alpha-OHE(1) or 16-ketoE(2) may be important for vascular health among postmenopausal women but not among similarly aged men. Am J Hypertens 2009; 22:1148-1153 (C) 2009 American Journal of Hypertension, Ltd.
C1 [Masi, Christopher M.] Univ Chicago, Gen Internal Med Sect, Chicago, IL 60637 USA.
[Masi, Christopher M.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Hawkley, Louise C.; Cacioppo, John T.] Univ Chicago, Ctr Cognit & Social Neurosci, Chicago, IL 60637 USA.
[Hawkley, Louise C.; Cacioppo, John T.] Univ Chicago, Dept Psychol, Chicago, IL 60637 USA.
[Xu, Xia; Veenstra, Timothy D.] NCI, Lab Prote & Analyt Technol, SAIC Frederick Inc, Adv Technol Program, Frederick, MD 21701 USA.
RP Masi, CM (reprint author), Univ Chicago, Gen Internal Med Sect, Chicago, IL 60637 USA.
EM cmasi@medicine.bsd.uchicago.edu
FU National Institute on Aging Career Development Award [5K08AG027200-02];
National Institute on Aging [R01 AG034052-01]; National Cancer
Institute, National Institutes of Health [N01-CO-12400]; Department of
Health and Human Services
FX This work was supported by a National Institute on Aging Career
Development Award 5K08AG027200-02 (principal investigator: C.M. Masi)
and a National Institute on Aging R01 AG034052-01 (principal
investigator: J.T. Cacioppo). This project has been funded in whole or
in part with federal funds from the National Cancer Institute, National
Institutes of Health, under Contract N01-CO-12400. The content of this
publication does not necessarily reflect the views or policies of the
Department of Health and Human Services, nor does mention of trade
names, commercial products, or organizations imply endorsement by the US
Government.
NR 17
TC 10
Z9 10
U1 0
U2 1
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0895-7061
J9 AM J HYPERTENS
JI Am. J. Hypertens.
PD NOV
PY 2009
VL 22
IS 11
BP 1148
EP 1153
DI 10.1038/ajh.2009.155
PG 6
WC Peripheral Vascular Disease
SC Cardiovascular System & Cardiology
GA 516IB
UT WOS:000271534400006
PM 19713943
ER
PT J
AU Solomon, BD
Pineda-Alvarez, DE
Balog, JZ
Hadley, D
Gropman, AL
Nandagopal, R
Han, JC
Hahn, JS
Blain, D
Brooks, B
Muenke, M
AF Solomon, Benjamin D.
Pineda-Alvarez, Daniel E.
Balog, Joan Z.
Hadley, Donald
Gropman, Andrea L.
Nandagopal, Radha
Han, Joan C.
Hahn, Jin S.
Blain, Delphine
Brooks, Brian
Muenke, Maximilian
TI Compound Heterozygosity for Mutations in PAX6 in a Patient With Complex
Brain Anomaly, Neonatal Diabetes Mellitus, and Microophthalmia
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE PAX6; microophthalmia; aniridia; neonatal diabetes mellitus
ID CRYSTAL-STRUCTURE; ANIRIDIA; GENE; HOMEODOMAIN; DNA
AB We report on a patient with trisomy 21, microophthalmia, neonatal diabetes mellitus, hypopituitarism, and a complex structural brain anomaly who was a member of a large bilineal family with eye anomalies. The patient inherited a different mutation in PAX6 from each parent and is the only known living and second reported patient with compound heterozygosity for mutations in PAX6. PAX6 is a transcription factor involved in eye and brain development and has roles in pancreatic and pituitary development. Clinical evaluation of the propositus and his parents demonstrated the effects of mutations of differing severity in multiple individuals. Published 2009 Wiley-Liss, Inc.(dagger)
C1 [Solomon, Benjamin D.; Pineda-Alvarez, Daniel E.; Balog, Joan Z.; Hadley, Donald; Gropman, Andrea L.; Muenke, Maximilian] NHGRI, NIH, Bethesda, MD 20892 USA.
[Gropman, Andrea L.] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Nandagopal, Radha; Han, Joan C.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Hahn, Jin S.] Stanford Univ, Palo Alto, CA 94304 USA.
[Blain, Delphine; Brooks, Brian] NEI, NIH, Bethesda, MD 20892 USA.
[Blain, Delphine] MedStar Res Inst, Hyattsville, MD USA.
RP Muenke, M (reprint author), NHGRI, NIH, Bldg 35,Room 1B-203,MSC 3717, Bethesda, MD 20892 USA.
EM mamuenke@mail.nih.gov
FU National Human Genome Research Institute; National Institutes of Health
FX Grant sponsor: National Human Genome Research Institute, National
Institutes of Health.
NR 18
TC 28
Z9 29
U1 0
U2 4
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD NOV
PY 2009
VL 149A
IS 11
BP 2543
EP 2546
DI 10.1002/ajmg.a.33081
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 517BL
UT WOS:000271587600031
PM 19876904
ER
PT J
AU Conde-Agudelo, A
Romero, R
AF Conde-Agudelo, Agustin
Romero, Roberto
TI Amniotic fluid embolism: an evidence-based review
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Review
DE amniotic fluid embolism; cardiovascular collapse; DIC; disseminated
intravascular coagulation; maternal death; maternal morbidity; maternal
mortality; perinatal mortality; pregnancy
ID DISSEMINATED INTRAVASCULAR COAGULATION; OF-THE-LITERATURE; MATERNAL
PULMONARY CIRCULATION; MONOCLONAL-ANTIBODY TKH-2; BLUNT
ABDOMINAL-TRAUMA; UNITED-STATES; HEMODYNAMIC-ALTERATIONS; ATYPICAL
PRESENTATION; TRANSESOPHAGEAL ECHOCARDIOGRAPHY; HISTOLOGICAL DIAGNOSIS
AB We reviewed the best evidence on amniotic fluid embolism (AFE). The estimated incidence of AFE is 1: 15,200 and 1: 53,800 deliveries in North America and Europe, respectively. The case fatality rate and perinatal mortality associated with AFE are 13-30% and 9-44%, respectively. Risk factors associated with increased risk of AFE include advanced maternal age, placental abnormalities, operative deliveries, eclampsia, polyhydramnios, cervical laceration, and uterine rupture. Hemodynamic response to AFE is biphasic, with initial pulmonary hypertension and right ventricular failure, followed by left ventricular failure. Promising therapies include selective pulmonary vasodilators and recombinant activated factor VIIa. Important topics for future research are presented.
C1 [Conde-Agudelo, Agustin; Romero, Roberto] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 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] Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI USA.
RP Conde-Agudelo, A (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Perinatol Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
FU 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 study 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 151
TC 29
Z9 37
U1 0
U2 5
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD NOV
PY 2009
VL 201
IS 5
AR 445.e1
DI 10.1016/j.ajog.2009.04.052
PG 13
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 514FO
UT WOS:000271379900012
PM 19879393
ER
PT J
AU Willinger, M
Ko, CW
Reddy, UM
AF Willinger, Marian
Ko, Chia-Wen
Reddy, Uma M.
TI Racial disparities in stillbirth risk across gestation in the United
States
SO AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
LA English
DT Article
DE racial disparity; stillbirth
ID FETAL-DEATH; PERINATAL-MORTALITY; ETHNIC-DIFFERENCES; AFRICAN-AMERICANS;
INFANT-MORTALITY; BIRTH-WEIGHT; PREGNANCY; RATES; AGE; CERTIFICATES
AB OBJECTIVE: We sought to determine factors associated with racial disparities in stillbirth risk.
STUDY DESIGN: Stillbirth hazard was analyzed using 5,138,122 singleton gestations from the National Center of Health Statistics perinatal mortality and birth files, 2001-2002.
RESULTS: Black women have a 2.2-fold increased risk of stillbirth compared with white women. The black/white disparity in stillbirth hazard at 20-23 weeks is 2.75, decreasing to 1.57 at 39-40 weeks. Higher education reduced the hazard for whites more than for blacks and Hispanics. Medical, pregnancy, and labor complications accounted for 30% of the hazard in blacks and 20% in whites and Hispanics. Congenital anomalies and small for gestational age contributed more to preterm stillbirth risk among whites than blacks. Pregnancy and labor conditions contributed more to preterm stillbirth risk among blacks than whites.
CONCLUSION: The excess stillbirth risk for blacks was greatest at preterm gestations, and factors contributing to stillbirth risk vary by race and gestational age.
C1 [Willinger, Marian; Reddy, Uma M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Pregnancy & Perinatol Branch, Ctr Dev Biol & Perinatal Med, NIH, Bethesda, MD USA.
[Ko, Chia-Wen] Natl Inst Deafness & Other Commun Disorders, Epidemiol & Biostat Program, NIH, Bethesda, MD USA.
RP Willinger, M (reprint author), NICHHD, Pregnancy & Perinatol Branch, Ctr Dev Biol & Perinatal Med, 6100 Execut Blvd,Room 4B03H, Rockville, MD 20852 USA.
EM willingm@mail.nih.gov
FU Intramural NIH HHS [Z99 HD999999]
NR 30
TC 14
Z9 14
U1 0
U2 3
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9378
J9 AM J OBSTET GYNECOL
JI Am. J. Obstet. Gynecol.
PD NOV
PY 2009
VL 201
IS 5
AR 469.e1
DI 10.1016/j.ajog.2009.06.057
PG 8
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 514FO
UT WOS:000271379900018
PM 19762004
ER
PT J
AU Sen, HN
Nussenblatt, RB
AF Sen, H. Nida
Nussenblatt, Robert B.
TI Sympathetic Ophthalmia: What Have We Learned?
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Editorial Material
ID TRENDS
C1 [Sen, H. Nida; Nussenblatt, Robert B.] NEI, NIH, Bethesda, MD 20892 USA.
RP Sen, HN (reprint author), NEI, NIH, 10 Ctr Dr,Bldg 10,Room 10N112, Bethesda, MD 20892 USA.
EM senh@nei.nih.gov
FU Intramural NIH HHS [Z99 EY999999]
NR 17
TC 10
Z9 10
U1 2
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD NOV
PY 2009
VL 148
IS 5
BP 632
EP 633
DI 10.1016/j.ajo.2009.07.024
PG 2
WC Ophthalmology
SC Ophthalmology
GA 518DA
UT WOS:000271669300002
PM 19878754
ER
PT J
AU Sen, HN
Levy-Clarke, G
Faia, LJ
Li, ZQ
Yeh, S
Barron, KS
Ryan, JG
Hammel, K
Nussenblatt, RB
AF Sen, H. Nida
Levy-Clarke, Grace
Faia, Lisa J.
Li, Zhuqing
Yeh, Steven
Barron, Karyl S.
Ryan, John G.
Hammel, Keri
Nussenblatt, Robert B.
TI High-dose Daclizumab for the Treatment of Juvenile Idiopathic
Arthritis-Associated Active Anterior Uveitis
SO AMERICAN JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID REFRACTORY CHILDHOOD UVEITIS; RHEUMATOID-ARTHRITIS;
RENAL-TRANSPLANTATION; NONINFECTIOUS UVEITIS; OCULAR COMPLICATIONS;
VISUAL OUTCOMES; ACUTE REJECTION; CLINICAL-TRIAL; RISK-FACTORS; THERAPY
AB PURPOSE: To provide preliminary data regarding the safety and efficacy of high-dose intravenous daclizumab (Zenapax; Roche Inc, Nutley, New Jersey, USA) thereapy for the treatment of juvenile idiopathic arthritis (JIA)-associated active anterior uveitis.
DESIGN: Interventional case series; open,label prospective, phase 11 pilot study.
METHODS: Six patients were recruited into the study and received daclizumab therapy at doses of 8 mg/kg at baseline, 4 mg/kg at week 2, and 2 mg/kg every 4 weeks thereafter, for a total of 52 weeks. The study was done at the National Eye Institute between June 29, 2005 and July 9, 2008. The primary outcome was a two-step decrease in inflammation grade assessed at week 12. Primary safety outcome was assessed at weeks 2 and 4. The ocular inflammation was assessed according to the Standardization of Uveitis Nomenclature criteria.
RESULTS: Four of the 6 participants achieved two,step reduction in anterior chamber cells according to Standardization of Uveitis Nomenclature Working Group grading scheme for anterior chamber cells 12 weeks into the study and met the primary efficacy endpoint. One additional patient responded to reinduction whereas 1 patient failed reinduction and was considered an ocular treatment failure. Visual acuity improved from a mean of 68 Early Treatment Diabetic Retinopathy Study letters in the worse eye to a mean of 79.6 letters (2 Snellen lines). Three participants were terminated before 52 weeks: First, because of a rash possibly induced by daclizumab; Second, because of ocular treatment failure; and Last, because of uncontrolled systemic manifestations of JIA.
CONCLUSION: High,dose intravenous daclizumab can help reduce active inflammation in active JIA-associated anterior uveitis; however, patients need to be monitored for potential side effects. Larger randomized trials are needed to better assess treatment effect and safety. (Am J Ophthalmol 2009;148:696-703. Published by Elsevier Inc.)
C1 [Sen, H. Nida; Levy-Clarke, Grace; Faia, Lisa J.; Li, Zhuqing; Yeh, Steven; Nussenblatt, Robert B.] NEI, NIH, Bethesda, MD 20892 USA.
[Barron, Karyl S.] NIAID, NIH, Bethesda, MD 20892 USA.
[Ryan, John G.] NIAMSD, NIH, Bethesda, MD 20892 USA.
[Hammel, Keri] EMMES Corp, Rockville, MD USA.
RP Sen, HN (reprint author), NEI, NIH, 10 Ctr Dr,Bldg 10,Rm 10N112, Bethesda, MD 20892 USA.
EM senh@nei.nih.gov
FU NATIONAL EYE INSTITUTE INTRAMURAL PROGRAM; NATIONAL INSTITUTE OF HEALTH,
Bethesda, Maryland
FX THIS STUDY WAS SUPPORTED BY THE NATIONAL EYE INSTITUTE INTRAMURAL
PROGRAM, NATIONAL INSTITUTE OF HEALTH, Bethesda, Maryland. The authors
indicate no financial conflict of interest. Involved in design and
conduct of study (G.L.C., R.B.N., K.B., J.R., L.J.F., S.Y., K.H.);
collection of data (H.N.S., L.J.F., S.Y.); management (R.B.N.), analysis
(H.N.S.), and interpretation of data (H.N.S., R.B.N., Z.L.); and
preparation (H.N.S., L.J.F.), review, or approval of the manuscript
(H.N.S., L.J.F., R.B.N.). The study was conducted at the National Eye
Institute, National Institutes of Health underan Investigational New
Drug (IND) application. The study protocol was reviewed and approved by
the Institutional Review Board of the National Eye Institute and all
procedures conformed to the tenets of the Declaration of Helsinki.
Clinical Trials registration: NCT00130637 (NEI protocol no.:
05-EI-0208).
NR 35
TC 31
Z9 31
U1 0
U2 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0002-9394
J9 AM J OPHTHALMOL
JI Am. J. Ophthalmol.
PD NOV
PY 2009
VL 148
IS 5
BP 696
EP 703
DI 10.1016/j.ajo.2009.06.003
PG 8
WC Ophthalmology
SC Ophthalmology
GA 518DA
UT WOS:000271669300010
PM 19664754
ER
PT J
AU Andersson, S
Sowjanya, P
Wangsa, D
Hjerpe, A
Johansson, B
Auer, G
Gravitt, PE
Larsson, C
Wallin, KL
Ried, T
Heselmeyer-Haddad, K
AF Andersson, Sonia
Sowjanya, Pavani
Wangsa, Darawalee
Hjerpe, Anders
Johansson, Bo
Auer, Gert
Gravitt, Patti E.
Larsson, Catharina
Wallin, Keng-Ling
Ried, Thomas
Heselmeyer-Haddad, Kerstin
TI Detection of Genomic Amplification of the Human Telomerase Gene TERC, a
Potential Marker for Triage of Women with HPV-Positive, Abnormal Pap
Smears
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; CERVICAL-CANCER PROGRESSION;
HUMAN-PAPILLOMAVIRUS TYPES; HIGH-RISK; EPITHELIAL-CELLS; UTERINE CERVIX;
VIRAL LOAD; CHROMOSOMAL-ABERRATIONS; RECURRENT PATTERN; IN-SITU
AB The vast majority of invasive cervical carcinomas harbor additional copies of the chromosome arm 3q, resulting in genomic amplification of the human telomerase gene TERC. Here, we evaluated TERC amplification in routinely collected liquid based cytology (LBC) samples with histologically confirmed diagnoses. A set of 78 LBC samples from a Swedish patient cohort were analyzed with a four-color fluorescence in situ hybridization probe panel that included TERC. Clinical follow-up included additional histological evaluation and Pap smears. Human papillomavirus status was available for all cases. The correlation of cytology, TERC amplification, human papillomavirus typing, and histological diagnosis showed that infection with high-risk human papillomavirus was detected in 64% of the LBC samples with normal histopathology, in 65% of the cervical intraepithelial neoplasia (CIN)1, 95% of the CIN2, 96% of the CIN3 lesions, and all carcinomas. Seven percent of the lesions with normal histopathology were positive for TERC amplification, 24% of the CIN1, 64% of the CIN2, 91% of the CIN3 lesions, and 100% of invasive carcinomas. This demonstrates that detection of genomic amplification of TERC in LBC samples can identify patients with histopathologically confirmed CIN3 or cancer. indeed, the proportion of TERC-positive cases increases with the severity of dysplasia. Among the markers tested, detection of TERC amplification in cytological samples has the highest combined sensitivity and specificity for discernment of low-grade from high-grade dysplasia and cancer. (Am J Pathol 2009, 175:1831-1847; DOI. 10.2353/ajpath.2009.090122)
C1 [Sowjanya, Pavani; Wangsa, Darawalee; Ried, Thomas; Heselmeyer-Haddad, Kerstin] NCI, Genet Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Andersson, Sonia] Karolinska Univ Hosp Huddinge, Karolinska Inst, Dept Clin Sci Intervent & Technol, Stockholm, Sweden.
[Hjerpe, Anders] Karolinska Univ Hosp Huddinge, Karolinska Inst, Div Obstet & Gynecol, Dept Lab Med, Stockholm, Sweden.
[Johansson, Bo] Karolinska Univ Hosp Huddinge, Karolinska Inst, Div Clin Virol, Dept Lab Med, Stockholm, Sweden.
[Wangsa, Darawalee] Karolinska Univ Hosp Solna, Karolinska Inst, Dept Oncol Pathol, Stockholm, Sweden.
[Gravitt, Patti E.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
RP Ried, T (reprint author), NCI, Genet Branch, Ctr Canc Res, NIH, 50 S Dr,Bldg 50,Rm 1306, Bethesda, MD 20892 USA.
EM riedt@mail.nih.gov
FU Swedish Cancer Foundation [CAN 2007/1044]; Swedish Research Council;
Medical Research Council; Cancer Society in Stockholm; Goran Gustafsson
Foundation; Stockholm County Council; Swedish Labor Market Insurance;
NIH, National Cancer Institute; NIH SPORE [P50 CA98252]
FX Supported by The Swedish Cancer Foundation (CAN 2007/1044), the Swedish
Research Council, the Medical Research Council, the Cancer Society in
Stockholm, the Goran Gustafsson Foundation, the Stockholm County
Council, and the Swedish Labor Market Insurance and the Intramural
Research Program of the NIH, National Cancer Institute. P. Gravitt and
P. Sowjanya were funded via the NIH SPORE P50 CA98252.
NR 41
TC 36
Z9 45
U1 0
U2 5
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD NOV
PY 2009
VL 175
IS 5
BP 1831
EP 1847
DI 10.2353/ajpath.2009.090122
PG 17
WC Pathology
SC Pathology
GA 515BH
UT WOS:000271440800007
PM 19880826
ER
PT J
AU Yuasa, T
Kondo, N
Yasuhara, R
Shimono, K
Mackeem, S
Pacifici, M
Iwamoto, M
Enomoto-Iwamoto, M
AF Yuasa, Takahito
Kondo, Naoki
Yasuhara, Rika
Shimono, Kengo
Mackeem, Susan
Pacifici, Maurizio
Iwamoto, Masahiro
Enomoto-Iwamoto, Motomi
TI Transient Activation of Wnt/beta-Catenin Signaling Induces Abnormal
Growth Plate Closure and Articular Cartilage Thickening in Postnatal
Mice
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID CHONDROCYTE DIFFERENTIATION; STEM/PROGENITOR CELLS; LIMB SKELETOGENESIS;
PROGENITOR CELLS; GENE-EXPRESSION; NOTCH RECEPTORS; SYNOVIAL JOINT;
SELF-RENEWAL; APOPTOSIS; TRANSCRIPTION
AB Wnt/beta-catenin signaling is required for skeletal development and organization and for function of the growth plate and articular cartilage. To further clarify these roles and their possible pathophysiological importance, we created a new transgenic mouse model in which Wnt/beta-catenin signaling can be activated in cartilage for specific periods of time. These transgenic mice expressed a constitutive active form of beta-catenin fused to a modified estrogen receptor ligand-binding domain under the control of cartilage-specific collagen 11 alpha 2 promoter/enhancer. Transient Wnt/beta-catenin signaling activation in young adult mice by tamoxifen injections induced growth retardation and severe deformities in knee joints. Tibial and femoral growth plates displayed an excessive number of apoptotic cells and eventually underwent abnormal regression. Articular cartilage exhibited an initial acute loss of proteoglycan matrix that was followed by increases in thickness, cell density, and cell proliferation. In reciprocal studies, we found that conditional ablation of beta-catenin in postnatal mice using a Col2-CreER strategy led to hypocellularity in articular cartilage, growth plate disorganization, and a severe reduction in bone volume. Together, these data provide evidence that Wnt/beta-catenin signaling has important and distinct roles in growth plate and articular cartilage and that postnatal dysregulation of this signaling pathway causes diverse structural and functional changes in the two cartilaginous structures. (Am J Pathol 2009, 175:1993-2003; DOI: 10.2353/ajpath.2009.081173)
C1 [Yuasa, Takahito; Kondo, Naoki; Yasuhara, Rika; Shimono, Kengo; Pacifici, Maurizio; Iwamoto, Masahiro; Enomoto-Iwamoto, Motomi] Thomas Jefferson Univ, Dept Orthoped Surg, Coll Med, Philadelphia, PA 19107 USA.
[Mackeem, Susan] NCI, Pathol Lab, Bethesda, MD 20892 USA.
RP Enomoto-Iwamoto, M (reprint author), Thomas Jefferson Univ, Dept Orthoped Surg, Coll Med, 1015 Walnut St,501 Curtis Bldg, Philadelphia, PA 19107 USA.
EM motomi.iwamoto@jefferson.edu
FU National Institute of Arthritis & Musculoskeletal Skin Diseases
[AR050507, AR046000]; National Institute on Aging [AG025868]
FX Supported by the National Institute of Arthritis & Musculoskeletal &
Skin Diseases (grants AR050507 and AR046000) and the National Institute
on Aging (grant AG025868).
NR 38
TC 36
Z9 36
U1 1
U2 6
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD NOV
PY 2009
VL 175
IS 5
BP 1993
EP 2003
DI 10.2353/ajpath.2009.081173
PG 11
WC Pathology
SC Pathology
GA 515BH
UT WOS:000271440800021
PM 19815716
ER
PT J
AU Bianco, C
Cotten, C
Lonardo, E
Strizzi, L
Baraty, C
Mancino, M
Gonzales, M
Watanabe, K
Nagaoka, T
Berry, C
Arai, AE
Minchiotti, G
Salomon, DS
AF Bianco, Caterina
Cotten, Catherine
Lonardo, Enza
Strizzi, Luigi
Baraty, Christina
Mancino, Mario
Gonzales, Monica
Watanabe, Kazuhide
Nagaoka, Tadahiro
Berry, Colin
Arai, Andrew E.
Minchiotti, Gabriella
Salomon, David S.
TI Cripto-1 Is Required for Hypoxia to Induce Cardiac Differentiation of
Mouse Embryonic Stem Cells
SO AMERICAN JOURNAL OF PATHOLOGY
LA English
DT Article
ID GROWTH-FACTOR; FACTOR 1-ALPHA; MAMMARY-GLAND; TUMOR-GROWTH;
COLON-CANCER; FACTOR-I; EXPRESSION; GENE; MORPHOGENESIS; ANGIOGENESIS
AB Cripto-1 is a membrane-bound protein that is highly expressed in embryonic stem cells and in human tumors. in the present study, we investigated the effect of low levels of oxygen, which occurs naturally in rapidly growing tissues, on Cripto-1 expression in mouse embryonic stem (mES) cells and in human embryonal carcinoma cells. During hypoxia, Cripto-1 expression levels were significantly elevated in mES cells and in Ntera-2 or NCCIT human embryonal carcinoma cells, as compared with cells growing with normal oxygen levels. The transcription factor hypoxia-inducible factor-1 alpha directly regulated Cripto-1 expression by binding to hypoxia-responsive elements within the promoter of mouse and human Cripto-1 genes in mES and NCCIT cells, respectively. Furthermore, hypoxia modulated differentiation of mES cells by enhancing formation of beating cardiomyocytes as compared with mES cells that were differentiated under normoxia. However, hypoxia failed to induce differentiation of mES cells into cardiomyocytes in the absence of Cripto-1 expression, demonstrating that Cripto-1 is required for hypoxia to fully differentiate mES cells into cardiomyocytes. Finally, cardiac tissue samples derived from patients who had suffered ischemic heart disease showed a dramatic increase in Cripto-1 expression as compared with nonischemic heart tissue samples, suggesting that hypoxia may also regulate Cripto-1 in vivo. (Ani J Pathol 2009, 175:2146-2158, DOI: 10.2353/ajpath.2009.090218)
C1 [Bianco, Caterina; Cotten, Catherine; Strizzi, Luigi; Baraty, Christina; Mancino, Mario; Gonzales, Monica; Watanabe, Kazuhide; Nagaoka, Tadahiro; Salomon, David S.] NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[Arai, Andrew E.] NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA.
[Lonardo, Enza; Berry, Colin; Minchiotti, Gabriella] CNR, Inst Genet & Biophys A Buzzati Traverso, Stem Cell Fate Lab, Naples, Italy.
RP Salomon, DS (reprint author), NCI, Mammary Biol & Tumorigenesis Lab, Ctr Canc Res, 37 Convent Dr,Bldg 37,Room 1118, Bethesda, MD 20892 USA.
EM Salomond@mail.nih.gov
RI Lonardo, Enza/A-8786-2011;
OI Nagaoka, Tadahiro/0000-0002-9391-0243
FU Intramural Research program of the National Institutes of Health;
National Cancer Institute; Center for Cancer Research; Associazione
Italiana per la Ricerca sul Cancro; Faculty of Medicine, University of
Glaskow
FX Supported by Intramural Research program of the National Institutes of
Health, National Cancer Institute, Center for Cancer Research, by a
grant from the Associazione Italiana per la Ricerca sul Cancro (to
G.M.), and by a grant of the Faculty of Medicine, University of Glaskow
(to C.B.).
NR 47
TC 33
Z9 33
U1 0
U2 3
PU AMER SOC INVESTIGATIVE PATHOLOGY, INC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3993 USA
SN 0002-9440
J9 AM J PATHOL
JI Am. J. Pathol.
PD NOV
PY 2009
VL 175
IS 5
BP 2146
EP 2158
DI 10.2353/ajpath.2009.090218
PG 13
WC Pathology
SC Pathology
GA 515BH
UT WOS:000271440800035
PM 19834060
ER
PT J
AU Grobman, WA
Lai, YL
Landon, MB
Spong, CY
Leveno, KJ
Rouse, DJ
Varner, MW
Moawad, AH
Simhan, HN
Harper, M
Wapner, RJ
Sorokin, Y
Miodovnik, M
Carpenter, M
O'Sullivan, MJ
Sibai, BM
Langer, O
Thorp, JM
Ramin, SM
Mercer, BM
AF Grobman, William A.
Lai, Yinglei
Landon, Mark B.
Spong, Catherine Y.
Leveno, Kenneth J.
Rouse, Dwight J.
Varner, Michael W.
Moawad, Atef H.
Simhan, Hyagriv N.
Harper, Margaret
Wapner, Ronald J.
Sorokin, Yoram
Miodovnik, Menachem
Carpenter, Marshall
O'Sullivan, Mary J.
Sibai, Baha M.
Langer, Oded
Thorp, John M.
Ramin, Susan M.
Mercer, Brian M.
TI Does Information Available at Admission for Delivery Improve Prediction
of Vaginal Birth after Cesarean?
SO AMERICAN JOURNAL OF PERINATOLOGY
LA English
DT Article
DE Trial of labor; vaginal birth after cesarean; prediction
ID LABOR
AB We sought to construct a predictive model for vaginal birth after cesarean (VBAC) that combines factors that can be ascertained only as the pregnancy progresses with those known at initiation of prenatal care. Using multivariable modeling, we constructed a predictive model for VBAC that included patient factors known at the initial prenatal visit as well as those that only become evident as the pregnancy progresses to the admission for delivery. We analyzed 9616 women. The regression equation for VBAC success included multiple factors that could not be known at the first prenatal visit. The area under the curve for this model was significantly greater (p<0.001) than that of a model that included only factors available at the first prenatal visit. A prediction model for VBAC success, which incorporates factors that can be ascertained only as the pregnancy progresses, adds to the predictive accuracy of a model that uses only factors available at a first prenatal visit.
C1 [Grobman, William A.] Northwestern Univ, Dept Obstet, Chicago, IL 60611 USA.
[Grobman, William A.] Northwestern Univ, Dept Gynecol, Chicago, IL 60611 USA.
[Lai, Yinglei] George Washington Univ, Ctr Biostat, Washington, DC USA.
[Landon, Mark B.] Ohio State Univ, Columbus, OH 43210 USA.
[Spong, Catherine Y.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
[Leveno, Kenneth J.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
[Rouse, Dwight J.] Univ Alabama, Birmingham, AL USA.
[Varner, Michael W.] Univ Chicago, Chicago, IL 60637 USA.
[Moawad, Atef H.] Univ Utah, Salt Lake City, UT USA.
[Simhan, Hyagriv N.] Univ Pittsburgh, Pittsburgh, PA USA.
[Harper, Margaret] Wake Forest Univ, Winston Salem, NC 27109 USA.
[Wapner, Ronald J.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA.
[Sorokin, Yoram] Wayne State Univ, Detroit, MI USA.
[Miodovnik, Menachem] Columbia Univ, New York, NY USA.
[Miodovnik, Menachem] Univ Cincinnati, Cincinnati, OH USA.
[Carpenter, Marshall] Brown Univ, Providence, RI 02912 USA.
[O'Sullivan, Mary J.] Univ Miami, Miami, FL USA.
[Sibai, Baha M.] Univ Tennessee, Memphis, TN USA.
[Langer, Oded] Univ Texas San Antonio, San Antonio, TX USA.
[Thorp, John M.] Univ N Carolina, Chapel Hill, NC USA.
[Ramin, Susan M.] Univ Texas Houston, Houston, TX USA.
[Mercer, Brian M.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
RP Grobman, WA (reprint author), 250 E Super St,Suite 05-2175, Chicago, IL 60611 USA.
EM w-grobman@northwestern.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 [HD21410, HD21414, HD27860, HD27861, HD27869, HD27905,
HD27915, HD27917, HD34116, HD34122, HD34136, HD34208, HD34210, HD40500,
HD40485, HD40544, HD40545, HD40560, HD40512, HD36801]
FX Supported by grants from the Eunice Kennedy Shriver National Institute
of Child Health and Human Development (HD21410, HD21414, HD27860,
HD27861, HD27869, HD27905, HD27915, HD27917, HD34116, HD34122, HD34136,
HD34208, HD34210, HD40500, HD40485, HD40544, HD40545, HD40560, HD40512,
and HD36801).
NR 7
TC 29
Z9 30
U1 0
U2 3
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0735-1631
J9 AM J PERINAT
JI Am. J. Perinatol.
PD NOV
PY 2009
VL 26
IS 10
BP 693
EP 701
DI 10.1055/s-0029-1239494
PG 9
WC Obstetrics & Gynecology; Pediatrics
SC Obstetrics & Gynecology; Pediatrics
GA 507VN
UT WOS:000270883400002
PM 19813165
ER
PT J
AU Muniyappa, R
Chen, H
Muzumdar, RH
Einstein, FH
Yan, X
Yue, LQ
Barzilai, N
Quon, MJ
AF Muniyappa, Ranganath
Chen, Hui
Muzumdar, Radhika H.
Einstein, Francine H.
Yan, Xu
Yue, Lilly Q.
Barzilai, Nir
Quon, Michael J.
TI Comparison between surrogate indexes of insulin sensitivity/resistance
and hyperinsulinemic euglycemic clamp estimates in rats
SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
LA English
DT Article
DE glucose clamp; calibration model; quantitative insulin-sensitivity check
index
ID HOMEOSTASIS MODEL ASSESSMENT; TYPE-2 DIABETIC-PATIENTS; FASTING
PLASMA-GLUCOSE; BETA-CELL FUNCTION; CHECK INDEX; CARDIOVASCULAR-DISEASE;
RECIPROCAL INDEX; VISCERAL FAT; RESISTANCE; MICE
AB Muniyappa R, Chen H, Muzumdar RH, Einstein FH, Yan X, Yue LQ, Barzilai N, Quon MJ. Comparison between surrogate indexes of insulin sensitivity/resistance and hyperinsulinemic euglycemic clamp estimates in rats. Am J Physiol Endocrinol Metab 297: E1023-E1029, 2009. First published August 25, 2009; doi: 10.1152/ajpendo.00397.2009.-Assessing insulin resistance in rodent models gives insight into mechanisms that cause type 2 diabetes and the metabolic syndrome. The hyperinsulinemic euglycemic glucose clamp, the reference standard for measuring insulin sensitivity in humans and animals, is labor intensive and technically demanding. A number of simple surrogate indexes of insulin sensitivity/resistance have been developed and validated primarily for use in large human studies. These same surrogates are also frequently used in rodent studies. However, in general, these indexes have not been rigorously evaluated in animals. In a recent validation study in mice, we demonstrated that surrogates have a weaker correlation with glucose clamp estimates of insulin sensitivity/resistance than in humans. This may be due to increased technical difficulties in mice and/or intrinsic differences between human and rodent physiology. To help distinguish among these possibilities, in the present study, using data from rats substantially larger than mice, we compared the clamp glucose infusion rate (GIR) with surrogate indexes, including QUICKI, HOMA, 1/HOMA, log (HOMA), and 1/fasting insulin. All surrogates were modestly correlated with GIR (r = 0.34-0.40). Calibration analyses of surrogates adjusted for body weight demonstrated similar predictive accuracy for GIR among all surrogates. We conclude that linear correlations of surrogate indexes with clamp estimates and predictive accuracy of surrogate indexes in rats are similar to those in mice (but not as substantial as in humans). This additional rat study (taken with the previous mouse study) suggests that application of surrogate insulin sensitivity indexes developed for humans may not be appropriate for determining primary outcomes in rodent studies due to intrinsic differences in metabolic physiology. However, use of surrogates may be appropriate in rodents, where feasibility of clamps is an obstacle and measurement of insulin sensitivity is a secondary outcome.
C1 [Muniyappa, Ranganath; Chen, Hui; Quon, Michael J.] NIH, Diabet Unit, NCCAM, Bethesda, MD 20892 USA.
[Yan, Xu; Yue, Lilly Q.] US FDA, Div Biostat, Ctr Devices & Radiol Hlth, Rockville, MD 20857 USA.
[Muzumdar, Radhika H.; Einstein, Francine H.; Barzilai, Nir] Albert Einstein Coll Med, Inst Aging Res, Bronx, NY 10467 USA.
[Muzumdar, Radhika H.; Einstein, Francine H.; Barzilai, Nir] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
RP Quon, MJ (reprint author), NIH, Diabet Unit, NCCAM, 9 Mem Dr,Bldg 9,Rm 1N-105 MSC 0920, Bethesda, MD 20892 USA.
EM quonm@nih.gov
RI Muzumdar, Radhika/D-9860-2014;
OI Quon, Michael/0000-0002-9601-9915; Quon , Michael /0000-0002-5289-3707
FU Intramural Research Program; National Center for Complementary and
Alternative Medicine; National Institutes of Health [K08-AG-027462,
P60-DK-20541, R01-AG-18381, T32-AG-23475, P01-AG-021654]; Albert
Einstein Diabetes Research and Training Center [P60-DK-20541]
FX This work was supported by the Intramural Research Program, the National
Center for Complementary and Alternative Medicine, and grants from the
National Institutes of Health (K08-AG-027462 and P60-DK-20541 to R. H.
Muzumdar; R01-AG-18381, T32-AG-23475, and P01-AG-021654 to N. Barzilai)
and the Core Laboratories of the Albert Einstein Diabetes Research and
Training Center (P60-DK-20541).
NR 30
TC 25
Z9 26
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0193-1849
J9 AM J PHYSIOL-ENDOC M
JI Am. J. Physiol.-Endocrinol. Metab.
PD NOV
PY 2009
VL 297
IS 5
BP E1023
EP E1029
DI 10.1152/ajpendo.00397.2009
PG 7
WC Endocrinology & Metabolism; Physiology
SC Endocrinology & Metabolism; Physiology
GA 509CL
UT WOS:000270990500007
PM 19706785
ER
PT J
AU Deschamps, AM
Murphy, E
AF Deschamps, Anne M.
Murphy, Elizabeth
TI Activation of a novel estrogen receptor, GPER, is cardioprotective in
male and female rats
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE Langendorff; ischemia-reperfusion; G-1; G protein-coupled receptor 30; G
protein-coupled estrogen receptor
ID PROTEIN-COUPLED RECEPTOR; GROWTH-FACTOR RECEPTOR; ISCHEMIA-REPERFUSION
INJURY; CORONARY-HEART-DISEASE; CARDIOVASCULAR-SYSTEM; POSTMENOPAUSAL
WOMEN; SELECTIVE AGONIST; SIGNAL STRENGTH; CANCER-CELLS; KINASE
AB Deschamps AM, Murphy E. Activation of a novel estrogen receptor, GPER, is cardioprotective in male and female rats. Am J Physiol Heart Circ Physiol 297: H1806-H1813, 2009. First published August 28, 2009; doi:10.1152/ajpheart.00283.2009.-Premenopausal females have a lower incidence of cardiovascular disease than their male counterparts, but the mechanism is unclear. Estrogen has been thought to signal through two nuclear receptors: estrogen receptor-alpha or estrogen receptor-beta; however, a third, membrane-bound receptor G protein-coupled estrogen receptor (GPER), has been identified and shown to bind estrogen with high affinity. To date, there is little information on GPER in the heart and no study has looked at the effect of GPER activation during myocardial ischemia-reperfusion (I/R). Therefore, the goal of this study was to determine whether activation of GPER is cardioprotective in rats. A highly specific GPER agonist, G-1, was administered to Sprague-Dawley (200-350 g) rat hearts 10 min before 20 min of ischemic followed by 120 min of reperfusion using a Langendorff model. Similar levels of GPER were found in both male and female rat hearts. With administration of 110 nM of G-1, postischemic contractile dysfunction was significantly reduced compared with untreated controls (43.8 +/- 4.3% vs. 26.9 +/- 2.1% of preischemic rate pressure product; P < 0.05). Additionally, infarct size was reduced in the G-1-treated animals when compared with control (18.8 +/- 2.7% vs. 32.4 +/- 2.1%; P < 0.05). These observations were demonstrated in both male and intact female rat hearts. Through Western blot analysis, it was demonstrated that G-1 induces the activation of both Akt and ERK1/2. Furthermore, the protection afforded by G-1 was blocked by coadministration of a phosphatidylinositol 3-kinase (PI3K) inhibitor (wortmannin, 100 nM). Taken together, the data show that G-1 activation of GPER improves functional recovery and reduces infarct size in isolated rat hearts following I/R through a PI3K-dependent, gender-independent mechanism.
C1 [Deschamps, Anne M.; Murphy, Elizabeth] NHLBI, NIH, Translat Med Branch, Lab Cardiac Physiol, Bethesda, MD 20892 USA.
RP Murphy, E (reprint author), NHLBI, NIH, Translat Med Branch, Lab Cardiac Physiol, Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM murphy1@mail.nih.gov
OI Deschamps, Anne/0000-0001-7415-1408
FU National Heart, Lung, and Blood Institute
FX These studies were supported by the National Heart, Lung, and Blood
Institute intramural program.
NR 37
TC 94
Z9 98
U1 0
U2 7
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP H1806
EP H1813
DI 10.1152/ajpheart.00283.2009
PG 8
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 511DF
UT WOS:000271143400032
PM 19717735
ER
PT J
AU Nomura-Kitabayashi, A
Phoon, CKL
Kishigami, S
Rosenthal, J
Yamauchi, Y
Abe, K
Yamamura, K
Samtani, R
Lo, CW
Mishina, Y
AF Nomura-Kitabayashi, Aya
Phoon, Colin K. L.
Kishigami, Satoshi
Rosenthal, Julie
Yamauchi, Yasutaka
Abe, Kuniya
Yamamura, Ken-ichi
Samtani, Rajeev
Lo, Cecilia W.
Mishina, Yuji
TI Outflow tract cushions perform a critical valve-like function in the
early embryonic heart requiring BMPRIA-mediated signaling in cardiac
neural crest
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE bone morphogenetic proteins; endocardial cushions; heart defects
congenital; heart development; ultrasound biomicroscopy
ID MORPHOGENETIC PROTEIN-RECEPTOR; ULTRASOUND BIOMICROSCOPY-DOPPLER;
ENDOCARDIAL CUSHION; MOUSE EMBRYOGENESIS; TRANSCRIPTION FACTOR;
CONDUCTION SYSTEM; GENE-EXPRESSION; NF-ATC; SEPTATION; MICE
AB Nomura-Kitabayashi A, Phoon CK, Kishigami S, Rosenthal J, Yamauchi Y, Abe K, Yamamura K, Samtani R, Lo CW, Mishina Y. Outflow tract cushions perform a critical valve-like function in the early embryonic heart requiring BMPRIA-mediated signaling in cardiac neural crest. Am J Physiol Heart Circ Physiol 297: H1617-H1628, 2009. First published August 28, 2009; doi:10.1152/ajpheart.00304.2009.-Neural crest-specific ablation of BMP type IA receptor (BMPRIA) causes embryonic lethality by embryonic day (E) 12.5, and this was previously postulated to arise from a myocardial defect related to signaling by a small population of cardiac neural crest cells (cNCC) in the epicardium. However, as BMP signaling via cNCC is also required for proper development of the outflow tract cushions, precursors to the semilunar valves, a plausible alternate or additional hypothesis is that heart failure may result from an outflow tract cushion defect. To investigate whether the outflow tract cushions may serve as dynamic valves in regulating hemodynamic function in the early embryo, in this study we used noninvasive ultrasound biomicroscopy-Doppler imaging to quantitatively assess hemodynamic function in mouse embryos with P0-Cre transgene mediated neural crest ablation of Bmpr1a (P0 mutants). Similar to previous studies, the neural crest-deleted Bmpr1a P0 mutants died at similar to E12.5, exhibiting persistent truncus arteriosus, thinned myocardium, and congestive heart failure. Surprisingly, our ultrasound analyses showed normal contractile indices, heart rate, and atrioventricular conduction in the P0 mutants. However, reversed diastolic arterial blood flow was detected as early as E11.5, with cardiovascular insufficiency and death rapidly ensuing by E12.5. Quantitative computed tomography showed thinning of the outflow cushions, and this was associated with a marked reduction in cell proliferation. These results suggest BMP signaling to cNCC is required for growth of the outflow tract cushions. This study provides definitive evidence that the outflow cushions perform a valve-like function critical for survival of the early mouse embryo.
C1 [Phoon, Colin K. L.] NYU, Pediat Cardiol Program, Sch Med, New York, NY 10016 USA.
[Nomura-Kitabayashi, Aya; Kishigami, Satoshi] Natl Inst Environm Hlth Sci, Reprod & Dev Toxicol Lab, NIH, Res Triangle Pk, NC USA.
[Rosenthal, Julie; Samtani, Rajeev; Lo, Cecilia W.] NHLBI, Dev Biol Lab, NIH, Bethesda, MD 20892 USA.
[Yamauchi, Yasutaka; Abe, Kuniya; Yamamura, Ken-ichi] Kumamoto Univ, Dept Dev Genet, Inst Mol Embryol & Genet, Kumamoto, Japan.
[Mishina, Yuji] Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA.
RP Phoon, CKL (reprint author), NYU, Pediat Cardiol Program, Sch Med, 160 E 32nd St,2nd Floor, New York, NY 10016 USA.
EM colin.phoon@med.nyu.edu
FU National Heart, Lung, and Blood Institute [K08-HL-04414]; American Heart
Association (Heritage Affiliate) [655907T, Z01-HL-005701]; National
Institute of Environmental Health Sciences [ES071003-10]; Japanese
Science Promotion Society; Ministry of Education, Culture, Sports,
Science, and Technology (Monkasho, Japan)
FX This work was supported by National Heart, Lung, and Blood Institute
Grants K08-HL-04414 and American Heart Association (Heritage Affiliate)
Grant-in-Aid No. 655907T (to C. K. L. Phoon) and Grant Z01-HL-005701 (to
C. W. Lo), the Intramural Research Program of the National Institute of
Environmental Health Sciences Grant ES071003-10, and a conditional gift
from RIKEN-Brain Science Institute to Y. Mishina. S. Kishigami was
supported in part by the Japanese Science Promotion Society. K. Yamamura
was supported in part by Grants-in-Aid from the Ministry of Education,
Culture, Sports, Science, and Technology (Monkasho, Japan).
NR 55
TC 21
Z9 21
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP H1617
EP H1628
DI 10.1152/ajpheart.00304.2009
PG 12
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 511DF
UT WOS:000271143400011
PM 19717734
ER
PT J
AU Ungvari, Z
Labinskyy, N
Mukhopadhyay, P
Pinto, JT
Bagi, Z
Ballabh, P
Zhang, CH
Pacher, P
Csiszar, A
AF Ungvari, Zoltan
Labinskyy, Nazar
Mukhopadhyay, Partha
Pinto, John T.
Bagi, Zsolt
Ballabh, Praveen
Zhang, Cuihua
Pacher, Pal
Csiszar, Anna
TI Resveratrol attenuates mitochondrial oxidative stress in coronary
arterial endothelial cells
SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
LA English
DT Article
DE vasoprotection; histone deacetylase; sirtuin 1
ID SMALL-MOLECULE ACTIVATORS; LIFE-SPAN; SUPEROXIDE-PRODUCTION; CALORIC
RESTRICTION; HYDROGEN-PEROXIDE; ENERGY-METABOLISM; SKELETAL-MUSCLE; LIVE
CELLS; IN-VIVO; SIRT1
AB Ungvari Z, Labinskyy N, Mukhopadhyay P, Pinto JT, Bagi Z, Ballabh P, Zhang C, Pacher P, Csiszar A. Resveratrol attenuates mitochondrial oxidative stress in coronary arterial endothelial cells. Am J Physiol Heart Circ Physiol 297: H1876-H1881, 2009. First published September 11, 2009; doi:10.1152/ajpheart.00375.2009. The production of hyperglycemia-induced mitochondrial reactive oxygen species (mtROS) is a key event in the development of diabetic complications. Because resveratrol, a naturally occurring polyphenol, has been reported to confer vasoprotection, improving endothelial function and preventing complications of diabetes, we investigated the effect of resveratrol on mtROS production in cultured human coronary arterial endothelial cells (CAECs). The measurement of MitoSox fluorescence showed that resveratrol attenuates both steady-state and high glucose (30 mM)-induced mtROS production in CAECs, an effect that was prevented by the knockdown of the protein deacetylase silent information regulator 2/sirtuin 1 (SIRT1), an intracellular target of resveratrol. An overexpression of SIRT1 mimicked the effects of resveratrol, attenuating mtROS production. Similar results were obtained in CAECs transfected with mitochondria-targeted H(2)O(2)-sensitive HyPer-Mito fluorescent sensor. Amplex red assay showed that resveratrol and SIRT1 overexpression significantly reduced cellular H(2)O(2) levels as well. Resveratrol upregulated MnSOD expression and increased cellular GSH content in a concentration-dependent manner (measured by HPLC coulometric analysis). These effects were attenuated by SIRT1 knockdown and mimicked by SIRT1 overexpression. We propose that resveratrol, via a pathway that involves the activation of SIRT1 and the upregulation of antioxidant defense mechanisms, attenuates mtROS production, suggesting the potential for new treatment approaches targeting endothelial mitochondria in metabolic diseases.
C1 [Ungvari, Zoltan; Labinskyy, Nazar; Bagi, Zsolt; Csiszar, Anna] New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA.
[Pinto, John T.] New York Med Coll, Dept Biochem, Valhalla, NY 10595 USA.
[Ballabh, Praveen] New York Med Coll, Dept Anat & Cell Biol & Pediat, Valhalla, NY 10595 USA.
[Ungvari, Zoltan; Csiszar, Anna] Univ Oklahoma, Hlth Sci Ctr, Dept Geriatr Med, Reynolds Oklahoma Ctr Aging, Oklahoma City, OK USA.
[Mukhopadhyay, Partha; Pacher, Pal] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD USA.
[Zhang, Cuihua] Univ Missouri, Dept Internal Med Med Pharmacol & Physiol & Nutr, Columbia, MO USA.
RP Csiszar, A (reprint author), New York Med Coll, Dept Physiol, Valhalla, NY 10595 USA.
EM zoltan-ungvari@ouhsc.edu; anna_csiszar@nymc.edu
RI MUKHOPADHYAY, PARTHA/G-3890-2010; Pacher, Pal/B-6378-2008
OI MUKHOPADHYAY, PARTHA/0000-0002-1178-1274; Pacher,
Pal/0000-0001-7036-8108
FU American Federation for Aging Research; American Diabetes Association;
American Heart Association [110350047A]; National Institutes of Health
(NIH) [HL-077256, HL-43023, CA-111842, RO1-HL-077566, RO1-HL-085119]
FX This work was supported by grants from the American Federation for Aging
Research (to A. Csiszar) and the American Diabetes Association (to Z.
Ungvari); by American Heart Association Grant 110350047A (to C. Zhang)
and National Institutes of Health (NIH) Grants HL-077256 and HL-43023
(to Z. Ungvari and A. Csiszar), CA-111842 (to J. PT. Pinto), and
RO1-HL-077566 and RO1-HL-085119 (to C. Zhang); and by the Intramural
Research Program of the NIH (to P. Pacher).
NR 50
TC 162
Z9 165
U1 2
U2 17
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 0363-6135
J9 AM J PHYSIOL-HEART C
JI Am. J. Physiol.-Heart Circul. Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP H1876
EP H1881
DI 10.1152/ajpheart.00375.2009
PG 6
WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular
Disease
SC Cardiovascular System & Cardiology; Physiology
GA 511DF
UT WOS:000271143400041
PM 19749157
ER
PT J
AU Meir, T
Levi, R
Lieben, L
Libutti, S
Carmeliet, G
Bouillon, R
Silver, J
Naveh-Many, T
AF Meir, Tomer
Levi, Ronen
Lieben, Liesbet
Libutti, Steven
Carmeliet, Geert
Bouillon, Roger
Silver, Justin
Naveh-Many, Tally
TI Deletion of the vitamin D receptor specifically in the parathyroid
demonstrates a limited role for the receptor in parathyroid physiology
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE serum calcium; calcium homeostasis; secondary hyperparathyroidism;
calcium receptor; parathyroid hormone
ID CALCIUM-SENSING RECEPTOR; EXTRACELLULAR CA2+-SENSING RECEPTOR; MINERAL
ION HOMEOSTASIS; VDR-KNOCKOUT MICE; SKELETAL PHENOTYPE; NUCLEAR
RECEPTOR; D METABOLITES; ABLATED MICE; HORMONE; GENE
AB Meir T, Levi R, Lieben L, Libutti S, Carmeliet G, Bouillon R, Silver J, Naveh-Many T. Deletion of the vitamin D receptor specifically in the parathyroid demonstrates a limited role for the receptor in parathyroid physiology. Am J Physiol Renal Physiol 297: F1192-F1198, 2009. First published August 19, 2009; doi: 10.1152/ajprenal.00360.2009.-1,25(OH)(2)D(3) decreases parathyroid hormone (PTH) gene transcription through the vitamin D receptor (VDR). Total body VDR(-/-) mice have high PTH levels, hypocalcemia, hypophosphatemia, and bone malformations. To investigate PTH regulation by the VDR specifically in the parathyroid, we generated parathyroid-specific VDR knockout mice (PT-VDR(-/-)). In both strains, there was a decrease in parathyroid calcium receptor (CaR) levels. The number of proliferating parathyroid cells was increased in the VDR(-/-) mice but not in the PT-VDR(-/-) mice. Serum PTH levels were moderately but significantly increased in the PT-VDR(-/-) mice with normal serum calcium levels. The sensitivity of the parathyroid glands of the PT-VDR(-/-) mice to calcium was intact as measured by serum PTH levels after changes in serum calcium. This indicates that the reduced CaR in the PT-VDR(-/-) mice enables a physiologic response to serum calcium. Serum C-terminal collagen crosslinks, a marker of bone resorption, were increased in the PT-VDR(-/-) mice with no change in the bone formation marker, serum osteocalcin, consistent with a resorptive effect due to the increased serum PTH levels in the PT-VDR(-/-) mice. Therefore, deletion of the VDR specifically in the parathyroid decreases parathyroid CaR expression and only moderately increases basal PTH levels, suggesting that the VDR has a limited role in parathyroid physiology.
C1 [Meir, Tomer; Levi, Ronen; Silver, Justin; Naveh-Many, Tally] Hadassah Hebrew Univ Hosp, Minerva Ctr Calcium & Bone Metab, Serv Nephrol, IL-91120 Jerusalem, Israel.
[Lieben, Liesbet; Carmeliet, Geert; Bouillon, Roger] NCI, Bethesda, MD 20892 USA.
[Libutti, Steven] Katholieke Univ Leuven, Lab Expt Med & Endocrinol, Louvain, Belgium.
RP Silver, J (reprint author), Hadassah Hebrew Univ Hosp, Minerva Ctr Calcium & Bone Metab, Serv Nephrol, POB 12000, IL-91120 Jerusalem, Israel.
EM silver@huji.ac.il; tally@cc.huji.ac.il
OI Lieben, Liesbet/0000-0002-3076-4947
FU Israel Academy of Sciences; D-Cure; Amgen
FX The work was supported in part by grants from the Israel Academy of
Sciences, D-Cure, and Amgen.
NR 37
TC 34
Z9 35
U1 0
U2 2
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP F1192
EP F1198
DI 10.1152/ajprenal.00360.2009
PG 7
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 514DO
UT WOS:000271374700007
PM 19692484
ER
PT J
AU Oppermann, M
Qin, Y
Lai, EY
Eisner, C
Li, LL
Huang, YN
Mizel, D
Fryc, J
Wilcox, CS
Briggs, J
Schnermann, J
Castrop, H
AF Oppermann, Mona
Qin, Yan
Lai, En Yin
Eisner, Christoph
Li, Lingli
Huang, Yuning
Mizel, Diane
Fryc, Justyna
Wilcox, Christopher S.
Briggs, Josephine
Schnermann, Jurgen
Castrop, Hayo
TI Enhanced tubuloglomerular feedback in mice with vascular overexpression
of A(1) adenosine receptors
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE single nephron glomerular filtration rate; smooth muscle;
juxtaglomerular apparatus
ID GLOMERULAR-FILTRATION RATE; RAT-KIDNEY; GENE-EXPRESSION; DEPENDENT
INHIBITION; AFFERENT ARTERIOLES; RENIN SECRETION; A(2A) RECEPTORS;
DEFICIENT MICE; MESSENGER-RNA; MOUSE STRAIN
AB Oppermann M, Qin Y, Lai EY, Eisner C, Li L, Huang Y, Mizel D, Fryc J, Wilcox CS, Briggs J, Schnermann J, Castrop H. Enhanced tubuloglomerular feedback in mice with vascular overexpression of A(1) adenosine receptors. Am J Physiol Renal Physiol 297: F1256-F1264, 2009. First published September 9, 2009; doi: 10.1152/ajprenal.00264.2009.-Adenosine 1 receptors (A1AR) in the kidney are expressed in the vasculature and the tubular system. Pharmacological inhibition or global genetic deletion of A1AR causes marked reductions or abolishment of tubuloglomerular feedback (TGF) responses. To assess the function of vascular A1AR in TGF, we generated transgenic mouse lines in which A1AR expression in smooth muscle was augmented by placing A1AR under the control of a 5.38-kb fragment of the rat smooth muscle alpha-actin promoter and first intron (12). Two founder lines with highest expression in the kidney [353 +/- 42 and 575 +/- 43% compared with the wild type (WT)] were used in the experiments. Enhanced expression of A1AR at the expected site in these lines was confirmed by augmented constrictor responses of isolated afferent arterioles to administration of the A1AR agonist N-6-cyclohexyladenosine. Maximum TGF responses (0-30 nl/min flow step) were increased from 8.4 +/- 0.9 mmHg in WT (n = 21) to 14.2 +/- 0.7 mmHg in A1AR-transgene (tg) 4 (n = 22; P < 0.0001), and to 12.6 +/- 1.2 mmHg in A1AR-tg7 (n = 12; P < 0.02). Stepwise changes in perfusion flow caused greater numerical TGF responses in A1AR-tg than WT in all flow ranges with differences reaching levels of significance in the intermediate flow ranges of 7.5-10 and 10-15 nl/min. Proximal-distal single-nephron glomerular filtration rate (SNGFR) differences (free-flow micropuncture) were also increased in A1AR-tg, averaging 6.25 +/- 1.5 nl/min compared with 2.6 +/- 0.51 nl/min in WT (P = 0.034). Basal plasma renin concentrations as well as the suppression of renin secretion after volume expansion were similar in A1AR-tg and WT mice, suggesting lack of transgene expression in juxtaglomerular cells. These data indicate that A1AR expression in vascular smooth muscle cells is a critical component for TGF signaling and that changes in renal vascular A1AR expression may determine the magnitude of TGF responses.
C1 [Castrop, Hayo] Univ Regensburg, Inst Physiol, D-93040 Regensburg, Germany.
[Oppermann, Mona; Qin, Yan; Eisner, Christoph; Li, Lingli; Huang, Yuning; Mizel, Diane; Fryc, Justyna; Schnermann, Jurgen] NIDDKD, Bethesda, MD 20892 USA.
[Briggs, Josephine] NIH, Natl Ctr Complementary & Alternat Med, Bethesda, MD 20892 USA.
[Oppermann, Mona] Childrens Hosp, Univ Med Ctr, Regensburg, Germany.
[Lai, En Yin; Wilcox, Christopher S.] Georgetown Univ, Div Nephrol & Hypertens, Washington, DC USA.
[Lai, En Yin; Wilcox, Christopher S.] Georgetown Univ, Cardiovasc Kidney Hypertens Inst, Washington, DC USA.
RP Castrop, H (reprint author), Univ Regensburg, Inst Physiol, Univ Str 31, D-93040 Regensburg, Germany.
EM hayo@castrop.com
RI Briggs, Josephine/B-9394-2009
OI Briggs, Josephine/0000-0003-0798-1190
FU NIDDK; Deutsche Forschungsgemeinschaft [SFB 699/A4]; NIH [DK-36079,
DK-49870, HL-68686-01]
FX This work was supported by the intramural research program of the NIDDK
and by a grant from the Deutsche Forschungsgemeinschaft (SFB 699/A4). C.
S. Wilcox was supported by NIH Grants DK-36079, DK-49870, and
HL-68686-01.
NR 35
TC 10
Z9 11
U1 0
U2 0
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP F1256
EP F1264
DI 10.1152/ajprenal.00264.2009
PG 9
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 514DO
UT WOS:000271374700014
PM 19741017
ER
PT J
AU Wangemann, P
Kim, HM
Billings, S
Nakaya, K
Li, XM
Singh, R
Sharlin, DS
Forrest, D
Marcus, DC
Fong, PY
AF Wangemann, Philine
Kim, Hyoung-Mi
Billings, Sara
Nakaya, Kazuhiro
Li, Xiangming
Singh, Ruchira
Sharlin, David S.
Forrest, Douglas
Marcus, Daniel C.
Fong, Peying
TI Developmental delays consistent with cochlear hypothyroidism contribute
to failure to develop hearing in mice lacking Slc26a4/pendrin expression
SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
LA English
DT Article
DE DFNB4; Pendred syndrome; thyroid; Tectb; bicarbonate
ID TYPE-2 IODOTHYRONINE DEIODINASE; ENLARGED VESTIBULAR AQUEDUCT; THYROID
EPITHELIAL-CELLS; PENDRED-SYNDROME GENE; APICAL IODIDE EFFLUX; SYNDROME
MOUSE MODEL; POSTNATAL-DEVELOPMENT; TECTORIAL MEMBRANE; CHLORIDE
CHANNEL; PDS MUTATIONS
AB Wangemann P, Kim HM, Billings S, Nakaya K, Li X, Singh R, Sharlin DS, Forrest D, Marcus DC, Fong P. Developmental delays consistent with cochlear hypothyroidism contribute to failure to develop hearing in mice lacking Slc26a4/pendrin expression. Am J Physiol Renal Physiol 297: F1435-F1447, 2009. First published August 19, 2009; doi:10.1152/ajprenal. 00011.2009.-Mutations of SLC26A4 cause an enlarged vestibular aqueduct, nonsyndromic deafness, and deafness as part of Pendred syndrome. SLC26A4 encodes pendrin, an anion exchanger located in the cochlea, thyroid, and kidney. The goal of the present study was to determine whether developmental delays, possibly mediated by systemic or local hypothyroidism, contribute to the failure to develop hearing in mice lacking Slc26a4 (Slc26a4(-/-)). We evaluated thyroid function by voltage and pH measurements, by array-assisted gene expression analysis, and by determination of plasma thyroxine levels. Cochlear development was evaluated for signs of hypothyroidism by microscopy, in situ hybridization, and quantitative RT-PCR. No differences in plasma thyroxine levels were found in Slc26a4(-/-) and sexmatched Slc26a4(+/-) littermates between postnatal day 5 (P5) and P90. In adult Slc26a4(-/-) mice, the transepithelial potential and the pH of thyroid follicles were reduced. No differences in the expression of genes that participate in thyroid hormone synthesis or ion transport were observed at P15, when plasma thyroxine levels peaked. Scala media of the cochlea was 10-fold enlarged, bulging into and thereby displacing fibrocytes, which express Dio2 to generate a cochlear thyroid hormone peak at P7. Cochlear development, including tunnel opening, arrival of efferent innervation at outer hair cells, endochondral and intramembraneous ossification, and developmental changes in the expression of Dio2, Dio3, and Tectb were delayed by 1-4 days. These data suggest that pendrin functions as a HCO(3)(-) transporter in the thyroid, that Slc26a4(-/-) mice are systemically euthyroid, and that delays in cochlear development, possibly due to local hypothyroidism, lead to the failure to develop hearing.
C1 [Wangemann, Philine; Kim, Hyoung-Mi; Billings, Sara; Nakaya, Kazuhiro; Li, Xiangming; Singh, Ruchira; Marcus, Daniel C.; Fong, Peying] Kansas State Univ, Dept Anat & Physiol, Manhattan, KS 66506 USA.
[Nakaya, Kazuhiro] Tohoku Univ, Dept Otolaryngol, Sendai, Miyagi 980, Japan.
[Sharlin, David S.; Forrest, Douglas] NIDDK, Bethesda, MD USA.
RP Wangemann, P (reprint author), Kansas State Univ, Dept Anat & Physiol, 205 Coles Hall, Manhattan, KS 66506 USA.
EM wange@vet.ksu.edu
RI Wangemann, Philine/N-2826-2013
FU National Institutes of Health (NIH) [NIH-R01-DC01098, NIH-R01-DC00212,
NIH-P20-RR017686]; College of Veterinary Medicine at Kansas State
University SFYI; National Institute of Diabetes and Digestive and Kidney
Diseases
FX We gratefully acknowledge the support by grants from the National
Institute on Deafness and Other Communication Disorders National
Institutes of Health (NIH)-R01-DC01098 to P. Wangemann and
NIH-R01-DC00212 to D. C. Marcus, grants from the National Institute for
Research Resources NIH-P20-RR017686-Project 2 to P. Fong,
NIH-P20-RR017686-Core B to D. C. Marcus, and NIH-P20-RR017686-Core C to
D. C. Marcus, and grants from College of Veterinary Medicine at Kansas
State University SFYI to P. Fong and SMILE to P. Wangemann. Furthermore,
the support of the intermural program at National Institute of Diabetes
and Digestive and Kidney Diseases at the NIH to D. Forrest is gratefully
acknowledged.
NR 66
TC 37
Z9 37
U1 0
U2 1
PU AMER PHYSIOLOGICAL SOC
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA
SN 1931-857X
J9 AM J PHYSIOL-RENAL
JI Am. J. Physiol.-Renal Physiol.
PD NOV
PY 2009
VL 297
IS 5
BP F1435
EP F1447
DI 10.1152/ajprenal.00011.2009
PG 13
WC Physiology; Urology & Nephrology
SC Physiology; Urology & Nephrology
GA 514DO
UT WOS:000271374700033
PM 19692489
ER
PT J
AU Rashid, JR
Spengler, RF
Wagner, RM
Melanson, C
Skillen, EL
Mays, RA
Heurtin-Roberts, S
Long, JA
AF Rashid, Jamila R.
Spengler, Robert F.
Wagner, Robin M.
Melanson, Cindi
Skillen, Elizabeth L.
Mays, Robert A., Jr.
Heurtin-Roberts, Suzanne
Long, Judith A.
TI Eliminating Health Disparities Through Transdisciplinary Research,
Cross-Agency Collaboration, and Public Participation
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
ID UNITED-STATES; TRENDS; SCIENCE; DISEASE
AB Despite efforts to the contrary, disparities in health and health care persist in the United States. To solve this problem, federal agencies representing different disciplines and perspectives are collaborating on a variety of transdisciplinary research initiatives. The most recent of these initiatives was launched in 2006 when the Centers for Disease Control and Prevention's Office of Public Health Research and the Department of Health and Human Services' Office of Minority Health brought together federal partners representing a variety of disciplines to form the Federal Collaboration on Health Disparities Research (FCHDR).
FCHDR collaborates with a wide variety of federal and nonfederal partners to support and disseminate research that aims to reduce or eliminate disparities in health and health care. Given the complexity involved in eliminating health disparities, there is a need for more transdisciplinary, collaborative research, and facilitating that research is FCHDR's mission. (Am J Public Health. 2009;99:1955-1961. doi:10.2105/AJPH.2009.167932)
C1 [Rashid, Jamila R.; Spengler, Robert F.; Wagner, Robin M.; Melanson, Cindi; Skillen, Elizabeth L.] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Heurtin-Roberts, Suzanne] Off Minor Hlth, Dept Hlth & Human Serv, Rockville, MD USA.
[Mays, Robert A., Jr.] NIH, Bethesda, MD 20892 USA.
[Long, Judith A.] Philadelphia VA Ctr Hlth Equ Res & Promot, Dept Vet Affairs, Philadelphia, PA USA.
RP Rashid, JR (reprint author), HHS, Off Minor Hlth, 1101 Wootton Pkwy,Suite 600, Rockville, MD 20852 USA.
EM jamila.rashid@hhs.gov
RI Heurtin-Roberts, Suzanne/D-7274-2013
NR 31
TC 16
Z9 16
U1 0
U2 9
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 NOV
PY 2009
VL 99
IS 11
BP 1955
EP 1961
DI 10.2105/AJPH.2009.167932
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 511ZD
UT WOS:000271209900012
PM 19762652
ER
PT J
AU Safran, MA
Mays, RA
Huang, LN
McCuan, R
Pham, PK
Fisher, SK
McDuffie, KY
Trachtenberg, A
AF Safran, Marc A.
Mays, Robert A., Jr.
Huang, Larke Nahme
McCuan, Ron
Pham, Phuong Kim
Fisher, Sylvia Kay
McDuffie, Kathleen Y.
Trachtenberg, Alan
TI Mental Health Disparities
SO AMERICAN JOURNAL OF PUBLIC HEALTH
LA English
DT Editorial Material
ID INTERNATIONAL DIAGNOSTIC INTERVIEW; DSM-IV; LIMITATIONS; PARADIGM;
VALIDITY; ILLNESS
AB Mental health disparities have received increased attention in the literature in recent years. After considering 165 different health disparity conditions, the Federal Collaborative for Health Disparities Research chose mental health disparity as one of four topics warranting its immediate national research attention. In this essay, we describe the challenges and opportunities encountered in developing a research agenda to address mental health disparities in the United States. Varying definitions of mental health disparity, the heterogeneity of populations facing such disparity, and the power, complexity, and intertwined nature of contributing factors are among the many challenges. We convey an evolving interagency approach to mental health disparities research and guidance for further work in the field. (Am J Public Health. 2009;99:1962-1966. doi:10.2105/AJPH.2009.167346)
C1 [Safran, Marc A.; McDuffie, Kathleen Y.] Ctr Dis Control & Prevent, Atlanta, GA 30333 USA.
[Mays, Robert A., Jr.; Pham, Phuong Kim] NIMH, NIH, Bethesda, MD 20892 USA.
[Huang, Larke Nahme; Fisher, Sylvia Kay] Subst Abuse & Mental Hlth Serv Adm, Rockville, MD USA.
[McCuan, Ron] Natl Inst Correct, Washington, DC USA.
[Trachtenberg, Alan] Indian Hlth Serv, Rockville, MD USA.
RP Safran, MA (reprint author), Ctr Dis Control & Prevent, 1600 Clifton Rd,Mail Stop E-44, Atlanta, GA 30333 USA.
EM MSafran@cdc.gov
NR 40
TC 26
Z9 26
U1 5
U2 9
PU AMER PUBLIC HEALTH ASSOC INC
PI WASHINGTON
PA 800 I STREET, NW, WASHINGTON, DC 20001-3710 USA
SN 0090-0036
J9 AM J PUBLIC HEALTH
JI Am. J. Public Health
PD NOV
PY 2009
VL 99
IS 11
BP 1962
EP 1966
DI 10.2105/AJPH.2009.167346
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 511ZD
UT WOS:000271209900013
PM 19820213
ER
PT J
AU Reddy, NM
Suryanaraya, V
Yates, MS
Kleeberger, SR
Hassoun, PM
Yamamoto, M
Liby, KT
Sporn, MB
Kensler, TW
Reddy, SP
AF Reddy, Narsa M.
Suryanaraya, Vegiraju
Yates, Melinda S.
Kleeberger, Steven R.
Hassoun, Paul M.
Yamamoto, Masayuki
Liby, Karen T.
Sporn, Michael B.
Kensler, Thomas W.
Reddy, Sekhar P.
TI The Triterpenoid CDDO-Imidazolide Confers Potent Protection against
Hyperoxic Acute Lung Injury in Mice
SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
LA English
DT Article
DE Nrf2; Keap1; antioxidants; stress response
ID RESPIRATORY-DISTRESS-SYNDROME; PERMEABLE RADICAL SCAVENGER; OXIDATIVE
STRESS; ORGAN INJURY; NRF2; INFLAMMATION; MECHANISMS; INDUCTION;
RESPONSES; OXIDANTS
AB Rationale: Oxygen supplementation (e.g., hyperoxia) is used to support critically ill patients with noninfectious and infectious acute lung injury (ALI); however, hyperoxia exposure can potentially further contribute to and/or perpetuate preexisting ALI. Thus, developing novel therapeutic agents to minimize the side effects of hyperoxia is essential to improve the health of patients with severe ALI and respiratory dysfunction. We have previously shown that mice with a genetic disruption of the Nrf2 transcription factor, which squelches cellular stress by up-regulating the induction of several antioxidant enzymes and proteins, have greater susceptibility to hyperoxic lung injury. Moreover, we have recently demonstrated that Nrf2-deficiency impairs the resolution of lung injury and inflammation after nonlethal hyperoxia exposure.
Objectives: To test the hypothesis that amplification of endogenous Nrf2 activity would prevent or dampen ALI induced by hyperoxia.
Methods: Here, we tested our hypothesis using a synthetic triterpenoid compound CDDO-imidazole (CDDO-Im) (1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl] imidazole) in Nrf2-sufficient and Nrf2-deficient mice subjected to hyperoxia-induced ALI.
Measurements and Main Results: We demonstrate that oral administration of CDDO-Im at a dose of 30 mu mol/kg body weight during the hyperoxic exposure is sufficient to markedly attenuate hyperoxia-induced ALI in Nrf2-sufficient but not Nrf2-deficient mice. This protection by the CDDO-Im against hyperoxic insult was accompanied by increased levels of Nrf2-regulated cytoprotective gene expression and reduced levels of DNA damage in the lung.
Conclusions: These results suggest that up-regulation of Nrf2 signaling by CDDO-Im or its analogs may provide a novel therapeutic strategy to minimize the adverse effects of hyperoxia.
C1 [Reddy, Narsa M.; Suryanaraya, Vegiraju; Yates, Melinda S.; Kensler, Thomas W.; Reddy, Sekhar P.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA.
[Kleeberger, Steven R.] Natl Inst Environm Hlth Sci, NIH, Res Triangle Pk, NC USA.
[Hassoun, Paul M.] Johns Hopkins Univ, Dept Med, Baltimore, MD USA.
[Yamamoto, Masayuki] Tohoku Univ, Dept Med Biochem, Sendai, Miyagi 980, Japan.
[Liby, Karen T.; Sporn, Michael B.] Dartmouth Coll, Hitchcock Med Ctr, Dartmouth Med Sch, Dept Pharmacol & Toxicol, Hanover, NH 03756 USA.
RP Reddy, SP (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Room E7610,615 N Wolfe St, Baltimore, MD 21205 USA.
EM sreddy@jhsph.edu
RI Yamamoto, Masayuki/A-4873-2010; Kensler, Thomas/D-8686-2014
OI Kensler, Thomas/0000-0002-6676-261X
FU National Institute of Health [HL66109, Est 1863, HL049441, SCCOR P50
HL073994, CA94076, P30 ES03819]; National Institutes of Health; National
Institute of Environmental Health Sciences
FX Supported by National Institute of Health grants HL66109 and Est 1863
(S.P.R.), HL049441 (P.M.H), SCCOR P50 HL073994 (S.P.R. and P.M.H.),
CA94076 (T.W.K.), P30 ES03819, and in part by the Intramural Research
Program of the National Institutes of Health, National Institute of
Environmental Health Sciences (S. R. K.).
NR 42
TC 30
Z9 30
U1 0
U2 1
PU AMER THORACIC SOC
PI NEW YORK
PA 1740 BROADWAY, NEW YORK, NY 10019-4374 USA
SN 1073-449X
J9 AM J RESP CRIT CARE
JI Am. J. Respir. Crit. Care Med.
PD NOV 1
PY 2009
VL 180
IS 9
BP 867
EP 874
DI 10.1164/rccm.200905-0670OC
PG 8
WC Critical Care Medicine; Respiratory System
SC General & Internal Medicine; Respiratory System
GA 512AX
UT WOS:000271215500011
PM 19679692
ER
PT J
AU Summers, RM
Swift, JA
Dwyer, AJ
Choi, JR
Pickhardt, PJ
AF Summers, Ronald M.
Swift, Jeffrey A.
Dwyer, Andrew J.
Choi, J. Richard
Pickhardt, Perry J.
TI Normalized Distance Along the Colon Centerline: A Method for Correlating
Polyp Location on CT Colonography and Optical Colonoscopy
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article; Proceedings Paper
CT Digestive Disease Week/110th Annual Meeting of the
American-Gastroenterological-Association
CY MAY 30-JUN 04, 2009
CL Chicago, IL
SP Amer Gastroenterol Assoc
DE colorectal cancer screening; colon polyp; CT colonography; optical
colonoscopy
ID CURVED CROSS-SECTIONS; FEASIBILITY; SYSTEM
AB OBJECTIVE. The ability to accurately locate a polyp found on CT colonography (CTC) at subsequent optical colonoscopy (OC) is an important part of the successful implementation of CTC for colorectal cancer screening. The purpose of this study was to determine whether a polyp's normalized distance along the colon centerline derived from CTC data can accurately predict its location on OC.
MATERIALS AND METHODS. The polyp population consisted of 152 polyps in 121 patients. CTC polyp findings were verified by same-day segmentally-unblinded OC. Each polyp's normalized distance along the colon centerline was computed by dividing its distance from the anorectal junction measured along the colon centerline by the length of the colon at CTC. The predicted polyp location at OC was computed by multiplying the normalized distance along the colon centerline by the colon length at OC (i.e., the distance to the cecum as determined at full colonoscope insertion). The differences between the true and predicted polyp locations at OC were compared using paired Student's t tests, linear regression, prediction interval assessment, and Bland-Altman analyses.
RESULTS. The differences between the true and predicted polyp locations at OC using the supine and prone CTC-normalized distances along the colon centerline were 2.2 +/- 10.5 cm (mean +/- SD; n = 136) and 1.5 +/- 10.5 cm (n = 135), respectively. The predicted location was within 10 cm of its true location for 71.3% (97/136) to 74.8% (101/135) of polyps and within 20 cm of its true location for 93.3% (126/135) to 93.4% (127/136) of polyps.
CONCLUSION. By computing the normalized distance along the colon centerline of a polyp found at CTC, the location of a polyp at OC can be predicted to within 10 cm (i.e., 1 colonoscope mark) for the majority of polyps.
C1 [Summers, Ronald M.; Swift, Jeffrey A.; Dwyer, Andrew J.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Choi, J. Richard] Walter Reed Army Med Ctr, Washington, DC 20307 USA.
[Pickhardt, Perry J.] Univ Wisconsin, Dept Radiol, Sch Med, Madison, WI 53706 USA.
RP Summers, RM (reprint author), NIH, Ctr Clin, Bldg 10,Rm 1C368X,MSC 1182, Bethesda, MD 20892 USA.
EM rms@nih.gov
FU Intramural NIH HHS [Z01 CL040003-05, Z01 CL040003-06, ZIA CL040003-07,
ZIA CL040003-08, ZIA CL040003-09]
NR 15
TC 17
Z9 18
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD NOV
PY 2009
VL 193
IS 5
BP 1296
EP 1304
DI 10.2214/AJR.09.2611
PG 9
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 508ST
UT WOS:000270956700015
PM 19843745
ER
PT J
AU Summers, RM
Liu, JM
Yao, JH
Brown, L
Choi, JR
Pickhardt, PJ
AF Summers, Ronald M.
Liu, Jiamin
Yao, Jianhua
Brown, Linda
Choi, J. Richard
Pickhardt, Perry J.
TI Automated Measurement of Colorectal Polyp Height at CT Colonography:
Hyperplastic Polyps Are Flatter Than Adenomatous Polyps
SO AMERICAN JOURNAL OF ROENTGENOLOGY
LA English
DT Article; Proceedings Paper
CT 94th Scientific Assembly and Annual Meeting of the
Radiological-Society-of-North-America
CY NOV 30-DEC 05, 2008
CL Chicago, IL
SP Radiol Soc N Amer
DE automated size measurement; colonoscopy; colorectal cancer screening; CT
colonography; optical colonoscopy
ID VIRTUAL COLONOSCOPY; ASYMPTOMATIC ADULTS; MISS RATE; IN-VITRO; COLON;
LESIONS; PREVALENCE; MANAGEMENT; MODEL; RATES
AB OBJECTIVE. Hyperplastic polyps are more difficult to detect than adenomatous polyps at CT colonography (CTC), and it has been theorized that this difference in detectability is because hyperplastic polyps are flatter. Using automated software that computes polyp height, we determined whether hyperplastic colonic polyps on CTC are indeed flatter than adenomatous polyps of comparable width.
MATERIALS AND METHODS. At three medical centers, 1,186 patients underwent oral contrast-enhanced CTC and same-day optical colonoscopy (OC) with segment unblinding for colorectal cancer screening. One hundred eighty-five of the patients had at least one hyperplastic or adenomatous polyp 6-10 mm visible at both OC and CTC, where size was determined by a calibrated guidewire at OC. To assess flatness, the heights of the polyps at CTC were measured using a validated automated software program. The heights and height-to-width ratios of the hyperplastic polyps were compared with those of the adenomatous polyps using a Student's t test (two-tailed, unpaired, unequal variance).
RESULTS. There were 176 adenomatous and 83 hyperplastic polyps visible at segment-unblinded OC. The fraction of these polyps that were measurable at CTC using the automated software was not significantly different for adenomatous versus hyperplastic polyps (158/176 [89.8%] vs 73/87 [83.9%], respectively; p = 0.2). The average height-to-width ratios using automated width measurements were 15% less for hyperplastic polyps: 0.39 +/- 0.20 (n = 158) and 0.33 +/- 0.19 (n = 73) for adenomatous and hyperplastic polyps, respectively (p = 0.03). When polyps of comparable OC size or CTC width were considered, the heights of hyperplastic polyps were up to 27% less than those of adenomatous polyps.
CONCLUSION. For 6-10 mm polyps of a given size as determined by OC or a given width at CTC, hyperplastic polyps tend to be flatter (i.e., have lower height) compared with adenomatous polyps.
C1 [Summers, Ronald M.; Liu, Jiamin; Yao, Jianhua; Brown, Linda] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Choi, J. Richard] Walter Reed Army Med Ctr, Washington, DC 20307 USA.
[Pickhardt, Perry J.] Univ Wisconsin, Dept Radiol, Sch Med, Madison, WI 53706 USA.
RP Summers, RM (reprint author), NIH, Ctr Clin, Bldg 10,Rm 1C368X,MSC 1182, Bethesda, MD 20892 USA.
EM rms@nih.gov
FU Intramural NIH HHS [Z01 CL040003-05, Z01 CL040003-06, ZIA CL040003-07,
ZIA CL040003-08, ZIA CL040003-09]
NR 32
TC 11
Z9 11
U1 0
U2 0
PU AMER ROENTGEN RAY SOC
PI RESTON
PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 USA
SN 0361-803X
J9 AM J ROENTGENOL
JI Am. J. Roentgenol.
PD NOV
PY 2009
VL 193
IS 5
BP 1305
EP 1310
DI 10.2214/AJR.09.2442
PG 6
WC Radiology, Nuclear Medicine & Medical Imaging
SC Radiology, Nuclear Medicine & Medical Imaging
GA 508ST
UT WOS:000270956700016
PM 19843746
ER
PT J
AU Anderson, JM
Lopez, J
Sogoba, N
Schrumpf, ME
Raffel, SJ
Schwan, TG
AF Anderson, Jennifer M.
Lopez, Job
Sogoba, Nafomon
Schrumpf, Merry E.
Raffel, Sandra J.
Schwan, Tom G.
TI TICK BORNE RELAPSING FEVER IN MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Anderson, Jennifer M.] NIH, Rockville, MD USA.
[Lopez, Job; Schrumpf, Merry E.; Raffel, Sandra J.; Schwan, Tom G.] NIH, Hamilton, MT USA.
[Sogoba, Nafomon] Malaria Res & Training Ctr, Bamako, Mali.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 11
BP 4
EP 4
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700012
ER
PT J
AU Keesen, TS
Antonelli, LR
Guimaraes, LH
Carvalho, EM
Dutra, WO
Gollob, KJ
AF Keesen, Tatjana S.
Antonelli, Lis R.
Guimaraes, Luiz H.
Carvalho, Edgar M.
Dutra, Walderez O.
Gollob, Kenneth J.
TI CD4+T CELLS SUBSETS IN HUMAN CUTANEOUS LEISHMANIASIS HAVE A DISTINCT
RECEPTOR REPERTOIRES AND CYTOKINE EXPRESSION
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Keesen, Tatjana S.; Dutra, Walderez O.; Gollob, Kenneth J.] Univ Fed Minas Gerais, Belo Horizonte, MG, Brazil.
[Antonelli, Lis R.] NIH, Bethesda, MD 20892 USA.
[Guimaraes, Luiz H.; Carvalho, Edgar M.] Univ Fed Bahia, Salvador, BA, Brazil.
RI Antonelli, Lis/G-2907-2012
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 37
BP 11
EP 11
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700038
ER
PT J
AU Shrestha, B
Brien, JD
Sukupolvi-Petty, S
O'Brien, K
Nelson, S
Pierson, TC
Diamond, MS
AF Shrestha, Bimmi
Brien, James D.
Sukupolvi-Petty, Soila
O'Brien, Kathryn
Nelson, Steevenson
Pierson, Theodore C.
Diamond, Michael S.
TI NEUTRALIZING ANTIBODIES AGAINST DENGUE VIRUS TYPE-1 MAP TO DOMAIN III OF
THE E PROTEIN AND PROTECT MICE FROM LETHAL CHALLENGE
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Shrestha, Bimmi; Brien, James D.; Sukupolvi-Petty, Soila; O'Brien, Kathryn; Diamond, Michael S.] Washington Univ, Sch Med, St Louis, MO USA.
[Nelson, Steevenson; Pierson, Theodore C.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 95
BP 27
EP 27
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700096
ER
PT J
AU Morens, DM
AF Morens, David M.
TI JOSEPH JAMES KINYOUN: FOUNDING FATHER OF AMERICAN MICROBIOLOGY
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Morens, David M.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 109
BP 31
EP 32
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700110
ER
PT J
AU Addo, R
Pillai, AD
Desai, SA
AF Addo, Rachel
Pillai, Ajay D.
Desai, Sanjay A.
TI PLASMODIUM FALCIPARUM CULTIVATION IN A SODIUM-FREE MEDIUM
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Addo, Rachel; Pillai, Ajay D.; Desai, Sanjay A.] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 147
BP 42
EP 42
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700147
ER
PT J
AU Onyamboko, MA
Atibu, J
Lokomba, V
Meshnick, S
Douoguih, M
Hemingway-Foday, J
Koch, M
Wesche, D
Capparelli, E
Fleckenstein, L
Ryder, R
Bose, C
Wright, L
Tshefu, A
AF Onyamboko, Marie A.
Atibu, Jef
Lokomba, Vicky
Meshnick, Steven
Douoguih, Macaya
Hemingway-Foday, Jennifer
Koch, Matthew
Wesche, David
Capparelli, Edmund
Fleckenstein, Larry
Ryder, Robert
Bose, Carl
Wright, Linda
Tshefu, Antoinette
TI PHARMACOKINETICS (PK) AND PHARMACODYNAMICS (PD) AND SAFETY OF ARTESUNATE
(AS) AND DIHYDROARTEMISININ (DHA) FOLLOWING A SINGLE ORAL DOSE OF
ARTESUNATE DURING THE 2(ND) AND 3(RD) TRIMESTER OF PREGNANCY
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Onyamboko, Marie A.; Atibu, Jef; Lokomba, Vicky; Tshefu, Antoinette] Kinshasa Sch Publ Hlth, Kinshasa, Zaire.
[Meshnick, Steven; Bose, Carl] Univ N Carolina, Chapel Hill, NC USA.
[Douoguih, Macaya] Aeras Global TB Vaccine Fdn, Rockville, MD USA.
[Hemingway-Foday, Jennifer; Koch, Matthew] RTI Int, Res Triangle Pk, NC USA.
[Wesche, David] Lundbeck Inc, Deerfield, IL USA.
[Capparelli, Edmund; Ryder, Robert] Univ Calif San Diego, San Diego, CA 92103 USA.
[Fleckenstein, Larry] Univ Iowa, Iowa City, IA USA.
[Wright, Linda] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 1
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 224
BP 63
EP 63
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700224
ER
PT J
AU Molina-Cruz, A
Ortega, C
Winikor, J
Rodrigues, J
Barillas-Mury, C
AF Molina-Cruz, Alvaro
Ortega, Corrie
Winikor, Jared
Rodrigues, Janneth
Barillas-Mury, Carolina
TI HOW DOES PLASMODIUM FALCIPARUM EVADE OF THE MOSQUITO IMMUNE SYSTEM
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Molina-Cruz, Alvaro; Ortega, Corrie; Winikor, Jared; Rodrigues, Janneth; Barillas-Mury, Carolina] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 237
BP 67
EP 67
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700237
ER
PT J
AU Nkhoma, ET
Mu, JB
Krause, MA
Diakite, SA
Kalilani, L
Rogerson, SJ
Fairhurst, RM
Meshnick, SR
AF Nkhoma, Ella T.
Mu, Jianbing
Krause, Michael A.
Diakite, Seidina A.
Kalilani, Linda
Rogerson, Stephen J.
Fairhurst, Rick M.
Meshnick, Steven R.
TI EFFECT OF THE A-FORM OF G6PD DEFICIENCY ON MATERNAL PLASMODIUM
FALCIPARUM PARASITEMIA AND PREGNANCY OUTCOMES
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Nkhoma, Ella T.; Meshnick, Steven R.] Univ N Carolina, Chapel Hill, NC USA.
[Mu, Jianbing; Krause, Michael A.; Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Diakite, Seidina A.] Univ Bamako, Dept Immunogenet, Bamako, Mali.
[Kalilani, Linda] Univ Malawi, Coll Med, Blantyre, Malawi.
[Rogerson, Stephen J.] Univ Melbourne, Dept Med, Parkville, Vic 3052, Australia.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 303
BP 86
EP 86
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700303
ER
PT J
AU Mahanty, S
Berns, AL
Scott, E
Lizak, M
Nash, T
AF Mahanty, Siddhartha
Berns, Abby L.
Scott, Erick
Lizak, Martin
Nash, Theodore
TI A RAT MODEL OF INTRACEREBRAL INFECTION WITH TAENIA CRASSICEPS FOR THE
STUDY OF INFLAMMATION ASSOCIATED WITH ANTHELMINTIC THERAPY IN
NEUROCYSTICERCOSIS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Mahanty, Siddhartha; Berns, Abby L.; Scott, Erick; Lizak, Martin; Nash, Theodore] NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 309
BP 88
EP 88
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700309
ER
PT J
AU Krolewiecki, AJ
Ramanathan, R
Fink, V
Won, K
Cajal, S
Juarez, M
Acosta, N
Lee, R
Lammie, P
Abraham, D
Nutman, T
AF Krolewiecki, Alejandro J.
Ramanathan, Roshan
Fink, Valeria
Won, Kimberly
Cajal, Silvana
Juarez, Marisa
Acosta, Norma
Lee, Rogan
Lammie, Patrick
Abraham, David
Nutman, Thomas
TI EVALUATION OF NEW SEROLOGIC TECHNIQUES FOR THE DIAGNOSIS OF
STRONGYLOIDES STERCORALIS INFECTIONS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Krolewiecki, Alejandro J.; Cajal, Silvana; Juarez, Marisa; Acosta, Norma] Inst Invest Enfermedades Trop, Oran, Argentina.
[Ramanathan, Roshan; Nutman, Thomas] NIH, Parasit Dis Lab, Bethesda, MD 20892 USA.
[Fink, Valeria] Fdn Huesped, Buenos Aires, DF, Argentina.
[Won, Kimberly; Lammie, Patrick] Ctr Dis Control & Prevent, Div Parasit Dis, Atlanta, GA USA.
[Lee, Rogan] Westmead Hosp, Inst Clin Pathol & Med Res, Westmead, NSW 2145, Australia.
[Abraham, David] Thomas Jefferson Univ, Dept Microbiol & Immunol, Kimmel Canc Ctr, Philadelphia, PA 19107 USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 312
BP 89
EP 89
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700312
ER
PT J
AU Eksi, S
Haile, Y
Morahan, BJ
Furuya, T
Suri, A
Jiang, HY
Su, XZ
Williamson, KC
AF Eksi, Saliha
Haile, Yoseph
Morahan, Belinda J.
Furuya, Tetsuya
Suri, Amreena
Jiang, Hongying
Su, Xinzhuan
Williamson, Kim C.
TI PERINUCLEAR PROTEIN, P. FALCIPARUM GAMETOCYTOGENESIS INDUCER 1, PFGYI1,
PLAYS AN IMPORTANT ROLE IN GAMETOCYTOGENESIS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Eksi, Saliha; Haile, Yoseph; Morahan, Belinda J.; Suri, Amreena; Williamson, Kim C.] Loyola Univ, Chicago, IL 60611 USA.
[Furuya, Tetsuya; Jiang, Hongying; Su, Xinzhuan] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 1
U2 3
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 316
BP 90
EP 90
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700316
ER
PT J
AU Ssekitoleko, R
Moore, CC
Jacob, ST
Pinkerton, R
Banura, P
Meya, D
Reynolds, SJ
Kenya-Mugisha, N
Mayanja-Kizza, H
Scheld, WM
AF Ssekitoleko, Richard
Moore, Christopher C.
Jacob, Shevin T.
Pinkerton, Relana
Banura, Patrick
Meya, David
Reynolds, Steven J.
Kenya-Mugisha, Nathan
Mayanja-Kizza, Harriet
Scheld, W. Michael
TI HYPOGLYCEMIA IS ASSOCIATED WITH MORTALITY IN UGANDAN PATIENTS WITH
SEVERE SEPSIS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Ssekitoleko, Richard] Mbarara Univ, Mbarara, Uganda.
[Moore, Christopher C.; Pinkerton, Relana; Scheld, W. Michael] Univ Virginia, Charlottesville, VA USA.
[Jacob, Shevin T.] Univ Washington, Seattle, WA 98195 USA.
[Banura, Patrick] Masaka Reg Referral Hosp, Masaka, Uganda.
[Meya, David; Mayanja-Kizza, Harriet] Makerere Univ, Kampala, Uganda.
[Reynolds, Steven J.] NIH, Bethesda, MD 20892 USA.
[Kenya-Mugisha, Nathan] Minist Hlth, Kampala, Uganda.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 322
BP 92
EP 92
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700322
ER
PT J
AU Bharti, N
Broutin, H
Grais, R
Djibo, A
Grenfell, B
AF Bharti, Nita
Broutin, Helene
Grais, Rebecca
Djibo, Ali
Grenfell, Bryan
TI SPATIAL PATTERNS OF MENINGITIS IN NIGER
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Bharti, Nita; Grenfell, Bryan] Penn State Univ, University Pk, PA 16802 USA.
[Broutin, Helene] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
[Grais, Rebecca] Epicentre, Paris, France.
[Djibo, Ali] Minist Sante, Direct Gen Sante Publ, Niamey, Niger.
NR 0
TC 0
Z9 0
U1 0
U2 3
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 325
BP 93
EP 93
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700325
ER
PT J
AU Cantey, PT
Richard, S
Richard, S
Dorkenoo, A
Sodahlon, Y
Mathieu, E
AF Cantey, Paul T.
Richard, Stephanie
Richard, Stephanie
Dorkenoo, Ameyo
Sodahlon, Yao
Mathieu, Els
TI PATIENT TREATMENT COSTS FOR MANAGEMENT OF LYMPHEDEMA AND ACUTE ATTACKS
IN TOGO
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Cantey, Paul T.; Mathieu, Els] Ctr Dis Control & Prevent, Div Parasit Dis, NCZVED, Atlanta, GA USA.
[Richard, Stephanie] Fogarty Int Ctr, Bethesda, MD USA.
[Richard, Stephanie] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Dorkenoo, Ameyo] Togo Natl Program Eliminat Lymphat Filariasis, Lome, Togo.
[Sodahlon, Yao] Mectizan Donat Program, Decatur, GA USA.
NR 0
TC 1
Z9 1
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 329
BP 94
EP 94
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700329
ER
PT J
AU Coulibaly, YI
Dembele, B
Konate, S
Dolo, H
Coulibaly, SY
Sanogo, D
Soumaoro, L
Coulibaly, ME
Doumbia, SS
Diallo, AA
Traore, SF
Keita, AD
Nutman, TB
Klion, AD
AF Coulibaly, Yaya I.
Dembele, Benoit
Konate, Siaka
Dolo, Housseini
Coulibaly, Siaka Y.
Sanogo, Dramane
Soumaoro, Lamine
Coulibaly, Michel E.
Doumbia, Salif S.
Diallo, Abdallah A.
Traore, Sekou F.
Keita, Adama D.
Nutman, Thomas B.
Klion, Amy D.
TI HIGH DOSE BIANNUAL ALBENDAZOLE AND IVERMECTIN SUPPRESS WUCHERERIA
BANCROFTI MICROFILARIAL LEVELS MORE EFFECTIVELY THAN STANDARD DOSE
ANNUAL TREATMENT
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Coulibaly, Yaya I.; Dembele, Benoit; Konate, Siaka; Dolo, Housseini; Coulibaly, Siaka Y.; Sanogo, Dramane; Soumaoro, Lamine; Coulibaly, Michel E.; Doumbia, Salif S.; Diallo, Abdallah A.; Traore, Sekou F.] Univ Bamako, Bamako, Mali.
[Keita, Adama D.] Hosp Point G, Bamako, Mali.
[Nutman, Thomas B.; Klion, Amy D.] NIAID, NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 332
BP 95
EP 95
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700332
ER
PT J
AU Ho, M
Beaudry, SD
White, A
Lee, K
Arie, T
Deitsch, K
Fairhurst, RM
AF Ho, May
Beaudry, Steven D.
White, Aaron
Lee, Kristine
Arie, Takayuki
Deitsch, Kirk
Fairhurst, Rick M.
TI EXPRESSION OF PLASMODIUM FALCIPARUM ERYTHROCYTE MEMBRANE PROTEIN 1
(PFEMP1) IS IRON-DEPENDENT
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 Univ Calgary, Dept Microbiol & Infect Dis, Calgary, AB, Canada.
NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
Cornell Univ, Weill Med Coll, Dept Microbiol & Immunol, New York, NY 10021 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 334
BP 95
EP 95
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700334
ER
PT J
AU Pillai, AD
Desai, SA
AF Pillai, Ajay D.
Desai, Sanjay A.
TI GENETIC VALIDATION OF THE PLASMODIAL SURFACE ANION CHANNEL AS AN
ANTIMALARIAL DRUG TARGET
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Pillai, Ajay D.; Desai, Sanjay A.] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 337
BP 96
EP 96
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700337
ER
PT J
AU Bokhari, AA
Desai, SA
AF Bokhari, Abdullah A.
Desai, Sanjay A.
TI GENETIC MAPPING IN TWO PLASMODIUM FALCIPARUM CROSSES IDENTIFIES A LOCUS
ENCODING THE PLASMODIAL SURFACE ANION CHANNEL
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Bokhari, Abdullah A.; Desai, Sanjay A.] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 340
BP 97
EP 97
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700340
ER
PT J
AU McQueen, PG
McKenzie, FE
AF McQueen, Philip G.
McKenzie, F. Ellis
TI IMMUNE CONSTRAINTS ON PARASITEMIA AND GAMETOCYTEMIA IN MALARIA: INSIGHT
FROM NUMERICAL STUDIES
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [McQueen, Philip G.; McKenzie, F. Ellis] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 342
BP 97
EP 98
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700342
ER
PT J
AU Singh, K
Gitti, RK
Gittis, AG
Nguyen, PG
Mohan, MJ
Gowda, DC
Gowda, DC
Tullo, G
Zhou, H
Fairhurst, R
Long, C
Garboczi, DN
AF Singh, Kavita
Gitti, Rossitza K.
Gittis, Apostolos G.
Nguyen, Phuc G.
Mohan, Michael J.
Gowda, D. Channe
Gowda, D. Channe
Tullo, Gregory
Zhou, Hong
Fairhurst, Rick
Long, Carole
Garboczi, David N.
TI STRUCTURAL AND BIOCHEMICAL CHARACTERIZATION OF THE BINDING REGION OF
PLASMODIUM FALCIPARUM VAR2CSA DBL3X WITH CHONDROITIN SULFATE A
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Singh, Kavita; Gittis, Apostolos G.; Nguyen, Phuc G.; Mohan, Michael J.; Gowda, D. Channe; Tullo, Gregory; Zhou, Hong; Fairhurst, Rick; Long, Carole; Garboczi, David N.] NIAID, NIH, Rockville, MD USA.
[Gitti, Rossitza K.] ECB Forens Analyt Branch, Aberdeen, MD USA.
[Gowda, D. Channe] Penn State Univ, Coll Med, Hershey, PA USA.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 344
BP 98
EP 98
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700344
ER
PT J
AU Durbin, AP
Whitehead, SS
Elwood, D
Kagucia, W
Thumar, B
Wanionek, KA
Pierro, D
Murphy, BR
Schmidt, AC
AF Durbin, Anna P.
Whitehead, Stephen S.
Elwood, Daniel
Kagucia, Wangeci
Thumar, Bhavin
Wanionek, Kimberli A.
Pierro, Dennis
Murphy, Brian R.
Schmidt, Alexander C.
TI SAFETY AND IMMUNOGENICITY OF A 2-DOSE REGIMEN OF RDEN1 Delta 30 DENGUE
SEROTYPE 1 VACCINE WITH BOOSTING AT FOUR VERSUS SIX MONTHS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Durbin, Anna P.; Elwood, Daniel; Kagucia, Wangeci; Thumar, Bhavin; Wanionek, Kimberli A.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
[Whitehead, Stephen S.; Pierro, Dennis; Murphy, Brian R.; Schmidt, Alexander C.] NIAID, NIH, Bethesda, MD 20892 USA.
RI Mavoa, Suzanne/B-5372-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 397
BP 114
EP 114
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700397
ER
PT J
AU Whitehead, SS
Schmidt, AC
McArthur, JH
Marron, JA
Elwood, D
Thumar, B
Wanionek, KA
Pierro, D
Blaney, JE
Murphy, BR
Durbin, AF
AF Whitehead, Stephen S.
Schmidt, Alexander C.
McArthur, Julie H.
Marron, Jennifer A.
Elwood, Daniel
Thumar, Bhavin
Wanionek, Kimberli A.
Pierro, Dennis
Blaney, Joseph E.
Murphy, Brian R.
Durbin, Anna F.
TI CLINICAL EVALUATION OF LIVE ATTENUATED DEN3 VACCINE CANDIDATES
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Whitehead, Stephen S.; Schmidt, Alexander C.; Pierro, Dennis; Blaney, Joseph E.; Murphy, Brian R.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
[McArthur, Julie H.; Marron, Jennifer A.; Elwood, Daniel; Thumar, Bhavin; Wanionek, Kimberli A.; Durbin, Anna F.] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
RI Mavoa, Suzanne/B-5372-2010
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 396
BP 114
EP 114
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700396
ER
PT J
AU Bosio, CF
Jarrett, CO
Hinnebusch, BJ
AF Bosio, Christopher F.
Jarrett, Clayton O.
Hinnebusch, B. Joseph
TI EFFECTS OF FLEA FEEDING ON EARLY INNATE IMMUNE EVENTS IN THE SKIN AND
TRANSMISSION OF YERSINIA PESTIS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Bosio, Christopher F.; Jarrett, Clayton O.; Hinnebusch, B. Joseph] NIAID, Rocky Mt Labs, Hamilton, MT 59840 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 418
BP 120
EP 120
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700418
ER
PT J
AU Doumbia, S
Faye, O
Oliveira, F
Anderson, JM
Traore, P
Diarra, S
Tall, K
Sissoko, IM
Diallo, D
Samake, S
Coulibaly, CA
Traore, B
Teixeira, C
Gomez, R
Soucko, C
Lawyer, P
Keita, S
Fairhurst, R
Kamhawi, S
Valenzuela, JL
AF Doumbia, Seydou
Faye, Ousmane
Oliveira, Fabiano
Anderson, Jennifer M.
Traore, Pierre
Diarra, Souleymane
Tall, Koureissi
Sissoko, Ibrahim M.
Diallo, Daouda
Samake, Sibiry
Coulibaly, Cheick Amadou
Traore, Bourama
Teixeira, Clarissa
Gomez, Regis
Soucko, Constance
Lawyer, Phil
Keita, Somita
Fairhurst, Rick
Kamhawi, Shaden
Valenzuela, Jesus L.
TI A COHORT-BASED STUDY OF LEISHMANIA MAJOR INFECTION AND CUTANEOUS
LEISHMANIASIS IN MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Doumbia, Seydou; Diarra, Souleymane; Sissoko, Ibrahim M.; Diallo, Daouda; Samake, Sibiry; Coulibaly, Cheick Amadou; Traore, Bourama; Soucko, Constance] Univ Bamako, Fac Med Pharm & Odontostomatol, Malaria Res & Training Ctr, Bamako, Mali.
[Faye, Ousmane; Traore, Pierre; Tall, Koureissi; Keita, Somita] Ctr Natl Appui Lutte Malad, Bamako, Mali.
[Oliveira, Fabiano; Anderson, Jennifer M.; Teixeira, Clarissa; Gomez, Regis; Lawyer, Phil; Fairhurst, Rick; Kamhawi, Shaden; Valenzuela, Jesus L.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
RI Oliveira, Fabiano/B-4251-2009
OI Oliveira, Fabiano/0000-0002-7924-8038
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 481
BP 137
EP 137
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700480
ER
PT J
AU Delgado, S
Neyra, RC
Machaca, VRQ
Juarez, JA
Verastegui, M
Bocangel, CD
Comrie, A
Naquira, C
del Carpio, JGC
Gilman, RH
Bern, C
Levy, MZ
AF Delgado, Stephen
Castillo Neyra, Ricardo
Quispe Machaca, Victor R.
Ancca Juarez, Jenny
Verastegui, Manuela
Bocangel, Cesar D.
Comrie, Andrew
Naquira, Cesar
Cornejo del Carpio, Juan G.
Gilman, Robert H.
Bern, Caryn
Levy, Michael Z.
TI SPATIO-TEMPORAL PERSPECTIVES ON PREVALENCE OF TRYPANOSOMA CRUZI
INFECTION IN PERI-URBAN AREQUIPA, PERU
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Delgado, Stephen; Comrie, Andrew] Univ Arizona, Tucson, AZ USA.
[Castillo Neyra, Ricardo; Quispe Machaca, Victor R.; Ancca Juarez, Jenny; Verastegui, Manuela; Bocangel, Cesar D.; Naquira, Cesar] Univ Peruana Cayetano Heredia, Lima, Peru.
[Cornejo del Carpio, Juan G.] Minist Salud, Direcc Reg, Arequipa, Peru.
[Gilman, Robert H.] Johns Hopkins Univ, Baltimore, MD USA.
[Bern, Caryn] Ctr Dis Control & Prevent, Atlanta, GA USA.
[Levy, Michael Z.] Fogarty Int Ctr, Bethesda, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 484
BP 138
EP 138
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700483
ER
PT J
AU Hernandez, Y
Kiphart, C
Joshi, MB
Dwyer, DM
AF Hernandez, Yunuen
Kiphart, Courtney
Joshi, Manju B.
Dwyer, Dennis M.
TI CHARACTERIZATION AND EXPRESSION OF A NOVEL SECRETORY NUCLEASE, LMEXNUCS,
IN THE HUMAN PATHOGEN LEISHMANIA MEXICANA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Hernandez, Yunuen; Kiphart, Courtney; Joshi, Manju B.; Dwyer, Dennis M.] NIAID, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 499
BP 142
EP 142
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700497
ER
PT J
AU Sissoko, MS
Assadou, MH
Kone, M
Karnate, B
Guindo, O
Diallo, A
Sagara, I
Guindo, MA
Saye, R
Fay, MP
Imeru, A
Pierce, MA
Dicko, A
Guindo, A
Diallo, DA
Doumbo, O
Miller, LH
Ellis, RD
AF Sissoko, Mahamadou S.
Assadou, Mahamadoun H.
Kone, Mamady
Karnate, Beh
Guindo, Ousmane
Diallo, Abdoulbaki
Sagara, Issaka
Guindo, Merapen A.
Saye, Renion
Fay, Michael P.
Imeru, Alemush
Pierce, Mark A.
Dicko, Alassane
Guindo, Aldiouma
Diallo, Dapa A.
Doumbo, Ogobara
Miller, Louis H.
Ellis, Ruth D.
TI MALARIA INCIDENCE IN INFANTS IN BANCOUMANA, MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Sissoko, Mahamadou S.; Assadou, Mahamadoun H.; Kone, Mamady; Karnate, Beh; Guindo, Ousmane; Diallo, Abdoulbaki; Sagara, Issaka; Guindo, Merapen A.; Saye, Renion; Dicko, Alassane; Guindo, Aldiouma; Diallo, Dapa A.; Doumbo, Ogobara] Univ Bamako, Malaria Res & Training Ctr, Fac Med Pharm & Odontostomatol, Bamako, Mali.
[Fay, Michael P.] NIAID, Biostat Res Branch, NIH, Bethesda, MD 20892 USA.
[Imeru, Alemush; Pierce, Mark A.; Miller, Louis H.; Ellis, Ruth D.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 541
BP 154
EP 154
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700539
ER
PT J
AU Ellis, RD
Sissoko, M
Assadou, MH
Guindo, MA
Saye, R
Kone, M
Kante, O
Kamate, B
Guindo, O
Sagara, I
Dicko, A
Imeru, A
Fay, MP
Pierce, M
Miller, L
Miura, K
Diallo, D
Doumbo, O
AF Ellis, Ruth D.
Sissoko, Mahamadou
Assadou, Mahamadoun H.
Guindo, Merapen A.
Saye, Renion
Kone, Mamady
Kante, Ousmane
Kamate, Beh
Guindo, Ousmane
Sagara, Issaka
Dicko, Alassane
Imeru, Alemush
Fay, Michael P.
Pierce, Mark
Miller, Louis
Miura, Kazutoyo
Diallo, Dapa
Doumbo, Ogobara
TI ANTIBODY LEVELS TO AMA1 AND MSP142 IN MALIAN INFANTS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Ellis, Ruth D.; Imeru, Alemush; Pierce, Mark; Miller, Louis; Miura, Kazutoyo] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
[Sissoko, Mahamadou; Assadou, Mahamadoun H.; Guindo, Merapen A.; Saye, Renion; Kone, Mamady; Kante, Ousmane; Kamate, Beh; Guindo, Ousmane; Sagara, Issaka; Dicko, Alassane; Diallo, Dapa; Doumbo, Ogobara] Univ Bamako, Fac Med Pharm & Dent, Malaria Res & Training Ctr, Bamako, Mali.
[Fay, Michael P.] NIAID, Biostat Res Branch, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 552
BP 157
EP 157
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700550
ER
PT J
AU Tachibana, M
Iriko, H
Muratova, O
Song, GH
Wu, YM
Sattabongkot, J
Takeo, S
Otsuki, H
Torii, M
Tsuboi, T
AF Tachibana, Mayumi
Iriko, Hideyuki
Muratova, Olga
Song, Guanhong
Wu, Yimin
Sattabongkot, Jetsumon
Takeo, Satoru
Otsuki, Hitoshi
Torii, Motomi
Tsuboi, Takafumi
TI IMMUNIZATION WITH N-TERMINAL REGION OF A GAMETOCYTE PROTEIN PFS230
SUCCESSFULLY INDUCE TRANSMISSION-BLOCKING ANTIBODIES AGAINST PLASMODIUM
FALCIPARUM
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Tachibana, Mayumi; Otsuki, Hitoshi; Torii, Motomi] Ehime Univ, Toon, Japan.
[Iriko, Hideyuki] Tottori Univ, Yonago, Tottori, Japan.
[Muratova, Olga; Song, Guanhong; Wu, Yimin] NIAID, Rockville, MD USA.
[Sattabongkot, Jetsumon] AF Res Inst Med Sci, Bangkok, Thailand.
[Takeo, Satoru; Tsuboi, Takafumi] Ehime Univ, Matsuyama, Ehime, Japan.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 562
BP 160
EP 160
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700560
ER
PT J
AU Miura, K
Perera, S
Brockley, S
Zhou, H
Aebig, JA
Moretz, SE
Miller, L
Sagara, I
Dicko, A
Ellis, RD
Long, C
AF Miura, Kazutoyo
Perera, Suwani
Brockley, Sarah
Zhou, Hong
Aebig, Joan A.
Moretz, Samuel E.
Miller, Louis
Sagara, Issaka
Dicko, Alassane
Ellis, Ruth D.
Long, Carole
TI PURIFIED IGGS WHICH ARE OBTAINED FROM MALIAN CHILDREN AND WHICH DO NOT
BIND TO APICAL MEMBRANE ANTIGEN 1(AMA1) INTERFERE WITH THE BIOLOGICAL
ACTIVITY OF AMA1-SPECIFIC IGGS AS JUDGED BY THE IN VITRO GROWTH
INHIBITION ASSAY
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Miura, Kazutoyo; Perera, Suwani; Brockley, Sarah; Aebig, Joan A.; Miller, Louis; Ellis, Ruth D.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
[Zhou, Hong; Moretz, Samuel E.; Long, Carole] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Sagara, Issaka; Dicko, Alassane] Univ Bamako, Fac Med Pharm & Dent, Malaria Res & Training Ctr, Bamako, Mali.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 565
BP 161
EP 161
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956700563
ER
PT J
AU Lehmann, T
Alpha, A
Diallo, M
Yaro, AS
Kassogue, Y
Dao, A
AF Lehmann, Tovi
Alpha, Adamou
Diallo, Moussa
Yaro, Alpha S.
Kassogue, Yaya
Dao, Adama
TI LONGEVITY OF ANOPHELES GAMBIAE SL UNDER NATURAL CONDITIONS USING A
MODIFIED MARK RELEASE RECAPTURE APPROACH
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Lehmann, Tovi] NIAID, NIH, Rockville, MD USA.
[Alpha, Adamou; Diallo, Moussa; Yaro, Alpha S.; Kassogue, Yaya; Dao, Adama] Univ Mali, Malaria Res & Training Ctr, Bamako, Mali.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 588
BP 167
EP 168
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701004
ER
PT J
AU Rodrigues, J
Dixit, R
Ortega, C
Molina-Cruz, A
Mury, CB
AF Rodrigues, Janneth
Dixit, Rajnikant
Ortega, Corrie
Molina-Cruz, Alvaro
Mury, Carolina Barillas
TI IMMUNOLOGICAL PRIMING IN ANOPHELES GAMBIAE: CAN MOSQUITOES 'LEARN' FROM
A CHALLENGE WITH PLASMODIUM?
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Rodrigues, Janneth; Dixit, Rajnikant; Ortega, Corrie; Molina-Cruz, Alvaro; Mury, Carolina Barillas] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 595
BP 169
EP 170
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701011
ER
PT J
AU Sogoba, N
Keita, M
Diakite, M
Diallo, M
Baber, I
Manoukis, NC
Traore, SF
Doumbia, S
Ribeiro, JM
AF Sogoba, Nafomon
Keita, Moussa
Diakite, Mahamadou
Diallo, M'Bouye
Baber, Ibrahima
Manoukis, Nicholas C.
Traore, Sekou F.
Doumbia, Seydou
Ribeiro, Jose M.
TI MALARIA TRANSMISSION ALONG THE NIGER RIVER IN A SUDAN SAVANNA AREA OF
MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Sogoba, Nafomon; Keita, Moussa; Diakite, Mahamadou; Diallo, M'Bouye; Baber, Ibrahima; Traore, Sekou F.; Doumbia, Seydou; Ribeiro, Jose M.] Univ Bamako, Malaria Res & Training Ctr, Fac Med Pharm & Odontostomatol, Bamako, Mali.
[Manoukis, Nicholas C.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 598
BP 170
EP 170
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701014
ER
PT J
AU Fink, DL
Klion, A
Nutman, TB
AF Fink, Doran L.
Klion, Amy
Nutman, Thomas B.
TI THE TRANSCRIPTOME OF LOA LOA L3 INFECTIVE LARVAE IN COMPARISON TO THE L3
TRANSCRIPTOMES OF THE OTHER MAJOR HUMAN PATHOGENIC FILARIAE
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Fink, Doran L.; Klion, Amy; Nutman, Thomas B.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
BP 192
EP 193
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701087
ER
PT J
AU Bennuru, S
Nutman, TB
AF Bennuru, Sasisekhar
Nutman, Thomas B.
TI DECODING THE INVASION AND MOLTING PROCESSES OF BRUGIA MALAYI L3 LARVAE
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Bennuru, Sasisekhar; Nutman, Thomas B.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
BP 193
EP 193
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701088
ER
PT J
AU Conrad, PA
VanWormer, E
Shapiro, K
Miller, M
Kreuder-Johnson, C
Tinker, T
Grigg, M
Largier, J
Carpenter, T
Mazet, JK
AF Conrad, Patricia A.
VanWormer, Elizabeth
Shapiro, Karen
Miller, Melissa
Kreuder-Johnson, Chris
Tinker, Tim
Grigg, Michael
Largier, John
Carpenter, Tim
Mazet, Jonna K.
TI TRACKING TOXOPLASMA GONDII FROM LAND TO SEA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Conrad, Patricia A.; VanWormer, Elizabeth; Shapiro, Karen; Kreuder-Johnson, Chris; Largier, John; Carpenter, Tim; Mazet, Jonna K.] Univ Calif Davis, Davis, CA 95616 USA.
[Miller, Melissa] Calif Dept Fish & Game, Santa Cruz, CA USA.
[Tinker, Tim] USGS, WERC, Santa Cruz, CA USA.
[Grigg, Michael] NIAID, Bethesda, MD 20892 USA.
RI Tinker, Martin/F-1277-2011; Mazet, Jonna/B-4811-2012
NR 0
TC 0
Z9 0
U1 0
U2 11
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 690
BP 198
EP 198
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701106
ER
PT J
AU Chretien, JP
Buczak, AL
Anyamba, A
Small, J
Philip, TL
Jessup, C
Nuckols, J
Leyk, S
Miller, M
Lewis, SH
AF Chretien, Jean-Paul
Buczak, Anna L.
Anyamba, Assaf
Small, Jennifer
Philip, Trudy L.
Jessup, Christine
Nuckols, John
Leyk, Stefan
Miller, Mark
Lewis, Sheri H.
TI FORECASTING CHOLERA EPIDEMICS IN AFRICA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Chretien, Jean-Paul] Walter Reed Army Inst Res, Silver Spring, MD 20771 USA.
[Buczak, Anna L.; Philip, Trudy L.; Lewis, Sheri H.] Johns Hopkins Univ, Appl Phys Lab, Laurel, MD 20892 USA.
[Anyamba, Assaf; Small, Jennifer] NASA, Goddard Space Flight Ctr, Greenbelt, MD 80309 USA.
[Jessup, Christine; Nuckols, John; Leyk, Stefan; Miller, Mark] NIH, Fogarty Int Ctr, Bethesda, MD USA.
[Leyk, Stefan] Univ Colorado, Dept Geography, Boulder, CO 80309 USA.
NR 0
TC 0
Z9 0
U1 1
U2 6
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 717
BP 206
EP 206
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701133
ER
PT J
AU Brayner-Santos, FA
Araujo, HR
Alves, LC
Pimenta, PF
AF Brayner-Santos, Fabio A.
Araujo, Helena R.
Alves, Luiz C.
Pimenta, Paulo F.
TI ULTRASTRUCTURAL STUDY OF AEDES ALBOPICTUS SKUSE, 1895 (DIPTERA:
CULICIDAE) HEMOCYTES
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Brayner-Santos, Fabio A.; Alves, Luiz C.] NIH, Rockville, MD USA.
[Araujo, Helena R.; Pimenta, Paulo F.] IRR, Belo Horizonte, MG, Brazil.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 755
BP 218
EP 219
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701171
ER
PT J
AU Alves, LC
Araujo, HR
Baryner-Santos, FA
Pimenta, PF
AF Alves, Luiz C.
Araujo, Helena R.
Baryner-Santos, Fabio A.
Pimenta, Paulo F.
TI CHARACTERIZATION OF HEMOCYTES FROM AEDES AEGYPTI AND AEDES ALBOPICTUS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Alves, Luiz C.; Baryner-Santos, Fabio A.] NIH, Rockville, MD USA.
[Araujo, Helena R.; Pimenta, Paulo F.] Inst Rene Rachou, Belo Horizonte, MG, Brazil.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 758
BP 219
EP 219
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701174
ER
PT J
AU Santiago, HC
Bennuru, S
Nutman, T
AF Santiago, Helton C.
Bennuru, Sasisekhar
Nutman, Thomas
TI STRUCTURAL AND IMMUNOLOGIC CROSS REACTIVITY AMONG ALLERGENS AND
HOMOLOGOUS HELMINTH ANTIGENS: LESSONS LEARNED FROM TROPOMYOSIN AND THEIR
IMPLICATION FOR THE HYGIENE HYPOTHESIS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Santiago, Helton C.; Bennuru, Sasisekhar; Nutman, Thomas] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 820
BP 236
EP 237
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701236
ER
PT J
AU Crivat, G
Sa, JM
Hwang, J
Tokumasu, F
Wellems, TE
AF Crivat, Georgeta
Sa, Juliana Martha
Hwang, Jeeseong
Tokumasu, Fuyuki
Wellems, Thomas E.
TI FLUORESCENCE MULTIPLEXING IMAGING FOR STUDYING PROTEIN TRAFFICKING IN
PLASMODIUM FALCIPARUM INFECTED HUMAN ERYTHROCYTES USING
TETRACYSTEINE-TAGGED KNOB-ASSOCIATED PROTEINS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Crivat, Georgeta; Hwang, Jeeseong] NIST, NIH, Rockville, MD USA.
[Sa, Juliana Martha; Tokumasu, Fuyuki; Wellems, Thomas E.] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 840
BP 242
EP 242
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701255
ER
PT J
AU Diakite, SAS
Doumbia, S
Lopera-Mesa, TM
Traore, K
Konate, D
Doumbia, M
Krause, MA
Diouf, A
Huaman, MC
Anderson, JM
Doumbia, S
Long, CA
Diakite, M
Fairhurst, RM
AF Diakite, Seidina A. S.
Doumbia, Saibou
Lopera-Mesa, Tatiana M.
Traore, Karim
Konate, Drissa
Doumbia, Mory
Krause, Michael A.
Diouf, Ababacar
Huaman, Maria Cecilia
Anderson, Jennifer M.
Doumbia, Seydou
Long, Carole A.
Diakite, Mahamadou
Fairhurst, Rick M.
TI RELATIONSHIPS BETWEEN HEMOGLOBIN/RED BLOOD CELL POLYMORPHISMS AND
HEMOGLOBIN LEVELS IN MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Diakite, Seidina A. S.; Doumbia, Saibou; Traore, Karim; Konate, Drissa; Doumbia, Mory; Doumbia, Seydou; Diakite, Mahamadou] Malaria Res & Training Ctr, Bamako, Mali.
[Lopera-Mesa, Tatiana M.; Krause, Michael A.; Diouf, Ababacar; Huaman, Maria Cecilia; Anderson, Jennifer M.; Long, Carole A.; Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 845
BP 243
EP 243
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701260
ER
PT J
AU Ostera, GR
Lukat-Rodgers, G
Tokumasu, F
Kumar, S
Rodgers, K
AF Ostera, Graciela R.
Lukat-Rodgers, Gudrun
Tokumasu, Fuyuki
Kumar, Sanjai
Rodgers, Kenton
TI ASSOCIATION OF NITRIC OXIDE WITH HEME IN PLASMODIUM FALCIPARUM FOOD
VACUOLES
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Ostera, Graciela R.; Tokumasu, Fuyuki] NIH, Rockville, MD USA.
[Lukat-Rodgers, Gudrun; Rodgers, Kenton] N Dakota State Univ, Fargo, ND 58105 USA.
[Kumar, Sanjai] US FDA, Ctr Biol Evaluat & Res, Rockville, MD 20857 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 844
BP 243
EP 243
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701259
ER
PT J
AU Mzayek, F
Deng, HY
Hadi, MA
Mave, V
Mather, FJ
Goodenough, C
Mushatt, DM
Lertora, JJ
Krogstad, D
AF Mzayek, Fawaz
Deng, Haiyan
Hadi, M. Azam
Mave, Vidya
Mather, Frances J.
Goodenough, Christopher
Mushatt, David M.
Lertora, Juan J.
Krogstad, Donald
TI RANDOMIZED CLINICAL TRIAL (RCT) WITH A CROSSOVER STUDY DESIGN TO EXAMINE
THE SAFETY AND PHARMACOKINETICS OF A 2100 MG DOSE OF AQ-13 AND THE
EFFECTS OF A STANDARD FATTY MEAL ON ITS BIOAVAILABILITY
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Mzayek, Fawaz] Univ Memphis, Memphis, TN 38152 USA.
[Deng, Haiyan; Hadi, M. Azam; Mave, Vidya; Mather, Frances J.; Goodenough, Christopher; Mushatt, David M.; Krogstad, Donald] Tulane Univ, Hlth Sci Ctr, New Orleans, LA 70118 USA.
[Lertora, Juan J.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
BP 252
EP 252
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701290
ER
PT J
AU Yuan, J
Johnson, R
Huang, RL
Wichterman, J
Jiang, HY
Hayton, K
Fidock, D
Wellems, T
Inglese, J
Austin, C
Su, XZA
AF Yuan, Jing
Johnson, Ronald
Huang, Ruiling
Wichterman, Jennifer
Jiang, Hongying
Hayton, Karen
Fidock, David
Wellems, Thomas
Inglese, James
Austin, Christopher
Su, Xinzhuan
TI SCREENING AND GENETIC MAPPING TARGETS OF DIFFERENTIAL CHEMICAL-RESPONSE
PHENOTYPES IN PLASMODIUM FALCIPARUM
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Yuan, Jing; Jiang, Hongying; Hayton, Karen; Wellems, Thomas; Su, Xinzhuan] NIAID, LMVR, NIH, Rockville, MD USA.
[Johnson, Ronald; Huang, Ruiling; Wichterman, Jennifer; Inglese, James; Austin, Christopher] NHGRI, NCGC, NIH, Rockville, MD USA.
[Fidock, David] Columbia Univ, New York, NY USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 888
BP 255
EP 256
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701303
ER
PT J
AU Richards, JS
Stanisic, DI
Michon, P
Dabod, E
Chitnis, CE
Narum, DE
Thompson, JK
Cowman, AF
Mueller, I
Beeson, JG
AF Richards, Jack S.
Stanisic, Danielle I.
Michon, Pascal
Dabod, Elijah
Chitnis, Chetan E.
Narum, David E.
Thompson, Jennifer K.
Cowman, Alan F.
Mueller, Ivo
Beeson, James G.
TI ANTIBODIES AGAINST THE ERYTHROCYTE BINDING ANTIGENS OF PLASMODIUM
FALCIPARUM ARE STRONGLY ASSOCIATED WITH PROTECTION AGAINST CLINICAL
MALARIA AND HIGH PARASITEMIA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Richards, Jack S.; Thompson, Jennifer K.; Cowman, Alan F.; Beeson, James G.] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Parkville, Vic 3050, Australia.
[Stanisic, Danielle I.; Michon, Pascal; Dabod, Elijah; Mueller, Ivo] Papua New Guinea Inst Med Res, Madang, Papua N Guinea.
[Chitnis, Chetan E.] Int Ctr Genet Engn & Biotechnol, New Delhi, India.
[Narum, David E.] NIH, Rockville, MD USA.
RI Mueller, Ivo/C-7251-2013; Cowman, Alan/C-7642-2013
OI Mueller, Ivo/0000-0001-6554-6889; Cowman, Alan/0000-0001-5145-9004
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 911
BP 262
EP 262
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701325
ER
PT J
AU Alvarenga, PH
Calvo, E
Francischetti, IM
Sa-Nunes, A
Ribeiro, JM
Andersen, JF
AF Alvarenga, Patricia H.
Calvo, Eric
Francischetti, Ivo M.
Sa-Nunes, Anderson
Ribeiro, Jose Marcos
Andersen, John F.
TI ANOPHELES STEPHENSI D7 L: A SALIVARY GLAND PROTEIN WITH BOTH
ANTI-INFLAMMATORY AND ANTIHEMOSTATIC EFFECT
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Alvarenga, Patricia H.; Calvo, Eric; Francischetti, Ivo M.; Sa-Nunes, Anderson; Ribeiro, Jose Marcos; Andersen, John F.] NIAID, NIH, Rockville, MD USA.
RI Sa-Nunes, Anderson/D-8667-2012
OI Sa-Nunes, Anderson/0000-0002-1859-4973
NR 0
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 945
BP 272
EP 273
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701359
ER
PT J
AU Takeo, S
Sakamoto, H
Kaneko, T
Tachibana, M
Miura, K
Varma, S
Sattabongkot, J
Torii, M
Tsuboi, T
AF Takeo, Satoru
Sakamoto, Hirokazu
Kaneko, Takamasa
Tachibana, Mayumi
Miura, Kazutoyo
Varma, Sudhir
Sattabongkot, Jetsumon
Torii, Motomi
Tsuboi, Takafumi
TI IDENTIFICATION OF NOVEL BLOOD-STAGE VACCINE CANDIDATES AGAINST
PLASMODIUM FALCIPARUM BY HIGH-THROUGHPUT IMMUNOSCREENING
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Takeo, Satoru; Sakamoto, Hirokazu; Kaneko, Takamasa; Tachibana, Mayumi; Torii, Motomi; Tsuboi, Takafumi] Ehime Univ, Matsuyama, Ehime 790, Japan.
[Miura, Kazutoyo] NIAID, MVDB, NIH, Rockville, MD USA.
[Varma, Sudhir] NIAID, BCBB, NIH, Bethesda, MD 20892 USA.
[Sattabongkot, Jetsumon] Armed Forces Res Inst Med Sci, Bangkok 10400, Thailand.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 944
BP 272
EP 272
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701358
ER
PT J
AU Coulibaly, MB
Diallo, B
Guindo, A
Traore, MM
Traore, SA
Konate, M
Anderson, JM
Lobo, NF
Besansky, NJ
Ribeiro, JM
Traore, SF
AF Coulibaly, Mamadou B.
Diallo, Brehima
Guindo, Amadou
Traore, Mohamed M.
Traore, Sekou A.
Konate, Mamadou
Anderson, Jennifer M.
Lobo, Neil F.
Besansky, Nora J.
Ribeiro, Jose M.
Traore, Sekou F.
TI GENE EXPRESSION PROFILE ASSOCIATED WITH BLOOD FEEDING AND PLASMODIUM
FALCIPARUM INFECTION IN THE MALARIA VECTOR ANOPHELES FUNESTUS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Coulibaly, Mamadou B.; Diallo, Brehima; Guindo, Amadou; Traore, Mohamed M.; Traore, Sekou A.; Konate, Mamadou; Traore, Sekou F.] Malaria Res & Training Ctr, Bamako, Mali.
[Anderson, Jennifer M.; Ribeiro, Jose M.] NIH, Bethesda, MD 20892 USA.
[Lobo, Neil F.; Besansky, Nora J.] Univ Notre Dame, Notre Dame, IN 46556 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 961
BP 277
EP 277
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701375
ER
PT J
AU Manoukis, NC
Sogoba, N
Diallo, M
Ribeiro, JM
AF Manoukis, Nicholas C.
Sogoba, Nafomon
Diallo, Moussa
Ribeiro, Jose M.
TI EVIDENCE OF PASSIVE DISPERSAL OF ANOPHELES GAMBIAE IN THE EARLY ADULT
PHASE
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Manoukis, Nicholas C.; Ribeiro, Jose M.] NIAID, Lab Malaria & Vector Res, NIH, Bethesda, MD 20892 USA.
[Sogoba, Nafomon; Diallo, Moussa] Fac Med, Malaria Res & Training Ctr, Bamako, Mali.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 972
BP 280
EP 280
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701386
ER
PT J
AU Kelly-Hope, LA
McKenzie, FE
AF Kelly-Hope, Louise A.
McKenzie, F. Ellis
TI ENVIRONMENTAL FACTORS ASSOCIATED WITH THE MALARIA VECTORS ANOPHELES
GAMBIAE S.L AND ANOPHELES FUNESTUS IN KENYA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Kelly-Hope, Louise A.] Univ Liverpool, Liverpool Sch Trop Med, Liverpool L3 5QA, Merseyside, England.
[McKenzie, F. Ellis] NIH, Fogarty Int Ctr, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 979
BP 282
EP 282
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701393
ER
PT J
AU Crompton, PD
Kayala, MA
Traore, B
Kayentao, K
Ongoiba, A
Weiss, GE
Molina, DM
Burk, CR
Waisberg, M
Jasinskas, A
Doumbo, S
Doumtabe, D
Kone, Y
Narum, DL
Liang, XW
Doumbo, OK
Miller, LH
Doolan, DL
Baldi, P
Felgner, PL
Pierce, SK
AF Crompton, Peter D.
Kayala, Matthew A.
Traore, Boubacar
Kayentao, Kassoum
Ongoiba, Aissata
Weiss, Greta E.
Molina, Douglas M.
Burk, Chad R.
Waisberg, Michael
Jasinskas, Algis
Doumbo, Safiatou
Doumtabe, Didier
Kone, Younoussou
Narum, David L.
Liang, Xiaowu
Doumbo, Ogobara K.
Miller, Louis H.
Doolan, Denise L.
Baldi, Pierre
Felgner, Philip L.
Pierce, Susan K.
TI PROFILING ANTIBODY RESPONSES TO P. FALCIPARUM INFECTION BY PROTEIN
MICROARRAY. A STRATEGY FOR IDENTIFYING NOVEL MALARIA VACCINE TARGETS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Crompton, Peter D.; Weiss, Greta E.; Waisberg, Michael; Pierce, Susan K.] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA.
[Kayala, Matthew A.; Baldi, Pierre] Univ Calif Irvine, Sch Informat & Comp Sci, Inst Genom & Bioinformat, Irvine, CA USA.
[Traore, Boubacar; Kayentao, Kassoum; Ongoiba, Aissata; Doumbo, Safiatou; Doumtabe, Didier; Kone, Younoussou; Doumbo, Ogobara K.] Univ Bamako, Malaria Res & Training Ctr, Fac Med Pharm & Dent, Bamako, Mali.
[Molina, Douglas M.; Liang, Xiaowu] Antigen Discovery Inc, Irvine, CA USA.
[Burk, Chad R.; Jasinskas, Algis; Felgner, Philip L.] Univ Calif Irvine, Dept Med, Div Infect Dis, Irvine, CA 92717 USA.
[Narum, David L.; Miller, Louis H.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD 20852 USA.
[Doolan, Denise L.] Queensland Inst Med Res, Mol Vaccinol Lab, Brisbane, Qld 4006, Australia.
RI Doolan, Denise/F-1969-2015; Crompton, Peter/N-1130-2016
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1007
BP 290
EP 290
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701421
ER
PT J
AU Diakite, SAS
Krause, MA
Traore, K
Lopera-Mesa, TM
Doumbia, S
Konate, D
Huaman, MC
Doumbia, M
Diouf, A
Anderson, JM
Doumbia, S
Long, CA
Fairhurst, RM
Diakite, M
AF Diakite, Seidina A. S.
Krause, Michael A.
Traore, Karim
Lopera-Mesa, Tatiana M.
Doumbia, Saibou
Konate, Drissa
Huaman, Maria Cecilia
Doumbia, Mory
Diouf, Ababacar
Anderson, Jennifer M.
Doumbia, Seydou
Long, Carole A.
Fairhurst, Rick M.
Diakite, Mahamadou
TI HEMOGLOBIN AND RED BLOOD CELL POLYMORPHISMS THAT CONFER PROTECTION
AGAINST SEVERE PLASMODIUM FALCIPARUM MALARIA ARE EXCEEDINGLY COMMON IN
MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Diakite, Seidina A. S.; Traore, Karim; Doumbia, Saibou; Konate, Drissa; Doumbia, Mory; Doumbia, Seydou; Diakite, Mahamadou] Malaria Res & Training Ctr, Bamako, Mali.
[Krause, Michael A.; Lopera-Mesa, Tatiana M.; Huaman, Maria Cecilia; Diouf, Ababacar; Anderson, Jennifer M.; Long, Carole A.; Fairhurst, Rick M.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1039
BP 299
EP 299
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701453
ER
PT J
AU Yusibov, V
Chichester, JA
Farrance, CE
Mett, V
Musiychuk, K
Shamloul, M
Sharma, S
Streatfield, S
Ugulava, N
Sauerwein, RW
Roeffen, W
Wu, YM
Muratova, O
Miller, LH
Holtzman, DA
AF Yusibov, Vidadi
Chichester, Jessica A.
Farrance, Christine E.
Mett, Vadim
Musiychuk, Konstantin
Shamloul, Moneim
Sharma, Satish
Streatfield, Stephen
Ugulava, Natalia
Sauerwein, Robert W.
Roeffen, Will
Wu, Yimin
Muratova, Olga
Miller, Louis H.
Holtzman, Douglas A.
TI ANTIBODIES TO PLANT-PRODUCED PLASMODIUM FALCIPARUM SEXUAL STAGE PROTEIN
PFS25 EXHIBIT TRANSMISSION BLOCKING ACTIVITY
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Yusibov, Vidadi; Chichester, Jessica A.; Farrance, Christine E.; Mett, Vadim; Musiychuk, Konstantin; Shamloul, Moneim; Sharma, Satish; Streatfield, Stephen; Ugulava, Natalia] Fraunhofer USA, Ctr Mol Biotechnol, Newark, DE USA.
[Sauerwein, Robert W.; Roeffen, Will] Radboud Univ Nijmegen, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Wu, Yimin; Muratova, Olga; Miller, Louis H.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
[Holtzman, Douglas A.] Bill & Melinda Gates Fdn, Seattle, WA USA.
RI Sauerwein, Robert/C-8519-2013; Roeffen, W.F.G./L-4607-2015
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1038
BP 299
EP 299
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701452
ER
PT J
AU Tozan, Y
Panicker, R
Darley, SR
Laxminarayan, R
Breman, JG
AF Tozan, Yesim
Panicker, Rajashree
Darley, Sarah R.
Laxminarayan, Ramanan
Breman, Joel G.
TI PRE-REFERRAL RECTAL ARTESUNATE IS COST-EFFECTIVE FOR TREATING SEVERE
CHILDHOOD MALARIA
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Tozan, Yesim] Boston Univ, Sch Publ Hlth, Boston, MA USA.
[Panicker, Rajashree; Darley, Sarah R.; Laxminarayan, Ramanan] Resources Future Inc, Washington, DC USA.
[Breman, Joel G.] NIH, Fogarty Int Ctr, Washington, DC USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1057
BP 305
EP 305
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701471
ER
PT J
AU Moretz, SE
Diouf, A
Zhou, H
Tullo, G
El Sahli, H
Keitel, W
Long, CA
AF Moretz, Samuel E.
Diouf, Ababacar
Zhou, Hong
Tullo, Gregory
El Sahli, Hanaa
Keitel, Wendy
Long, Carole A.
TI ANALYSIS OF THE BIOLOGICAL FUNCTION OF ANTIBODIES ELICITED FOLLOWING
IMMUNIZATION OF MALARIA-NAIVE SUBJECTS WITH A PLASMODIUM FALCIPARUM
ERYTHROCYTE-BINDING ANTIGEN 175 (EBA175) VACCINE
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Moretz, Samuel E.; Diouf, Ababacar; Zhou, Hong; Tullo, Gregory; Long, Carole A.] NIAID, Lab Malaria & Vector Res, Rockville, MD USA.
[El Sahli, Hanaa; Keitel, Wendy] Baylor Coll Med, Houston, TX 77030 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1067
BP 308
EP 308
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701481
ER
PT J
AU McCarthy, JS
Marjason, J
Elliott, S
Fahey, P
Malkin, E
Tierney, E
Cross, N
Richards, JS
Boyle, M
Bang, G
Long, C
Druilhe, P
Beeson, J
Anders, RF
AF McCarthy, James S.
Marjason, Joanne
Elliott, Suzanne
Fahey, Paul
Malkin, Elissa
Tierney, Eveline
Cross, Nadia
Richards, Jack S.
Boyle, Michelle
Bang, Gilles
Long, Carole
Druilhe, Pierre
Beeson, James
Anders, Robin F.
TI A PHASE 1 TRIAL OF A BIVALENT MSP2 BLOOD-STAGE MALARIA VACCINE
FORMULATED WITH MONTANIDE ISA 720
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [McCarthy, James S.] Univ Queensland, Queensland Inst Med Res, Brisbane, Qld 20892, Australia.
[Marjason, Joanne; Elliott, Suzanne] Q Pharm Pty Ltd, Brisbane, Qld, Australia.
[Fahey, Paul; Malkin, Elissa; Tierney, Eveline] PATH Malaria Vaccine Initiat, Bethesda, MD USA.
[Cross, Nadia; Richards, Jack S.; Boyle, Michelle; Beeson, James] Walter & Eliza Hall Inst Med Res, Melbourne, Vic, Australia.
[Long, Carole] NIAID, NIH, Bethesda, MD USA.
[Bang, Gilles; Druilhe, Pierre] Inst Pasteur, Paris, France.
[Anders, Robin F.] La Trobe Univ, Dept Biochem, Melbourne, Vic, Australia.
NR 0
TC 0
Z9 0
U1 1
U2 1
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1076
BP 310
EP 311
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701490
ER
PT J
AU Miura, K
Zhou, H
Diouf, A
Tullo, G
Aebig, JA
Miller, LH
Saul, A
Doumbo, OK
Sagara, I
Dicko, A
Long, CA
Ellis, RD
AF Miura, Kazutoyo
Zhou, Hong
Diouf, Ababacar
Tullo, Gregory
Aebig, Joan A.
Miller, Louis H.
Saul, Allan
Doumbo, Ogobara K.
Sagara, Issaka
Dicko, Alassane
Long, Carole A.
Ellis, Ruth D.
TI IMPACT OF PLASMODIUM FALCIPARUM APICAL MEMBRANE ANTIGEN 1-COMBINATION
1/ALHYDROGEL VACCINE ON GROWTH-INHIBITORY ACTIVITY OF ANTIBODIES IN
CHILDREN IN MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Miura, Kazutoyo; Aebig, Joan A.; Miller, Louis H.; Saul, Allan; Ellis, Ruth D.] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
[Zhou, Hong; Diouf, Ababacar; Tullo, Gregory; Long, Carole A.] NIAID, Lab Malaria & Vector Res, NIH, Rockville, MD USA.
[Doumbo, Ogobara K.; Sagara, Issaka; Dicko, Alassane] Univ Bamako, Malaria Res & Training Ctr, Fac Med Pharm & Dent, Bamako, Mali.
RI Saul, Allan/I-6968-2013
OI Saul, Allan/0000-0003-0665-4091
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1075
BP 310
EP 310
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701489
ER
PT J
AU Mahapatra, L
Dembele, B
Metenou, S
Konate, S
Dolo, H
Coulibaly, ME
Soumaoro, L
Panka, R
Chaussabel, D
Coulibaly, SY
Sanogo, D
Doumbia, SS
Diallo, AA
Nutman, TB
Mahanty, S
Semnani, RT
AF Mahapatra, Lily
Dembele, Benoit
Metenou, Simon
Konate, Siaka
Dolo, Housseini
Coulibaly, Michel E.
Soumaoro, Lamine
Panka, Rungnapa
Chaussabel, Damien
Coulibaly, Siaka Y.
Sanogo, Dramane
Doumbia, Salif Seriba
Diallo, Abdallah A.
Nutman, Thomas B.
Mahanty, Siddhartha
Semnani, Roshanak Tolouei
TI INCREASED POPULATIONS OF CIRCULATING MYELOID AND PLASMACYTOID DENDRITIC
CELLS IN PATENT FILARIAL INFECTIONS
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Mahapatra, Lily; Metenou, Simon; Nutman, Thomas B.; Mahanty, Siddhartha; Semnani, Roshanak Tolouei] NIAID, NIH, Bethesda, MD 20892 USA.
[Dembele, Benoit; Konate, Siaka; Dolo, Housseini; Coulibaly, Michel E.; Soumaoro, Lamine; Coulibaly, Siaka Y.; Sanogo, Dramane; Doumbia, Salif Seriba; Diallo, Abdallah A.] Univ Bamako, FMPOS, Filariasis Unit, Bamako, Mali.
[Panka, Rungnapa; Chaussabel, Damien] Baylor Univ, Baylor Inst Immunol Res, Dallas, TX USA.
RI Metenou, Simon/C-1101-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1081
BP 312
EP 312
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701495
ER
PT J
AU Babu, S
Bhat, SQ
Kumar, P
Anuradha, R
Kumaran, P
Gopi, PG
Kolappan, C
Kumaraswami, V
Nutman, TB
AF Babu, Subash
Bhat, Sajid Q.
Kumar, Pavan
Anuradha, R.
Kumaran, Paul
Gopi, P. G.
Kolappan, C.
Kumaraswami, V.
Nutman, Thomas B.
TI ATTENUATION OF TLR EXPRESSION AND FUNCTION IN LATENT TUBERCULOSIS BY
COEXISTENT FILARIAL INFECTION WITH RESTORATION FOLLOWING ANTIFILARIAL
CHEMOTHERAPY
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Babu, Subash; Bhat, Sajid Q.; Kumar, Pavan; Anuradha, R.] NIH TRC ICER, Madras, Tamil Nadu, India.
[Kumaran, Paul; Gopi, P. G.; Kolappan, C.; Kumaraswami, V.] TB Res Ctr, Madras, Tamil Nadu, India.
[Nutman, Thomas B.] NIH, Bethesda, MD 20892 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1085
BP 313
EP 314
PG 2
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701499
ER
PT J
AU Dembele, B
Metenou, S
Dolo, H
Konate, S
Coulibaly, SY
Sanogo, D
Mahanty, S
Coulibaly, ME
Soumaoro, L
Doumbia, SS
Diallo, AA
Guindo, MA
Diallo, DA
Traore, SF
Coulibaly, YI
Nutman, TB
Klion, AD
AF Dembele, Benoit
Metenou, Simon
Dolo, Housseini
Konate, Siaka
Coulibaly, Siaka Y.
Sanogo, Dramane
Mahanty, Siddhartha
Coulibaly, Michel E.
Soumaoro, Lamine
Doumbia, Salif S.
Diallo, Abdallah A.
Guindo, Merepin A.
Diallo, Dapa A.
Traore, Sekou F.
Coulibaly, Yaya I.
Nutman, Thomas B.
Klion, Amy D.
TI PRE-EXISTING FILARIAL INFECTION INFLUENCES CYTOKINE PRODUCTION DURING
ACUTE MALARIA IN CHILDREN AND YOUNG ADULTS IN A COENDEMIC REGION OF MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Dembele, Benoit; Dolo, Housseini; Konate, Siaka; Coulibaly, Siaka Y.; Sanogo, Dramane; Coulibaly, Michel E.; Soumaoro, Lamine; Doumbia, Salif S.; Diallo, Abdallah A.; Guindo, Merepin A.; Diallo, Dapa A.; Traore, Sekou F.; Coulibaly, Yaya I.] Univ Bamako, Bamako, Mali.
[Metenou, Simon; Mahanty, Siddhartha; Nutman, Thomas B.; Klion, Amy D.] NIAID, NIH, Bethesda, MD 20892 USA.
RI Metenou, Simon/C-1101-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1083
BP 313
EP 313
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701497
ER
PT J
AU Metenou, S
Dembele, B
Konate, S
Dolo, H
Soumaoro, L
Diallo, AA
Coulibaly, ME
Coulibaly, SY
Sanogo, D
Coulibaly, YI
Traore, SF
Mahanty, S
Klion, AD
Nutman, TB
AF Metenou, Simon
Dembele, Benoit
Konate, Siaka
Dolo, Housseini
Soumaoro, Lamine
Diallo, Abdallah A.
Coulibaly, Michel E.
Coulibaly, Siaka Y.
Sanogo, Dramane
Coulibaly, Yaya I.
Traore, Sekou F.
Mahanty, Siddhartha
Klion, Amy D.
Nutman, Thomas B.
TI PATENT FILARIAL INFECTION MODULATES THE QUALITY OF T CELL RESPONSES TO
MALARIAL ANTIGENS IN MALARIA/FILARIAL CO-ENDEMIC VILLAGE OF MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Metenou, Simon; Mahanty, Siddhartha; Klion, Amy D.; Nutman, Thomas B.] NIH, Bethesda, MD 20892 USA.
[Dembele, Benoit; Konate, Siaka; Dolo, Housseini; Soumaoro, Lamine; Diallo, Abdallah A.; Coulibaly, Michel E.; Coulibaly, Siaka Y.; Sanogo, Dramane; Coulibaly, Yaya I.; Traore, Sekou F.] Univ Bamako, Filaria Unit, FMPOS, Bamako, Mali.
RI Metenou, Simon/C-1101-2013
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1084
BP 313
EP 313
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701498
ER
PT J
AU Lisk, G
Desai, SA
AF Lisk, Godfrey
Desai, Sanjay A.
TI A GENE LINKED TO A NEW ANTIMALARIAL DRUG RESISTANCE MECHANISM: REDUCED
UPTAKE BY INFECTED ERYTHROCYTES
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Lisk, Godfrey; Desai, Sanjay A.] NIAID, NIH, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1108
BP 320
EP 320
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701522
ER
PT J
AU Ellis, RD
Sagara, I
Durbin, A
Dicko, A
Shaffer, D
Pierce, M
Miller, L
Assadou, MH
Kone, M
Kamate, B
Guindo, O
Fay, MP
Diallo, D
Doumbo, OK
Emmanuel, E
Millum, J
AF Ellis, Ruth D.
Sagara, Issaka
Durbin, Anna
Dicko, Alassane
Shaffer, Donna
Pierce, Mark
Miller, Louis
Assadou, Mahamadoun H.
Kone, Mamady
Kamate, Beh
Guindo, Ousmane
Fay, Michael P.
Diallo, Dapa
Doumbo, Ogobara K.
Emmanuel, Ezekiel
Millum, Joseph
TI COMPARING THE QUALITY OF INFORMED CONSENT IN THE UNITED STATES AND MALI
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Meeting Abstract
CT 58th Annual Meeting of the
American-Society-of-Tropical-Medicine-and-Hygiene
CY NOV 18-22, 2009
CL Washington, DC
SP Amer Soc Trop Med & Hyg
C1 [Ellis, Ruth D.; Pierce, Mark; Miller, Louis] NIAID, Malaria Vaccine Dev Branch, NIH, Rockville, MD USA.
[Sagara, Issaka; Dicko, Alassane; Assadou, Mahamadoun H.; Kone, Mamady; Kamate, Beh; Guindo, Ousmane; Diallo, Dapa; Doumbo, Ogobara K.] Univ Bamako, Malaria Res & Training Ctr, Fac Med Pharm & Dent, Bamako, Mali.
[Durbin, Anna; Shaffer, Donna] Johns Hopkins Ctr Immunizat Res, Washington, DC USA.
[Fay, Michael P.] NIAID, Biostat Res Branch, NIH, Rockville, MD USA.
[Emmanuel, Ezekiel] NIH, Clin Ctr Dept Bioeth, Bethesda, MD 20892 USA.
[Millum, Joseph] NIH, Clin Ctr Dept Bioeth, Fogarty Int Ctr, Rockville, MD USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
SU S
MA 1137
BP 328
EP 328
PG 1
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WK
UT WOS:000271956701551
ER
PT J
AU Wright, PF
Durbin, AP
Whitehead, SS
Ikizler, MR
Henderson, S
Blaney, JE
Thumar, B
Ankrah, S
Rock, MT
McKinney, BA
Murphy, BR
Schmidt, AC
AF Wright, Peter F.
Durbin, Anna P.
Whitehead, Stephen S.
Ikizler, Mine R.
Henderson, Susan
Blaney, Joseph E.
Thumar, Bhavin
Ankrah, Sharon
Rock, Michael T.
McKinney, Brett A.
Murphy, Brian R.
Schmidt, Alexander C.
TI Phase 1 Trial of the Dengue Virus Type 4 Vaccine Candidate rDEN4 Delta
30-4995 in Healthy Adult Volunteers
SO AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE
LA English
DT Article
ID 3' UNTRANSLATED REGION; HUMAN LIVER-CELLS; YELLOW-FEVER;
HEMORRHAGIC-FEVER; SHOCK SYNDROME; IMMUNOGENICITY; SAFETY; ATTENUATION;
FORMULATIONS; ANTIBODY
AB rDEN4 Delta 30-4995 is a live attenuated dengue virus type 4 (DENV4) vaccine candidate specifically designed as a further attenuated derivative of the rDEN4 Delta 30 parent virus. In a previous study, 5 of 20 vaccinees who received 10(5) plaque-forming units (PFU) of rDEN4 Delta 30 developed a transient elevation of the serum alanine aminotransferase (ALT) level and an asymptomatic maculopapular rash developed in 10 of 20. In the current study, 28 healthy adult volunteers were randomized to receive 10(5) PFU of rDEN4 Delta 30-4995 (20) or placebo (8) as a single subcutaneous injection. The vaccine was safe, well-tolerated, and immunogenic.An asymptomatic generalized maculopapular rash and elevations in ALT levels were observed in 10% of the rDEN4 Delta 30-4995 vaccinees. None of the rDEN4 Delta 30-4995 vaccinees became viremic, yet 95% developed a four-fold or greater increase in neutralizing antibody titers. Thus, rDEN4 Delta 30-4995 was demonstrated to be safe, highly attenuated, and immunogenic. However, an asymptomatic localized erythematous rash at the injection site was seen in 17/20 rDEN4 Delta 30-4995 vaccinees. Therefore, alternative DENV4 vaccine strains were selected for further clinical development.
C1 [Whitehead, Stephen S.; Blaney, Joseph E.; Murphy, Brian R.; Schmidt, Alexander C.] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA.
Dartmouth Med Sch, Dept Pediat, Lebanon, NH 03756 USA.
Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37232 USA.
[Durbin, Anna P.; Thumar, Bhavin] Johns Hopkins Sch Pulb Hlth, Ctr Immunizat Res, Baltimore, MD 21205 USA.
Johns Hopkins Bloomberg Sch Pulb Hlth, Ctr Immunizat Res, Dept Int Hlth, Baltimore, MD USA.
[Henderson, Susan; Ankrah, Sharon; Rock, Michael T.] Vanderbilt Univ, Div Pediat Infect Dis, Nashville, TN 37232 USA.
[McKinney, Brett A.] Univ Alabama, Sch Med, Dept Genet, Birmingham, AL 35294 USA.
RP Schmidt, AC (reprint author), NIAID, Infect Dis Lab, NIH, 50 South Dr,Room 6511, Bethesda, MD 20892 USA.
EM peter.f.wright@dartmouth.edu; adurbin@jhsph.edu;
swhitehead@niaid.nih.gov; mine.ikizler@vanderbilt.edu;
shende8@emory.edu; jblaney@niaid.nih.gov; bthumar@jhsph.edu;
sharon.n.ankrah@vanderbilt.edu; michael.rock@vanderbilt.edu;
brett.mckinney@gmail.com; bmurphy@niaid.nih.gov; as337y@nih.gov
FU National Institutes of Allergy and Infectious Diseases; National
Institutes of Health; Johns Hopkins Bloomberg School of Public Health;
Vanderbilt University Medical Center
FX This study was supported by the Intramural Research Program of the
National Institutes of Allergy and Infectious Diseases, National
Institutes of Health, in part through a contract with the Johns Hopkins
Bloomberg School of Public Health and a subcontract with Vanderbilt
University Medical Center.
NR 45
TC 29
Z9 30
U1 0
U2 0
PU AMER SOC TROP MED & HYGIENE
PI MCLEAN
PA 8000 WESTPARK DR, STE 130, MCLEAN, VA 22101 USA
SN 0002-9637
J9 AM J TROP MED HYG
JI Am. J. Trop. Med. Hyg.
PD NOV
PY 2009
VL 81
IS 5
BP 834
EP 841
DI 10.4269/ajtmh.2009.09-0131
PG 8
WC Public, Environmental & Occupational Health; Tropical Medicine
SC Public, Environmental & Occupational Health; Tropical Medicine
GA 521WI
UT WOS:000271956500019
PM 19861619
ER
PT J
AU Titus, SA
Beacham, D
Shahane, SA
Southall, N
Xia, MH
Huang, RL
Hooten, E
Zhao, Y
Shou, L
Austin, CP
Zheng, W
AF Titus, Steven A.
Beacham, Daniel
Shahane, Sampada A.
Southall, Noel
Xia, Menghang
Huang, Ruili
Hooten, Elizabeth
Zhao, Yong
Shou, Louie
Austin, Christopher P.
Zheng, Wei
TI A new homogeneous high-throughput screening assay for profiling compound
activity on the human ether-a-go-go-related gene channel
SO ANALYTICAL BIOCHEMISTRY
LA English
DT Article
DE Human ether-a-go-go-related gene (hERG); Quantitative high-throughput
screening (qHTS); FluxOR; Thallium flux; Baculovirus; BacMam
ID HERG POTASSIUM CHANNEL; FLUORESCENCE QUENCHING TECHNIQUE; DRUG
DISCOVERY; CARDIAC-ARRHYTHMIA; QT PROLONGATION; K+ CHANNELS; DE-POINTES;
DROSOPHILA; MUTATIONS; CELLS
AB Long QT syndrome, either inherited or acquired from drug treatments, can result in ventricular arrhythmia (torsade de pointes) and sudden death. Human ether-a-go-go-related gene (hERG) channel inhibition by drugs is now recognized as a common reason for the acquired form of long QT syndrome. It has been reported that more than 100 known drugs inhibit the activity of the hERG channel. Since 1997, several drugs have been withdrawn from the market due to the long QT syndrome caused by hERG inhibition. Food and Drug Administration regulations now require safety data on hERG channels for investigative new drug (IND) applications. The assessment of compound activity on the hERG channel has now become an important part of the safety evaluation in the process of drug discovery. During the past decade, several in vitro assay methods have been developed and significant resources have been used to characterize hERG channel activities. However, evaluation of compound activities on hERG have not been performed for large compound collections due to technical difficulty, lack of throughput, and/or lack of biological relevance to function. Here we report a modified form of the FluxOR thallium flux assay, capable of measuring hERG activity in a homogeneous 1536-well plate format. To validate the assay, we screened a 7-point dilution series of the LOPAC 1280 library collection and reported rank order potencies of ten common hERG inhibitors. A correlation was also observed for the hERG channel activities of 10 known hERG inhibitors determined in this thallium flux assay and in the patch clamp experiment. Our findings indicate that this thallium flux assay can be used as an alternative method to pro. le large-volume compound libraries for compound activity on the hERG channel. Published by Elsevier Inc.
C1 [Titus, Steven A.; Shahane, Sampada A.; Southall, Noel; Xia, Menghang; Huang, Ruili; Shou, Louie; Austin, Christopher P.; Zheng, Wei] NHGRI, NIH, Chem Genom Ctr, Bethesda, MD 20892 USA.
[Beacham, Daniel] Life Technol, Cellular Syst Div, Eugene, OR 97403 USA.
[Hooten, Elizabeth; Zhao, Yong] Cerep, Redmond, WA 98052 USA.
RP Zheng, W (reprint author), NHGRI, NIH, Chem Genom Ctr, 9800 Med Ctr Dr, Bethesda, MD 20892 USA.
EM wzheng@mail.nih.gov
RI Southall, Noel/H-8991-2012; Zheng, Wei/J-8889-2014
OI Southall, Noel/0000-0003-4500-880X; Zheng, Wei/0000-0003-1034-0757
FU NIH; National Human Genome Research Institute
FX This research was supported by the Molecular Libraries Initiative of the
NIH Roadmap for Medical Research and the Intramural Research Programs of
the National Human Genome Research Institute. The authors thank Paul
Shinn for assistance with compound management. The authors also thank
Shouming Du of Hamamatsu for technical support with the FDSS 7000
kinetic plate reader; Michael O'Grady, Matt Robers, and George Hanson of
Invitrogen/Life Technologies and Blake Anson of Cellular Dynamics for
technical assistance; and Darryl Leja for help with artwork.
NR 44
TC 30
Z9 30
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 0003-2697
J9 ANAL BIOCHEM
JI Anal. Biochem.
PD NOV 1
PY 2009
VL 394
IS 1
BP 30
EP 38
DI 10.1016/j.ab.2009.07.003
PG 9
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Analytical
SC Biochemistry & Molecular Biology; Chemistry
GA 534GH
UT WOS:000272883900005
PM 19583963
ER
PT J
AU Chikkaveeraiah, BV
Bhirde, A
Malhotra, R
Patel, V
Gutkind, JS
Rusling, JF
AF Chikkaveeraiah, Bhaskara V.
Bhirde, Ashwin
Malhotra, Ruchika
Patel, Vyomesh
Gutkind, J. Silvio
Rusling, James F.
TI Single-Wall Carbon Nanotube Forest Arrays for Immunoelectrochemical
Measurement of Four Protein Biomarkers for Prostate Cancer
SO ANALYTICAL CHEMISTRY
LA English
DT Article
ID ELECTROCHEMICAL DETECTION; ANALYTICAL PERFORMANCE; SENSOR ARRAYS;
ANTIGEN; IMMUNOSENSORS; PROTEOMICS; MARKERS; AMPLIFICATION; IMMUNOASSAY;
CHALLENGES
AB Protein arrays that measure multiple protein cancer biomarkers in clinical samples hold great promise for reliable early cancer detection. Herein, we report a prototype 4-unit electrochemical immunoarray based on single-wall carbon nanotube forests for the simultaneous detection of multiple protein biomarkers for prostate cancer. Immunoarray procedures were designed to measure prostate specific antigen (PSA), prostate specific membrane antigen (PSMA), platelet factor-4 (PF-4), and interleukin-6 (IL-6) simultaneously in a single serum sample. All of these proteins are elevated in serum of patients with prostate cancer, but they have widely different relative levels of serum concentration. Horseradish peroxidase (HRP) was used as label on detection (secondary) antibodies in a sandwich immunoassay scheme. Biotinylated secondary antibodies (Ab(2)) that bind specifically to streptavidin-HRP conjugates provided 14-16 labels per antibody and gave the necessary higher sensitivity required for PF-4 and IL-6 detection at physiological levels. Conventional singly labeled Ab(2)-HRP conjugates were sufficient for PSA and PSMA detection. Immunoarrays were used to measure four biomarkers in clinical human serum samples of prostate cancer patients and controls with excellent correlation to referee enzyme-linked immunosorbent (ELISA) assays.
C1 [Chikkaveeraiah, Bhaskara V.; Bhirde, Ashwin; Malhotra, Ruchika; Rusling, James F.] Univ Connecticut, Dept Chem, Storrs, CT 06269 USA.
[Chikkaveeraiah, Bhaskara V.; Bhirde, Ashwin; Malhotra, Ruchika; Rusling, James F.] Univ Connecticut, Inst Mat Sci, Storrs, CT 06269 USA.
[Rusling, James F.] Univ Connecticut, Ctr Hlth, Dept Cell Biol, Farmington, CT 06032 USA.
[Rusling, James F.] Natl Univ Ireland, Sch Chem, Galway, Ireland.
[Patel, Vyomesh; Gutkind, J. Silvio] Natl Inst Dent & Craniofacial Res, Oral & Phatyngeal Canc Branch, NIH, Bethesda, MD 20892 USA.
RP Rusling, JF (reprint author), Univ Connecticut, Dept Chem, 55 N Eagleville Rd, Storrs, CT 06269 USA.
EM james.rusling@uconn.edu
RI Gutkind, J. Silvio/A-1053-2009
FU NIEHS/NIH [ES013557]; Intramural Research Program; NIDCR; NIH
FX This work was supported by PHS Grant ES013557 from NIEHS/NIH and
partially by the Intramural Research Program, NIDCR, NIH. We thank Debra
Rood and Lawrence K. Silbart for assistance with ELISA measurements.
NR 39
TC 92
Z9 94
U1 3
U2 40
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0003-2700
J9 ANAL CHEM
JI Anal. Chem.
PD NOV 1
PY 2009
VL 81
IS 21
BP 9129
EP 9134
DI 10.1021/ac9018022
PG 6
WC Chemistry, Analytical
SC Chemistry
GA 577AL
UT WOS:000276191900066
PM 19775154
ER
PT J
AU Moyo, VM
Mvundura, E
Khumalo, H
Gangaidzo, IT
Saungweme, T
Nouraie, M
Rouault, TA
Gomo, ZAR
Gordeuk, VR
AF Moyo, Victor M.
Mvundura, Elisha
Khumalo, Hlosukwazi
Gangaidzo, Innocent T.
Saungweme, Thokozile
Nouraie, Mehdi
Rouault, Tracey A.
Gomo, Zvenyika A. R.
Gordeuk, Victor R.
TI Serum ferritin concentrations in Africans with low dietary iron
SO ANNALS OF HEMATOLOGY
LA English
DT Article
DE African iron overload; Iron status; Ferritin; Dietary iron
ID ERYTHROCYTE SEDIMENTATION-RATE; HEREDITARY HEMOCHROMATOSIS; OVERLOAD;
POPULATION; GENE; FORTIFICATION; DEFICIENCY; NUTRITION; AMERICAN; BEER
AB In the setting of high dietary, several studies have provided evidence for a strong effect of both high dietary iron and an unidentified genetic locus on iron stores in Africans. To investigate whether these effects are discernible in the setting of low dietary iron, serum ferritin concentrations were measured in 194 Zimbabwean men > 30 years of age and 299 postmenopausal women who consumed a non-iron-fortified diet and who did not drink iron-rich traditional beer or other alcoholic beverages. Comparisons were made with non-alcohol drinking African-Americans studied in the third National Health and Nutritional Examination Survey (NHANES III) who consume an iron-fortified diet. As stratified by age and sex, serum ferritin concentrations were significantly lower in the 493 Zimbabweans studied than in 1,380 comparable African-Americans (P < 0.0005). Nevertheless, nine Zimbabwean subjects (1.8% of all cases) had modestly elevated serum ferritin concentrations not associated with evidence of inflammation or hepatic dysfunction. These data suggest that mild serum ferritin concentration elevations may occur among Zimbabweans not exposed to high dietary iron and that iron fortification of the diet may have substantial effects on serum ferritin concentration.
C1 [Nouraie, Mehdi; Gordeuk, Victor R.] Howard Univ, Dept Med, Washington, DC 20060 USA.
[Nouraie, Mehdi; Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20060 USA.
[Moyo, Victor M.] Ortho Biotech LLC, Clin Affairs, Oncol Hematol, Bridgewater, NJ USA.
[Mvundura, Elisha] Georgetown Hosp, Dept Obstet & Gynecol, Washington, DC USA.
[Khumalo, Hlosukwazi] Univ Witwatersrand, Fac Hlth Sci, Johannesburg, South Africa.
[Gangaidzo, Innocent T.; Saungweme, Thokozile] Univ Zimbabwe, Sch Med, Dept Med, Harare, Zimbabwe.
[Rouault, Tracey A.] NICHHD, Cell Biol & Metab Branch, Bethesda, MD 20892 USA.
RP Gordeuk, VR (reprint author), Howard Univ, Dept Med, 2041 Georgia Ave NW, Washington, DC 20060 USA.
EM vgordeuk@howard.edu
FU NIH [UH1-HL03679-07]; Office of Research on Minority Health; Howard
University General Clinical Research Center [MO1-RR10284]; National
Institute of Child Health and Human Development [1-HD-3-3196]; J.F.
Kapnek Charitable Trust (Philadelphia, PA); University of Zimbabwe
(Harare, Zimbabwe)
FX This study was supported in part by the NIH research grant no.
UH1-HL03679-07 from the National Heart, Lung and Blood Institute and the
Office of Research on Minority Health and by Howard University General
Clinical Research Center grant no. MO1-RR10284, by National Institute of
Child Health and Human Development contract no. 1-HD-3-3196, by a grant
from the J.F. Kapnek Charitable Trust (Philadelphia, PA), and by a grant
allocation from the Research Board of the University of Zimbabwe
(Harare, Zimbabwe).
NR 34
TC 5
Z9 5
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0939-5555
J9 ANN HEMATOL
JI Ann. Hematol.
PD NOV
PY 2009
VL 88
IS 11
BP 1131
EP 1136
DI 10.1007/s00277-009-0718-6
PG 6
WC Hematology
SC Hematology
GA 495SX
UT WOS:000269916400010
PM 19259672
ER
PT J
AU Marenne, G
Chanock, S
Rothman, N
Rodriguez-Santiago, B
Rico, D
Pita, G
Perez-Jurado, L
Valencia, A
Jacobs, K
Pisano, DG
Diaz-Uriarte, R
Earl, J
Garcia-Closas, M
Silverman, D
Kogevinas, M
Genin, E
Real, FX
Malats, N
AF Marenne, Gaelle
Chanock, Stephen
Rothman, Nathaniel
Rodriguez-Santiago, Benjamin
Rico, Daniel
Pita, Guillermo
Perez-Jurado, Luis
Valencia, Alfonso
Jacobs, Kevin
Pisano, David G.
Diaz-Uriarte, Ramon
Earl, Julie
Garcia-Closas, Montserrat
Silverman, Debra
Kogevinas, Manolis
Genin, Emmanuelle
Real, Francisco X.
Malats, Nuria
TI CNV assessment using the Illumina Infinium 1M platform: Agreement
according to algorithm and source of DNA
SO ANNALS OF HUMAN GENETICS
LA English
DT Meeting Abstract
CT European Mathematical Genetics Meeting
CY MAY 14-15, 2009
CL Munich, GERMANY
C1 [Marenne, Gaelle; Rico, Daniel; Pita, Guillermo; Valencia, Alfonso; Pisano, David G.; Diaz-Uriarte, Ramon; Earl, Julie; Real, Francisco X.; Malats, Nuria] Spanish Natl Canc Res Ctr CNIO, Madrid, Spain.
[Chanock, Stephen; Rothman, Nathaniel; Jacobs, Kevin; Garcia-Closas, Montserrat; Silverman, Debra] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Rodriguez-Santiago, Benjamin; Perez-Jurado, Luis] Univ Pompeu Fabra, Fac Ciencies Salut, Barcelona, Spain.
[Kogevinas, Manolis] CREAL IMIM, Hosp Mar, Barcelona, Spain.
[Marenne, Gaelle; Genin, Emmanuelle] INSERM, UMR S946, Fdn Jean Dausset CEPH, Paris, France.
[Genin, Emmanuelle] Univ Paris Diderot, Paris, France.
RI Genin, Emmanuelle/C-4974-2013; Valencia, Alfonso/I-3127-2015; Perez
Jurado, Luis Alberto/M-7706-2015; Kogevinas, Manolis/C-3918-2017;
Pisano, David/N-5817-2014
OI Genin, Emmanuelle/0000-0003-4117-2813; Valencia,
Alfonso/0000-0002-8937-6789; Pisano, David/0000-0002-4895-4124
NR 0
TC 0
Z9 0
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0003-4800
J9 ANN HUM GENET
JI Ann. Hum. Genet.
PD NOV
PY 2009
VL 73
BP 660
EP 660
PG 1
WC Genetics & Heredity
SC Genetics & Heredity
GA 505VL
UT WOS:000270726900017
ER
PT J
AU Minig, L
Biffi, R
Zanagnolo, V
Attanasio, A
Beltrami, C
Bocciolone, L
Botteri, E
Colombo, N
Iodice, S
Landoni, F
Peiretti, M
Roviglione, G
Maggioni, A
AF Minig, Lucas
Biffi, Roberto
Zanagnolo, Vanna
Attanasio, Anna
Beltrami, Carmen
Bocciolone, Luca
Botteri, Edoardo
Colombo, Nicoletta
Iodice, Simona
Landoni, Fabio
Peiretti, Michele
Roviglione, Giovanni
Maggioni, Angelo
TI Reduction of Postoperative Complication Rate with the Use of Early Oral
Feeding in Gynecologic Oncologic Patients Undergoing a Major Surgery: A
Randomized Controlled Trial
SO ANNALS OF SURGICAL ONCOLOGY
LA English
DT Article
ID QUALITY-OF-LIFE; NORTHERN EUROPEAN COUNTRIES; ENTERAL NUTRITION;
OVARIAN-CANCER; MATERNAL SATISFACTION; QUESTIONNAIRE MODULE; SURGICAL
PATIENTS; CESAREAN-SECTION; CLINICAL IMPACT; FOOD-INTAKE
AB A randomized controlled trial was performed to assess the outcome of early oral postoperative feeding (EOF) compared with traditional oral feeding (TOF) in gynecologic oncology patients undergoing a complex laparotomy, including upper abdominal surgery.
Patients aged 18-75 years, undergoing an elective laparotomy and with a preoperative suspicion of gynecologic malignancy, were eligible. Exclusion criteria included infectious conditions, intestinal obstruction, severe malnutrition, American Society of Anesthesiologists score a parts per thousand yen4, intestinal resection, and postoperative stay in the intensive care unit lasting > 24 h. Patients allocated to EOF received liquid diet in the first postoperative day and then regular diet. Patients received traditional feeding scheme until resolution of postoperative ileus to start liquid diet. The primary end-point of the trial was length of hospital stay.
Between January 1, 2007, and November 17, 2007, a total of 143 patients were randomized to receive either EOF or TOF. Hospital stay for patients who received EOF (n = 71) was 4.7 vs. 5.8 days for the TOF group (n = 72) (P = 0.006). The mean level of postoperative satisfaction was significantly higher in the EOF group (82.8 vs. 71.7 mm, P a parts per thousand currency sign 0.001). Patients who received the TOF scheme had significantly higher overall postoperative complications (39 vs. 17% in EOF group, P = 0.003) and infective complications (14% in TOF group vs. 3% in EOF group, P = 0.017). Variables such as nausea and vomiting, analgesic and antiemetic requirement as well as level of pain and quality of life were not different between groups.
On the basis of these findings, the policy of EOF should be used after a complex gynecologic oncologic laparotomy.
C1 [Minig, Lucas; Zanagnolo, Vanna; Bocciolone, Luca; Colombo, Nicoletta; Landoni, Fabio; Peiretti, Michele; Roviglione, Giovanni; Maggioni, Angelo] European Inst Oncol, Dept Gynecol, Milan, Italy.
[Biffi, Roberto] European Inst Oncol, Abdominopelv Surg Dept, Milan, Italy.
[Attanasio, Anna] European Inst Oncol, Dept Anesthesiol, Milan, Italy.
[Beltrami, Carmen] European Inst Oncol, Gynecol Nurses Dept, Milan, Italy.
[Botteri, Edoardo; Iodice, Simona] European Inst Oncol, Div Epidemiol & Biostat, Milan, Italy.
[Minig, Lucas] NCI, Div Canc Treatment & Diag, NIH, Bethesda, MD 20892 USA.
RP Minig, L (reprint author), European Inst Oncol, Dept Gynecol, Milan, Italy.
EM lucasminig@yahoo.com
NR 47
TC 20
Z9 21
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1068-9265
J9 ANN SURG ONCOL
JI Ann. Surg. Oncol.
PD NOV
PY 2009
VL 16
IS 11
BP 3101
EP 3110
DI 10.1245/s10434-009-0681-4
PG 10
WC Oncology; Surgery
SC Oncology; Surgery
GA 510LE
UT WOS:000271089200018
PM 19760046
ER
PT J
AU Jonsson, H
Helgadottir, GP
Aspelund, T
Eiriksdottir, G
Sigurdsson, S
Ingvarsson, T
Harris, TB
Launer, L
Gudnason, V
AF Jonsson, H.
Helgadottir, G. P.
Aspelund, T.
Eiriksdottir, G.
Sigurdsson, S.
Ingvarsson, T.
Harris, T. B.
Launer, L.
Gudnason, V.
TI Hand osteoarthritis in older women is associated with carotid and
coronary atherosclerosis: the AGES Reykjavik study
SO ANNALS OF THE RHEUMATIC DISEASES
LA English
DT Article
ID BONE-MARROW EDEMA; MYOCARDIAL-INFARCTION; RISK-FACTORS; KLOTHO GENE;
DISEASE; POPULATION; PREVALENCE; ROTTERDAM; MORTALITY; ADULTS
AB Objective: There is evidence that atherosclerosis may contribute to the initiation or progression of osteoarthritis. To test this hypothesis, the presence and severity of hand osteoarthritis (HOA) was compared with markers of atherosclerotic vascular disease in an elderly population.
Patients and Methods: The AGES Reykjavik Study is a population-based multidisciplinary study of ageing in the elderly population of Reykjavik. In a study of 2264 men ( mean age 76 years; SD 6) and 3078 women ( mean age 76 years; SD 6) the severity of HOA, scored from photographs, was compared with measures of atherosclerosis. These included carotid intimal thickness and plaque severity, coronary calcifications (CAC) and aortic calcifications and reported cardiac and cerebrovascular events.
Results: After adjustment for confounders, both carotid plaque severity and CAC were significantly associated with HOA in women, with an odds ratio of 1.42 (95% CI 1.14 to 1.76, p=0.002) for having CAC and 1.25 ( 95% CI 1.04 to 1.49, p=0.016) for having moderate or severe carotid plaques. Both carotid plaques and CAC also exhibited significant linear trends in relation to HOA severity in women in the whole AGES Reykjavik cohort (p<0.001 and p=0.027, respectively, for trend). No significant associations were seen in men. Despite this evidence of increased atherosclerosis, women with HOA did not report proportionally more previous cardiovascular or cerebrovascular events.
Conclusions: The results indicate a linear association between the severity of HOA and atherosclerosis in older women. The pathological process of HOA seems to have some components in common with atherosclerosis. Prospective studies may help elucidate the possible mechanisms of this relationship.
C1 [Jonsson, H.] Landspitalinn Univ Hosp, Dept Rheumatol, IS-108 Reykjavik, Iceland.
[Aspelund, T.] Univ Iceland, Iceland Heart Assoc, Reykjavik, Iceland.
[Ingvarsson, T.] Akureyri Cent Hosp, Akureyri, Iceland.
[Harris, T. B.; Launer, L.] NIA, Bethesda, MD 20892 USA.
RP Jonsson, H (reprint author), Landspitalinn Univ Hosp, Dept Rheumatol, IS-108 Reykjavik, Iceland.
EM helgijon@landspitali.is
RI Aspelund, Thor/F-4826-2011; Aspelund, Thor/C-5983-2008; Gudnason,
Vilmundur/K-6885-2015
OI Aspelund, Thor/0000-0002-7998-5433; Gudnason,
Vilmundur/0000-0001-5696-0084
FU National Institutes of Health [N01AG-12100]; NIA Intramural Research
Program, Hjartavernd ( the Icelandic Heart Association); Althingi ( the
Icelandic Parliament); Icelandic Osteoarthritis Fund; University of
Iceland Science Fund
FX This study has been funded by National Institutes of Health contract
N01AG-12100, the NIA Intramural Research Program, Hjartavernd ( the
Icelandic Heart Association) and the Althingi ( the Icelandic
Parliament). The study was also supported by the Icelandic
Osteoarthritis Fund and the University of Iceland Science Fund.
NR 29
TC 45
Z9 47
U1 1
U2 5
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-4967
J9 ANN RHEUM DIS
JI Ann. Rheum. Dis.
PD NOV
PY 2009
VL 68
IS 11
BP 1696
EP 1700
DI 10.1136/ard.2008.096289
PG 5
WC Rheumatology
SC Rheumatology
GA 505NP
UT WOS:000270700900008
PM 19033292
ER
PT J
AU Cook, MB
Greenwood, DC
Hardie, LJ
Forman, D
Wild, CP
AF Cook, Michael B.
Greenwood, Darren C.
Hardie, Laura J.
Forman, David
Wild, Christopher P.
TI On the Association Between Body Mass Index and Barrett's Esophagus
SO ANNALS OF THORACIC SURGERY
LA English
DT Letter
ID METAANALYSIS
C1 [Cook, Michael B.] NCI, Div Canc Epidemiol & Genet, Rockville, MD 20852 USA.
[Greenwood, Darren C.] Univ Leeds, Div Biostat, Ctr Biostat & Epidemiol, Leeds Inst Genet Hlth & Therapeut, Leeds LS2 9JT, W Yorkshire, England.
[Wild, Christopher P.] Int Agcy Res Canc, F-69372 Lyon, France.
[Forman, David] Leeds Inst Genet Hlth & Therapeut, Ctr Biostat & Epidemiol, Canc Epidemiol Grp, Leeds, W Yorkshire, England.
[Hardie, Laura J.] Leeds Inst Genet Hlth & Therapeut, Ctr Biostat & Epidemiol, Mol Epidemiol Unit, Leeds, W Yorkshire, England.
RP Cook, MB (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,EPS 5012, Rockville, MD 20852 USA.
EM cookmich@mail.nih.gov; d.c.greenwood@leeds.ac.uk;
laura.j.hardie@leeds.ac.uk; d.forman@leeds.ac.uk; director@iarc.fr
RI Greenwood, Darren/C-3220-2008; Cook, Michael/A-5641-2009
OI Greenwood, Darren/0000-0001-7035-3096; Cook, Michael/0000-0002-0533-7302
FU Intramural NIH HHS [NIH0013132602]; PHS HHS [NIH0013132602]
NR 2
TC 0
Z9 0
U1 0
U2 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0003-4975
J9 ANN THORAC SURG
JI Ann. Thorac. Surg.
PD NOV
PY 2009
VL 88
IS 5
BP 1728
EP 1728
PG 1
WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery
SC Cardiovascular System & Cardiology; Respiratory System; Surgery
GA 512AZ
UT WOS:000271215700077
PM 19853166
ER
PT J
AU Tulloch-Reid, M
Skarulis, MC
Sherman, SI
Sarlis, NJ
Santarpia, L
AF Tulloch-Reid, Marshall
Skarulis, Monica C.
Sherman, Steven I.
Sarlis, Nicholas J.
Santarpia, Libero
TI Long-term Eradication of Locally Recurrent Invasive Follicular Thyroid
Carcinoma after Taxane-based Concomitant Chemoradiotherapy
SO ANTICANCER RESEARCH
LA English
DT Article
DE Aerodigestive tract; external beam; radioiodine; radiosensitizer;
radiotherapy; paclitaxel; taxane; carboplatin
ID SQUAMOUS-CELL CARCINOMA; CONCURRENT WEEKLY DOCETAXEL; BEAM
RADIATION-THERAPY; PHASE-II TRIAL; HYPERFRACTIONATED RADIOTHERAPY;
SURGICAL-MANAGEMENT; BOOST RADIATION; NECK-CANCER; HEAD; DEATH
AB A 46-year-old woman with history of radioiodine-refractory follicular thyroid carcinoma (FTC) presented with locally recurrent, high-risk, invasive disease. She was treated with paclitaxel/carboplatin concomitant chemoradiotherapy (CRT), which was well tolerated, resulting in complete remission and freedom from residual or recurrent FTC for longer than 5 years until her last follow-up at age 52. This case highlights the possibility of combining taxane-based chemotherapy with definitive radiotherapy (as CRT) for the management of locally aggressive recurrences in poorly differentiated thyroid carcinoma, thereby resulting in rapid and persistent disease eradication. Even in the light of recent data on the potential benefit of novel targeted therapy agents in poorly differentiated thyroid carcinoma, this approach in similar clinical settings deserves future investigation.
C1 [Sherman, Steven I.; Sarlis, Nicholas J.; Santarpia, Libero] Univ Texas MD Anderson Canc Ctr, Dept Endocrine Neoplasia & Hormonal Disorders, Houston, TX 77030 USA.
[Tulloch-Reid, Marshall; Skarulis, Monica C.] NIDDKD, NIH, Bethesda, MD 20892 USA.
[Santarpia, Libero] Hosp Prato, Translat Res Unit, Florence, Italy.
[Santarpia, Libero] Ist Toscana Tumori, Florence, Italy.
RP Santarpia, L (reprint author), Univ Texas MD Anderson Canc Ctr, Dept Endocrine Neoplasia & Hormonal Disorders, Houston, TX 77030 USA.
EM lsantarp@mdanderson.org
RI Tulloch-Reid, Marshall/E-4383-2012;
OI Santarpia, Libero/0000-0001-6777-1449; Sherman,
Steven/0000-0002-3079-5153
FU Intramural NIH HHS [ZIA DK047053-04]
NR 50
TC 2
Z9 2
U1 0
U2 0
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
ATHENS 19014, GREECE
SN 0250-7005
J9 ANTICANCER RES
JI Anticancer Res.
PD NOV
PY 2009
VL 29
IS 11
BP 4665
EP 4671
PG 7
WC Oncology
SC Oncology
GA 538SC
UT WOS:000273203300046
PM 20032418
ER
PT J
AU Christen-Zaech, S
Imoto, K
Khan, SG
Oh, KS
Tamura, D
DiGiovanna, JJ
Boyle, J
Patronas, NJ
Schiffmann, R
Kraemer, KH
Paller, AS
AF Christen-Zaech, Stephanie
Imoto, Kyoko
Khan, Sikandar G.
Oh, Kyu-Seon
Tamura, Deborah
DiGiovanna, John J.
Boyle, Jennifer
Patronas, Nickolas J.
Schiffmann, Raphael
Kraemer, Kenneth H.
Paller, Amy S.
TI Unexpected Occurrence of Xeroderma Pigmentosum in an Uncle and Nephew
SO ARCHIVES OF DERMATOLOGY
LA English
DT Article
ID GROUP-A PATIENTS; DNA-REPAIR GENE; COCKAYNE-SYNDROME; XPAC GENE;
MUTATIONS; DAMAGE; TRICHOTHIODYSTROPHY; DISORDERS; NEURODEGENERATION;
POPULATION
AB Background: Xeroderma pigmentosum (XP) is a rare autosomal recessive disorder characterized by a decreased ability to repair DNA damaged by UV radiation and the early development of cutaneous and ocular malignant neoplasms. Approximately 20% of patients with XP also develop progressive neurologic degeneration.
Observations: We describe a boy who was found to have XP after a severe burn following minimal sun exposure. His maternal uncle, now age 20 years, had been diagnosed with XP after a similar sunburn in infancy. The uncle has the typical skin pigmentary findings of XP along with severe progressive neurologic involvement. Although the infant's parents were not known to be blood relatives, the infant and his affected uncle proved to be compound heterozygotes for the same 2 frameshift mutations in the XPA DNA repair gene (c.288delT and c.349_353del). After the diagnosis of XP in the infant, genealogic investigation identified a common Dutch ancestor for both of his grandfathers 5 generations back.
Conclusions: Counseling families at risk for a rare inherited disease is not always straightforward. The sociocultural and demographic backgrounds of the families must be considered for evaluation of risk assessment.
C1 [Christen-Zaech, Stephanie; Paller, Amy S.] Northwestern Univ, Feinberg Sch Med, Dept Dermatol, Chicago, IL 60611 USA.
[Christen-Zaech, Stephanie; Paller, Amy S.] Northwestern Univ, Feinberg Sch Med, Dept Pediat, Chicago, IL 60611 USA.
[Imoto, Kyoko; Khan, Sikandar G.; Oh, Kyu-Seon; Tamura, Deborah; DiGiovanna, John J.; Boyle, Jennifer; Kraemer, Kenneth H.] NCI, DNA Repair Sect, Basic Res Lab, Ctr Canc Res, Bethesda, MD 20892 USA.
[DiGiovanna, John J.] Brown Univ, Warren Alpert Med Sch, Dept Dermatol, Div Dermatopharmacol, Providence, RI 02912 USA.
[Patronas, Nickolas J.] NIH, Dept Radiol, Ctr Clin, Bethesda, MD 20892 USA.
[Schiffmann, Raphael] NINDS, NIH, Bethesda, MD 20892 USA.
RP Paller, AS (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Dermatol, 676 N St Clair St,Ste 1600, Chicago, IL 60611 USA.
EM apaller@northwestern.edu
FU Intramural Research Program of the NIH; Center for Cancer Research, NCI
FX Funding/Support: This research was supported in part by the Intramural
Research Program of the NIH, Center for Cancer Research, NCI.
NR 32
TC 3
Z9 3
U1 0
U2 1
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-987X
J9 ARCH DERMATOL
JI Arch. Dermatol.
PD NOV
PY 2009
VL 145
IS 11
BP 1285
EP 1291
PG 7
WC Dermatology
SC Dermatology
GA 520ZS
UT WOS:000271889100010
PM 19917958
ER
PT J
AU Chodick, G
Kleinerman, RA
Stovall, M
Abramson, DH
Seddon, JM
Smith, SA
Tucker, MA
AF Chodick, Gabriel
Kleinerman, Ruth A.
Stovall, Marilyn
Abramson, David H.
Seddon, Johanna M.
Smith, Susan A.
Tucker, Margaret A.
TI Risk of Cataract Extraction Among Adult Retinoblastoma Survivors
SO ARCHIVES OF OPHTHALMOLOGY
LA English
DT Article
ID RADIATION-THERAPY; RADIOTHERAPY; SURGERY; IRRADIATION; GENE
AB Objective: To investigate the risk of cataract extraction among adult retinoblastoma survivors.
Design: A retrospective cohort study was performed on retinoblastoma survivors who received the diagnosis from 1914 to 1984 and were interviewed in 2000. Lens doses were estimated from radiotherapy records. The cumulative time interval to cataract extraction between dose groups was compared using the log-rank test and Cox regression.
Results: Seven hundred fifty-three subjects (828 eyes) were available for analysis for an average of 32 years of follow-up. During this period, 51 cataract extractions were reported. One extraction was reported in an eye with no radiotherapy compared with 36 extractions in 306 eyes with 1 course of radiotherapy and 14 among 38 eyes with 2 or 3 treatments. The average time interval to cataract extraction in irradiated eyes was 51 years (95% confidence interval [ CI], 48-54) following 1 treatment and 32 years (95% CI, 27-37) after 2 or 3 treatments. Eyes exposed to a therapeutic radiation dose of 5 Gy or more had a 6-fold increased risk (95% CI, 1.3-27.2) of cataract extraction compared with eyes exposed to 2.5 Gy or less.
Conclusions: The results emphasize the importance of ophthalmologic examination of retinoblastoma survivors who have undergone radiotherapy. The risk of cataract extraction in untreated eyes with retinoblastoma is comparable with the risk of the general population.
C1 [Chodick, Gabriel; Kleinerman, Ruth A.; Tucker, Margaret A.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
[Stovall, Marilyn; Smith, Susan A.] Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
[Abramson, David H.] Mem Sloan Kettering Canc Ctr, Ophthalm Oncol Serv, New York, NY 10021 USA.
[Seddon, Johanna M.] Tufts Med Ctr, Ophthalm Epidemiol & Genet Serv, New England Eye Ctr, Boston, MA USA.
RP Chodick, G (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Bethesda, MD 20892 USA.
EM hodik_g@mac.org.il
OI Kleinerman, Ruth/0000-0001-7415-2478
FU National Institutes of Health; National Cancer Institute; Division of
Cancer Epidemiology and Genetics
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, the National Cancer Institute, Division
of Cancer Epidemiology and Genetics.
NR 36
TC 3
Z9 3
U1 0
U2 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA
SN 0003-9950
J9 ARCH OPHTHALMOL-CHIC
JI Arch. Ophthalmol.
PD NOV
PY 2009
VL 127
IS 11
BP 1500
EP 1504
PG 5
WC Ophthalmology
SC Ophthalmology
GA 516ZY
UT WOS:000271583700012
PM 19901216
ER
PT J
AU Sikdar, S
Shah, JP
Gebreab, T
Yen, RH
Gilliams, E
Danoff, J
Gerber, LH
AF Sikdar, Siddhartha
Shah, Jay P.
Gebreab, Tadesse
Yen, Ru-Huey
Gilliams, Elizabeth
Danoff, Jerome
Gerber, Lynn H.
TI Novel Applications of Ultrasound Technology to Visualize and
Characterize Myofascial Trigger Points and Surrounding Soft Tissue
SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION
LA English
DT Article
DE Myofascial pain syndromes; Rehabilitation; Sonoelastography; Trigger
points, myofascial; Ultrasonography
ID MAGNETIC-RESONANCE ELASTOGRAPHY; HUMAN SKELETAL-MUSCLE; TAUT BANDS;
PAIN; PREVALENCE; TENSION
AB Objective: To apply ultrasound (US) imaging techniques to better describe the characteristics of myofascial trigger points (MTrPs) and the immediately adjacent soft tissue.
Design: Four sites in each patient were labeled based on physical examination as active myofascial trigger points (A-MTrPs; spontaneously painful), latent myofascial trigger points (L-MTrPs; nonpainful), or normal myofascial tissue. US examination was performed on each subject by a team blinded to the physical findings. A 12 similar to 5MHz US transducer was used. Vibration sonoelastography (VSE) was performed by color Doppler variance imaging while simultaneously inducing vibrations (similar to 92Hz) with a handheld massage vibrator. Each site was assigned a tissue imaging score as follows: 0, uniform. echogenicity and stiffness; 1, focal hypoechoic region with stiff nodule; 2, multiple hypoechoic regions with stiff nodules. Blood flow in the neighborhood of MTrPs was assessed using Doppler imaging. Each site was assigned a blood flow waveform score as follows: 0, normal arterial flow in muscle; 1, elevated diastolic flow; 2, high-resistance flow waveform with retrograde diastolic flow.
Setting: Biomedical research center.
Participants: Subjects (N=9) meeting Travell and Simons' criteria for MTrPs in a taut band in the upper trapezius.
Interventions: Not applicable.
Main Outcome Measures: MTrPs were evaluated by (1) physical examination, (2) pressure algometry, and (3) three types of US imaging including gray-scale (2-dimensional [2D] US), VSE, and Doppler.
Results: MTrPs appeared as focal, hypoechoic regions on 2D US, indicating local changes in tissue echogenicity, and as focal regions of reduced vibration amplitude on VSE, indicating a localized, stiff nodule. MTrPs were elliptical, with a size of.16 +/- 11cm(2). There were no significant differences in size between A-MTrPs and L-MTrPs. Sites containing MTrPs were more likely to have a higher tissue imaging score compared with normal myofascial tissue (P<002). Small arteries (or enlarged arterioles) near A-MTrPs showed retrograde flow in diastole, indicating a highly resistive vascular bed. A-MTrP sites were more likely to have a higher blood flow score compared with L-MTrPs (P<.021).
Conclusions: Preliminary findings show that, under the conditions of this investigation, US imaging techniques can be used to distinguish myofascial tissue containing MTrPs from normal myofascial tissue (lacking trigger points). US enables visualization and some characterization of MTrPs and adjacent soft tissue.
C1 [Sikdar, Siddhartha] George Mason Univ, Dept Elect & Comp Engn, Fairfax, VA 22030 USA.
[Gerber, Lynn H.] George Mason Univ, Ctr Study Chron Illness & Disabil, Fairfax, VA 22030 USA.
[Shah, Jay P.; Gebreab, Tadesse; Yen, Ru-Huey; Gilliams, Elizabeth; Danoff, Jerome; Gerber, Lynn H.] NIH, Dept Rehabil Med, Bethesda, MD 20892 USA.
RP Sikdar, S (reprint author), George Mason Univ, Dept Elect & Comp Engn, 4400 Univ Dr,MS 1G5, Fairfax, VA 22030 USA.
EM ssikdar@gmu.edu
OI Sikdar, Siddhartha/0000-0002-6426-2320
FU National Institutes of Health (NIH)
FX Supported by the Intramural Research Program, National Institutes of
Health (NIH), and the Clinical Center and Office of the Director, NIH.
NR 34
TC 102
Z9 106
U1 2
U2 19
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0003-9993
J9 ARCH PHYS MED REHAB
JI Arch. Phys. Med. Rehabil.
PD NOV
PY 2009
VL 90
IS 11
BP 1829
EP 1838
DI 10.1016/j.apmr.2009.04.015
PG 10
WC Rehabilitation; Sport Sciences
SC Rehabilitation; Sport Sciences
GA 520XC
UT WOS:000271881900003
PM 19887205
ER
PT J
AU Rider, LG
Lachenbruch, PA
Monroe, JB
Ravelli, A
Cabalar, I
Feldman, BM
Villalba, ML
Myones, BL
Pachman, LM
Rennebohm, RM
Reed, AM
Miller, FW
AF Rider, Lisa G.
Lachenbruch, Peter A.
Monroe, Jason B.
Ravelli, Angelo
Cabalar, Imelda
Feldman, Brian M.
Villalba, Maria L.
Myones, Barry L.
Pachman, Lauren M.
Rennebohm, Robert M.
Reed, Ann M.
Miller, Frederick W.
CA IMACS Grp
TI Damage Extent and Predictors in Adult and Juvenile Dermatomyositis and
Polymyositis as Determined With the Myrositis Damage Index
SO ARTHRITIS AND RHEUMATISM
LA English
DT Article
ID SYSTEMIC-LUPUS-ERYTHEMATOSUS; IDIOPATHIC INFLAMMATORY MYOPATHIES;
COLLABORATING-CLINICS/AMERICAN-COLLEGE; 3 ETHNIC-GROUPS; MULTICENTER
COHORT; INITIAL VALIDATION; DISEASE-ACTIVITY; CHILDHOOD-ONSET;
RISK-FACTORS; ASSOCIATION
AB Objective. We undertook this study to validate the Myositis Damage Index (MDI) in juvenile and adult myositis, to describe the degree and types of damage and to develop predictors of damage.
Methods. Retrospective MDI evaluations and prospective assessment of disease activity and illness features were conducted. Patients with juvenile-onset disease (n = 143) were evaluated a median of 18 months after diagnosis; 135 patients were assessed 7-9 months later, and 121 were last assessed a median of 82 months after diagnosis. Ninety-six patients with adult-onset dermatomyositis or polymyositis had a baseline assessment a median of 30 months after diagnosis; 77 patients had a 6-month followup evaluation, and 55 had a final assessment a median of 60 months after diagnosis.
Results. Damage was present in 79% of juvenile patients and in 97% of adult patients. In juveniles, scarring, contractures, persistent weakness, muscle dysfunction, and calcinosis were most frequent (23-30%) at the last evaluation. In adults, muscle atrophy, muscle dysfunction, and muscle weakness were most frequent (74-84%). MDI severity correlated with physician-assessed global damage, serum creatinine, and muscle atrophy on magnetic resonance imaging, and in juveniles also with functional disability and weakness. MDI damage scores and frequency were highest in patients with a chronic illness course and in adult patients who died. Predictors of damage included functional disability, duration of active disease, disease severity at diagnosis, physician-assessed global disease activity, and illness features, including ulcerations in children and pericarditis in adults.
Conclusion. Damage is common in myositis after a median duration of 5 years in patients with adult-onset disease and 6.8 years in patients with juvenile-onset disease. The MDI has good content, construct, and predictive validity in juvenile and adult myositis.
C1 [Rider, Lisa G.] Natl Inst Environm Hlth Sci, Environm Autoimmun Grp, NIH, Bethesda, MD 20892 USA.
[Lachenbruch, Peter A.] Oregon State Univ, Corvallis, OR 97331 USA.
[Ravelli, Angelo] Univ Genoa, Genoa, Italy.
[Ravelli, Angelo] IRCCS G Gaslini, Genoa, Italy.
[Cabalar, Imelda] NIAMS, NIH, Bethesda, MD USA.
[Feldman, Brian M.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Feldman, Brian M.] Univ Toronto, Toronto, ON, Canada.
[Villalba, Maria L.] FDA, Ctr Drug Evaluat & Res, Silver Spring, MD USA.
[Myones, Barry L.] Texas Childrens Hosp, Houston, TX 77030 USA.
[Myones, Barry L.] Baylor Coll Med, Houston, TX 77030 USA.
[Pachman, Lauren M.] Childrens Mem Hosp, Chicago, IL 60614 USA.
[Pachman, Lauren M.] Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA.
[Rennebohm, Robert M.] Columbus Childrens Hosp, Columbus, OH 43205 USA.
[Rennebohm, Robert M.] Ohio State Univ, Columbus, OH USA.
[Reed, Ann M.] Mayo Clin, Rochester, MN USA.
RP Rider, LG (reprint author), Natl Inst Environm Hlth Sci, Environm Autoimmun Grp, NIH, CRC 4-2332,MSC 1301,10 Ctr Dr, Bethesda, MD 20892 USA.
EM riderl@mail.nih.gov
RI Feldman, Brian/A-8586-2011; Harris-Love, Michael/J-1359-2014; RAVELLI,
ANGELO/J-8161-2016;
OI Harris-Love, Michael/0000-0002-1842-3269; RAVELLI,
ANGELO/0000-0001-9658-0385; Rider, Lisa/0000-0002-6912-2458
FU National Institute of Environmental Health Sciences; National Institute
of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH
[1R-21-AR-048349-01]; Cure JM Foundation; Arthritis Foundation
FX Supported in part by the intramural research programs of the National
Institute of Environmental Health Sciences and the National Institute of
Arthritis and Musculoskeletal and Skin Diseases (NIAMS), NIH. Dr.
Lachenbruch's work was supported in part by a grant from the Cure JM
Foundation. Dr. Pachman's work was supported in part by a grant from the
Arthritis Foundation. The work of Dr. Reed and that of contributors from
the International Myositis Assessment and Clinical Studies Group who are
not employed by the US government was supported by the NIH (NIAMS grant
1R-21-AR-048349-01).
NR 35
TC 40
Z9 44
U1 0
U2 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0004-3591
EI 1529-0131
J9 ARTHRITIS RHEUM-US
JI Arthritis Rheum.
PD NOV
PY 2009
VL 60
IS 11
BP 3425
EP 3435
DI 10.1002/art.24904
PG 11
WC Rheumatology
SC Rheumatology
GA 519QF
UT WOS:000271781400032
PM 19877055
ER
PT J
AU Benjamin, D
Chabris, C
Glaeser, E
Gudnason, V
Harris, T
Laibson, D
Launer, L
Purcell, S
Smith, A
AF Benjamin, Daniel
Chabris, Christopher
Glaeser, Edward
Gudnason, Vilmundur
Harris, Tamara
Laibson, David
Launer, Lenore
Purcell, Shaun
Smith, Albert
TI Genetic influences on economic behavior
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [Benjamin, Daniel] Cornell Univ, Ithaca, NY 14853 USA.
[Chabris, Christopher] Union Coll, Schenectady, NY USA.
[Glaeser, Edward; Laibson, David] Harvard Univ, Cambridge, MA 02138 USA.
[Harris, Tamara; Launer, Lenore] NIA, Bethesda, MD 20892 USA.
RI Gudnason, Vilmundur/K-6885-2015
OI Gudnason, Vilmundur/0000-0001-5696-0084
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 636
EP 636
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300016
ER
PT J
AU Chester, C
Horwitz, B
Spotts, EL
Ganiban, J
Lichtenstein, P
Reiss, D
Neiderhiser, JM
AF Chester, Charlene
Horwitz, Brianna
Spotts, Erica L.
Ganiban, Jody
Lichtenstein, Paul
Reiss, David
Neiderhiser, Jenae M.
TI Quality of sibling relationships in middle adulthood: Genetic and
environmental Influences
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [Chester, Charlene; Horwitz, Brianna; Neiderhiser, Jenae M.] Penn State Univ, University Pk, PA 16802 USA.
[Spotts, Erica L.] NIA, Bethesda, MD 20892 USA.
[Ganiban, Jody] George Washington Univ, Washington, DC 20052 USA.
[Lichtenstein, Paul] Karolinska Inst, S-10401 Stockholm, Sweden.
[Reiss, David] Yale Univ, New Haven, CT 06520 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 641
EP 642
PG 2
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300034
ER
PT J
AU de Moor, MHM
Boomsma, DI
de Geus, EJC
Willemsen, G
Hottenga, JJ
Distel, MA
Abecasis, GR
Terracciano, A
McCrae, RR
Costa, PT
Hartman, CA
Spinhoven, P
Penninx, BW
Esko, T
Allik, J
Realo, A
Metspalu, A
Hansell, NK
Medland, SE
Wray, NR
Wright, MJ
Martin, NG
Amin, N
Aulchenko, YS
Janssens, AC
Oostra, BA
van Duijn, CM
AF de Moor, Marleen H. M.
Boomsma, Dorret, I
de Geus, Eco J. C.
Willemsen, Gonneke
Hottenga, Jouke-Jan
Distel, Marijn A.
Abecasis, Goncalo R.
Terracciano, Antonio
McCrae, Robert R.
Costa, Paul T.
Hartman, Catharina A.
Spinhoven, Philip
Penninx, Brenda W.
Esko, Tonu
Allik, Jueri
Realo, Anu
Metspalu, Andres
Hansell, Narelle K.
Medland, Sarah E.
Wray, Naomi R.
Wright, Margie J.
Martin, Nicholas G.
Amin, Najaf
Aulchenko, Yurii S.
Janssens, A. Cecile
Oostra, Ben A.
van Duijn, Cornelia M.
TI Meta-analysis of genome-wide association results in > 10.000 individuals
for the big five personality traits
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [de Moor, Marleen H. M.; Boomsma, Dorret, I; de Geus, Eco J. C.; Willemsen, Gonneke; Hottenga, Jouke-Jan; Distel, Marijn A.] Vrije Univ Amsterdam, Dept Biol Psychol, NL-1081 BT Amsterdam, Netherlands.
[Abecasis, Goncalo R.] Univ Michigan, Dept Biostat, Ctr Stat Genet, Ann Arbor, MI 48109 USA.
[Terracciano, Antonio; McCrae, Robert R.; Costa, Paul T.] NIA, NIH, Baltimore, MD 21224 USA.
[Hartman, Catharina A.] Univ Groningen, Dept Psychiat, Groningen, Netherlands.
[Spinhoven, Philip] Leiden Univ, Dept Psychiat & Psychol, Leiden, Netherlands.
[Penninx, Brenda W.] VU Univ Med Ctr Amsterdam, Inst Neurosci, EMGO Inst, Dept Psychiat, Amsterdam, Netherlands.
[Esko, Tonu] Univ Tartu, Inst Mol & Cell Biol, Estonian Bioctr, EE-50410 Tartu, Estonia.
[Allik, Jueri; Realo, Anu] Univ Tartu, Inst Psychol, EE-50410 Tartu, Estonia.
[Metspalu, Andres] Univ Tartu, Estonian Bioctr, Inst Mol & Cell Biol, EE-50410 Tartu, Estonia.
[Hansell, Narelle K.; Medland, Sarah E.; Wray, Naomi R.; Wright, Margie J.; Martin, Nicholas G.] Queensland Inst Med Res, Brisbane, Qld 4006, Australia.
[Amin, Najaf; Aulchenko, Yurii S.; Janssens, A. Cecile; van Duijn, Cornelia M.] Erasmus Univ, Med Ctr, Dept Epidemiol & Biostat, NL-3000 CA Rotterdam, Netherlands.
[Oostra, Ben A.] Erasmus Univ, Med Ctr, Dept Clin Genet, NL-3000 CA Rotterdam, Netherlands.
RI Allik, Juri/D-5609-2009; terracciano, antonio/B-1884-2008; Aulchenko,
Yurii/M-8270-2013; Realo, Anu/M-9524-2016; Hansell, Narelle/A-4553-2016;
OI Allik, Juri/0000-0002-8358-4747; Aulchenko, Yurii/0000-0002-7899-1575;
Hansell, Narelle/0000-0002-8229-9741; de Geus, Eco/0000-0001-6022-2666
NR 0
TC 3
Z9 3
U1 1
U2 14
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 643
EP 643
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300038
ER
PT J
AU Evrony, HK
Ganiban, JM
Haddad, SK
Lichtenstein, P
Spotts, E
Reiss, D
Neiderhiser, JM
AF Evrony, Hilah K.
Ganiban, Jody M.
Haddad, Suzanne K.
Lichtenstein, Paul
Spotts, Erica
Reiss, David
Neiderhiser, Jenae M.
TI Personality accounting for genetic and environmental associations
between recalled parenting and marital satisfaction
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [Evrony, Hilah K.; Ganiban, Jody M.; Haddad, Suzanne K.] George Washington Univ, Washington, DC USA.
[Lichtenstein, Paul] Karolinska Inst, Stockholm, Sweden.
[Spotts, Erica] NIA, Bethesda, MD 20892 USA.
[Reiss, David] Yale Univ, New Haven, CT USA.
[Neiderhiser, Jenae M.] Penn State Univ, University Pk, PA 16802 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 649
EP 649
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300054
ER
PT J
AU Horwitz, B
Ganiban, J
Spotts, E
Reiss, D
Lichtenstein, P
Neiderhiser, J
AF Horwitz, Briana
Ganiban, Jody
Spotts, Erica
Reiss, David
Lichtenstein, Paul
Neiderhiser, Jenae
TI The role of parent's personality and family relationships in explaining
global family conflict
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [Horwitz, Briana; Neiderhiser, Jenae] Penn State Univ, University Pk, PA 16802 USA.
[Ganiban, Jody] George Washington Univ, Washington, DC 20052 USA.
[Spotts, Erica] NIA, Bethesda, MD 20892 USA.
[Reiss, David] Yale Univ, New Haven, CT 06520 USA.
[Lichtenstein, Paul] Karolinska Inst, S-10401 Stockholm, Sweden.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 657
EP 657
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300075
ER
PT J
AU Narusyte, J
Andershed, AK
Neiderhiser, J
D'Onofrio, B
Reiss, D
Spotts, E
Ganiban, J
Lichtenstein, P
AF Narusyte, Jurgita
Andershed, Anna-Karin
Neiderhiser, Jenae
D'Onofrio, Brian
Reiss, David
Spotts, Erica
Ganiban, Jody
Lichtenstein, Paul
TI Parental criticism and externalizing behavior problems in adolescents:
The role of environment and genotype-environment correlation
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [Narusyte, Jurgita; Lichtenstein, Paul] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
[Andershed, Anna-Karin] Univ Orebro, Dept Behav Social & Legal Sci, Orebro, Sweden.
[Neiderhiser, Jenae] Penn State Univ, Dept Psychol, University Pk, PA 16802 USA.
[D'Onofrio, Brian] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN USA.
[Reiss, David] Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT USA.
[Spotts, Erica] NIA, NIH, Bethesda, MD 20892 USA.
[Ganiban, Jody] George Washington Univ, Dept Psychol, Washington, DC 20052 USA.
NR 0
TC 0
Z9 0
U1 0
U2 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 672
EP 672
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300120
ER
PT J
AU Walum, H
Westberg, L
Henningsson, S
Neiderhiser, JM
Reiss, D
Igl, W
Ganiban, JM
Spotts, EL
Pedersen, NL
Eriksson, E
Lichtenstein, P
AF Walum, Hasse
Westberg, Lars
Henningsson, Susanne
Neiderhiser, Jenae M.
Reiss, David
Igl, Wilmar
Ganiban, Jody M.
Spotts, Erica L.
Pedersen, Nancy L.
Eriksson, Elias
Lichtenstein, Paul
TI Genetic variation in the vasopressin receptor 1a gene (AVPR1A) is
associated with pair-bonding behavior in humans
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 39th Annual Meeting of the Behavior-Genetics-Association
CY JUN 17-20, 2009
CL Mineapolis, MN
SP Behav Genet Assoc
C1 [Walum, Hasse; Igl, Wilmar; Pedersen, Nancy L.; Lichtenstein, Paul] Karolinska Inst, Dept Med Epidemiol & Biostat, S-10401 Stockholm, Sweden.
[Westberg, Lars; Henningsson, Susanne; Eriksson, Elias] Univ Gothenburg, Inst Neurosci & Physiol, Dept Pharmacol, Gothenburg, Sweden.
[Neiderhiser, Jenae M.] Penn State Univ, Dept Psychol, University Pk, PA 16802 USA.
[Reiss, David] Yale Univ, Yale Child Study Ctr, New Haven, CT 06520 USA.
[Ganiban, Jody M.] George Washington Univ, Dept Psychol, Washington, DC 20052 USA.
[Spotts, Erica L.] NIA, Behav & Social Res Program, Bethesda, MD 20892 USA.
NR 0
TC 1
Z9 1
U1 2
U2 20
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2009
VL 39
IS 6
BP 689
EP 689
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 522VL
UT WOS:000272027300168
ER
PT J
AU Lebedeva, NA
Rechkunova, NI
Agama, K
Pommier, Y
Lavrik, OI
AF Lebedeva, N. A.
Rechkunova, N. I.
Agama, K.
Pommier, Y.
Lavrik, O. I.
TI Interaction of DNA topoisomerase 1 with DNA intermediates and proteins
of base excision repair
SO BIOCHEMISTRY-MOSCOW
LA English
DT Article
DE DNA topoisomerase 1; DNA repair; base excision repair factors
ID POSTTRANSLATIONAL MODIFICATION; CLEAVABLE COMPLEXES; ABASIC SITES;
DAMAGE; CAMPTOTHECIN; REPLICATION; INHIBITORS; ENZYMES; KU
AB The interaction of human recombinant DNA topoisomerase 1 (Top1) with linear and circular DNA structures containing a nick or short gap but lacking a specific Top1 recognition site was studied. The effect of key excision repair proteins on formation of the Top1 covalent adduct with the DNA repair intermediates was shown. Partial inhibition of the Top1-DNA-adduct formation upon addition of poly(ADP-ribose) polymerase 1 in the absence of NAD(+) was shown, whereas in the presence of NAD(+) formation of a high molecular weight product, most likely corresponding to poly(ADP)-ribosylated Top1-DNA adduct, was observed. The data show that the key base excision repair proteins can influence formation of suicide Top1-DNA adducts. Top1 was identified by immunoprecipitation in the bovine testis nuclear extract as the protein forming the main modification product with nick-containing DNA.
C1 [Lebedeva, N. A.; Rechkunova, N. I.; Lavrik, O. I.] Inst Chem Biol & Fundamental Med, Novosibirsk 630090, Russia.
[Lebedeva, N. A.] Novosibirsk State Univ, Novosibirsk 630090, Russia.
[Agama, K.; Pommier, Y.] NCI, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Lavrik, OI (reprint author), Inst Chem Biol & Fundamental Med, Pr Akad Lavrentieva 8, Novosibirsk 630090, Russia.
EM lavrik@niboch.nsc.ru
RI Lebedeva, Natalya /G-4758-2013; Rechkunova, Nadezda /G-5093-2013;
Lavrik, Olga /G-4641-2013
FU Russian Foundation for Basic Research [07-04-00389, 09-04-91320];
HRJRG-102; Russian Academy of Sciences program; "Leading Research
Schools" [652.2008]; FTsPK [2009-1.1-201-018-002]; CRDF-BRHE
[RNP.2.2.2.3.10031]
FX This work was supported by the Russian Foundation for Basic Research
(grants 07-04-00389 and 09-04-91320), HRJRG-102, the Russian Academy of
Sciences program "Molecular and Cell Biology", program "Leading Research
Schools" (652.2008), FTsPK (State contract 2009-1.1-201-018-002), and
CRDF-BRHE (RNP.2.2.2.3.10031).
NR 29
TC 3
Z9 3
U1 1
U2 7
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 NOV
PY 2009
VL 74
IS 11
BP 1278
EP 1284
DI 10.1134/S0006297909110157
PG 7
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 522DQ
UT WOS:000271978400015
PM 19916945
ER
PT J
AU Balaban, RS
AF Balaban, Robert S.
TI The role of Ca2+ signaling in the coordination of mitochondrial ATP
production with cardiac work
SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
LA English
DT Review
DE Dehydrogenase; F1-FO-ATPase; Membrane potential; Oxidative
phosphorylation; NADH; Oxygen consumption; Sarcoplasmic reticulum;
Starling effect; Energy homeostasis; Aralar; Citrin
ID CYTOCHROME-C-OXIDASE; PERFUSED RAT-HEART; 2-OXOGLUTARATE DEHYDROGENASE
COMPLEX; CALCIUM-BINDING PROTEIN; P-31 NMR-SPECTROSCOPY; INTRACELLULAR
CALCIUM; OXIDATIVE-PHOSPHORYLATION; PYRUVATE-DEHYDROGENASE;
OXYGEN-CONSUMPTION; IN-VIVO
AB The heart is capable of balancing the rate of mitochondrial ATP production with utilization continuously over a wide range of activity. This results in a constant phosphorylation potential despite a large change in metabolite turnover. The molecular mechanisms responsible for generating this energy homeostasis are poorly understood. The best candidate for a cytosolic signaling molecule reflecting ATP hydrolysis is Ca2+. Since Ca2+ initiates and powers muscle contraction as well as serves as the primary substrate for SERCA, Ca2+ is an ideal feed-forward signal for priming ATP production. With the sarcoplasmic reticulum to cytosolic Ca2+ gradient near equilibrium with the free energy of ATP, cytosolic Ca2+ release is exquisitely sensitive to the cellular energy state providing a feedback signal. Thus, Ca2+ can serve as a feed-forward and feedback regulator of ATP production. Consistent with this notion is the correlation of cytosolic and mitochondrial Ca2+ with work in numerous preparations as well as the localization of mitochondria near Ca2+ release sites. How cytosolic Ca2+ signaling might regulate oxidative phosphorylation is a focus of this review. The relevant Ca2+ sensitive sites include several dehydrogenases and substrate transporters together with a post-translational modification of F1-FO-ATPase and cytochrome oxidase. Thus, Ca2+ apparently activates both the generation of the mitochondrial membrane potential as well as utilization to produce ATP. This balanced activation extends the energy homeostasis observed in the cytosol into the mitochondria matrix in the never resting heart. Published by Elsevier B.V.
C1 NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA.
RP Balaban, RS (reprint author), NHLBI, Cardiac Energet Lab, NIH, Bethesda, MD 20892 USA.
EM rsb@nih.gov
FU Intramural NIH HHS [Z01 HL004601-20]
NR 145
TC 97
Z9 101
U1 1
U2 18
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0005-2728
EI 0006-3002
J9 BBA-BIOENERGETICS
JI Biochim. Biophys. Acta-Bioenerg.
PD NOV
PY 2009
VL 1787
IS 11
SI SI
BP 1334
EP 1341
DI 10.1016/j.bbabio.2009.05.011
PG 8
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 492KI
UT WOS:000269654000006
PM 19481532
ER
PT J
AU Lobanov, AV
Hatfield, DL
Gladyshev, VN
AF Lobanov, Alexey V.
Hatfield, Dolph L.
Gladyshev, Vadim N.
TI Eukaryotic selenoproteins and selenoproteomes
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
LA English
DT Review
DE Selenocysteine; Selenoprotein; Selenoproteome; SECIS element
ID SELENOCYSTEINE INSERTION SYSTEM; SECIS ELEMENTS; THIOREDOXIN REDUCTASE;
ONE CODON; IDENTIFICATION; PROTEIN; EVOLUTION; FAMILY; SELENIUM; ELEGANS
AB Selenium is an essential trace element for which both beneficial and toxic effects in human health have been described. It is now clear that the importance of having adequate amounts of this micronutrient in the diet is primarily due to the fact that selenium is required for biosynthesis of selenocysteine, the twenty first naturally occurring amino acid in protein. In this review, we provide an overview of eukaryotic selenoproteins and selenoproteomes, which are sets of selenoproteins in these organisms. In eukaryotes, selenoproteins show a mosaic occurrence, with some organisms, such as vertebrates and algae, having dozens of these proteins, while other organisms, such as higher plants and fungi, having lost all selenoproteins during evolution. We also discuss selenoprotein functions and evolutionary trends in the use of these proteins in eukaryotes. Functional analysis of selenoproteins is critical for better understanding of the role of selenium in human health and disease. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Lobanov, Alexey V.; Gladyshev, Vadim N.] Univ Nebraska, Dept Biochem, Lincoln, NE 68588 USA.
[Lobanov, Alexey V.; Gladyshev, Vadim N.] Univ Nebraska, Redox Biol Ctr, Lincoln, NE 68588 USA.
[Hatfield, Dolph L.] NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Gladyshev, VN (reprint author), Univ Nebraska, Dept Biochem, Lincoln, NE 68588 USA.
EM vgladyshev1@unl.edu
RI Gladyshev, Vadim/A-9894-2013
FU Intramural NIH HHS [ZIA BC010767-04]; NIGMS NIH HHS [R01 GM061603]
NR 33
TC 116
Z9 123
U1 4
U2 36
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-4165
J9 BBA-GEN SUBJECTS
JI Biochim. Biophys. Acta-Gen. Subj.
PD NOV
PY 2009
VL 1790
IS 11
BP 1424
EP 1428
DI 10.1016/j.bbagen.2009.05.014
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 515GA
UT WOS:000271454600005
PM 19477234
ER
PT J
AU Hatfield, DL
Yoo, MH
Carlson, BA
Gladyshev, VN
AF Hatfield, Dolph L.
Yoo, Min-Hyuk
Carlson, Bradley A.
Gladyshev, Vadim N.
TI Selenoproteins that function in cancer prevention and promotion
SO BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
LA English
DT Review
DE Selenoprotein; 15 kDa selenoprotein; Tumorigenesis; Thioredoxin
reductase 1
ID THIOREDOXIN REDUCTASE; ENDOPLASMIC-RETICULUM; 15-KDA SELENOPROTEIN;
SELENIUM-COMPOUNDS; TRANSGENIC MICE; SELENOCYSTEINE; GENE;
CHEMOPREVENTION; DEFICIENCY; EXPRESSION
AB Of the many health benefits attributed to selenium, the one that has received the most attention is its role in cancer prevention. Selenium-containing proteins (selenoproteins) have been shown in recent years to have roles in cancer prevention. However, selenoproteins have diverse functions and their view as antioxidants is oversimplified. Some selenoproteins appear to have a split personality in having roles both in preventing and promoting cancer. The contrasting roles of one selenoprotein, thioredoxin reductase 1, in cancer are discussed in detail, but as also noted, at least one other selenoprotein may also have such a dual function. In addition, we discuss examples of inhibition of cancer development by selenoprotein deficiency in mouse models. These studies highlight the complex nature of selenium in relation to cancer. Published by Elsevier B.V.
C1 [Hatfield, Dolph L.; Yoo, Min-Hyuk; Carlson, Bradley A.] NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
[Gladyshev, Vadim N.] Univ Nebraska, Dept Biochem, Lincoln, NE 68588 USA.
[Gladyshev, Vadim N.] Univ Nebraska, Redox Biol Ctr, Lincoln, NE 68588 USA.
RP Hatfield, DL (reprint author), NCI, Mol Biol Selenium Sect, Lab Canc Prevent, Ctr Canc Res,NIH, Bldg 37,Room 6032A, Bethesda, MD 20892 USA.
EM hatfield@mail.nih.gov
RI Gladyshev, Vadim/A-9894-2013
FU Intramural Research Program of the National Institutes of Health;
National Cancer Institute; Center for Cancer Research
FX This research was supported by the Intramural Research Program of the
National Institutes of Health, National Cancer Institute, Center for
Cancer Research and NIH grants awarded to VNG.
NR 53
TC 59
Z9 61
U1 0
U2 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-4165
J9 BBA-GEN SUBJECTS
JI Biochim. Biophys. Acta-Gen. Subj.
PD NOV
PY 2009
VL 1790
IS 11
BP 1541
EP 1545
DI 10.1016/j.bbagen.2009.03.001
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 515GA
UT WOS:000271454600018
PM 19272412
ER
PT J
AU Ogawa, M
Regino, CAS
Seidel, J
Green, MV
Xi, WZ
Williams, M
Kosaka, N
Choyke, PL
Kobayashi, H
AF Ogawa, Mikako
Regino, Celeste A. S.
Seidel, Jurgen
Green, Michael V.
Xi, Wenze
Williams, Mark
Kosaka, Nobuyuki
Choyke, Peter L.
Kobayashi, Hisataka
TI Dual-Modality Molecular Imaging Using Antibodies Labeled with
Activatable Fluorescence and a Radionuclide for Specific and
Quantitative Targeted Cancer Detection
SO BIOCONJUGATE CHEMISTRY
LA English
DT Article
ID MONOCLONAL-ANTIBODIES; INDOCYANINE GREEN; OVARIAN-CANCER; PROBE; AGENT;
EXPRESSION; METASTASES; CONJUGATE; VISION; LIGHT
AB Multimodality molecular imaging should have potential for compensating the disadvantages and enhancing the advantages of each modality. Nuclear imaging is superior to optical imaging in whole body imaging and in quantification due to good tissue penetration of gamma rays. However, target specificity can be compromised by high background signal due to the always signal ON feature of nuclear probes. In contrast, optical imaging can be superior in target-specific imaging by employing target-specific signal activation systems, although it is not quantitative because of signal attenuation. In this study, to take advantage of the mutual cooperation of each modality, multimodality imaging was performed by a combination of quantitative radiolabeled probe and an activatable optical probe. The monoclonal antibodies, panitumumab (anti-HER1) and trastuzumab (anti-HER2), were labeled with In-111 and ICG and tested. in both HER1 and HER2 tumor bearing mice by the cocktail injection of radiolabeled and optical probes and by the single injection of a dual-labeled probe. The optical and nuclear images were obtained over 6 days after the conjugates injection. The fluorescence activation properties of ICG labeled antibodies were also investigated by in vitro microscopy. In vitro microscopy demonstrated that there was no fluorescence signal with either panitumumab-ICG or trastuzumab-ICG, when the probes were bound to cell surface antigens but were not yet internalized. After the conjugates were internalized into the cells, both conjugates showed bright fluorescence signal only in the target cells. These results show that both conjugates work as activatable probes. In in vivo multimodality imaging by injection of a cocktail of radio-optical probes, only the target specific tumor was visualized by optical imaging. Meanwhile, the biodistribution profile of the injected antibody was provided by nuclear imaging. Similar results were obtained with radio and optical dual-labeled probes, and it is confirmed that pharmacokinetic properties did not affect the results above. Here, we could characterize the molecular targets by activatable optical probes and visualize the delivery of targeting molecules quantitatively by radioactive probes. Multimodality molecular imaging combining activatable optical and radioactive probes has great potential for simultaneous visualization, characterization, and measurement of biological processes.
C1 [Ogawa, Mikako; Regino, Celeste A. S.; Seidel, Jurgen; Green, Michael V.; Xi, Wenze; Williams, Mark; Kosaka, Nobuyuki; Choyke, Peter L.; Kobayashi, Hisataka] 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, Bldg 10,Room 1B40,MSC1088, 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 43
TC 59
Z9 62
U1 1
U2 28
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 NOV
PY 2009
VL 20
IS 11
BP 2177
EP 2184
DI 10.1021/bc900362k
PG 8
WC Biochemical Research Methods; Biochemistry & Molecular Biology;
Chemistry, Multidisciplinary; Chemistry, Organic
SC Biochemistry & Molecular Biology; Chemistry
GA 520FP
UT WOS:000271826600020
PM 19919110
ER
PT J
AU Blasi, G
Hariri, AR
Alce, G
Taurisano, P
Sambataro, F
Das, S
Bertolino, A
Weinberger, DR
Mattay, VS
AF Blasi, Giuseppe
Hariri, Ahmad R.
Alce, Guilna
Taurisano, Paolo
Sambataro, Fabio
Das, Saumitra
Bertolino, Alessandro
Weinberger, Daniel R.
Mattay, Venkata S.
TI Preferential Amygdala Reactivity to the Negative Assessment of Neutral
Faces
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Amygdala; cingulate; facial expressions; fMRI; prefrontal cortex; social
decision making
ID PREFRONTAL CORTEX; EMOTIONAL STIMULI; COGNITIVE CONTROL; LATERAL
AMYGDALA; FEAR; UNCERTAINTY; BRAIN; FMRI; CONNECTIVITY; NEUROBIOLOGY
AB Background: Prior studies suggest that the amygdala shapes complex behavioral responses to socially ambiguous cues. We explored human amygdala function during explicit behavioral decision making about discrete emotional facial expressions that can represent socially unambiguous and ambiguous cues.
Methods: During functional magnetic resonance imaging, 43 healthy adults were required to make complex social decisions (i.e., approach or avoid) about either relatively unambiguous (i.e., angry, fearful, happy) or ambiguous (i.e., neutral) facial expressions. Amygdala activation during this task was compared with that elicited by simple, perceptual decisions (sex discrimination) about the identical facial stimuli.
Results: Angry and fearful expressions were more frequently judged as avoidable and happy expressions most often as approachable. Neutral expressions were equally judged as avoidable and approachable. Reaction times to neutral expressions were longer than those to angry, fearful, and happy expressions during social judgment only. Imaging data on stimuli judged to be avoided revealed a significant task by emotion interaction in the amygdala. Here, only neutral facial expressions elicited greater activity during social judgment than during sex discrimination. Furthermore, during social judgment only, neutral faces judged to be avoided were associated with greater amygdala activity relative to neutral faces that were judged as approachable. Moreover, functional coupling between the amygdala and both dorsolateral prefrontal (social judgment > sex discrimination) and cingulate (sex discrimination > social judgment) cortices was differentially modulated by task during processing of neutral faces.
Conclusions: Our results suggest that increased amygdala reactivity and differential functional coupling with prefrontal circuitries may shape complex decisions and behavioral responses to socially ambiguous cues.
C1 [Mattay, Venkata S.] NIMH, Clin Brain Disorders Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Blasi, Giuseppe; Taurisano, Paolo; Bertolino, Alessandro] Univ Bari, Dept Neurol & Psychiat Sci, Psychiat Neurosci Grp, Bari, Italy.
[Hariri, Ahmad R.] Duke Univ, Dept Psychol & Neurosci, Durham, NC USA.
[Hariri, Ahmad R.] Duke Univ, Inst Genome Sci & Policy, Durham, NC USA.
RP Mattay, VS (reprint author), NIMH, Clin Brain Disorders Branch, NIH, Dept Hlth & Human Serv, Bldg 10,Ctr Dr,Room 3C-108, Bethesda, MD 20892 USA.
EM vsm@mail.nih.gov
RI Sambataro, Fabio/E-3426-2010; Hariri, Ahmad/D-5761-2011; Bertolino,
Alessandro/O-6352-2016
OI Sambataro, Fabio/0000-0003-2102-416X; Bertolino,
Alessandro/0000-0002-1251-1380
FU Intramural NIH HHS [Z01 MH002905-01]
NR 39
TC 34
Z9 34
U1 4
U2 15
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD NOV 1
PY 2009
VL 66
IS 9
BP 847
EP 853
DI 10.1016/j.biopsych.2009.06.017
PG 7
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 512BH
UT WOS:000271216800006
PM 19709644
ER
PT J
AU Dichter, GS
Felder, JN
Petty, C
Bizzell, J
Ernst, M
Smoski, MJ
AF Dichter, Gabriel S.
Felder, Jennifer N.
Petty, Christopher
Bizzell, Joshua
Ernst, Monique
Smoski, Moria J.
TI The Effects of Psychotherapy on Neural Responses to Rewards in Major
Depression
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Cingulate gyrus; depression; fMRI; orbital frontal cortex; reward;
striatum
ID PRIMATE CAUDATE-NUCLEUS; BRAIN METABOLIC-CHANGES; COGNITIVE-BEHAVIOR
THERAPY; MEDIAL PREFRONTAL CORTEX; SLEEP-DEPRIVATION; DECISION-MAKING;
ANTIDEPRESSANT TREATMENT; ESCAPE PERFORMANCE; ANTERIOR CINGULATE;
GLUCOSE-METABOLISM
AB Background: Unipolar major depressive disorder (MDD) is characterized by anomalous neurobiological responses to pleasant stimuli, a pattern that may be linked to symptoms of anhedonia. However, the potential for psychotherapy to normalize neurobiological responses to pleasant stimuli has not been evaluated.
Methods: Twelve adults with and 15 adults without MDD participated in two identical functional magnetic resonance imaging scans that used a Wheel of Fortune task. Between scans, MDD outpatients received Behavioral Activation Therapy for Depression, a psychotherapy modality designed to increase engagement with rewarding stimuli and reduce avoidance behaviors.
Results: Seventy-five percent of adults with MDD were treatment responders, achieving post-treatment Hamilton Rating Scale for Depression score of six or below. Relative to changes in brain function in the matched nondepressed group, psychotherapy resulted in functional changes in structures that mediate responses to rewards, including the paracingulate gyrus during reward selection, the right caudate nucleus (i.e., the dorsal striatum), during reward anticipation, and the paracingulate and orbital frontal gyri during reward feedback. There was no effect of diagnostic status or psychotherapy on in-scanner task-related behavioral responses.
Conclusions: Behavioral Activation Therapy for Depression, a psychotherapy modality designed to increase engagement with rewarding stimuli and reduce avoidance behaviors, results in improved functioning of unique reward structures during different temporal phases of responses to pleasurable stimuli, including the dorsal striatum during reward anticipation.
C1 [Dichter, Gabriel S.; Bizzell, Joshua] Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA.
[Dichter, Gabriel S.; Felder, Jennifer N.; Bizzell, Joshua] Univ N Carolina, Sch Med, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA.
[Dichter, Gabriel S.; Bizzell, Joshua] Duke Univ, Med Ctr, Duke UNC Brain Imaging & Anal Ctr, Durham, NC USA.
[Dichter, Gabriel S.; Smoski, Moria J.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC USA.
[Petty, Christopher] Durham VA Med Ctr, Mental Illness Res Educ & Clin Ctr, Durham, NC USA.
[Ernst, Monique] NIMH, Mood & Anxiety Disorders Program, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Dichter, GS (reprint author), Univ N Carolina, Sch Med, Dept Psychiat, CB 3366,101 Manning Dr, Chapel Hill, NC 27599 USA.
EM dichter@med.unc.edu
RI Dichter, Gabriel/K-6726-2015;
OI Dichter, Gabriel/0000-0003-3407-5417; Felder,
Jennifer/0000-0002-4598-7836
FU University of North Carolina neurodevelopmental Disorders Research
Center; National Institute of Mental Health (NIMH) [T32-MH070448, K23
MH087754, K23 MH081285]; National Alliance for Research on Schizophrenia
and Depression (NARSAD) Young Investigator award; Duke University
Medical Center; National Institute of Child Health & Development (NICHD)
[K12 HD043446, T32-HD40127]; University of North Carolina-Chapel Hill;
National Institutes of Health National Center for Research Resources
[K12 RR023248]; [MH078145]
FX We would like to thank Todd Harshharger and Syam Gadde for assistance
with image analysis; Prue Cuper Shian-Ling Keng, and Justin Woodlief for
assistance with data collection; and magnetic resonance imaging
technologists Susan Music, Natalie Gautkin, and Talagnair Venkatraman
for assistance with data acquisition. This research was supported by
MH078145 to GSD. Assistance for this study was provided by the
Neuroimaging Core of the University of North Carolina neurodevelopmental
Disorders Research Center. The author MJS was supported by National
Institute of Mental Health (NIMH) T32-MH070448, a National Alliance for
Research on Schizophrenia and Depression (NARSAD) Young Investigator
award, a carrier development award from Duke University Medical Center,
National Institute of Child Health & Development (NICHD), K12 HD043446,
and NIMH K23 MH087754. The author GSD was supported by Postdoctoral
Research in Neurodevelopmental Disorders, NICHD T32-HD40127, NARSAD
Young Investigator awards, a career development award from University of
North Carolina-Chapel Hill, National Institutes of Health National
Center for Research Resources K12 RR023248 and NIMH K23 MH081285. The
authors reported no biomedical financial interests or Potential
conflicts of interest.
NR 96
TC 92
Z9 96
U1 7
U2 20
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD NOV 1
PY 2009
VL 66
IS 9
BP 886
EP 897
DI 10.1016/j.biopsych.2009.06.021
PG 12
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 512BH
UT WOS:000271216800011
PM 19726030
ER
PT J
AU Netzel-Arnett, S
Bugge, TH
Hess, RA
Carnes, K
Stringer, BW
Scarman, AL
Hooper, JD
Tonks, ID
Kay, GF
Antalis, TM
AF Netzel-Arnett, Sarah
Bugge, Thomas H.
Hess, Rex A.
Carnes, Kay
Stringer, Brett W.
Scarman, Anthony L.
Hooper, John D.
Tonks, Ian D.
Kay, Graham F.
Antalis, Toni M.
TI The Glycosylphosphatidylinositol-Anchored Serine Protease PRSS21
(Testisin) Imparts Murine Epididymal Sperm Cell Maturation and
Fertilizing Ability
SO BIOLOGY OF REPRODUCTION
LA English
DT Article
DE decapitated sperm; easily decapitated sperm; epididymis; fertilizing
ability; male reproductive tract; PRSS21; serine protease; sperm; sperm
maturation; testisin
ID EPITHELIAL SODIUM-CHANNELS; TYROSINE PHOSPHORYLATION; MOUSE SPERMATOZOA;
VOLUME REGULATION; ZONA-PELLUCIDA; MAMMALIAN SPERMATOZOA; IN-VIVO; MICE;
CAPACITATION; GENE
AB An estimated 25%-40% of infertile men have idiopathic infertility associated with deficient sperm numbers and quality. Here, we identify the membrane-anchored serine protease PRSS21, also known as testisin, to he a novel proteolytic factor that directs epididymal sperm cell maturation and sperm-fertilizing ability. PRSS21-deficient spermatozoa show decreased motility, angulated and curled tails, fragile necks, and dramatically increased susceptibility to decapitation. These defects reflect aberrant maturation during passage through the epididymis, because histological and electron microscopic structural analyses showed an increased tendency for curled and detached tails as spermatozoa transit from the corpus to the cauda epididymis. Cauda epididymal spermatozoa deficient in PRSS21 fail to mount a swelling response when exposed to hypotonic conditions, suggesting an impaired ability to respond to osmotic challenges facing maturing spermatozoa in the female reproductive tract. These data suggest that aberrant regulation of PRSS21 may underlie certain secondary male infertility syndromes, such as "easily decapitated" spermatozoa in humans.
C1 [Netzel-Arnett, Sarah; Antalis, Toni M.] Univ Maryland, Sch Med, Ctr Vasc & Inflammatory Dis, Baltimore, MD 21201 USA.
[Netzel-Arnett, Sarah; Antalis, Toni M.] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA.
[Bugge, Thomas H.] Natl Inst Dent & Craniofacial Res, Proteases & Tissue Remodeling Unit, NIH, Bethesda, MD USA.
[Hess, Rex A.; Carnes, Kay] Univ Illinois, Dept Vet Biosci, Urbana, IL 61801 USA.
[Stringer, Brett W.; Tonks, Ian D.; Kay, Graham F.] Queensland Inst Med Res, Herston, Qld 4006, Australia.
[Scarman, Anthony L.; Hooper, John D.] Queensland Univ Technol, Inst Hlth & Biomed Innovat, Kelvin Grove, Qld, Australia.
RP Antalis, TM (reprint author), Univ Maryland, Sch Med, Ctr Vasc & Inflammatory Dis, 800 W Baltimore St, Baltimore, MD 21201 USA.
EM tantalis@som.umaryland.edu
RI Kay, Graham/A-4130-2011; Hooper, John/B-4153-2011; Hooper,
John/C-1481-2016
OI Hooper, John/0000-0003-1054-8486
FU Lance Armstrong Foundation; National Institutes of Health (NIH)
[CA098369, HL084387, HL07698]; NIH Intramural program; Department of
Defense [DAMD-17-02-1-0693]; National Health and Medical Research
Council; Consortium for Industrial Collaboration in Contraceptive
Research (CICCR); program of Contraceptive Research and Development
(CONRAD); Eastern Virginia Medical School; Nationa Institute of Child
Health and Human Development (NICHD) Brain Nationa Institute of Child
Health and Human Development (NICHD) Brain and Tissue Bank for
Developmental Disorders at the University of Maryland School of
Medicine; NICHD [N01-HD-4-3368, N01-HD-4-3383]
FX Supported by the Lance Armstrong Foundation (T.M.A.); National
Institutes of Health (NIH) grants CA098369 and HL084387 to T.M.A. and
HL07698 to S.N.-A., the NIH Intramural program (T.H.B.); Department of
Defense grant DAMD-17-02-1-0693 to T.H.B.; and the National Health and
Medical Research Council (T.M.A. and G.F.K.) Partial support was
provided by Consortium for Industrial Collaboration in Contraceptive
Research (CICCR), a program of Contraceptive Research and Development
(CONRAD), Eastern Virginia Medical School, to R.A.H. The views expressed
by the authors do not necessarily reflect the views of CONRAD or CICCR.
The Nationa Institute of Child Health and Human Development (NICHD)
Brain and Tissue Bank for Developmental Disorders at the University of
Maryland School of Medicine and NICHD contracts N01-HD-4-3368 and
N01-HD-4-3383 are acknowledged for deidentified human tissues.
NR 77
TC 29
Z9 32
U1 0
U2 3
PU SOC STUDY REPRODUCTION
PI MADISON
PA 1603 MONROE ST, MADISON, WI 53711-2021 USA
SN 0006-3363
J9 BIOL REPROD
JI Biol. Reprod.
PD NOV
PY 2009
VL 81
IS 5
BP 921
EP 932
DI 10.1095/biolreprod.109.076273
PG 12
WC Reproductive Biology
SC Reproductive Biology
GA 509PP
UT WOS:000271030700013
PM 19571264
ER
PT J
AU Donohue, SR
Varnas, K
Jia, ZS
Gulyas, B
Pike, VW
Halldin, C
AF Donohue, Sean R.
Varnas, Katarina
Jia, Zhisheng
Gulyas, Balazs
Pike, Victor W.
Halldin, Christer
TI Synthesis and in vitro autoradiographic evaluation of a novel
high-affinity radioiodinated ligand for imaging brain cannabinoid
subtype-1 receptors
SO BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
LA English
DT Article
DE SPECT; PET; CB(1) receptors; Radioiodination; Radioligand
ID CB1 RECEPTORS; RAT-BRAIN; CANDIDATE RADIOLIGANDS; VIVO; SCHIZOPHRENIA;
LOCALIZATION; BINDING; ANTAGONIST; DISCOVERY; DENSITY
AB There is strong interest to study the involvement of brain cannabinoid subtype-1 (CB(1)) receptors in neuropsychiatric disorders with single photon emission computed tomography ( SPECT) and a suitable radioligand. Here we report the synthesis of a novel high-affinity radioiodinated CB(1) receptor ligand ([(125)I]8, [(125)I]1-(2-iodophenyl)-4-cyano-5-(4-methoxyphenyl)-N-(piperidin-1-yl)-1H-pyrazole-3-carboxylate, [(125)I] SD7015). By autoradiography in vitro, [(125)I]8 showed selective binding to CB(1) receptors on human brain postmortem cryosections and now merits labeling with iodine-123 for further evaluation as a SPECT radioligand in non-human primate. (c) 2009 Elsevier Ltd. All rights reserved.
C1 [Donohue, Sean R.; Pike, Victor W.] NIMH, Mol Imaging Branch, NIH, Bethesda, MD 20892 USA.
[Donohue, Sean R.; Varnas, Katarina; Jia, Zhisheng; Gulyas, Balazs; Halldin, Christer] Karolinska Hosp, Karolinska Inst, Dept Clin Neurosci, Psychiat Sect, S-17176 Stockholm, Sweden.
RP Donohue, SR (reprint author), Johns Hopkins PET Ctr, Div Nucl Med, Nelson B1-122,600 N Wolfe St, Baltimore, MD 21287 USA.
EM Sean_Donohue@tracer.nm.jhu.edu
RI Gulyas, Balazs/F-9508-2015
FU National Institutes of Health; National Institute of Mental Health
(NIMH) [ZO1MH002793]; University of Carolina at Chapel Hill [NO1MH32004]
FX S. R. D. and V. W. P. were supported by the Intramural Research Program
of the National Institutes of Health, specifically the National
Institute of Mental Health (NIMH), project number ZO1MH002793. We thank
the NIMH Psychoactive Drug Screening Program (PDSP) for performing
binding assays and Siv Eriksson for the excellent technical assistance
with autoradiographic experiments. The PDSP is directed by Bryan L.
Roth, PhD, with project officer Jamie Driscoll ( NIMH) at the University
of Carolina at Chapel Hill ( contract NO1MH32004).
NR 26
TC 13
Z9 13
U1 0
U2 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0960-894X
J9 BIOORG MED CHEM LETT
JI Bioorg. Med. Chem. Lett.
PD NOV 1
PY 2009
VL 19
IS 21
BP 6209
EP 6212
DI 10.1016/j.bmcl.2009.08.092
PG 4
WC Chemistry, Medicinal; Chemistry, Organic
SC Pharmacology & Pharmacy; Chemistry
GA 503SX
UT WOS:000270561300048
PM 19767206
ER
PT J
AU Topol, I
Collins, J
Polyakov, I
Grigorenko, B
Nemukhin, A
AF Topol, Igor
Collins, Jack
Polyakov, Igor
Grigorenko, Bella
Nemukhin, Alexander
TI On photoabsorption of the neutral form of the green fluorescent protein
chromophore
SO BIOPHYSICAL CHEMISTRY
LA English
DT Article
DE Green fluorescent protein; Photoabsorption spectra; Quantum
calculations; Protein matrix influence
ID ELECTRONIC EXCITATIONS; GAS-PHASE; ABSORPTION-SPECTRUM; PROTONATION
STATES; GFP; ISOMERIZATION; CONSISTENT; VARIANTS; DYNAMICS; COLOR
AB We present results of theoretical studies of the photoabsorption band corresponding to the vertical electronic transition S(0)-S(1) between first two singlet states of the model chromophore from the green fluorescent protein (GFP) in its neutral form. Predictions of quantum chemical approaches including ab initio and semi-empirical approximations are compared for the model systems which mimic the GFP chromophore in different environments. We provide evidences that the protein matrix in GFP accounts for a fairly large shift of about 40 nm in the S(0)-S(1) absorption band as compared to the gas phase. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Topol, Igor; Collins, Jack] SAIC Fredenick Inc, Adv Biomed Comp Ctr, Informat Syst Program, NCI Frederick, Frederick, MD 21702 USA.
[Polyakov, Igor; Grigorenko, Bella; Nemukhin, Alexander] Moscow MV Lomonosov State Univ, Dept Chem, Moscow 119991, Russia.
[Nemukhin, Alexander] Russian Acad Sci, NM Emanuel Inst Biochem Phys, Moscow 119334, Russia.
RP Topol, I (reprint author), SAIC Fredenick Inc, Adv Biomed Comp Ctr, Informat Syst Program, NCI Frederick, Frederick, MD 21702 USA.
EM topol@ncifcrf.gov
RI Nemukhin, Alexander/P-9662-2015
FU National Cancer Institute, National Institutes of Health
[HHSN261200800001E]; Russian Foundation [07-03-00059]
FX We thank the staff and administration of the Advanced Biomedical
Computing Center for their support of this project. This project has
been funded in whole or in part with federal funds from the National
Cancer Institute, National Institutes of Health, under contract number
HHSN261200800001E. The content of this publication does not necessarily
reflect the views or policies of the Department of Health and Human
Services, nor does mention of trade names, commercial products, or
organization imply endorsement by the U.S. Government. This work is
partly supported by the Russian Foundation for Basic Research (project #
07-03-00059).
NR 35
TC 19
Z9 19
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0301-4622
J9 BIOPHYS CHEM
JI Biophys. Chem.
PD NOV
PY 2009
VL 145
IS 1
BP 1
EP 6
DI 10.1016/j.bpc.2009.08.002
PG 6
WC Biochemistry & Molecular Biology; Biophysics; Chemistry, Physical
SC Biochemistry & Molecular Biology; Biophysics; Chemistry
GA 512AA
UT WOS:000271212800001
PM 19720446
ER
PT J
AU Hall, D
Edskes, H
AF Hall, Damien
Edskes, Herman
TI A model of amyloid's role in disease based on fibril fracture
SO BIOPHYSICAL CHEMISTRY
LA English
DT Article
DE Amyloid kinetics; Amyloid toxicity; Fibril fracture; Toxic oligomer
hypothesis; Solid mass hypothesis
ID ALZHEIMERS-DISEASE; MISFOLDING DISEASES; STRUCTURAL BASIS; POTENTIAL
ROLES; IN-VITRO; PROTEIN; BETA; MECHANISM; TOXICITY; NEURODEGENERATION
AB Although the correlative evidence relating the presence of amyloid fibrils and certain disease states (e.g. Alzheimer's disease and Type 2 Diabetes) is overwhelming, a direct causative role for amyloid has proved harder to establish. Current thinking links a narrow region of the aggregate protein size distribution, the so called 'early aggregate' domain to cellular toxicity. A troubling feature of this theory however is that the nucleated reaction mechanism by which amyloid formation is believed to occur results in a very low number concentration of early aggregates which are rapidly extended to form amyloid fibrils. Ibis situation means that the concentration of early aggregates is very low at the time when they are supposedly at their most toxic. Here we adopt a novel explicit simulation strategy to examine a kinetic regime involving nucleated growth combined with fibril fragmentation under which this situation can be reversed so as to produce a high number concentration of small on-pathway toxic aggregates. Dependent upon the rate of fragmentation, the time scale for generation of toxic early aggregates may be coupled. uncoupled or disassociated from the time scale for the appearance of amyloid fibrils. Furthermore the model presents itself as a biochemical 'switch' transitioning between modes of amyloid induced cell death dependent upon either specific amyloid toxicity or non-specific solid mass induced tissue damage. (C) 2009 Elsevier B.V. All rights reserved.
C1 [Hall, Damien] Univ Tsukuba, Inst Basic Med Sci, Lab 225 B, Tsukuba, Ibaraki 3058577, Japan.
[Edskes, Herman] Natl Inst Diabet Digest & Kidney Dis, Lab Biochem & Genet, NIH, Lab 226, Bethesda, MD 20892 USA.
RP Hall, D (reprint author), Univ Tsukuba, Inst Basic Med Sci, Lab 225 B, Bldg D,1-1-1 Tennodai, Tsukuba, Ibaraki 3058577, Japan.
EM damienhall@md.tsukuba.ac.jp; edskes@helix.nih.gov
RI Hall, Damien/D-9927-2012
OI Hall, Damien/0000-0003-1538-7618
FU Intramural NIH HHS [Z99 DK999999]
NR 51
TC 11
Z9 11
U1 1
U2 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0301-4622
J9 BIOPHYS CHEM
JI Biophys. Chem.
PD NOV
PY 2009
VL 145
IS 1
BP 17
EP 28
DI 10.1016/j.bpc.2009.08.004
PG 12
WC Biochemistry & Molecular Biology; Biophysics; Chemistry, Physical
SC Biochemistry & Molecular Biology; Biophysics; Chemistry
GA 512AA
UT WOS:000271212800003
PM 19735971
ER
PT J
AU Aviner, S
Garty, BZ
Rachmel, A
Baris, HN
Sidransky, E
Shuffer, A
Attias, J
Yaniv, Y
Cohen, IJ
AF Aviner, Shraga
Garty, Ben-Zion
Rachmel, Avinoam
Baris, Hagit N.
Sidransky, Ellen
Shuffer, Avinoam
Attias, Joseph
Yaniv, Yisaac
Cohen, Ian J.
TI Type 2 Gaucher disease occurs in Ashkenazi Jews but is surprisingly rare
SO BLOOD CELLS MOLECULES AND DISEASES
LA English
DT Article
DE Type 2 Gaucher disease; Ashkenazi Jews; Glucocerebrosidase; Lysosomal
storage disorder
ID GLUCOCEREBROSIDASE GENE; PHENOTYPE; MUTATIONS
AB Patients with Gaucher disease (GD) are divided into three types based on the presence and rate of progression of the neurologic manifestations. While type 1 GD has a strong predilection in the Jewish Ashkenazi population, both other types lack such a propensity. We report the occurrence of type 2 GD (GD2) in four pregnancies in two Jewish families in Israel (in one case the mother was not Ashkenazi but was from a Sfaradi Jewish family) and also review seven additional cases of GD2 in Ashkenazi Jewish families reported in the literature. Phenotypically, GD2 in Ashkenazi Jews does not differ significantly from this form in other ethnic groups. Genotypic analysis of probands from the two Israeli families demonstrates that each carried two heterozygous glucocerebrosidase mutations. We could find no explanation why GD2 is so rare in the Jewish Ashkenazi population but we could hypothesize that homozygosity for certain Ashkenazi alleles might be lethal, leading to a lower than expected frequency of GD2 and noted that no cases of homozygous L444P has ever been described in Ashkenazi Jews (C) 2009 Elsevier Inc. All rights reserved.
C1 [Aviner, Shraga] Barzilai Govt Hosp, Dept Pediat, IL-78278 Ashqelon, Israel.
[Aviner, Shraga] Ben Gurion Univ Negev, Fac Hlth Sci, Beer Sheva, Israel.
[Garty, Ben-Zion] Schneider Childrens Med Ctr, Dept Pediat B, Petah Tiqwa, Israel.
[Garty, Ben-Zion; Rachmel, Avinoam; Baris, Hagit N.; Shuffer, Avinoam; Attias, Joseph; Yaniv, Yisaac; Cohen, Ian J.] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel.
[Rachmel, Avinoam] Schneider Childrens Med Ctr, Dept Pediat A, Petah Tiqwa, Israel.
[Baris, Hagit N.] Beilinson Med Ctr, Rabin Med Ctr, Raphael Recanati Genet Inst, Petah Tiqwa, Israel.
[Sidransky, Ellen] NHGRI, Sect Mol Neurogenet, Med Genet Branch, NIH, Bethesda, MD 20892 USA.
[Shuffer, Avinoam] Schneider Childrens Med Ctr, Dept Neurol, Petah Tiqwa, Israel.
[Attias, Joseph] Schneider Childrens Med Ctr, Inst Clin Neurophysiol, Petah Tiqwa, Israel.
[Yaniv, Yisaac; Cohen, Ian J.] Schneider Childrens Med Ctr, Dept Pediat Hematol & Oncol, Petah Tiqwa, Israel.
RP Aviner, S (reprint author), Barzilai Govt Hosp, Dept Pediat, 2 Hahistadrut St, IL-78278 Ashqelon, Israel.
EM aviners@barzi.health.gov.il
RI Cohen, Ian/H-3358-2013
FU National Human Genome Research Institute, National Institutes of Health
FX Ellen Sidransky's contribution to this work was funded by the Intramural
Research Program of the National Human Genome Research Institute,
National Institutes of Health.
NR 21
TC 4
Z9 4
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 1079-9796
J9 BLOOD CELL MOL DIS
JI Blood Cells Mol. Dis.
PD NOV-DEC
PY 2009
VL 43
IS 3
BP 294
EP 297
DI 10.1016/j.bcmd.2009.08.004
PG 4
WC Hematology
SC Hematology
GA 515PO
UT WOS:000271484600012
PM 19734074
ER
PT J
AU Williams-Gray, CH
Evans, JR
Goris, A
Foltynie, T
Ban, M
Robbins, TW
Brayne, C
Kolachana, BS
Weinberger, DR
Sawcer, SJ
Barker, RA
AF Williams-Gray, Caroline H.
Evans, Jonathan R.
Goris, An
Foltynie, Thomas
Ban, Maria
Robbins, Trevor W.
Brayne, Carol
Kolachana, Bhaskar S.
Weinberger, Daniel R.
Sawcer, Stephen J.
Barker, Roger A.
TI The distinct cognitive syndromes of Parkinson's disease: 5 year
follow-up of the CamPaIGN cohort
SO BRAIN
LA English
DT Article
DE Parkinson's disease; dementia; cognitive deficits;
microtubule-associated protein tau; catechol-O-methyltransferase
ID PROGRESSIVE SUPRANUCLEAR PALSY; POSITRON-EMISSION-TOMOGRAPHY;
ALZHEIMERS-DISEASE; ALPHA-SYNUCLEIN; MAPT LOCUS; LEWY BODY; TAU-GENE;
DOPAMINE TRANSPORTER; VAL(158)MET GENOTYPE; PREFRONTAL CORTEX
AB Cognitive abnormalities are common in Parkinson's disease, with important social and economic implications. Factors influencing their evolution remain unclear but are crucial to the development of targeted therapeutic strategies. We have investigated the development of cognitive impairment and dementia in Parkinson's disease using a longitudinal approach in a population-representative incident cohort (CamPaIGN study, n = 126) and here present the 5-year follow-up data from this study. Our previous work has implicated two genetic factors in the development of cognitive dysfunction in Parkinson's disease, namely the genes for catechol-O-methyltransferase (COMT Val(158)Met) and microtubule-associated protein tau (MAPT) H1/H2. Here, we have explored the influence of these genes in our incident cohort and an additional cross-sectional prevalent cohort (n = 386), and investigated the effect of MAPT H1/H2 haplotypes on tau transcription in post-mortem brain samples from patients with Lewy body disease and controls. Seventeen percent of incident patients developed dementia over 5 years [incidence 38.7 (23.9-59.3) per 1000 person-years]. We have demonstrated that three baseline measures, namely, age >= 72 years, semantic fluency less than 20 words in 90 s and inability to copy an intersecting pentagons figure, are significant predictors of dementia risk, thus validating our previous findings. In combination, these factors had an odds ratio of 88 for dementia within the first 5 years from diagnosis and may reflect the syndrome of mild cognitive impairment of Parkinson's disease. Phonemic fluency and other frontally based tasks were not associated with dementia risk. MAPT H1/H1 genotype was an independent predictor of dementia risk (odds ratio = 12.1) and the H1 versus H2 haplotype was associated with a 20% increase in transcription of 4-repeat tau in Lewy body disease brains. In contrast, COMT genotype had no effect on dementia, but a significant impact on Tower of London performance, a frontostriatally based executive task, which was dynamic, such that the ability to solve this task changed with disease progression. Hence, we have identified three highly informative predictors of dementia in Parkinson's disease, which can be easily translated into the clinic, and established that MAPT H1/H1 genotype is an important risk factor with functional effects on tau transcription. Our work suggests that the dementing process in Parkinson's disease is predictable and related to tau while frontal-executive dysfunction evolves independently with a more dopaminergic basis and better prognosis.
C1 [Williams-Gray, Caroline H.; Evans, Jonathan R.; Barker, Roger A.] Univ Cambridge, Ctr Brain Repair, Dept Clin Neurosci, Cambridge CB2 0PY, England.
[Goris, An; Ban, Maria; Sawcer, Stephen J.] Univ Cambridge, Neurol Unit, Dept Clin Neurosci, Cambridge CB2 0PY, England.
[Goris, An] Katholieke Univ Leuven, Lab Neuroimmunol, Sect Expt Neurol, Leuven, Belgium.
[Foltynie, Thomas] UCL, Inst Neurol, Sobell Dept Motor Neurosci & Movement Disorders, London WC1E 6BT, England.
[Robbins, Trevor W.] Univ Cambridge, Dept Expt Psychol, Cambridge CB2 0PY, England.
[Brayne, Carol] Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB2 0PY, England.
[Kolachana, Bhaskar S.; Weinberger, Daniel R.] NIMH, Genes Cognit & Psychosis Program, Intramural Res Program, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Williams-Gray, CH (reprint author), Univ Cambridge, Cambridge Ctr Brain Repair, Dept Clin Neurosci, Forvie Site,Robinson Way, Cambridge CB2 0PY, England.
EM chm27@cam.ac.uk
RI Goris, An/F-2943-2010
OI Goris, An/0000-0002-1276-6682
FU Medical Research Council [RG38582]; Parkinson's Disease Society [RG39
906]; National Institutes of Health; Patrick Berthoud Clinical Research
Fellowship; Foundation-Flanders (FWO-Vlaanderen)
FX This work was supported by grants from Medical Research Council
(RG38582, RAB) and the Parkinson's Disease Society (RG39 906, RAB), and
the National Institutes of Health Research Biomedical Research Centre
Award to the University of Cambridge. C. H. W. G. was supported by a
Patrick Berthoud Clinical Research Fellowship, and held a Raymond and
Beverly Sackler Studentship. A. G. is a Postdoctoral Fellow of the
Research Foundation-Flanders (FWO-Vlaanderen). The sponsors had no role
in study design, or collection, analysis and interpretation of data.
NR 72
TC 306
Z9 313
U1 3
U2 30
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD NOV
PY 2009
VL 132
BP 2958
EP 2969
DI 10.1093/brain/awp245
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 514JB
UT WOS:000271389300007
PM 19812213
ER
PT J
AU Rowland, JH
Meyerowitz, BE
Crespi, CM
Leedham, B
Desmond, K
Belin, TR
Ganz, PA
AF Rowland, Julia H.
Meyerowitz, Beth E.
Crespi, Catherine M.
Leedham, Beth
Desmond, Katherine
Belin, Thomas R.
Ganz, Patricia A.
TI Addressing intimacy and partner communication after breast cancer: a
randomized controlled group intervention
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Body image; Breast cancer; Partner communication; Sexuality; Survivor
ID QUALITY-OF-LIFE; BODY CHANGE STRESS; LONG-TERM; PSYCHOLOGICAL
ADJUSTMENT; ADJUVANT CHEMOTHERAPY; PSYCHOSOCIAL CONCERNS; DYADIC
ADJUSTMENT; COMMUNITY SAMPLE; SEXUAL PROBLEMS; YOUNGER WOMEN
AB While quality of life for most breast cancer survivors (BCS) returns to normal by 1 year post-treatment, problems in sexual function and intimacy often persist. The present study tested the efficacy of a 6-week psycho-educational group intervention in improving BCS's sexual well-being. We conducted a mailed survey of BCS 1-5 years post-diagnosis to identify a sample of women who reported moderately severe problems in body image, sexual function or partner communication, and were deemed eligible for the randomized intervention trial. Using a pre-randomized design, 70% (n = 284) were assigned to a 6-week psycho-educational group intervention and 30% (n = 127) were assigned to a control condition (print material only); however, only 83 BCS agreed to participate in the intervention. Four months post-intervention, the intervention and control groups were not significantly different on the primary outcome of emotional functioning; however, BCS randomized to the intervention group were more likely to report improvements in relationship adjustment and communication as well as increased satisfaction with sex compared to controls. Members of the intervention group who were the least satisfied with their sexual relationship appeared to improve the most. Although modest in its effects, this intervention can be delivered in standard clinical settings. Having an identified treatment may help reduce physician reluctance to ask BCS about problems in intimacy and as appropriate, refer them for timely help.
C1 [Crespi, Catherine M.; Ganz, Patricia A.] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Div Canc Prevent & Control Res, Los Angeles, CA 90095 USA.
[Rowland, Julia H.] NCI, Off Canc Survivorship, Bethesda, MD 20892 USA.
[Rowland, Julia H.] NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Meyerowitz, Beth E.] Univ So Calif, Dept Psychol, Los Angeles, CA 90089 USA.
[Crespi, Catherine M.; Belin, Thomas R.] Univ Calif Los Angeles, Dept Biostat, Los Angeles, CA 90095 USA.
[Desmond, Katherine] Univ Calif Los Angeles, Ctr Community Hlth, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
RP Ganz, PA (reprint author), Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Div Canc Prevent & Control Res, 650 Charles Young Dr S,A2-125 CHS, Los Angeles, CA 90095 USA.
EM rowlandj@mail.nih.gov; meyerow@rcf.usc.edu; ccrespi@ucla.edu;
tbelin@mednet.ucla.edu; pganz@mednet.ucla.edu
OI Crespi, Catherine/0000-0002-6150-2181
FU National Cancer Institute, National Institutes of Health, Department of
Health and Human Services [R01CA63028]; National Institutes of Health
[CA016042]
FX This study was supported by Public Health Service grant R01CA63028 to
Dr. Ganz from the National Cancer Institute, National Institutes of
Health, Department of Health and Human Services and National Institutes
of Health grant CA016042 which supported part of Dr. Crespi's salary.
The authors wish to thank Barbara Bass, Pamela W. Black, Bonnie A.
Cesak, Romaine Clifton, Karin M. Johnson, Shirley Otis-Greene, Dominica
T. Roth and Deborah S. Kulp for their work as leaders of the
intervention groups.
NR 54
TC 31
Z9 33
U1 1
U2 10
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD NOV
PY 2009
VL 118
IS 1
BP 99
EP 111
DI 10.1007/s10549-009-0398-x
PG 13
WC Oncology
SC Oncology
GA 505YI
UT WOS:000270737800011
PM 19390963
ER
PT J
AU Sigurdson, AJ
Bhatti, P
Chang, SC
Rajaraman, P
Doody, MM
Bowen, L
Simon, SL
Weinstock, RM
Linet, MS
Rosenstein, M
Stovall, M
Alexander, BH
Preston, DL
Struewing, JP
AF Sigurdson, Alice J.
Bhatti, Parveen
Chang, Shih-chen
Rajaraman, Preetha
Doody, Michele M.
Bowen, Laura
Simon, Steven L.
Weinstock, Robert M.
Linet, Martha S.
Rosenstein, Marvin
Stovall, Marilyn
Alexander, Bruce H.
Preston, Dale L.
Struewing, Jeffery P.
TI Polymorphisms in estrogen biosynthesis and metabolism-related genes,
ionizing radiation exposure, and risk of breast cancer among US
radiologic technologists
SO BREAST CANCER RESEARCH AND TREATMENT
LA English
DT Article
DE Estrogen biosynthesis; Polymorphisms; Ionizing radiation; Interaction;
Risk factors; Casecontrol; Radiologic technologists
ID THERAPY
AB Ionizing radiation-associated breast cancer risk appears to be modified by timing of reproductive events such as age at radiation exposure, parity, age at first live birth, and age at menopause. However, potential breast cancer risk modification of low to moderate radiation dose by polymorphic estrogen metabolism-related gene variants has not been routinely investigated. We assessed breast cancer risk of 12 candidate variants in 12 genes involved in steroid metabolism, catabolism, binding, or receptor functions in a study of 859 cases and 1,083 controls within the US radiologic technologists (USRT) cohort. Using cumulative breast dose estimates from a detailed assessment of occupational and personal diagnostic ionizing radiation exposure, we investigated the joint effects of genotype on the risk of breast cancer. In multivariate analyses, we observed a significantly decreased risk of breast cancer associated with the CYP3A4 M445T minor allele (rs4986910, OR = 0.3; 95% CI 0.1-0.9). We found a borderline increased breast cancer risk with having both minor alleles of CYP1B1 V432L (rs1056836, CC vs. GG, OR = 1.2; 95% CI 0.9-1.6). Assuming a recessive model, the minor allele of CYP1B1 V432L significantly increased the dose-response relationship between personal diagnostic X-ray exposure and breast cancer risk, adjusted for cumulative occupational radiation dose (p(interaction) = 0.03) and had a similar joint effect for cumulative occupational radiation dose adjusted for personal diagnostic X-ray exposure (pinteraction = 0.06). We found suggestive evidence that common variants in selected estrogen metabolizing genes may modify the association between ionizing radiation exposure and breast cancer risk.
C1 [Sigurdson, Alice J.; Bhatti, Parveen; Rajaraman, Preetha; Doody, Michele M.; Simon, Steven L.; Linet, Martha S.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Chang, Shih-chen] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, Bethesda, MD 20892 USA.
[Chang, Shih-chen] AstraZeneca, Wilmington, DE USA.
[Bowen, Laura] Informat Management Syst, Silver Spring, MD USA.
[Weinstock, Robert M.] Res Triangle Inst, Bethesda, MD USA.
[Stovall, Marilyn] Univ Texas MD Anderson Canc Ctr, Dept Radiat Phys, Houston, TX 77030 USA.
[Alexander, Bruce H.] Univ Minnesota, Div Environm Hlth Sci, Minneapolis, MN USA.
[Preston, Dale L.] HiroSoft Int Corp, Seattle, WA USA.
[Struewing, Jeffery P.] NCI, Lab Populat Genet, Ctr Canc Res, NIH,DHHS, Bethesda, MD 20892 USA.
RP Sigurdson, AJ (reprint author), NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,DHHS, 6120 Execut Blvd,EPS 7060,MSC 7238, Bethesda, MD 20892 USA.
EM sigurdsa@mail.nih.gov
RI Struewing, Jeffery/I-7502-2013
OI Struewing, Jeffery/0000-0002-4848-3334
FU National Institutes of Health
FX We are grateful to the radiologic technologists who participated in the
USRT study; Jerry Reid of the American Registry of Radiologic
Technologists for continued support of this study; and Diane Kampa and
Allison Iwan of the University of Minnesota for data collection and
study coordination. This study was supported by the Intramural Research
Program of the Division of Cancer Epidemiology and Genetics, National
Cancer Institute, National Institutes of Health.
NR 21
TC 7
Z9 8
U1 1
U2 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0167-6806
EI 1573-7217
J9 BREAST CANCER RES TR
JI Breast Cancer Res. Treat.
PD NOV
PY 2009
VL 118
IS 1
BP 177
EP 184
DI 10.1007/s10549-009-0307-3
PG 8
WC Oncology
SC Oncology
GA 505YI
UT WOS:000270737800019
PM 19214745
ER
PT J
AU Campbell, A
Minniti, CP
Nouraie, M
Arteta, M
Rana, S
Onyekwere, O
Sable, C
Ensing, G
Dham, N
Luchtman-Jones, L
Kato, GJ
Gladwin, MT
Castro, OL
Gordeuk, VR
AF Campbell, Andrew
Minniti, Caterina P.
Nouraie, Mehdi
Arteta, Manuel
Rana, Sohail
Onyekwere, Onyinye
Sable, Craig
Ensing, Gregory
Dham, Niti
Luchtman-Jones, Lori
Kato, Gregory J.
Gladwin, Mark T.
Castro, Oswaldo L.
Gordeuk, Victor R.
TI Prospective evaluation of haemoglobin oxygen saturation at rest and
after exercise in paediatric sickle cell disease patients
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE sickle cell disease; paediatric; oxygen saturation; six-minute walk;
pulmonary hypertension
ID REGURGITANT JET VELOCITY; PULSE OXIMETRY; PULMONARY-HYPERTENSION; CHEST
SYNDROME; LUNG-FUNCTION; CHILDREN; ANEMIA; DESATURATION;
STANDARDIZATION; HYPOXEMIA
AB P>Low steady state haemoglobin oxygen saturation in patients with sickle cell anaemia has been associated with the degree of anaemia and haemolysis. How much pulmonary dysfunction contributes to low saturation is not clear. In a prospective study of children and adolescents with sickle cell disease aged 3-20 years at steady state and matched controls, 52% of 391 patients versus 24% of 63 controls had steady state oxygen saturation < 99% (P < 0 center dot 0001), 9% of patients versus no controls had saturation < 95% (P = 0 center dot 008) and 8% of patients versus no controls had exercise-induced reduction in saturation >= 3%. Decreasing haemoglobin concentration (P < 0 center dot 001) and increasing haemolysis (P < 0 center dot 003) but not pulmonary function tests were independent predictors of both lower steady-state saturation and exercise-induced reduction in saturation. Neither history of stroke nor history of acute chest syndrome was significantly associated with lower steady-state oxygen saturation or exercise-induced reduction in saturation. Tricuspid regurgitation velocity was higher in patients with lower steady state haemoglobin oxygen saturation (P = 0 center dot 003) and with greater decline in oxygen saturation during the six-minute walk (P = 0 center dot 022). In conclusion, lower haemoglobin oxygen saturation is independently associated with increasing degrees of anaemia and haemolysis but not pulmonary function abnormalities among children and adolescents with sickle cell disease.
C1 [Gordeuk, Victor R.] Howard Univ, Ctr Sickle Cell Dis, Washington, DC 20001 USA.
[Campbell, Andrew; Arteta, Manuel; Ensing, Gregory] Univ Michigan, Ann Arbor, MI 48109 USA.
[Minniti, Caterina P.; Kato, Gregory J.] NHLBI, Bethesda, MD 20892 USA.
[Minniti, Caterina P.; Kato, Gregory J.] NIH, Dept Crit Care Med, Bethesda, MD 20892 USA.
[Sable, Craig; Dham, Niti; Luchtman-Jones, Lori] Childrens Natl Med Ctr, Washington, DC 20010 USA.
[Gladwin, Mark T.] Univ Pittsburgh, Med Ctr, Pittsburgh, PA USA.
RP Gordeuk, VR (reprint author), Howard Univ, Ctr Sickle Cell Dis, 1840th St,Room 201, Washington, DC 20001 USA.
EM vgordeuk@howard.edu
RI Kato, Gregory/I-7615-2014
OI Kato, Gregory/0000-0003-4465-3217
FU Intramural NIH HHS [Z01 CL008098-02, Z01 CL008098-01, ZIA HL006016-01,
ZIA HL006016-02]; NCRR NIH HHS [2MOI RR10284-10, M01 RR010284]; NHLBI
NIH HHS [1 R01 HL079912-02, 2 R25 HL003679-08, R01 HL079912, R25
HL003679]
NR 32
TC 27
Z9 28
U1 0
U2 6
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2009
VL 147
IS 3
BP 352
EP 359
DI 10.1111/j.1365-2141.2009.07854.x
PG 8
WC Hematology
SC Hematology
GA 505VT
UT WOS:000270727900009
PM 19694721
ER
PT J
AU Anderson, LA
Landgren, O
Engels, EA
AF Anderson, Lesley A.
Landgren, Ola
Engels, Eric A.
TI Common community acquired infections and subsequent risk of chronic
lymphocytic leukaemia
SO BRITISH JOURNAL OF HAEMATOLOGY
LA English
DT Article
DE chronic lymphocytic leukaemia; infection; risk factors; epidemiology
ID RECEPTORS; ZOSTER
AB Emerging evidence supports a role for immune-related factors in the causation of chronic lymphocytic leukaemia (CLL). Using the population-based U. S. Surveillance Epidemiology and End Results-Medicare database, 10 171 elderly CLL patients and 122 531 frequency-matched controls were identified in order to evaluate several community acquired infections associated with subsequent CLL risk. Odds ratios (ORs) were adjusted for gender, age, race, calendar year and number of physician claims. CLL risk was increased following Medicare claims for sinusitis (OR = 1.11; 95% CI = 1.05-1.17), pharyngitis (OR = 1.15; 1.08-1.22), bronchitis (OR = 1.14; 1.08-1.19), pneumonia(OR = 1.17; 1.11-1.24), influenza (OR = 1.10; 1.01-1.19), cellulitis (OR = 1.08; 1.02-1.14) and herpes zoster (OR = 1.26; 1.15-1.37). Associations with pneumonia and cellulitis remained significant when the 5-year period before diagnosis/control selection was excluded. CLL risk increased with increasing severity/frequency of pneumonia (P = 0.005), cellulitis (P < 0.001) and herpes zoster (P < 0.001). Our findings suggest that common infections may play a role in CLL aetiology. Alternatively, the associations might reflect an underlying immune disturbance present several years prior to CLL diagnosis.
C1 [Anderson, Lesley A.] Queens Univ Belfast, Canc Epidemiol & Prevent Res Grp, Ctr Publ Hlth, Belfast BT12 6BJ, Antrim, North Ireland.
[Landgren, Ola; Engels, Eric A.] NCI, Div Canc Epidemiol & Genet, Rockville, MD USA.
[Landgren, Ola] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
RP Anderson, LA (reprint author), Queens Univ Belfast, Canc Epidemiol & Prevent Res Grp, Ctr Publ Hlth, Mulhouse Bldg,Grosvenor Rd, Belfast BT12 6BJ, Antrim, North Ireland.
EM l.anderson@qub.ac.uk
OI Anderson, Lesley/0000-0002-1000-3649
FU Intramural Research Programme of the National Cancer Institute; Research
and Development Office, Northern Ireland; Cancer Prevention Fellowship
Programme; Office of Preventive Oncology; National Cancer Institute;
Surveillance, Epidemiology and End Results (SEER)-Medicare database
FX This study was supported by the Intramural Research Programme of the
National Cancer Institute. The Research and Development Office, Northern
Ireland, funded Dr. Lesley Anderson to participate in the Cancer
Prevention Fellowship Programme, Office of Preventive Oncology, National
Cancer Institute. This study used the linked Surveillance, Epidemiology
and End Results (SEER)-Medicare database. The interpretation and
reporting of these data are the sole responsibility of the authors. The
authors acknowledge the efforts of the Applied Research Programme, NCI;
the Office of Research, Development and Information, Centres for
Medicare and Medicaid Services; Information Management Services, Inc.;
and the SEER Programme tumour registries in the creation of the
SEER-Medicare database. The authors thank Winnie Ricker and Ruth
Parsons, Information Management Services, Rockville, MD for constructing
the dataset, and our colleagues on the SMAHRT Study, who provided advice
and assistance with the SEER-Medicare dataset.
NR 20
TC 30
Z9 31
U1 0
U2 2
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1048
J9 BRIT J HAEMATOL
JI Br. J. Haematol.
PD NOV
PY 2009
VL 147
IS 4
BP 444
EP 449
DI 10.1111/j.1365-2141.2009.07849.x
PG 6
WC Hematology
SC Hematology
GA 512IN
UT WOS:000271240900003
PM 19725826
ER
PT J
AU Bottos, J
Miller, RH
Belfort, RN
Macedo, AC
Belfort, R
Grigg, ME
AF Bottos, J.
Miller, R. H.
Belfort, R. N.
Macedo, A. C.
Belfort, R., Jr.
Grigg, M. E.
CA UNIFESP Toxoplasmosis Grp
TI Bilateral retinochoroiditis caused by an atypical strain of Toxoplasma
gondii
SO BRITISH JOURNAL OF OPHTHALMOLOGY
LA English
DT Article
ID OCULAR TOXOPLASMOSIS; GLOBAL REASSESSMENT; MEMORIAL-LECTURE; SOUTHERN
BRAZIL; GENOTYPE; DISEASE; INFECTION; HUMANS; GENE
AB Background: A 53-year-old man presented with an acute bilateral posterior uveitis with extensive necrotising retinochoroiditis but without chorioretinal scarring. A thorough workup did not reveal any underlying disease. The possibilities of atypical ocular toxoplasmosis as well as herpetic retinal necrosis were considered and specific therapy instituted, with little improvement. The patient died within 2 months as result of an undifferentiated squamous cell carcinoma.
Methods: Histopathological examination, immunohistochemistry and multilocus polymerase chain reaction confirmed Toxoplasma gondii infection of the retina
Results: Macroscopic examination of enucleated globe showed extensive retinal necrosis and vitreous detachment. Histological examination of retinal tissue identified numerous round-to-elliptical toxoplasmic cysts within the retina, with retinal necrosis and minimal choroidal inflammation. Immunohistochemical analyses confirmed that the cysts were due to T gondii. DNA extracted from formalin-fixed, paraffin-embedded tissue sections was subjected to multilocus polymerase chain reaction (PCR) analysis at the following typing loci: SAG1, SAG2, SAG3, SAG4, B1, NTS2, GRA6 and GRA7. DNA sequencing of positive PCR products at the NTS2, SAG1 and GRA7 loci confirmed the presence of a non-archetypal strain of T gondii infecting the eye of the patient experiencing a severe, atypical ocular toxoplasmosis
Conclusion: A highly divergent, non-archetypal strain of T gondii was responsible for causing a severe, atypical bilateral retinochoroiditis in a patient from Brazil.
C1 [Bottos, J.; Belfort, R. N.; Macedo, A. C.; Belfort, R., Jr.] Univ Fed Sao Paulo, Vis Inst, Dept Ophthalmol, BR-04044010 Sao Paulo, Brazil.
[Miller, R. H.; Grigg, M. E.] NIAID, Parasit Dis Lab, Mol Parasitol Unit, NIH, Bethesda, MD 20892 USA.
[Belfort, R. N.] McGill Univ, Dept Ophthalmol, Henry C Witelson Ocular Pathol Lab, Montreal, PQ H3A 2T5, Canada.
RP Bottos, J (reprint author), Univ Fed Sao Paulo, Vis Inst, Dept Ophthalmol, Rua Mirassol 236 Ap 22, BR-04044010 Sao Paulo, Brazil.
EM jubottos@gmail.com
RI Belfort Jr, Rubens/E-2252-2012
OI Belfort Jr, Rubens/0000-0002-8422-3898
FU FADA-UNIFESP; CNPq; NIH; NIAID
FX This work was supported by the Intramural Research Program of the NIH
and NIAID. MEG is a scholar of the Canadian Institute for Advanced
Research (CIFAR) Program for Integrated Microbial Biodiversity.
NR 19
TC 15
Z9 15
U1 0
U2 2
PU B M J PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0007-1161
J9 BRIT J OPHTHALMOL
JI Br. J. Ophthalmol.
PD NOV
PY 2009
VL 93
IS 11
BP 1546
EP 1550
DI 10.1136/bjo.2009.162412
PG 5
WC Ophthalmology
SC Ophthalmology
GA 510MF
UT WOS:000271091900028
PM 19666926
ER
PT J
AU Boknik, P
Grote-Wessels, S
Barteska, G
Jiang, M
Muller, FU
Schmitz, W
Neumann, J
Birnbaumer, L
AF Boknik, P.
Grote-Wessels, S.
Barteska, G.
Jiang, M.
Mueller, F. U.
Schmitz, W.
Neumann, J.
Birnbaumer, L.
TI Genetic disruption of G proteins, G(i2)alpha or G(o)alpha, does not
abolish inotropic and chronotropic effects of stimulating muscarinic
cholinoceptors in atrium
SO BRITISH JOURNAL OF PHARMACOLOGY
LA English
DT Article
DE acetylcholine; carbachol; muscarinic cholinoceptors; G proteins;
parasympathomimetics; vagal stimulation
ID OVEREXPRESSING A(1)-ADENOSINE RECEPTORS; SINOATRIAL NODE CELLS;
NITRIC-OXIDE SYNTHASE; VENTRICULAR MYOCYTES; ADENOSINE RECEPTOR;
PERTUSSIS-TOXIN; CYCLIC-AMP; ACETYLCHOLINE-RECEPTORS; MEDIATED
INHIBITION; SIGNAL-TRANSDUCTION
AB Background and purpose:
Classically, stimulation of muscarinic cholinoceptors exerts negative inotropic and chronotropic effects in the atrium of mammalian hearts. These effects are crucial to the vagal regulation of the heart beat. This effect is assumed to be mediated via GTP binding (G) proteins, because they can be abolished by Pertussis toxin. However, it is unknown which G proteins are involved.
Experimental approach:
We studied contractility in isolated left or right atrium from genetically manipulated mice with deletion of one of two G proteins, either of the alpha subunit of G(i2) protein (G(i2)alpha) or of the alpha subunit of G(o) protein (G(o)alpha). Preparations were stimulated with carbachol alone or after pretreatment with the beta-adrenoceptor agonist isoprenaline. For comparison, the effects of carbachol on L-type Ca2+-channels in isolated ventricular cardiomyocytes were studied.
Key results:
The negative inotropic and chronotropic effects of carbachol alone or in the presence of isoprenaline were identical in atria from knockout or wild-type mice. However, the effect of carbachol on isoprenaline-activated L-type Ca2+-channel in isolated ventricular cardiomyocytes was greatly attenuated in both types of knockout mice studied.
Conclusions and implications:
These data imply that there is either redundancy of G proteins for signal transduction or that Pertussis toxin-sensitive proteins other than G(i2)alpha and G(o)alpha mediate the vagal stimulation in the atrium. Moreover, different G proteins mediate the effect of carbachol in ventricle compared with atrium.
C1 [Boknik, P.; Grote-Wessels, S.; Barteska, G.; Mueller, F. U.; Schmitz, W.] Univ Munster, Inst Pharmakol & Toxikol, Univ Klinikum Munster, D-48149 Munster, Germany.
[Jiang, M.] Univ Calif Los Angeles, Dept Mol & Med Pharmacol, Los Angeles, CA USA.
[Neumann, J.] Univ Halle Wittenberg, Inst Pharmakol & Toxikol, Halle, Germany.
[Birnbaumer, L.] NIEHS, NIH, Dept Human & Hlth Serv, Res Triangle Pk, NC 27709 USA.
RP Boknik, P (reprint author), Univ Munster, Inst Pharmakol & Toxikol, Univ Klinikum Munster, Domagkstr 12, D-48149 Munster, Germany.
EM boknik@uni-muenster.de
FU NIH [Z01-ES-101643, DK069771]
FX This work was supported in part by the Intramural Research Program of
the NIH to LB (Z01-ES-101643) and by the NIH grant to MJ (DK069771).
NR 55
TC 9
Z9 9
U1 1
U2 1
PU WILEY-BLACKWELL
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 0007-1188
J9 BRIT J PHARMACOL
JI Br. J. Pharmacol.
PD NOV
PY 2009
VL 158
IS 6
BP 1557
EP 1564
DI 10.1111/j.1476-5381.2009.00441.x
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 512QC
UT WOS:000271263900015
PM 19906118
ER
PT J
AU Adams, PC
Barton, JC
McLaren, GD
Acton, RT
Speechley, M
McLaren, CE
Reboussin, DM
Leiendecker-Foster, C
Harris, EL
Snively, BM
Vogt, T
Sholinsky, P
Thomson, E
Dawkins, FW
Gordeuk, VR
Eckfeldt, JH
AF Adams, Paul C.
Barton, James C.
McLaren, Gordon D.
Acton, Ronald T.
Speechley, Mark
McLaren, Christine E.
Reboussin, David M.
Leiendecker-Foster, Catherine
Harris, Emily L.
Snively, Beverly M.
Vogt, Thomas
Sholinsky, Phyliss
Thomson, Elizabeth
Dawkins, Fitzroy W.
Gordeuk, Victor R.
Eckfeldt, John H.
TI Screening for iron overload: Lessons from the HEmochromatosis and IRon
Overload Screening (HEIRS) Study
SO CANADIAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Review
DE Haemochromatosis; Hemochromatosis; HFE; Iron overload
ID HFE C282Y HOMOZYGOTES; HEREDITARY HEMOCHROMATOSIS; COST-EFFECTIVENESS;
FAMILY-HISTORY; SERUM FERRITIN; PRIMARY-CARE; POPULATION; PREVALENCE
AB BACKGROUND: The HEmochromatosis and IRon Overload Screening (HEIRS) Study provided data on a racially, ethnically and geographically diverse cohort of participants in North America screened from primary care populations.
METHODS: A total of 101,168 participants were screened by testing for HFE C282Y and H63D Mutations, and measuring serum ferritin concentration and transferrin saturation. In the present review, lessons from the HEIRS Study are highlighted in the context of the principles of screening for a medical disease as previously outlined by the World Health Organization.
RESULTS: Genetic testing is well accepted, with minimal risk of discrimination. Transferrin saturation has high biological variability and relatively low sensitivity to detect HFE C282Y homozygotes, which limits its role as a screening rest. Symptoms attributable to HFE C282Y homozygosity are no more common in individuals identified by Population screening than in control subjects.
CONCLUSIONS: Generalized Population screening in a primary care population as performed in the HEIRS Study is not recommended. There may be a role for focused screening ill Caucasian men, with some debate regarding genotyping followed by phenotyping, or phenotyping followed by genotyping.
C1 [Adams, Paul C.] London Hlth Sci Ctr, Dept Med, London, ON, Canada.
[Barton, James C.] So Iron Disorders Ctr, Birmingham, AL USA.
[McLaren, Gordon D.] VA Long Beach Healthcare Syst, Long Beach, CA USA.
[McLaren, Christine E.] Univ Calif Irvine, Dept Epidemiol, Irvine, CA 92717 USA.
[Acton, Ronald T.] Univ Alabama, Dept Microbiol, Birmingham, AL 35294 USA.
[Reboussin, David M.; Snively, Beverly M.] Wake Forest Univ, Bowman Gray Sch Med, Div Publ Hlth Sci, Winston Salem, NC USA.
[Leiendecker-Foster, Catherine; Eckfeldt, John H.] Univ Minnesota, Dept Lab Med, Minneapolis, MN 55455 USA.
[Leiendecker-Foster, Catherine; Eckfeldt, John H.] Univ Minnesota, Dept Pathol, Minneapolis, MN 55455 USA.
[Harris, Emily L.] Natl Inst Dent & Craniofacial Res, Translat Genom Res Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD USA.
[Vogt, Thomas; Gordeuk, Victor R.] Kaiser Permanente Ctr Hlth Res, Honolulu, HI USA.
[Sholinsky, Phyliss] NHLBI, Dept Epidemiol & Biostat, Epidemiol Branch, Bethesda, MD 20892 USA.
[Thomson, Elizabeth] NHGRI, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Dawkins, Fitzroy W.] Howard Univ, Dept Med, Washington, DC 20059 USA.
RP Adams, PC (reprint author), Univ Western Ontario, Univ Hosp, Dept Med, 339 Windermere Rd, London, ON N6A 5A5, Canada.
EM padams@uwo.ca
FU National Heart, Lung, and Blood Institute; University of Minnesota,
Minneapolis, Minnesota [N01-HC05185]; Howard University, Washington DC
[N01-HC05186, N01-CM-07003-74]; University of Alabama, Birmingham,
Alabama [N01-HC05188]; Kaiser Permanente Center for Health Research
[N01-C05189]; University of California, Irvine, California
[N01-HC05190]; London Health Sciences Centre, London, Ontario
[N01-HC05191]; Wake Forest University, Winston-Salem, North Carolina
[N01-C05192]; University of Alabama at Birmingham General Clinical
Research Center (GCRC) [M01-RR00032]; Howard University GCRC
[M01-RR10284]; University of California, Irvine UCSD/UCI Satellite GCRC
[M01-RR00827]; National Center for Research Resources, National
Institutes of Health (Bethesda, Maryland); National Heart, Lung, and
Blood Institute, and the Office of Research on Minority Health (VRG)
[UH1-HL03679-05]; Southern Iron Disorders Center (Birmingham, Alabama)
FX The HEIRS Study was initiated and funded by the National Heart, Lung,
and Blood Institute, in conjunction with the National Human Genome
Research Institute (Bethesda, Maryland). The study is supported by
contracts N01-HC05185 (University of Minnesota, Minneapolis, Minnesota);
N01-HC05186, N01-CM-07003-74, and Minority CCOP (Howard University,
Washington DC); N01-HC05188 (University of Alabama, Birmingham,
Alabama); N01-C05189 (Kaiser Permanente Center for Health Research);
N01-HC05190 (University of California, Irvine, California); N01-HC05191
(London Health Sciences Centre, London, Ontario); and N01-C05192 (Wake
Forest University, Winston-Salem, North Carolina). Additional support
was provided by the University of Alabama at Birmingham General Clinical
Research Center (GCRC) grant M01-RR00032, Howard University GCRC grant
M01-RR10284, and the University of California, Irvine UCSD/UCI Satellite
GCRC grant M01-RR00827, sponsored by the National Center for Research
Resources, National Institutes of Health (Bethesda, Maryland); Howard
University Research Scientist Award UH1-HL03679-05 from the National
Heart, Lung, and Blood Institute, and the Office of Research on Minority
Health (VRG); and Southern Iron Disorders Center (Birmingham, Alabama)
(JCB, RTA).
NR 24
TC 8
Z9 8
U1 0
U2 3
PU PULSUS GROUP INC
PI OAKVILLE
PA 2902 S SHERIDAN WAY, OAKVILLE, ONTARIO L6J 7L6, CANADA
SN 0835-7900
J9 CAN J GASTROENTEROL
JI Can. J. Gastroenterol.
PD NOV
PY 2009
VL 23
IS 11
BP 769
EP 772
PG 4
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 522JL
UT WOS:000271993700006
PM 19893773
ER
PT J
AU Doria-Rose, VP
Marcus, PM
Szabo, E
Tockman, MS
Melamed, MR
Prorok, PC
AF Doria-Rose, V. Paul
Marcus, Pamela M.
Szabo, Eva
Tockman, Melvyn S.
Melamed, Myron R.
Prorok, Philip C.
TI Randomized Controlled Trials of the Efficacy of Lung Cancer Screening by
Sputum Cytology Revisited A Combined Mortality Analysis From the Johns
Hopkins Lung Project and the Memorial Sloan-Kettering Lung Study
SO CANCER
LA English
DT Article
DE lung cancer; screening; sputum cytology; chest X-ray
ID DETECTION PROGRAM; NEW-YORK; CARCINOMA; SMOKERS; ATYPIA; COHORT
AB BACKGROUND: Two randomized controlled trials of lung cancer screening initiated in the 1970s, the Johns Hopkins Lung Project and the Memorial Sloan Kettering Lung Study, compared 1 arm that received annual chest x-ray and 4-monthly sputum cytology (dual-screen) to a second arm that received annual chest x-ray only. Previous publications from these trials reported similar lung cancer mortality between the 2 groups. However, these findings were based on incomplete follow-up, and each trial on its own was under-powered to detect a modest mortality benefit. METHODS: The authors estimated the efficacy of lung cancer screening with sputum cytology in an intention to screen analysis of lung cancer mortality, using combined data from these trials (n = 20,426). RESULTS: Over 1/2 of squamous cell lung cancers diagnosed in the dual screen group were identified by cytology these cancers tended to be more localized than squamous cancers diagnosed in the X-ray only arm. After 9 years of follow-up, lung cancer mortality was slightly lower in the dual-screen in the X-ray only arm (rate ratio [RR], 0.88; 95% CI, 0.54-1.14) and in the heaviest smokers (RR, 0.81, 95% CI, 0.67-1.00). There were also fewer deaths from large cell carcinoma in the dual-screen group although the reason for this is unclear. CONCLUSIONS: These data are suggestive of a model benefit of sputum cytology screening although we cannot rule out chance as an explanation for these findings. Cancer 2009;115:5007-17. (C) 2009 American Cancer Society.
C1 [Doria-Rose, V. Paul; Marcus, Pamela M.; Prorok, Philip C.] NCI, Biometry Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Doria-Rose, V. Paul] NCI, Canc Prevent Fellowship Program, Ctr Canc Training, NIH, Bethesda, MD 20892 USA.
[Szabo, Eva] NCI, Lung & Upper Aerodigest Canc Res Grp, Canc Prevent Div, NIH, Bethesda, MD 20892 USA.
[Tockman, Melvyn S.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Risk Assessment Detect & Intervent Program,Dept C, Tampa, FL 33612 USA.
[Melamed, Myron R.] New York Med Coll, Dept Pathol, Valhalla, NY 10595 USA.
RP Doria-Rose, VP (reprint author), NCI, Biometry Res Grp, Canc Prevent Div, NIH, 6130 Execut Blvd,Suite 3131, Bethesda, MD 20892 USA.
EM doriarop@mail.nih.gov
OI Doria-Rose, Vincent/0000-0002-8802-5143
FU National Cancer Institute [NO1-CN-45007, N01-CB-92172, N01-CN-45037,
M01-RR-00035-21, RR00722]
FX The trials were supported by the following grants and contracts from the
National Cancer Institute: NO1-CN-45007 (Memorial Sloan-Kettering Lung
Study) and N01-CB-92172, N01-CN-45037, M01-RR-00035-21, and RR00722
(Johns Hopkins Lung Project).
NR 28
TC 23
Z9 24
U1 1
U2 6
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0008-543X
EI 1097-0142
J9 CANCER-AM CANCER SOC
JI Cancer
PD NOV 1
PY 2009
VL 115
IS 21
BP 5007
EP 5017
DI 10.1002/cncr.24545
PG 11
WC Oncology
SC Oncology
GA 511LY
UT WOS:000271167900017
PM 19637354
ER
PT J
AU Moore, SC
Peters, TM
Ahn, J
Park, Y
Schatzkin, A
Albanes, D
Hollenbeck, A
Leitzmann, MF
AF Moore, Steven C.
Peters, Tricia M.
Ahn, Jiyoung
Park, Yikyung
Schatzkin, Arthur
Albanes, Demetrius
Hollenbeck, Albert
Leitzmann, Michael F.
TI Age-Specific Physical Activity and Prostate Cancer Risk Among White Men
and Black Men
SO CANCER
LA English
DT Article
DE physical activity; prostate; cancer; epidemiology
ID UNITED-STATES; SEX-HORMONES; LARGE COHORT; AMERICAN; HEALTH; DIET
AB BACKGROUND: The relation of physical activity across the lifespan to risk of prostate cancer has not been thoroughly investigated, particularly among black men. The authors investigated physical activity, including activity during different age periods and of various intensities, in relation to prostate cancer incidence among white men and black men. METHODS: In total, 160,006 white men and 3671 black men ages 51 years to 72 years who were enrolled in the National Institutes of Health-AARP Diet and Health Study reported their time spent per week engaging in physical activity during ages 15 to 18 years, 19 years to 29 years, 35 years to 39 years, and during the past 10 years. Cox regression models were used to examine physical activity, categorized by intensity (moderate or vigorous, light, and total), in relation to prostate cancer risk. RESULTS: During 7 years of follow-up, 9624 white men and 371 black men developed prostate cancer. Among white men, physical activity had no association with prostate cancer regardless of age period or activity intensity. Among black men, engaging in >= 4 hours of moderate/vigorous intensity physical activity versus infrequent activity during ages 19 years to 29 years was related to a 35% lower risk of prostate cancer (relative risk, 0.65; 95% confidence interval [95% CI], 0.43-0.99 [P(trend) = .01]). Frequent moderate/vigorous physical activity at ages 35 years to 39 years also potentially was related to reduced prostate cancer risk (relative risk, 0.59; 95% Cl, 0.36-0.96 [P(trend) = .15]). CONCLUSIONS: Regular physical activity may reduce prostate cancer risk among black men, and activity during young adulthood may yield the greatest benefit. This novel finding needs confirmation in additional studies. Cancer 2009;115:5060-70. Published 2009 by the American Cancer Society.*
C1 [Moore, Steven C.; Peters, Tricia M.; Ahn, Jiyoung; Park, Yikyung; Schatzkin, Arthur; Albanes, Demetrius; Leitzmann, Michael F.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Hollenbeck, Albert] AARP, Washington, DC USA.
RP Moore, SC (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd, Bethesda, MD 20892 USA.
EM moorest@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015; Moore, Steven/D-8760-2016;
OI Moore, Steven/0000-0002-8169-1661; Park, Yikyung/0000-0002-6281-489X
FU National Institutes of Health, National Cancer Institute [TU2CA105666]
FX Supported by the Intramural Research Program of the National Institutes
of Health, National Cancer Institute, and by grant TU2CA105666 (to
S.C.M.).
NR 25
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U1 0
U2 1
PU JOHN WILEY & SONS INC
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 0008-543X
J9 CANCER
JI Cancer
PD NOV 1
PY 2009
VL 115
IS 21
BP 5060
EP 5070
DI 10.1002/cncr.24538
PG 11
WC Oncology
SC Oncology
GA 511LY
UT WOS:000271167900022
PM 19645029
ER
PT J
AU Mohla, S
Stearns, V
Sathyamoorthy, N
Rosenfeld, MG
Nelson, P
AF Mohla, Suresh
Stearns, Vered
Sathyamoorthy, Neeraja
Rosenfeld, Michael G.
Nelson, Peter
TI The biology of hormone refractory breast and prostate cancer An NCI
workshop report
SO CANCER BIOLOGY & THERAPY
LA English
DT Editorial Material
DE hormone refractory cancer; steroid receptors; breast cancer; prostate
cancer
ID ANDROGEN-RECEPTOR; GENE-EXPRESSION; THERAPEUTIC IMPLICATIONS; TAMOXIFEN
RESISTANCE; CELLS; GROWTH; MECHANISMS; TESTOSTERONE; NUCLEAR; PATHWAY
AB The molecular regulation of growth and progression of hormone refractory breast and prostate cancers remains challenging. The Division of Cancer Biology, NCI organized a small "think tank" style workshop and invited scientists in relevant areas to assess the state of science on the biology of hormone refractory tumors and to identify potential research opportunities to enhance a better understanding of the molecular regulation of these tumors. The meeting, held on May 27-29, 2008 in Bethesda, MD, was co-chaired by Drs. Michael Geoffrey Rosenfeld and Michael Press. While expression of estrogen or progesterone receptors (ER/PR) is required for benefit from endocrine manipulations, many women with breast cancer will not respond to primary endocrine manipulations despite ER/PR expression, and others acquire resistance while on treatment. Understanding the mechanisms that lead to Hormone Refractory Breast Cancer (HRBC) and defining interventions that may modulate the resistance to endocrine therapy are currently lacking. In contrast to breast cancers, the vast majority of both early and advanced prostate carcinomas exhibit androgen-pathway activity at diagnosis and the vast majority respond to treatments designed to inhibit AR-signaling. However, after initial benefit, advanced prostate cancers regularly progress to a clinical state termed Castration Resistant Prostate Cancer (CRPC) that reflects a diverse array of molecular events maintaining AR signaling. The workshop focused on both common and unique features of hormone refractory breast and prostate cancer with an orientation toward defining major research questions, delineating opportunities and recommending strategies for overcoming barriers to progress in understanding these important clinical disease states.
C1 [Mohla, Suresh; Sathyamoorthy, Neeraja] NCI, Div Canc Biol, Bethesda, MD 20892 USA.
[Stearns, Vered] Johns Hopkins Sch Med, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA.
[Rosenfeld, Michael G.] Univ Calif San Diego, Howard Hughes Med Inst, San Diego, CA 92103 USA.
[Nelson, Peter] Fred Hutchinson Canc Res Ctr, Seattle, WA 98104 USA.
RP Mohla, S (reprint author), NCI, Div Canc Biol, Bethesda, MD 20892 USA.
EM mohlas@mail.nih.gov
NR 36
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U1 0
U2 2
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD NOV 1
PY 2009
VL 8
IS 21
BP 1975
EP 1985
DI 10.4161/cbt.8.21.9918
PG 11
WC Oncology
SC Oncology
GA 533BF
UT WOS:000272796200003
PM 19783900
ER
PT J
AU Jonsson, JG
Sissung, TM
Figg, WD
AF Jonsson, Johann G.
Sissung, Tristan M.
Figg, William D.
TI A genomic strategy for predicting androgen receptor activity in prostate
tumors
SO CANCER BIOLOGY & THERAPY
LA English
DT Editorial Material
DE genomic strategy; androgen receptor; activity; AR signature; prostate
tumors; ADT; CRPC
ID CANCER; CASTRATION; THERAPY
AB Mendiratta et al. have developed an AR signature for prostate cancer that is based on the expression of 300 genes. The AR signature is decreased with androgen deprivation therapy, and in the development of androgen independent prostate cancer, however significant inter-individual variation in AR activity was noted. Decreased AR activity was also related to the expression of SRC kinase, and sensitivity to dasatinib. The work by Mendiratta et al. may be useful to determine the AR status of tumors in order to inform therapy and individualize treatment.
C1 [Sissung, Tristan M.; Figg, William D.] NCI, Clin Pharmacol Program, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Jonsson, Johann G.] Univ Iceland, Fac Pharmaceut Sci, Reykjavik, Iceland.
RP Figg, WD (reprint author), NCI, Clin Pharmacol Program, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
EM wdfigg@helix.nih.gov
RI Figg Sr, William/M-2411-2016
NR 10
TC 1
Z9 1
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD NOV 1
PY 2009
VL 8
IS 21
BP 2002
EP 2003
DI 10.4161/cbt.8.21.10180
PG 2
WC Oncology
SC Oncology
GA 533BF
UT WOS:000272796200006
PM 19838047
ER
PT J
AU Yang, SX
Kummar, S
Steinberg, SM
Murgo, AJ
Gutierrez, M
Rubinstein, L
Nguyen, D
Kaur, G
Chen, AP
Giranda, VL
Tomaszewski, JE
Doroshow, JH
AF Yang, Sherry X.
Kummar, Shivaani
Steinberg, Seth M.
Murgo, Anthony J.
Gutierrez, Martin
Rubinstein, Larry
Nguyen, Dat
Kaur, Gurmeet
Chen, Alice P.
Giranda, Vincent L.
Tomaszewski, Joseph E.
Doroshow, James H.
CA Natl Canc Inst Phase 0 Working Grp
TI Immunohistochemical detection of poly(ADP-ribose) polymerase inhibition
by ABT-888 in patients with refractory solid tumors and lymphomas
SO CANCER BIOLOGY & THERAPY
LA English
DT Article
DE ABT-888; immunohistochemistry; PARP; solid tumors and lymphomas; Phase 0
clinical trial
ID ADP-RIBOSE POLYMERASE; METASTATIC BREAST-CANCER; 0 CLINICAL-TRIAL;
ERLOTINIB TREATMENT; DNA-REPAIR; EXPRESSION; GLYCOHYDROLASE; DEATH;
CELLS
AB Purpose: Targeting the poly (ADP-ribose) polymerase (PAPARP) pathway for cancer treatment has been an active area of pre-clinical and clinical research. We aimed to determine whether the PAPARP inhibitor ABT-888 hits its therapeutic target in tumors by immunohistochemistry during a Phase 0 trial conducted at the National Cancer Institute.
Experimental design: The expression of poly (ADP-ribose) (PAR) and full size PAPARP-1 were quantitatively examined by immunohistochemistry in paraffin-embedded tumor biopsies at baseline and 3-24 h after a single oral dose (25 or 50 mg) of ABT-888.
Results: Baseline PAR levels were moderate to high in three patients with non-Hodgkin lymphomas, and one each with small cell lung cancer, squamous cell carcinoma of the tongue and melanoma; low in two patients with cutaneous T-cell lymphoma and one with adenocarcinoma of external ear canal. A significant decrease in PAR (median decrease 30.2, range -13.1 to -69.8) was achieved after drug administration (n = 6 pairs; p = 0.03), whereas an increase in PAPARP-1 expression was observed in five of the six tumors. This resulted in a decrease in the ratio of PAR to PARP-1 in tumor biopsies (median -6.76, range -0.41 to -22.59; p = 0.03).
Conclusions: ABT-888 hits its therapeutic target by significantly reducing PAR levels and the ratio of PAR to PARP-1 in human tumor cells detected by immunohistochemistry. Baseline tumor PAPAR levels vary considerably among patients who entered this Phase 0 study. This underscores a need to investigate baseline PAPAR levels in association with response in future preclinical and clinical studies.
C1 [Yang, Sherry X.; Rubinstein, Larry; Nguyen, Dat; Kaur, Gurmeet; Chen, Alice P.; Tomaszewski, Joseph E.; Doroshow, James H.] NCI, Div Canc Treatment & Diag, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Kummar, Shivaani; Murgo, Anthony J.; Gutierrez, Martin] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Steinberg, Seth M.] NCI, Biostat & Data Management Sect, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Doroshow, James H.] NCI, Mol Pharmacol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Giranda, Vincent L.] Abbott Labs, Chicago, IL USA.
RP Yang, SX (reprint author), NCI, Div Canc Treatment & Diag, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
EM yangxia@mail.nih.gov; doroshoj@mail.nih.gov
FU Division of Cancer Treatment and Diagnosis, National Cancer Institute
(NCI) [N01-CO-12400]
FX Funded in part by the Division of Cancer Treatment and Diagnosis,
National Cancer Institute (NCI) and the NCI Contract N01-CO-12400.
NR 28
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Z9 16
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4047
J9 CANCER BIOL THER
JI Cancer Biol. Ther.
PD NOV 1
PY 2009
VL 8
IS 21
BP 2004
EP 2009
DI 10.4161/cbt.8.21.9917
PG 6
WC Oncology
SC Oncology
GA 533BF
UT WOS:000272796200007
PM 19823047
ER
PT J
AU Tsilidis, KK
Helzlsouer, KJ
Smith, MW
Grinberg, V
Hoffman-Bolton, J
Clipp, SL
Visvanathan, K
Platz, EA
AF Tsilidis, Konstantinos K.
Helzlsouer, Kathy J.
Smith, Michael W.
Grinberg, Victoriya
Hoffman-Bolton, Judith
Clipp, Sandra L.
Visvanathan, Kala
Platz, Elizabeth A.
TI Association of common polymorphisms in IL10, and in other genes related
to inflammatory response and obesity with colorectal cancer
SO CANCER CAUSES & CONTROL
LA English
DT Article
DE Inflammation; Obesity; Colorectal cancer; Genetic epidemiology;
Prospective study
ID C-REACTIVE PROTEIN; SINGLE-NUCLEOTIDE POLYMORPHISMS; COLON-CANCER; CRP
LEVELS; INTERLEUKIN-10-DEFICIENT MICE; CARDIOVASCULAR EVENTS; INSULIN
SENSITIVITY; PLASMA ADIPONECTIN; SEQUENCE VARIANTS; PROMOTER REGION
AB Objective and methods The association of 17 candidate single nucleotide polymorphisms (SNPs) in IL10 and other immune response genes (CRP, TLR4, IL6, IL1B, IL8, TNF, RNASEL) and genes related to obesity (PPARG, TCF7L2, ADIPOQ, LEP) with colorectal cancer was investigated. Haplotype tagging SNPs were chosen for IL10, CRP, and TLR4. Incident colorectal cancer cases (n = 208) and matched controls (n = 381) were identified between baseline in 1989 and 2003 among participants in the CLUE II cohort. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using conditional logistic regression.
Results Compared with the AA genotype at the candidate IL10-1082 locus (rs1800896), carrying one (OR, 0.79; 95% CI, 0.53-1.18) or two (OR, 0.58; 95% CI, 0.35-0.95) G alleles, a known higher producer of the anti-inflammatory cytokine IL-10, was associated with lower risk of colorectal cancer (p(trend) = 0.03). Statistically significant associations with colorectal cancer were observed for three tagSNPs in IL10 (rs1800890, rs3024496, rs3024498) and one common haplotype, but these associations were due to high linkage disequilibrium with IL10-1082. Two CRP haplotypes (global p = 0.04) and TLR4 tagSNPs (rs7873784, rs11536891), but not TLR4 haplotypes, were associated with colorectal cancer.
Conclusions Our study suggests that polymorphisms in IL10, and also possibly in CRP and other genes related to immune response or obesity may be associated with colorectal cancer.
C1 [Tsilidis, Konstantinos K.; Helzlsouer, Kathy J.; Hoffman-Bolton, Judith; Clipp, Sandra L.; Visvanathan, Kala; Platz, Elizabeth A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA.
[Helzlsouer, Kathy J.] St Johns Mercy Med Ctr, Weinberg Ctr Womens Hlth & Med, Prevent & Res Ctr, Baltimore, MD USA.
[Helzlsouer, Kathy J.; Hoffman-Bolton, Judith; Clipp, Sandra L.] Johns Hopkins Bloomberg Sch Publ Hlth, George W Comstock Ctr Publ Hlth Res & Prevent, Hagerstown, MD USA.
[Helzlsouer, Kathy J.; Visvanathan, Kala; Platz, Elizabeth A.] Johns Hopkins Med Inst, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA.
[Grinberg, Victoriya] NCI Frederick, SAIC Frederick Inc, Adv Technol Program, Lab Mol Technol, Frederick, MD USA.
RP Platz, EA (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, 615 N Wolfe St,Rm E6132, Baltimore, MD 21205 USA.
EM eplatz@jhsph.edu
RI Smith, Michael/B-5341-2012
FU NCI NIH HHS [K07 CA111948, K07 CA111948-01A1]
NR 68
TC 81
Z9 81
U1 0
U2 8
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 0957-5243
J9 CANCER CAUSE CONTROL
JI Cancer Causes Control
PD NOV
PY 2009
VL 20
IS 9
BP 1739
EP 1751
DI 10.1007/s10552-009-9427-7
PG 13
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 511VF
UT WOS:000271198400022
PM 19760027
ER
PT J
AU Rixe, O
Franco, SX
Yardley, DA
Johnston, SR
Martin, M
Arun, BK
Letrent, SP
Rugo, HS
AF Rixe, Olivier
Franco, Sandra X.
Yardley, Denise A.
Johnston, Stephen R.
Martin, Miguel
Arun, Banu K.
Letrent, Stephen P.
Rugo, Hope S.
TI A randomized, phase II, dose-finding study of the pan-ErbB receptor
tyrosine-kinase inhibitor CI-1033 in patients with pretreated metastatic
breast cancer
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE CI-1033; Pan-ErbB receptor tyrosine-kinase inhibitor; Metastatic breast
cancer; Efficacy; Safety
ID PLUS CAPECITABINE; ORAL CL-1033; MULTICENTER; TRIAL; EFFICACY; FAMILY;
SAFETY
AB To evaluate the efficacy and safety of the pan-ErbB receptor tyrosine-kinase inhibitor CI-1033 in metastatic breast cancer (MBC).
Patients with measurable, progressive, or recurrent MBC whose primary tumor expressed a parts per thousand yen1 ErbB receptor were randomized to the following CI-1033 regimens: 50 mg (arm A) or 150 mg (arm B) daily without rest period, or 450 mg/day x 14 days every 21 days (arm C). The primary endpoint was 1-year progression-free survival (PFS).
Overall, 194 patients were treated. One-year PFS estimates were 3.8, 2.0, and 4.6%; median PFS was 61, 56, and 58 days; and investigator-assessed overall response rates were 1.5, 1.5, and 7.3%, in arms A, B, and C, respectively. Response duration was 110-419 days. In arm C, response (18.8 vs. 2.6%) and 1-year overall survival rates (86.7 vs. 47.5%) were greater in patients with HER2-positive versus HER2-negative tumors. The incidence of grade 3/4 adverse events (AEs) was dose-dependent, affecting 10.3, 48.6, and 80.4% of patients in arms A, B and C, respectively. The most common grade 3/4, treatment-related AEs were diarrhea, asthenia, and stomatitis. Arm C enrollment was prematurely discontinued due to a high frequency of grade 3/4 AEs.
Single-agent CI-1033 did not show clinically meaningful activity in heavily pretreated patients with MBC expressing a parts per thousand yen1 ErbB receptor. Antitumor activity was observed in arm C patients with HER2-positive tumors. However, only the 50 mg dose was well tolerated, and the highest dose reached unacceptable levels of toxicity.
C1 [Rixe, Olivier] NCI, Med Oncol Branch, Ctr Canc Res, Bethesda, MD 20892 USA.
[Rixe, Olivier] Hop La Pitie Salpetriere, APHP, Paris, France.
[Franco, Sandra X.] Mem Canc Inst, Hollywood, FL USA.
[Yardley, Denise A.] Sarah Cannon Res Inst, Nashville, TN USA.
[Johnston, Stephen R.] Royal Marsden Hosp, London SW3 6JJ, England.
[Martin, Miguel] Hosp Clin San Carlos, Madrid, Spain.
[Arun, Banu K.] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA.
[Letrent, Stephen P.] Pfizer Global Res & Dev, San Diego, CA USA.
[Rugo, Hope S.] Univ Calif San Francisco, Helen Diller Family Comprehens Canc Ctr, San Francisco, CA 94143 USA.
RP Rixe, O (reprint author), NCI, Med Oncol Branch, Ctr Canc Res, Bldg 10,Room 13N240 10 Ctr Dr, Bethesda, MD 20892 USA.
EM rixeo@mail.nih.gov
OI MARTIN, MIGUEL/0000-0001-9237-3231
FU ACUMED(R) (Tytherington, UK); Pfizer Inc. [MI 48105]
FX The authors thank the study center staff, participating patients, and
the clinical trial team for expert collaboration. We also thank Dr
Patrice Herait for expert manuscript preparation assistance and
acknowledge editorial support from ACUMED (R) (Tytherington, UK) with
funding from Pfizer Inc. This study was supported by Pfizer, Inc.,
Clinical Research Department, 2800 Plymouth Road, Ann Arbor, MI 48105,
USA.
NR 25
TC 29
Z9 29
U1 0
U2 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
EI 1432-0843
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD NOV
PY 2009
VL 64
IS 6
BP 1139
EP 1148
DI 10.1007/s00280-009-0975-z
PG 10
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 485HU
UT WOS:000269112600010
PM 19294387
ER
PT J
AU Shibata, SI
Doroshow, JH
Frankel, P
Synold, TW
Yen, Y
Gandara, DR
Lenz, HJ
Chow, WA
Leong, LA
Lim, D
Margolin, KA
Morgan, RJ
Somlo, G
Newman, EM
AF Shibata, Stephen I.
Doroshow, James H.
Frankel, Paul
Synold, Timothy W.
Yen, Yun
Gandara, David R.
Lenz, Heinz-Josef
Chow, Warren A.
Leong, Lucille A.
Lim, Dean
Margolin, Kim A.
Morgan, Robert J.
Somlo, George
Newman, Edward M.
TI Phase I trial of GTI-2040, oxaliplatin, and capecitabine in the
treatment of advanced metastatic solid tumors: a California Cancer
Consortium Study
SO CANCER CHEMOTHERAPY AND PHARMACOLOGY
LA English
DT Article
DE GTI-2040; Oxaliplatin; Capecitabine; Ribonucleotide reductase;
Pharmacokinetics
ID MAMMALIAN RIBONUCLEOTIDE REDUCTASE; KINASE-C-ALPHA; M2 MESSENGER-RNA;
ORNITHINE DECARBOXYLASE; COMPLEMENT ACTIVATION; COLORECTAL-CANCER;
GENE-EXPRESSION; ANTISENSE; PROTEIN; SUBUNIT
AB GTI-2040 is a 20-mer antisense oligonucleotide targeting the mRNA of ribonucleotide reductase M2. It was combined with oxaliplatin and capecitabine in a phase I trial in patients with advance solid tumors based on previous studies demonstrating potentiation of chemotherapy with ribonucleotide reductase inhibitors.
Patients at least 18 years of age with advanced incurable solid tumors and normal organ function as well as a Karnofsky performance status of a parts per thousand yen60% were eligible. One prior chemotherapy regimen for advanced disease or relapse within 12 months of adjuvant chemotherapy was required. Patients could have received prior fluoropyrimidines, including capecitabine, but not oxaliplatin. Treatment cycles were 21 days. In each cycle, GTI-2040 was given as a continuous intravenous infusion over 14 days, oxaliplatin as a 2-h intravenous infusion on day 1, and capecitabine orally twice a day for 14 days. In cycle 1 only, oxaliplatin and capecitabine were started on day 2 to allow ribonucleotide reductase mRNA levels to be measured with and without oxaliplatin and capecitabine. Doses were escalated in cohorts of three patients using a standard 3 + 3 design until the maximum tolerated dose was established, defined as no more than one first-cycle dose-limiting toxicity among six patients treated at a given dose level.
The maximum tolerated dose was estimated to be the combination of GTI-2040 3 mg/kg per day for 14 days, capecitabine 600 mg/m(2) twice daily for 14 days, and oxaliplatin 100 mg/m(2) every 21 days. Dose-limiting toxicities were hematologic. GTI-2040 pharmacokinetics, obtained at steady-state on days 7 and 14, showed the high inter-patient variability previously reported. Two of six patients had stable disease at the maximum tolerated dose and one patient, with heavily pre-treated non-small cell lung cancer, had a partial response at a higher dose level. In samples from a limited number of patients, there was no clear decrease in ribonucleotide reductase expression in peripheral blood mononuclear cells during treatment.
A combination of GTI-2040, capecitabine and oxaliplatin is feasible in patients with advanced solid tumors.
C1 [Shibata, Stephen I.; Doroshow, James H.; Frankel, Paul; Synold, Timothy W.; Yen, Yun; Chow, Warren A.; Leong, Lucille A.; Lim, Dean; Margolin, Kim A.; Morgan, Robert J.; Somlo, George; Newman, Edward M.] City Hope Comprehens Canc Ctr, Dept Med Oncol, Duarte, CA 91010 USA.
[Gandara, David R.] Univ Calif Davis, Ctr Canc, Sacramento, CA 95817 USA.
[Lenz, Heinz-Josef] Univ So Calif, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Doroshow, James H.] NCI, Div Canc Treatment & Diag, Bethesda, MD 20892 USA.
RP Shibata, SI (reprint author), City Hope Comprehens Canc Ctr, Dept Med Oncol, 1500 E Duarte Rd, Duarte, CA 91010 USA.
EM sshibata@coh.org
FU NCI NIH HHS [U01 CA062505, U01 CA062505-17, P30 CA033572]
NR 32
TC 6
Z9 6
U1 0
U2 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0344-5704
J9 CANCER CHEMOTH PHARM
JI Cancer Chemother. Pharmacol.
PD NOV
PY 2009
VL 64
IS 6
BP 1149
EP 1155
DI 10.1007/s00280-009-0977-x
PG 7
WC Oncology; Pharmacology & Pharmacy
SC Oncology; Pharmacology & Pharmacy
GA 485HU
UT WOS:000269112600011
PM 19322566
ER
PT J
AU Laiyemo, AO
Kamangar, F
Marcus, PM
Taylor, PR
Virtamo, J
Albanes, D
Stolzenberg-Solomon, RZ
AF Laiyemo, Adeyinka O.
Kamangar, Farin
Marcus, Pamela M.
Taylor, Philip R.
Virtamo, Jarmo
Albanes, Demetrius
Stolzenberg-Solomon, Rachael Z.
TI Serum pepsinogen level, atrophic gastritis and the risk of incident
pancreatic cancer-A prospective cohort study
SO CANCER EPIDEMIOLOGY
LA English
DT Article
DE Serum pepsinogen; Atrophic gastritis; Pancreatic cancer
ID HELICOBACTER-PYLORI INFECTION; ULCER
AB Background: Pancreatic cancer is a highly fatal disease without screening tests. Studies have suggested possible etiologic similarities between gastric and pancreatic cancers. Atrophic gastritis, a pre-malignant condition for gastric cancer, is characterized by low serum pepsinogen I (SPGI) level. We hypothesized that low SPGI level may be associated with an increased risk of pancreatic cancer and be a useful biomarker for the disease. Methods: Our analytic cohort included 20,962 participants in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) who had SPGI level measured. Of these, 1663 (7.9%) subjects had low SPGI levels (<25 mu g/l) and were invited for gastroscopy which was completed in 1059 (63.7%) participants. Atrophic gastritis was histologically confirmed in 1006 (95.0%) subjects. We used Cox proportional hazards regression to calculate the hazard ratios (HR) and 95% confidence intervals (CI) for pancreatic cancer. Results: During follow-up of up to 16.3 years (mean = 10.8 years; 226,325 person-years), 227 incident pancreatic cancers were diagnosed. The incidence rates were 9.9, 11.3, and 12.7 per 10,000 person-years of follow-up for participants with normal pepsinogen level (>= 25 mu g/l, low pepsinogen level and histologically confirmed atrophic gastritis, respectively. Compared to subjects with normal pepsinogen levels, there was no statistically significant increased risk of pancreatic cancer among subjects with low pepsinogen level (adjusted HR = 1.01; 95% CI: 0.63-1.62) or those with histologically confirmed atrophic gastritis (adjusted HR = 1.13; 95% CI: 0.66-1.95). Conclusions: Atrophic gastritis, serological or histological, is not associated with increased risk of pancreatic cancer. These findings do not provide any evidence for potential usefulness of SPGI for pancreatic cancer screening. Published by Elsevier Ltd.
C1 [Laiyemo, Adeyinka O.] NCI, Canc Prevent Fellowship Program, Biometry Res Grp, Canc Prevent Div,Off Prevent Oncol,NIH, Bethesda, MD 20892 USA.
[Kamangar, Farin; Albanes, Demetrius; Stolzenberg-Solomon, Rachael Z.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Kamangar, Farin] Morgan State Univ, Dept Publ Hlth Anal, Sch Community Hlth & Policy, Baltimore, MD 21239 USA.
[Taylor, Philip R.] NCI, Genet Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
RP Laiyemo, AO (reprint author), NCI, Canc Prevent Fellowship Program, Biometry Res Grp, Canc Prevent Div,Off Prevent Oncol,NIH, 6130 Executive Blvd,Suite 3131, Bethesda, MD 20892 USA.
EM laiyemoa@mail.nih.gov
RI Albanes, Demetrius/B-9749-2015
FU National Institutes of Health, Division of Cancer Epidemiology and
Genetics, National Cancer Institute; Division of Cancer Prevention,
National Institutes of Health, Department of Health and Human Services
FX This study was supported by the Intramural Research Program of the
National Institutes of Health, Division of Cancer Epidemiology and
Genetics, National Cancer Institute, and the Division of Cancer
Prevention, National Institutes of Health, Department of Health and
Human Services. The funding agency had a role in the design and
reporting of the study and in the decision to submit the manuscript for
publication and approved the final version of the manuscript.
NR 26
TC 3
Z9 3
U1 0
U2 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1877-7821
J9 CANCER EPIDEMIOL
JI Cancer Epidemiol.
PD NOV
PY 2009
VL 33
IS 5
BP 368
EP 373
DI 10.1016/j.canep.2009.09.001
PG 6
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 538EY
UT WOS:000273168300009
PM 19800305
ER
PT J
AU Platz, EA
Till, C
Goodman, PJ
Parnes, HL
Figg, WD
Albanes, D
Neuhouser, ML
Klein, EA
Thompson, IM
Kristal, AR
AF Platz, Elizabeth A.
Till, Cathee
Goodman, Phyllis J.
Parnes, Howard L.
Figg, William D.
Albanes, Demetrius
Neuhouser, Marian L.
Klein, Eric A.
Thompson, Ian M., Jr.
Kristal, Alan R.
TI Men with Low Serum Cholesterol Have a Lower Risk of High-Grade Prostate
Cancer in the Placebo Arm of the Prostate Cancer Prevention Trial
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID FOLLOW-UP; STATIN USE; PLASMA-CHOLESTEROL; NATIONAL-HEALTH; FINASTERIDE;
COHORT; DRUGS; ASSOCIATION; POPULATION; SENSITIVITY
AB Background: Several prospective studies suggest that use of cholesterol owe ring statin drugs is inversely associated with advanced stage and possibly high-grade prostate cancer. One study reported that men with low cholesterol had a lower risk of high-grade prostate cancer. Given these findings, we investigated the association between low serum cholesterol and prostate cancer risk in the Prostate Cancer Prevention Trial.
Methods: We conducted a cohort study of 5,586 men ages >= 55 years who were randomized to the placebo arm of the Prostate Cancer Prevention Trial between 1993 and 1996. Serum cholesterol was measured enzy-matically at entry. By the end of follow-up, 1,251 prostate cancer cases were confirmed. We used logistic regression to calculate the multivariable odds ratio (OR) of total, and Gleason 2 to 6 (n = 993), 7 (n = 199), and 8 to 10 (n = 59) prostate cancer comparing low serum (normal, <200 mg/dL) to high-serum (borderline and elevated cholesterol, >= 200 mg/dL) cholesterol.
Results: Men with low cholesterol had a lower risk of Gleason 8 to 10 prostate cancer [OR, 0.41; 95% confidence interval (CI), 0.22-0.77] than men with high cholesterol. No association was present for prostate cancer overall (OR, 0.97; 95% CI, 0.85-1.11), Gleason 2 to 6 disease (OR, 1.03; 95% CI, 0.89-1.18), or Gleason 7 disease (OR, 0.93; 95% CI, 0.69-1.24).
Conclusion: These prospective results support that men with low cholesterol have a reduced risk of high-grade prostate cancer. These and other contemporary data that suggest that cholesterol metabolism should be investigated further in the etiology of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2807-13)
C1 [Platz, Elizabeth A.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, James Buchanan Brady Urol Inst, Baltimore, MD 21205 USA.
[Platz, Elizabeth A.] Johns Hopkins Med Inst, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD 21205 USA.
[Till, Cathee; Goodman, Phyllis J.] Fred Hutchinson Canc Res Ctr, SW Oncol Grp, Ctr Stat, Seattle, WA 98104 USA.
[Parnes, Howard L.] NCI, Canc Prevent Div, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Figg, William D.] NCI, Med Oncol Branch, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Albanes, Demetrius] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Neuhouser, Marian L.; Kristal, Alan R.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Canc Prevent Program, Seattle, WA 98104 USA.
[Klein, Eric A.] Cleveland Clin, Lerner Coll Med, Ctr Clin & Translational Res, Cleveland, OH 44106 USA.
[Thompson, Ian M., Jr.] Univ Texas Hlth Sci Ctr San Antonio, Dept Urol, San Antonio, TX 78229 USA.
RP Platz, EA (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, James Buchanan Brady Urol Inst, Room E6132,615 N Wolfe St, Baltimore, MD 21205 USA.
EM eplatz@jhsph.edu
RI Albanes, Demetrius/B-9749-2015; Figg Sr, William/M-2411-2016;
OI Kristal, Alan/0000-0002-7329-1617
FU NIH [P01 CA108964, U10 CA37429, P50 CA58236]
FX Grant support: National Cancer Institute, NIH, (P01 CA108964, U10
CA37429, and P50 CA58236).
NR 30
TC 79
Z9 80
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
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 2807
EP 2813
DI 10.1158/1055-9965.EPI-09-0472
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600002
PM 19887582
ER
PT J
AU Ahn, J
Lim, U
Weinstein, SJ
Schatzkin, A
Hayes, RB
Virtamo, J
Albanes, D
AF Ahn, Jiyoung
Lim, Unhee
Weinstein, Stephanie J.
Schatzkin, Arthur
Hayes, Richard B.
Virtamo, Jarmo
Albanes, Demetrius
TI Prediagnostic Total and High-Density Lipoprotein Cholesterol and Risk of
Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SERUM-CHOLESTEROL; LUNG-CANCER; HDL-CHOLESTEROL; BLOOD-CHOLESTEROL;
PLASMA-LIPIDS; LIVER-CANCER; MORTALITY; METABOLISM; CELL; ASSOCIATION
AB Background: Circulating total cholesterol has been inversely associated with cancer risk; however, the role of reverse causation and the associations for high-density lipoprotein (HDL) cholesterol have not been fully characterized. We examined the relationship between serum total and HDL cholesterol and risk of overall and site-specific cancers among 29,093 men in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study cohort.
Methods: Fasting serum total and HDL cholesterol were assayed at baseline, and 7,545 incident cancers were identified during up to 18 years of follow-up. Multivariable proportional hazards models were conducted to estimate relative risks (RR).
Results: Higher serum total cholesterol concentration was associated with decreased risk of cancer overall (RR for comparing high versus low quintile, 0.85; 95% confidence interval, 0.79-0.91; P trend <0.001; >276.7 versus <203.9 mg/dL), and the inverse association was particularly evident for cancers of the lung and liver. These associations were no longer significant, however, when cases diagnosed during the first 9 years of follow-up were excluded. Greater HDL cholesterol was also associated with decreased risk of cancer (RR for high versus low quintile, 0.89; 95% confidence interval, 0.83-0.97; P trend = 0.01; >55.3 versus <36.2 mg/dL). The inverse association of HDL cholesterol was evident for cancers of lung, prostate, liver, and the hematopoietic system, and the associations of HDL cholesterol with liver and lung cancers remained after excluding cases diagnosed within 12 years of study entry.
Conclusion: Our findings suggest that prior observations regarding serum total cholesterol and cancer are largely explained by reverse causation. Although chance and reverse causation may explain some of the inverse HDL associations, we cannot rule out some etiologic role for this lipid fraction. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2814-21)
C1 [Albanes, Demetrius] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA.
[Virtamo, Jarmo] Natl Inst Hlth & Welf, Dept Chron Dis Prevent, Helsinki, Finland.
RP Albanes, D (reprint author), NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH, EPS 3044, Bethesda, MD 20892 USA.
EM daa@nih.gov
RI Albanes, Demetrius/B-9749-2015;
OI Hayes, Richard/0000-0002-0918-661X
FU NIH; Division of Cancer Epidemiology and Genetics; National Cancer
Institute; Department of Health and Human Services and Public Health
Service [N01-CN-45165, N01-RC45035, N01-RC-37004]
FX Intramural Research Program of the NIH, Division of Cancer Epidemiology
and Genetics, National Cancer Institute, Department of Health and Human
Services and Public Health Service contracts N01-CN-45165, N01-RC45035,
and N01-RC-37004.
NR 38
TC 68
Z9 71
U1 1
U2 9
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
EI 1538-7755
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 2814
EP 2821
DI 10.1158/1055-9965.EPI-08-1248
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600003
PM 19887581
ER
PT J
AU Sue, LY
Schairer, C
Ma, XM
Williams, C
Chang, SC
Millers, AB
McCarty, CA
Willcox, BJ
Ziegler, RG
AF Sue, Laura Y.
Schairer, Catherine
Ma, Xiaomei
Williams, Craig
Chang, Shih-Chen
Millers, Anthony B.
McCarty, Catherine A.
Willcox, Bradley J.
Ziegler, Regina G.
TI Energy Intake and Risk of Postmenopausal Breast Cancer: An Expanded
Analysis in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening
Trial (PLCO) Cohort
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID FOOD FREQUENCY QUESTIONNAIRES; DIETARY-FAT; CALORIC RESTRICTION;
BALANCE; WOMEN; ADOLESCENCE; ASSOCIATION; VALIDATION; MECHANISMS;
PREVENTION
AB Although animal experiments have consistently shown a positive relationship between breast cancer and energy intake, evidence from human studies remains inconclusive. In the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial cohort, 29,170 women, ages 55 to 75 years, who successfully completed a food frequency questionnaire (FFQ) at entry (1993-2001), were followed through 2007, and 1,319 incident breast cancers were ascertained (median time from FFQ completion to diagnosis, 4.4 years). Women in the highest quartile of energy intake, relative to the lowest, had modestly, but significantly, increased breast cancer risk [multivariate relative risk (RR), 1.21; 95% confidence interval (95% CI), 1.03-1.42; P(trend) = 0.03]. The inclusion of body mass index and physical activity in the model reduced risk slightly (RR, 1.18; 95% CI, 1.00-1.39; P(trend) = 0.07). However, in similar analyses using energy intake from a FFQ administered approximately five years after entry (27,428 women; 806 incident breast cancers; median time from FFQ completion to diagnosis, 2.7 years), women in the highest and lowest quartiles of energy intake had similar risk. When follow-up time after the first FFQ was divided into three 4-year periods, the multivariate RRs for high versus low energy intake increased from 1.21 to 1.37 to 1.55 with increasing time since dietary assessment. Although the divergent results for the two FFQs could be due to subtle questionnaire differences, our findings suggest a modest positive association between energy intake and postmenopausal breast cancer that strengthens with time since dietary assessment. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2842-50)
C1 [Sue, Laura Y.] NCI, Div Canc Epidemiol & Genet, NIH, DHHS, Bethesda, MD 20892 USA.
[Ma, Xiaomei] Yale Univ, Sch Publ Hlth, Dept Epidemiol & Publ Hlth, New Haven, CT USA.
[Williams, Craig] Informat Management Serv Inc, Rockville, MD USA.
[Chang, Shih-Chen] AstraZeneca, Wilmington, DE USA.
[Millers, Anthony B.] Univ Toronto, Dalla Lana Sch Publ Hlth, Toronto, ON, Canada.
[McCarty, Catherine A.] Marshfield Clin Fdn Med Res & Educ, Ctr Human Genet, Marshfield, WI 54449 USA.
[Willcox, Bradley J.] Pacific Hlth Res Inst, Honolulu, HI USA.
RP Sue, LY (reprint author), NCI, Div Canc Epidemiol & Genet, NIH, DHHS, 6120 Execut Blvd,EPS 6113, Bethesda, MD 20892 USA.
EM suel@mail.nih.gov
FU Intramural NIH HHS [Z01 CP010169-06]
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 2842
EP 2850
DI 10.1158/1055-9965.EPI-09-0087
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600007
PM 19843674
ER
PT J
AU Eliassen, AH
Ziegler, RG
Rosner, B
Veenstra, TD
Roman, JM
Xu, X
Hankinson, SE
AF Eliassen, A. Heather
Ziegler, Regina G.
Rosner, Bernard
Veenstra, Timothy D.
Roman, John M.
Xu, Xia
Hankinson, Susan E.
TI Reproducibility of Fifteen Urinary Estrogens and Estrogen Metabolites
over a 2-to 3-Year Period in Premenopausal Women
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID BREAST-CANCER-CELLS; CHROMATOGRAPHY-MASS SPECTROMETRY; STEROID-HORMONE
CONCENTRATIONS; POSTMENOPAUSAL WOMEN; ENDOGENOUS ESTROGEN; MCF-7 CELLS;
RISK; ESTRADIOL; RECEPTOR; SERUM
AB Endogenous estrogens play an integral role in the etiology of breast, endometrial, and, possibly, ovarian cancers. Estrogen metabolism yields products that are potentially both estrogenic and genotoxic, yet individual metabolic patterns are just beginning to be explored in epidemiologic studies. Within the Nurses' Health Study 11, we examined reproducibility of 15 urinary estrogens and estrogen metabolites (EM) among 110 premenopausal women with three luteal-phase urine samples collected over 3 years. EM were measured by a recently developed high-performance liquid chromatography-tandem mass spectrometry (LC-MS2) method with high sensitivity, specificity, and precision. We assessed Spearman correlations and intraclass correlation coefficients (ICC) across the three samples. Correlations between urinary estrone or estradiol and EM were only modest (r = 0.1-0.5). The 2- and 4-hydroxylation pathways were highly correlated (r = 0.9) but weakly inversely correlated with the 16-hydroxylation pathway (r = -0.2). Within-woman reproducibility over time was fairly high for the three pathways, with ICCs ranging from 0.52 (16-hydroxylation pathway) to 0.72 (2-hydroxylation pathway). ICCs were similarly high for 2-catechols and the individual catechols (ICCs = 0.58-0.72). Individual and grouped methylated 2-catechols had fairly high ICCs (0.51-0.62), but methylated 4-catechols had low ICCs (0.14-0.27). These data indicate that, in general, urinary EM levels vary substantially among individuals compared with intraindiviual variability. Within-person reproducibility over time for most EM measures is comparable to or better than that for well-vetted biomarkers such as plasma cholesterol and, in postmenopausal women, estradiol. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2860-8)
C1 [Eliassen, A. Heather; Rosner, Bernard; Hankinson, Susan E.] Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA.
[Eliassen, A. Heather; Rosner, Bernard; Hankinson, Susan E.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
[Rosner, Bernard] Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA.
[Hankinson, Susan E.] Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA.
[Ziegler, Regina G.] NCI, Div Canc Epidemiol & Genet, Epidemiol & Biostat Program, Bethesda, MD 20892 USA.
[Veenstra, Timothy D.; Roman, John M.; Xu, Xia] NCI, Sci Applicat Int Corp Frederick Inc, Adv Technol Program, Lab Prote & Analyt Technol, Frederick, MD 21701 USA.
RP Eliassen, AH (reprint author), Brigham & Womens Hosp, Dept Med, Channing Lab, 181 Longwood Ave, Boston, MA 02115 USA.
EM heather.eliassen@channing.harvard.edu
FU National Cancer Institute [CA67262, CA50385, HHSN261200800001E]; Harvard
Medical School
FX National Cancer Institute research grants CA67262 and CA50385, the
Harvard Medical School Eleanor and Miles Shore Fellowship for Scholars
in Medicine, the National Cancer Institute Intramural Funding Program of
the Division of Cancer Epidemiology and Genetics, and federal funds from
the National Cancer Institute awarded under contract HHSN261200800001E
to Science Applications international Corporation-Frederick. The content
of this publication does not necessarily reflect the views or policies
of the U.S. Department of Health and Human Services, nor does mention of
trade names, commercial products, or organizations imply endorsement by
the U.S. Government.
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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 NOV
PY 2009
VL 18
IS 11
BP 2860
EP 2868
DI 10.1158/1055-9965.EPI-09-0591
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600009
PM 19843676
ER
PT J
AU Boukheris, H
Curtis, RE
Land, CE
Dores, GM
AF Boukheris, Houda
Curtis, Rochelle E.
Land, Charles E.
Dores, Graca M.
TI Incidence of Carcinoma of the Major Salivary Glands According to the WHO
Classification, 1992 to 2006: A Population-Based Study in the United
States
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID SQUAMOUS-CELL CARCINOMA; PAROTID-GLAND; RISK-FACTORS; CANCER INCIDENCE;
TUMORS; EPIDEMIOLOGY; SURVIVAL; REGION; TRENDS; RATES
AB Background: Carcinomas of the major salivary glands (M-SGC) comprise a morphologically diverse group of rare tumors of largely unknown cause. To gain insight into etiology, we evaluated incidence of M-SGC using the WHO classification schema (WHO-2005).
Methods: We calculated age-adjusted incidence rates (IR) and IR ratios (IRR) for M-SGC diagnosed between 1992 and 2006 in the Surveillance, Epidemiology and End Results Program.
Results: Overall, 6,391 M-SGC (IR, 11.95/1,000,000 person-years) were diagnosed during 1992 to 2006. Nearly 85% of cases (n = 5,370; IR, 10.00) were encompassed within WHO-2005, and among these, males had higher IRs than females [IRR, 1.51; 95% confidence interval (95% CI), 1.43-1.60]. Squamous cell (IR, 3.44) and mucoepidermoid (IR, 3.23) carcinomas occurred most frequently among males, whereas mucoepidermoid (IR, 2.67), acinic cell (IR, 1.57), and adenoid cystic (IR, 1.40) carcinomas were most common among females. Mucoepidermoid, acinic cell, and adenoid cystic carcinomas predominated in females through age similar to 50 years; thereafter, IRs of acinic cell and adenoid cystic carcinomas were nearly equal among females and males, whereas IRs of mucclepidermoid carcinoma among males exceeded IRs among females (IRR, 1.57; 95% CI, 1.38-1.78). Except for mucoepidermoid and adenoid cystic carcinomas, which occurred equally among all races, other subtypes had significantly lower incidence among Blacks and Asians/Pacific Islanders than among Whites. Adenoid cystic carcinoma occurred equally in the submandibular and parotid glands, and other M-SGC histologic subtypes evaluated had 77% to 98% lower IRS in the submandibular gland. Overall M-SGC IRs remained stable during 1992 to 2006.
Conclusion: Distinct incidence patterns according to histologic subtype suggest that M-SGC are a diverse group of neoplasms characterized by etiologic and/or biological heterogeneity with varying susceptibility by gender and race. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2899-906)
C1 [Dores, Graca M.] Dept Vet Affairs Med Ctr, Med Serv, Oklahoma City, OK USA.
[Boukheris, Houda; Curtis, Rochelle E.; Land, Charles E.; Dores, Graca M.] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD USA.
RP Dores, GM (reprint author), Dept Vet Affairs Med Ctr, Med Serv 111, 921 NE 13th St, Oklahoma City, OK 73104 USA.
EM doresg@mail.nih.gov
FU National Cancer Institute/NIH; Department of Health and Human Services;
Department of Veterans Affairs
FX Intramural Research Program of the National Cancer Institute/NIH,
Department of Health and Human Services, and Department of Veterans
Affairs.
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 2899
EP 2906
DI 10.1158/1055-9965.EPI-09-0638
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600015
PM 19861510
ER
PT J
AU Fedirko, V
Bostick, RM
Flanders, WD
Long, Q
Sidelnikov, E
Shaukat, A
Daniel, CR
Rutherford, RE
Woodard, JJ
AF Fedirko, Veronika
Bostick, Roberd M.
Flanders, W. Dana
Long, Qi
Sidelnikov, Eduard
Shaukat, Aasma
Daniel, Carrie R.
Rutherford, Robin E.
Woodard, Jill Joelle
TI Effects of Vitamin D and Calcium on Proliferation and Differentiation In
Normal Colon Mucosa: a Randomized Clinical Trial
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID EPITHELIAL-CELL PROLIFERATION; FAT DAIRY FOODS; COLORECTAL ADENOMAS;
DIETARY CALCIUM; P21(WAF1/CIP1) EXPRESSION; SUPPLEMENTAL CALCIUM; RECTAL
MUCOSA; CANCER; CARCINOGENESIS; NEOPLASIA
AB To investigate the potential efficacy of calcium and vitamin D in reducing risk for colorectal neoplasms and to develop "treatable" phenotypic biomarkers of risk for colorectal neoplasms, we conducted a pilot, randomized, double-blind, placebo-controlled, 2 x 2 factorial clinical trial to test the effects of these agents on cell cycle markers in the normal colorectal mucosa. Ninety-two men and women with at least one pathology-confirmed colorectal adenoma were treated with 2 g/day calcium and/or 800 IU/day vitamin D(3) versus placebo over 6 months. Overall expression and distributions of p21(waf1/cip1) (marker of differentiation), MIB-1 (marker of short-term proliferation), and hTERT (marker of long-term proliferation) in colorectal crypts in the normal-appearing rectal mucosa were detected by automated immunohistochemistry and quantified by image analysis. In the calcium, vitamin D, and calcium plus vitamin D groups relative to the placebo, p21 expression increased by 201% (P = 0.03), 242% (P = 0.005), and 25% (P = 0.47), respectively, along the full lengths of colorectal crypts after 6 months of treatment. There were no statistically significant changes in the expression of either MIB-1 or hTERT in the crypts overall; however, the proportion of hTERT, but not MIB-1, expression that extended into the upper 40% of the crypts was reduced by 15% (P = 0.02) in the vitamin D plus calcium group relative to the placebo. These results indicate that calcium and vitamin D promote colorectal epithelial cell differentiation and may "normalize" the colorectal crypt proliferative zone in sporadic adenoma patients, and support further investigation of calcium and vitamin D as chemopreventive agents against colorectal neoplasms. (Cancer Epidemiol Biomarkers Prev 2009;18(11):2933-41)
C1 [Fedirko, Veronika; Bostick, Roberd M.; Flanders, W. Dana; Sidelnikov, Eduard; Woodard, Jill Joelle] Emory Univ, Dept Epidemiol, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.
[Fedirko, Veronika; Bostick, Roberd M.; Flanders, W. Dana; Long, Qi; Sidelnikov, Eduard; Woodard, Jill Joelle] Emory Univ, Winship Canc Inst, Atlanta, GA 30322 USA.
[Flanders, W. Dana; Long, Qi] Emory Univ, Rollins Sch Publ Hlth, Dept Biostat & Bioinformat, Atlanta, GA 30322 USA.
[Rutherford, Robin E.] Emory Univ, Sch Med, Div Digest Dis, Atlanta, GA 30322 USA.
[Shaukat, Aasma] Univ Minnesota, GI Div, Dept Med, Minneapolis, MN USA.
[Daniel, Carrie R.] NCI, Nutr Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Bostick, RM (reprint author), Emory Univ, Dept Epidemiol, Rollins Sch Publ Hlth, 1518 Clifton Rd NE, Atlanta, GA 30322 USA.
EM rmbosti@sph.emory.edu
FU National Cancer Institute; NIH [R01 CA104637]; Georgia Cancer Coalition
Distinguished Scholar; Franklin Foundation; Georgia Cancer Coalition
FX National Cancer Institute, NIH grant R01 CA104637 (R.M. Bostick),
Georgia Cancer Coalition Distinguished Scholar award (R.M. Bostick), and
the Franklin Foundation. The National Cancer Institute, the Georgia
Cancer Coalition, and the Franklin Foundation had no influence on the
design of the study; the collection, analysis, and interpretation of the
data; the decision to submit the manuscript for publication; or the
writing of the manuscript.
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 2933
EP 2941
DI 10.1158/1055-9965.EPI-09-0239
PG 9
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600020
PM 19861511
ER
PT J
AU Gaudet, MM
Campan, M
Figueroa, JD
Yang, XHR
Lissowska, J
Peplonska, B
Brinton, LA
Rimm, DL
Laird, PW
Garcia-Closas, M
Sherman, ME
AF Gaudet, Mia M.
Campan, Mihaela
Figueroa, Jonine D.
Yang, Xiaohong R.
Lissowska, Jolanta
Peplonska, Beata
Brinton, Louise A.
Rimm, David L.
Laird, Peter W.
Garcia-Closas, Montserrat
Sherman, Mark E.
TI DNA Hypermethylation of ESR1 and PGR in Breast Cancer: Pathologic and
Epidemiologic Associations
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID ESTROGEN-RECEPTOR-ALPHA; GENE-EXPRESSION; HORMONE-RECEPTOR; METHYLATION
ANALYSIS; PROTEIN EXPRESSION; MESSENGER-RNA; CPG ISLANDS; PROGESTERONE;
CELLS; PROMOTERS
AB Improved understanding of the etiology of estrogen receptor-alpha (ER alpha)-negative and progesterone receptor (PR)-negative breast cancers may permit improved risk prediction. In vitro studies implicate DNA hypermethylation of the ER alpha and PR promoters in the pathogenesis of ER alpha-negative and PR-negative tumors, but results are not definitive. We evaluated 200 invasive breast cancers selected from a population-based case-control study. DNA extracted from fixed tumor tissue cores was tested using MethyLight to assess DNA methylation at four CpG islands: ESR1 promoters A and B; PGR promoters A and B; and a CpG shore, ESR1 promoter C. DNA methylation results were compared with levels of ER alpha and PR, tumor characteristics, and breast cancer risk factors. We observed mild to moderate DNA methylation levels in most tumors for ESR1 promoters A and B and PGR promoter B, and a few tumors showed mild methylation in PGR promoter A. In contrast, ESR1 promoter C showed a wide range of methylation and was weakly correlated with lower expression levels of ER alpha (beta = -0.26; P < 0.0001) and PR (beta = -0.25; P < 0.0001). The percentage of tumors with methylated PGR promoters A and B was significantly higher for tumors with low ER alpha (A, Fisher's test P = 0.0001; B, P = 0.033) and PR levels (A, P = 0.0006; B, P = 0.001). Our data suggest that the relationships between DNA methylation of ESR1 and PGR promoters and protein expression are weak and unlikely to represent a predominant mechanism of receptor silencing. In contrast to CpG islands, ESR1 promoter C showed a wider range of methylation levels and inverse associations with ER alpha and PR expression. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3036-43)
C1 [Gaudet, Mia M.] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10461 USA.
[Campan, Mihaela; Laird, Peter W.] Univ So Calif, Keck Sch Med, Dept Surg, Los Angeles, CA 90033 USA.
[Laird, Peter W.] Univ So Calif, Keck Sch Med, Dept Biochem & Mol Biol, Los Angeles, CA 90033 USA.
[Laird, Peter W.] Univ So Calif, Keck Sch Med, Epigenome Ctr, Los Angeles, CA 90033 USA.
[Laird, Peter W.] Univ So Calif, Keck Sch Med, Kenneth Norris Jr Comprehens Canc Ctr, Los Angeles, CA 90033 USA.
[Figueroa, Jonine D.; Yang, Xiaohong R.; Lissowska, Jolanta; Brinton, Louise A.; Garcia-Closas, Montserrat; Sherman, Mark E.] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Lissowska, Jolanta] M Sklodowska Curie Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
[Peplonska, Beata] Nofer Inst Occupat Med, Dept Occupat & Environm Epidemiol, Lodz, Poland.
[Rimm, David L.] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06510 USA.
RP Gaudet, MM (reprint author), Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Belfer Bldg,Room 1303E,1300 Morris Pk Ave, Bronx, NY 10461 USA.
EM mia.gaudet@einstein.yu.edu
RI Peplonska, Beata/F-6004-2010; Laird, Peter/G-8683-2012; Garcia-Closas,
Montserrat /F-3871-2015; Brinton, Louise/G-7486-2015;
OI Garcia-Closas, Montserrat /0000-0003-1033-2650; Brinton,
Louise/0000-0003-3853-8562; Lissowska, Jolanta/0000-0003-2695-5799
FU National Cancer Institute, NIH
FX Grant support: The intramural program of the National Cancer Institute,
NIH.
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 3036
EP 3043
DI 10.1158/1055-9965.EPI-09-0678
PG 8
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600034
PM 19861523
ER
PT J
AU Dong, LM
Shu, XO
Gao, YT
Milne, G
Ji, BT
Yang, G
Li, HL
Rothman, N
Zheng, W
Chow, WH
Abnet, CC
AF Dong, Linda M.
Shu, Xiao-Ou
Gao, Yu-Tang
Milne, Ginger
Ji, Bu-Tian
Yang, Gong
Li, Hong-Lan
Rothman, Nathaniel
Zheng, Wei
Chow, Wong-Ho
Abnet, Christian C.
TI Urinary Prostaglandin E-2 Metabolite and Gastric Cancer Risk in the
Shanghai Women's Health Study
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; EXPRESSION; ESOPHAGEAL;
METAANALYSIS; INHIBITION; CARCINOMA; ASPIRIN; CYCLOOXYGENASE-2;
ADENOCARCINOMAS; COLON
AB Chronic inflammation has been implicated in the etiology of gastric cancer. Prostaglandin E-2 (PGE(2)) is one of the major end-products of the cyclooxygenase-2 pathway, an enzyme that is an important mediator of inflammation. Using a novel method of quantifying the primary urinary metabolite of PGE(2) (PGE-M; 11 alpha-hydroxy-9,15-dioxo-2,3,4,5-tetranorprostane-1,20-dioic acid), we evaluated urinary PGE-M concentrations in association with subsequent risk of development of gastric cancer in the Shanghai Women's Health Study, a large population-based prospective cohort, using a nested case-control study design. Controls were matched (1:1) to 153 gastric cancer cases by menopausal status; age, time, and date of sample collection; time interval since last meal; and availability of urine sample. Odds ratios (95% confidence intervals) were calculated using conditional logistic regression adjusted for potential confounders. Baseline urinary PGE-M levels were slightly higher among gastric cancer cases with a median of 6.4 ng/mg creatinine (interquartile range, 3.4-11.2) compared with 5.4 ng/mg creatinine among controls (interquartile range, 2.8-9.0), but this difference was not statistically significant (P = 0.34, Wilcoxon). With increasing quartiles of urinary PGE-M levels, the odds ratios (95% confidence intervals) for risk of gastric cancer increased in quartiles 2 to 4: 1.00 (0.48-2.08), 1.40 (0.67-2.91), and 1.98 (0.95-4.13), with a statistically significant test for trend (P = 0.04). The association persisted after additional adjustment for Helicobacter pylori status and was slightly strengthened among non-nonsteroidal anti-inflammatory drug users, subjects with positive H. pylori status, and for cases diagnosed within 46 months after study enrollment. Our findings suggest that higher levels of urinary PGE-M, a marker of inflammation, may be associated with gastric cancer risk. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3075-8)
C1 [Dong, Linda M.; Ji, Bu-Tian; Rothman, Nathaniel; Chow, Wong-Ho; Abnet, Christian C.] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA.
[Shu, Xiao-Ou; Milne, Ginger; Yang, Gong; Zheng, Wei] Vanderbilt Univ, Sch Med, Dept Med & Pharmacol, Nashville, TN 37212 USA.
[Gao, Yu-Tang; Li, Hong-Lan] Shanghai Canc Inst, Dept Epidemiol, Shanghai, Peoples R China.
RP Dong, LM (reprint author), NCI, Div Canc Epidemiol & Genet, 6120 Execut Blvd,MSC 7240, Bethesda, MD 20892 USA.
EM donglm@mail.nih.gov
RI Liao, Linda/B-3960-2011; Milne, Ginger/D-7648-2014; Abnet,
Christian/C-4111-2015
OI Milne, Ginger/0000-0003-3890-151X; Abnet, Christian/0000-0002-3008-7843
FU NIH [R01 CA70867]; Intramural Research Program [N02 CP1101066]
FX Grant support: NIH research grant R01 CA70867 and Intramural Research
Program contract N02 CP1101066.
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 3075
EP 3078
DI 10.1158/1055-9965.EPI-09-0680
PG 4
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600040
PM 19861525
ER
PT J
AU Prentice, RL
Huang, Y
Hinds, DA
Peters, U
Pettinger, M
Cox, DR
Beilharz, E
Chlebowski, RT
Rossouw, JE
Caan, B
Ballinger, DG
AF Prentice, Ross L.
Huang, Ying
Hinds, David A.
Peters, Ulrike
Pettinger, Mary
Cox, David R.
Beilharz, Erica
Chlebowski, Rowan T.
Rossouw, Jacques E.
Caan, Bette
Ballinger, Dennis G.
TI Variation in the FGFR2 Gene and the Effects of Postmenopausal Hormone
Therapy on Invasive Breast Cancer
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; ESTROGEN PLUS PROGESTIN; CONJUGATED EQUINE
ESTROGENS; RANDOMIZED CONTROLLED-TRIAL; INITIATIVE CLINICAL-TRIAL;
SUSCEPTIBILITY LOCI; AFRICAN-AMERICAN; WOMEN; RISK; DESIGN
AB Background: Breast cancer concern is a major reason for the recent marked reduction in use of postmenopausal hormone therapy, although equally effective means of controlling menopausal symptoms are lacking. Single nucleotide polymorphisms (SNP) in the fibroblast growth factor receptor 2 (FGFR2) gene are substantially associated with postmenopausal breast cancer risk and could influence hormone therapy effects.
Participants and Methods: We interrogated eight SNPs in intron 2 of the FGFR2 gene for 2,166 invasive breast cancer cases from the Women's Health Initiative clinical trial and one-to-one matched controls to confirm an association with breast cancer risk. We used case-only analyses to examine the dependence of estrogen plus progestin and estrogen-alone odds ratios on SNP genotype.
Results: Seven FGFR2 SNPs, including six in a single linkage disequilibrium region, were found to associate strongly (p < 10(-7)) with breast cancer risk. SNP rs3750817 (minor allele T with frequency 0.39) had an estimated per-minor-allele odds ratio of 0.78, and was not in such strong linkage disequilibrium with the other SNPs. The genotype of this SNP related significantly (P < 0.05) to hormone therapy odds ratios. For estrogen plus progestin, the odds ratios (95% confidence intervals) at 0, 1, and 2 minor SNP alleles were 1.52 (1.14-2.02), 1.33 (1.01-1.75), and 0.69 (0.41-1.17), whereas the corresponding values for estrogen alone were 0.74 (0.51-1.09), 0.99 (0.68-1.44), and 0.34 (0.15-0.76).
Conclusions: Postmenopausal women having T-F genotype for SNP rs3750817 have a reduced breast cancer risk and seem to experience comparatively favorable effects of postmenopausal hormone therapy. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3079-85)
C1 [Prentice, Ross L.] Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, Seattle, WA 98109 USA.
[Hinds, David A.; Cox, David R.; Beilharz, Erica; Ballinger, Dennis G.] Perlegen Sci Inc, Mountain View, CA USA.
[Chlebowski, Rowan T.] Harbor UCLA Res & Educ Inst, Torrance, CA USA.
[Rossouw, Jacques E.] NIH, Bethesda, MD 20892 USA.
[Caan, Bette] Kaiser Permanente, Div Res, Oakland, CA USA.
RP Prentice, RL (reprint author), Fred Hutchinson Canc Res Ctr, Div Publ Hlth Sci, 1100 Fairview Ave N,M3-A410,POB 19024, Seattle, WA 98109 USA.
EM rprentic@fhcrc.org
FU National Heart, Lung, and Blood Institute; NIH, U.S. Department of
Health and Human Services [HHSN268200764314C, N01WH22110, 24152,
32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-19, 32122, 42107-26,
42129-32, 44221]; National Cancer Institute [CA53996]
FX Grant support: National Heart, Lung, and Blood Institute; NIH, U.S.
Department of Health and Human Services (contracts HHSN268200764314C,
N01WH22110, 24152, 32100-2, 32105-6, 32108-9, 32111-13, 32115, 32118-19,
32122, 42107-26, 42129-32, and 44221). Clinical Trials Registration:
ClinicalTrials.gov identifier: NCT00000611. National Cancer Institute
grant CA53996 (R.L Prentice and Y Huang).
NR 37
TC 44
Z9 44
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
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 3079
EP 3085
DI 10.1158/1055-9965.EPI-09-0611
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600041
PM 19861516
ER
PT J
AU Hou, LF
Savage, SA
Blaser, MJ
Perez-Perez, G
Hoxha, M
Dioni, L
Pegoraro, V
Dong, LM
Zatonski, W
Lissowska, J
Chow, WH
Baccarelli, A
AF Hou, Lifang
Savage, Sharon A.
Blaser, Martin J.
Perez-Perez, Guillermo
Hoxha, Mirjam
Dioni, Laura
Pegoraro, Valeria
Dong, Linda M.
Zatonski, Witold
Lissowska, Jolanta
Chow, Wong-Ho
Baccarelli, Andrea
TI Telomere Length in Peripheral Leukocyte DNA and Gastric Cancer Risk
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Article
ID HELICOBACTER-PYLORI; OXIDATIVE STRESS; STOMACH-CANCER; CHROMOSOME
INSTABILITY; GENETIC POLYMORPHISMS; PREDISPOSITION FACTOR; CELLULAR
SENESCENCE; CIGARETTE-SMOKING; BLADDER-CANCER; BLOOD CELLS
AB Telomere length reflects lifetime cumulative oxidative stress from environmental exposures, such as cigarette smoking and chronic inflammation. Shortened telomere length is thought to cause genomic instability and has been associated with several cancers. We examined the association of telomere length in peripheral leukocyte DNA with gastric cancer risk as well as potential confounding factors and risk modifiers for telomere length-related risk. In a population-based study of gastric cancer conducted in a high-risk population in Warsaw, Poland, between 1994 and 1996, we measured relative telomere length in 300 cases and 416 age- and gender-matched controls using quantitative real-time PCR. Among controls, telomeres were significantly shorter in association with aging (P < 0.001), increasing pack-years of cigarette smoking (P = 0.02), decreasing fruit intake (P = 0.04), and Helicobacter pylori positivity (P = 0.03). Gastric cancer cases had significantly shorter telomere length (mean +/- SD relative telomere length, 1.25 +/- 0.34) than controls (1.34 +/- 0.35; P = 0.0008). Gastric cancer risk doubled [odds ratio (OR), 2.04; 95% confidence interval (95% Cl), 1.33-3.13] among subjects in the shortest compared with the highest quartile of telomere length (P(trend) < 0.001). Telomere length-associated risks were higher among individuals with the lowest risk profile, those H. pylori-negative (OR, 5.45; 95% CI, 2.10-14.1), nonsmokers (OR, 3.07; 95% Cl, 1.71-5.51), and individuals with high intake of fruits (OR, 2.43; 95% Cl, 1.46-4.05) or vegetables (OR, 2.39; 95% Cl, 1.51-3.81). Our results suggest that telomere length in peripheral leukocyte DNA was associated with H. pylori positivity, cigarette smoking, and dietary fruit intake. Shortened telomeres increased gastric cancer risk in this high-risk Polish population. (Cancer Epidemiol Biomarkers Prev 2009;18(11):3103-9)
C1 [Hou, Lifang] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA.
[Hou, Lifang] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA.
[Savage, Sharon A.; Dong, Linda M.; Chow, Wong-Ho] NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
[Blaser, Martin J.; Perez-Perez, Guillermo] NYU, Dept Med & Microbiol, New York, NY USA.
[Hoxha, Mirjam; Dioni, Laura; Pegoraro, Valeria; Baccarelli, Andrea] Univ Milan, Dept Environm & Occupat Hlth, Ctr Mol & Genet Epidemiol, Maggiore Policlin Hosp,Mangiagalli & Regina Elena, Milan, Italy.
[Zatonski, Witold; Lissowska, Jolanta] M Sklodowska Curie Mem Canc Ctr, Dept Canc Epidemiol & Prevent, Warsaw, Poland.
[Zatonski, Witold; Lissowska, Jolanta] Inst Oncol, Warsaw, Poland.
RP Hou, LF (reprint author), Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, 680 N Lake Shore Dr,Suite 1102, Chicago, IL 60611 USA.
EM l-hou@northwestern.edu
RI Liao, Linda/B-3960-2011; Savage, Sharon/B-9747-2015;
OI Savage, Sharon/0000-0001-6006-0740; Baccarelli,
Andrea/0000-0002-3436-0640; Lissowska, Jolanta/0000-0003-2695-5799;
Perez Perez, Guillermo /0000-0002-0131-5798
FU Division of Cancer Epidemiology and Genetics, National Cancer
Institute/NIH; Diane Better Program for Human Microbial Diversity; NIH
[R01GM63270]
FX Grant support: Intramural Research Program of the Division of Cancer
Epidemiology and Genetics, National Cancer Institute/NIH; Diane Better
Program for Human Microbial Diversity; and NIH grant R01GM63270.
NR 59
TC 59
Z9 59
U1 1
U2 2
PU AMER ASSOC CANCER RESEARCH
PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1055-9965
J9 CANCER EPIDEM BIOMAR
JI Cancer Epidemiol. Biomarkers Prev.
PD NOV
PY 2009
VL 18
IS 11
BP 3103
EP 3109
DI 10.1158/1055-9965.EPI-09-0347
PG 7
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600044
PM 19861514
ER
PT J
AU Kiviniemi, MT
Hay, JL
James, AS
Lipkus, IM
Meissner, HI
Stefanek, M
Studts, JL
Bridges, JFP
Close, DR
Erwin, DO
Jones, RM
Kaiser, K
Kash, KM
Kelly, KM
Lee, SJC
Purnell, JQ
Siminoff, LA
Vadaparampil, ST
Wang, C
AF Kiviniemi, Marc T.
Hay, Jennifer L.
James, Aimee S.
Lipkus, Isaac M.
Meissner, Helen I.
Stefanek, Michael
Studts, Jamie L.
Bridges, John F. P.
Close, David R.
Erwin, Deborah O.
Jones, Resa M.
Kaiser, Karen
Kash, Kathryn M.
Kelly, Kimberly M.
Lee, Simon J. Craddock
Purnell, Jason Q.
Siminoff, Laura A.
Vadaparampil, Susan T.
Wang, Catharine
TI Decision Making about Cancer Screening: An Assessment of the State of
the Science and a Suggested Research Agenda from the ASPO Behavioral
Oncology and Cancer Communication Special Interest Group
SO CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
LA English
DT Review
ID NONPOLYPOSIS COLORECTAL-CANCER; BREAST-CANCER; CONJOINT-ANALYSIS; HEALTH
LITERACY; INFORMED CHOICE; OVARIAN-CANCER; UNITED-STATES; RISK; WOMEN;
WORRY
C1 [Kiviniemi, Marc T.] SUNY Coll Buffalo, Dept Hlth Behav, Buffalo, NY 14222 USA.
[Hay, Jennifer L.] Mem Sloan Kettering Canc Ctr, Dept Psychiat & Behav Sci, New York, NY 10021 USA.
[James, Aimee S.] Washington Univ, Dept Surg, St Louis, MO USA.
[Lipkus, Isaac M.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC USA.
[Meissner, Helen I.] NIH, Off Behav & Social Sci Res, Bethesda, MD 20892 USA.
[Stefanek, Michael] Emory Univ, Rollins Sch Publ Hlth, Atlanta, GA 30322 USA.
[Studts, Jamie L.] Univ Kentucky, Coll Med, Dept Behav Sci, Lexington, KY 40536 USA.
[Bridges, John F. P.] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Hlth Policy & Management, Baltimore, MD USA.
[Close, David R.] Joe A Arrington Canc Res & Treatment Ctr, Lubbock, TX USA.
[Erwin, Deborah O.] Roswell Pk Canc Inst, Buffalo, NY 14263 USA.
[Jones, Resa M.] Virginia Commonwealth Univ, Dept Epidemiol & Community Hlth, Sch Med, Richmond, VA USA.
[Jones, Resa M.] Virginia Commonwealth Univ, Massey Canc Ctr, Richmond, VA USA.
[Kaiser, Karen] Univ Illinois, Inst Hlth Res & Policy, Chicago, IL USA.
[Kash, Kathryn M.] Thomas Jefferson Univ, Jefferson Sch Populat Hlth, Philadelphia, PA 19107 USA.
[Kelly, Kimberly M.] Ohio State Univ, Dept Mol Virol, Columbus, OH 43210 USA.
[Lee, Simon J. Craddock] Univ Texas SW Med Ctr Dallas, Dept Clin Sci, Dallas, TX 75390 USA.
[Lee, Simon J. Craddock] Univ Texas SW Med Ctr Dallas, Simmons Canc Ctr, Dallas, TX 75390 USA.
[Purnell, Jason Q.] Washington Univ, Hlth Commun Res Lab, St Louis, MO USA.
[Siminoff, Laura A.] Virginia Commonwealth Univ, Dept Social & Behav Hlth, Sch Med, Richmond, VA USA.
[Vadaparampil, Susan T.] Univ S Florida, Dept Interdisciplinary Oncol, Tampa, FL USA.
[Vadaparampil, Susan T.] Univ S Florida, Coll Med, H Lee Moffitt Canc Ctr & Res Inst, Tampa, FL 33612 USA.
[Wang, Catharine] Boston Univ, Sch Publ Hlth, Dept Community Hlth Sci, Boston, MA USA.
RP Kiviniemi, MT (reprint author), SUNY Coll Buffalo, Dept Hlth Behav, 314 Kimball Tower,3435 Main St, Buffalo, NY 14222 USA.
EM mtk8@buffalo.edu
RI Lee, Simon/B-2443-2008; Siminoff, Laura /H-6277-2012; Kiviniemi,
Marc/B-8513-2013;
OI Kiviniemi, Marc/0000-0002-1299-8416; James, Aimee/0000-0002-1411-9307;
Wang, Catharine/0000-0001-8584-2781; Lee, Simon J.
Craddock/0000-0001-6345-1237
FU NCI NIH HHS [K07 CA106225, K07 CA106225-04, K07 CA131103, K07
CA131103-02, K07CA106225, R25 CA057699, R25 CA057699-14]; PHS HHS
[R25TCA57699-14]
NR 72
TC 8
Z9 8
U1 4
U2 14
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 NOV
PY 2009
VL 18
IS 11
BP 3133
EP 3137
DI 10.1158/1055-9965.EPI-18-11-ASPO
PG 5
WC Oncology; Public, Environmental & Occupational Health
SC Oncology; Public, Environmental & Occupational Health
GA 516SJ
UT WOS:000271562600049
PM 19900944
ER
PT J
AU Lee, TY
Kim, YH
Yoon, SW
Choi, JC
Yang, JM
Kim, CJ
Schiller, JT
Sung, MH
Poo, H
AF Lee, Tae-Young
Kim, Yang-Hyun
Yoon, Sun-Woo
Choi, Jai-Chul
Yang, Jai-Myung
Kim, Chul-Joong
Schiller, John T.
Sung, Moon-Hee
Poo, Haryoung
TI Oral administration of poly-gamma-glutamate induces TLR4-and dendritic
cell-dependent antitumor effect
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE Poly-gamma-glutamate; MyD88; TLR4; Anti-tumor effect; Dendritic cell
ID TOLL-LIKE RECEPTOR-4; SIGNALING PATHWAYS; GENE-EXPRESSION; IMMUNITY;
INNATE; ACTIVATION; FAMILY; MYD88; MICE; LIPOPOLYSACCHARIDE
AB Previously, we reported that the oral administration of high molecular mass poly-gamma-glutamate (gamma-PGA) induced antitumor immunity but the mechanism underlying this antitumor activity was not understood. In the present study, we found that application of high molecular mass gamma-PGA induced secretion of tumor necrosis factor (TNF)-alpha from the bone-marrow-derived macrophages of wild type (C57BL/6 and C3H/HeN) and Toll-like receptor 2 knockout (TLR2(-/-)) mice, but not those of myeloid differentiation factor 88 knockout (MyD88(-/-)) and TLR4-defective mice (C3H/HeJ). Production of interferon (IFN)-gamma-inducible protein 10 (IP-10) in response to treatment with gamma-PGA was almost abolished in C3H/HeJ mice. In contrast to LPS, gamma-PGA induced productions of TNF-alpha and IP-10 could not be blocked by polymyxin B. Furthermore, gamma-PGA-induced interleukin-12 production was also impaired in immature dendritic cells (iDCs) from MyD88(-/-) and C3H/HeJ mice. Downregulation of MyD88 and TLR4 expression using small interfering RNA (siRNA) significantly inhibited gamma-PGA-induced TNF-alpha secretion from the RAW264.7 cells. gamma-PGA-mediated intracellular signaling was markedly inhibited in C3H/HeJ cells. The antitumor effect of gamma-PGA was completely abrogated in C3H/HeJ mice compared with control mice (C3H/HeN) but significant antitumor effect was generated by the intratumoral administration of C3H/HeN mice-derived iDCs followed by 2,000 kDa gamma-PGA in C3H/HeJ. These findings strongly suggest that the antitumor activity of gamma-PGA is mediated by TLR4.
C1 [Lee, Tae-Young; Kim, Yang-Hyun; Yoon, Sun-Woo; Poo, Haryoung] Korea Res Inst Biosci & Biotechnol, BioNanotechnol Res Ctr, Mucosal Immunol Lab, Taejon 305806, South Korea.
[Choi, Jai-Chul; Sung, Moon-Hee] BioLeaders Corp, Taejon, South Korea.
[Kim, Yang-Hyun; Yang, Jai-Myung] Sogang Univ, Dept Life Sci, Seoul, South Korea.
[Kim, Chul-Joong] Chungnam Natl Univ, Coll Vet Med, Taejon, South Korea.
[Schiller, John T.] NCI, Cellular Oncol Lab, NIH, Bethesda, MD 20892 USA.
[Sung, Moon-Hee] Kookmin Univ, Dept Bio & Nanochem, Seoul, South Korea.
RP Poo, H (reprint author), Korea Res Inst Biosci & Biotechnol, BioNanotechnol Res Ctr, Mucosal Immunol Lab, Taejon 305806, South Korea.
EM haryoung@kribb.re.kr
FU Korea Health 21 RD Project [A050562]; National R&D Program for Cancer
Control [0720510]; Ministry of Health & Welfare, Republic of Korea;
KRIBB Initiative program
FX We thank Dr S. Akira and Dr S. Uemastu for MyD88-/- and
TLR2-/- mice, Dr J. Y. Lee and Dr Kate Fitzgerald for IRF3
luciferase plasmid, and Dr H. Kuroda for helpful advices. This work was
supported by grants of the Korea Health 21 R&D Project ( A050562) and
National R&D Program for Cancer Control ( 0720510), Ministry of Health &
Welfare, Republic of Korea and a grant from KRIBB Initiative program to
H. Poo.
NR 39
TC 30
Z9 31
U1 1
U2 5
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 NOV
PY 2009
VL 58
IS 11
BP 1783
EP 1796
DI 10.1007/s00262-009-0689-4
PG 14
WC Oncology; Immunology
SC Oncology; Immunology
GA 485HW
UT WOS:000269112900006
PM 19294383
ER
PT J
AU di Bari, MG
Lutsiak, MEC
Takai, S
Mostbock, S
Farsaci, B
Semnani, RT
Wakefield, LM
Schlom, J
Sabzevari, H
AF di Bari, Maria Giovanna
Lutsiak, M. E. Christine
Takai, Shinji
Mostbock, Sven
Farsaci, Benedetto
Semnani, Roshanak Tolouei
Wakefield, Lalage M.
Schlom, Jeffrey
Sabzevari, Helen
TI TGF-beta modulates the functionality of tumor-infiltrating CD8(+) T
cells through effects on TCR signaling and Spred1 expression
SO CANCER IMMUNOLOGY IMMUNOTHERAPY
LA English
DT Article
DE T cells; Tolerance/suppression/anergy; Tumor immunity; Signal
transduction
ID ANTITUMOR IMMUNITY; GROWTH; ACTIVATION; TRANSDUCTION; SUPPRESSION;
INDUCTION; CD4(+); PHOSPHORYLATION; MECHANISMS; GENERATION
AB This study demonstrates that CD8(+) T cells in the tumor microenvironment display reduced functionality and hyporesponsiveness. TGF-beta contributed markedly to the tumor-infiltrating CD8(+) T cells' (TILs) reduced functionality, which could be reversed using a small molecule TGF-beta inhibitor. Upon T-cell receptor (TCR) activation, the activation of ITK and ERK kinases were reduced in CD8(+) TILs, as compared to splenic CD8(+) T cells: TGF-beta inhibitor could reverse this phenomenon. This study demonstrates for the first time the association of the Spred-1 gene, an inhibitor of the Ras/MAPK pathway, with CD8(+) TILs and TGF-beta activity. Spred-1 was upregulated in CD8(+) TILs and TGF-beta enhanced the expression of Spred-1 in effector/memory CD8(+) T cells and not in rested/memory CD8(+) T cells. Based on these findings, this study supports the hypothesis that TGF-beta mediates an inhibitory mechanism on CD8(+) TILs involving TCR-signaling blockade and the upregulation of Spred-1, thus implicating Spred-1 as a potential new target for future anti-tumor immune studies.
C1 [di Bari, Maria Giovanna; Lutsiak, M. E. Christine; Takai, Shinji; Mostbock, Sven; Farsaci, Benedetto; Schlom, Jeffrey; Sabzevari, Helen] NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[Semnani, Roshanak Tolouei] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA.
[Wakefield, Lalage M.] NCI, Lab Canc Biol & Genet, NIH, Bethesda, MD 20892 USA.
RP Schlom, J (reprint author), NCI, Tumor Immunol & Biol Lab, Ctr Canc Res, NIH, 10 Ctr Dr,Room 8B09,MSC 1750, Bethesda, MD 20892 USA.
EM js141c@nih.gov
RI Farsaci, Benedetto/L-9837-2014
OI Farsaci, Benedetto/0000-0001-8275-2561
FU National Institutes of Health Intramural Program; Center for Cancer
Research; National Cancer Institute
FX We thank Judith DiPietro for technical assistance, Lajuan Chase for
mouse work and Debra Weingarten for editorial assistance in the
preparation of this manuscript. This work was supported by the National
Institutes of Health Intramural Program, Center for Cancer Research,
National Cancer Institute.
NR 41
TC 13
Z9 13
U1 0
U2 1
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 NOV
PY 2009
VL 58
IS 11
BP 1811
EP 1820
DI 10.1007/s00262-009-0692-9
PG 10
WC Oncology; Immunology
SC Oncology; Immunology
GA 485HW
UT WOS:000269112900009
PM 19319531
ER
PT J
AU Kristinsson, SY
Landgren, O
Rajkumar, VS
AF Kristinsson, Sigurdur Yngvi
Landgren, Ola
Rajkumar, Vincent S.
TI Novel Therapies in Multiple Myeloma for Newly Diagnosed Nontransplant
Candidates
SO CANCER JOURNAL
LA English
DT Review
DE multiple myeloma; therapy; prognosis
ID STEM-CELL TRANSPLANTATION; LENALIDOMIDE PLUS DEXAMETHASONE; UNDETERMINED
SIGNIFICANCE; MONOCLONAL GAMMOPATHY; ELDERLY-PATIENTS; AUTOLOGOUS
TRANSPLANTATION; COMBINATION CHEMOTHERAPY; 1ST-DEGREE RELATIVES;
THALIDOMIDE ANALOGS; RANDOMIZED-TRIAL
AB In the twenty-first century, melphalan-prednisone can no longer be regarded as the standard treatment of multiple myeloma patients not eligible for high-dose melphalan followed by autologous stern cell transplantation. The introduction of thalidomide, lenalidomide, and bortezomib has improved the arsenal of therapeutic options in multiple myeloma. Indeed, randomized studies have shown that melphalan-prednisone-thalidomide and melphalan-prednisone-bortezomib are superior to melphalan-prednisone alone. III addition, other combinations, including lenalidomide, are under study. III this review, we discuss the role of novel therapies in multiple myeloma in elderly multiple myeloma patients. Important aspects, such as toxicity and the role of prognostic factors, are also addressed.
C1 [Rajkumar, Vincent S.] Mayo Clin, Div Hematol, Rochester, MN 55905 USA.
[Kristinsson, Sigurdur Yngvi] Karolinska Univ, Hosp Solna, Dept Med, Div Hematol, Stockholm, Sweden.
[Kristinsson, Sigurdur Yngvi] Karolinska Inst, Stockholm, Sweden.
[Landgren, Ola] NCI, Div Med Oncol, Med Oncol Branch, Ctr Canc Res,NIH, Bethesda, MD 20892 USA.
RP Rajkumar, VS (reprint author), Mayo Clin, Div Hematol, Rochester, MN 55905 USA.
EM rajkumar.vincent@mayo.edu
RI Kristinsson, Sigurdur /M-2910-2015;
OI Kristinsson, Sigurdur /0000-0002-4964-7476; Rajkumar, S.
Vincent/0000-0002-5862-1833
FU National Cancer Institute, Bethesda, MD [CA62242, CA107476]
FX Supported in part by National Cancer Institute, Bethesda, MD, grants
CA62242 and CA107476.
NR 63
TC 3
Z9 3
U1 0
U2 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1528-9117
J9 CANCER J
JI Cancer J.
PD NOV-DEC
PY 2009
VL 15
IS 6
BP 473
EP 478
PG 6
WC Oncology
SC Oncology
GA 535EW
UT WOS:000272951000005
PM 20010166
ER
PT J
AU Anastasiadou, E
Vaeth, S
Cuomo, L
Boccellato, F
Vincenti, S
Cirone, M
Presutti, C
Junker, S
Winberg, G
Frati, L
Wade, PA
Faggioni, A
Trivedi, P
AF Anastasiadou, Eleni
Vaeth, Signe
Cuomo, Laura
Boccellato, Francesco
Vincenti, Sara
Cirone, Mara
Presutti, Carlo
Junker, Steffen
Winberg, Gosta
Frati, Luigi
Wade, Paul A.
Faggioni, Alberto
Trivedi, Pankaj
TI Epstein-Barr virus infection leads to partial phenotypic reversion of
terminally differentiated malignant B cells
SO CANCER LETTERS
LA English
DT Article
DE EBV; Latency; Myeloma; Differentiation
ID LATENT GENE-EXPRESSION; EFFUSION LYMPHOMA-CELLS; NON-HODGKINS-LYMPHOMA;
BURKITTS-LYMPHOMA; MULTIPLE-MYELOMA; TCL1 EXPRESSION; PLASMA-CELLS; EBV
LATENCY; IN-VIVO; DISRUPTION
AB The B cell lymphomas associated with Epstein-Barr virus (EBV) are not limited to any specific stage of B cell differentiation but covers widely different B cell phenotypes. In vitro infection of the virus negative tumors with a recombinant EBV strain has provided important insights into virus-tumor interaction. Here, we investigated the interaction between EBV and terminally differentiated tumor derived B cells, namely multiple myeloma (MM). The in vitro EBV infected MM expressed restricted viral latency. Acquisition of the virus was accompanied by a partial reprogramming to a mature B cell phenotype. Thus. the plasma cell markers syndecan-1 (CD138), Blimp1 and MUM1 were downregulated, while expression of HLADR, CIITA and TCL1, which are normally not expressed in plasmacytoid cells, was upregulated. The silenced transcription factor gene encoding Pax5 and its target BLNK were activated. Significantly. the free lambda light chains secreted in the medium were reduced in EBV infected MM clones. Collectively, these results suggest that the restricted EBV latency can cause at least partial phenotypic reversion of terminally differentiated B tumor cells. We suggest that the restricted EBV latent gene expression may not only be the consequence but the cause of the mature B cell phenotype, actively participating in the virus persistence. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
C1 [Anastasiadou, Eleni; Boccellato, Francesco; Cirone, Mara; Frati, Luigi; Faggioni, Alberto; Trivedi, Pankaj] Univ Roma La Sapienza, Ist Pasteur Fdn Cenci Bolognetti, Dept Expt Med & Pathol, I-00161 Rome, Italy.
[Vaeth, Signe; Junker, Steffen] Aarhus Univ, Dept Human Genet, Aarhus, Denmark.
[Cuomo, Laura] San Filippo Neri Hosp, Dept Clin Pathol, I-00135 Rome, Italy.
[Vincenti, Sara; Presutti, Carlo] Univ Roma La Sapienza, Dept Genet & Mol Biol, I-00185 Rome, Italy.
[Winberg, Gosta] Karolinska Inst, MTC, Stockholm, Sweden.
[Wade, Paul A.] NIEHS, Mol Carcinogenesis Lab, Res Triangle Pk, NC 27709 USA.
RP Trivedi, P (reprint author), Univ Roma La Sapienza, Ist Pasteur Fdn Cenci Bolognetti, Dept Expt Med & Pathol, Viale Regina Elena 324, I-00161 Rome, Italy.
EM alberto.faggioni@uniroma1.it; Pankaj.Trivedi@uniroma1.it
RI Winberg, Gosta/I-5686-2013;
OI Winberg, Gosta/0000-0002-3371-4056
FU MIUR; Associazione Italiana per la ricerca sul Cancro (AIRC); Fondazione
Italiana per la sclerosi multipla (FISM); Ministero della Sanita,
progetto AIDS; National Institute of Environmental Health Science, NIH;
Danish Cancer Society; NOVO Foundation; Danish Medical Research Council;
Eva and Henry Fraenkel Memorial Foundation
FX This work was partially supported by Grants from MIUR and Associazione
Italiana per la ricerca sul Cancro (AIRC), Fondazione Italiana per la
sclerosi multipla (FISM) and from Ministero della Sanita, progetto AIDS.
PW was supported by the Intramural Research Program of the National
Institute of Environmental Health Science, NIH. S.J is supported by
Danish Cancer Society, the NOVO Foundation, Danish Medical Research
Council, and the Eva and Henry Fraenkel Memorial Foundation. We thank
Dr. J. Epstein, Little Rock University, Arkansas, USA for CAG MM cell
line 173 and Dr. Kenzo Takada for the recombinant EBV. Sandro Valia and
Paola Ottaviani are acknowledged for technical help and photographic
work.
NR 27
TC 13
Z9 13
U1 0
U2 1
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0304-3835
J9 CANCER LETT
JI Cancer Lett.
PD NOV 1
PY 2009
VL 284
IS 2
BP 165
EP 174
DI 10.1016/j.canlet.2009.04.025
PG 10
WC Oncology
SC Oncology
GA 503JQ
UT WOS:000270530700007
PM 19481340
ER
PT J
AU Steele, VE
Rao, CV
Zhang, YT
Patlolla, J
Boring, D
Kopelovich, L
Juliana, MM
Grubbs, CJ
Lubet, RA
AF Steele, Vernon E.
Rao, Chinthalapally V.
Zhang, Yuting
Patlolla, Jagan
Boring, Daniel
Kopelovich, Levy
Juliana, M. Margaret
Grubbs, Clinton J.
Lubet, Ronald A.
TI Chemopreventive Efficacy of Naproxen and Nitric Oxide-naproxen in Rodent
Models of Colon, Urinary Bladder, and Mammary Cancers
SO CANCER PREVENTION RESEARCH
LA English
DT Article
ID NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ABERRANT CRYPT FOCI;
CYCLO-OXYGENASE-2 INHIBITORS; CYCLOOXYGENASE-2 INHIBITOR; PRENEOPLASTIC
LESIONS; RANDOMIZED-TRIALS; CELECOXIB; CARCINOGENESIS; PREVENTION;
AGENTS
AB Nonsteroidal anti-inflammatory drugs (NSAID) have been highly effective in preventing colon, urinary bladder, and skin cancer preclinically, and also in clinical trials of colon adenoma formation. However, certain NSAIDs cause gastrointestinal ulceration and may increase cardiovascular events. Naproxen seems to cause the lowest cardiovascular events of the common NSAIDs other than aspirin. Nitric oxide (NO)-naproxen was tested based on the finding that adding a NO group to NSAIDs may help alleviate GI toxicity. In the azoxymethane-induced rat colon aberrant crypt foci (ACF) model, naproxen administered at 200 and 400 ppm in the diet reduced mean ACFs in the colon by about 45% to 60%, respectively. NO-naproxen was likewise administered in the diet at roughly equimolar doses (300 and 600 ppm) and reduced total ACF by 20% to 40%, respectively. In the hydroxybutyl (butyl) nitrosamine rat urinary bladder cancer model, NO-naproxen was given at 183 or 550 ppm in the diet, and naproxen at 128 ppm. The NO-naproxen groups had 77% and 73% decreases, respectively, in the development of large urinary bladder tumors, whereas the 128 ppm naproxen group also showed a strong decrease (69%). If treatments were started 3 months after hydroxybutyl (butyl) nitrosamine, NO-naproxen (550 ppm) and naproxen (400 ppm) were also highly effective (86-94% decreases). In the methylnitrosourea-induced mammary cancer model in rats, NO-naproxen and naproxen showed nonsignificant inhibitions (12% and 24%) at 550 and 400 ppm, respectively. These data show that both naproxen and NO-naproxen are effective agents against urinary bladder and colon, but not mammary, carcinogenesis.
C1 [Steele, Vernon E.; Boring, Daniel; Kopelovich, Levy; Lubet, Ronald A.] NIH, Chemoprevent Agent Dev Res Grp, Canc Prevent Div, Bethesda, MD USA.
[Rao, Chinthalapally V.; Zhang, Yuting; Patlolla, Jagan] Univ Oklahoma, Inst Canc, OUHSC, Oklahoma City, OK USA.
[Juliana, M. Margaret; Grubbs, Clinton J.] Univ Alabama, Birmingham, AL USA.
RP Steele, VE (reprint author), NCI, Execut Plaza N,Room 2118,6130 Execut Blvd, Rockville, MD 20852 USA.
EM Steelev@mail.nih.gov
FU National Cancer Institute [NCI-CN53300, NCI-CN43301]
FX Grant support: National Cancer Institute Contracts NCI-CN53300 and
NCI-CN43301.
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 1940-6207
J9 CANCER PREV RES
JI Cancer Prev. Res.
PD NOV
PY 2009
VL 2
IS 11
BP 951
EP 956
DI 10.1158/1940-6207.CAPR-09-0080
PG 6
WC Oncology
SC Oncology
GA 515HG
UT WOS:000271458400006
PM 19892664
ER
PT J
AU Turk, D
Hall, MD
Chu, BF
Ludwig, JA
Fales, HM
Gottesman, MM
Szakacs, G
AF Tuerk, Dora
Hall, Matthew D.
Chu, Benjamin F.
Ludwig, Joseph A.
Fales, Henry M.
Gottesman, Michael M.
Szakacs, Gergely
TI Identification of Compounds Selectively Killing Multidrug-Resistant
Cancer Cells
SO CANCER RESEARCH
LA English
DT Article
ID TUMOR-SCREENING DATABASE; ANTICANCER DRUG SCREEN; P-GLYCOPROTEIN;
LEUKEMIA-CELLS; RIBONUCLEOTIDE REDUCTASE; IRON CHELATORS; KB CELLS;
INHIBITORS; LINES; AGENTS
AB There is a great need for the development of novel chemotherapeutic agents that overcome the emergence of multidrug resistance (MDR) in cancer. We catalogued the National Cancer Institute's DTP drug repository in search of compounds showing increased toxicity in MDR cells. By comparing the sensitivity of parental cell lines with MDR derivatives, we identified 22 compounds possessing MDR-selective activity. Analysis of structural congeners led to the identification of 15 additional drugs showing increased toxicity in Pgp-expressing cells. Analysis of MDR-selective compounds led to the formulation of structure activity relationships and pharmacophore models. This data mining coupled with experimental data points to a possible mechanism of action linked to metal chelation. Taken together, the discovery of the MDR-selective compound set shows the robustness of the developing field of MDR-targeting therapy as a new strategy for resolving Pgp-mediated MDR. [Cancer Res 2009;69(21):8293-301]
C1 [Tuerk, Dora; Szakacs, Gergely] Hungarian Acad Sci, Inst Enzymol, H-1113 Budapest, Hungary.
[Hall, Matthew D.; Chu, Benjamin F.; Gottesman, Michael M.] NCI, Cell Biol Lab, Bethesda, MD 20892 USA.
[Fales, Henry M.] NHLBI, Biophys Chem Lab, Bethesda, MD 20892 USA.
[Ludwig, Joseph A.] Univ Texas MD Anderson Canc Ctr, Dept Sarcoma Med Oncol, Houston, TX 77030 USA.
RP Szakacs, G (reprint author), Hungarian Acad Sci, Inst Enzymol, Karolina Ut 29, H-1113 Budapest, Hungary.
EM szakacs@biomembrane.hu
RI Szakacs, Gergely/A-2580-2009; Hall, Matthew/B-2132-2010
OI Szakacs, Gergely/0000-0002-9311-7827;
FU OTKA [PF60435]; EMBO-SDIG; Marie Curie [046560, 041547]; NIH; Janos
Bolyai Scholarship; Leukemia and Lymphoma Society
FX Grant support: OTKA (PF60435), EMBO-SDIG, and Marie Curie grants
(046560, 041547) as well as the Intramural Research Program of the NIH.
G. Szakacs is the recipient of a Janos Bolyai Scholarship and a Special
Fellow Award from the Leukemia and Lymphoma Society.; The costs of
publication of this article were defrayed in part by the payment of page
charges. This article must therefore be hereby marked advertisement in
accordance with 18 U.S.C. Section 1734 solely to indicate this fact.; We
thank the NCI DTP for generation of the database used in this study and
Zsuzsanna Sebestyen for the technical help.
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8293
EP 8301
DI 10.1158/0008-5472.CAN-09-2422
PG 9
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000011
PM 19843850
ER
PT J
AU Moore, SC
Rajaraman, P
Dubrow, R
Darefsky, AS
Koebnick, C
Hollenbeck, A
Schatzkin, A
Leitzmann, MF
AF Moore, Steven C.
Rajaraman, Preetha
Dubrow, Robert
Darefsky, Amy S.
Koebnick, Corinna
Hollenbeck, Albert
Schatzkin, Arthur
Leitzmann, Michael F.
TI Height, Body Mass Index, and Physical Activity in Relation to Glioma
Risk
SO CANCER RESEARCH
LA English
DT Article
ID BRAIN-TUMORS; CANCER STATISTICS; GROWTH-FACTORS; INSULIN; COHORT;
ADULTS; VALIDITY; WEIGHT; SYSTEM; HEALTH
AB Whether energy balance during early life and/or adulthood is related to glioma risk is unknown. We therefore investigated height, body mass index (BMI), and physical activity in relation to glioma risk in the prospective NIH-AARP Diet and Health Study. Participants completed a baseline questionnaire (sent in 1995-1996) inquiring about height, weight, and potential confounders. A second questionnaire (sent in 1996) inquired about physical activity during ages 15 to 18, 19 to 29, and 35 to 39 years and the past 10 years and body weight at ages 18, 35, and 50 years. During follow-up from 1995/1996 to 2003, we documented 480 cases of glioma among 499,437 respondents to the baseline questionnaire and 257 cases among 305,681 respondents to the second questionnaire. Glioma risk among tall persons (>= 1.90 m) was twice that of short persons [<1.60 m; multivariate relative risk (RR), 2.12; 95% confidence interval (95% CI), 1.18-3.81; P-trend = 0.006]. Risk among participants who were obese (BMI 30.0-34.9 kg/m(2)) at age 18 years was nearly four times that of persons of normal weight (BMI 18.5-24.9 kg/m(2)) at age 18 years (RR, 3.74; 95% CI, 2.03-6.90; P-trend = 0.003); 11 cases were obese at age 18 years. Risk among participants who were active during ages 15 to IS years was 36% lower than that of persons who were inactive during ages 15 to 18 years (RR, 0.64; 95% CI, 0.44-0.93; P-trend = 0.02). BMI and physical activity after age 18 years were unrelated to glioma risk. Adult height, BMI during adolescence, and physical activity during adolescence were each associated with glioma risk, supporting a role for early-life energy balance in glioma carcinogenesis. [Cancer Res 2009;69(21):8349-55]
C1 [Moore, Steven C.; Schatzkin, Arthur] NCI, Nutr Epidemiol Branch, NIH, Dept Hlth & Human Serv, Rockville, MD USA.
[Rajaraman, Preetha] NCI, Radiat Epidemiol Branch, Div Canc Epidemiol & Genet, NIH,Dept Hlth & Human Serv, Rockville, MD USA.
[Dubrow, Robert; Darefsky, Amy S.] Yale Univ, Sch Med, Yale Sch Publ Hlth, New Haven, CT USA.
[Koebnick, Corinna] Kaiser Permanente So Calif, Dept Res & Evaluat, Pasadena, CA USA.
[Hollenbeck, Albert] AARP, Washington, DC USA.
[Leitzmann, Michael F.] Univ Regensburg, Med Ctr, Dept Epidemiol & Prevent Med, Regensburg, Germany.
RP Moore, SC (reprint author), 6120 Execut Blvd, Bethesda, MD 20892 USA.
EM moorest@mail.nih.gov
RI Koebnick, Corinna/P-4767-2016; Moore, Steven/D-8760-2016
OI Koebnick, Corinna/0000-0001-8274-0309; Moore, Steven/0000-0002-8169-1661
FU NIH/National Cancer Institute
FX Grant support: Intramural Research Program of the NIH/National Cancer
Institute.; The costs of publication of this article were defrayed in
part by the payment of page charges. This article must therefore be
hereby marked advertisement in accordance with 18 U.S.C. Section 1734
solely to indicate this fact.; We thank the participants in the NIH-AARP
Diet and Health Study for outstanding cooperation.; S.C. Moore had full
access to all of the data in the study and takes responsibility for the
integrity of the data and the accuracy of the data analysis.; Cancer
incidence data from the Atlanta metropolitan area were collected by the
Georgia Center for Cancer Statistics, Department of Epidemiology,
Rollins School of Public Health, Emory University. Cancer incidence data
from California were collected by the California Department of Health
Services, Cancer Surveillance Section. Cancer incidence data from the
Detroit metropolitan area were collected by the Michigan Cancer
Surveillance Program, Community Health Administration, State of
Michigan. The Florida cancer incidence data used in this report were
collected by the Florida Cancer Data System under contract to the
Department of Health. The views expressed herein are solely those of the
authors and do not necessarily reflect those of the contractor or
Department of Health. Cancer incidence data from Louisiana were
collected by the Louisiana Tumor Registry, Louisiana State University
Medical Center in New Orleans. Cancer incidence data from New Jersey
were collected by the New Jersey State Cancer Registry, Cancer
Epidemiology Services, New Jersey State Department of Health and Senior
Services. Cancer incidence data from North Carolina were collected by
the North Carolina Central Cancer Registry. Cancer incidence data from
Pennsylvania were supplied by the Division of Health Statistics and
Research, Pennsylvania Department of Health, Harrisburg, Pennsylvania.
The Pennsylvania Department of Health specifically disclaims
responsibility for any analyses, interpretations or conclusions.
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8349
EP 8355
DI 10.1158/0008-5472.CAN-09-1669
PG 7
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000018
PM 19808953
ER
PT J
AU Collier, LS
Adams, DJ
Hackett, CS
Bendzick, LE
Akagi, K
Davies, MN
Diers, MD
Rodriguez, FJ
Bender, AM
Tieu, C
Matise, I
Dupuy, AJ
Copeland, NG
Jenkins, NA
Hodgson, JG
Weiss, WA
Jenkins, RB
Largaespada, DA
AF Collier, Lara S.
Adams, David J.
Hackett, Christopher S.
Bendzick, Laura E.
Akagi, Keiko
Davies, Michael N.
Diers, Miechaleen D.
Rodriguez, Fausto J.
Bender, Aaron M.
Tieu, Christina
Matise, Ilze
Dupuy, Adam J.
Copeland, Neal G.
Jenkins, Nancy A.
Hodgson, J. Graeme
Weiss, William A.
Jenkins, Robert B.
Largaespada, David A.
TI Whole-Body Sleeping Beauty Mutagenesis Can Cause Penetrant
Leukemia/Lymphoma and Rare High-Grade Glioma without Associated
Embryonic Lethality
SO CANCER RESEARCH
LA English
DT Article
ID TUMOR-SUPPRESSOR; INSERTIONAL MUTAGENESIS; SOMATIC MUTAGENESIS; SITE
PREFERENCES; GENE DISCOVERY; TRANSPOSON; CANCER; MOUSE; CELLS; MICE
AB The Sleeping Beauty (SB) transposon system has been used as a somatic mutagen to identify candidate cancer genes. In previous studies, efficient leukemia/lymphoma formation on an otherwise wild-type genetic background occurred in mice undergoing whole-body mobilization of transposons, but was accompanied by high levels of embryonic lethality. To explore the utility of SB for large-scale cancer gene discovery projects, we have generated mice that carry combinations of different transposon and transposase transgenes. We have identified a transposon/transposase combination that promotes highly penetrant leukemia/lymphoma formation on an otherwise wild-type genetic background, yet does not cause embryonic lethality. Infiltrating gliomas also occurred at lower penetrance in these mice. SB-induced or accelerated tumors do not harbor large numbers of chromosomal amplifications or deletions, indicating that transposon mobilization likely promotes tumor formation by insertional mutagenesis of cancer genes, and not by promoting wide-scale genomic instability. Cloning of transposon insertions from lymphomas/leukemias identified common insertion sites at known and candidate novel cancer genes. These data indicate that a high mutagenesis rate can be achieved using SB without high levels of embryonic lethality or genomic instability. Furthermore, the SB system could be used to identify new genes involved in lymphomagenesis/leukemogenesis. [Cancer Res 2009;69(21):8429-37]
C1 [Collier, Lara S.; Bendzick, Laura E.; Davies, Michael N.; Diers, Miechaleen D.; Largaespada, David A.] Univ Minnesota, Dept Genet Cell Biol & Dev, Mason Canc Ctr, Minneapolis, MN USA.
[Matise, Ilze] Univ Minnesota, Mason Canc Ctr Histopathol Core, Minneapolis, MN USA.
[Adams, David J.] Wellcome Trust Sanger Inst, Cambridge, England.
[Hackett, Christopher S.; Hodgson, J. Graeme; Weiss, William A.] Univ Calif San Francisco, San Francisco, CA 94143 USA.
[Akagi, Keiko] NCI, Mouse Canc Genet Program, Frederick, MD 21701 USA.
[Rodriguez, Fausto J.; Bender, Aaron M.; Tieu, Christina; Jenkins, Robert B.] Mayo Clin, Div Expt Pathol, Rochester, MN USA.
[Dupuy, Adam J.] Univ Iowa, Dept Cell Biol & Anat, Iowa City, IA USA.
[Copeland, Neal G.; Jenkins, Nancy A.] Natl Univ Singapore, Inst Mol & Cell Biol, Singapore 117548, Singapore.
RP Collier, LS (reprint author), Univ Wisconsin, 4117 Rennebohm Hall, Madison, WI 53705 USA.
EM lcollier@wisc.edu; larga002@umn.edu
RI ASTAR, IMCB/E-2320-2012; Largaespada, David/C-9832-2014;
OI Weiss, William/0000-0003-2230-9132
FU American Cancer Society predoctoral fellowship; Minnesota Department of
Employment and Economic Development [SPAP-05-0013-P-FY06,
R01CA113636-01A1, R01NS055750]; Cancer Research-UK; Wellcome Trust;
[K01CA122183]
FX Grant support: K01CA122183 and an American Cancer Society predoctoral
fellowship (L.S. Collier), Minnesota Department of Employment and
Economic Development SPAP-05-0013-P-FY06 (D.A. Largaespada and R.B.
Jenkins), R01CA113636-01A1 (D.A. Largaespada), R01NS055750 (IA A.
Weiss), Cancer Research-UK, and the Wellcome Trust (DJ. Adams).
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PI PHILADELPHIA
PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA
SN 0008-5472
EI 1538-7445
J9 CANCER RES
JI Cancer Res.
PD NOV 1
PY 2009
VL 69
IS 21
BP 8429
EP 8437
DI 10.1158/0008-5472.CAN-09-1760
PG 9
WC Oncology
SC Oncology
GA 514OA
UT WOS:000271403000027
PM 19843846
ER
PT J
AU Ryan, BM
O'Donovan, N
Duffy, MJ
AF Ryan, Brid M.
O'Donovan, Norma
Duffy, Michael J.
TI Survivin: A new target for anti-cancer therapy
SO CANCER TREATMENT REVIEWS
LA English
DT Review
DE Survivin; BIRC5; IAP; Cancer; Treatment
ID SQUAMOUS-CELL CARCINOMA; PROSTATE-CANCER CELLS; HUMAN-MELANOMA CELLS;
CHEMOPREVENTIVE AGENT RESVERATROL; CHROMOSOMAL PASSENGER COMPLEX;
RIBOZYME-MEDIATED INHIBITION; TRAIL-INDUCED APOPTOSIS; TUMOR-ANTIGEN
SURVIVIN; NEGATIVE BREAST-CANCER; DRUG-INDUCED APOPTOSIS
AB Survivin is one of the most cancer-specific proteins identified to date, being upregulated in almost all human tumors. Biologically, survivin has been shown to inhibit apoptosis, enhance proliferation and promote angiogenesis. Because of its upregulation in malignancy and its key role in apoptosis, proliferation and angiogenesis, survivin is currently attracting considerable attention as a new target for anti-cancer therapies. In several animal model systems, downregulation of survivin or inactivation of its function has been shown to inhibit tumor growth. Strategies under investigation to target survivin include antisense oligonucleotides, siRNA, ribozymes, immunotherapy and small molecular weight molecules. The translation of these findings to the clinic is currently ongoing with a number of phase I/II clinical trials targeting survivin in progress. These include use of the antisense oligonucleotide LY2181308, the low molecular weight molecule inhibitor YM155 and survivin-directed autologous cytotoxic T lymphocytes. The optimum use of survivin antagonists in the treatment of cancer is likely to be in combination with conventional cancer therapies. (C) 2009 Elsevier Ltd. All rights reserved.
C1 [Ryan, Brid M.] NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, NIH, Bethesda, MD 20892 USA.
[Ryan, Brid M.] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA.
[O'Donovan, Norma] Dublin City Univ, Natl Inst Cellular Biotechnol, Dublin 9, Ireland.
[Duffy, Michael J.] St Vincents Univ Hosp, Dept Pathol & Lab Med, Dublin 4, Ireland.
[Duffy, Michael J.] Univ Coll Dublin, Conway Inst, Sch Med & Med Sci, Dublin 4, Ireland.
RP Ryan, BM (reprint author), NCI, Canc Prevent Fellowship Program, Off Prevent Oncol, NIH, Bethesda, MD 20892 USA.
EM ryanb@mail.nih.gov; norma.odonovan@dcu.ie; michael.j.duffy@ucd.ie
RI O'Donovan, Norma/B-6710-2013;
OI O'Donovan, Norma/0000-0003-1113-3872; Ryan, Brid/0000-0003-0038-131X
FU Irish Cancer Society; Health Research Board of Ireland [PRP/2005/35]
FX The authors' work on survivin was supported by the Irish Cancer Society
and the Health Research Board of Ireland (Project No. PRP/2005/35). The
authors declare no conflicts of interest.
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U2 58
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 0305-7372
J9 CANCER TREAT REV
JI Cancer Treat. Rev.
PD NOV
PY 2009
VL 35
IS 7
BP 553
EP 562
DI 10.1016/j.ctrv.2009.05.003
PG 10
WC Oncology
SC Oncology
GA 523TV
UT WOS:000272098400004
PM 19559538
ER
PT J
AU Itano, O
Yang, K
Fan, KH
Kurihara, N
Shinozaki, H
Abe, S
Jin, B
Gravaghi, C
Edelmann, W
Augenlicht, L
Kopelovich, L
Kucherlapati, R
Lamprecht, S
Lipkin, M
AF Itano, Osamu
Yang, Kan
Fan, Kunhua
Kurihara, Naoto
Shinozaki, Hiroharu
Abe, Sadanori
Jin, Bo
Gravaghi, Claudia
Edelmann, Winfried
Augenlicht, Leonard
Kopelovich, Levy
Kucherlapati, Raju
Lamprecht, Sergio
Lipkin, Martin
TI Sulindac effects on inflammation and tumorigenesis in the intestine of
mice with Apc and Mlh1 mutations
SO CARCINOGENESIS
LA English
DT Article
ID FAMILIAL ADENOMATOUS POLYPOSIS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS;
LONG-TERM TREATMENT; P38 MAP-KINASES; OXIDATIVE STRESS; RECTAL-CANCER;
COLORECTAL ADENOMAS; BOWEL-DISEASE; MOUSE; CELLS
AB We have previously reported that sulindac, a non-steroidal anti-inflammatory drug, inhibited tumor formation in the small intestine but increased tumors in the colon of Apc(Min/+) mice, a model of human familial adenomatous polyposis. To further explore intestinal regional responses, we studied effects of sulindac on additional gene-targeted mouse models of human intestinal tumorigenesis; these were (i) Apc(1638N/+) mouse (chain termination mutation in exon 15 of the Apc gene); (ii) Mlh1(+/-) mouse (DNA mismatch repair deficiency, a mouse model of human hereditary non-polyposis colorectal cancer) and (iii) double-heterozygous Mlh1(+/-)Apc(1638N/+) mutant mouse. Mice were fed AIN-76A control diet with or without 0.02% sulindac for 6 months. Intestinal regional tumor incidence, multiplicity, volume and degree of inflammation were used as end points. The results showed the following: (i) sulindac inhibited tumor development in the small intestine of Apc(1638N/+) mice; (ii) in contrast, sulindac increased tumors in the small intestine of Mlh1 mutant mice, a neoplastic effect which persisted in heterozygous compound Mlh1(+/-)Apc(1638N/+) mutant mice; (iii) sulindac increased tumors in the cecum of all mice regardless of genetic background; (iv) sulindac decreased inflammation in the small intestine of Apc(1638N/+) mice, but it increased inflammation in the small intestine of Mlh1(+/-) mice and Mlh1(+/-)Apc(1638N/+) mice and (v) sulindac enhanced inflammation in the cecum of all mutant mice. Findings indicate that the effects of sulindac in the intestine of these mutant mouse models are probably related to genetic background and appear to be associated with its inflammatory-inducing response.
C1 [Itano, Osamu; Yang, Kan; Fan, Kunhua; Kurihara, Naoto; Shinozaki, Hiroharu; Abe, Sadanori; Gravaghi, Claudia; Lamprecht, Sergio; Lipkin, Martin] Cornell Univ, Weill Med Coll, Dept Med, Strang Canc Res Lab,Div Gastroenterol & Hepatol, New York, NY 10021 USA.
[Jin, Bo; Edelmann, Winfried] Albert Einstein Coll Med, Dept Cell Biol, Bronx, NY 10467 USA.
[Augenlicht, Leonard] Montefiore Med Ctr, Dept Oncol, Bronx, NY 10467 USA.
[Kucherlapati, Raju] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
[Kopelovich, Levy] NCI, Canc Prevent Div, Bethesda, MD 20852 USA.
RP Lipkin, M (reprint author), Cornell Univ, Weill Med Coll, Dept Med, Strang Canc Res Lab,Div Gastroenterol & Hepatol, New York, NY 10021 USA.
EM mal2019@med.cornell.edu
FU National Cancer Institute; National Institutes of Health [NO1-CN-15116,
NO1-CN-43308, RO1 CA 87559]
FX National Cancer Institute; National Institutes of Health (NO1-CN-15116,
NO1-CN-43308, RO1 CA 87559).
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U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD NOV
PY 2009
VL 30
IS 11
BP 1923
EP 1926
DI 10.1093/carcin/bgp200
PG 4
WC Oncology
SC Oncology
GA 524YB
UT WOS:000272179200014
PM 19755659
ER
PT J
AU Shi, SL
Yoon, DY
Hodge-Bell, KC
Bebenek, IG
Whitekus, MJ
Zhang, RX
Cochran, AJ
Huerta-Yepez, S
Yim, SH
Gonzalez, FJ
Jaiswal, AK
Hankinson, O
AF Shi, Shengli
Yoon, Diana Y.
Hodge-Bell, Kimberly C.
Bebenek, Ilona G.
Whitekus, Michael J.
Zhang, Ruixue
Cochran, Alistair J.
Huerta-Yepez, Sara
Yim, Sun-Hee
Gonzalez, Frank J.
Jaiswal, Anil K.
Hankinson, Oliver
TI The aryl hydrocarbon receptor nuclear translocator (Arnt) is required
for tumor initiation by benzo[a]pyrene
SO CARCINOGENESIS
LA English
DT Article
ID MOUSE SKIN; AH RECEPTOR; INCREASES SUSCEPTIBILITY; DEFICIENT MICE;
CARCINOGENESIS; HYDROXYLASE; DISRUPTION; INDUCTION; PROTEIN; GENE
AB Benzo[a]pyrene (B[a]P) is a ligand for the aryl hydrocarbon receptor (Ahr). After binding ligand, Ahr dimerizes with the aryl hydrocarbon receptor nuclear translocator (Arnt) protein, and the dimer upregulates the transcription of Cyp1a1, Cyp1b1 and other enzymes involved in the metabolic activation of B[a]P. Arnt null mice die in utero. Mice in which Arnt deletion occurs constitutively in the epidermis die perinatally. In the current study, mice were developed in which the Arnt gene could be deleted specifically in adult skin epidermis. This deletion had no overt pathological effect. Homozygosity for a null reduced nicotinamide adenine dinucleotide (phosphate): quinone oxidoreductase allele was introduced into the above mouse strain to render it more susceptible to tumor initiation by B[a]P. Deletion of Arnt in the epidermis of this strain completely prevented the induction of skin tumors in a tumor initiation-promotion protocol in which a single topical application of B[a]P acted as the tumor-initiating event, and tumor promotion was provided by repeated topical applications of 12-O-tetradecanoyl phorbol-13-acetate (TPA). In contrast, deletion of Arnt did not prevent the induction of skin tumors in a protocol also using TPA as the promoter but using as the initiator N-methyl-N'-nitro-N-nitrosoguanidine, whose activity is unlikely to be affected by the activity of Ahr, Arnt or their target genes. These observations demonstrate that Arnt is required for tumor initiation by B[a]P in this system.
C1 [Shi, Shengli; Yoon, Diana Y.; Hodge-Bell, Kimberly C.; Bebenek, Ilona G.; Whitekus, Michael J.; Zhang, Ruixue; Cochran, Alistair J.; Hankinson, Oliver] Univ Calif Los Angeles, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
[Shi, Shengli; Yoon, Diana Y.; Hodge-Bell, Kimberly C.; Bebenek, Ilona G.; Whitekus, Michael J.; Zhang, Ruixue; Cochran, Alistair J.; Hankinson, Oliver] Univ Calif Los Angeles, Jonsson Comprehens Canc Ctr, Los Angeles, CA 90095 USA.
[Bebenek, Ilona G.; Hankinson, Oliver] Univ Calif Los Angeles, Mol Toxicol Program, Los Angeles, CA 90095 USA.
[Huerta-Yepez, Sara] Hosp Infantil Mexico Dr Federico Gomez, Colonia Doctores 06720, DF, Mexico.
[Yim, Sun-Hee; Gonzalez, Frank J.] NCI, Lab Metab, Bethesda, MD 20892 USA.
[Jaiswal, Anil K.] Univ Maryland, Sch Med, Baltimore, MD 21201 USA.
RP Hankinson, O (reprint author), Univ Calif Los Angeles, Dept Pathol & Lab Med, Los Angeles, CA 90095 USA.
EM ohank@mednet.ucla.edu
FU NIH [RO1 CA93471, RO1 CA28868]; National Cancer Institute
FX NIH (RO1 CA93471); an underrepresented minority supplement (RO1 CA93471
to K. H. B.); NIH (RO1 CA28868); National Cancer Institute Intramural
Research Program to F.J.G. and S.H.-Y.
NR 29
TC 14
Z9 15
U1 1
U2 2
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0143-3334
J9 CARCINOGENESIS
JI Carcinogenesis
PD NOV
PY 2009
VL 30
IS 11
BP 1957
EP 1961
DI 10.1093/carcin/bgp201
PG 5
WC Oncology
SC Oncology
GA 524YB
UT WOS:000272179200019
PM 19755658
ER
PT J
AU Perry, TE
Song, MJ
Despres, DJ
Kim, SM
San, H
Yu, ZX
Raghavachari, N
Schnermann, J
Cannon, RO
Orlic, D
AF Perry, Tashera E.
Song, Minjung
Despres, Daryl J.
Kim, Soo Mi
San, Hong
Yu, Zu-Xi
Raghavachari, Nalini
Schnermann, Jurgen
Cannon, Richard O., III
Orlic, Donald
TI Bone marrow-derived cells do not repair endothelium in a mouse model of
chronic endothelial cell dysfunction
SO CARDIOVASCULAR RESEARCH
LA English
DT Article
DE Stem cells; Bone marrow transplantation; Endothelial NOS deficiency;
Hypertension
ID NITRIC-OXIDE SYNTHASE; PROGENITOR CELLS; POSTNATAL VASCULOGENESIS;
STEM-CELLS; BLOOD; NEOVASCULARIZATION; MOBILIZATION; CONTRIBUTE;
ISCHEMIA; ANGIOGENESIS
AB Aims Bone marrow (BM)-derived endothelial progenitor cells (EPCs) in the circulation replace damaged vascular endothelium. We assessed the hypothesis that a BM transplant from healthy animals would restore normal arterial endothelium and prevent hypertension in young endothelial nitric oxide synthase-deficient (eNOS(-/-)) mice.
Methods and results Radiation or busulfan-induced BM ablation in eNOS(-/-) mice on day 6, day 14, or day 28 was followed by a BM transplant consisting of enhanced green fluorescent protein positive (EGFP(+)) cells from C57BL/6J mice. Peripheral blood cell chimerism was always greater than 85% at 4 months after BM transplant. Molecular assays of heart, kidney, and liver revealed low-level chimerism in all treatment groups, consistent with residual circulating EGFP+ blood cells. When aorta, coronary, renal, hepatic, and splenic arteries in BM-transplanted eNOS(-/-) mice were examined by confocal microscopy, there were no EGFP- or eNOS-positive endothelial cells detected in these vessels in any of the treatment groups. Likewise, telemetry did not detect any reduction in blood pressure. Thus, no differences were observed in our measurements using several different treatment protocols.
Conclusion We found no evidence for BM-derived EPIC renewal of endothelium in this eNOS-deficient mouse model of a chronic vascular disease or in wild-type mice during postnatal growth. Hence, renewal of chronic dysfunctional endothelium and endothelial homeostasis may be dependent on resident vascular progenitor cells.
C1 [Perry, Tashera E.; Song, Minjung; Cannon, Richard O., III; Orlic, Donald] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA.
[Despres, Daryl J.] Natl Inst Neurol Disorders & Stroke, Mouse Imaging Facil, NIH, Bethesda, MD USA.
[Kim, Soo Mi; Schnermann, Jurgen] NIDDK, Kidney Dis Branch, NIH, Bethesda, MD USA.
[San, Hong] NHGRI, NIH, Bethesda, MD 20892 USA.
RP Orlic, D (reprint author), NHLBI, Translat Med Branch, NIH, 9000 Rockville Pike,Bldg 10-CRC,Room 6-3130, Bethesda, MD 20892 USA.
EM dorlic@nhlbi.nih.gov
FU NHLBI, National Institutes of Health, Bethesda, MD, USA
FX This work was supported by the intramural research program of the NHLBI,
National Institutes of Health, Bethesda, MD, USA. Funding to pay the
Open Access charges was provided by the NHLBI, National Institutes of
Health.
NR 28
TC 37
Z9 38
U1 0
U2 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0008-6363
J9 CARDIOVASC RES
JI Cardiovasc. Res.
PD NOV 1
PY 2009
VL 84
IS 2
BP 317
EP 325
DI 10.1093/cvr/cvp215
PG 9
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 514VD
UT WOS:000271422900020
PM 19578071
ER
PT J
AU Lederman, RJ
AF Lederman, Robert J.
TI Legs bend: Why Dynamic Angiography Is Important
SO CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS
LA English
DT Editorial Material
ID ARTERY; DISEASE
C1 NHLBI, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
RP Lederman, RJ (reprint author), NHLBI, Div Intramural Res, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM lederman@nih.gov
OI lederman, robert/0000-0003-1202-6673
FU Intramural NIH HHS [ZIA HL005062-07, ZID HL006061-03]
NR 7
TC 1
Z9 1
U1 0
U2 0
PU WILEY-LISS
PI HOBOKEN
PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA
SN 1522-1946
J9 CATHETER CARDIO INTE
JI Catheter. Cardiovasc. Interv.
PD NOV 1
PY 2009
VL 74
IS 5
BP 799
EP 799
DI 10.1002/22268
PG 1
WC Cardiac & Cardiovascular Systems
SC Cardiovascular System & Cardiology
GA 515UD
UT WOS:000271497500019
PM 19856463
ER
PT J
AU Khatami, M
AF Khatami, Mahin
TI Inflammation, Aging, and Cancer: Tumoricidal Versus Tumorigenesis of
Immunity
SO CELL BIOCHEMISTRY AND BIOPHYSICS
LA English
DT Review
DE Unresolved inflammation; Aging; Cancer; Innate and adaptive immunity;
Autoimmune and neurodegenerative diseases; Stem cells; Hormonal change
ID COLONY-STIMULATING FACTOR; NF-KAPPA-B; TUMOR-ASSOCIATED MACROPHAGES;
CENTRAL-NERVOUS-SYSTEM; ALTERNATIVELY ACTIVATED MACROPHAGES; PIGMENT
EPITHELIAL-CELLS; C-REACTIVE PROTEIN; DENDRITIC CELLS; MAST-CELLS;
STEM-CELLS
AB Acute inflammation is a highly regulated defense mechanism of immune system possessing two well-balanced and biologically opposing arms termed apoptosis ('Yin') and wound healing ('Yang') processes. Unresolved or chronic inflammation (oxidative stress) is perhaps the loss of balance between 'Yin' and 'Yang' that would induce co-expression of exaggerated or 'mismatched' apoptotic and wound healing factors in the microenvironment of tissues ('immune meltdown'). Unresolved inflammation could initiate the genesis of many age-associated chronic illnesses such as autoimmune and neurodegenerative diseases or tumors/cancers. In this perspective 'birds' eye' view of major interrelated co-morbidity risk factors that participate in biological shifts of growth-arresting ('tumoricidal') or growth-promoting ('tumorigenic') properties of immune cells and the genesis of chronic inflammatory diseases and cancer will be discussed. Persistent inflammation is perhaps a common denominator in the genesis of nearly all age-associated health problems or cancer. Future challenging opportunities for diagnosis, prevention, and/or therapy of chronic illnesses will require an integrated understanding and identification of developmental phases of inflammation-induced immune dysfunction and age-associated hormonal and physiological readjustments of organ systems. Designing suitable cohort studies to establish the oxido-redox status of adults may prove to be an effective strategy in assessing individual's health toward developing personal medicine for healthy aging.
C1 NCI, NIH, Bethesda, MD 20892 USA.
RP Khatami, M (reprint author), NCI, NIH, Bethesda, MD 20892 USA.
EM mkgoodness@aol.com
NR 237
TC 33
Z9 34
U1 0
U2 4
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1085-9195
J9 CELL BIOCHEM BIOPHYS
JI Cell Biochem. Biophys.
PD NOV
PY 2009
VL 55
IS 2
BP 55
EP 79
DI 10.1007/s12013-009-9059-2
PG 25
WC Biochemistry & Molecular Biology; Biophysics; Cell Biology
SC Biochemistry & Molecular Biology; Biophysics; Cell Biology
GA 495WO
UT WOS:000269926100001
PM 19672563
ER
PT J
AU Chavakis, T
Orlova, VV
Langer, HF
AF Chavakis, Triantafyllos
Orlova, Valeria V.
Langer, Harald F.
TI A possible crosstalk between DNA repair pathways and angiogenesis
SO CELL CYCLE
LA English
DT Editorial Material
ID DAMAGE RESPONSE; HISTONE H2AX; C-MYC; HYPOXIA; OXYGEN; ATM;
PHOSPHORYLATION; REOXYGENATION; RECOGNITION; INSTABILITY
C1 [Chavakis, Triantafyllos; Orlova, Valeria V.; Langer, Harald F.] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA.
RP Chavakis, T (reprint author), NCI, Expt Immunol Branch, NIH, Bldg 10, Bethesda, MD 20892 USA.
EM chavakist@mail.nih.gov
RI Orlova, Valeria/C-6065-2014
OI Orlova, Valeria/0000-0002-1169-2802
FU Intramural NIH HHS [NIH0012066627, Z01 BC010664-03]
NR 24
TC 3
Z9 3
U1 0
U2 0
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1538-4101
J9 CELL CYCLE
JI Cell Cycle
PD NOV 1
PY 2009
VL 8
IS 21
BP 3438
EP 3439
DI 10.4161/cc.8.21.9750
PG 2
WC Cell Biology
SC Cell Biology
GA 525LX
UT WOS:000272218600003
PM 19838053
ER
PT J
AU Kino, T
Su, YA
Chrousos, GP
AF Kino, Tomoshige
Su, Yan A.
Chrousos, George P.
TI Human glucocorticoid receptor isoform beta: recent understanding of its
potential implications in physiology and pathophysiology
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Review
DE Cytoplasmic to nuclear translocation; Glucocorticoid receptor;
Ligand-binding pocket; Microarray; Splicing isoform; Zebrafish
ID DOMINANT-NEGATIVE ACTIVITY; LIGAND-BINDING DOMAIN; TRANSCRIPTIONAL
ACTIVITY; MESSENGER-RNA; RESISTANCE/HYPERSENSITIVITY SYNDROMES;
COACTIVATOR PROTEINS; ACTIVATION DOMAIN; SPLICE VARIANT; GENE VARIANT;
DNA-BINDING
AB The human glucocorticoid receptor (GR) gene expresses two splicing isoforms alpha and beta through alternative use of specific exons 9 alpha and 9 beta. In contrast to the classic receptor GR alpha, which mediates most of the known actions of glucocorticoids, the functions of GR beta have been largely unexplored. Owing to newly developed methods, for example microarrays and the jellyfish fluorescence proteins, we and others have recently revealed novel functions of GR beta. Indeed, this enigmatic GR isoform influences positively and negatively the transcriptional activity of large subsets of genes, most of which are not responsive to glucocorticoids, in addition to its well-known dominant negative effect against GR alpha-mediated transcriptional activity. A recent report suggested that the "ligand-binding domain" of GR beta is active, forming a functional ligand-binding pocket associated with the synthetic compound RU 486. In this review, we discuss the functions of GR beta, its mechanisms of action, and its pathologic implications.
C1 [Kino, Tomoshige] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Clin Res Ctr, Bethesda, MD 20892 USA.
[Su, Yan A.] GenProMarkers Inc, Rockville, MD 20850 USA.
[Chrousos, George P.] Univ Athens, Dept Pediat 1, Athens 11527, Greece.
RP Kino, T (reprint author), Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Program Reprod & Adult Endocrinol, NIH, Clin Res Ctr, Bldg 10,Rm 1E-3140,10 Ctr Dr MSC 1109, Bethesda, MD 20892 USA.
EM kinot@mail.nih.gov
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development, National Institutes of Health, Bethesda, MD
FX Literary work of this article was funded partly by the Intramural
Research Program of the Eunice Kennedy Shriver National Institute of
Child Health and Human Development, National Institutes of Health,
Bethesda, MD.
NR 75
TC 65
Z9 67
U1 1
U2 10
PU BIRKHAUSER VERLAG AG
PI BASEL
PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD NOV
PY 2009
VL 66
IS 21
BP 3435
EP 3448
DI 10.1007/s00018-009-0098-z
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 504QQ
UT WOS:000270632600004
PM 19633971
ER
PT J
AU Kang, XZ
Chao, DM
Gu, QB
Ding, GH
Wang, YW
Balboni, G
Lazarus, LH
Xia, Y
AF Kang, Xuezhi
Chao, Dongman
Gu, Quanbao
Ding, Guanghong
Wang, Yingwei
Balboni, Gianfranco
Lazarus, Lawrence H.
Xia, Ying
TI delta-Opioid receptors protect from anoxic disruption of Na+ homeostasis
via Na+ channel regulation
SO CELLULAR AND MOLECULAR LIFE SCIENCES
LA English
DT Article; Proceedings Paper
CT Beijing Joint Conference of Physiological Science
CY 2008
CL Beijing, PEOPLES R CHINA
DE delta-Opioid receptor; Na+ channels; Na+ influx; Hypoxia; Cortex
ID RAT HIPPOCAMPAL SLICES; SENSITIVE SODIUM-CHANNELS; APOPTOTIC NEURONAL
DEATH; NULL MUTANT MOUSE; FOREBRAIN ISCHEMIA; IN-VITRO; GLUCOSE
DEPRIVATION; K+ HOMEOSTASIS; BRAIN; MODEL
AB Hypoxic/ischemic disruption of ionic homeostasis is a critical trigger of neuronal injury/death in the brain. There is, however, no promising strategy against such pathophysiologic change to protect the brain from hypoxic/ischemic injury. Here, we present a novel finding that activation of delta-opioid receptors (DOR) reduced anoxic Na+ influx in the mouse cortex, which was completely blocked by DOR antagonism with naltrindole. Furthermore, we co-expressed DOR and Na+ channels in Xenopus oocytes and showed that DOR expression and activation indeed play an inhibitory role in Na+ channel regulation by decreasing the amplitude of sodium currents and increasing activation threshold of Na+ channels. Our results suggest that DOR protects from anoxic disruption of Na+ homeostasis via Na+ channel regulation. These data may potentially have significant impacts on understanding the intrinsic mechanism of neuronal responses to stress and provide clues for better solutions of hypoxic/ischemic encephalopathy, and for the exploration of acupuncture mechanism since acupuncture activates opioid system.
C1 [Chao, Dongman; Xia, Ying] Yale Univ, Sch Med, New Haven, CT 06520 USA.
[Kang, Xuezhi; Gu, Quanbao; Ding, Guanghong] Shanghai Res Ctr Acupuncture & Meridians, Shanghai, Peoples R China.
[Wang, Yingwei] Shanghai Jiao Tong Univ, Coll Med, Shanghai 200030, Peoples R China.
[Balboni, Gianfranco] Univ Cagliari, Cagliari, Italy.
[Lazarus, Lawrence H.] Natl Inst Environm Hlth Sci, Res Triangle Pk, NC USA.
RP Xia, Y (reprint author), Yale Univ, Sch Med, 333 Cedar St,LMP 3107, New Haven, CT 06520 USA.
EM ying.xia@yale.edu
RI Kang, Xuezhi/L-6719-2016
OI Kang, Xuezhi/0000-0002-0582-2244
FU Intramural NIH HHS [Z01 ES090053-21, Z01 ES100472-06]; NCCIH NIH HHS
[AT004422]; NICHD NIH HHS [HD34852, R01 HD034852]
NR 50
TC 17
Z9 18
U1 0
U2 5
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 1420-682X
J9 CELL MOL LIFE SCI
JI Cell. Mol. Life Sci.
PD NOV
PY 2009
VL 66
IS 21
BP 3505
EP 3516
DI 10.1007/s00018-009-0136-x
PG 12
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 504QQ
UT WOS:000270632600008
PM 19756387
ER
PT J
AU Ibarra, JA
Steele-Mortimer, O
AF Ibarra, J. Antonio
Steele-Mortimer, Olivia
TI Salmonella- the ultimate insider. Salmonella virulence factors that
modulate intracellular survival
SO CELLULAR MICROBIOLOGY
LA English
DT Review
ID ENTERICA SEROVAR TYPHIMURIUM; III SECRETION SYSTEM; PHOSPHOTHREONINE
LYASE ACTIVITY; EPITHELIAL-CELLS; SEROTYPE TYPHIMURIUM; INTESTINAL
COLONIZATION; PATHOGENICITY ISLAND-1; COORDINATED REGULATION; BACTERIAL
FLAGELLIN; VACUOLAR MEMBRANE
AB P>Salmonella enterica serovar Typhimurium is a common facultative intracellular pathogen that causes food-borne gastroenteritis in millions of people worldwide. Intracellular survival and replication are important virulence determinants and the bacteria can be found in a variety of phagocytic and non-phagocytic cells in vivo. Invasion of host cells and intracellular survival are dependent on two type III secretion systems, T3SS1 and T3SS2, each of which translocates a distinct set of effector proteins. However, other virulence factors including ion transporters, superoxide dismutase, flagella and fimbriae are also involved in accessing and utilizing the intracellular niche.
C1 [Ibarra, J. Antonio; Steele-Mortimer, Olivia] NIAID, Intracellular Parasites Lab, NIH, Rocky Mt Labs, Hamilton, MT USA.
RP Steele-Mortimer, O (reprint author), NIAID, Intracellular Parasites Lab, NIH, Rocky Mt Labs, Hamilton, MT USA.
EM omortimer@niaid.nih.gov
FU Intramural Research Program (DIR) of the NIH, NIAID
FX We apologize to all those whose work is not cited, or has not been
adequately acknowledged, due to space limitations. Research in O.S.-M.'s
laboratory is supported by the Intramural Research Program (DIR) of the
NIH, NIAID.
NR 84
TC 121
Z9 125
U1 3
U2 29
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-5814
J9 CELL MICROBIOL
JI Cell Microbiol.
PD NOV
PY 2009
VL 11
IS 11
BP 1579
EP 1586
DI 10.1111/j.1462-5822.2009.01368.x
PG 8
WC Cell Biology; Microbiology
SC Cell Biology; Microbiology
GA 504UE
UT WOS:000270642400004
PM 19775254
ER
PT J
AU Knodler, LA
Winfree, S
Drecktrah, D
Ireland, R
Steele-Mortimer, O
AF Knodler, Leigh A.
Winfree, Seth
Drecktrah, Dan
Ireland, Robin
Steele-Mortimer, Olivia
TI Ubiquitination of the bacterial inositol phosphatase, SopB, regulates
its biological activity at the plasma membrane
SO CELLULAR MICROBIOLOGY
LA English
DT Article
ID IV SECRETION SYSTEMS; HOST-CELL MEMBRANES; SALMONELLA-ENTERICA;
EPITHELIAL-CELLS; CONTAINING VACUOLES; EFFECTOR PROTEINS;
MASS-SPECTROMETRY; ESCHERICHIA-COLI; MAMMALIAN-CELLS; GENE-EXPRESSION
AB P>The Salmonella type III effector, SopB, is an inositol polyphosphate phosphatase that modulates host cell phospholipids at the plasma membrane and the nascent Salmonella-containing vacuole (SCV). Translocated SopB persists for many hours after infection and is ubiquitinated but the significance of this covalent modification has not been investigated. Here we identify by mass spectrometry six lysine residues of SopB that are mono-ubiquitinated. Substitution of these six lysine residues with arginine, SopB-K6R, almost completely eliminated SopB ubiquitination. We found that ubiquitination does not affect SopB stability or membrane association, or SopB-dependent events in SCV biogenesis. However, two spatially and temporally distinct events are dependent on ubiquitination, downregulation of SopB activity at the plasma membrane and prolonged retention of SopB on the SCV. Activation of the mammalian pro-survival kinase Akt/PKB, a downstream target of SopB, was intensified and prolonged after infection with the SopB-K6R mutant. At later times, fewer SCV were decorated with SopB-K6R compared with SopB. Instead SopB-K6R was present as discrete vesicles spread diffusely throughout the cell. Altogether, our data show that ubiquitination of SopB is not related to its intracellular stability but rather regulates its enzymatic activity at the plasma membrane and intracellular localization.
C1 [Knodler, Leigh A.; Winfree, Seth; Drecktrah, Dan; Ireland, Robin; Steele-Mortimer, Olivia] NIAID, Intracellular Parasites Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
RP Knodler, LA (reprint author), NIAID, Intracellular Parasites Lab, Rocky Mt Labs, NIH, Hamilton, MT 59840 USA.
EM lknodler@niaid.nih.gov
FU Taplin Mass Spectrometry Facility, Harvard Medical School for LC/MS-MS;
Intramural Research Program (DIR) of NIH, NIAID
FX We are grateful to Jean Celli for his helpful comments, Ross Tomaino at
the Taplin Mass Spectrometry Facility, Harvard Medical School for
LC/MS-MS analysis, Mark Jepson and Julian Downward for providing
plasmids, Sandra Marcus for providing recombinant SopB, Anita Mora and
Gary Hettrick for graphics assistance and the Genomics Core Facility at
Rocky Mountain Laboratories for DNA sequence analysis. This research is
supported by the Intramural Research Program (DIR) of NIH, NIAID.
NR 69
TC 40
Z9 40
U1 0
U2 4
PU WILEY-BLACKWELL PUBLISHING, INC
PI MALDEN
PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA
SN 1462-5814
J9 CELL MICROBIOL
JI Cell Microbiol.
PD NOV
PY 2009
VL 11
IS 11
BP 1652
EP 1670
DI 10.1111/j.1462-5822.2009.01356.x
PG 19
WC Cell Biology; Microbiology
SC Cell Biology; Microbiology
GA 504UE
UT WOS:000270642400010
PM 19614667
ER
PT J
AU Cooper, G
Gilbert, K
Greidinger, E
James, J
Pfau, J
Reinlib, L
Richardson, B
Rose, N
AF Cooper, Glinda
Gilbert, Kathleen
Greidinger, Eric
James, Judith
Pfau, Jean
Reinlib, Leslie
Richardson, Bruce
Rose, Noel
TI Recent advances and opportunities in research on lupus: environmental
influences and mechanisms of disease
SO CIENCIA & SAUDE COLETIVA
LA English
DT Review
DE Apoptosis; Epstein-Barr virus; Silica; Systemic lupus erythematosus;
Trichloroethylene
ID EPSTEIN-BARR-VIRUS; ZEALAND MIXED MICE; T-CELL-ACTIVATION;
KINASE-C-DELTA; SYSTEMIC AUTOIMMUNE-DISEASE; TUMOR-NECROSIS-FACTOR;
RESISTANT B10.A MICE; APOPTOTIC CELLS; ALVEOLAR MACROPHAGES; MURINE
MODEL
AB We summarize research on mechanisms through which environmental agents may affect the pathogenesis of lupus, discuss three exposures that have been the focus of research in this area, and propose recommendations for new research initiatives. We examined studies pertaining to key mechanistic events and specific exposures. Apoptosis leading to increased production or decreased clearance of immunogenic intracellular self-antigens and defective apoptosis of autoreactive immune cells both have been implicated in the loss of self-tolerance. The adjuvant or bystander effect is also needed to produce a sustained autoimmune response. Activation of toll-like receptors is one mechanism through which these effects may occur. Abnormal DNA methylation may contribute to the pathogenesis of lupus. Each of the specific exposures has been shown, in humans or in mice, to act upon one or more of these pathogenic steps. Specific recommendations for the continued advancement of our understanding of environmental influences on lupus and other autoimmune diseases include the development and use of mouse models with varying degrees of penetrance and manifestations of disease, identification of molecular or physiologic targets of specific exposures, development and use of improved exposure assessment methodologies, and multisite collaborations designed to examine understudied environmental exposures in humans.
C1 [Cooper, Glinda] US EPA, Natl Ctr Environm Assessment, Washington, DC 20460 USA.
[Gilbert, Kathleen] Univ Arkansas Med Sci, Dept Microbiol & Immunol, Little Rock, AR 72205 USA.
[Greidinger, Eric] Univ Miami, Miller Sch Med, Div Rheumatol, Coral Gables, FL 33124 USA.
[James, Judith] Oklahoma Med Res Fdn, Arthrit & Immunol Program, Oklahoma City, OK USA.
[Pfau, Jean] Univ Montana, Dept Biomed & Pharmaceut Sci, Ctr Environm Hlth Sci, Missoula, MT 59812 USA.
[Reinlib, Leslie] NIEHS, Div Extramural Res & Training, NIH, Bethesda, MD USA.
[Richardson, Bruce] Univ Michigan, Ann Arbor, MI 48109 USA.
[Rose, Noel] Johns Hopkins Univ, Johns Hopkins Ctr Autoimmune Dis, Dept Pathol, Baltimore, MD 21218 USA.
RP Cooper, G (reprint author), US EPA, Natl Ctr Environm Assessment, 1200 Penn Ave NW, Washington, DC 20460 USA.
EM cooper.glinda@epa.gov
NR 107
TC 6
Z9 6
U1 0
U2 3
PU ABRASCO
PI RIO DE JANEIRO
PA RUA HESPERIA, 16-PARTE MANGUINHOS, RIO DE JANEIRO, 21050-040, BRAZIL
SN 1413-8123
J9 CIENC SAUDE COLETIVA
JI Cienc. Saude Coletiva
PD NOV-DEC
PY 2009
VL 14
IS 5
BP 1865
EP 1876
PG 12
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 511KH
UT WOS:000271162500028
PM 19851599
ER
PT J
AU Marques, A
Brown, MR
Fleisher, TA
AF Marques, Adriana
Brown, Margaret R.
Fleisher, Thomas A.
TI Natural Killer Cells in Chronic Lyme Disease Reply
SO CLINICAL AND VACCINE IMMUNOLOGY
LA English
DT Letter
ID EXPRESSION; PATTERNS; GENDER; TRIAL
C1 [Marques, Adriana] NIAID, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA.
[Brown, Margaret R.; Fleisher, Thomas A.] NIH, Serv Immunol, Dept Lab Med, Ctr Clin, Bethesda, MD 20892 USA.
RP Marques, A (reprint author), NIAID, Lab Clin Infect Dis, NIH, 9000 Rockville Pike, Bethesda, MD 20892 USA.
EM amarques@niaid.nih.gov
NR 12
TC 0
Z9 0
U1 0
U2 2
PU AMER SOC MICROBIOLOGY
PI WASHINGTON
PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA
SN 1556-6811
J9 CLIN VACCINE IMMUNOL
JI Clin. Vaccine Immunol.
PD NOV
PY 2009
VL 16
IS 11
BP 1704
EP 1706
PG 3
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 514DE
UT WOS:000271373700026
ER
PT J
AU Terabe, M
Ambrosino, E
Takaku, S
O'Konek, JJ
Venzon, D
Lonnin, S
McPherson, JM
Berzofsky, JA
AF Terabe, Masaki
Ambrosino, Elena
Takaku, Shun
O'Konek, Jessica J.
Venzon, David
Lonnin, Scott
McPherson, John M.
Berzofsky, Jay A.
TI Synergistic Enhancement of CD8(+) T Cell-Mediated Tumor Vaccine Efficacy
by an Anti-Transforming Growth Factor-beta Monoclonal Antibody
SO CLINICAL CANCER RESEARCH
LA English
DT Article
ID HIGH-AVIDITY CTL; TGF-BETA; IMMUNE-RESPONSE; DOWN-REGULATION; MYELOID
CELLS; NK CELLS; IN-VITRO; ABROGATION; DISEASE; MOUSE
AB Purpose: Transforming growth factor-beta (TGF-beta) is an immunosuppressive cytokine, having direct suppressive activity against conventional CD4(+) and CD8(+)T cells and natural killer cells, thereby inhibiting tumor immunosurveillance. Here, we investigated possible synergy between anti-TGF-beta (1D11) and a peptide vaccine on induction of antitumor immunity, and the mechanisms accounting for synergistic efficacy.
Experimental Design: The effect of combination treatment with a peptide vaccine and anti-TGF-beta was examined in a subcutaneous TC1 tumor model, as well as the mechanisms of protection induced by this treatment.
Results: Anti-TGF-beta significantly and synergistically improved vaccine efficacy as measured by reduction in primary tumor growth, although anti-TGF-beta alone had no impact. The number of tumor antigen-specific CTL with high functional avidity as measured by IFN-gamma production and lytic activity was significantly increased in vaccinated mice by TGF-beta neutralization. Although TGF-beta is known to play a critical role in CD4(+)Foxp3(+) Treg cells, Treg depletion/suppression by an anti-CD25 monoclonal antibody (PC61) before tumor challenge did not enhance vaccine efficacy, and adding anti-TGF-beta did not affect Treg numbers in lymph nodes or tumors or their function. Also, TGF-beta neutralization had no effect on interleukin-17-producing T cells, which are induced by TGF-beta and interleukin-6. Absence of type II NKT cells, which induce myeloid cells to produce TGF-beta, was not sufficient to eliminate all sources of suppressive TGF-beta. Finally, the synergistic protection induced by anti-TGF-beta vaccine augmentation was mediated by CD8(+) T cells since anti-CD8 treatment completely abrogated the effect.
Conclusions: These results suggest that TGF-beta blockade may be useful for enhancing cancer vaccine efficacy. (Clin Cancer Res 2009;15(21):6560-9)
C1 [Terabe, Masaki; Ambrosino, Elena; Takaku, Shun; O'Konek, Jessica J.; Berzofsky, Jay A.] NCI, Vaccine Branch, NIH, Bethesda, MD 20892 USA.
[Venzon, David] NCI, Biostat & Data Management Sect, NIH, Bethesda, MD 20892 USA.
[Lonnin, Scott; McPherson, John M.] Genzyme Corp, Framingham, MA 01701 USA.
RP Terabe, M (reprint author), NCI, Vaccine Branch, NIH, Bldg 10,Room 61312,9000 Rockville Pike, Bethesda, MD 20892 USA.
EM terabe@mail.nih.gov
FU NIH; National Cancer Institute; Center for Cancer Research
FX Intramural Research Program of the NIH, National Cancer Institute,
Center for Cancer Research. National Cancer Institute has a Cooperative
Research and Development Agreement with Genzyme Cooperation. The costs
of publication of this article were defrayed in part by the payment of
page charges. This article must therefore be hereby marked advertisement
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
NR 44
TC 69
Z9 70
U1 0
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 NOV 1
PY 2009
VL 15
IS 21
BP 6560
EP 6569
DI 10.1158/1078-0432.CCR-09-1066
PG 10
WC Oncology
SC Oncology
GA 513CP
UT WOS:000271300200013
PM 19861451
ER
EF